FitSugar

Yoga and Running: Opposites Attract

FitSugar — Thu, 20 Sep 2007 11:45:00 -0700

Yoga is great for stretching and toning your muscles, and increasing flexibility, but as far as a great cardio workout for your heart, it doesn't quite cut it.

That's why running is the perfect complement to yoga. It's practically the opposite of yoga on the exercise scale. Nothing gets the blood flowing and your heart pumping like a good run. On an average mile run, your foot will hit the ground 1,000 times. The force of impact can be 3 to 4 times your weight, so it's no wonder that many runners complain of lower back and knee pain, tight hips and hamstrings, and sore feet.

Running works your lower body brilliantly, but it leaves your upper body in the dust. This imbalance is what can cause so many problems for runners, so that's where yoga comes in. Yoga works your upper body (another reason I love vinyasas) and stretches out tight muscles. It also increases flexibility, which can prevent injury, so you'll be able to run for many years to come. Running and yoga can work as a team to keep your muscles strong and supple, and your bones in alignment.

Although both can be quite meditative and relaxing, neither one is a substitute for the other. Whether you focus more on running or yoga, try to strike a balance since the two compliment each other so well.

Fit's Tips: If you are a die-hard runner, try to remember to make time for stretching before or after your runs. You might even want to throw a weekly yoga class into your routine. On the other hand, if you are more into gentle exercise like yoga and stretching, you've got to remember to work your heart too. Add 20 minutes of heart pumping exercise (it doesn't have to be running), 2-3 times a week. Incorporating cardio and yoga will make your body and mind stronger and more balanced.

Celebrate Daylight Saving Time With a Morning Workout

FitSugar — Sat, 31 Oct 2009 03:30:05 -0700

It's that time of year again, where we "fall back," and turn our clocks back one hour. I love gaining an extra hour this one time of the year, so make the most of it. Don't just go through your day as usual, because you'll never even realize you received that extra 60 minutes.

Since most people complain that they don't have time to exercise, my advice is to get up in the morning when you normally do, and spend your freebie hour working out. It's a great habit to get into, especially if you love exercising outdoors. Mornings will be brighter, so it's safer to exercise before work, since it'll most likely be dark by the time you get home. Here are some ways to sweat it out for an hour:

Call a friend and go on a long, brisk walk. You'll burn 236 calories.
Pick up the pace and go on a relaxing run. An hour burns 473 calories.
Hit a mountain trail. An hour-long hike burns 355 calories.
Hop on your bike and tour a new spot in your neighborhood. After an hour, you'll have burned 473 calories.
Do a strength-training session and burn 177 calories after an hour.
Take a heart-pumping cardio class at your gym. You'll burn an astounding 414 calories.

Don't forget to change your clocks before you go to bed tonight. Daylight saving time officially ends at 2 a.m., Sunday, Nov. 1. Enjoy your hour!

Class Act: Skinny Jeans Fitness Workout

FitSugar — Tue, 20 Oct 2009 14:43:33 -0700

I won't lie, the name caught my attention: Skinny Jeans Workout, a place where denim and my hamstrings collide. I find the fashion / fitness connection slightly amusing, but the 45 minute class left me more than slightly sweaty. It truly is a sculpting workout that borrows from a diverse array of fitness methods. We did lunges of all sorts, from the basic forward variety to the criss-crossing curtsy lunge. We did squat variations. We even did multiple Warrior 3s. My legs and glutes were worked from all angles ensuring that every fiber was taxed. There were sections of the workout that felt rather balletic too; these moves really worked the deep glute muscles that help lift the seat. The class kept moving, and my heart rate stayed pumping for most of the class. The first 35 minutes of the class are standing and there is an emphasis on standing tall and keeping your chest open, since part of looking good in your skinny jeans is postural. I have heard that slouching can make a person look 10 pounds heavier. The ab work is very Pilates based, with cuing to keep the abs pulled to the spine - a phrase you can't make it through a Pilates session without hearing repeatedly.

I will definitely take this class again and recommend it. This class is currently offered at many Equinox locations, but look for a version at a gym near you.

P.L.O.W. - Heart Pumping Love Songs For Cardio

FitSugar — Sat, 14 Feb 2009 03:30:00 -0800

Most love songs are soft and sweet, but when it comes to cardio I need a beat to keep me going. In honor of Valentine's Day I made a lovely playlist of love songs that are a little more rocking and ready to keep you pumped up during cardio. Why not exercise your heart today, before celebrating this day dedicated to hearts? This mix is about 33 minutes long that ends with a sweet song by Nick Drake to help you cool down and stretch.

To hear the music mix, click on the black triangle when you read more.

Cardio Love Songs

Source

Heart failure

FitSugar — Wed, 08 Oct 2008 17:35:10 -0700

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Permanent Implantable Heart Approved

In 2006, the FDA approved the first permanent artificial heart. The AbiCor is intended for patients who are not eligible for heart transplants and who are only expected to survive about a month without medical treatment. Patients who received the AbiCor have survived, on average, about 5 months.

Statin Drug Approved for Heart Failure

In 2006, the FDA approved the cholesterol drug atorvastatin (Lipitor) to reduce the risks of hospitalization for heart failure in patients with heart disease.

Drug Research

The investigational drug tolvaptan improved symptoms in patients hospitalized with severe heart failure and fluid build-up in the lungs, according to several 2007 Journal of the American Medical Association (JAMA) studies. However, the drug did not reduce the risks of re-hospitalization and death.

Preserved Versus Reduced Ejection Fraction

Heart failure with preserved left-ventricular ejection fraction (LVEF) is becoming more common, suggests several 2006 studies published in JAMA and the New England Journal of Medicine. Unfortunately, this type of heart failure is less well studied than reduced LVEF. Experts are urging that more studies be conducted to determine better treatment options for preserved LVEF. Both types of heart failure have high mortality rates.

Systolic Blood Pressure Predictor of Mortality

Patients who are admitted to the hospital with heart failure and low systolic blood pressure have a poorer chance of survival than patients admitted with high blood pressure, indicates a 2006 JAMA study.

Diet and Lifestyle Factors

Daily consumption of whole-grain breakfast cereals may reduce the risk for heart failure, suggests research presented at a 2007 American Heart Association conference on heart disease prevention.
A drink or two a day is associated with lower risk of heart failure, indicates a 2006 Journal of the American College of Cardiology study. However, heavy alcohol consumption can increase the risk for heart failure.

Introduction

To understand what occurs in heart failure, it is useful to be familiar with the anatomy of the heart and how it works. The heart is composed of two independent pumping systems, one on the right side, and the other on the left. Each has two chambers, an atrium and a ventricle. The ventricles are the major pumps in the heart.

The external structures of the heart include the ventricles, atria, arteries, and veins. Arteries carry blood away from the heart while veins carry blood into the heart. The vessels colored blue indicate the transport of blood with relatively low content of oxygen and high content of carbon dioxide. The vessels colored red indicate the transport of blood with relatively high content of oxygen and low content of carbon dioxide.

The Right Side of the Heart. The right system receives blood from the veins of the whole body. This is "used" blood, which is poor in oxygen and rich in carbon dioxide.

The right atrium is the first chamber that receives blood.
The chamber expands as its muscles relax to fill with blood that has returned from the body.
The blood enters a second muscular chamber called the right ventricle.
The right ventricle is one of the heart's two major pumps. Its function is to pump the blood into the lungs.
The lungs restore oxygen to the blood and exchange it with carbon dioxide, which is exhaled.

The Left Side of the Heart. The left system receives blood from the lungs. This blood is now oxygen rich.

The oxygen-rich blood returns through veins coming from the lungs (pulmonary veins) to the heart.
It is received from the lungs in the left atrium, the first chamber on the left side.
Here, it moves to the left ventricle, a powerful muscular chamber that pumps the blood back out to the body.
The left ventricle is the strongest of the heart's pumps. Its thicker muscles need to perform contractions powerful enough to force the blood to all parts of the body.
This strong contraction produces systolic blood pressure (the first and higher number in blood pressure measurement). The lower number ( diastolic blood pressure) is measured when the left ventricle relaxes to refill with blood between beats.
Blood leaves the heart through the ascending aorta, the major artery that feeds blood to the entire body.

The Valves. Valves are muscular flaps that open and close so blood will flow in the right direction. There are four valves in the heart:

The tricuspid regulates blood flow between the right atrium and the right ventricle.
The pulmonary valve opens to allow blood to flow from the right ventricle to the lungs.
The mitral valve regulates blood flow between the left atrium and the left ventricle.
The aortic valve allows blood to flow from the left ventricle to the ascending aorta.

Click the icon to see an image of the internal structures of the heart.

The Heart's Electrical System. The heartbeats are triggered and regulated by the conducting system, a network of specialized muscle cells that form an independent electrical system in the heart muscles. These cells are connected by channels that pass chemically caused electrical impulses.

Click the icon to see an image of the conduction system of the heart.

Heart failure is not a disease. It is a condition or process in which the heart is unable to pump enough blood to meet the needs of the body's tissues. The heart doesn't "fail" in the sense of ceasing to beat (as occurs during a heart attack). Rather, it weakens, usually over the course of months or years, so that it is unable to pump out all the blood that enters its chambers. As a result, fluids tend to build up in the lungs and tissues, causing congestion. This condition used to be called "congestive heart failure," but the name was officially changed to heart failure in 2005.

Ways the Heart Can Fail. Heart failure can occur in several ways:

The muscles of the heart pumps (ventricles) become thin and weakened. They stretch (dilate) to the extent that they cannot pump the blood with enough force to reach all the body's tissues.
The heart muscles stiffen or thicken. Here, they lose elasticity and cannot relax. Insufficient blood enters the chamber, so not enough blood is pumped out into the body to serve its needs.
Sometimes the valves of the heart are abnormal. (Valves open or close to control the flow of blood entering or leaving the heart). They may narrow, such as in aortic stenosis, causing a back up of blood, or they may close improperly so that blood leaks back into the heart. The mitral valve (which regulates blood flow between the two chambers on the left side of the heart) often becomes leaky in severe heart failure -- a condition called mitral regurgitation.

Click the icon to see an image of the valves of the heart.

The very mechanisms that the body uses to compensate for inefficient heart pumping can, over time, change the architecture of the heart (called remodeling) and finally lead to irreversible problems.

The specific effects of heart failure on the body depend on whether it occurs on the left or right side. Over time, however, in either form of heart failure, the organs in the body do not receive enough oxygen and nutrients, and the body's wastes are removed slowly. Eventually, vital systems break down.

Failure on the Left Side (Left-Ventricular Heart Failure). Failure on the left side of the heart is more common than failure on the right side. The failure can be a result of abnormal systolic (contraction) or diastolic (relaxation) action:

Systolic. Systolic heart failure is a pumping problem. In systolic failure, the heart muscles weaken and cannot pump enough blood throughout the body. The left ventricle is usually stretched (dilated). Fluid backs up and accumulates in the lungs (pulmonary edema). Systolic heart failure typically occurs in men between the ages of 50 - 70 years who have had a heart attack.
Diastolic. Diastolic heart failure is a filling problem. When the left ventricle muscle becomes stiff and cannot relax properly between heartbeats, the heart cannot fill fully with blood. When this happens, fluid entering the heart backs up. This causes the veins in the body and tissues surrounding the heart to swell and become congested. Patients with diastolic failure are typically women, overweight, and elderly, and have high blood pressure and diabetes.

Failure on the Right Side (Right-Ventricular Heart Failure). Failure on the right side of the heart is most often a result of failure on the left. Because the right ventricle receives blood from the veins, failure here causes the blood to back up. As a result, the veins in the body and tissues surrounding the heart to swell. This causes swelling in the feet, ankles, legs, and abdomen.

Ejection Fraction. To help determine the severity of left-sided heart failure, doctors use an ejection fraction (EF) calculation, also called a left-ventricular ejection fraction (LVEF). This is the percentage of the blood pumped out from the left ventricle during each heartbeat. An ejection fraction of 50 - 75% is considered normal. Patients with left-ventricular heart failure are classified as either having a preserved ejection fraction (greater than 50%) or a reduced ejection fraction (less than 50%).

In general, systolic heart failure has been thought to be associated with a reduced ejection fraction, whereas diastolic heart failure was associated with a preserved (normal) ejection fraction. However, several 2006 studies indicated that diastolic heart failure can occur regardless of the ejection fraction, although it is more common in patients with a preserved ejection fraction. Mortality rates among patients with reduced LVEF and preserved LVEF are similar.

Although reduced LVEF heart failure is better studied, and its treatment goals more clearly defined, several important 2006 studies suggest that preserved LVEF heart failure is becoming increasingly common. The studies, published in the Journal of the American Medical Association and the New England Journal of Medicine, indicated that patients with preserved LVEF heart failure are more likely to be female and older, and have a history of high blood pressure and atrial fibrillation (a disturbance in heart rhythm). Experts are now urging that more studies focus on patients with preserved LVEF so that better treatment options can be established.

Causes

Heart failure has many causes and can evolve in different ways.

It can be a direct, last-stage result of heart damage from one or more of several heart or circulation diseases.
It can occur over time as the heart tries to compensate for abnormalities caused by these conditions, a condition called remodeling.

In all cases, the weaker pumping action of the heart means that less blood is sent to the kidneys. The kidneys respond by retaining water and salt. This in turn increases edema (fluid buildup) in the body, which causes widespread damage.

Uncontrolled high blood pressure (hypertension) is also a major cause of heart failure even in the absence of a heart attack. In fact, about 75% of cases of heart failure start with hypertension. It generally develops as follows:

The heart muscles thicken to make up for increased blood pressure.
The force of the heart muscle contractions weaken over time, and the muscles have difficulty relaxing. This prevents the normal filling of the heart with blood.

[See In-Depth Report #14:High blood pressure.]

Hypertension is a disorder characterized by consistently high blood pressure. Generally, high blood pressure consists of systolic blood pressure (the "top" number, which represents the pressure generated when the heart beats) higher than 140, or diastolic blood pressure (the "bottom" number, which represents the pressure in the vessels when the heart is at rest) over 90.

Coronary artery disease is the end result of a complex process called atherosclerosis (commonly called "hardening of the arteries"). It is the most common cause of heart attack and involves the build-up of unhealthy cholesterol in the arteries, with inflammation and injury in the cells of the blood vessels. The arteries narrow and become brittle. Heart failure in such cases most often results from a pumping defect in the left side of the heart. [See In-Depth Report #3: Coronary artery disease and angina ; and In-Depth Report #23: Cholesterol.]

Click the icon to see an image of atherosclerosis.

People now often survive heart attacks, but eventually many develop heart failure from the physical damage done to the heart muscles by the attack. Ironically, heart attack recovery is probably one of the major factors in the dramatic increase in heart failure cases over the past decade. On an encouraging note, however, new therapies that are reducing the severity of heart attacks may help stabilize heart failure rates. [See In-Depth Report #12: Heart attack.]

The valves of the heart control the flow of blood leaving and entering the heart. Abnormalities can cause blood to back up or leak back into the heart.

Click the icon to see an image of the heart valves.

In the past, rheumatic fever, which scars the heart valves and prevents them from closing, was a major cause of death from heart failure. Fortunately, antibiotics have relegated this disease to a minor cause of heart failure. Birth defects may also cause abnormal valvular development. Although more children born with heart defects are now living to adulthood, they still face a higher than average risk for heart failure as they age.

Cardiomyopathy is disease that damages the heart muscles and leads to heart failure. There are several different types. Injury to the heart muscles may cause the heart muscles to thin out (dilate) or become too thick (become hypertrophic). In either case, the heart doesn't pump correctly.

Dilated Cardiomyopathy. Dilated cardiomyopathy involves an enlarged heart ventricle. The muscles thin out, reducing the pumping action, usually on the left side. Although this condition is associated with genetic factors, the direct cause often is not known. (This is called idiopathic dilated cardiomyopathy.) Research strongly indicates that viruses, such as Coxsackie virus, or other infections may be at the base of this condition. Experts think that an autoimmune response occurs in which infection-fighting antibodies attack a person's own proteins in the heart, mistaking them for foreign substances.

Click the icon to see an image of dilated cardiomyopathy.

Hypertrophic Cardiomyopathy. In hypertrophic cardiomyopathy, the heart muscles become thick and contract with difficulty. Some research indicates that this occurs because of a genetic defect that causes a loss of power in heart muscle cells and, subsequently, lower pumping strength. To compensate for this power loss, the heart muscle cells grow. This condition, rare in the general population, is often the cause of sudden death in young athletes.

Click the icon to see an image of hypertrophic cardiomyopathy.

High blood pressure, heart attacks, or other initial processes that impair the pumping actions of the heart trigger a number of hormonal and neurochemical mechanisms to correct imbalances in pressure and blood flow. Unfortunately, while these corrective responses help in the short term, they increase the work of the heart. The mechanisms are now viewed as major contributors to the end stages of heart failure. Some are described briefly in the following sections.

Remodeling. The heart responds to high blood pressure and overload by enlarging in order to increase blood input. This leads to structural damage called remodeling:

In order to accommodate the increased blood input, the heart muscle cells elongate. The muscular walls of the heart that they form become thinner and inefficient.
The muscle cells undergo other changes that result in calcium loss. Calcium is a mineral that is crucial for healthy heart contractions.
The thinner heart muscles and the impaired heart contractions further weaken the heart's pump.
Mitral valve regurgitation is a possible outcome of remodeling. The mitral valve regulates blood flow between the two chambers on the left side of the heart. In response to remodeling, the structural changes in the heart may distort the mitral valve so that the blood leaks backward into the left atrium of the heart instead of flowing out into the body's circulation.
These changes are generally irreversible, although heart pacemakers and certain drugs, including beta-blockers and ACE inhibitors, may reverse some of the remodeling in some patients.

Activation of the Sympathetic Nervous System. The sympathetic nervous system consists of the nerve cells that automatically govern and regulate the beating heart.

This nervous system responds to the failing heart pump by signaling the release of stress hormones, in particular a powerful one called norepinephrine.
These hormones flood the heart, causing it to beat even faster.
These rapid heart beats, although intended to accommodate the weakened pumping actions, only accelerate the damage.

The Renin-Angiotensin-Aldosterone System (RAAS). The renin-angiotensin-aldosterone system (RAAS) is a group of hormones that are responsible for the opening and narrowing of blood vessels and retention of fluids. They also affect cell development in the heart.

The RAAS hormones are called into action by the failing heart.
They respond to the lower blood volume of the weakened heart by constricting the blood vessels and retaining fluids and sodium.
The heart then works harder to pump blood through these narrowed vessels. Blood pressure, then, is forced to increase, which creates a vicious cycle.

Immune System Response. The immune system may also compound the damage. In response to injury in the heart muscle cells or in other parts of the body that occurs as the heart fails, the immune system releases factors intended to protect these areas.

In excess, however, they can cause inflammation and damage.

The most important of these factors are called cytokines. Active cytokines include tumor necrosis factor (TNF) and possibly interleukins 1 and 6.
High levels of these cytokines have been observed in patients with the most severe classes of heart failure.
They may play an important role in the process leading to remodeling. High levels of these cytokines may actually trigger muscle cell growth and enlargement of the heart.

Other Players. Other molecules or compounds have been identified that might play a positive or negative role in the process of the failing heart.

Natriuretic peptides are a family of compounds released to counterbalance the effects of RAAS. Atrial natriuretic peptide (ANP) is a specific member of this family that opens blood vessels and counteracts the sodium-retaining properties of aldosterone (one of the RAAS hormones). It is of particular interest to researchers looking for new treatments.
Endothelin is a powerful protein involved in blood vessel constriction, cell proliferation and build-up, and other negative effects on the heart.
Nitric oxide is important for blood vessel dilation and elasticity.

Symptoms

Many symptoms of heart failure result from the congestion that develops as fluid backs up into the lungs and leaks into the tissues. Other symptoms result from inadequate delivery of oxygen-rich blood to the body's tissues. Since heart failure can progress rapidly, it is essential to consult a doctor immediately if any of the following symptoms are detected.

Fatigue and shortness of breath (dyspnea) are the first symptoms. They are caused by fluid in the lungs. Patients typically report that they feel out of breath after mild exertion. It is unlike the breathlessness of angina, which feels like a heavy weight pressing on the chest.

Fluid retention. Patients may complain of leg or abdominal swelling.
Wheezing or cough. Patients may have asthma-like wheezing or a dry hacking cough that occurs a few hours after lying down, but then stops after the patient sits up.
Central sleep apnea. This disorder results when the brain fails to signal the muscles to breathe during sleep. It occurs in up to half of people with heart failure. Sleep apnea causes disordered breathing at night. If heart failure progresses, the apnea may be so acute that a person, unable to breathe, may awaken from sleep in panic.
Loss of muscle mass. Over time, patients may lose muscle weight due to low cardiac output.

Ultimately, fluid in the lungs may build up. This is called pulmonary edema. When this happens, symptoms become more severe.

In addition to shortness of breath, patients sometimes have a cough that produces a pinkish froth.
Patients may experience a bubbling sensation in the lungs and feel as if they are drowning.
Typically, the skin is clammy and pale, sometimes nearly blue. This is a life-threatening situation, and the patient must go immediately to an emergency room.

Fatigue. As with left-side heart failure, an early symptom of right-side (right-ventricular) failure is extreme tiredness.
Fluid accumulation. This first occurs in the feet, then the ankles and legs, and finally in the abdomen. The liver may also be enlarged.
Weight gain. Although appetites are often depressed, patients with heart failure gain weight because they retain salt and water.
Loss of muscle mass.

Risk Factors

Nearly 5 million Americans currently suffer from heart failure. About 550,000 new cases of heart failure are now diagnosed each year. In 1970 there were only 250,000 new cases, so the annual numbers have risen dramatically. Such numbers represent an increasingly older population. Although there has been a dramatic increase over the last several decades in the number of people who suffer from heart failure, survival rates have been improving greatly.

Coronary artery disease and high blood pressure are the main causes of heart failure. Other diseases that damage or weaken the heart muscle or heart valves can also cause heart failure. Heart failure is most common in people over age 65, African-Americans, and women.

Heart failure is the most common reason for hospitalization in the elderly, and as the population ages, the incidence of heart failure is rising dramatically. According to one report, it occurs at a rate of about 10 in 1,000 people after age 65. The positive implication is, however, that people are living longer with heart failure.

Men are at higher risk for heart failure than women, although the difference narrows with age. Women also have a better survival rate than men do when heart failure is caused by valvular heart disease, high blood pressure, or alcohol abuse. (Some studies indicate that this is because men may be more susceptible to the process of heart muscle-cell remodeling, a damaging effect of hypertension.)

The survival rates of women and men are more similar, however, when heart failure evolves from coronary artery disease or heart attack. Women are much more likely to develop heart failure after a heart attack than men. In such cases, some evidence suggests that the reasons for this may include less aggressive approach to treatment for the initial heart conditions.

African-Americans are at higher risk for heart failure than Caucasians, and studies have reported that they tend to do much worse. In a 2003 study, however, in which Caucasians and African-Americans had comparable treatment, African-Americans actually had lower 1-year mortality rates (with slightly higher rates of rehospitalizations). Some evidence suggests that African-Americans are more often likely than Caucasians to develop diastolic heart failure (a failure of the heart muscle to relax normally), which is often a precursor to systolic heart failure (impaired ability to pump blood). Caucasians tend to develop systolic heart failure first.

According to a 2006 New England Journal of Medicine study, people whose parents had heart failure have a greatly increased risk of developing heart failure, particularly left-ventricular systolic heart failure. Earlier studies have suggested that a family history of early heart failure caused by cardiomyopathies (diseases that damage the heart muscle) may also predispose people to the disease. Researchers are looking for changes in specific genes that might regulate systems involved in heart failure and so increase susceptibility in certain populations.

Chronic alcohol abuse can damage the heart muscles, can cause hypertension, and may prove to be one cause of idiopathic dilated cardiomyopathy. Moderate alcohol consumption, on the other hand (generally defined as 2 drinks a day for men and 1 drink for women), may protect against heart failure. Non-drinkers, though, are not advised to begin drinking.

Coronary artery disease. More than 60% of heart failure cases may be due to coronary artery disease and its risk factors (smoking, sedentary living, obesity).
Heart attack. The injured heart after an attack is at high risk for failure. The improved survival rates from heart attack over the past decades have actually been responsible for the dramatic increase in heart failure rates.
High blood pressure. Hypertension is a significant risk factor and is present in 75% of patients with heart failure.
Diabetes. People with diabetes are at high risk for heart failure, particularly if they also have coronary artery disease. Even blood sugar abnormalities that precede diabetes increase the risk.
Obesity. Obesity is associated with both hypertension and type 2 diabetes, conditions that place people at risk for heart failure. Evidence strongly suggests that obesity itself is a major risk factor for heart failure, particularly in women. In a major 2002 study, about 14% of heart failure cases in women and 11% in men could be attributed to obesity. Both overweight and obese women had a significantly higher than normal risk for heart failure. Only obesity led to a significant risk in men.
Valvular heart disease. Specific valvular conditions that are common in patients with heart failure include aortic stenosis and mitral regurgitation.
Severe emphysema. Chronic obstructive pulmonary disease is a major risk factor for right-side heart failure.

Emphysema is a lung disease involving damage to the air sacs (alveoli).There is progressive destruction of alveoli and the surrounding tissue that supports them. As the disease gets worse, large air cysts take the place of normal lung tissue. Air is trapped in the lungs.

Cardiomyopathies due to various causes, including birth defects, HIV infection, and other infections.
In rare cases, heart failure can occur in women around the time of childbirth, a condition called peripartum cardiomyopathy.

Click the icon to see an image of peripartum cardiomyopathy.

An overactive thyroid (hyperthyroidism) or underactive thyroid (hypothyroidism) can have severe effects on the heart and increase the risk for heart failure.
Amyloidosis. A starchy protein (amyloid) that builds up in tissues and organs can lead to heart failure.
Surviving childhood cancers. Survivors face a risk for developing heart failure in later years, particularly those treated with chemotherapies such as doxorubicin. Newer cancer advances may reduce this risk.
Acute myocarditis. This rare viral infection involves the heart muscle and can produce temporary but potentially life-threatening heart failure.

Long-term use of anabolic steroids (male hormones used to build muscle mass) increases the risk for heart failure. The drug itraconazole (Sporanox), used to treat skin, nail, or other fungal infections, has been linked to heart failure. In 2006, the FDA warned that the cancer drug imatinib (Gleevec) has been associated with heart failure cases. Most patients who took imatinib and developed heart failure had a history of diabetes, high blood pressure, or heart disease.

Complications

At least 20% of hospitalizations in older adults are due to heart failure. For people over age 65, it is the number one cause of death, with nearly 290,000 people dying from this disease each year. Nevertheless, although heart failure produces very high mortality rates, treatment advances in hypertension, heart surgeries, and heart pacemakers are improving survival rates.

The most serious and life-threatening complications of heart failure are:

Arrhythmias (irregular beatings of the heart)
Acute pulmonary edema (fluid in the lungs)

Left-side heart failure tends to be more severe than right-side heart failure, particularly when it is associated with the following conditions:

Coronary artery disease
HIV infection
Amyloidosis (a metabolic disorder than can lead to organ failure)
Chemotherapy that uses the drug doxorubicin

The outlook is better in patients with left-side heart failure associated with:

Idiopathic cardiomyopathy (the cause is unknown)
Heart failure due to childbirth

Weight Issues. If patients with heart failure are overweight to begin with, their condition tends to be more severe. Once heart failure develops, however, an important indicator of a worsening condition is the occurrence of cardiac cachexia, which is unintentional rapid weight loss (a loss of at least 7.5% of normal weight within 6 months).

Impaired Kidney Function. Heart failure weakens the heart’s ability to pump blood. This can affect other parts of the body including the kidneys (which in turn can lead to fluid build-up). Decreased kidney function is common in patients with heart failure, both as a complication of heart failure and as a complication of other diseases associated with heart failure (such as diabetes). Studies suggest that in patients with heart failure, impaired kidney function increases the risks for heart complications including hospitalization and death.

Congestion (Fluid Buildup). In left-sided heart failure, fluid builds up first in the lungs. Later, as right-sided heart failure develops, fluid builds up in the legs, feet, and abdomen. According to one study, patients with severe symptoms who had congestion (fluid buildup) had poorer survival rates than those without fluid build up. Two-year survival rates were 87% in those who were congestion-free compared to 41 - 67% in patients with various signs of congestion (such as swelling, difficulty breathing when lying down, and weight gain from fluid buildup). Fluid buildup is treated with lifestyle measures, such as reducing salt in the diet, as well as drugs, such as diuretics. Sometimes, for hospitalized patients, an ultrafiltration device is used to remove excess water and salt from the body (see Surgery and Devices).

Atrial Fibrillation. This abnormal rhythm is a rapid quivering beat in the upper chambers of the heart. It is a major cause of stroke and very dangerous in people with heart failure.

Left Bundle Branch Block. Left bundle-branch block is an abnormality in electrical conduction in the heart. It develops in about 30% of patients with heart failure and is a major risk factor for serious adverse heart events.

Systolic Blood Pressure. An important 2006 study indicated that patients who arrive at the hospital with heart failure and low systolic blood pressure have a poorer prognosis than those who arrive with high systolic blood pressure. Researchers think that high systolic blood pressure may be a signal for unique clinical characteristics.

Sleep Apnea. With this disorder, a person stops breathing during the night, perhaps hundreds of times, usually for periods of 10 seconds or longer. It is a very strong risk factor for heart failure, and patients with apnea have a higher mortality rate than those who do not.

Depression. The presence of depression indicates a poorer outlook for the heart. Studies indicate that depression may have adverse biologic effects on the immune and nervous systems, blood clotting, blood pressure, blood vessels, and heart rhythms.

Seasonal and Daily Patterns. Studies have shown that more emergency room visits and higher mortality rates occur during winter months and on Mondays in patients with heart failure. One factor in this higher risk may be sudden and strenuous exertion, particularly snow-shoveling, which is associated with a risk for heart attack in people with heart problems.

Diagnosis

Doctors can often make a preliminary diagnosis of heart failure by medical history and careful physical examination.

The medical history risks for heart failure include:

High blood pressure
Diabetes
Poor cholesterol levels
Heart or peripheral vascular disease
Sleep apnea
Thyroid problems
Obesity
Lifestyle factors (smoking, alcohol use)

The following physical signs, along with medical history, strongly suggest heart failure:

Enlarged heart
Irregular heart sounds
Abnormal sounds in the lungs
Swelling or tenderness of the liver
Fluid retention in legs and abdomen
Elevation of pressure in the veins of the neck

Both blood and urine tests are used to check for problems with the liver and kidneys and to detect signs of diabetes. Lab tests can measure:

Cholesterol and lipid levels
Blood sugar (glucose)
Red blood cell count (to rule out anemia)
Blood sugar levels
Thyroid function

Urine tests can be used to assess the presence of a protein called albumin. Albumin in the urine is usually a sign of kidney disease, but even tiny amounts (microalbumin) signal an increased risk for heart failure in people with and without diabetes.

The exercise stress test measures heart rate, blood pressure, and oxygen consumption while a patient is performing physically, usually walking on a treadmill. It is an important diagnostic component in determining heart failure symptoms. Doctors also use exercise tests to gauge long-term outlook and the effects of particular treatments.

An electrocardiogram (ECG) cannot diagnose heart failure, but it can indicate underlying heart problems. It is sometimes called an EKG. The test is simple and painless to perform. It may be used to diagnose:

Enlargement of the heart muscle, which may help to determine long-term outlook
The presence of coronary artery disease
Abnormal cardiac rhythms. A rhythm pattern called a prolonged QT interval, for example, might predict people with heart failure who are at risk for severe complications and would need more aggressive therapies.

The major benefit of an ECG is that it can help determine which patients do not need an echocardiogram, a more accurate (but more expensive) diagnostic test.

The electrocardiogram (ECG, EKG) is used extensively to diagnose heart disease, from congenital heart disease in infants to myocardial infarction and myocarditis in adults. There are several different types of electrocardiograms.

The best diagnostic test for heart failure is echocardiography. Echocardiography is a noninvasive, entirely safe test that uses ultrasound to image the heart as it is beating. Cardiac ultrasounds provide the following information:

Accurate indications of valve function
The amount of blood flow through the heart's chambers
The location of the failure and where it has occurred

Doctors use information from the echocardiogram for calculating the ejection fraction (how much blood is pumped out during each heartbeat), which is important for determining the severity of heart failure.

Radionuclide Ventriculography. Radionuclide ventriculography is an imaging technique that uses a tiny amount of radioactive material (called a trace element). The substance is injected into a patient. As it passes through the bloodstream it is picked up on x-rays. This is a very important imaging technique for patients with heart failure. It is very sensitive in revealing heart enlargement or evidence of fluid accumulation around the heart and lungs. It is typically used in concert with angiography.

Magnetic Resonance Imaging. Magnetic resonance imaging (MRI) scans that use contrast dyes to improve resolution are proving helpful for identifying patients with irreversible heart damage. Damage appears as very bright areas on the scan.

Doctors may recommend angiography if they suspect that blockage of the arteries is contributing to heart failure. This procedure is invasive.

A thin tube called a catheter is inserted into one of the large arteries in the arm or leg.
It is gently guided through the artery until it reaches the heart.
The catheter measures internal blood pressure at various locations, giving the doctor a comprehensive picture of the extent and nature of the heart failure.
Dye is then injected through the tube into the heart.
X-rays called angiograms are taken as the dye moves through the heart and arteries.
These images help locate problems in the heart's pumping action or blockage in the arteries.

Major complications of angiography are rare (about 0.1%) but can occur. They include stroke, heart attacks, and kidney damage. The more experienced the medical center in this procedure, the lower the risk.

Click the icon to see an image of cardiac catheterization.

Researchers are looking for biologic factors (called biomarkers) that will confirm a diagnosis or suggest a better or worse prognosis. Many are under investigation.

Tumor Necrosis Factor. Elevated levels of tumor necrosis factor (TNF) may be a very strong and accurate predictor of a poor outlook. This immune substance is known to be a potent substance in the inflammatory process.

Natriuretic Peptides. Natriuretic peptides are substances that help regulate salt and water balance in the body. Levels of these peptides increase as heart failure symptoms worsen. Blood tests for brain natriuretic peptide (BNP) are now used to help diagnose heart failure. There are two types of BNP tests: The enzyme-linked immunosorbent assay (ELISA) and the radioimmunosorbent assay (RIA). Research from 2006 suggested that the ELISA test may be more accurate, but it is also more expensive.

BNP testing can be very helpful in correctly diagnosing heart failure in patients who come to the emergency room complaining of shortness of breath (dyspnea). A 2006 study indicated that this test can also help predict which patients with dyspnea are at greatest risk of dying within a year from heart failure.

Brain Metabolites. High levels of a compound called N-acetylaspartate, generated as a byproduct of chemical processes in the brain, may indicate a poor outlook.

Treatment

Guidelines for evaluating the severity of heart failure and determining treatments use a staging system that is similar to the one used for major cancers:

Stage A: Patients are at high risk for heart failure, but there is no evidence of structural damage to the heart. Risk factors include high blood pressure, heart diseases, diabetes, obesity, metabolic syndrome, and previous use of medications that damage the heart (such as some chemotherapy).
Stage B: Patients have a structural heart abnormality but no symptoms of heart failure. Abnormalities include left ventricular hypertrophy and low ejection fraction, asymptomatic valvular heart disease, and a previous heart attack.
Stage C: Patients have a structural abnormality and current or previous symptoms of heart failure, including shortness of breath, fatigue, and difficulty exercising.
Stage D: Patients have end-stage symptoms that do not respond to standard treatments.

According to expert guidelines, the first step in managing heart failure is to treat the primary conditions causing or complicating heart failure. These include:

Coronary artery disease. Treatment includes a healthy diet, exercise, smoking cessation, medications, and, possibly, bypass or angioplasty. [See In-Depth Report #3: Coronary artery disease and angina.]
Cholesterol and lipid problems. Treatments include lifestyle management and medications, especially statins. [See In-Depth Report #23: Cholesterol.]
High blood pressure. A normal systolic blood pressure is considered below 120 mm Hg, and a normal diastolic blood pressure is below 80 mm Hg. Patients with diabetes or chronic kidney disease should maintain blood pressure readings of 130/80 or less, while other patients with high blood pressure should aim for readings no higher than 140/90. Effective reduction of blood pressure reduces the risk of heart failure by 30 - 50%. [See In-Depth Report #14: High blood pressure.]
Diabetes. Treating diabetes is extremely important for reducing the risk for heart disease. ACE inhibitors are especially beneficial, particularly for people with diabetes. Recent research suggests that metformin, a drug used to treat diabetes, may also help prevent heart failure. [See In-Depth Report #60: Diabetes - type 2; and In-Depth Report #9: Diabetes - type 1.]
Valvular abnormalities such as aortic stenosis and mitral regurgitation. Surgery may be required.
Abnormal health rhythms (arrhythmias). Ventricular assisted devices, notably biventricular pacers (BVPs), are proving to be important in preventing hospitalizations for patients with these conditions.
Anemia. Giving erythropoietin (EPO) and iron injections to patients with heart failure and underlying anemia not only reverses the anemia, but may markedly improve heart symptoms as well. [See In-Depth Report #57: Anemia.]
Thyroid function. Various medications are used to treat overactive thyroid (hyperthyroidism) or underactive thyroid (hypothyroidism). [See In-Depth Report #38: Hypothyroidism.]
Sleep apnea. Continuous positive airway pressure (CPAP) is an effective treatment for sleep apnea. CPAP may help reduce systolic blood pressure and improve left ventricular systolic function. [See In-Depth Report#65:Sleep apnea.]

Click the icon to see an image of CPAP treatment.

Treatments for patients with Stage B risk for heart failure include all of the treatments recommended in Stage A. In addition, the following types of drugs and devices may be recommended for some patients. These include:

Angiotensin-converting enzyme (ACE) inhibitors for patients with a recent or past history of heart attack. Also for patients who have not had a heart attack if they have a low left ventricular ejection fraction (LVEF) and no heart failure symptoms. A reduced LVEF indicates that the heart’s left ventricle is not pumping blood efficiently.
Beta blockers for patients with a recent or past history of heart attack. Also for patients who have not had a heart attack but who do have reduced LVEF without heart failure symptoms.
Angiotensin-receptor blockers (ARBs) for patients who have had a heart attack or have low LVEF, but who cannot take ACE inhibitors.
Implantable defibrillators for patients who have weakened heart pumps (ischemic cardiomyopathy), who had a heart attack more than 40 days prior, and who have low LVEF.

Treat conditions as recommended in Stage A plus:

Restrict dietary salt. Lowering salt in the diet can help diuretics work better.
ACE inhibitors, beta blockers, and diuretics are recommended for most patients.
ARBs are recommended for patients who cannot tolerate ACE inhibitors.
Aldosterone inhibitors or digitalis may be used for some patients.
A hydralazine and nitrate combination (BiDil) may be used for African-American patients who are taking an ACE inhibitor and beta blocker and who still have heart failure symptoms.
Avoid drugs that can worsen heart failure symptoms. These include nonsteroidal anti-inflammatory drugs (NSAIDs), most calcium channel blockers, and most drugs used to treat irregular heart rhythms (arrhythmia).
Exercise training for appropriate patients.
Biventricular pacemakers and implantable defibrillators for some patients.

Treatment includes appropriate measures used for Stages A, B, and C plus:

Heart transplantation referral for appropriate patients.
Left-ventricular assist devices (LVADs) as permanent therapy for patients who are not candidates for heart transplants. LVADs are surgically implanted to help pump blood through the body.
Hospice and end-of-life care information for patients and families.

Medications

Many different medications are used in the treatment of heart failure. They include:

Angiotensin-converting enzyme (ACE) inhibitors
Angiotensin-receptor blockers (ARBs)
Beta blockers
Diuretics
Aldosterone blockers
Digitalis
Hydralazine and nitrates
Statins
Nesiritide (Natrecor)
Aspirin

Angiotensin-converting enzyme (ACE) inhibitors are among the most important drugs for treating patients with heart failure. ACE inhibitors open blood vessels and decrease the workload of the heart. They are used to treat high blood pressure but can also help improve heart and lung muscle function. Major studies suggest that ACE inhibitors may reduce the risk of death, heart attack, and hospital admissions by 28% in patients with existing heart failure.

ACE inhibitors are particularly important for patients with diabetes. A large study reported that patients with diabetes who took these drugs had fewer heart attacks and lower overall mortality rates than patients who took other types of high blood pressure medications. ACE inhibitors may also help slow progression of kidney disease, in addition to controlling blood pressure.

Doctors sometimes avoid giving aspirin to patients who are taking ACE inhibitors due to concerns that this drug combination can cause kidney problems. A 2005 study of patients with both coronary artery disease and heart failure indicated that an aspirin and ACE inhibitor combination is not harmful, and that aspirin can significantly reduce mortality risk for these patients.

Choosing an ACE inhibitor. ACE inhibitors treat Stage A high-risk conditions such as high blood pressure, heart disease, and diabetic nerve disorders (neuropathy). They also treat Stage B patients who have had a heart attack or who have left ventricular systolic disorder, and Stage C patients with heart failure. Specific brands and stages include:

Benazepril (Lotrel) -- (Stage A)
Captopril (Capoten) -- (Stages A, B, C)
Enalapril (Vasotec) -- (Stages A, B, C)
Fosinopril (Monopril) -- (Stages A, C)
Lisinopril (Prinivil, Zestril) -- (Stages A, B, C)
Moexipril (Univasc) -- (Stage A)
Perindopril (Aceon) -- (Stage A)
Quinapril (Accupril) -- (Stages A, C)
Ramipril (Altace) -- (Stages A, B, C)
Trandolapril (Mavik) -- (Stages A, B, C)

Side Effects of ACE Inhibitors:

Low blood pressure is the main side effect of ACE inhibitors. This can be severe in some patients, especially at the start of therapy.
Irritating cough is a common side effect, which some people find intolerable. Although all ACE inhibitors can have this side effect, sometimes switching to another brand will reduce this symptom.
Although ACE inhibitors can protect against kidney disease, they also increase potassium retention in the kidneys. This increases the risk for cardiac arrest if potassium levels become too high. Because of this action, they are not generally given with potassium-sparing diuretics or potassium supplements.
A rare but severe side effect is granulocytopenia, which is an extreme reduction in infection-fighting white blood cells.
In very rare cases, patients suffer a sudden and severe allergic reaction called angioedema that causes swelling in the eyes and mouth and may close off the throat.

Patients who have difficulty tolerating ACE inhibitor side effects are usually switched to an angiotensin-receptor blocker (ARB).

ARBs, also known as angiotensin II receptor antagonists, are similar to ACE inhibitors in their ability to open blood vessels and lower blood pressure. They may have fewer or less-severe side effects than ACE inhibitors, especially coughing, and are sometimes prescribed as an alternative to ACE inhibitors. Some patients with heart failure take an ACE inhibitor along with an ARB.

Brands and Indications. ARBs are used to treat Stage A high-risk conditions such as high blood pressure and diabetic nerve disorders (neuropathy). They are also used to treat Stage B patients who have had a heart attack or who have left ventricular systolic disorder, and Stage C patients with heart failure. Specific brands, and the stage of heart failure they are used for, are listed below.

Candesartan (Atacand) -- (Stages A, C)
Eprosartan (Teveten) -- (Stage A)
Irbesartan (Avapro) -- (Stage A)
Losartan (Cozaar) -- (Stages A, B)
Olmesartan (Benicar) -- (Stage A)
Telmisartan (Micardis) -- (Stage A)
Valsartan (Diovan) -- (Stages A, B, C)

Common Side Effects

Low blood pressure
Dizziness and lightheadedness
Raised potassium levels
Drowsiness

Beta blockers are almost always used in combination with other drugs, such as ACE inhibitors and diuretics. They help slow heart rate and lower blood pressure. Research presented at the 2006 American College of Cardiology meeting indicated that beta-blockers are an important treatment for most patients with left ventricular heart failure. Data from the study found that the beta blocker carvedilol (Coreg) significantly lowered the risk of death or rehospitalization within 3 - 6 months after hospital discharge.

Beta blockers can help patients with heart failure by:

Treating high blood pressure, angina, arrhythmias, and preventing heart attack in high-risk patients.
Preventing left ventricular remodeling in patients with enlarged heart chambers and weakened heart muscles (dilated cardiomyopathy), and in those who have suffered a first heart attack.
Blocking inflammatory immune factors called cytokines, including tumor necrosis factor (TNF). TNF may play a key role in the process leading to heart failure.
Preventing norepinephrine (adrenaline) from binding to heart cells. Elevated levels of norepinephrine, a stress hormone, can overstimulate the failing heart and are associated with severe heart failure.

Brands and Indications. Beta blockers treat Stage A high blood pressure. They are also treat Stage B patients (both those who have had a heart attack and those who have not had a heart attack but who have heart damage). Recent guidelines identify three drugs best for treating Stage C patients with heart failure. Specific brands and stages include:

Acebutolol (Sectral) -- (Stage A)
Atenolol (Tenormin) -- (Stages A, B)
Betaxolol (Kerlone) -- (Stage A)
Bisoprolol (Zebeta) -- (Stages A, C)
Cartelol (Cartrol) -- (Stage A)
Carvedilol (Coreg) -- (Stages A, B, C)
Labetalol (Trandate) -- (Stage A)
Metoprolol succinate (Toprol XL) -- (Stages A, C)
Metoprolol tartrate (Lopressor) -- (Stages A, B)
Nadolol (Corgard) -- (Stage A)
Penbutolol (Levatol) -- (Stage A)
Pindolol (Visken) -- (Stage A)
Propranolol (Inderal) -- (Stages A, B)
Timolol (Blocadren, Timolide) -- (Stages A, B)

Beta Blocker Concerns

Do not abruptly stop taking these drugs. The sudden withdrawal of beta blockers can rapidly increase heart rate and blood pressure. Your doctor may want you to slowly decrease the dose before stopping completely.
Beta blockers are categorized as non-selective or selective. Non-selective beta blockers such as carvedilol and propranolol can narrow bronchial airways. Patients with asthma, emphysema, or chronic bronchitis should not use these beta blockers.
Beta blockers can lower HDL (“good”) cholesterol.
These drugs can hide warning signs of low blood sugar (hypoglycemia) in patients with diabetes.
Beta blockers are usually used in combination with ACE inhibitors, but the two drugs are not started at the same time. Research presented at the 2005 European Society of Cardiology meeting indicates that either a beta blocker or an ACE inhibitor can be prescribed at first, and the other drug added on later.

Common Side Effects

Fatigue and lethargy
Vivid dreams and nightmares
Depression
Memory loss
Dizziness and lightheadedness
Reduced ability to exercise
Coldness in extremities (legs, toes, arms, hands)

Check with your doctor about any side effects. Do not stop taking these drugs on your own.

Diuretics cause the kidneys to rid the body of excess salt and water. Fluid retention is a major symptom of heart failure. Aggressive use of diuretics can help eliminate excess body fluids, while reducing hospitalizations and improving exercise capacity. These drugs are also important to help prevent heart failure in patients with high blood pressure. In addition, certain diuretics, notably spironolactone (Aldactone), block aldosterone, a hormone involved in heart failure. This drug class is beneficial for patients in late stages of heart failure (Stages C and D).

Diuretic Types and Brands. Diuretics come in many brands and are generally inexpensive. Some need to be taken once a day, some twice a day. Treatment is usually started at a low dose and gradually increased. Diuretics are virtually always used in combination with other drugs, especially ACE inhibitors and beta blockers. There are three main types of diuretics:

Potassium-sparing diuretics. These include amiloride (Midamor), spironolactone (Aldactone), and triamterene (Dyrenium).
Thiazide diuretics. These include chlorothiazide (Diuril), chlorthalidone (Hygroton), indapamide (Lozol), hydrochlorothiazide (Esidrix, HydroDiuril), and metolazone (Mykrox, Zaroxolyn).
Loop diuretics. Because loop diuretics act faster than other diuretics it is important to avoid dehydration and potassium loss. Loop diuretics include bumentanide (Bumex), furosemide (Lasix), and torsemide (Demadex).

Problems with Diuretics. Loop and thiazide diuretics deplete the body's supply of potassium, which, if left untreated, increases the risk for arrhythmias. Arrhythmias are heart rhythm disturbances that can, in rare instances, lead to cardiac arrest. In such cases, doctors will prescribe lower doses of the current diuretic, recommend potassium supplements, or use potassium-sparing diuretics either alone or in combination with a thiazide. Potassium-sparing drugs have their own risks, which include dangerously high levels of potassium in people with existing elevated levels of potassium or in those with damaged kidneys. However, all diuretics are generally more beneficial than harmful.

Common Side Effects

Fatigue
Depression and irritability
Urinary incontinence
Reduced sexual drive

Aldosterone is a hormone that is critical in controlling the body's balance of salt and water. Excessive levels may play important roles in hypertension and heart failure. Drugs that block aldosterone are prescribed for some patients with Stage C heart failure.

Spironolactone (Aldactone, Spirinol) is both a potassium-sparing diuretic and an aldosterone blocker. A major study of patients with heart failure found that spironolactone reduced death rate by 30%. Like all medications for heart failure, it must be used with care; elevated potassium levels are a potential risk of therapy.
Eplerenone (Inspra), a newer aldosterone blocker, has been specifically approved for treatment of heart failure. It is prescribed for patients who have heart failure following a heart attack. Its actions are similar to potassium-sparing diuretics and, like these drugs, it poses some risk for high potassium levels.

Digitalis is derived from the foxglove plant. It has been used to treat heart disease since the 1700s. Digoxin (Lanoxin) is the most commonly prescribed digitalis preparation. Digoxin decreases heart size and reduces certain heart rhythm disturbances (arrhythmias).

Unfortunately, digitalis does not reduce mortality rates, although it does reduce hospitalizations and worsening of heart failure. Controversy has been ongoing for more than 100 years over whether the benefits of digitalis outweigh its risks and adverse effects.

Digitalis may be useful for patients with left-ventricular systolic dysfunction who do not respond to other drugs (diuretics, ACE inhibitors). It is also used for patients who have atrial fibrillation.

Digitalis does not appear to help patients with left-ventricular diastolic heart failure. It may be harmful in patients with right-ventricular heart failure and those who stop taking digoxin after using it in combination with ACE inhibitors.

Side Effects and Problems. While digitalis is generally a safe drug, it can have toxic side effects due to overdose or other accompanying conditions. The most serious side effects are arrhythmias (abnormal heart rhythms that can be life-threatening). Early signs of toxicity may be irregular heartbeat, nausea and vomiting, stomach pain, fatigue, visual disturbances (such as yellow vision, seeing halos around lights, flickering or flashing of lights), and emotional and mental disturbances.

Many factors increase the chance for side effects.

Advanced age
Low blood potassium levels (which may be caused by diuretics)
Hypothyroidism
Anemia
Valvular heart disease
Impaired kidney function

Digitalis also interacts with many other drugs, including quinidine, amiodarone, verapamil, flecainide, amiloride, and propafenone.

A blood test that monitors drug levels in patients taking the drug can limit the rate of toxicity to about 2%. For most patients with mild-to-moderate heart failure, low-dose digoxin may be as effective as higher doses. If side effects are mild, patients should still consider continuing with digitalis if they experience other benefits.

Hydralazine and nitrates are two older drugs that help relax arteries and veins, thereby reducing the heart's workload and allowing more blood to reach the tissues. In 2005, the FDA approved BiDil, a drug that combines isosorbide dinitrate and hydralazine. BiDil is approved to specifically treat heart failure in African-Americans. African-Americans have a particularly high risk for heart failure. BiDil is the first drug approved for a specific racial group. The Food and Drug Administration (FDA) based its approval on a landmark 2004 study published in the New England Journal of Medicine, which showed that African-Americans who took the drug were 43% more likely to survive heart failure than patients who took placebo. Some experts suggest that BiDil could also benefit other racial groups.

Statins are important drugs used to lower cholesterol and to prevent heart disease leading to heart failure. These drugs include lovastatin (Mevacor), pravastatin (Pravachol), simvastatin (Zocor), fluvastatin (Lescol), atorvastatin (Lipitor), and rosuvastatin (Crestor). In 2007, the FDA approved atorvastatin to reduce the risks for hospitalization for heart failure in patients with heart disease.

In a 2006 Journal of the American Medical Association study, patients with heart failure who began taking a statin drug had a 24% lower relative risk of death and a 21% lower relative risk of hospitalization for heart failure than patient who did not take a statin. Statins appeared to help these patients regardless of whether or not they had co-existing coronary heart disease.

Aspirin is a type of non-steroid anti-inflammatory (NSAID). A 2005 study in the Journal of the American College of Cardiology indicated that aspirin is important for preventing heart failure death in patients with heart disease, and can safely be used with ACE inhibitors. However, some research has suggested that NSAIDs may increase the risk of heart failure for patients with a history of heart disease, especially when used in combination with ACE inhibitors or diuretics. Patients with heart disease should ask their doctor which NSAIDs are right for them.

Nesiritide treats patients who have arrived at a hospital with decompensated heart failure. Decompensated heart failure is a life-threatening condition in which the heart fails over the course of minutes or a few days, often as the result of a heart attack or sudden and severe heart valve problems. However, nesiritide may cause serious kidney damage.

In 2005, the FDA released recommendations from an expert panel concerning the appropriate and inappropriate use of nesiritide. The panel emphasized that nesiritide should be used to treat only patients with decompensated heart failure who have shortness of breath (dyspnea) and trouble breathing. The drug should not be a replacement for diuretics.

Despite these warnings, some doctors have prescribed nesiritide “off-label” to treat patients with severe heart failure outside of a hospital setting. Research presented at the 2007 American College of Cardiology annual conference criticized this practice by demonstrating that nesiritide plus standard treatment does not reduce the risk of heart- or kidney-related death or hospitalization. In addition, the research suggested some concerns about nesiritide’s overall safety.

Tolvaptan. Tolvaptan is an investigational drug that is being studied in combination with standard therapy for treatment of heart failure. It is especially being investigated for acute decompensated heart failure, a type of heart failure categorized by fluid build-up in the lungs (pulmonary edema) for which there are few available treatments. In patients hospitalized with heart failure, tolvaptan plus standard drugs improved breathing problems (dyspnea) and reduced fluid accumulation (edema) and body weight, according to two studies published in 2007 in the Journal of the American Medical Association. However, the drug did not appear to reduce the risk of re-hospitalization or death.

Levosimendan. Levosimendan is an experimental inotropic drug that is being investigated as a treatment for severely ill patients with heart failure. It belongs to a new class of drugs called calcium sensitizers that may help improve heart contractions and blood flow. Clinical trials suggest that levosimendan may improve survival in patients hospitalized for heart failure. The drug also appears to reduce levels of BNP (brain natriuretic peptide), a chemical marker for heart failure severity.

Prograf. Tacrolimus (Prograf) was approved in 2006 to help prevent organ rejection in patients who have received a heart transplant. The drug suppresses the immune system. Patients who receive this drug are at increased risk of developing lymphoma (a cancer of the immune system).

Surgery and Devices

Revascularization surgery helps to restore blood flow to the heart. It can treat blocked arteries in patients with coronary artery disease and may help selected patients with heart failure. Surgery types include coronary artery bypass graft (CABG) and percutaneous coronary intervention (PCI). CABG is a traditional type of open heart surgery. PCI, also called angioplasty, uses a catheter to inflate a balloon inside the artery. A metal stent may also be inserted during a PCI procedure. [See In-Depth Report#03:Coronary artery disease.]

A 2006 study suggested that early treatment with revascularization surgery may be particularly important for patients with systolic heart failure, a condition that occurs when the heart does not pump out enough blood. This condition has a very high death rate. Researchers found that CABG or PCI surgery halved the risk of dying compared to standard drug therapy. Patients in the study first underwent a positron emission tomography (PET) test to determine if they would be good candidates for surgery.

Click the icon to see an illustrated series detailing coronary artery balloon angioplasty.

Click the icon to see an illustrated series detailing heart bypass surgery.

In appropriate patients, mitral valve surgery may significantly reduce the severity of heart failure. In a study of 92 patients with late-stage heart failure and faulty valves, reconstruction of the heart's mitral valve drastically improved heart function.

An experimental mesh "heart sock" is being investigated as an adjunct to mitral valve repair surgery. Research presented at the 2004 American Heart Association Scientific Sessions suggested that the device reduced the progression of heart failure and halved the need for transplant surgery. The "sock" helps realign the shape of the heart and improve heart function. To date, it has been tested in patients with dilated cardiomyopathy.

Ventricular Remodeling. Ventricular remodeling (also called partial left ventriculectomy or the Batista procedure, after its inventor) may allow some patients with dilated cardiomyopathy to avoid a heart transplant.

The procedure involves the following:

The surgeon first performs ventriculectomy, which is the removal of a section of healthy heart muscle weighing about 3 ounces.
The surgeon then reshapes the heart to a more normal size and form.
Any faulty heart valves are repaired.

Ventricular remodeling is still relatively new, and mortality rates are very high. Studies on long-term improvement are mixed. More research is needed to target the patients who would most benefit.

Patients who suffer from severe heart failure and whose symptoms do not improve with drug therapy or mechanical assistance may be candidates for heart transplantation. Some 3,600 people are awaiting a transplant, although only about 2,000 operations are performed each year.

The most important factor for heart transplant eligibility is overall health. Chronological age is less important. Most heart transplant candidates are between the ages of 50 – 64 years. About 72% of transplant patients are male, and 70% are white.

While the risks of this procedure are high, the 1-year survival rate is about 86% for men and 84% for women. The 3-year survival rate is 78% for men and 75% for women. Five years after a heart transplant, about 71% of men and 67% of women remain alive. In general, the highest risk factors for death 3 or more years after a transplant operation are coronary artery disease and the adverse effects (infection and certain cancers) of immunosuppressive drugs used in the procedure. The rejection rates in older people appear to be similar to those of younger patients.

In 2004, the FDA approved a temporary artificial heart (Syncardia) intended to keep patients alive in the hospital while they waited for a heart transplant. In 2006, the FDA approved the first permanent implantable artificial heart (AbiCor). The AbiCor is available only for patients who are not eligible for a heart transplant and who are not expected to live more than a month without medical treatment. The device requires a large chest cavity, which means that most women will not be eligible for it. Of the 14 men who have received the AbiCor, the average survival was less than 5 months after surgery. Only one patient was discharged from the hospital. The device’s manufacturer is working on a new model that it hopes will extend survival by as long as 5 years.

A growing array of heart devices and machines are changing the face of heart failure treatment. They have gained widespread acceptance for use as a bridge to transplant in patients who are on medications but still have severe symptoms and are awaiting a donor heart. Increasingly, though, doctors are exploring the possibility that such devices may be satisfactory treatments themselves, forestalling the need for a transplant altogether in some patients.

Ventricular Assist Devices (VADs). Ventricular assist devices are machines that help improve pumping actions. Several models with slightly different features are in use or under investigation. Some include the following:

Left ventricular assist device (LVAD) are used for patients whose heartbeat has slowed dangerously (a condition called bradycardia) to help take over the pumping action of the failing heart. Studies suggest that in some people the use of an LVAD may allow some of the damaged heart muscle to heal, perhaps even helping some patients avoid heart transplants. These devices are also being studied in combination with drug therapy to help recover heart function and improve patients’ chances for survival. Until recently, these machines required remaining in the hospital. Smaller battery-powered LVAD units, however, are allowing many patients to leave the hospital and are proving to be effective bridges to heart transplants in adults. The HeartMate, for example, a portable LVAD about the size of a portable CD player (2 in. by 4 in.), is implanted in the upper abdomen. The implanted device plugs into an external power base, which is used when the patient is at rest to recharge the battery and provide continuous power.
Fully implanted miniature artificial pumps that assist the heart (not replace it) are also being tested. The DeBakey ventricular assist device (VAD) for example, is a tiny heart pump that weighs less than 4 ounces. It has been approved in Europe and is being tested in the United States. The Jarvik 2000 heart pump is also showing promise.
The intra-aortic balloon pump (IABP) is helpful for maintaining heart function in people with left-side failure waiting for transplants and in those who develop a sudden and severe deterioration of heart function. The IABP is an implanted thin balloon that is usually inserted into the artery in the leg and threaded up to the aorta leading from the heart. Its pumping action is generated by inflating and deflating the balloon at certain rates. Usually, it is used only for short periods, but some studies indicate that patients may be able to use it safely for somewhat longer periods (an average duration of 23 days in one study).

There are risks involved with many of these devices, including bleeding, blood clots, and right-side heart failure. Infections are a particular hazard.

Pacers (Pacemakers). Pacers, or pacemakers, help regulate the heart’s beating action, especially when the heart beats too slowly. Biventricular pacers (BVPs) are a special type of pacemaker used for patients with heart failure. Because BVPs help the heart’s left and right chambers beat together, this treatment is called cardiac resynchronization therapy (CST). BVPs may particularly help heart failure patients who have left bundle branch block, a condition in which the electrical impulses in the heart do not follow their normal pattern. In general, BVPs are recommended for patients with moderate-to-severe heart failure. A small 2006 study suggested that a defibrillator may be better suited for patients with moderate heart failure, while indicating a BVP might be best for patients with severe heart failure.

Implantable Cardioverter-Defibrillators. Devices called implantable cardioverter-defibrillators (ICDs), which are sometimes combined with pacemakers, work well for preventing arrhythmias (abnormal heart rhythms) in heart failure patients. Studies have also found them effective in preventing sudden death from severe rhythm disturbances in patients with weakened hearts from previous arrhythmias and in patients with genetic hypertrophic cardiomyopathy. Patients who have an ICD should avoid taking fish oil supplements. A 2005 Journal of the American Medical Association study found that omega-3 fatty acid supplements may increase the risk of rapid heart beat (ventricular tachycardia) or irregular heart rhythm (ventricular fibrillation) in some of these patients.

ICDs have many benefits, and recent expert guidelines recommend that they be used in more patients with heart failure. However, in June 2005, certain ICD models and biventricular pacemaker-defibrillators were recalled by the manufacturer because of a circuitry flaw that prevents the devices from delivering therapeutic electrical shocks when needed. The problem may result in patient death. Although the FDA did not make any specific recommendations, the agency encourages patients who may have such a device to ask their doctor if they should have it removed or replaced.

In April 2006, two studies published in the Journal of the American Medical Association evaluated data concerning the safety and reliability of implantable pacemakers and defibrillators. The studies found that from 1990 – 2002, pacemakers became increasingly reliable. From 1998 – 2002, ICDs had a significantly higher rate of malfunction than pacemakers, although the reliability of ICDs appeared to improve from 2003 – 2004.

In October 2006, the U.S. Heart Rhythm Society issued recommendations for doctors, manufacturers, and the FDA to help improve communication concerning performance and recalls of ICDs and pacemakers. Experts stress that the chance of an ICD or pacemaker saving a person’s life far outweigh the possible risks of these devices failing.

Ultrafiltration devices are used in hospitals to pump excess water and salt from the body. Catheters are inserted into several of the patient’s veins. The catheters are connected to a blood filter device. Blood is withdrawn through one of the catheters and filtered in the device to remove excess fluid. The filtered blood is then returned to the patient through another catheter. A 2006 study reported that ultrafiltration devices may work better than diuretic drugs for patients with acute decompensated heart failure (ADHF). ADHF is heart failure that has rapidly deteriorated so that patients require immediate hospitalization.

Lifestyle Changes

Between 30 - 47% of patients who require hospitalization for heart failure are back in the hospital within 6 months. Many people return because of lifestyle factors such as poor diet, failure to comply with medications, and social isolation.

In one study, elderly people who had no emotional support at home had triple the risk of a heart attack after hospitalization for heart failure than those who did have such support. (Women had eight times the risk.) In another study, the greatest risk factor for death and readmission to the hospital after a first hospitalization was being single, regardless of the health of the patient at discharge. A third study confirmed that a strong marriage predicted long-term survival. Evidence continues to mount that programs that offer intensive follow-up to ensure that the patient complies with lifestyle changes and medication regimens at home are reducing rehospitalization rates and improving survival. Patients without available rehabilitation programs should seek support from local and national heart associations and groups.

Patients should weigh themselves each morning and keep a record. Any changes are important:

A sudden increase in weight of more than 2 - 3 pounds may indicate fluid accumulation and should prompt an immediate call to the doctor.
Rapid wasting weight loss over a few months is a very serious sign and may indicate the need for surgical intervention.

Whole Grains. Evidence suggests that daily consumption of whole grain foods may help prevent heart failure. In research presented at a 2007 American Heart Association conference, people who ate whole-grain breakfast cereals seven or more times a week had a 28% lower risk of developing heart failure than those who never ate these cereals.

Mediterranean Diet. Evidence suggests that the Mediterranean diet helps protect the heart and may even reduce the risk for heart failure after a first heart attack. The diet emphasizes whole grains, fish, olive oil, garlic, and moderate daily intake of wine. There are several variations to the Mediterranean diet but general recommendations include:

Limit red meats.
Limit dairy products.
Eat moderate amounts of fish and poultry. Fish is the diet’s main protein source. Some studies suggest that fish is the primary heart-protective ingredient in this diet. However, patients who have an implantable defibrillator should not take fish oil supplements. A 2005 study suggested that these supplements may worsen heart rhythm problems in some patients.
Eat plenty of fresh fruits and vegetables, nuts, legumes, beans, and whole grains.
Daily glass or two of wine. Light-to-moderate alcohol use may reduce the risk for heart failure, (but heavy alcohol consumption is a risk factor).
Plenty of fresh fruits and vegetables, as well as nuts, legumes, beans, and whole grains.

DASH Diet. The Dietary Approaches to Stop Hypertension (DASH) diet is an important lifestyle step in managing blood pressure. It may also be useful for many patients with heart failure. This diet is not only rich in important nutrients and fiber but also includes foods that contain two and a half times the amounts of electrolytes, potassium, calcium, and magnesium found in the average American diet.

Potassium-rich foods, which are important for patients with heart failure, include bananas, oranges, prunes, cantaloupes, carrots, spinach, celery, alfalfa, mushrooms, lima beans, potatoes, avocados, and broccoli. However, patients who take potassium-sparing diuretics or ACE inhibitors, and those with kidney dysfunction, may have to restrict their potassium intake.

The DASH diet is rich in whole grains and fresh fruits and vegetables. It stresses avoiding saturated fats, as any healthy diet does, although it includes calcium-rich dairy products that are non- or low-fat. When choosing fats, the diet recommends monounsaturated oils such as olive or canola oil.

Salt Restriction. People with high blood pressure are generally urged to restrict salt, although certain people may be more susceptible to its effects. For example, a high intake of salt may be an independent risk factor for the development of heart failure in people who are overweight. All patients with heart failure should limit their salt intake, and in severe cases, very stringent salt restriction may be necessary. Patients should not add salt to their cooking and their meals. They should also avoid foods high in sodium. These salty foods include ham, bacon, hot dogs, lunch meats, prepared snack foods, dry cereal, cheese, canned soups, soy sauce, and condiments. Some patients may need to reduce their water intake as well. People with high cholesterol levels or diabetes require additional dietary precautions. [See In-Depth Report #43: Heart-healthy diet. ]

People with heart failure used to be discouraged from exercising. Now, experts think that exercise, when performed under medical supervision, is extremely important for many patients with stable conditions. Studies have reported that patients with stable conditions who engage in regular moderate exercise (three times a week) experience a better quality of life and lower mortality rates than those who do not exercise.

The following guidelines are critical:

Experts warn that exercise is not appropriate for all patients with heart failure. If you have heart failure, always consult your doctor before starting an exercise program.
People who are approved for, but not used to, exercise should start with 5 - 15 minutes of easy exercise with frequent breaks. Although the goal is to build up to 30 - 45 minutes of walking, swimming, or low-impact aerobic exercises three to five times every week, even shorter times spent exercising are useful.

Studies report benefits from specific exercises:

Progressive strength training may be particularly useful for patients with heart failure since it strengthens muscles, which commonly deteriorate in this disorder. Strength training typically uses light weights, weight machines, or even the body's weight (leg raises or sit-ups, for example). Even performing daily handgrip exercises can improve blood flow through the arteries.
Patients who exercise regularly using supervised treadmill and stationary-bicycle exercises can increase their exercise capacity by 14 - 36%. In one study, patients as old as 91 years increased their oxygen consumption significantly after 6 months of supervised treadmill and stationary bicycle exercises. Exercising the legs may help correct problems in heart muscles. In one study, patients who did leg extension exercises for 8 weeks had higher levels of an enzyme involved in forming new blood vessels. Exercise has also been associated with reduced inflammation in blood vessels.
Dancing may be a fun and beneficial alternative to standard aerobic exercise, according to research presented at the 2006 annual meeting of the American Heart Association. In a study of patients with stable chronic heart failure, dancing helped improve cardiopulmonary fitness, arterial elasticity, and quality of life. Patients in the study danced fast and slow waltzes for 21 minutes, three times a week.

Bed rest may be required in cases of severe heart failure. To reduce congestion in the lungs, the patient's upper body should be elevated. For most patients, resting in an armchair is better than lying in bed. Relaxing and contracting leg muscles is important to prevent clots. As the patient improves, a doctor will progressively recommend more activity.

Experts have traditionally recommended that people with heart failure avoid warm baths, which can increase the heart rate. Some studies now report that carefully controlled bathing for short periods may not be harmful and may actually be beneficial, reducing irregular heart beats and increasing cardiac output and ejection fraction. Warm water may behave like a vasodilating drug, opening up the vessels gently and improving circulation. In clinical trials, patients sat in warm water or a dry sauna for 10 minutes, with their bodies tilted at a 45 degree angle.

Warning Note: Prolonged periods in hot or even warm conditions can be dangerous. Any patient with heart failure should consult their doctor first, not bathe unaccompanied, and be sure that the temperature does not go above 106° Fahrenheit for water bathing or 140° Fahrenheit for dry saunas.

Stress reduction techniques, such as meditation and relaxation response methods, may have direct physical benefits for lowering stress hormones. These hormones include cortisol, which suppresses the immune system, and norepinephrine (also known as adrenaline), the chemical messenger associated with heart dysfunction.

Patients with heart failure may resort to alternative remedies. Such remedies are often ineffective and may have severe or toxic effects. Of particular note for patients with heart failure is an interaction between St. John's wort (an herbal medicine used for depression) and digoxin (a heart drug). St. John's wort can significantly interfere with this drug.

Arginine. Some evidence suggests that arginine (also called L-arginine) may have some benefit. This amino acid appears to reduce endothelin, a protein that causes blood vessel constriction and is found in high amounts in patients with heart failure. It can have adverse effects, however, including gastrointestinal problems. It can also lower blood pressure and change levels of certain chemicals and electrolytes in the body. It may increase the risk for bleeding. Some people have an allergic reaction to it, which in same cases may be severe. It may worsen asthma.

Coenzyme Q10 and Vitamin E. Small studies have suggested that coenzyme Q10 (CoQ10) may help patients with heart failure, particularly when combined with vitamin E. CoQ10 is a vitamin-like substance found in organ meats and soybean oil. More recent studies, however, have found that CoQ10 and vitamin E do not help the heart or prevent heart disease. According to a 2005 Journal of the American Medical Association study, vitamin E supplements can actually increase the risk of heart failure, especially for patients with diabetes or vascular diseases.

Crataegus Extract. An herbal remedy, Crataegus Extract WS1442, which is made from the leaves of the Crataegus tree, may have antioxidant properties that can help patients with heart failure. In a study presented at the 2007 American College of Cardiology annual meeting, over 2,000 patients with severe heart failure were randomized to receive either Crataegus Extract or placebo (plus standard drug treatment) for 2 years. The researchers noted a 20% reduction in heart-related deaths among patients who received the extract, and suggested that the herb extended patients’ lives by 4 months during the first 18 months of the study.

Other Vitamins and Supplements. A wide variety of other vitamins (thiamin, B6, and C), minerals (calcium, magnesium, zinc, manganese, copper, selenium), nutritional supplements (carnitine, creatine), and herbal remedies (hawthorn) have been proposed as treatments for heart failure. None have been adequately tested. There is no evidence that a particular vitamin or supplement can cure heart failure. In any case, vitamins are best consumed through the food sources contained in a healthy diet.

Generally, manufacturers of herbal remedies and dietary supplements do not need FDA approval to sell their products. Just like a drug, herbs and supplements can affect the body's chemistry, and therefore have the potential to produce side effects that may be harmful. There have been several reported cases of serious and even lethal side effects from herbal products. Always check with your doctor before using any herbal remedies or dietary supplements.

Resources

www.nhlbi.nih.gov -- National Heart, Lung, and Blood Institute
www.americanheart.org -- American Heart Association
www.acc.org -- American College of Cardiology
www.hfsa.org -- Heart Failure Society of America
www.heartfailure.org -- Heart Failure Online
www.unos.org -- United Network for Organ Sharing
www.organdonor.org -- National Transplant Society
www.organdonor.gov -- US government organ donor site

References

Ahmed A, Rich MW, Fleg JL, Zile MR, Young JB, Kitzman DW, et al. Effects of digoxin on morbidity and mortality in diastolic heart failure: the ancillary digitalis investigation group trial. Circulation. 2006 Aug 1;114(5):397-403.

Battaglia M, Pewsner D, Juni P, Egger M, Bucher HC, Bachmann LM. Accuracy of B-type natriuretic peptide tests to exclude congestive heart failure: systematic review of test accuracy studies. Arch Intern Med. 2006 May 22;166(10):1073-80.

Bhatia RS, Tu JV, Lee DS, Austin PC, Fang J, Haouzi A, et al. Outcome of heart failure with preserved ejection fraction in a population-based study. N Engl J Med. 2006 Jul 20;355(3):260-9.

Birks EJ, Tansley PD, Hardy J, George RS, Bowles CT, Burke M, et al. Left ventricular assist device and drug therapy for the reversal of heart failure. N Engl J Med. 2006 Nov 2;355(18):1873-84.

Bryson CL, Mukamal KJ, Mittleman MA, Fried LP, Hirsch CH, Kitzman DW, et al. The association of alcohol consumption and incident heart failure: the Cardiovascular Health Study. J Am Coll Cardiol. 2006 Jul 18;48(2):305-11.

Bursi F, Weston SA, Redfield MM, Jacobsen SJ, Pakhomov S, Nkomo VT, et al. Systolic and diastolic heart failure in the community. JAMA. 2006 Nov 8;296(18):2209-16.

Carlson MD, Wilkoff BL, Maisel WH, Carlson MD, Ellenbogen KA, Saxon LA, et al. Recommendations from the Heart Rhythm Society Task Force on Device Performance Policies and Guidelines Endorsed by the American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) and the International Coalition of Pacing and Electrophysiology Organizations (COPE). Heart Rhythm. 2006 Oct;3(10):1250-73.

Davis BR, Piller LB, Cutler JA, Furberg C, Dunn K, Franklin S, et al. Role of diuretics in the prevention of heart failure: the Antihypertensive andLipid-Lowering Treatment to Prevent Heart Attack Trial. Circulation. 2006 May 9;113(18):2201-10. Epub 2006 May 1.

Gheorghiade M, Abraham WT, Albert NM, Greenberg BH, O'Connor CM, She L, et al. Systolic blood pressure at admission, clinical characteristics, and outcomes inpatients hospitalized with acute heart failure. JAMA. 2006 Nov 8;296(18):2217-26.

Gheorghiade M, Konstam MA, Burnett JC Jr, Grinfeld L, Maggioni AP, Swedberg K, et al. Short-term clinical effects of tolvaptan, an oral vasopressin antagonist, in patients hospitalized for heartfFailure: the EVEREST clinical status trials. JAMA. 2007 Mar 25; [Epub ahead of print]

Go AS, Lee WY, Yang J, Lo JC, Gurwitz JH. Statin therapy and risks for death and hospitalization in chronic heart failure. JAMA. 2006 Nov 1;296(17):2105-11.

Hildebrandt P. Systolic and nonsystolic heart failure: equally serious threats. JAMA. 2006 Nov 8;296(18):2259-60.

Konstam MA, Gheorghiade M, Burnett JC Jr, Grinfeld L, Maggioni AP, Swedberg K, et al. Effects of oral tolvaptan in patients hospitalized for worsening heart failure: the EVEREST Outcome Trial. JAMA. 2007 Mar 25; [Epub ahead of print]

Lee DS, Pencina MJ, Benjamin EJ, Wang TJ, Levy D, O'Donnell CJ, et al. Association of parental heart failure with risk of heart failure in offspring. N Engl J Med. 2006 Jul 13;355(2):138-47.Maisel WH. Pacemaker and ICD generator reliability: meta-analysis of device registries. JAMA. 2006 Apr 26;295(16):1929-34.

Maisel WH, Moynahan M, Zuckerman BD, Gross TP, Tovar OH, Tillman DB, et al. Pacemaker and ICD generator malfunctions: analysis of Food and Drug Administration annual reports. JAMA. 2006 Apr 26;295(16):1901-6.

Mueller C, Laule-Kilian K, Schindler C, Klima T, Frana B, Rodriguez D, et al. Cost-effectiveness of B-type natriuretic peptide testing in patients with acute dyspnea. Arch Intern Med. 2006 May 22;166(10):1081-7.

Owan TE, Hodge DO, Herges RM, Jacobsen SJ, Roger VL, Redfield MM. Trends in prevalence and outcome of heart failure with preserved ejection fraction. N Engl J Med. 2006 Jul 20;355(3):251-9.

Review Date:
4/11/2007
Reviewed By:
Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

A.D.A.M., Inc. is accredited by URAC, also known as the American Accreditation HealthCare Commission (www.urac.org). URAC's accreditation program is an independent audit to verify that A.D.A.M. follows rigorous standards of quality and accountability. A.D.A.M. is among the first to achieve this important distinction for online health information and services. Learn more about A.D.A.M.'s editorial policy, editorial process and privacy policy. A.D.A.M. is also a founding member of Hi-Ethics and subscribes to the principles of the Health on the Net Foundation (www.hon.ch).

A.D.A.M. Copyright

The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed medical professional should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are provided for information only -- they do not constitute endorsements of those other sites. © 1997-2009 A.D.A.M., Inc. Any duplication or distribution of the information contained herein is strictly prohibited.

adam.com

Body Knowledge: Red Blood, Blue Veins?

FitSugar — Thu, 24 Sep 2009 03:00:18 -0700

There is a common misconception among kids that blood, as it courses through our veins on its return trip back to the heart, is blue.

When you look at your arms you see blue veins, but this is a trick of light, or rather a problem with wavelengths. According to Live Science, the blue waves of light are not absorbed by your skin, unlike red light waves, so blue is the color you see because it bounces back.

So what does happen to your blood as it moves about your body? Learn the details by reading more.

Heart attack and acute coronary syndrome

FitSugar — Wed, 08 Oct 2008 17:34:57 -0700

In This Report

Highlights
Introduction
Symptoms
Prognosis
Risk Factors
Diagnosis
Treatment
Medications
Surgery
Rehabilitation
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Drug Approval

In 2006, the FDA approved the use of clopidogrel (Plavix) for patients who have had a STEMI heart attack and who will not be having angioplasty. A STEMI is a very severe type of heart attack caused by sudden and total artery blockage.

Angioplasty and Stents

Surgery with angioplasty and stents that is performed more than 3 days after a heart attack offers no advantage over standard drug therapy for clinically stable patients, indicates an important 2006 New England Journal of Medicine study. Experts recommend that this procedure be performed to open blocked arteries within 12 hours of a heart attack.

Drug-Coated Stents

Drug-coated stents may be better than bare metal stents for patients who have had a STEMI heart attack, suggest several New England Journal of Medicine studies. However, recent research has raised concern that these types of stents increase the risk for blood clots.
Patients who have a drug-coated stent must take aspirin and clopidogrel (Plavix) for at least 1 year after the stent is inserted, according to an important 2007 advisory from the American Heart Association (AHA). The combination of these drugs can help prevent blood clots.

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

NSAIDs such as acetaminophen (Tylenol), ibuprofen (Advil) should be used with caution by patients who have had a heart attack:

In 2007, the AHA warned that NSAIDs (with the exception of aspirin) and COX-2 inhibitors increase the risk of heart attack and stroke. The AHA is recommending that doctors change the way they prescribe these pain relievers for patients who have or are at risk for heart disease.
A 2006 Journal of the American Medical Association study suggested that the prescription NSAID diclofenac (Cataflam) carries a higher risk for heart attack than other NSAIDs.

Introduction

The heart is the human body's hardest working organ. Throughout life it continuously pumps blood enriched with oxygen and vital nutrients through a network of arteries to all parts of the body's tissues. In order to perform the arduous task of pumping blood to the rest of the body, the heart muscle itself needs a plentiful supply of oxygen-rich blood, which is provided through a network of coronary arteries. These arteries carry oxygen-rich blood to the heart's muscular walls (the myocardium).

Coronary artery disease is the most common cause of heart attacks. Coronary artery disease is the end result of a complex process called atherosclerosis (commonly called "hardening of the arteries"). This causes blockage of arteries (ischemia) and prevents oxygen-rich blood from reaching the heart. A full-blown heart attack occurs when blood flow to the myocardium is blocked and tissue death occurs from loss of oxygen, severely damaging the heart. The medical term for heart attack is myocardial infarction. [See In-Depth Report #3: Coronary artery disease.]

Click the icon to see an image of atherosclerosis.

Heart attack (or myocardial infarction) is the most serious outcome of atherosclerosis. It can occur as a result of one or two effects of atherosclerosis:

(1) If the artery becomes completely blocked and ischemia becomes so extensive that oxygen-bearing tissues around the heart die.

(2) If the plaque itself develops fissures or tears. Blood platelets adhere to the site to seal off the plaque, and a blood clot (thrombus) forms. A heart attack can then occur if the formed blood clot completely blocks the passage of oxygen-rich blood to the heart.

Click the icon to see an image of an acute myocardial infarction.

Angina is the primary symptom of coronary artery disease and is typically experienced as chest pain. There are two kinds of angina:

Stable Angina is predictable chest pain that can usually be managed with lifestyle measures and medications, such as low-dose aspirin.
Unstable angina is a much more serious situation than stable angina that is often an intermediate stage between stable angina and a heart attack. Unstable angina is part of a condition called acute coronary syndrome.

Acute coronary syndrome (ACS) is a severe and sudden heart condition that requires aggressive treatment, but has not developed into a full blown heart attack. Acute coronary syndrome includes:

Unstable angina. Unstable angina is a much more serious situation than stable angina. It is often an intermediate stage between stable angina and a heart attack.
NSTEMI (non ST-segment elevation myocardial infarction). This condition, also called non Q-wave myocardial infarction, is diagnosed when blood tests and ECGs suggest a developing heart attack. The injury in the arteries is less severe than with a full-blown heart attack.

Symptoms

ANYONE WHO BELIEVES THEY ARE HAVING A HEART ATTACK SHOULD IMMEDIATELY CALL THE EMERGENCY MEDICAL SYSTEM (911 IN THE UNITED STATES).

In people with known heart disease, any unusual chest pain or other symptoms of heart attack that do not clear up with medications are signals to go to the hospital. The degree of pain and the specific symptoms before a heart attack vary greatly among individuals. Onset can be abrupt, gradual, or intermittent.

Chest Pain. People with heart disease or risk factors should be concerned about any chest pain, usually precipitated by exercise or stress, that interrupts normal activities and does not clear up after resting or taking angina medications. Chest symptoms might be experienced as follows:

Pain is typically felt as a crushing weight against the chest, accompanied by profuse sweating. The pain may radiate to the left shoulder and arm, the neck or jaw, and even infrequently to the right arm. The arm may be tingling or numb.
Some people may have only a tingling sensation or a sense of fullness, squeezing, or pressure in the chest.
In some patients with a history of heart disease, chest pain is mild. Such patients may have experienced unexplained fatigue, depression, and ill health within a month of a heart attack.

Although chest pain is the classic symptom, it occurs in only about half of patients with a heart attack.

Other Common Symptoms. Other common symptoms of a heart attack include:

Nausea, vomiting, and cold sweats
A feeling of indigestion or heartburn
Fainting
A great fear of impending death, a phenomena known as angor animi

Uncommon Symptoms. Some studies suggest that nearly half of patients with heart attack do not have chest pain as the primary symptom. Common atypical symptoms of a heart attack include:

Shortness of breath
Cardiac arrest
Dizziness, weakness, and fainting
Abdominal pain

Patients most likely to have atypical symptoms are women and the very elderly (although they can certainly have classic heart attack symptoms as well.)

In one study, 52% of elderly people with acute coronary syndrome had atypical symptoms that included shortness of breath, nausea, profuse sweating, pain in the arms, and fainting. Such symptoms were more likely to occur in people with personal or family history of heart disease.
Before a heart attack, women are more likely than men to be nauseous and experience pain high in the abdomen or chest. Their first symptom may be extreme fatigue after physical activity rather than chest pain. Chest pain in women is also more likely to be caused by non-heart problems than in men.

Symptoms That Are Less Likely to Indicate a Heart Attack. The following are symptoms that are more likely to be due to causes other than a heart event:

Sharp pain brought on by lung movements or coughing
Pain that is mainly or only in the middle or lower abdomen
Pain that can be pinpointed with the top of one finger
Pain that can be reproduced by moving or pressing on the chest wall or arms
Pain that is constant and lasts for hours (although no one should wait hours if they suspect they are having a heart attack)
Pain that is very brief and lasts for a few seconds
Pain that spreads to the legs

The presence of these symptoms, however, does not always rule out a serious heart event.

Chest pain is a very common symptom in the emergency room, but heart problems account for only 10% to a third of all episodes. High on the list of other causes of chest pain are the following:

The most common causes of chest pain are muscular and bone problems. Problems affecting the ribs and chest muscles include injured muscles, fractures, arthritis, spasms, and infections.
Anxiety attacks
Gastrointestinal disorders (gallstone attacks, peptic ulcer disease, hiatal hernia, heartburn)
Asthma
Spasm in the coronary artery
Abnormalities of the heart muscle itself
Rupture of the aorta, collapsed lung, acute inflammation of the heart, or a blood clot in the lung
Hyperthyroidism
Anemia
Vasculitis (a group of disorders that cause inflammation of the blood vessels)
Exposure to high altitudes (rare)

Immediately call 911 or the local emergency number.

If patients have been previously diagnosed with angina, they should take one nitroglycerin dose either as an under-the-tongue tablet or in spray form at the onset of symptoms. They should take another dose every 5 minutes up to three doses or when the pain is relieved, whichever comes first.

It should be noted, however, that only 20% of heart attacks occur in patients with long-standing angina.

Anyone who has heart disease or risk factors for it and experiences heart attack symptoms should immediately contact emergency services.

The patient should chew an aspirin (250 - 500 mg) and be sure that emergency health providers are informed of this so an additional dose is not given.

Patients who experience chest pain should go immediately to the nearest emergency room, preferably traveling by ambulance. They should not drive themselves.

Prognosis

Each year, an estimated 650,000 Americans will suffer a first heart attack, and 450,000 will have a recurrent episode. Currently, half of the men and 63% of the women who died of heart disease had no warning prior to their fatal attacks.

Heart attacks may be rapidly fatal, evolve into a chronic disabling condition, or lead to full recovery. The long-term prognosis for both length and quality of life after a heart attack depends on its severity and the preventive measures taken afterward.

About 88% of patients under age 65 who experience a heart attack can expect to return to work. About 12,600,000 Americans who have had heart attacks, angina, or both are alive today. However, within 6 years of a heart attack, 18% of men and 35% of women have a recurrent attack. And, about 22% of men and 46% of women develop heart failure.

Although no tests can absolutely predict whether another heart attack will occur, experts estimate that up to 30% of fatal attacks, and many follow-up surgeries, could be avoided with healthy lifestyle changes and adherence to medical treatments. Two-thirds of patients who have suffered a heart attack, however, do not take the necessary steps to prevent another.

Higher Risk Individuals. A heart attack is always more serious in certain people:

Elderly (particularly those who are thinner)
People with a history of heart disease or risk factors for heart disease
People with heart failure
People with diabetes
People on long-term dialysis

Women are more likely to die after a heart attack than men. The risk is highest in younger women (although in the younger population, the risk for having a first heart attack and then dying from it is very low). It is still unclear why heart attacks are more severe in this group.

Factors Occurring at the Time of a Heart Attack That Increase Severity. The presence of other conditions during a heart attack can contribute to a poorer outlook:

Arrhythmias (disturbed heart rhythms). A dangerous arrhythmia called ventricular fibrillation is a major cause of short-term death from heart attack. Such arrhythmias are more likely to occur within the first 4 hours and are associated with a high mortality rate. Patients who are successfully treated, however, have the same long-term prognosis as those who do not experience such arrhythmias.
Signs of severe physical damage to the heart may indicate a poorer outlook.
Shock. This very dangerous condition is associated with very low blood pressure, reduced urine levels, and cellular abnormalities. Shock occurs in about 7% of heart attacks. The incidence has not declined over recent years, although its survival rates have improved.
Heart block, also called atrioventricular (AV) block, is a condition in which the electric conduction of nerve impulses to specialized muscles in the heart is slowed or interrupted. Although heart block is dangerous, it can be treated effectively with a pacemaker, and it rarely causes any long-term complications in patients who survive it.

Heart attacks and acute coronary syndrome pose a high risk for stroke. According to a major 2002 study, the risk for stroke after heart attack is 2.5% in the first 6 months and 5% per year thereafter. In the study, patients with a higher risk (about 4%) for stroke within 6 months of a heart attack were older (over age 75), African-American, had a history of stroke, atrial fibrillation, hypertension, diabetes, or peripheral artery disease. Most people who fall into these categories have more than one of these risk factors.

Risk Factors

About 25% of all Americans have one or more risk factors for heart disease, increasing their risk for heart attack. Most risk factors for heart disease are related to lifestyle. Some risk factors, (such as age, gender, and ethnicity) cannot be changed. Nevertheless, overall risks can be reduced with healthy lifestyle changes. [See In-Depth Report #3: Coronary artery disease.]

The American Heart Association's guidelines for preventing heart disease recommend:

Improve Cholesterol. People with at least two risk factors and a 10-year risk for heart disease or stroke of more than 20% should aim for LDL levels of less than 100 mg/dl. Statins are now used in more cases.

Keep Blood Pressure Low. People in normal health should have a blood pressure reading of 120/80 mm Hg or less. According to new guidelines, blood pressure readings of 120/80 are considered normal, readings of 140/90 or higher indicate hypertension, and readings in between the two are called pre-hypertension. Patients with diabetes or chronic kidney disease should maintain blood pressure readings of 130/80 mm Hg or less, while others should be no higher than 140/90 mm Hg.

Exercise. Everyone in normal health should engage in at least moderate physical activity for a minimum of 30 minutes on most -- if not all -- days of the week.

Healthy Diet. Everyone should aim for a diet that contains a healthy balance of fruits, vegetables, grains, fish, nuts, legumes, poultry, lean meat, and low-fat dairy items. Avoid saturated fats and trans-fatty acids.

Quit Smoking. Also avoid exposure to second-hand smoke.

Maintain Weight. People should aim for a BMI index of 18.5 - 24.9.

Take Aspirin. People at high risk for heart disease should take a low-dose aspirin every day, unless they have medical reasons to avoid aspirin.

Control Diabetes. People with diabetes should aim for fast blood glucose levels of less than 110 mg/dl and hemoglobin A1C of less than 7%.

Control Atrial Fibrillation. People with atrial fibrillation should use anticoagulants to reduce the risk for blood clots.

The approach for managing acute coronary syndrome involves lifestyle changes and medications. Experts have come up with a mnemonic device (ABCDE) for remembering the factors that are fundamental for management of acute coronary syndrome:

A. Antiplatelets, anticoagulants, and ACE inhibitors

B. Blood pressure and beta-blockers

C. Cholesterol-lowering drugs (typically statins) and cigarettes (stopping)

D. Diet and diabetes control

E. Exercise and education

Age. About 85% of people who die from heart disease are over the age of 65.

Gender. Coronary artery disease and heart attacks are much more common in middle-aged men. Women have, on average, 10 - 15 more years of heart disease-free life than do men, but as women age, they catch up to men. Women are more likely to have angina than men are. Younger women with heart disease often do not have the same symptoms as their male counterparts and may be less likely to be diagnosed correctly. They are also more likely than men are to die after a heart attack. Evidence suggests that this is because women tend to be older and sicker than men at the time of a first attack. A 2002 study indicated, however, that with early aggressive treatment women with acute coronary syndrome do as well or better than men with the same condition and treatments.

Ethnicity. Of all major ethnic groups, African-American women face the highest risk for death from heart disease, and their rate of heart attacks is increasing. (Mortality rates in men do not differ much by race.) Native American men have a lower risk for heart disease than Caucasian men, and Hispanics have the lowest risk for heart disease of all major American population groups.

Timing of Heart Attack. A 2007 study suggested that patients who are admitted to a hospital on a weekend are less likely to receive aggressive heart attack treatment and less likely to survive than patients who are treated on a weekday. However, no one can predict when a heart attack will occur. The most important point is to get treatment quickly, regardless of the day of the week. And, if you think you having a heart attack, call an ambulance -- or have someone call for you -- to ensure prompt treatment. Do not drive yourself.

Cholesterol. Cholesterol is a white, powdery substance that is found in all animal cells and in animal-based foods (not in plants). In spite of its bad press, cholesterol is an essential nutrient necessary for many functions. However, when certain cholesterol levels rise in the blood, they can have dangerous consequences, depending on the type of cholesterol.

Low-density lipoprotein (LDL) cholesterol is the "bad" cholesterol responsible for many heart problems. Triglycerides are another type of lipid (fat molecule) that can be bad for the heart. High-density lipoprotein (HDL) cholesterol is the "good" cholesterol that helps protect against heart disease. Doctors test for a "total cholesterol" profile that includes measurements for LDL, HDL, and triglycerides. The ratio of these lipids can affect heart disease risk. [See In-Depth Report #23: Cholesterol.]

Cholesterol Goals. In 2004, the National Cholesterol Education Program updated its clinical practice guidelines. The new recommendations set lower treatment goals for LDL levels based on a patient's risk factors for heart disease.

These risk factors include:

Having a first-degree female relative diagnosed with heart disease before age 65 or a first-degree male relative diagnosed before age 55
Being male and over age 45 or female and over age 55
Cigarette smoking
Diabetes
High blood pressure
Metabolic syndrome (risk factors associated with obesity such as low HDL levels and high triglycerides)

Having two or more of these risk factors indicates a greater than 20% chance of having a heart attack within 10 years.


Risk Level	Goal (d/L)	OptimalGoal(d/L)
Very High Risk	70	70
High Risk	100	70
Moderate Risk	130	100
Low Risk	160	130

LDL cholesterol, together with other risk factors for heart disease, is the best determinant for whether cholesterol therapy is needed and whether it is working properly. In particular, the new guidelines emphasize lower LDL levels and earlier treatment for people with coronary artery disease, or other forms of atherosclerosis, and diabetes.


Total Cholesterol Goals	LDL Goals	HDL Goals	Triglyceride Goals
Less than 200 mg/dL is desirable. Between 200 and 239 is borderline. Over 240 is high.	70 mg/dL or less is the new goal for very high-risk patients (recent heart attack; current active or unstable cardiovascular or cerebrovascular disease; or two multiple risk factors as defined above.) Below 100 mg/dl is optimal for everyone. It should be the goal for high-risk people including those with existing heart disease, diabetes, or two or more risk factors for heart disease; 70 mg/dL is an optimal goal for these individuals. 130 mg/dl or below for people with two or more risk factors; 100 mg/dL is the optimal goal. 160 mg/dl or less for people at less risk (one or zero risk factors); 130 mg/dL is an optimal goal. Anything over 160 is high, with levels over 190 being very high. LDL levels over 190 require medication even with no other cardiac risk factors present.	Levels above 40 mg/dL are desirable; levels above 60 mg/dL are optimal.	Below 150 mg/dL is normal. 150-199 is borderline high. 200-499 is high. Over 500 is very high.
*Risk factors for heart disease include a family history of early heart problems before age 55 for men (before age 65 for women), smoking, high blood pressure, diabetes, being older (over 45 for men and 55 for women), and having HDL levels below 35 mg/dl. People with two or more of these risk factors may have a 10-year risk of heart attack that exceeds 20%, and may therefore need to aim for LDL levels of 100 mg/dL or below.

Other Lipids. Elevated levels of other fatty molecules (lipids) are also now thought to be important indicators of heart disease risk. Studies are finding an elevated risk for angina and first heart attacks in people with elevated levels of lipoprotein(a), or lp(a). This lipoprotein falls somewhere in density between HDL and LDL and may have some properties that increase the risk for blood clots. Some experts suggest, however, that high levels of lp(a) may merely be markers of late-stage atherosclerosis, not a cause.

High blood pressure, or hypertension, has long been a proven cause of coronary artery disease. Blood pressure is categorized as normal, prehypertensive, and hypertensive (which is further divided as Stage 1 or 2 according to severity). High blood pressure is generally considered to be a blood pressure reading greater than or equal to 140 mm Hg (systolic) or greater than or equal to 90 mm Hg (diastolic). Blood pressure readings in the prehypertension category (120 - 139 systolic or 80 - 89 diastolic) indicate an increased risk for developing hypertension. [See Blood Pressure Ranges table.]

A normal blood pressure reading is 120/80 mm Hg or lower. Most people with high blood pressure should aim for a goal of below 140/90 mm Hg. Patients with certain health problems should aim lower (blood pressure in patients with kidney disease, heart failure, or diabetes should be equal to or lower than 130/80 mm Hg.) [See In-Depth Report #14: High blood pressure.]


Blood Pressure Category	Ranges for Most Adults (systolic/diastolic)
Normal Blood Pressure (systolic/diastolic)	Systolic below 120 mm Hg Diastolic below 80 mm Hg
Prehypertension (Formerly Classified as Normal to High-Normal Blood Pressure)	Systolic 120 to 139 mm Hg Diastolic 80 to 89 mm Hg (NOTE: 139/89 or below should be the minimum goal for everyone. People with diabetes or chronic kidney disease should strive for 130/80 or less.)
Mild Hypertension (Stage 1)	Systolic 140 to 159 mm Hg Diastolic 90 to 99 mm Hg
Moderate-to-Severe Hypertension (Stage 2)	Systolic over 160 mm Hg and/or Diastolic over 100 mm Hg
Note: If one of the measurements is in a higher category than the other, the higher measurement is usually used to determine the stage. For example, if systolic pressure is 165 (Stage 2) and diastolic is 92 (Stage 1), the patient would still be diagnosed with Stage 2 hypertension. It should be strongly noted that a high systolic pressure should be a major focus of concern in most adults.

American obesity is at epidemic levels in all age groups. The effect of obesity on cholesterol levels is complex. Although obesity does not appear to be strongly associated with overall cholesterol levels, among obese individuals triglyceride levels are usually high while HDL (beneficial cholesterol) levels tend to be low, both risk factors for heart disease. Obesity, in any case, has other effects (hypertension, increase in inflammation) that pose major risks to the heart.

Obesity is particularly hazardous when it is one of the components of the metabolic syndrome. This syndrome is diagnosed when three of the following are present: abdominal obesity, low HDL cholesterol, high triglyceride levels, high blood pressure, and insulin resistance. Metabolic syndrome is a pre-diabetic condition that is significantly associated with heart disease and higher mortality rates from all causes. A 2002 study estimated that 24% of the population now has this condition. Obesity is highly linked with type 2 diabetes, in any case. And diabetes itself poses a significant risk for high cholesterol levels and heart disease. [See In-Depth Report #53: Weight control and diet.]

People who are sedentary are almost twice as likely to suffer heart attacks as are people who exercise regularly. Exercise has several effects that benefit the heart and circulation, including improving cholesterol and lipid levels, reducing inflammation in the arteries, assisting weight loss programs, and helping to keep blood vessels flexible and open. Studies continue to show that physical activity and avoiding high-fat foods are the two most successful means of reaching and maintaining heart healthy levels of fitness and weight.

Experts have been attempting to define how much exercise is needed to produce heart benefits. In 2002, a well-conducted study on overweight adults confirmed previous research that reported beneficial changes in cholesterol and lipid levels even when people performed low amounts of moderate or high intensity exercise (walking or jogging 12 miles a week). However, more intense exercise is required to significantly change cholesterol levels, notably by increasing HDL (the so-called good cholesterol). Overweight people who have trouble losing pounds can still achieve considerable heart benefits by exercising. Resistance (weight) training has also been associated with heart protection. Exercises that train and strengthen the chest muscles may prove to be very important for patients with angina.

Some studies suggest that people may gain the greatest heart protection benefit from the total daily amount of energy they expend, rather than from the length of a single exercise session. Therefore, the best way to exercise may be in multiple short bouts of intense exercise, which can be particularly helpful for older people.

Sudden strenuous exercise (such as snow shoveling and mowing lawns) can put people at risk for angina and heart attack. Activities that involve raising the arms above the head may also be risky. Patients with angina should never exercise shortly after eating. People with risk factors for heart disease should seek medical clearance and a detailed exercise prescription. And all people, including healthy individuals, should listen carefully to their bodies for signs of distress as they exercise. [See In-Depth Report #29: Exercise.]

Heart disease and stroke are the leading causes of death in people with diabetes. People with diabetes are at risk for the following heart-risk conditions, and the more of these conditions they have, the worse the outlook:

High blood pressure (hypertension) --up to 75% of cardiovascular problems in people with diabetes may be due to hypertension.
Very unhealthy cholesterol and lipid balances (high triglyceride levels and lower high density lipoprotein).
Blood clotting problems.
Impaired nerve function (neuropathy), which can also damage the heart. In fact, some experts estimate that the mortality rates from neuropathy-related heart conditions ranges from 15 - 53%.

Patients with both diabetes and heart disease may have a higher risk for silent ischemia, a condition in which people have blocked arteries but do not experience the angina, the chest pain that signals heart disease [See In-Depth Report #9: Diabetes - type 1 ; or In-Depth Report #60: Diabetes - type 2.]

Smokers in their 30s and 40s have a heart-attack rate that is five times higher than their nonsmoking peers. Cigarette smoking may be directly responsible for at least 20% of all deaths from heart disease, or about 120,000 deaths annually. Smoking cigars may increase the risk of early death from heart disease, although evidence is much stronger for cigarette smoking. Although heavy cigarette smokers are at greatest risk, a 2002 study suggested that people who smoke as few as three cigarettes a day are at higher risk for blood vessel abnormalities that endanger the heart. Regular exposure to passive smoke also increases the risk of heart disease in nonsmokers. [See In-Depth Report #41: Smoking.]

Eating habits can either protect or hurt the heart. Experts generally agree on the following heart-smart recommendations:

Choose fiber-rich food (whole grains, legumes, nuts) as the main source of carbohydrates, along with a high intake of fresh fruits and vegetables.
Avoid saturated fats (found mostly in animal products) and trans fatty acids (found in hydrogenated fats and many commercial products and fast foods). Choose unsaturated fats, particularly omega-3 fatty acids (found in vegetable and fish oils).
In selecting proteins, choose soy, legumes, poultry, and fish over meat. Fat free and low fat dairy products (skimmed milk, yogurt) are also healthy choices.
Controlling weight, quitting smoking, and exercising are essential companions of any diet program.

After starting any heart healthy diet, it generally takes an average of 3 - 6 months before any noticeable reduction in cholesterol occurs, although some people have reported better levels in as few as 4 weeks. An intensive program may be necessary to achieve significant improvements in cholesterol levels and to reduce other heart risk factors. [See In-Depth Report #43: Heart-healthy diet.]

Stress. The effects of mental stress on heart disease are controversial. Stress can affect the heart when it activates the sympathetic nervous system (the automatic part of the nervous system that affects many organs, including the heart). Some studies suggest an association between acute stress and a higher risk for serious cardiac events, such as heart rhythm abnormalities and heart attacks, in people with heart disease. However, not all studies report strong evidence that stress has any effect on the heart, particularly in people without any history of heart disease. [See In-Depth Report #31: Stress.]

Depression. Depression increases the severity of heart attack and may even impair a patient's response to medication for heart disease. Although people with heart disease may certainly become depressed, this does not explain entirely the link between the two problems. The data now suggest that depression itself may be a true risk factor for heart disease as well as its increased severity. Several studies have suggested that depression has biologic effects on the heart, including blood clotting and heart rate. A study in 2001, for example, reported an association between depression and a greater risk for death from heart problems even in people without a history of heart disease. A 2002 study reported a higher risk for heart failure in women -- although not in men -- with depression. The more severe the depression, the more dangerous to the health, although even mild depression, including feelings of hopelessness, experienced over many years, may harm the heart, even in people with no early signs of heart disease. [See In-Depth Report #8: Depression.]

Benefits of Moderate Drinking. Several studies have found heart protection from moderate intake of alcohol (one or two glasses a day). Moderate alcohol consumption can help boost HDL levels. Alcohol may also prevent blood clots and inflammation. Although red wine is most often cited for healthful properties, any type of alcoholic beverage appears to have similar benefit.

Adverse Effects of Heavy Drinking on the Heart. By contrast, heavy drinking harms the heart; heart disease is the leading cause of death in alcoholics. Evidence suggests that people who consume more than three drinks a day have abnormal blood clotting factors. Heavy alcohol consumption can raise blood pressure, and binge drinking may increase the risk for hemorrhagic stroke (caused by bleeding in the brain). Large doses of alcohol can trigger irregular heartbeats, which can be dangerous in people with existing heart disease.

Pregnant women and people who can't drink moderately should not drink at all.

In 2005, the FDA warned that all nonsteroidal anti-inflammatory drugs (NSAIDs) -- with the exception of aspirin -- carry heart risks. NSAIDs and COX-2 inhibitors may increase the risk for death in patients who have experienced a heart attack. The risk is greatest at higher dosages, but not necessarily for length of time. According to a 2006 Danish study of heart attack survivors, patients do not need to take NSAIDs for long periods of time to be at risk.

NSAIDs include nonprescription drugs like ibuprofen (Advil, Motrin) and prescription drugs like diclofenac (Cataflam, Voltaren). Celecoxib (Celebrex) is currently the only COX-2 inhibitor that is available in the U.S. It has been linked to cardiovascular risks such as heart attack and stroke. Patients who have had heart attacks should talk to their doctors before taking any of these drugs.

A 2006 comprehensive report from the U.S. Agency for Healthcare Quality and Research indicated that both NSAIDs and COX-2 inhibitors pose similar risks for heart attacks. The report found that one particular NSAID, naproxen (Aleve, Naprosyn), may present less risk of heart attack for some patients, but other studies have contradicted this finding. A 2006 Journal of the American Medical Association study suggested that diclofenac (Voltaren, Cataflam) poses a higher risk for heart attack than other NSAIDs.

In 2007, the American Heart Association issued a scientific statement encouraging doctors to change the way they prescribe pain relief medication for patients with or who are at risk for heart disease. The AHA recommends that patients first try non-drug methods of pain relief (physical therapy, exercise, weight loss to reduce stress on joints, and heat or cold therapy). If these methods don’t work, patients should take the lowest possible dose of acetaminophen (Tylenol) or aspirin. COX-2 inhibitors, such as celecoxib (Celebrex), should be the last resort.

Anemia. Anemia has adverse effects on the heart and increases the severity of cardiac conditions, including heart failure and heart attacks.

Iron Overload. An inherited disease called hemochromatosis, in which the intestinal tract absorbs too much iron from food, has been associated with atherosclerosis and heart attack. About 10% of Caucasians carry the gene. There is no strong evidence that excess iron levels in people without hemochromatosis can contribute to heart disease.

Sleep Apnea. Obstructive sleep apnea is a condition in which tissues in the upper throat collapse at intervals during sleep, thereby blocking the passage of air. It has been strongly associated with high blood pressure and obesity, but is also associated with heart disease and heart attacks, regardless of these risk factors. Some evidence suggests that obstructive apneas cause an increase in stiffness and inflammation in the arteries.

Pregnancy Complications. Although women of child-bearing age are generally at low risk of heart attack, pregnancy can increase the risk for women with certain health conditions. Pregnant women who have diabetes, high blood pressure, or coronary artery disease are at greater risk of having a heart attack than healthy pregnant women. Smoking can increase the risk of heart attack during pregnancy by eight times. Pregnant women who are over 40 years old are at much greater risk than younger women.

Diagnosis

When a patient comes to the hospital with chest pain, the following diagnostic steps are usually taken to determine any heart problems, and, if present, their severity.

The patient will report all symptoms so that a health professional can rule out either a non-heart problem or possible other serious accompany conditions.
An electrocardiogram (ECG) reading is taken, which records the waves made the heart. It is the key tool for determining if heart problems are causing chest pain and, if so, how severe they are.
Blood tests showing elevated levels of certain factors (troponins and CK-MB) indicate heart damage. (The doctor will not wait for results, however, before administering treatment if a heart attack is strongly suspected.)
Imaging tests, including echocardiogram and perfusion scintigraphy, help rule out a heart attack if there is any question.

An electrocardiogram (ECG or EKG) measures and records the electrical activity of the heart. The waves measured by the ECG correspond to the contraction and relaxation pattern of the different parts of the heart. Specific waves seen on an ECG are named with letters:

P. The P wave is associated with the contractions of the atria (the two chambers in the heart that receive blood from outside).
QRS. The QRS is a series of waves associated with ventricular contractions. (The ventricles are two major pumping chambers in the heart.)
T and U. These waves follow the ventricular contractions.

Click the icon to see an image of a normal sinus rhythm.

Doctors use a term called the P-Q or P-R interval, which is the time taken for an electrical impulse to travel from the atria to the ventricle.

The most important wave patterns in diagnosing and determining treatment for a heart attack are called ST elevations and Q waves.

Elevated ST Segments: Heart Attack. Elevated ST segments are strong indicators of a heart attack in patients with symptoms and other indicators. They suggest that an artery to the heart is blocked and that the full thickness of the heart muscle is damaged. When this finding coincides with a heart attack, the condition is sometimes referred to as either as a Q-wave myocardial infarction or a STEMI (ST-segment elevation myocardial infarction). STEMI heart attacks are very severe and usually have complete artery blockage. ST-elevations are strong indicators for aggressive treatments (thrombolytic drugs or angioplasty) to reopen blood vessels. (ST segment elevations do not always mean the patient has a heart attack. Also, some patients do not have elevated ST segments. Other factors are important in making a diagnosis.)

Non-Elevated ST Segments: Angina and Acute Coronary Syndrome. A depressed or horizontal ST wave suggests some blockage and the presence of a heart disease, even if there is no angina present. It occurs in about half of patients with other signs of a heart event. This finding, however, is not very accurate, particularly in women, and can occur without heart problems. In such cases, laboratory tests are needed to determine the extent, if any, of heart damage. In general, one of the following conditions may be present:

Stable Angina (blood test results or other tests show no serious problems and chest pain resolves). Most patients with angina can go home. (Between 25 - 50% of people who have angina or silent ischemia have normal ECG readings.)
Acute Coronary Syndrome (ACS). This includes severe and sudden heart conditions that require aggressive treatment but have not developed into a full-blown heart attack. ACS, refers to either unstable angina or NSTEMI (non ST-segment elevation myocardial infarction) -- also referred to as non Q-wave myocardial infarction. Unstable angina is potentially serious, and chest pain is persistent, but blood tests do not show markers for heart attack. With NSTEMI, the blood tests suggest a developing heart attack, but most likely, injury in the arteries is less serious than with a full-blown heart attack.

Nuclear ventriculography (also known as a radionuclide test) uses radioactive materials called tracers to make heart chambers and blood vessels visible. The procedure is noninvasive. It is a reliable measure of severe heart events and can help identify if damage has occurred from a heart attack. A radioactive isotope such as thallium (or technetium) is injected into the patient's vein. The radioactive isotope attaches to red blood cells and passes through the heart in the circulating blood. The isotope can then be traced through the heart using special cameras or scanners. The images may be combined with an electrocardiogram. The patient is tested while resting, then tested again during an exercise stress test. If the scan detects damage, more images are taken 3 or 4 hours later. Damage due to a prior heart attack will persist when the heart scan is repeated. Injury caused by angina, however, will have resolved by that time.

Angiography is an invasive test. It is used for patients who show strong evidence for severe obstruction on stress and other tests and for patients with acute coronary syndrome.

A narrow tube is inserted into an artery, usually in the leg or arm, and then threaded up through the body to the coronary arteries.
A dye is injected into the tube, and an x-ray records the flow of dye through the arteries.
This process provides a map of the coronary circulation, revealing any blocked areas.

Click the icon to see an image of cardiac catheterization.

Click the icon to see an image of dye injected into the coronary arteries.

Major complications include stroke, heart attacks, and kidney damage. These risks are very low (about 0.1%), however, if the procedure is done in an experienced medical center (one that performs at least 300 of these operations every year). Allergic reactions can also occur. The procedure is expensive, and between 10 - 30% of patients who have this procedure have normal results.

Magnetic Resonance Angiography (MRA). MRA is a very promising noninvasive imaging technique that can provide three-dimensional images of the major arteries to the heart and identify disease with high accuracy. Experts believe this approach will eventually be a good alternative to angiography.

Tests that measure kidney function can help predict which patients are at greatest risk of heart attack, stroke, or death from heart disease. Kidney tests measure proteins in the blood that are filtered through the kidneys. These proteins include creatinine and blood urea nitrogen (BUN). A more recent type of kidney test measures the protein cystatin C. Recent research suggests that the cystatin C kidney test may be better at predicting cardiovascular risks in elderly patients.

When heart cells become damaged, they release different enzymes and other molecules into the blood stream. Elevated levels of such markers of heart damage in the blood or urine may help predict a heart attack in patients with severe chest pain and help determine treatment. Some markers include:

Troponins. The proteins cardiac troponin T and I are released when the heart muscle is damaged. Both are proving to be among the best diagnostic indications of heart attacks. They help to identify many individuals with ACS who might otherwise be misdiagnosed.
Creatine kinase myocardial band (CK-MB). CK-MB has been a standard marker, but the MB fraction is not as accurate as troponin levels, since elevated levels can appear in people without heart injury.
Myoglobin. Myoglobin is a protein found in heart muscles. It is released early in the injured heart and may be useful in combination with CK-MB and the troponins.
Newer biomarkers, including C-reactive protein (CRP), homocysteine, B-type natriuretic peptide (BNP), urinary albumin, and fibrinogen.

Several 2006 studies that evaluated how well biomarkers predict the risk of heart events concluded that they do not provide much more useful information than standard risk factors (high blood pressure, unhealthy cholesterol levels, diabetes). At this time, most experts feel that these standard disease risk factors provide the best predictors of the likelihood of developing coronary artery disease, heart attack, or stroke.

Treatment

Treatment options will depend on whether the patient has angina, acute coronary syndrome, or a full-blown heart attack.

Patients who are diagnosed with acute coronary syndrome (ACS) may be at risk for a heart attack. ACS refers to either unstable angina or NSTEMI (non ST-segment elevation myocardial infarction). Unstable angina is potentially serious and chest pain is persistent, but blood tests do not show markers for heart attack. With NSTEMI, the blood tests suggest a developing heart attack, but most likely, injury in the arteries is less serious than with a full-blown heart attack.

Doctors use a patient's medical history, various tests, and the presence of certain factors to help predict which ACS patients are most at risk for developing a more serious condition. The degree of chest pain itself is not necessarily useful for determining the actual damage in the heart.

Depending on how severe the condition is, the patient is then given either medical treatments or more invasive approaches, such as angioplasty. Some experts believe that even if patients with ACS are only given drug therapy, they should still be transferred to centers equipped for angioplasty.

Early supportive treatments are similar for patients who have ACS or those who have had a heart attack.

Oxygen. Oxygen is almost always administered right away, usually through a tube that enters through the nose. The patient is given aspirin if one was not taken at home.

Medications for Relieving Symptoms.

Nitroglycerin. Most patients will receive nitroglycerin after a heart attack, usually under the tongue. Nitroglycerin decreases blood pressure and dilates the blood vessels around the heart, increasing blood flow. Nitroglycerin may be given intravenously in certain cases (recurrent angina, congestive heart failure, or high blood pressure). Some evidence suggests that intravenous administration may help reduce long-term heart muscle changes that can occur after a heart attack. (Patients with very low blood pressure or severely slow heart rate will not receive nitroglycerin.)
Morphine. Morphine not only relieves pain and reduces anxiety but also dilates blood vessels, aiding the circulation of blood and oxygen to the heart. Morphine can decrease blood pressure and slow down the heart. In patients in which such effects may worsen their heart attacks, other drugs such as meperidine (Demerol) or nalbuphine (Nubain) may be used.

Anticlotting Medications. Appropriate anticlotting medications are started immediately in all patients.

Aspirin (antiplatelet drug) should be taken immediately after a heart attack. It can be either swallowed or chewed, but chewing provides more rapid benefit. If the patient has not taken an aspirin at home, it will be given at the hospital.
Clopidogrel (a stronger antiplatelet drug) is usually given along with other anticlotting drugs. It is sometimes used in place of aspirin.
Heparin (an anticoagulant) is usually given to moderate- to high-risk patients. Low-molecular weight heparin (LMWH), such as enoxaparin, is now recommended over standard heparin. Fondaparinux (Arixtra) is another type of blood thinner that is showing promise for treating patients with STEMI (ST-elevation myocardial infarction), a severe type of heart attack. Fondaparinux may also be better than enoxaparin for patients with acute coronary syndrome (ACS).
Glycoprotein IIb/IIIa inhibitors (antiplatelet drugs), most often tirofiban, are added for patients undergoing angioplasty. These drugs include tirofiban (Aggrastat) and abciximab (ReoPro). They are also beneficial for nonsurgical patients with ACS, notably NSTEMI (non ST-segment elevation myocardial infarction).

After a heart attack, clots form in the injured artery within 4 - 6 hours in 90% of patients. Opening a clotted artery as quickly as possible is the best approach to improving survival.

The standard medical and surgical solutions for opening arteries are:

Angioplasty, also called percutaneous coronary intervention (PCI), is standard procedure for opening the arteries. Coronary artery bypass graft (CABG) is sometimes used as an alternative to angioplasty. Angioplasty should be performed no later than 12 hours after a heart attack.
Thrombolytics are known as blood-clot-busting drugs and are the standard medications used to open the arteries. They are administered as soon as possible in centers where angioplasty is not available or in patients who are not good candidates for angioplasty.

The best candidates for either thrombolytic therapy or angioplasty are:

Adults younger than 75 years old with elevated ST segments or indications of bundle branch block (an ECG reading showing an interruption in the electrical pathway within the heart).
Patients whose symptoms occur within 12 hours of treatment.

Specific Candidates for Emergency Angioplasty. Most patients who meet the criteria for either thrombolytic drugs or angioplasty do better with angioplasty (although only in centers equipped to do this procedure).

Good candidates for angioplasty include:

Elderly patients (including those over age 75) who meet the criteria for both approaches tend to do better with angioplasty than thrombolytic therapy
Patients with diabetes who meet the criteria for both approaches
Patients under age 75 who go into shock, provided that angioplasty can be performed within 18 hours of shock (There is no advantage for patients over 75 who are in shock.)

As with thrombolytic treatments, angioplasty is most effective when performed within 12 hours of symptoms, and the sooner the better. Unfortunately not all communities have centers experienced in the procedure. The experience of the medical center's staff is critical for optimal benefits, and not all surgeons are experienced in angioplasty. However, the procedure is becoming increasingly available, and overall mortality rates are improving over time with angioplasty. Patients or their families should be sure their surgeon has performed at least 75 of these procedures and that the medical center has performed at least 200.

Specific Candidates or Non-Candidates for Thrombolytics. People who meet the criteria for either thrombolytics or angioplasty may benefit from thrombolytic drugs even if they have high-risk conditions such as diabetes, high systolic blood pressure less than 180 mm Hg, or a history of heart attack.

Several studies report that women do worse after thrombolytic therapy. Evidence indicates, however, that they are generally older and have more serious medical conditions when they seek treatment. One study also reported that women were given these drugs an average of 14 minutes later than men were. Women on thrombolytic therapy still do better than those not given these drugs. The bottom line is that thrombolytic therapy is life-saving, and appropriate candidates, regardless of age or gender, should not be denied this therapy.

Thrombolytics should be avoided or used with great caution in the following patients:

People older than age 75 -- a 2000 study suggested that their risk of death was 38% higher than patients in their age group who were not given therapy; a higher risk exists in such older patients even if they are otherwise healthy.
Patients with elevated ST segments whose symptoms have continued beyond 12 hours
Pregnant women
People who have experienced recent trauma (especially head injury) or invasive surgery
People with active peptic ulcers
Patients who have been given prolonged CPR
Current users of anticoagulants

Thrombolytics should not be used in the following patients:

Patients who have experienced any recent major bleeding
Patients with low ST segments
Patients with a history of stroke
Patients with uncontrolled high blood pressure

After a heart attack, the patient may need a number of different medications, depending on their risk factors for a future heart attack:

Beta-blockers reduce the oxygen demand of the heart by slowing the heart rate and lowering arterial pressure. They have been proven to help improve survival in patients who have had a heart attack.
Angiotensin converting enzyme (ACE) inhibitors should be given on the first day to all patients, unless there are medical reasons for not taking them.
Calcium channel blockers may provide relief in patients with unstable angina whose symptoms do not respond to nitrates and beta blockers. They are also useful for patients with Prinzmetal's angina.
Statins. Statins are important cholesterol lowering drugs that are beneficial for patients who have experienced a heart attack. They may also have heart-protective properties that go beyond lowering cholesterol.
Atropine. Atropine may be given for a very low heart rate (bradycardia) or signs of atrioventricular (AV) block, in which electric conduction of nerve impulses to specialized muscles in the heart is slowed or interrupted.

Severely ill patients, particularly those in cardiogenic shock (a dangerous condition that includes a drop in blood pressure and other abnormalities) or with heart failure, will be monitored closely and stabilized. Oxygen is administered, and fluids are given or replaced when it is appropriate to either increase or reduce blood pressure. Such patients may be given dopamine, dobutamine, or both. Other treatments depend on the specific condition.

Heart failure. Intravenous furosemide may be administered. Patients may also be given nitrates, and ACE inhibitors, unless they have a severe drop in blood pressure or other conditions that preclude them. Clot-busting drugs or angioplasty may be appropriate and life-saving in many of these patients, although heart failure patients are less likely to be given these treatments.

Cardiogenic Shock. A procedure called intra-aortic balloon counterpulsation (IABP) is proving to help these patients when used in combination with thrombolytic therapy. IABP involves inserting a catheter containing a balloon, which is inflated and deflated within the artery to boost blood pressure. Left ventricular assist devices and early angioplasty might be considered.

An important study published in 2006 in the Journal of the American Medical Association indicated that early surgical intervention is important for patients who have cardiogenic shock. The study found that patients who had angioplasty or bypass surgery within 6 hours of a heart attack complicated by shock had greatly improved odds for long-term survival compared to patients who received intensive medical therapy with clot-busting drugs.

An arrhythmia is a deviation from the heart's normal beating pattern caused when the heart muscle is deprived of oxygen and is a dangerous side effect of a heart attack. A very fast or slow rhythmic heart rate often occurs in patients who have had a heart attack, and is not usually a dangerous sign.

Premature beats or very fast arrhythmias called tachycardia, however, may be predictors of ventricular fibrillation. This is a lethal rhythm abnormality, in which the ventricles of the heart beat so rapidly that they do not actually contract but quiver ineffectually. The pumping action necessary to keep blood circulating is lost.

Preventing Ventricular Fibrillation. People who develop ventricular fibrillation do not always experience warning arrhythmias, and to date, there are no effective drugs for preventing arrhythmias during a heart attack.

Potassium and magnesium levels should be monitored and maintained.
Intravenous beta-blockers followed by oral administration of the drugs may help prevent arrhythmias in certain patients.

Treating Ventricular Fibrillation.

Defibrillators. Patients who develop ventricular arrhythmias are given electrical shocks with defibrillators to restore normal rhythms. Some studies suggest that implantable cardioverter-defibrillators (ICDs) may prevent further arrhythmias in heart attack survivors of these events who are at risk for further arrhythmias. Patients with ICDs should not take fish oil supplements, as they may increase the risk of ventricular fibrillation.
Antiarrhythmic Drugs. Antiarrhythmic drugs include lidocaine, procainamide, or amiodarone. Amiodarone or another antiarrhythmic drug may be used afterward to prevent future events.

Managing Other Arrhythmias. People with an arrhythmia called atrial fibrillation have a higher risk for stroke after a heart attack and should be treated with anticoagulants such as warfarin (Coumadin). Other rhythm disturbances called bradyarrhythmias (very slow rhythm disturbances) frequently develop in association with a heart attack and may be treated with atropine or pacemakers.

[For more information on atrial fibrillation, ICDs, and pacemakers see In-Depth Report #45: Stroke.]

Medications

Thrombolytic, also called clot-busting or fibrinolytic, drugs are now mainstays in the early treatment of many patients with heart attacks. These drugs dissolve the clot, or thrombus, responsible for causing artery blockage and heart-muscle tissue death.

The standard thrombolytic drugs are recombinant tissue plasminogen activators or rt-PAs. They include alteplase (Activase) and reteplase (Retavase). Both are similar in effectiveness, although reteplase is easier to administer. Tenecteplase (TNKase), a newer drug, can be delivered more rapidly than alteplase, and to date, survival rates are similar. Streptokinase (Kabikinase, Streptase) is sometimes used but is somewhat less effective that the others.

The sooner that thrombolytic drugs are given after a heart attack, the better. The benefits of thrombolytics are highest within the first 3 hours. They can still help if given within 12 hours of a heart attack.

A thrombolytic drug, such as alteplase or tenecteplase, is typically given by IV along with heparin, an anticoagulant drug. (Heparin, like aspirin, cannot destroy existing blood clots but can prevent clots from reforming after they are broken up.) Enoproxin, a form of heparin called low-molecular weight heparin, may be more beneficial than standard heparin.

Other anticlotting drugs are being tested in combination with thrombolytic drugs for emergency treatment following a severe heart attack. Several 2005 studies have indicated that the antiplatelet drug clopidogrel (Plavix) can help prevent arteries from reclosing, and a second heart attack, when given along with aspirin and thrombolytic drugs. The studies evaluated patients who received thrombolytic drugs for treatment of STEMI (severe heart attacks with complete artery blockage).

Hemorrhagic stroke, usually occurring during the first day, is the most serious complication of thrombolytic therapy, but fortunately it is rare. Streptokinase given without heparin poses the lowest risk (although it is also less effective than other regimens in restoring blood flow). In general, the mortality rate from bleeding is only 3 in 1,000 patients treated with thrombolytics, whereas 39 patients in 1,000 would die without these clot-busting drugs. Recent evidence suggests that the survival benefits of thrombolytic therapy, particularly in combination with aspirin, last for years.

Anti-clotting drugs that inhibit or break up blood clots are used at every stage of heart disease. They are generally classified as either antiplatelets or anticoagulants. All anti-clotting therapies carry the risk of bleeding, which can lead to dangerous situations, including stroke.

Anti-platelet Drugs. These drugs prevent formation of blood platelets. Platelets are very small disc-shaped blood cells that are important for blood-clotting.

Aspirin. Aspirin is an antiplatelet drug. It is the most common anti-clotting drug and nearly anyone with heart disease is advised to take it daily in low dose.
Thienopyridines. Clopidogrel (Plavix) and ticlopidine (Ticlid) are thienopyridines, another type of anti-platelet drug.
Glycoprotein IIb/IIIa Inhibitors. These powerful blood-thinning drugs include abciximab (ReoPro), eptifibatide (Integrilin), tirofiban (Aggrastat), and lamifiban. They are administered intravenously in the hospital and are used with angioplasty and stent placement. They are proving to be helpful for ACS patients with NSTEMI (non ST-segment elevation myocardial infarction).

Anticoagulants. Anticoagulants thin blood. They include:

Heparin
Fondaparinux (Arixtra)
Warfarin (Coumadin)
Direct thrombin inhibitors such as argatroban (Novastan), danaparoid (Orgaran), and lepirudin (Refludan)

How Anti-Clotting Drugs Are Used For Heart Attacks. Unlike the thrombolytic (clot-busting) drugs, which are used to break up blood clots during a heart attack, anti-clotting drugs are used to prevent blood clots from forming in the first place. Such drugs are sometimes used along with thrombolytics, immediately after a heart attack, and also as on-going maintenance to prevent a heart attack.

Aspirin is given immediately, and heparin is usually started during or at the end of the thrombolytic infusion.
Clopidogrel (Plavix) is given along with aspirin, heparin, and thrombolytic (“clot busting”) drugs as emergency treatment following a heart attack and to prepare for angioplasty surgery. In 2006, the FDA approved clopidogrel for patients who have had a STEMI heart attack and who are not going to have angioplasty. Clopidogrel is also helpful for patients with acute coronary syndrome. A 2006 study suggested that clopidogrel plus aspirin may not work better than aspirin alone in preventing a first heart attack. However, many studies show that clopidogrel is an important treatment for patients who have already had a heart attack. Clopidogrel and aspirin may reduce the risk of a second heart attack by 30%. The combination of clopidogrel (or ticlopidine) and aspirin is essential for patients who have a drug-eluting stent. In 2007, the American Heart Association recommended that patients with drug-eluting stents take this drug combination for at least 1 year after the stent is inserted to reduce the risks of blood clots.

All of these drugs pose a risk for bleeding. [See In-Depth Report #03: Coronary artery disease.]

Beta-blockers reduce the oxygen demand of the heart by slowing the heart rate and lowering pressure in the arteries. They are effective for reducing deaths from heart disease. These drugs include propranolol (Inderal), carvedilol (Coreg), bisoprolol (Zebeta), acebutolol (Sectral), atenolol (Tenormin), labetalol (Normodyne, Trandate), metoprolol (Lopressor, Toprol-XL), and esmolol (Brevibloc).

Administration During a Heart Attack. The beta-blocker metoprolol is given through an IV within the first few hours of a heart attack to reduce the destruction of heart tissue. However, a study suggests that emergency intravenous use of metoprolol may increase the risk of cardiac shock.

Prevention After a Heart Attack. Beta-blockers taken by mouth are also used on a long-term basis (“maintenance therapy”) after a first heart attack to help prevent future heart attacks.

Side Effects. Beta-blocker side effects include fatigue, lethargy, vivid dreams and nightmares, depression, memory loss, and dizziness. They can lower HDL (“good”) cholesterol. Beta-blockers are categorized as non-selective or selective. Non-selective beta-blockers such as carvedilol and propranolol can narrow bronchial airways. These beta-blockers should not be used by patients with asthma, emphysema, or chronic bronchitis.

Patients should not abruptly stop taking these drugs. The sudden withdrawal of beta-blockers can rapidly increase heart rate and blood pressure. The doctor may want the patient to slowly decrease the dose before stopping completely.

In 2004, the National Cholesterol Education Program issued updated recommendations on how to control cholesterol levels. These guidelines emphasize that patients should lower their LDL (“bad”) cholesterol and recommend that more people take LDL-lowering medication. Lowering LDL cholesterol and raising HDL (“good”) cholesterol can significantly reduce the risk of heart disease. Several different types of drugs (statins, bile-acid binding resins, niacin, and fibrates) are used to treat cholesterol. [See In-Depth Report #23: Cholesterol.]

Statins are the most important of these drugs. Brands include lovastatin (Mevacor), pravastatin (Pravachol), simvastatin (Zocor), fluvastatin (Lescol), atorvastatin (Lipitor), and rosuvastatin (Crestor). A major analysis of over 200 studies found that statins reduced the risk for heart problems by 60% and stroke by 17%. A 2005 review found that the more that statins lower LDL, the more they reduce CAD and other heart disease risks.

An important 2006 study found that aggressive treatment with statins may have the potential to reverse coronary artery disease. In the study, rosuvastatin reduced fatty plaque in the arteries in addition to improving LDL and HDL cholesterol levels. However, a follow-up 2007 study of rosuvastatin indicated that while the drug slowed the rate of atherosclerotic progression, it did not reverse heart disease. Future studies will continue to investigate this issue.

A 2006 review of studies indicated that early, intensive therapy with statins can help reduce the risk of death, unstable angina, and revascularization (surgery to restore blood flow) for patients with acute coronary syndrome. The review indicated that statins work best when they are prescribed within 14 days of hospitalization for acute coronary syndrome. The researchers found that the effect of statins began about 4 months after starting drug therapy and that benefits lasted up to 2 years.

Side effects of statins may include stomach upset, headaches, skin rashes, muscle aches, sexual dysfunction, drowsiness, dizziness, nausea, constipation, and peripheral neuropathy (numbness or tingling in the hands and feet).

The main safety concern with statins is an uncommon condition called myopathy, which can cause muscle and joint pain and possible muscle damage. Doctors will immediately stop statin therapy if myopathy occurs. Patients should talk to their doctor about any unusual muscle discomfort or weakness or if their urine becomes brown-colored. Statins can also affect the liver, particularly at higher doses, so patients taking these drugs should receive regular liver function tests.

Angiotensin converting enzyme (ACE) inhibitors are important drugs for treating patients who have had a heart attack, particularly for patients at risk for heart failure. These drugs are commonly used to treat hypertension and are recommended as first-line treatment for people with diabetes and kidney damage.

ACE inhibitors include captopril (Capoten), ramipril (Altace), enalapril (Vasotec), quinapril (Accupril), benazepril (Lotensin), perindopril (Aceon), and lisinopril (Prinivil, Zestril).

Magnesium has blood-thinning properties and may help open blood vessels. It is important to correct any magnesium deficiencies in patients (such as those who are taking diuretics).

Flu Shots. Influenza vaccinations may help protect patients against another heart attack during flu season.

Antibiotics. Researchers have investigated antibiotics for treating patients with heart disease and past infection of the bacteria Chlamydia pneumoniae. Results from several large-scale clinical trials, published in 2003 in the Journal of the American Medical Association (JAMA) and presented in 2004 at the European Society of Cardiology annual meeting, suggest that antibiotic treatment provides no benefit in preventing heart attack or other cardiac events in patients with coronary artery disease. While it is still possible that C. pneumoniae may play a role in triggering inflammatory responses associated with ACS, antibiotic therapy is no longer considered appropriate for treatment or prevention of heart disease.

Stem Cell Therapy. Researchers are investigating whether infusions of adult stem cells can help improve outcomes in patients who have a heart attack. Results from three small trials, published in 2006 in the New England Journal of Medicine, suggested that stem cell therapy may have some benefits in improving heart function. None of the studies reported treatment complications. Research presented at the 2007 American College of Cardiology annual meeting discussed intravenous stem cell therapy with Provacel (a commercial stem cell preparation). In the small study, patients who received Provacel had fewer adverse events (such as arrhythmia) and improved heart, lung, and overall function compared to patients who received placebo. Patients in the study received a Provacel infusion within 10 days of having a heart attack.

Surgery

Percutaneous coronary intervention (PCI), also called angioplasty, and coronary artery bypass graft surgery are the standard operations for opening narrowed or blocked arteries. They are known as revascularization procedures.

Emergency angioplasty is the standard procedure for heart attacks. It should be performed within 12 hours of a heart attack. Clot-buster drugs can help prevent damage, but must be given with 1 hour of a heart attack.
Coronary bypass surgery is typically used as elective surgery for patients with blocked arteries. It may be used after a heart attack if angioplasty or thrombolytics fail or are not appropriate. It is usually not performed for a few days to allow recovery of the heart muscles.

Click the icon to see an illustrated series detailing a heart bypass surgery.

Percutaneous coronary intervention (PCI), also called angioplasty, involves procedures such as percutaneous transluminal coronary angioplasty (PTCA) that help open the blocked artery. A typical angioplasty procedure involves the following steps:

Click the icon to see an image of an angioplasty.

The cardiologist threads a narrow catheter (a tube) containing a fiber into the blocked vessel.
The cardiologist opens the blocked vessel using balloon angioplasty, in which a tiny deflated balloon is passed through the catheter to the vessel.
The balloon is inflated to compress the plaque against the walls of the artery, flattening it out so that blood can once again flow through the blood vessel freely.
The balloon is inflated to compress the plaque against the walls of the artery, flattening it out so that blood can once again flow through the blood vessel freely.
To keep the artery open afterwards, doctors use a device called a coronary stent, an expandable metal mesh tube that is implanted during angioplasty at the site of the blockage.
Once in place, the stent pushes against the wall of the artery to keep it open. Stenting is improving results in patients with heart attack who have emergency angioplasty. It also significantly prevents reclosure and reduces heart attack rates in patients with ACS.

Experts recommend that appropriate patients receive angioplasty and stenting within 90 minutes after having a heart attack and no later than 12 hours following an attack. Although some hospitals have been performing angioplasty and stenting for up to a month following a heart attack, a landmark 2006 study found that delayed surgical intervention is not helpful for most patients. The Occluded Artery Trial (OAT), published in the New England Journal of Medicine, reported that balloon angioplasty and stenting failed to prevent heart complications in patients who received the procedure 3 – 28 days after a heart attack. The trial compared angioplasty to medications (aspirin, ACE inhibitors, beta-blockers, statins, clopidogrel).

Experts are now recommending delayed angioplasty and stenting only for patients who are unstable or who continue to have chest pain following a heart attack. This procedure may also be appropriate for patients who cannot tolerate beta-blocker drugs, which are commonly prescribed to help improve survival after a heart attack.

Complications occur in about 10% of patients (about 80% within the first day). Serious side effects include heart attack and the need for additional surgery. Best results occur in hospital settings with experienced teams and backup. Women who have angioplasty after a heart attack have a higher risk of death than men.

Reclosure and Blockage During or Shortly after Angioplasty. Reclosure of the artery often occurs during or shortly after angioplasty. A number of anticlotting drugs are used to reduce this risk. Clopidogrel (Plavix) is often given along with aspirin and thrombolytic drugs (such as abciximab) in the days before angioplasty surgery, to help prevent heart attack or stroke following surgery. Research suggests that abciximab (ReoPro) is especially helpful for patients with acute coronary syndrome.

Prevention of Restenosis. Narrowing or reclosing of the artery (restenosis) occurs within a year of angioplasty in many angioplasty patients, often requiring a repeat operation. In restenosis, the narrowing of the artery is usually due to scarring, not blood clots. Drug-eluting stents, which are coated with sirolimus (Rapamune) or paclitaxel (Taxol), can help prevent restenosis. Several 2006 studies indicated that this type of stent may be better than a bare metal stent for patients who have experienced a STEMI heart attack. However, because drug-eluting stents reduce arterial tissue growth, they can increase the risks of blood clots.

In February 2007, the American Heart Association and other professional organization issued an extremely important joint advisory statement. The statement advises that all patients who have drug-eluting stents must continue to take aspirin and clopidogrel (or, rarely,) ticlopidine for at least 1 year after the stent is inserted to reduce the risk of blood clots. Clopidogrel and ticlopidine are thienopyridine drugs that, like aspirin, help prevent blood platelets from clumping together. It is very important that patients who have drug-eluting stents take both aspirin and a thienopyridine drug. If for some reason patients cannot take a thienopyridine drug, they should receive a bare metal stent instead of a drug-eluting stent. [See In-Depth Report #03: Coronary artery disease.]

Click the icon to see an illustrated series detailing balloon angioplasty.

Coronary artery bypass graft surgery (CABG) is the alternative elective procedure to angioplasty for opening blocked arteries in patients with severe angina, particularly those who have two or more blocked arteries. It is a very invasive procedure, however:

The chest is opened, and the blood is rerouted through a lung-heart machine.
The heart is stopped during the procedure.
Segments of veins or arteries taken from elsewhere in the patient's body are fashioned into grafts, which are used to reroute the blood. The blood vessel grafts are placed in front of and beyond the blocked arteries, so the blood flows through the new vessels around the blockage.

Mortality rates with this procedure after a heart attack are much higher (6%) than when it is used electively (1 - 2%). How or when it should be used after a heart attack, then, is controversial. A 2002 study attempted to determine which patients are at highest risk for poor results from CABG after a heart attack. The study found higher risks for women, patients over age 75, and those with heart failure or other severe heart problems.

Rehabilitation

Lifestyle measures, particularly dietary factors, are equally important in preventing heart attacks and must be strenuously adhered to.

Physical rehabilitation is extremely important after a heart attack. It has been associated with a 25% reduction in mortality rates at 3 years. Rehabilitation may include:

Leg exercises may start as early as the first day. The patient usually sits in a chair on the second day, and begins to walk on the second or third day.
Most patients undergo low-level exercise tolerance tests early in their recovery. One study suggests that exercise testing within 3 days after a relatively minor attack may allow patients to go home earlier.
After 8 - 12 weeks, many patients, even those with heart failure, benefit from supervised exercise programs. Health professionals should provide the patient with schedules for low-level aerobic home-activity. Strength (resistance) training is also important. Tai Chi, a Chinese martial art, appears to be very beneficial and safe for people after a heart attack. It should be noted that the risk for serious heart events during rehabilitation is very low.

Patients generally return to work in about 2 months, although timing can vary depending on the severity of the condition.

Sexual activity after a heart attack carries a very low risk and is believed to be safe, particularly in people who had exercised regularly before the attack. In any case, the feelings of intimacy and love that accompany healthy sex can help offset depression, a far greater risk for a future attack.

Major depression affects between 15 - 23% of patients with ACS or heart attacks. Many studies suggest that depression is a major predictor for increased mortality in both women and men. (One reason may be that depressed patients are less likely to comply with their heart medications.)

Psychotherapeutic techniques, especially cognitive behavioral therapies, are very helpful. Doctors have been reluctant to prescribe antidepressant drugs after ACS or a heart attack because older antidepressants tended to have adverse effects on the heart. Newer antidepressants may be safer. Studies on sertraline (Zoloft), one of the selective serotonin reuptake inhibitor (SSRI) antidepressants, have not reported harmful effects for patients who have had a heart attack. It is not yet clear if other SSRIs are equally safe and effective.

Resources

www.nhlbi.nih.gov -- National Heart, Lung, and Blood Institute
www.acc.org -- American College of Cardiology
www.americanheart.org -- American Heart Association

References

Antman EM, Bennett JS, Daugherty A, Furberg C, Roberts H, Taubert KA. Use of nonsteroidal antiinflammatory drugs: an update for clinicians: a scientific statement from the American Heart Association. Circulation. 2007 Mar 27;115(12):1634-42. Epub 2007 Feb 26.

Assmus B, Honold J, Schachinger V, Britten MB, Fischer-Rasokat U, et al. Transcoronary transplantation of progenitor cells after myocardial infarction. N Engl J Med. 2006 Sep 21;355(12):1222-32.

Chou R, Helfland M, Peterson K, Dana T, Roberts C. Comparative Effectiveness and Safety of Analgesics for Osteoarthritis. Comparative Effectiveness Review No. 4. (Prepared by the Oregon Evidence-based Practice Center under Contract No. 290-02-0024.) Rockville, MD: Agency for Healthcare Quality and Research. September 2006.

Crouse JR 3rd, Raichlen JS, Riley WA, Evans GW, Palmer MK, O'Leary DH, et al. Effect of rosuvastatin on progression of carotid intima-media thickness in low-risk individuals with subclinical atherosclerosis: the METEOR Trial. JAMA. 2007 Mar 28;297(12):1344-53. Epub 2007 Mar 25.

Eisenstein EL, Anstrom KJ, Kong DF, Shaw LK, Tuttle RH, Mark DB, et al. Clopidogrel use and long-term clinical outcomes after drug-eluting stent implantation. JAMA. 2007 Jan 10;297(2):159-68. Epub 2006 Dec 5.

Folsom AR, Chambless LE, Ballantyne CM, Coresh J, Heiss G, Wu KK, et al. An assessment of incremental coronary risk prediction using C-reactive protein and other novel risk markers: the atherosclerosis risk in communities study. Arch Intern Med. 2006 Jul 10;166(13):1368-73.

Gislason GH, Jacobsen S, Rasmussen JN, Rasmussen S, Buch P, Friberg J, et al. Risk of death or reinfarction associated with the use of selectivecyclooxygenase-2 inhibitors and nonselective nonsteroidal antiinflammatory drugs after acute myocardial infarction. Circulation. 2006 Jun 27;113(25):2906-13. Epub 2006 Jun 19.

Grines CL, Bonow RO, Casey DE Jr, Gardner TJ, Lockhart PB, Moliterno DJ, et al. Prevention of premature discontinuation of dual antiplatelet therapy in patients with coronary artery stents: a science advisory from the American Heart Association, American College of Cardiology, Society for Cardiovascular Angiography and Interventions, American College of Surgeons, and American Dental Association, with representation from the American College of Physicians. Circulation. 2007 Feb 13;115(6):813-8. Epub 2007 Jan 15.

Hulten E, Jackson JL, Douglas K, George S, Villines TC. The effect of early, intensive statin therapy on acute coronary syndrome: a meta-analysis of randomized controlled trials. Arch Intern Med. 2006 Sep 25;166(17):1814-21.

Hochman JS, Lamas GA, Buller CE, Dzavik V, Reynolds HR, Abramsky SJ, et al. Coronary intervention for persistent occlusion after myocardial infarction. N Engl J Med. 2006 Dec 7;355(23):2395-407. Epub 2006 Nov 14.

Hochman JS, Sleeper LA, Webb JG, Dzavik V, Buller CE, Aylward P, et al. Early revascularization and long-term survival in cardiogenic shock complicating acute myocardial infarction. JAMA. 2006 Jun 7;295(21):2511-5.

Kearney PM, Baigent C, Godwin J, Halls H, Emberson JR, Patrono C. Do selective cyclo-oxygenase-2 inhibitors and traditional non-steroidal anti-inflammatory drugs increase the risk of atherothrombosis? Meta-analysis of randomised trials. BMJ. 2006 Jun 3;332(7553):1302-8.

Kostis WJ, Demissie K, Marcella SW, Shao YH, Wilson AC, Moreyra AE. Weekend versus weekday admission and mortality from myocardial infarction. N Engl J Med. 2007 Mar 15;356(11):1099-109.

Laarman GJ, Suttorp MJ, Dirksen MT, van Heerebeek L, Kiemeneij F, Slagboom T, et al. Paclitaxel-eluting versus uncoated stents in primary percutaneous coronary intervention. N Engl J Med. 2006 Sep 14;355(11):1105-13.

Lloyd-Jones DM, Liu K, Tian L, Greenland P. Narrative review: Assessment of C-reactive protein in risk prediction for cardiovascular disease. Ann Intern Med. 2006 Jul 4;145(1):35-42.

Lunde K, Solheim S, Aakhus S, Arnesen H, Abdelnoor M, Egeland T, et al. Intracoronary injection of mononuclear bone marrow cells in acute myocardial infarction. N Engl J Med. 2006 Sep 21;355(12):1199-209.

McGettigan P, Henry D. Cardiovascular risk and inhibition of cyclooxygenase: a systematic review of the observational studies of selective and nonselective inhibitors of cyclooxygenase2. JAMA. 2006 Oct 4;296(13):1633-44. Epub 2006 Sep 12.

Nicholls SJ, Tuzcu EM, Sipahi I, Grasso AW, Schoenhagen P, Hu T, et al. Statins, high-density lipoprotein cholesterol, and regression of coronary atherosclerosis. JAMA. 2007 Feb 7;297(5):499-508.

Schachinger V, Erbs S, Elsasser A, Haberbosch W, Hambrecht R, Holschermann H, et al. Intracoronary bone marrow-derived progenitor cells in acute myocardial infarction. N Engl J Med. 2006 Sep 21;355(12):1210-21.

Spaulding C, Henry P, Teiger E, Beatt K, Bramucci E, Carrie D, et al. Sirolimus-eluting versus uncoated stents in acute myocardial infarction. N Engl J Med. 2006 Sep 14;355(11):1093-104.

Spertus JA, Kettelkamp R, Vance C, Decker C, Jones PG, Rumsfeld JS, et al. Prevalence, predictors, and outcomes of premature discontinuation of thienopyridine therapy after drug-eluting stent placement: results from the PREMIER registry. Circulation. 2006 Jun 20;113(24):2803-9. Epub 2006 Jun 12.

Wang TJ, Gona P, Larson MG, Tofler GH, Levy D, Newton-Cheh C, et al. Multiple biomarkers for the prediction of first major cardiovascular events and death. N Engl J Med. 2006 Dec 21;355(25):2631-9.

Review Date:
4/16/2007
Reviewed By:
Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

A.D.A.M. Copyright

adam.com

Coronary artery disease

FitSugar — Wed, 08 Oct 2008 17:35:07 -0700

In This Report

Highlights
Introduction
Prognosis
Risk Factors
Diagnosis
Managing Heart Disease
Anti-Clotting Medications...
Other Medications
Surgery
Coronary Artery Bypass Graf...
Angioplasty and Stents
Other Treatments
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Angioplasty Versus Drugs

Angioplasty works no better than drug therapy (high blood pressure, cholesterol, anti-platelet, and other medication) in preventing heart attack and stroke in patients with stable coronary artery disease (CAD), according to an important New England Journal of Medicine study. Experts still recommend angioplasty for patients with unstable or severe CAD.

Stents

Stents coated with drugs may have a slightly higher risk of causing blood clots than bare metal stents, according to FDA meetings held in late 2006. Researchers still need to conduct more research before reaching final conclusions.
Drug-coated stents work well when they are used for patients with specific types of heart conditions, indicate several studies published in the New England Journal of Medicine. However, problems may develop when these stents are used for “off-label” purposes. Experts are also concerned that both bare metal and drug-coated stents may be used too frequently.
Patients who receive a drug-coated stent must take both aspirin and an anti-platelet thienopyridine drug (usually clopidogrel) for at least 1 year after the stent is inserted, advises an important statement from the American Heart Association. Patients who cannot take a thienopyridine drug should receive a bare metal stent instead of a drug-coated stent.

Anti-Bleeding Drugs for Coronary Artery Bypass Graft (CAGB)

Aprotinin (Trasylol), a drug used to control bleeding during CABG, is more dangerous than other types of anti-bleeding drugs, according to a 2007 study in the Journal of the American Medical Association. Many experts now recommend against its use.

Diagnosis

Blood tests for biomarkers do not provide much more predictive information than standard disease risk factors, suggest several recent studies. In a 2006 study published in the New England Journal of Medicine, researchers found that risk factors such as high blood pressure, high cholesterol, and diabetes are still the best methods for predicting the likelihood of heart disease and heart-related death.

Introduction

In order to perform the difficult task of pumping blood to the rest of the body, the heart muscle itself needs a plentiful supply of oxygen-rich blood, which is provided through a network of coronary arteries. These arteries carry oxygen-rich blood to the heart's muscular walls (the myocardium).

Click the icon to see an image of the anterior heart arteries.

If blood flow to the myocardium is interrupted, an injury known as an infarct occurs. This is also known as myocardial infarction or, more commonly, a heart attack.

Click the icon to see an animation about coronary artery disease.

Coronary artery disease is the end result of a complex process called atherosclerosis (commonly called "hardening of the arteries"). This causes blockage of arteries (ischemia ) and prevents oxygen-rich blood from reaching the heart. There are many steps in the process leading to atherosclerosis, some not fully understood.

Click the icon to see an image of atherosclerosis.

Increasingly, however, researchers are studying the interactions between cholesterol and processes known as oxidation and the inflammatory response.

Cholesterol and Lipoproteins. The story begins with cholesterol and sphere-shaped bodies called lipoproteins that transport cholesterol.

Cholesterol is a white, crystalline substance that is found in all animal cells and in animal-based foods. It is critical for many functions, but under certain conditions cholesterol can have harmful effects.
The lipoproteins that transport cholesterol are referred to by their size. The most commonly known are low-density lipoproteins (LDL) and high density lipoproteins (HDL). LDL is often referred to as the "bad" cholesterol and HDL as the "good" cholesterol.

Click the icon to see an image of cholesterol inside an artery.

Oxidation. The damaging process called oxidation is an important trigger in the atherosclerosis story.

Oxidation is a chemical process in the body caused by the release of unstable particles known as oxygen-free radicals. It is one of the normal processes in the body, but under certain conditions (such as exposure to cigarette smoke or other environment stresses) these free radicals are overproduced.
In excess amounts, they can be very dangerous, causing damaging inflammation and even affecting genetic material in cells.
In heart disease, free radicals are released in artery linings and oxidize low-density lipoproteins (LDL). The oxidized LDL is the basis for cholesterol build-up on the artery walls and damage leading to heart disease.

Inflammatory Response. For the arteries to harden there must be a persistent reaction in the body that causes ongoing harm. Researchers now believe that this reaction is an immune process known as the inflammatory response. The following is one theory about how the inflammatory response contributes to heart disease:

The injuries to the arteries during oxidation signal the immune system to release white blood cells (particularly those called neutrophils and macrophages) at the site. These factors initiate the inflammatory response.
Macrophages literally "eat" foreign debris, in this case oxidized LDL cholesterol.
The process converts LDL cholesterol into foamy material that attaches to the smooth muscle cells of the arteries. The cholesterol becomes mushy and accumulates on artery walls.
Over time the cholesterol dries and forms a hard plaque, which causes further injury to the walls of the arteries.
In response to this additional harm, the immune system releases other factors called cytokines. These are powerful inflammatory molecules that attract more white blood cells and perpetuate the whole cycle, causing persistent injury to the arteries.

Click the icon to see an image of atherosclerosis.

Evidence is growing that the inflammatory response may be present not only in local plaques in single arteries but also throughout the arteries leading to the heart.

Blockage in the Arteries. Eventually these calcified (hardened) arteries become narrower (a condition known as stenosis).

As this narrowing and hardening process continues, blood flow slows and prevents sufficient oxygen-rich blood from reaching the heart.
Such oxygen deprivation in vital cells is called ischemia. When it affects the coronary arteries, it causes injury to the tissues of the heart.
Injured inner vessel walls also fail to produce enough nitric oxide, a substance critical for maintaining blood vessel elasticity. (Nitric oxide has complex effects and may increase inflammation in the arteries.)
These narrow and inelastic arteries not only slow down blood flow but also become vulnerable to injury and tears.

Click the icon to see an image of coronary artery blockage

The End Result: Heart Attack. Heart attack can occur as a result of one or two effects of atherosclerosis.

(1) If the artery becomes completely blocked and ischemia becomes so extensive that oxygen-bearing tissues around the heart die.

Click the icon to see an image of the developmental process of atherosclerosis.

Angina is the primary symptom of coronary artery disease and, in severe cases, of a heart attack. It is typically experienced as chest pain and occurs when the heart muscle does not get as much blood (hence as much oxygen) as it needs for a given level of work (ischemia). Angina is usually referred to as one of two states:

Click the icon to see an image about angina.

Stable Angina (which is predictable)
Unstable Angina (which is less predictable and a sign of a more serious situation)

Angina itself is not a disease. Much evidence indicates that onset of angina less than 48 hours before a heart attack may be protective, possibly by conditioning the heart to resist the damage resulting from the attack. Angina may be experienced in different ways and can be mild, moderate, or severe.

Click the icon to see an image of angina.

Specific factors are typically considered in determining whether symptoms indicate angina:

Quality of the pain. Angina pain is typically described by patients as squeezing, heavy, suffocating, or griplike. It is rarely described as stabbing or burning. Changing one's position or breathing in and out does not affect the pain. The intensity of the pain does not always relate to the severity of the medical problem. Some people may feel a crushing pain from mild ischemia, while others might experience only mild discomfort from severe ischemia. In some cases, the patient experiences shortness of breath, fatigue, or palpitations instead of pain. In others, the ischemia is entirely asymptomatic ("silent ischemia").
Duration. A typical angina attack lasts minutes. If it is more fleeting or lasts for hours, it is probably not angina.
Location. Pain is usually in the chest under the breast bone. It often radiates to the neck, jaw, or left shoulder and arm. Less commonly, patients report symptoms that radiate to the right arm or back.
Triggers of Angina. Angina is usually triggered by physical exertion, emotional stress, or exposure to cold.
Factors that Relieve Angina. Angina is usually relieved by rest or by taking nitroglycerine under the tongue.

Stable Angina. Stable angina is predictable chest pain. Although less serious than unstable angina, it can be extremely painful. It is usually relieved by rest and responds well to medical treatment (typically nitroglycerin). Any event that increases oxygen demand can cause an angina attack. Some typical triggers include:

Exercise
Cold weather
Emotional tension
Large meals

Angina attacks can occur at any time during the day, but most occur between 6 a.m. and noon.

Unstable Angina and Acute Coronary Syndrome. Unstable angina is a much more serious situation and is often an intermediate stage between stable angina and a heart attack, in which an artery leading to the heart (a coronary artery) becomes completely blocked. A patient is usually diagnosed with unstable angina under one or more of the following conditions:

Pain awakens a patient or occurs during rest.
A patient who has never experienced angina has severe or moderate pain during mild exertion (walking two level blocks or climbing one flight of stairs).
Stable angina has progressed in severity and frequency within a 2-month period, and medications are less effective in relieving its pain.

Unstable angina is now usually discussed as part of a condition called acute coronary syndrome (ACS). ACS also includes people with a condition called NSTEMI (non ST-segment elevation myocardial infarction) -- also referred to as non-Q wave heart attack. With NSTEMI, the blood tests suggest a developing heart attack. These conditions are less severe than heart attacks but may develop into full-blown attacks without aggressive treatment. [See In-Depth Report #12: Heart attack and acute coronary syndrome.]

Prinzmetal's Angina. A third type of angina, called variant or Prinzmetal's angina, is caused by a spasm of a coronary artery. It almost always occurs when the patient is at rest. About two-thirds of people with it have severe atherosclerosis in at least one major blood vessel. Irregular heartbeats are common, but the pain is generally relieved immediately with standard treatment.

Click the icon to see an image of a coronary artery spasm.

Silent Ischemia. Some people with severe coronary artery disease do not experience angina pain. This condition is known as silent ischemia, which some experts attribute to abnormal processing of heart pain by the brain. This is a dangerous condition because patients have no warning signs of heart disease. Some studies suggest that people with silent ischemia experience higher complication and mortality rates than those with angina pain. (Angina pain may actually protect the heart by conditioning it before a heart attack.)

Syndrome X. Syndrome X is a condition that occurs when patients have atypical angina chest pain. Their electrocardiograms are abnormal during a stress test, but they have no signs of blocked arteries. It is more likely to occur in women. Although it unclear what causes this condition, imaging tests suggest that Syndrome X may also be caused by ischemia, as is angina.

Prognosis

According to a 2007 report, nearly 16 million Americans have coronary artery disease. In the U.S., coronary artery disease is the leading killer of both men and women. In 2004, nearly 500,000 people died because of CAD. On the positive side, heart attack mortality rates have been declining. Half of men and 63% of women who die of heart disease do not have angina or other warning symptoms prior to their fatal attacks. Although at this time no tests can reliably predict whether a heart attack will occur, experts estimate that up to 30% of fatal attacks and many follow-up surgeries could be avoided with healthy lifestyle changes and by sticking to medical treatments. Two-thirds of patients who have suffered a first heart attack, however, do not take the necessary steps to prevent another.

The following syndromes suggest different degrees of severity among patients with heart disease.

Stable Angina. This condition can usually be managed with lifestyle measures and medications, such as low-dose aspirin. The more severe the angina, however, the greater the chance for progressing to a more serious condition.

Acute Coronary Syndromes (ACS). ACS includes severe and sudden heart conditions that require aggressive treatment but have not developed into a full-blown heart attack. ACS refers to either unstable angina or NSTEMI (non ST-segment elevation myocardial infarction). NSTEMI is also known as non Q-wave myocardial infarction.

Angina is a specific type of pain in the chest caused by inadequate blood flow through the blood vessels (coronary vessels) of the heart muscle (myocardium).

Unstable angina is potentially serious and chest pain is persistent, but blood tests do not show markers for heart attack.
With NSTEMI, the blood tests suggest a developing heart attack, but, most likely, injury in the arteries is less serious than with a full-blown heart attack.

Most discussions of the treatment of unstable angina now refer to acute coronary syndrome. Doctors use the presence of a number of factors to help predict which ACS patients are most at risk for developing a heart attack.

First, patients are categorized by whether they have a history of heart disease or risk factors for heart disease (such as diabetes, high blood pressure, peripheral artery disease) or other complicating conditions (such as lung disease, heart failure). The doctor also evaluates the severity of the angina. Other factors that pose a high risk for ACS include:

Age 65 years or older
Evidence of severe heart tissue injury
Having a lighter weight
Having a history of severe chronic angina
Having abnormal lung sounds called rales (a bubbling or crackling sound) on examination
ST-segment deviation
Having either very slow or very fast heat beats
Having very low blood pressure

Heart Attack. A full-blown heart attack occurs with severe damage to the heart, which blocks oxygen.

ANYONE WHO BELIEVES THEY ARE HAVING A HEART ATTACK SHOULD IMMEDIATELY CALL THE EMERGENCY MEDICAL SYSTEM (911 IN THE UNITED STATES).

People with known heart disease and any unusual chest pain or other symptoms of heart attack that do not clear up with medications should go to the hospital. The degree of pain and the specific symptoms before a heart attack vary greatly among individuals. Symptoms can be abrupt, gradual, or intermittent.

Pain is typically felt as a crushing weight against the chest, accompanied by profuse sweating. The pain may radiate to the left shoulder and arm, the neck or jaw, and even infrequently to the right arm. The arm may be tingling or numb.
Some people may have only a tingling sensation or a sense of fullness, squeezing, or pressure in the chest.
In some patients with a history of heart disease, chest pain is mild. Such patients may have experienced unexplained fatigue, depression, and ill health within a month of a heart attack. Although chest pain is the classic symptom, it occurs in only about half of patients with a heart attack.

Other Common Symptoms.

Nausea, vomiting, and cold sweats
A feeling of indigestion or heartburn
Fainting
A great fear of impending death, a phenomena known as angor animi

Atypical Symptoms. Some studies suggest that nearly half of patients with heart attack do not have chest pain as the primary symptom. Common atypical symptoms of a heart attack include:

Shortness of breath
Cardiac arrest
Dizziness, weakness, and fainting
Abdominal pain

Patients most likely to have atypical symptoms are women and the very elderly (although they can certainly have classic heart attack symptoms as well).

In one study, 52% of elderly people with acute coronary syndrome had atypical symptoms that included shortness of breath, nausea, profuse sweating, pain in the arms, and fainting. Such symptoms were more likely to occur in people with personal or family history of heart disease.
Before a heart attack, women are more likely than men to be nauseous and experience pain high in the abdomen or chest. Their first symptom may be extreme fatigue after physical activity rather than chest pain. Chest pain in women is also more likely to be caused by non-heart problems than in men.

Symptoms That Are Less Likely to Indicate a Heart Attack. The following symptoms are less likely to be due to a heart attack:

Sharp pain brought on by lung movements or coughing
Pain that is mainly or only in the middle or lower abdomen
Pain that can be pinpointed with the top of one finger
Pain that can be reproduced by moving or pressing on the chest wall or arms
Pain that is constant and lasts for hours (although no one should wait hours if they suspect they are having a heart attack)
Pain that is very brief and lasts for a few seconds
Pain that spreads to the legs

However, the presence of these symptoms does not always rule out a serious heart event.

Chest pain is a very common symptom in the emergency room, but heart problems account for only 10 - 33% of all episodes.

The most common causes of chest pain are muscular and bone problems. Problems affecting the ribs and chest muscles include injured muscles, fractures, arthritis, spasms, and infections.

Other causes of chest pain include:

Anxiety attacks
Gastrointestinal disorders (gallstone attacks, peptic ulcer disease, hiatal hernia, heartburn)
Asthma
Spasm in the coronary artery
Abnormalities of the heart muscle
Rupture of the aorta
Collapsed lung
Acute inflammation of the heart
Blood clot in the lung
High thyroid levels (hyperthyroidism)
Anemia
Vasculitis (a group of disorders that cause inflammation of the blood vessels)
Exposure to high altitudes (rare)

Individuals who experience symptoms of a heart attack should take the following actions:

For angina patients, take one nitroglycerin dose either as an under-the-tongue tablet or in spray form at the onset of symptoms. Take another dose every 5 minutes up to three doses or when the pain is relieved, whichever comes first.
Call 911 or the local emergency number. This should be the first action taken if angina patients continue to experience chest pain after taking the full three doses of nitroglycerin. However, only 20% of heart attacks occur in patients with long-standing angina. Therefore, anyone who has heart disease or risk factors for it and experiences heart attack symptoms should contact emergency services.
The patient should chew an aspirin (250 - 500 mg) and be sure that emergency health providers are informed of this so an additional dose is not given.
Patients with chest pain should go immediately to the nearest emergency room, preferably traveling by ambulance. They should not drive themselves.

Click the icon to see an image about heart attack symptoms.

Click the icon to see another image about heart attack symptoms.

Risk Factors

Over 13 million Americans have had angina, a heart attack, or both. Each year, about 1.2 million people will experience a serious heart event. About 25% of all Americans have one or more risk factors for heart disease. Most risk factors for heart disease are related to lifestyle and environmental factors.

Over the past decades, heart disease rates declined in both men and women as they quit smoking and improved dietary habits. This rate, however, has stabilized in recent years, most likely because of the dramatic increase in obesity in the U.S. and other industrialized nations. There have also been minimal changes in other risk factors, including smoking, sedentary behavior, and blood pressure control. Some risk factors cannot be changed, including age, gender, and genetics. Nevertheless, their effects can still be modified with healthy lifestyle changes.

Heart disease may be prevented with a healthy diet and regular exercise, and by quitting smoking if you smoke. Follow your health care provider's recommendations for the treatment and prevention of heart disease.

The American Heart Association guidelines for preventing heart disease recommend:

Keep Blood Pressure Low. People in normal health should have a blood pressure reading of 120/80 mm Hg or less. According to the latest guidelines, blood pressure readings of 120/80 are considered normal, readings of 140/90 or higher indicate hypertension, and readings in between the two are called pre-hypertension. Patients with diabetes or chronic kidney disease should maintain blood pressure readings of 130/80 mm Hg or less, while others should be no higher than 140/90 mm Hg.

Exercise. Everyone in normal health should engage in at least moderate physical activity for a minimum of 30 minutes on most, if not all, days of the week.

Quit Smoking. Also avoid exposure to secondhand smoke.

Maintain Weight. People should aim for a BMI index of 18.5 - 24.9.

Taking Aspirin. People whose risk for heart disease within 10 years is 10% or more should take a low-dose aspirin every day, unless they have medical reasons to avoid aspirin.

Control Diabetes. People with diabetes should aim for fast blood glucose levels of less than 110 mg/dl and hemoglobin A1C or less than 7%.

Control Atrial Fibrillation. People with atrial fibrillation should use anticoagulants to reduce the risk for blood clots.

Age. About 85% of people who die from heart disease are over the age of 65.

In 2007, the American Heart Association issued updated guidelines focusing on prevention of heart disease in women. The new guidelines recommend:

Healthy diet (fresh fruits and vegetables, low-fat dairy products, salt and saturated fat restrictions, alcohol moderation)
Eating oily fish (such as salmon) at least twice a week. Women with existing heart disease should consider taking fish oil supplements of 850 – 1,000 mg eicosapentaenoic acid (EPA) and docosahexaenoic acid (DPA).
Increased physical activity (60 – 90 minutes, preferably 7 days a week)
Quitting smoking
Low-dose aspirin therapy for all women age 65 years and older who can safely take aspirin. High-risk women may require 75 – 325 mg / day; lower-risk women may benefit from 81 mg a day or 100 mg every other day.

Genetic Factors. Genetics are involved in increasing the likelihood of developing important risk factors such as diabetes and high blood pressure. For example, one genetic variant called apolipoprotein E4 (ApoE4) affects cholesterol levels, particularly those associated with heart disease.

Ethnicity. African-American women face the highest risk for death from heart disease, and their rate of heart attacks is increasing. (Mortality rates in men do not differ much by race.) Native American men have a lower risk for heart disease than Caucasian men, and Hispanics have the lowest risk for heart disease of all major American population groups.

African-Americans face a number of biologic and social dangers to their hearts.

They have a higher prevalence of diabetes and hypertension than do Caucasians.
They tend to have poorer diets, higher stress levels, and less access to health care.
All African-Americans risk discrimination in obtaining optimal treatments, but women may be at particular risk for unequal treatment. In one study in which female actors portrayed heart patients, African-American women were 60% less likely to receive aggressive (and expensive) diagnostic tests than African-American men or any Caucasians, even though they presented with similar symptoms.
While African-Americans comprise 13% of the U.S. population, African-Americans have comprised only 2 - 9% of subjects in most major research trials, so knowledge about their specific risks is limited.
Some African-Americans with coronary artery disease appear to have a genetic trait that increases the danger of triglycerides, which may be particularly hazardous for women.

Click the icon to see an image about ethnicity and heart disease risks.

Cholesterol. In spite of its bad press, cholesterol is an essential nutrient necessary for many cellular functions. However, when certain cholesterol levels rise in the blood, they can have dangerous consequences, depending on the type of cholesterol. Low-density lipoprotein (LDL) cholesterol is the "bad" cholesterol responsible for many heart problems. Triglycerides are another type of lipid (fat molecule) that can be bad for the heart. High-density lipoprotein (HDL) cholesterol is the "good" cholesterol that helps protect against heart disease. Doctors test for a "total cholesterol" profile that includes measurements for LDL, HDL, and triglycerides. The ratio of these lipids can affect heart disease risk.

For example, according to one study, men with total cholesterol levels over 240 mg/dl have a risk that is two to four times higher than men whose cholesterol is below 200. A number of studies have demonstrated that reducing LDL and total cholesterol levels and boosting high-density lipoprotein (HDL) levels can improve survival and prevent heart attacks in people with and without heart disease.

It is very difficult to measure LDL levels by themselves, but LDL levels can be reliably calculated by the Friedewald formula: LDL=TC-HDL-TG/5. (LDL=low-density lipoprotein; TC= total cholesterol; HDL=high-density lipoprotein; TG=triglycerides.)

Click the icon to see an image about serum cholesterol.

These risk factors include:

Having a first-degree female relative diagnosed with heart disease before age 65 or a first-degree male relative diagnosed before age 55
Being male and over age 45 or female and over age 55
Cigarette smoking
Diabetes
High blood pressure
Metabolic syndrome (risk factors associated with obesity such as low HDL levels and high triglycerides

Having two or more of these risk factors indicates a greater than 20% chance of having a heart attack within 10 years.


Risk Level	Goal (d/L)	Optimal Goal(d/L)
Very High Risk	70	70
High Risk	100	70
Moderate Risk	130	100
Low Risk	160	130


Total Cholesterol Goals	LDL Goals	HDL Goals	Triglyceride Goals
Less than 200 mg/dL is desirable. Between 200 and 239 is borderline. Over 240 is high.	70 mg/dL or less is the new goal for very high-risk patients (recent heart attack; current active or unstable cardiovascular or cerebrovascular disease; or two multiple risk factors as defined above.) Below 100 mg/dl is optimal for everyone. It should be the goal for high-risk people including those with existing heart disease, diabetes, or two or more risk factors for heart disease; 70 mg/dL is an optimal goal for these individuals. 130 mg/dl or below for people with two or more risk factors; 100 mg/dL is the optimal goal. 160 mg/dl or less for people at less risk (one or zero risk factors); 130 mg/dL is the optimal goal. Anything over 160 is high with levels over 190 being very high. LDL levels over 190 require medication even with no other cardiac risk factors present.	Levels above 40 mg/dL are desirable; levels above 60 mg/DL are optimal.	Below 150 mg/dL is normal. 150-199 is borderline high. 200-499 is high. Over 500 is very high.
*Risk factors for heart disease include a family history of early heart problems before age 55 for men, before age 65 for women, smoking, high blood pressure, diabetes, being older (over 45 for men and 55 for women), and having HDL levels below 35 mg/dl. People with two or more of these risk factors may have a 10-year risk of heart attack that exceeds 20%, and may therefore need to aim for LDL levels of 100 mg/dL or below.

[See In-Depth Report #23: Cholesterol; and In-Depth Report #43: Heart-healthy diet.]

Click the icon to see an image about hypertension.


Blood Pressure Category	Ranges for Most Adults (systolic/diastolic)
Normal Blood Pressure (systolic/diastolic)	Systolic below 120 mm Hg Diastolic below 80 mm Hg
Prehypertension (Formerly Classified as Normal to High-Normal Blood Pressure)	Systolic 120 to 139 mm Hg Diastolic 80 to 89 mm Hg (NOTE: 139/89 or below should be the minimum goal for everyone. People with diabetes or chronic kidney disease should strive for 130/80 or less.)
Mild Hypertension (Stage 1)	Systolic 140 to 159 mm Hg Diastolic 90 to 99 mm Hg
Moderate-to-Severe Hypertension (Stage 2)	Systolic over 160 mm Hg and/or Diastolic over 100 mm Hg
Note: If one of the measurements is in a higher category than the other, the higher measurement is usually used to determine the stage. For example, if systolic pressure is 165 (Stage 2) and diastolic is 92 (Stage 1), the patient would still be diagnosed with Stage 2 hypertension. A high systolic pressure should be a major focus of concern in most adults.

American obesity is at epidemic levels in all age groups. The effect of obesity on cholesterol levels is complex. Although obesity does not appear to be strongly associated with overall cholesterol levels, among obese individuals triglyceride levels are usually high while HDL (beneficial cholesterol) levels tend to be low, both risk factors for heart disease. Obesity has other effects (hypertension, increase in inflammation) that pose major risks to the heart.

Click the icon to see an image of childhood obesity.

Obesity is particularly hazardous when it is one of the components of the metabolic syndrome. This syndrome is diagnosed when three of the following are present: abdominal obesity, low HDL cholesterol, high triglyceride levels, high blood pressure, and insulin resistance. Metabolic syndrome is a pre-diabetic condition that is significantly associated with heart disease and higher mortality rates from all causes. A 2002 study estimated that 24% of the population now has this condition. Obesity is highly linked with type 2 diabetes, and diabetes itself poses a significant risk for high cholesterol levels and heart disease.

Some obese patients with coronary artery disease may consider having bariatric surgery (stomach bypass) to lose excess weight. The weight lost after surgery can help improve blood pressure, cholesterol, blood sugar and other factors associated with CAD. A 2005 study reported that bariatric surgery is safe for patients with CAD who cannot lose weight with diet and exercise, which should always be tried first.

[See In-Depth Report #53: Weight control and diet.]

People who are sedentary are almost twice as likely to suffer heart attacks as are people who exercise regularly. Exercise has a number of effects that benefit the heart and circulation, including:

Improving cholesterol and lipid levels
Reducing inflammation in the arteries
Assisting weight loss programs
Helping to keep blood vessels flexible and open

Studies continue to show that physical activity and avoiding high-fat foods are the two most successful means of reaching and maintaining heart healthy levels of fitness and weight.

Click the icon to see an image about exercise.

Click the icon to see an image about hypertension and lifestyle changes.

Some studies suggest that for the greatest heart protection, it is not the duration of a single exercise session that counts but the total daily amount of energy expended. Therefore, the best way to exercise may be in multiple short bouts of intense exercise, which can be particularly helpful for older people.

Sudden strenuous exercise (such as snow shoveling and mowing lawns) puts many people at risk for angina and heart attack. Activities that involve raising the arms above the head may also be risky. Patients with angina should never exercise shortly after eating. People with risk factors for heart disease should seek medical clearance and a detailed exercise prescription. And all people, including healthy individuals, should listen carefully to their bodies for signs of distress as they exercise. [See In-Depth Report #29: Exercise.]

High blood pressure (hypertension). Up to 75% of cardiovascular problems in people with diabetes may be due to hypertension.
Very unhealthy cholesterol and lipid balances (high triglyceride levels and lower HDL).
Blood clotting problems.
Impaired nerve function (neuropathy), which can also damage the heart. Some experts estimate that the mortality rates from neuropathy-related heart conditions range from 15 - 53%.

People with both diabetes and heart disease may have a higher risk for silent ischemia, a condition in which people have blocked arteries but do not experience the angina, the chest pain that signals heart disease. [See In-Depth Report #9: Diabetes - type 1; or In-Depth Report #60: Diabetes - type 2.]

Peripheral artery disease (PAD) occurs when atherosclerosis affects the extremities, particularly the feet and legs. The major risk factors for heart disease and stroke are also the most important risk factors for PAD. (The combination of such conditions with PAD also produces more severe forms of heart or circulatory disease.) Although signs of heart disease are detected in only 20 - 40% of patients with PAD after an initial diagnosis, studies suggest that when intense heart-diagnostics tests are performed, such as angiography or thallium stress tests, co-existing heart disease is detected in up to 90% of all PAD patients. [See In-Depth Report #102: Peripheral artery disease.]

Eating habits can be protective or dangerous to the heart. Avoiding saturated fats and trans-fatty acids is particularly important for controlling cholesterol.

Diet plays an important role in the health of the heart. In 2006, the American Heart Association (AHA) issued revised diet and lifestyle recommendations. The current guidelines recommend:

Balance calorie intake and physical activity to achieve or maintain a healthy body weight. (Controlling weight, quitting smoking, and exercising regularly are essential companions of any diet program. Try to get at least 30 minutes, and preferably 60 – 90 minutes, of daily exercise.)
Consume a diet rich in a variety of vegetables and fruits. Vegetables and fruits that are deeply colored (spinach, carrots, peaches, berries) are especially recommended as they have the highest micronutrient content.
Choose whole-grain, high-fiber foods. These include fruits, vegetables, and legumes (beans). Good whole grain choices include whole wheat, oats/oatmeal, rye, barley, brown rice, buckwheat, bulgur, millet, and quinoa.
Consume fish, especially oily fish, at least twice a week (about 8 ounces/week). Oily fish such as salmon, mackerel, and sardines are rich in the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Consumption of these fatty acids is linked to reduced risk of sudden death and death from coronary artery disease.
Limit daily intake of saturated fat (found mostly in animal products) to less than 7% of total calories, trans fat (found in hydrogenated fats, commercially baked products, and many fast foods) to less than 1% of total calories, and cholesterol (found in eggs, dairy products, meat, poultry, fish, shellfish) to less than 300 mg per day. Choose lean meats and vegetable alternatives (such as soy). Select fat-free and low-fat dairy products. Grill, bake, or broil fish, meat, and skinless poultry.
Use little or no salt in your foods. Reducing salt can lower blood pressure and decrease the risk of heart disease and heart failure.
Cut down on beverages and foods that contain added sugars (corn syrups, sucrose, glucose, fructose, maltrose, dextrose, concentrated fruit juice, honey.)
If you consume alcohol, do so in moderation. The AHA recommends limiting alcohol to no more than 2 drinks per day for men and 1 drink per day for women.

[See In-Depth Report #43: Heart-healthy diet.]

Depression. Depression increases the severity of heart attack and may even worsen a patient's response to medication for heart disease. Although people with heart disease may become depressed, this does not explain entirely the link between the two problems. Data suggest that depression itself may be a risk factor for heart disease as well as its increased severity.

A number of studies indicate that depression has biologic effects on the heart, including blood clotting and heart rate. One study, for example, reported an association between depression and a greater risk for death from heart problems even in people without a history of heart disease. Even mild depression, which includes feelings of hopelessness experienced over many years, may harm the heart. A 2007 study suggested that depressive symptoms (fatigue, loss of appetite) may be a sign of thickening arteries, the early stage of coronary artery disease. [See In-Depth Report #8: Depression.]

Adverse Effects of Heavy Drinking. By contrast, heavy drinking harms the heart. In fact, heart disease is the leading cause of death in alcoholics. Evidence suggests that people who consume more than three drinks a day have abnormal blood clotting factors. Heavy alcohol consumption can raise blood pressure, and binge drinking may increase the risk for hemorrhagic stroke (caused by bleeding in the brain). Large doses of alcohol can trigger irregular heartbeats, which can be dangerous in people with existing heart disease.

Pregnant women and people who can't drink moderately should not drink at all.

Homocysteine and Vitamin B Deficiencies. Deficiencies in the B vitamins folate (known also as folic acid), B6, and B12 have been associated with a higher risk for heart disease in some studies. Such deficiencies produce higher blood levels of homocysteine, an amino acid that has been associated with a higher risk for heart disease, stroke, and heart failure. Researchers have been studying whether vitamin B supplements can reduce homocysteine levels and, consequently, heart disease risks.

Several major 2006 studies indicated that while B vitamin supplements do help lower homocysteine levels, they have no effect on heart disease outcomes. The studies, published in the New England Journal of Medicine, examined patients who had either recently had a heart attack or suffered from diabetes or heart disease. Results showed a similar number of heart attacks and strokes among patients who took B vitamins and those who received placebo. Some experts think that homocysteine may be a marker for heart disease rather than a cause of it.

Click the icon to see the benefits of vitamin B.

Click the icon to see the food sources of vitamin B.

C-Reactive Protein. C-reactive protein is a product of the inflammatory process. Evidence increasingly suggests that high levels may predict future heart disease. It is not known if the protein plays any causal role or whether it is simply a marker for other factors in the disease process.

C. pneumoniae and Other Infectious Organisms. Some microorganisms and viruses have been under suspicion for triggering the inflammation and damage in the arteries that contribute to heart disease. The strongest evidence to date supports a possible role from Chlamydia (C.) pneumoniae (a non-bacterial organism that causes mild pneumonia in young adults). C. pneumoniae has been detected in plaques in the arteries of patients with heart disease. In some studies, evidence of previous infection has been associated with a higher risk for heart events.

Other studies also suggest that cytomegalovirus (CMV), a common virus, may have similar effects. Many people, however, have been infected with these organisms, and no clear association has been found with any of these infections.(H. pylori, the bacteria that causes peptic ulcers, has also been studied for heart effects, but evidence is very weak on any link.)

Erectile Dysfunction. Recent research suggests that erectile dysfunction may be a warning sign of coronary artery disease, even in men who are not considered at risk for the condition. Some studies indicate that men with erectile dysfunction have higher levels of C-reactive protein and more symptoms of atherosclerosis than men without erectile problems.

Periodontal Disease. A number of studies support an association between periodontal disease and cardiovascular disorders. According to a 2003 major analysis, periodontal (gum) disease is associated with a 20% higher risk for ischemic stroke and heart disease. (The added risk may be even higher in adults under 65.) Recent evidence is pointing to the inflammatory response as the common element.

Click the icon to see an image of gum disease.

Anemia. Anemia has adverse effects on the heart and increases the severity of cardiac conditions, including heart failure and heart attacks. A 2002 study suggested that anemia may even be a risk factor for heart disease itself. Blood transfusions after a heart attack improve survival rates in elderly patients who are anemic.

Iron Overload. An inherited disease called hemochromatosis, in which the intestinal tract absorbs too much iron from food, has been associated with atherosclerosis and heart attack. About 10% of Caucasians carry the gene for this condition. There is no strong evidence that excess iron levels in people without hemochromatosis can contribute to heart disease.

Some inborn or natural conditions are not risk factors themselves but have been associated with a higher incidence of heart disease or its consequences:

Factors Before Birth and In Infancy. Low weight at birth and in the womb has been associated with later heart disease in a few studies. Some suggest, however, that this may just reflect poor nutrition in the mother, which appears to affect life-long risk.

Seasonal Differences. More deaths from heart disease occur in December and January, and the fewest in the summertime. Although lower temperatures and snow shoveling may play a role in some cases, more winter deaths have been reported even in warm regions. Holiday stress or fewer daylight hours have been suggested as other reasons for these higher winter rates.

Physical Characteristics. Male pattern baldness, hair in the ear canals, and creased earlobes are associated with a higher risk for heart disease in Caucasian males.

Click the icon to see an image of an ear lobe crease.

Diagnosis

Many tests can diagnose possible heart disease. The choice of which (and how many) tests to perform depends on the patient's risk factors, history of heart problems, and current symptoms. Usually the tests begin with the simplest and may progress to more complicated ones.

Doctors routinely check for high blood pressure and unhealthy cholesterol levels in all older adults. Specific tests are also important in people who may have risk factors or symptoms of diabetes. Doctors may also test for homocysteine, the protein albumin, and blood clotting factors, especially fibrinogen.

An electrocardiogram (ECG) measures and records the electrical activity of the heart. Between 25 - 50% of people who suffer from angina or have silent ischemia, however, have normal ECG readings. The waves measured by the ECG correspond to the contraction and relaxation pattern of the different parts of the heart. Specific waves seen on an ECG are named with letters:

The electrocardiogram (ECG, EKG) is used extensively in the diagnosis of heart disease, from congenital heart disease in infants to myocardial infarction and myocarditis in adults. Several different types of electrocardiogram exist.

P. The P wave is associated with the contractions of the atria (the two chambers in the heart that receive blood from outside).
QRS. The QRS is a series of waves associated with ventricular contractions. (The ventricles are the two major pumping chambers in the heart.)
T and U. These waves follow the ventricular contractions.

The most important wave patterns in diagnosing and determining treatment for heart disease and heart attack are called ST elevations and Q waves.

A depressed or horizontal ST wave suggests some blockage and the presence of a heart disease, even if there is no angina present. (This finding, however, is not very accurate, particularly in women, and can occur without heart problems).
ST elevations and Q waves are the most important wave patterns in diagnosing and determining treatment for a heart attack. They suggest that an artery to the heart is blocked, and that the full thickness of the heart muscle is damaged. ST segment elevations do not always mean the patient has a heart attack. And, some heart attack patients do not have elevated ST segments. Other factors are important in making a diagnosis.

The primary value of exercise stress tests is not to detect coronary artery disease but to help determine the severity and predict the outcome of an existing heart condition. It is considered for the following people:

Patients with possible or probable angina and low or intermediate risk for adverse heart events.
Selected adults who do not have symptoms of heart disease but are at moderate risk to high risk for developing heart disease (a 10 - 20% chance within 10 years). Moreover, heart blockage without angina (silent ischemia) may suggest a more severe condition, at least in men.

Basic Procedure. A stress test (exercise tolerance test) monitors the patient's heart rhythms, blood pressure, and clinical status. It can tell how well the heart handles work and if parts of the heart have decreased blood supply. A typical stress test involves:

The patient walks on a treadmill or rides a stationary bicycle. Exercise continues until the heart is beating at least 85% of its maximum rate, until symptoms of heart trouble occur (changes in blood pressure, heart rhythm abnormalities, angina, fatigue), or the patient simply wants to stop.
For patients who cannot exercise, the doctor may administer dobutamine or arbutamine, which are drugs that simulate the stress of exercise.
An ECG is used to monitor heart rhythms during a stress test. (An echocardiogram or more advanced imaging technique may also be used to visualize the actions of the heart and blood flow.)

More than 25% of patients stop exercising before they reach their own maximum limits because of fear of a heart event. Patients should be reassured that the activities performed in the test under the guidance of a professional are safe.

Interpreting Results. To accurately assess heart problems, experts look at a number of findings derived from the ECG and other tools during exercise. They include:

Exercise capacity. This is a measure of a person's capacity to reach certain metabolic rates.
Heart rate and ST waves. On ECGs, doctors specifically look for abnormalities in part of the wave tracing called an ST segment. A certain type of ST segment depression may suggest the presence of heart disease. However, gender, drugs and other medical conditions can affect the ST segment. Using a measurement that adjusts the ST segment to heart rate improves accuracy.
Dukes Treadmill Score. This important score uses the number of minutes a patient can exercise and other factors that are present in patients with exercise-limiting angina.
Heart rate recovery.
Chronotropic index. This is the percentage of the heart-rate reserve that is used during the exercise. A result of 80% or less suggests a significant risk for serious heart problems in most patients.
Changes in systolic blood pressure.

Using these and other measures, doctors can determine risk fairly accurately, particularly for men of any age with chronic stable angina. The test has limitations, however, and some are significant. For example, a 2002 study indicated that in patients with suspected unstable angina the chances for a future adverse heart event remain high even if the exercise test shows low risk. In addition, for many reasons, the test is less accurate in women, and an echocardiogram may be a more accurate procedure for them. About 10% of patients, particularly younger people, will have false positive test results. In such cases, test results indicate abnormalities when there are no heart problems.

An echocardiogram is a noninvasive test that uses ultrasound images of the heart. This test is more expensive than an ECG, but it can be very valuable, particularly when used with a stress test, to detect the location and extent of heart muscle damage. It appears to be more accurate for women than ECG stress tests, but at this time it is not routinely recommended as a replacement for most women.

Computed tomography (CT) scans used alone or with ECG may be used to detect calcium deposits on the arterial walls, which are strong indicators of current and future coronary artery disease. The presence of calcium does not always signify narrowing of the arteries. But, the absence of calcification in the arteries indicates the patient has no risk for heart disease.

Advanced CT techniques are improving accuracy:

Click the icon to see an image of a CT scan.

Electron Beam Computed Tomography. Electron beam computed tomography (EBCT) is a CT technique that scans the heart so quickly that the motion of the heart appears frozen. This procedure identifies calcification and stratifies cardiac risk accurately.
Multidetector Computed Tomography. Another CT technique called multidetector computed tomography (MDCT) is able to take pictures of the entire heart in 1 millimeter slices in the time it takes for a patient to hold one breath. A 2006 study indicated that MDCT tends to have a high “false-positive” rate (indicating disease when it is not actually there), but for some patients the test may be helpful in ruling out coronary artery disease.

Some expert groups recommend CT scans in selected patients who have an intermediate risk (10 - 20% chance of heart disease within 10 years). For some of these patients, EBCT may be preferred over exercise stress testing, but most experts recommend a stress test as the main diagnostic tool. In general, the use of these expensive imaging tests is probably not very helpful for people at low or high risk. (For people with high risk, the additional information from these tests would not add much value.) More research is needed to determine the benefits of CT scanning in specific individuals.

Radionuclide procedures use imaging techniques and computer analyses to plot and detect the passage of radioactive tracers through the region of the heart. Such tracing elements are typically given intravenously. Radionuclide imaging is useful for diagnosing and determining:

Severity of unstable angina when less expensive diagnostic approaches are unavailable or unreliable
Severity of chronic coronary artery disease
Success of surgeries for coronary artery disease.
Whether a heart attack has occurred

Various imaging techniques may be used with radionuclide procedures, including:

Planar scintigraphy uses a special overhead camera and is the oldest scanning technique.
Single-photon emission computed tomography (SPECT) uses a camera that rotates around the patient and takes pictures of "slices" of the heart. It is more accurate than planar imaging in precisely locating problems in the arteries.
Positron-emission tomographic (PET) scanners employ multiple rings that surround the patients, which detect and record atomic particles (photons) that are emitted by the tracer elements (such as radioactive oxygen, nitrogen, or carbon). It is more expensive and less widely available than SPECT.

Myocardial Perfusion (Blood Flow) Imaging Test (also called the Thallium Stress Test). This radionuclide test is typically used with an exercise stress test to determine blood flow to the heart muscles. It is a reliable measure of severe heart events. It may be useful in determining the need for angiography if CT scans have detected calcification in the arteries. About a minute before the patient is ready to stop exercising, the doctor administers a radioactive tracer into the intravenous line. (Tracers include thallium, technetium, or sestamibi.) Immediately afterwards, the patient lies down for a heart scan, usually with a planar scintigraphy or with SPECT. If the scan detects damage, more images are taken 3 or 4 hours later. Damage due to a prior heart attack will persist when the heart scan is repeated. Injury caused by angina, however, will have resolved by that time.

Radionuclide Angiography. This is a technique for visualizing the chambers and major blood vessels of the heart. It uses an injected radioactive tracer and can be performed during exercise, at rest, or with use of stress-inducing drugs. It is an excellent test for assessing the heart's pumping action and for determining the severity of coronary artery disease. It is an alternative to echocardiograms in certain situations.

Click the icon to see an internal view of the heart.

Click the icon to see an image of a MRI.

Angiography is an invasive test. It is used for patients who show strong evidence for severe obstruction on stress and other tests, and for patients with acute coronary syndrome.

A narrow tube is inserted into an artery, usually in the leg or arm, and then threaded up through the body to the coronary arteries.
A dye is injected into the tube, and an x-ray records the flow of dye through the arteries.
This process provides a map of the coronary circulation, revealing any blocked areas.

Click the icon to see an image of dye in the coronary artery.

When heart cells become damaged, they release different enzymes and other molecules into the bloodstream. Elevated levels of such markers of heart damage in the blood or urine may help predict a heart attack in patients with severe chest pain and help determine treatment. Some of these factors include:

Troponins. The proteins cardiac troponin T and I are released when the heart muscle is damaged. Both are proving to be among the best diagnostic indications of heart attacks. They help to identify many individuals with ACS who might otherwise be misdiagnosed.
Creatine kinase myocardial band (CK-MB). CK-MB has been a standard marker, but the MB fraction is not as accurate as troponin levels, since elevated levels can appear in people without heart injury.
Myoglobin. Myoglobin is a protein found in heart muscles. It is released early in the injured heart, and it may be useful in combination with CK-MB and the troponins.
Newer biomarkers, including C-reactive protein (CRP), homocysteine, B-type natriuretic peptide (BNP), urinary albumin, and fibrinogen.

Several 2006 studies that evaluated how well biomarkers predict risk of heart events concluded that they do not provide much more useful information than standard risk factors (high blood pressure, unhealthy cholesterol levels, diabetes). At this time, most experts feel that these standard disease risk factors provide the best predictors of the likelihood of developing coronary artery disease, heart attack, or stroke.

Managing Heart Disease

The approach for managing any degree of coronary artery disease involves lifestyle changes. Depending on severity and individual conditions, patients may need one or more medications, surgery, or both.

Healthy diet, regular exercise and quitting smoking if you are a smoker may prevent heart disease. Follow your health care provider's recommendations for treatment and prevention of heart disease.

Experts have come up with a mnemonic device (ABCDE) for remembering 10 factors that are fundamental for management of stable angina and coronary artery disease:

A. Aspirin and anti-angina drugs

B. Blood pressure and beta-blockers

C. Cholesterol-lowering drugs (typically statins) and cigarettes (stopping)

D. Diet and diabetes control

E. Exercise and education

Unstable angina is now usually classified with non-Q myocardial infarction as acute coronary syndrome (ACS) in professional discussions of treatments. ACS usually requires more aggressive treatments, including surgery. [ACS is more fully discussed in In-Depth Report #12: Heart attack and acute coronary syndrome.]

Click the icon to see an image about angina.

Anti-Clotting Medications

A thrombus is a blood clot that forms in a vessel and remains there. An embolism is a clot that travels from the site where it formed to another location in the body. Thrombi or emboli can lodge in a blood vessel and block the flow of blood in that location depriving tissues of normal blood flow and oxygen. This can result in damage, destruction (infarction), or even death of the tissues (necrosis) in that area.

Antiplatelet Drugs. These drugs prevent formation of blood platelets. Platelets are very small disc-shaped blood cells that are important for blood clotting.

Aspirin. Aspirin is an antiplatelet. It is the most common anti-clotting drug. Nearly anyone with existing heart disease or at risk for it is advised to take a low-dose aspirin every day.
Thienopyridines. Clopidogrel (Plavix) and ticlopidine (Ticlid) are thienopyridines, another type of anti-platelet drug.
Glycoprotein IIb/IIIa Inhibitors. These powerful blood-thinning drugs include abciximab (ReoPro, Centocor), eptifibatide (Integrilin), tirofiban (Aggrastat), and lamifiban. They are administered intravenously in the hospital and are used after angioplasty surgery and stent placement.

Click the icon to see an image about blood.

Anticoagulants. Anticoagulants help thin blood and include:

Heparin
Warfarin (Coumadin)
Direct thrombin inhibitors

Aspirin. Aspirin is known as a nonsteroidal anti-inflammatory drug (NSAID). It stops blood platelets, which are major clotting factors, from sticking together to form a blood clot. A daily low-dose aspirin (75 - 325 mg) is usually the first choice for preventing heart disease in high-risk individuals. Aspirin can prevent by 25 – 50% the risk of heart attacks and death in people with existing heart disease and a history of heart attack. It also reduces the risk for stroke. According to a 2006 review, aspirin works equally well for both men and women.

Click the icon to see an image about stomach ulcers.

Side effects from prolonged use of aspirin may include stomach ulcers and bleeding. (There may be a slight increased risk for bleeding-related strokes, which are very uncommon, however. Furthermore, this risk may be outweighed by protection against the more common type of stroke, which is caused by artery blockage.)

Clopidogreland Ticlopidine. Clopidogrel (Plavix) and ticlopidine (Ticlide) are anti-platelet drugs known as thienopyridines. When taken with aspirin, these drugs can significantly reduce the risk for heart attack and stroke in patients with acute coronary syndrome (unstable angina or early signs of heart attack). The combination of aspirin and a thienopyridine is essential for patients who have a drug-eluting stent. According to a 2007 American Heart Association advisory, patients who have a drug-eluting stent must take both aspirin and a thienopyridine for at least 1 year after the stent is inserted. Many experts recommend clopidogrel instead of ticlopidine because ticlopidine has been associated with dangerous blood disorders, particularly thrombocytopenia.

Clopidogrel is also recommended for patients who are undergoing angioplasty. For patients having coronary bypass surgery, it should be withheld for at least 5 -7 days prior to surgery because of a significant bleeding risk. Researchers are investigating whether clopidogrel and aspirin together are better than aspirin alone in reducing the risks following coronary bypass surgery. A 2006 study suggested that for some patients with heart disease, clopidogrel plus aspirin does not work better than aspirin alone for preventing a first heart attack or stroke.

Click the icon to see an image of the developmental process of atherosclerosis.

Click the icon to see an image about atherosclerosis.

Anticoagulants are drugs that prevent or delay blood coagulation and the formation of blood clots. Heparin has been the standard anticoagulant, but a number of drugs are now available that are proving to be better choices in many cases.

Standard (Unfractionated) Heparin. The heparin referred to as unfractionated heparin has been the standard for years and is used alone or in combination with aspirin for managing unstable angina. It is no longer the recommended first choice, however, for this patient group. It must be intravenously administered and monitored with frequent blood tests. The major complication is thrombocytopenia (a severe drop in platelets). This condition is extremely serious and can become life-threatening, particularly with bleeding in various body tissues. Alternatives include low-molecular weight heparin and direct thrombin inhibitors.

Low-Molecular Weight Heparin. Enoxaparin (Lovenox), dalteparin (Fragmin), tinzaparin (Innohep) are drugs known as low-molecular weight heparins (LMWHs). Many doctors now recommend these drugs over standard heparin for patients with unstable angina (unless bypass surgery is being planned). They have similar rates of survival, recurring angina, and bleeding as standard heparin. However, they pose lower risks for heart attack, repeat angioplasties, and thrombocytopenia. They require injections but do not require the ongoing monitoring that standard heparin does. Patients may even be able to self-administer LMWHs as people with diabetes do insulin.

Warfarin. Warfarin (Coumadin) is an oral anticoagulant. It prevents clots by inhibiting vitamin K. Warfarin is used with aspirin after a heart attack to prevent another one and to prevent blood clots in patients with atrial fibrillation. Warfarin is also proving to be more effective than aspirin for preventing heart attacks in patients with acute coronary syndromes. Warfarin therapy poses a dangerous risk for bleeding and blood coagulation must be monitored with frequent blood tests.

Direct Thrombin Inhibitors (DTIs). Direct thrombin inhibitors are a more recent group of anti-coagulants. The first DTI was hirudin, a natural substance derived from the saliva of leeches. New forms include argatroban (Novastan), bivalirudin (Angiomax), danaparoid (Orgaran), lepirudin (Refludan), desirudin (Revasc), and ximelagatran (Exanta). Many of these drugs are used along with warfarin and may be good options for patients who develop thrombocytopenia with heparin use. DTIs may prove to be superior to standard heparin for patients with acute coronary syndrome.

Other Medications

Nitrates have been used in the treatment of angina for over 100 years. These drugs release nitric oxide, thereby relaxing the smooth muscles in blood vessels. Many nitrate preparations are available. The most commonly used are nitroglycerin, isosorbide dinitrate, and isosorbide mononitrate. Nitrates can be absorbed from the gastrointestinal tract (oral tablet), skin (ointment or patch), or from under the tongue (sublingual tablet or spray).

Rapid Acting Nitrates. Rapid-acting nitrates are used to treat acute attacks. Nitroglycerin is the most widely used drug for this purpose. It can be administered under the tongue (sublingually or as a spray) or pocketed between the upper lip and gum (buccally) and can relieve angina within minutes. The procedure for taking nitroglycerin during an attack is as follows:

At the onset of an angina attack, the patient administers one sublingual or buccal tablet or one metered dose of the spray.
If the pain is not relieved within 5 minutes the patient takes a second dose; a third can be taken after another 5 minutes if symptoms persist.
If pain continues after a total of three doses in 15 minutes, the patient should go immediately to the nearest emergency room.

Nitroglycerin is very volatile so its potency can be easily lost. Patients should take the following precautions:

Keep no more than 100 tablets on hand, stored in their original container.
When first opened, the cotton filler should be discarded, and the cap screwed on tightly immediately after each use.
A supply should always be kept close at hand in case of an attack, with the rest kept in a cool dry place.

Intermediate to Long-Term Nitrates. Sublingual tablets of isosorbide dinitrate have a somewhat slower onset of action than nitroglycerin and are useful for preventing exercise angina. Ointments, patches, and oral tablets are used for longer-term prevention of angina attacks:

Transdermal patches are applied in the morning to any hair- or injury-free area on the chest, back, stomach, thigh, or upper arm. Hands should be washed after each patch or ointment application, and sites of application should be rotated to avoid skin irritation.
Nitroglycerin ointment is applied by measuring out an even amount on an applicator paper and then placing, not rubbing or massaging, it on the chest, stomach, or thigh. Any ointment that remains from the previous application should be removed.

Long-acting forms may lose their effectiveness over time, so doctors generally schedule nitrate-free breaks to prevent tolerance. Some concern exists that nitrate-free periods might increase the risk for angina and adverse heart events. One large study, however, found no increased danger when patients used a nitroglycerine patch with scheduled breaks. The use of high blood pressure drugs known as ACE inhibitors may help prevent tolerance to nitrates.

Side Effects. Nitrates have many side effects, some of which can be serious.

Common side effects of nitrates include headaches, dizziness, nausea and vomiting, blurred vision, fast heartbeat, sweating, and flushing on the face and neck. Low blood pressure and dizziness can be relieved by lying down with the legs elevated. These effects are significantly worsened by alcohol, beta-blockers, calcium channel blockers, sildenafil (Viagra), and certain antidepressants. The doctor may prescribe medicines to lessen these side effects. Patients should contact their doctor if these side effects are persistent or severe.

Serious side effects requiring immediate medical help include fever, joint or chest pain, sore throat, skin rash (especially on the face), unusual bleeding or bruising, weight gain, and swelling of the ankles.

Withdrawal. Withdrawal from nitrates should be gradual. Abrupt termination may cause angina attacks.

Beta-blockers are useful for preventing angina attacks and reducing high blood pressure. They reduce the heart's oxygen demand by slowing the heart rate and lowering blood pressure. They are recognized for reducing deaths from heart disease and from heart surgeries, including angiography and coronary bypass. Beta-blockers are the drugs of choice for older patients with stable angina and may also be beneficial for people with silent ischemia. They are, however, less useful for the treatment of Prinzmetal’s angina. Beta-blockers are often prescribed along with other drugs such as nitrates, calcium channel blockers, or statins. A 2006 study suggested that beta-blockers and statins may help stabilize coronary artery disease and prevent the development of heart attacks.

Specific Beta-blockers. Beta-blockers include propranolol (Inderal), carvedilol (Coreg), bisoprolol (Zebeta), acebutolol (Sectral), atenolol (Tenormin), labetalol (Normodyne, Trandate), metoprolol (Lopressor, Toprol-XL), and esmolol (Brevibloc). A nasal spray form of propranolol appears to be very helpful in reducing exercise-induced angina attacks.

Side Effects. Beta-blocker side effects include fatigue, lethargy, vivid dreams and nightmares, depression, memory loss, and dizziness. They can lower HDL (“good”) cholesterol. Beta blockers are categorized as non-selective or selective. Non-selective beta blockers such as carvedilol and propranolol can narrow bronchial airways. These beta-blockers should not be used by patients with asthma, emphysema, or chronic bronchitis.

Patients should never abruptly stop taking these drugs. The sudden withdrawal of beta-blockers can rapidly increase heart rate and blood pressure. The doctor may advise a patient to slowly decrease the dose before stopping completely.

Calcium channel blockers reduce heart rate and slightly dilate the blood vessels of the heart, thereby decreasing oxygen demand and increasing oxygen supply. They also reduce blood pressure. CCBs vary chemically, however, and although some are helpful, others may even be dangerous for certain patients with angina.

Click the icon to see an image of the anterior heart arteries.

Long-acting nifedipine (Adalat, Procardia) and nisoldipine (Sular) and newer CCBs, such as amlodipine (Norvasc) and nicardipine (Cardene), may be beneficial for some patients with angina. They can be considered alone for patients who cannot tolerate beta-blockers, but may provide the best results when used in combination with a beta-blocker. Studies suggest that they reduce the need for repeat angioplasties. Their effects on other outcomes, including mortality rates and heart attack, are less clear.
Short-acting CCBs, including short-acting forms of verapamil, diltiazem, nifedipine, and nicardipine, are helpful for many patients with Prinzmetal's angina. However, short-acting forms of certain CCBs, such as nifedipine and nisoldipine, have been associated with severe and even dangerous side effects, including an increase in heart attacks and sudden death in some patients with unstable angina. They also increase the risk for adverse effects in patients with stable angina. Short-acting CCBs are, therefore, not used for stable or unstable angina.

There is no strong evidence that any calcium channel blockers improve survival rates. Overdose can cause dangerously low blood pressure and slow heart beats. Patients with heart failure have a higher risk for death with these drugs and should not take them. No one taking any calcium channel blocker should withdraw abruptly because such action could dangerously increase the risk of high blood pressure. Note: Grapefruit and Seville oranges boost the effects of CCBs, sometimes to toxic levels. (Regular oranges do not appear to pose any hazard.)

Angiotensin converting enzyme (ACE) inhibitors are important heart-protective drugs, particularly for people with diabetes and high blood pressure. They reduce the production of angiotensin, a chemical that causes arteries to narrow, and so are commonly used to lower blood pressure. They may also reduce risk for heart attack, stroke, complications of diabetes, and death in patients at high risk for heart disease.

ACE inhibitors include captopril (Capoten), ramipril (Altace), enalapril (Vasotec), quinapril (Accupril), benazepril (Lotensin), perindopril (Aceon), and lisinopril (Prinivil, Zestril).

Side Effects. Side effects of ACE inhibitors are uncommon but may include an irritating cough, excessive drops in blood pressure, and allergic reactions. In the past, doctors sometimes avoided giving aspirin to patients who were taking ACE inhibitors because the combination was believed to cause kidney problems. But, a 2005 study of patients with both coronary artery disease and heart failure found that taking aspirin and ACE inhibitord together is safe. The researchers also noted that taking aspirin with an ACE inhibitor can significantly reduce the risk of death for older patients with CAD and heart failure. [See In-Depth Report #14: High blood pressure.]

In 2004, the National Cholesterol Education Program issued updated recommendations on how to control cholesterol levels. These guidelines emphasize that patients should lower their LDL (“bad”) cholesterol and recommend that more people take LDL-lowering medication. Lowering LDL cholesterol and raising HDL (“good”) cholesterol can significantly reduce the risks of heart disease. Several different types of drugs (statins, bile-acid binding resins, niacin, and fibrates) are used to treat cholesterol. [See In-Depth Report #23: Cholesterol.]

The main safety concern with statins is an uncommon condition called myopathy, which can cause muscle and joint pain and possible muscle damage. Doctors will immediately stop statin therapy if myopathy occurs. Patients should talk to their doctor about any unusual muscle discomfort or weakness, or if their urine becomes brown-colored. Statins can also affect the liver, particularly at higher doses, so patients taking these drugs should receive regular liver function tests.

Click the icon to see an image of cholesterol.

Influenza Vaccinations (Flu Shots). Evidence suggests influenza vaccinations help protect against adverse heart events (including after heart surgeries), stroke, and death from all causes in the elderly. Still, studies suggest that only two-thirds of at risk people are vaccinated, mostly because of unwarranted fears of ineffectiveness or adverse effects.

Antibiotics. Researchers have investigated antibiotics for treating patients with heart disease and past infection of the bacteria Chlamydia pneumoniae. Results from several recent large-scale clinical trials suggest that antibiotic treatment provides no benefit in preventing heart attack or other cardiac events in patients with coronary artery disease. In addition, a 2006 study indicated that short-term treatment with the antibiotic clarithromycin may increase the risk for death in patients with coronary artery disease. While it is still possible that C. pneumoniae may play a role in triggering inflammatory responses associated with ACS, antibiotic therapy is no longer considered appropriate for treatment or prevention of heart disease.

Ranolazine (Ranexa) was approved in 2006 for treatment of chronic angina. It is recommended for patients who have not responded to other angina drugs. Ranolazine is taken in combination with amlodipine, beta blockers, or nitrates. The drug appears to work better in men than in women

Gene Therapy and Angiogenesis. Proteins known as growth factors are being investigated for their ability to grow new blood vessels for supplying oxygen to the heart. After promising small trials, two large studies of genetically engineered forms of vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF [GenerX]) failed to detect any benefits. Studies on therapies that actually genetically encode these proteins are underway.

Testosterone Supplements. Some trials using testosterone supplements or patches have reported improved exercise-induced blood flow in the coronary arteries and improvement in angina in some cases. Supplements of this male hormone, however, may increase the risk for prostate cancer. Experts suggest that testosterone be used only in older men with significant deficiencies in testosterone.

Selective Estrogen-Receptor Modulators (SERMs). Selective estrogen-receptor modulators (SERMs), including raloxifene (Evista), have been designed to produce the benefits of estrogen without its risks. They are thought to act like estrogen in some tissues but behave like estrogen blockers (antiestrogens) in others. Raloxifene may have some heart benefits, although it poses a risk for deep vein blood clots, which may have long-term implications for patients with heart problems. A major study is underway to determine its effects on the heart.

Surgery

Surgery is usually recommended for patients who have:

Unstable angina that does not respond promptly to medical treatment
Severe recurrent episodes of angina that last more than 20 minutes
Acute coronary syndrome
Severe coronary artery disease (severe angina, multi-artery involvement, evidence of ischemia), particularly if abnormalities are evident in the left ventricle of the heart, the main pumping chamber

Atherosclerosis is a disease of the arteries in which fatty material is deposited in the vessel wall, resulting in narrowing and eventual impairment of blood flow. Severely restricted blood flow in the arteries to the heart muscle leads to symptoms such as chest pain. Atherosclerosis shows no symptoms until a complication occurs.

Researchers have been investigating whether surgery offers any advantages if used as an early treatment for mild angina. A major analysis in 2003 reported that the use of angioplasty in patients with mild heart blockage did not reduce the risk for heart attack or death over the long term. A landmark 2007 study found that angioplasty was no better than drug therapy for preventing heart attack and stroke in patients with stable coronary artery disease. (For more information, see Angioplasty and Stents.)

Two effective surgical procedures for heart patients are:

Coronary artery bypass grafting (commonly called bypass or CABG)
Percutaneous coronary intervention (commonly called angioplasty or PCI), usually with coronary artery stent placement

Click the icon to see an image about bypass grafting.

Each of these procedures is described below.

Studies have generally reported similar survival rates with either procedure. There are some differences, however, and decision often depends on individual conditions. Patients considering surgery should discuss all options and risks with their doctor. No surgical procedure cures coronary artery disease, and patients must continue to rigorously maintain a healthy lifestyle and any necessary medications. For some patients, lifestyle changes and medications may be able to control the disease without surgery or angioplasty.

Considerations for Choosing Angioplasty with Stent Placement. Angioplasty has the following advantages for most patients. It is:

Less invasive than bypass. (Although a minimally invasive variation of bypass surgery may reduce this distinction.)
Less expensive than bypass. (Although the postoperative need for more medications and the high risk for repeat procedures to reopen the artery may reduce the long-term difference in cost between the two procedures.)
Life-saving emergency procedure for many patients with heart attacks. (The use of bypass after a heart attack has much higher mortality rates than when it is used electively and its use is controversial in heart attack patients.)

It has the following disadvantages:

The blood vessels can close up again (restenosis) so that patients require additional procedures. (New blood thinning drugs, coronary stent coatings, and radiation treatments may help to significantly reduce restenosis rates. However, there is also some indication that stents, especially drug-eluting stents, may increase the risk for blood clots.)
It is not as appropriate as bypass for many patients with angina (people with diabetes, elderly patients, or those with multi-vessel blockage). Increasingly, however, angioplasty is proving to be as safe and as effective as bypass in many high-risk patients. Patients should be sure to discuss with their doctors the relevant risks and benefits of angioplasty and bypass.

Considerations for Choosing Bypass. Bypass is usually the appropriate procedure in patients with high-risk conditions, such as:

Multi-vessel blockage. (In one report comparing surgery to angioplasty in patients with two or three blocked vessels, the mortality rate 1 year after bypass was 0.8% and after angioplasty was 2.5%. About 80% of patients in the study were men.)
Diabetes. (Bypass produces significantly higher survival rates in these patients. Some experts believe angioplasty should rarely, if ever, be used in this population.)
Being elderly.
Certain structural features, such as a left main artery narrowed by 50% or more or a very long diseased portion of the artery.

Considerations for Women. Studies have reported higher mortality rates in women than in men after any heart surgery. Some experts theorize that on average women may be older and sicker when they have a heart operation. A 2002 study, however, suggested that when women with acute coronary syndromes are given the same aggressive and early treatment as men are, their survival rates are equal or even better.

In addition to angioplasty and bypass procedures, a number of other procedures are available or under investigation for coronary artery disease. They include:

Atherectomy
Myocardial Laser Revascularization
Enhanced External Counterpulsation (EECP)

Coronary Artery Bypass Graft Surgery

Coronary artery bypass graft surgery (CABG) is a good alternative to angioplasty for many patients, but it is very invasive. The surgery involves the following processes:

Click the icon to see an animation about CABG.

The chest is opened, and the blood is rerouted through a lung-heart machine.
The heart is stopped during the procedure.
Large blood vessels supply the grafts, which are used to reroute the blood. The blood vessel grafts are transplanted in front of and beyond the blocked arteries, so the blood flows through the new vessels around the blockage.
The standard grafts now use arteries taken from the chest wall. Studies are reporting that with such grafts arteries remain open in 90% of cases after 15 years.
In general, patients with triple bypass procedures stay in the hospital for 5 days. Those with one-vessel bypass may be able to go home in 3 days.

Click the icon to see an illustrated series detailing a heart bypass surgery.

In spite of the invasive nature of this procedure, elective bypass procedures produce better long-term survival rates than angioplasty, particularly in patients with diabetes and multi-vessel blockage. Overall mortality rates after this procedure range from 1% to slightly over 2%. The risk for stroke or heart attack after a bypass operation ranges from 1.3 - 5%. Finding a surgeon who performs at least 100 of the procedures a year helps reduce the risk for complications.

Blood clots may form in the new graft, closing it up or narrowing the treated vessel over time. Therapy with aspirin and other anti-clotting drugs help keep the graft open and working properly. For long-term prevention of closure, as well as for slowing progression of atherosclerosis, aggressive treatment with cholesterol-lowering drugs may be more beneficial than standard anti-clotting drugs.

Bleeding is also a potential complication of CABG. Anti-bleeding (also called hemorrhage-sparing) drugs are sometimes used to limit blood loss in patients who undergo this surgery. In 2006, concerns were raised about one of these drugs, aprotinin (Trasylol). Data suggested that aprotinin seriously increased the risks for kidney failure, heart failure, and stroke.

An important study, published in 2007 in the Journal of the American Medical Association, compared aprotinin with two anti-fibrinolytic drugs, aminocaproic acid (Amicar) and tranexamic acid (Cyklokapron), which are also used to control blood loss. The study of nearly 4,000 patients who had CABG found that over a 5-year period, the death rate for patients who took aprotinin was 21%, and patients had a 48% increased risk of dying. By comparison, the death rate was 16% for aminocaproic acid, 15% for tranexamic acid, and 13% for no anti-bleeding drug. Because aprotinin is more expensive as well as potentially more dangerous than other anti-bleeding drugs, experts are now recommending against its use in CABG.

Minimally invasive bypass (also called buttonhole or keyhole bypass) surgeries are exciting advances in basic bypass surgery. Studies indicate good success of these procedures for patients with disease in single vessels. They are also being investigated for multiple vessels.

One variation of minimally invasive bypass uses a four-inch incision. The surgeon works on the front of the heart while it is beating slowly. To date, there have been no differences in cardiac events or later mental complications between this so-called off-pump procedure and the standard bypass procedure.
In another variation, the heart is stopped, and the patient is put on a machine that reroutes the blood through a device that keeps it oxygenated. Fiberoptic scopes and instruments are passed through a number of finger-sized incisions. The surgeon works on all sides of the heart, guided by a video image from a tiny camera inserted through a 4-inch incision.
Some advanced heart centers now use robotic systems, which allow the surgeon to perform extremely delicate maneuvers on tiny vessels through pencil-size incisions. They are not yet used for the whole bypass process.

Eventually, minimally invasive bypass procedures may prove to be less expensive, require a shorter hospital stay, and have fewer complications than conventional coronary artery bypass surgery -- or even angioplasty. At this time, however, they are experimental procedures, performed in only a few medical centers for select candidates. Long term-success rates are unknown.

Angioplasty and Stents

Percutaneous coronary intervention (PCI), also called angioplasty, involves procedures such as percutaneous transluminal coronary angioplasty (PTCA) that help open the blocked artery.

Click the icon to see an animation about percutaneous transluminal coronary angioplasty.

A typical angioplasty procedure follows these steps:

The cardiologist threads a narrow catheter (a tube) containing a catheter into the blocked vessel.
The doctor opens the blocked vessel using balloon angioplasty, in which the surgeon passes a tiny deflated balloon through the catheter to the vessel.
The balloon is inflated to compress the plaque against the walls of the artery, flattening it out so that blood can once again flow through the blood vessel freely.
In order to keep the artery open afterwards, surgeons use a device called a coronary stent, an expandable metal mesh tube that is implanted during angioplasty at the site of the blockage. (In some cases, a stent may be used as the initial opening device instead of balloon angioplasty.)
Once in place, the stent pushes against the wall of the artery to keep it open.

Click the icon to see an animation about percutaneous transluminal coronary angioplasty.

Complications occur in about 10% of patients (about 80% within the first day). Outcomes are better in hospital settings with experienced teams and backup.

Click the icon to see an illustrated series detailing coronary artery balloon angioplasty surgery.

The most important long-term complication is reclosure (restenosis), which can lead to heart attack if not treated with a repeat procedure. Stenting and other advances have helped significantly in preventing reclosure and reducing heart attack rates. Nevertheless, a repeat procedure is still needed to restore the opening in 10 - 15% of procedures that use stents.

PCI (angioplasty) has been proven to help reduce the frequency of angina attacks. It is commonly recommended for patients who have critically blocked arteries or have already had a recent, acute heart attack. PCI can also help improve survival and prevent heart attacks in patients with acute coronary syndrome (ACS). However, doctors have been uncertain about angioplasty’s benefits for survival and heart attack prevention in lower-risk patients with stable coronary artery disease.

In 2007, a landmark study was published in the New England Journal of Medicine and presented at the 2007 meeting of the American College of Cardiology. The COURAGE study found that PCI works no better than standard heart medication (drugs to control blood pressure, lower cholesterol, and prevent blood clots) in preventing heart attack, stroke, and hospitalization in patients with stable coronary artery disease. Based on this study’s findings, experts are now recommending angioplasty only for patients who have severe heart disease. For patients with stable heart disease, drug therapy may be sufficient enough treatment and allow them to safely defer having surgery.

Angioplasty is less invasive than bypass surgery, requiring only one night in the hospital. Recuperation takes about a week. Chest pain after the procedure is very common and usually due to problems other than ischemia. Mild chest pain is even more common when a stent is used, possibly because the artery is stretched.

Reclosure of the artery during or shortly after angioplasty often occurs. A number of anti-clotting drugs are used to help prevent this.

Aspirin and the anti-platelet drug clopidogrel (Plavix) are often used to prevent reclosure during the procedure.
A high dose of the anticoagulant heparin is typically given before the operation.
Intravenous glycoprotein IIb/IIIa inhibitors, powerful drugs that block platelets, also prevent reclosure after stenting in many high-risk patients, and evidence now strongly suggests that they reduce rates of heart attack and death. Eptifibatide (Integrilin) and tirofiban (Aggrastat) are the standard drugs used during angioplasty. They may be most effective if administered during angioplasty, rather than beforehand.

All of these drugs pose a risk for bleeding complications.

Narrowing or reclosing of the artery (restenosis) can occur within a year of angioplasty or even longer in 15 - 60% of angioplasty patients. Coronary stents, anti-clotting drugs, and other advances have reduced these events significantly, but have not eliminated the problem. Theories for the cause of restenosis include:

The release of oxidants (damaging unstable particles) at the surgical site may cause injury and activate immune factors that produce cellular overgrowth in smooth muscles of the blood vessels.
Other activities, including scarring, may remodel and narrow the blood vessels. (This is most likely the reason for restenosis in patients with stents.)

Symptoms of restenosis include chest pain on exertion. (Heart attacks, however, do not usually occur with such events.) The narrowing of the artery in this case is not due to blood clots, so anti-clotting drugs are not useful. Restenosis usually requires a repeat operation. A number of approaches, mostly investigative, have been developed to prevent restenosis after angioplasty.

Drug-Coated Stents. Stents coated with the drugs sirolimus (Rapamune) or paclitaxel (Taxol) have been increasingly used in the last several years. Drug-eluting stents (as they are also called) can help prevent restenosis. However, because drug-eluting stents reduce arterial tissue growth, they can increase the risks of blood clots. In late 2006, the FDA held several meetings to discuss the increased risks of blood clots associated with drug-eluting stents. The committees found that drug-eluting stents do appear to have a small increased risk of blood clots compared to bare metal stents, but not enough research has been conducted to fully determine their risks for heart attack and death.

Five studies published in the New England Journal of Medicine in March 2007 indicated that drug-eluting stents are safe and effective for patients with coronary artery disease when they are used for FDA-approved indications. Problems have arisen when these stents are used for “off-label” purposes in patients with more complicated health problems. There is still some concern as to whether all stents (both bare metal and drug eluting) are used too frequently for patients who may be better served by drugs or bypass surgery.

In February 2007, the American Heart Association and other professional organization issued an extremely important joint advisory statement. The statement advises that all patients who have drug-eluting stents must continue to take aspirin and clopidogrel (or, rarely, ticlopidine) for at least 1 year after the stent is inserted to reduce the risk of blood clots. Clopidogrel and ticlopidine are thienopyridine drugs that, like aspirin, help prevent blood platelets from clumping together. It is very important that patients who have drug-eluting stents take both aspirin and a thienopyridine drug. If for some reason patients cannot take a thienopyridine drug, they should receive a bare metal stent instead of a drug-eluting stent.

Coronary Artery Brachytherapy. Radiation treatment called coronary artery brachytherapy (Gamma One, Beta-Cath) can slow the cell growth in the arteries that causes restenosis. With this approach, any blockage in the stent is first removed, and a tube with an inflatable balloon is inserted. The surgeon then implants a temporary device that delivers radiation. Brachytherapy has shown excellent results in preventing restenosis and significantly reducing heart events and improving survival. Brachytherapy is also showing promise in preventing restenosis in stented artery grafts that were put in place after bypass surgery and later failed. However, several 2006 studies in the Journal of the American Medical Association indicated that drug-coated stents may work better than brachytherapy in preventing restenosis in failed stents. In these studies, the drug-coated stents were inserted inside the original bare metal stents.

Medications. A number of medications are being studied for prevention of restenosis, although benefits to date have been modest. Other drugs under investigation include statins, various anti-clotting drugs, and B vitamins.

Other Procedures. Other procedures under investigation to keep the arteries open use ultrasound, "soft" x-rays, and cryotherapy (very low temperatures).

Other Treatments

Transmyocardial laser revascularization (TMLR) applies laser energy directly to areas in the heart where blockage has occurred, creating 10 - 50 tiny channels. TMLR is recommended for patients with severe angina who have not responded to surgical bypass or angioplasty procedures. TMLR is not suitable for patients who have severely damaged heart muscles. A variant called percutaneous transmyocardial laser revascularization uses a small laser (a holmium YAG laser), which is smaller than the device used in TMLR and does not require open chest surgery and a general anesthetic.

Patients report improved symptoms and exercise tolerance. Both procedures carry risks for serious complications, however, including some that can be life-threatening. It is not clear if either TMLR procedure improves survival, and, in one study, the quality of life afterwards was less than with standard heart surgeries.

A noninvasive technique called enhanced external counterpulsation (EECP) has been used successfully by over a million people in China. The technique uses an air pump that inflates and deflates pressurized cuffs around the legs, causing blood to be pushed into the heart.

EECP may help patients with angina who have not had pain relief from nitrate drugs and who do not qualify as candidates for bypass or angioplasty. In different studies, it has relieved angina in over 75% of patients who used it and reduced the need for medication. The benefits persist, and there is some evidence that it produces actual cellular changes that benefit the heart. In 2002, the FDA approved EECP for the treatment of heart failure but some insurance companies still consider its use “experimental” and will not pay for it. EECP is not recommended for patients with arrhythmia, serious heart valve problems, or peripheral artery disease.

Atherectomy procedures clear the narrowed arteries by using an approach called debulking. All of these procedures use a catheter (a thin tube) that is inserted into an artery (usually in the groin) and threaded up to the blockage. Devices are inserted through the tube to remove the plaque. They include:

Rotational atherectomy, which uses a tiny cutter spinning at 2,500 rpm
Extractional atherectomy, which "shaves" the plaque
Directional atherectomy, which slices the plaques

Although they are successful in opening arteries, they offer no advantages over standard angioplasty and are used only for special cases.

Resources

www.nhlbi.nih.gov -- National Heart, Lung, and Blood Institute
www.americanheart.org -- American Heart Association
www.acc.org -- American College of Cardiology

References

Boden WE, O'Rourke RA, Teo KK, Hartigan PM, Maron DJ, Kostuk WJ, et al. Optimalmedical therapy with or without PCI for stable coronary disease. N Engl J Med. 2007 Mar 26; [Epub ahead of print]

Garcia MJ, Lessick J, Hoffmann MH; CATSCAN Study Investigators. Accuracy of 16-row multidetector computed tomography for the assessment of coronary artery stenosis. JAMA. 2006 Jul 26;296(4):403-11.

Kastrati A, Mehilli J, Pache J, Kaiser C, Valgimigli M, Kelbaek H, et al. Analysis of 14 trials comparing sirolimus-eluting stents with bare-metal stents. N Engl J Med. 2007 Mar 8;356(10):1030-9. Epub 2007 Feb 12.

Lagerqvist B, James SK, Stenestrand U, Lindback J, Nilsson T, Wallentin L; SCAAR Study Group. Long-term outcomes with drug-eluting stents versus bare-metal stents in Sweden. N Engl J Med. 2007 Mar 8;356(10):1009-19. Epub 2007 Feb 12.

Lloyd-Jones DM, Liu K, Tian L, Greenland P. Narrative review: Assessment of C-reactive protein in risk prediction for cardiovascular disease. Ann Intern Med. 2006 Jul 4;145(1):35-42.

Maisel WH. Unanswered questions--drug-eluting stents and the risk of late thrombosis. N Engl J Med. 2007 Mar 8;356(10):981-4. Epub 2007 Feb 12.

Mangano DT, Miao Y, Vuylsteke A, Tudor IC, Juneja R, Filipescu D, et al. Mortality associated with aprotinin during 5 years following coronary artery bypass graft surgery. JAMA. 2007 Feb 7;297(5):471-9.

Mangano DT, Tudor IC, Dietzel C; Multicenter Study of Perioperative Ischemia Research Group; Ischemia Research and Education Foundation. The risk associated with aprotinin in cardiac surgery. N Engl J Med. 2006 Jan 26;354(4):353-65.

Mauri L, Hsieh WH, Massaro JM, Ho KK, D'Agostino R, Cutlip DE. Stent thrombosis in randomized clinical trials of drug-eluting stents. N Engl J Med. 2007 Mar 8;356(10):1020-9. Epub 2007 Feb 12.

Mosca L, Banka CL, Benjamin EJ, Berra K, Bushnell C, Dolor RJ, et al. Evidence-based guidelines for cardiovascular disease prevention in women: 2007 update. Circulation. 2007 Mar 20;115(11):1481-501.

Nicholls SJ, Tuzcu EM, Sipahi I, Grasso AW, Schoenhagen P, Hu T, et al. Statins, high-density lipoprotein cholesterol, and regression of coronary atherosclerosis. JAMA. 2007 Feb 7;297(5):499-508.

Rosamond W, Flegal K, Friday G, Furie K, Go A, Greenlund K, et al. Heart disease and stroke statistics--2007 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2007 Feb 6;115(5):e69-171. Epub 2006 Dec 28.

Spaulding C, Daemen J, Boersma E, Cutlip DE, Serruys PW. A pooled analysis of data comparing sirolimus-eluting stents with bare-metal stents. N Engl J Med. 2007 Mar 8;356(10):989-97. Epub 2007 Feb 12.

Stewart JC, Janicki DL, Muldoon MF, Sutton-Tyrrell K, Kamarck TW. Negative emotions and 3-year progression of subclinical atherosclerosis. Arch Gen Psychiatry. 2007 Feb;64(2):225-33.

Stone GW, Moses JW, Ellis SG, Schofer J, Dawkins KD, Morice MC, et al. Safety and efficacy of sirolimus- and paclitaxel-eluting coronary stents. N Engl J Med. 2007 Mar 8;356(10):998-1008. Epub 2007 Feb 12.

Wang TJ, Gona P, Larson MG, Tofler GH, Levy D, Newton-Cheh C, et al. Multiple biomarkers for the prediction of first major cardiovascular events and death. N Engl J Med. 2006 Dec 21;355(25):2631-9.

Review Date:
4/16/2007
Reviewed By:
Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

A.D.A.M. Copyright

adam.com

High blood pressure

FitSugar — Wed, 08 Oct 2008 17:35:08 -0700

In This Report

Highlights
Introduction
Diagnosis
Causes
Risk Factors
Complications
Symptoms
Treatment
Lifestyle Changes
Medications
Classes of Medications
Resources
References

HEALTH GUIDE REFERENCE FROM A.D.A.M

Highlights

Drug Approval

In 2007, the FDA approved a new type of high blood pressure drug. Aliskiren (Tekturna) blocks renin, a kidney enzyme that is associated with blood pressure regulation. Aliskiren can be taken alone or in combination with other blood pressure drugs, but it should not be used during pregnancy.

Drug Concerns

ACE inhibitors should never be taken during the second or third trimesters of pregnancy. An important 2006 New England Journal of Medicine study extended these concerns by reporting that ACE inhibitors may cause major heart birth defects during the first trimester. Although this research is still preliminary, the FDA and the American Heart Association now recommend that women who are pregnant or considering becoming pregnant switch to another type of blood pressure drug.
Nonsteroidal anti-inflammatory drugs (NSAIDs) may increase the risk of developing high blood pressure in men, suggests a 2007 Archives of Internal Medicine study. Previous research indicated that these non-prescription painkillers increase high blood pressure risk in women.

Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT)

The ALLHAT trial has been the most important long-running clinical study for evaluating the effects of high blood pressure medications. One of its most critical findings established the importance of thiazide-type diuretics as first-line treatment for high blood pressure. Recent trial results indicate:

Diuretics are very helpful for preventing heart failure in patients with high blood pressure. In a 2006 Circulation study, diuretics outperformed ACE inhibitors and calcium channel blockers in reducing heart failure risk.
Thiazide-type diuretics may slightly increase the risk of developing diabetes more than other drug classes but their blood pressure-lowering benefits outweigh the risks, according to a 2006 Archives of Internal Medicine study. The study found that all types of blood pressure medications increase blood sugar levels and diabetes risk.

Introduction

High blood pressure, also called hypertension, is elevated pressure of the blood in the arteries. Hypertension results from two major factors, which can be present independently or together:

The heart pumps blood with excessive force
The body's smaller blood vessels (known as the arterioles) narrow, so that blood flow exerts more pressure against the vessels' walls

Blood pressure is the force applied against the walls of the arteries as the heart pumps blood through the body. The pressure is determined by the force and amount of blood pumped and the size and flexibility of the arteries.

Although the body can tolerate increased blood pressure for months and even years, eventually the heart may enlarge (a condition called hypertrophy), which is a major factor in heart failure.

Click the icon to see an image of hypertrophic cardiomyopathy.

Such pressure can also injure blood vessels in the heart, kidneys, the brain, and the eyes.

Two numbers are used to describe blood pressure: the systolic pressure (the higher and first number) and the diastolic pressure (the lower and second number). Health dangers from blood pressure may vary among different age groups and depending on whether systolic or diastolic pressure (or both) is elevated. A third measurement, pulse pressure, may also be important as an indicator of severity.

Blood pressure is measured in millimeters of mercury (mm Hg). According to current adult guidelines, blood pressure is categorized as normal, prehypertensive, and hypertensive (which is further divided into Stage 1 and 2, according to severity). People in normal health should have a blood pressure reading of 120/80 mm Hg or less. High blood pressure is generally considered to be a blood pressure reading greater than or equal to 140 mm Hg (systolic) or greater than or equal to 90 mm Hg (diastolic). Blood pressure readings in the prehypertension category (120-139 systolic or 80-89 diastolic) indicate an increased risk for developing hypertension.

Current guidelines for children are based on percentile ranges for a child’s body size. Hypertension is defined as average systolic and diastolic readings that are greater than the 95th percentile for gender, age, and height on at least three occasions. Prehypertension in children is diagnosed when average systolic or diastolic blood pressure levels are at least in the 90th percentile but less than the 95th percentile. For adolescents, as with adults, blood pressure readings greater than 120/80 are considered prehypertensive. Increasing rates of childhood obesity have lead to higher than average blood pressure levels in children.

American expert groups recommend treating any blood pressure above normal. Some experts are concerned, however, that such guidelines may unnecessarily increase the use of anti-hypertensive drugs. It is important that patients establish a relationship with a doctor whom they trust, to help them determine individual blood pressure goals and treatment regimens. For some patients, a decrease of a few points in blood pressure may not be worth the side effects caused by higher doses of anti-hypertensive drugs.

Systolic Blood Pressure. The systolic pressure (the first and higher number) is the force that blood exerts on the artery walls as the heart contracts to pump out the blood. High systolic pressure is now known to be a greater risk factor than diastolic pressure for heart, kidney, and circulatory complications and for death, particularly in middle-aged and elderly adults. The wider the spread between the systolic and diastolic measurements, the greater the danger.

Elevated systolic pressure may pose a significant danger for heart events and stroke events even when diastolic is normal -- a condition called isolated systolic hypertension. Isolated systolic hypertension is the most common form of hypertension in people older than age 50. In one study, it comprised 87% of hypertension cases in people between ages 50 and 59.

Diastolic Blood Pressure. The diastolic pressure (the second and lower number) is the measurement of force as the heart relaxes to allow the blood to flow into the heart. High diastolic pressure is a strong predictor of heart attack and stroke in young adults.

Pulse Pressure. Pulse pressure is the difference between the systolic and the diastolic readings. It appears to be an indicator of stiffness and inflammation in the blood-vessel walls. The greater the difference between systolic and diastolic numbers, the stiffer and more injured the vessels are thought to be. Although not yet used by doctors to determine treatment, evidence suggests that it may prove to be a strong predictor of heart problems, particularly in older adults. Some studies suggest that in people over 45 years old, every 10 mm Hg increase in pulse pressure increases the risk for stroke rises by 11%, cardiovascular disease by 10%, and overall mortality by 16%. (In younger adults the risks are even higher.)

Click the icon to see an animation about blood pressure.

Some experts categorize hypertension into the following types:

Essential Hypertension. Essential hypertension is also known as primary or idiopathic hypertension. About 90% of all high blood pressure cases are this type. The causes of essential hypertension are unknown but are based on complex processes in all major organs and systems, including the heart, blood vessels, nerves, hormones, and the kidneys.

Secondary Hypertension. Secondary hypertension comprises about 5% of high blood pressure cases. In this condition, the cause has been identified.

Isolated Systolic Hypertension. This occurs when systolic hypertension is over 140 mm Hg but diastolic pressure is normal. It is related to arteriosclerosis (hardening of the arteries).

Click the icon to see an image of atherosclerosis.

Pregnancy Induced Hypertension. This condition occurs during pregnancy if blood pressure increases by more than 15 mm Hg above normal.

White Coat Hypertension. This form of hypertension is elevated blood pressure that occurs only during a visit to the doctor's office, but not at home. It is a factor in about 20% of patients with mild hypertension. Although previously considered a relatively harmless condition, research now suggests that white-coat hypertension shares certain features with essential hypertension. Studies have even suggested that white-coat hypertension actually may pose a risk for future heart problems, although the increased danger appears to be small compared with the risk in those with steady mild hypertension.


Blood Pressure Category	Ranges for Most Adults (systolic/diastolic)
Normal Blood Pressure (systolic/diastolic)	Systolic below 120 mm Hg Diastolic below 80 mm Hg
Prehypertension (Formerly Normal to High-Normal Blood Pressure)	Systolic 120 - 139 mm Hg Diastolic 80 - 89 mm Hg (NOTE: 139/89 or below should be the minimum goal for everyone. People with diabetes or chronic kidney disease should strive for 130/80 or less.)
Mild Hypertension (Stage 1)	Systolic 140 - 159 mm Hg Diastolic 90 - 99 mm Hg
Moderate to Severe Hypertension (Stage 2)	Systolic over 160 mm Hg or Diastolic over 100 mm Hg
Note: If one of the measurements is in a higher category than the other, the higher measurement is usually used to determine the stage. For example, if systolic pressure is 165 (Stage 2) and diastolic is 92 (Stage 1), the patient would still be diagnosed with Stage 2 hypertension. It should be strongly noted that a high systolic pressure compared to a normal or low diastolic pressure should be a major focus of concern in most adults.

Diagnosis

Most physical exams include a blood pressure measurement. Patients should not smoke or drink caffeinated beverages within 30 minutes before their blood pressure measurement.

The standard instrument used to measure blood pressure is called a mercury sphygmomanometer. Measurements are given as units of mercury, which has filled the central column in standard sphygmomanometers for years. (Some people view the mercury sphygmomanometer as an environmental health hazard, but modern devices are designed to prevent mercury spillage.)
An inflatable cuff with a meter attached is placed around the patient's arm over the artery while the patient is seated. The inflated cuff briefly interrupts the flow of blood in the artery, which then resumes as the cuff is slowly deflated.
The person taking the blood pressure listens through a stethoscope for so-called Korotkoff sounds, which first appear as blood begins to flow through the artery and then change in tone and volume as the cuff is deflated.
If a first blood pressure reading is above normal, the health professional may take two or more measurements separated by 2 minutes with the patient sitting or lying down. Another measurement may be taken after the patient has been standing for 2 minutes.

To measure blood pressure, your doctor uses an instrument called a "sphygmomanometer," more often referred to as a blood pressure cuff. The cuff is wrapped around your upper arm and inflated to stop the flow of blood in your artery. As the cuff is slowly deflated, your doctor uses a stethoscope to listen to the blood pumping through the artery. These pumping sounds register on a gauge attached to the cuff. The first pumping sound your doctor hears is recorded as the systolic pressure, and the last sound is the diastolic pressure.

Although this test has been used for more than 90 years, it is not completely accurate or sensitive. The following factors can cause a falsely low pressure reading:

An arm cuff that is too wide
Recent exercise
Not smoking for a while after heavy, long-term smoking

Falsely high pressure can result from:

An arm cuff that is too small
Talking during the test
Recently consuming foods or beverages (such as coffee) that raise blood pressure

Office blood pressure readings taken by a doctor are more likely to be higher than readings measured at home. This so-called white-coat hypertension requires additional readings by a nurse or by the patient. Home monitoring improves the accuracy of a simple office measurement. An average of all the measurements will be considered in the diagnosis of hypertension. If high normal or high blood pressure persists, further tests should be performed to determine if the organs are affected.

Other Blood-Pressure Monitors. Alternative pressure-measuring aneroid and electronic devices are available. Aneroid instruments are round, compass-like devices that use a metal spring to measure blood pressure and are often used by doctors. Electronic devices are typically used for home monitoring.

Monitoring Equipment. A number of home tests are available for checking blood pressure between doctor visits. A doctor may loan a patient a portable unit that records blood pressure during a full day's activity. This test, known as ambulatory monitoring, is particularly useful for those who experience wide blood pressure swings, such as those who have white-coat hypertension or show resistance to drug therapy. According to one study, accurately measuring blood pressure at home over a full day was a significantly better predictor of cardiovascular risk than standard office-based measurements. To improve clinical outcomes, devices are now available that allow 24-hour ambulatory blood pressure monitoring and electronically store results for analysis by the doctor. It is not clear if their added benefits justify their expense, however.

Cuffs and Stethoscopes. Manual cuffs and stethoscopes are fairly accurate, but they require practice to use. The cuff must be the right size (one size does not fit all). Devices that use a digital readout and a cuff that can be electronically inflated and deflated are proving to be as accurate as a stethoscope.

Blood Pressure Variations at Home. In general, everyone's blood pressure varies in the same way throughout a given day. In monitoring at home, it is important to note these changes:

Blood pressure is usually highest at work.
It drops slightly at home.
It then normally dips to its lowest level during sleep. There are important exceptions. Certain people have a condition called nondipper hypertension, in which blood pressure does not fall at night. Postmenopausal women appear to be at particular risk for this phenomenon, and it may pose a special danger for heart disease and stroke (particularly in older African-American women). It has also been linked to salt-sensitivity and insulin resistance.

Click the icon to see an image of stroke.

Upon waking, pressure in most people typically increases suddenly. In people with severe high blood pressure, this is the highest risk period for heart attack and stroke.

Click the icon to see an image of a heart attack.

Some studies have reported that when patients record and report their own blood pressure, they are unreliable and don't always tell the truth. Despite the difficulties and controversy surrounding this issue, home blood pressure monitoring has been shown to encourage patients to use measures that control their blood pressure and thereby reduce the risk of cardiovascular events.

Click the icon to see an image about monitoring blood pressure.

If blood pressure is elevated, the doctor will check the patient's pulse rate, examine the neck for distended veins or an enlarged thyroid gland, check the heart for enlargement and murmurs, and examine the abdomen and the eyes.

Click the icon to see an image of the thyroid gland.

If hypertension is suspected, the doctor should obtain the following information:

A family and personal medical history, especially incidence of high blood pressure, stroke, heart problems, kidney disease, or diabetes.
Risk factors for heart disease and stroke, including tobacco use, salt intake, obesity, physical inactivity, and unhealthy cholesterol levels.
Any medications being taken.
Any symptom that might indicate so-called secondary hypertension (that is, caused by another disorder). Such symptoms include headache, heart palpitations, excessive sweating, muscle cramps or weakness, or excessive urination.
Any emotional or environmental factors that could affect blood pressure.

If a physical examination indicates hypertension, additional tests may help determine whether it is secondary hypertension or essential hypertension (no other disorder is present) and whether organ damage is present. They include the following:

Blood tests and a urinalysis. (Performed to check for a number of factors, including potassium levels, cholesterol, blood sugar, infection, kidney function, and other possible problems. Measuring blood levels of the protein creatinine, for example, is important for all hypertensive patients in order to determine kidney damage. Higher concentrations may also be an indicator of heart disease.)

An electrocardiogram (ECG).

Click the icon to see an image of an electrocardiogram.

An exercise stress test. This could be important for those with borderline hypertension. Stress-induced blood pressure in such patients has been associated with a risk for left ventricular hypertrophy, a serious complication in which the muscles on the left side of the heart become enlarged. Studies also suggest that an excessive rise in systolic pressure during exercise indicates a risk for coronary artery disease, and stroke.

Click the icon to see an image of blood pressure tests.

Causes

Hypertension is referred to as essential (primary) when the doctor is unable to identify a specific cause. It is by far the most common type of high blood pressure. The causes of this type are unknown but are likely to be a complex combination of genetic, environmental, and other factors.

Genetic Factors. A number of genetic factors or interactions between genes play a major role in essential hypertension. Experts think that the chromosomes (13 and 18) house the genes responsible for blood pressure regulation, although pinning down the range of specific genes involved in hypertension is more difficult.

Abnormalities in the Angiotensin-Renin-Aldosterone System. Genes under intense study are those that regulate a group of hormones known collectively as the angiotensin-renin-aldosterone system. This system influences all aspects of blood pressure control, including blood vessel contraction, sodium and water balance, and cell development in the heart.

Experts believed that this system evolved millions of years ago to protect early humans during drought or stress by retaining salt and water and narrowing blood vessels to ensure adequate blood flow and repair injured tissue. With industrialization, however, this system wreaks havoc on modern humans by intensifying the effects of high-salt diets and sedentary lifestyle. Of particular importance in these harmful responses are the hormone aldosterone and a peptide (a component of proteins) called angiotensin II.

Inherited Abnormalities in the Sympathetic Nervous System. Studies suggest that some people with essential hypertension may inherit abnormalities of the sympathetic nervous system. This is the part of the autonomic nervous system that controls heart rate, blood pressure, and the diameter of the blood vessels.

Insulin Resistance and Type 2 Diabetes. Hypertension is strongly associated with diabetes, both type 1 and type 2. Kidney damage is generally the cause of high blood pressure in type 1 diabetes. Obesity and insulin resistance are the factors associated with hypertension in type 2 diabetes, the more common type. People with type 2 diabetes generally have normal or high levels of insulin, a critical hormone in the metabolism of sugar. However, they are unable to use the insulin, the condition called insulin resistance. Without insulin, blood glucose (sugar) levels rise, the hallmark of diabetes.

Some research indicates that obesity is the one common element linking insulin, type 2 diabetes, and high blood pressure. Obesity is common in both type 2 diabetes and hypertension. Oddly, however, studies have found a stronger association between hypertension and insulin resistance in thin patients as well as overweight people with type 2 diabetes. Some research indicates that insulin resistance may cause sodium retention, a contributor to high blood pressure.

In any case, regardless of the causal connections, people who have insulin resistance or full-blown diabetes plus hypertension have a significantly greater chance for heart attack, kidney disease, and stroke than people who have only high blood pressure.

Obesity. Obesity on its own has a number of possible effects that could lead to hypertension. It may blunt certain actions of insulin that open blood vessels, and it may cause structural changes in the kidney and abnormal handling of sodium. It is also associated with alterations in the systems that regulate blood flow.

Low Levels of Nitric Oxide. The gas nitric oxide can be produced in the body, where it affects the smooth muscle cells that line blood vessels; it helps keep them relaxed, flexible. It may also help prevent blood clotting. Low levels of nitric oxide have been observed in people with high blood pressure (particularly in African-Americans) and may be an important factor in essential hypertension.

Secondary hypertension has recognizable causes, which are usually treatable or reversible.

Medical Conditions. A number of medical conditions can cause secondary high blood pressure:

Kidney disease is the most common cause of secondary hypertension, particularly in older people.
Sleep apnea, a disorder in which breathing halts briefly but repeatedly during sleep, is now highly associated with hypertension. A weak but still higher than normal association with high blood pressure has even been observed in those who snore or have mild sleep apnea. The relationship between sleep apnea and hypertension has been thought to be largely due to obesity, but major studies are finding a higher rate of hypertension in people with sleep apnea regardless of their weight. Treating sleep apnea with a device known as nasal continuous positive airway pressure (CPAP) may have modest benefits blood pressure as well.

CPAP is an airway treatment using slight positive pressure during inhalation to increase the volume of inspired air and to decrease the work of breathing.

Other medical conditions that contribute to temporary hypertension are pregnancy, cirrhosis, and Cushing's disease.

Click the icon to see an image of cirrhosis of the liver.

Medications. Certain prescription and over-the-counter drugs can cause temporary high blood pressure. They include:

Corticosteroids
Acetaminophen (Tylenol)
Nonsteroidal anti-inflammatory drugs (NSAIDs) -- such as ibuprofen (Motrin), naproxen (Aleve), and aspirin -- may cause secondary hypertension as well as other complications. In one important study, women who used an NSAID for 5 or more days a month had a significantly higher risk for hypertension. The more often they used these drugs, the higher the risk. A 2007 study indicated that NSAIDs also increase the risk for hypertension in men. A 2005 study found that NSAIDs increase the risk for kidney failure, and that the risk is significantly greater for all patients with hypertension. Patients who took diuretics along with NSAIDs had 11.6 times the risk of developing acute kidney failure compared to non-NSAID users. The relative risk for calcium channel blockers and NSAIDs was 7.8. The researchers advised that NSAIDs should be used with caution in patients with hypertension or heart failure.
Cold medicines containing pseudoephedrine have also been found to increase blood pressure in hypertensive people, although they appear to pose no danger for those with normal blood pressure.
Oral contraceptives ("the pill") increase the risk for high blood pressure, particularly in women who are older, obese, smokers, or some combination. Stopping the pill nearly always reduces blood pressure, although a recent study suggested that oral contraceptives may produce a small but significant increase in diastolic pressure that persists in some older women who have been off the pill for years.

Alcohol, Cigarettes, and Coffee

An estimated 10% of hypertension cases are caused by alcohol abuse (three or more alcohol drinks a day), with heavier drinkers having higher pressure. Women may be more sensitive than men to the blood pressure effects of alcohol. Moderate drinking (one or two drinks a day) has benefits for the heart and may even protect against some types of stroke. In particular, red wine may have chemicals that help blood pressure.
Smoking. Smoking is a major risk factor. One study reported that smokers have blood pressures up to 10 points higher than nonsmokers.
Caffeine. In healthy people with normal blood pressure, drinking a couple of cups of coffee a day is unlikely to do any harm. A high intake of coffee may be harmful in people with hypertension and may even increase their risk for stroke.

Other Causes of Secondary High Blood Pressure

Stress
Intense workouts (snow shoveling, jogging, speed walking, tennis, heavy lifting, heavy gardening)

Risk Factors

During the last decade, the number of Americans with high blood pressure has increased by 30%. Over 65 million American adults now have high blood pressure, and this condition affects close to 1 billion people worldwide. Less than half of these people are on medication, however, and only about half of this group have their blood pressure under good control with such drugs. Older people are less likely to be treated adequately. The majority of people with high blood pressure have the mild type, but even this condition requires attention.

Age is the major risk factor of hypertension. Blood pressure increases with age in both men and women, and in fact, the lifetime risk for hypertension is nearly 90%. Two-thirds of Americans over age 60 have hypertension. Older women (60 years and above) currently have the highest rates of hypertension, and mortality rates from hypertension are higher in women than in men. Hypertension is also becoming more common in children and teenagers.

Compared to Caucasians, African Americans have 1.8 times the rate of fatal stroke, 1.5 times the risk for fatal heart disease, and 4.2 times the rates of end-stage kidney disease. In general, about 34% of African American men and women have hypertension; it may account for over 40% of all deaths in this group.

The prevalence of high blood pressure among African Americans is among the highest in the world. The rates of hypertension in Hispanic Americans, Caucasians, and Native Americans are about equivalent (ranging from 24 - 27%). The rate is much lower in Asian/ Pacific Islanders (9.7% in men and 8.4% in women). However, nearly 75% of older Japanese American men are hypertensive.

A number of theories have addressed the reasons for this difference:

African Americans may have lower levels of nitric oxide and higher levels of a peptide called endothelin-1 (ET-1) than Caucasians. Nitric oxide keeps blood vessels flexible and open and ET-1 narrows blood vessels.
African Americans have a higher risk for an impaired response to angiotensin (Ang II), which is a peptide important in regulating salt and water balances. African Americans are more likely to be salt-sensitive than other groups.
Social and income disparities and dietary issues may explain many of the differences in blood pressure rates observed between ethnic groups. For example, while African Americans have a disproportionately high rate of hypertension, one study in rural African villages, where diets are rich in fish, reported only a 3% rate of high blood pressure among inhabitants. Another study reported that Caucasian as well as African Americans in the Southeast have a higher incidence of hypertension and stroke than people in other U.S. regions. The Southeast also has a higher rate of obesity, stress, anxiety, and depression, and diets low in potassium and high in salt, all related to a lower socioeconomic level.
African Americans have a higher prevalence of risk factors (cardiovascular disease, obesity, diabetes and kidney disease) that are associated with hypertension.

In any case, hypertension appears to be dangerously undertreated in major minority groups. Inadequately controlled hypertension is the major factor for the higher mortality rate from heart disease among African Americans, and special treatment considerations need to be addressed in this population. A 2003 treatment consensus statement released by the International Society on Hypertension in Blacks (ISHIB) advises that many African Americans may need at least two medications to help lower their blood pressure. The ISHIB's "15 over 10" rule recommends combination therapy for any patient whose blood pressure exceeds their desired goal by 15 mm Hg systolic or 10 mm Hg diastolic.

Obesity. About one-third of patients with high blood pressure are overweight. Even moderately obese adults have double the risk of hypertension than people with normal weights. Moreover, the increase in blood pressure in aging Americans may be due primarily to weight gain. (In other cultures old age does not necessarily coincide with weight gain or high blood pressure.) Children and adolescents who are obese are at greater risk for high blood pressure when they reach adulthood.

Thinness. Interestingly, thin people with hypertension are at higher risk for heart attacks and stroke than obese people with high blood pressure. Experts think that thin people with hypertension are likely to have conditions such as an enlarged heart or stiff arteries that cause the blood pressure to rise and also pose greater dangers to health.

Low Birth Weight. Low birth weight, particularly in girls, has been associated with high blood pressure in both childhood and adulthood. One study suggested that breast-feeding these babies may help reduce this risk. Another study reported high levels of stress hormones in babies with low birth weight, which could increase the risk for high blood pressure later on. Low birth weight is also associated with subsequent obesity, a major contributor to hypertension.

Up to 75% of cardiovascular problems in people with diabetes may be due to hypertension. There are strong biologic links between insulin resistance (with or without diabetes) and hypertension. It is unclear which condition causes the other. Some experts believe angiotensin may be the common factor linking diabetes and high blood pressure. This natural chemical not only influences all aspects of blood pressure control but also interferes with insulin's normal metabolic signaling. People with diabetes or chronic kidney disease need to reduce their blood pressure to 130/80 mm Hg or lower to protect the heart and help prevent other complications common to both diseases. Lowering systolic pressure may be particularly important for people with diabetes.

Spouses. Studies suggest that spouses of people with high blood pressure are at a much higher risk as well. Such findings indicate that dietary and environmental factors play a role in this disease. Some evidence also indicates that higher risk in spouses may be due to people often choosing mates who are similar to them.

Family History and Genetics. Essential hypertension may be inherited in 30 - 60% of cases. According to one study, being a brother or sister of someone with premature coronary artery disease is a greater risk factor for hypertension than having a parent with the disease. A family history of heart disease is considered to be a major risk factor for high blood pressure in adults under age 65.

Atherosclerosis is a common disorder of the arteries. Fat, cholesterol, and other substances collect in the walls of arteries. Larger accumulations are called atheromas or plaque and can damage artery walls and block blood flow. Severely restricted blood flow in the heart muscle leads to symptoms such as chest pain.

People who are anxious or depressed may have over twice the risk for high blood pressure than those without these problems.

Mental Stress. Recent evidence confirms the association between stress and hypertension. In one 20-year study, men who periodically measured highest on the stress scale were twice as likely to have high blood pressure as those with normal stress. The effects of stress on blood pressure in women were less clear. Job stress and lack of career success have been specifically linked to high blood pressure in both men and women.

Anxiety. Studies suggest that anxiety is a risk factor for hypertension, particularly in women.

Depression. Mounting evidence suggests that depression has physiological effects that impair the heart and that it contributes to destructive behaviors, such as weight gain, smoking, or alcohol abuse. In one study, those who scored highest on a depression test had about twice the risk of high blood pressure as those with the lowest score. This link was particularly strong in African Americans. Depression was the strongest risk factor in this group.

Blood pressure levels tend to be lowest during the morning and midday hours and highest at the end of the day. Seasonal changes also affect blood pressure, with hypertension increasing during cold months and declining during the summer. Blood pressure readings can vary by as much as 40% depending on the time of day and season.

Complications

Hypertension places stress on several organs (called target organs), including the kidneys, eyes, and heart, causing them to deteriorate over time. High blood pressure contributes to 75% of all strokes and heart attacks. It is particularly deadly in African-Americans.

Research suggests that prehypertension is also a serious risk factor for heart complications. A 2005 study found that people with prehypertension are three times more likely to have a heart attack, and nearly twice as likely to develop coronary artery disease as people with normal blood pressure.

Hypertension is a disorder characterized by chronically high blood pressure. It must be monitored, treated and controlled by medication, lifestyle changes, or a combination of both.

Malignant hypertension, an emergency condition resulting from untreated primary hypertension, can be lethal.

About two-thirds of people who suffer a first stroke have moderate elevated blood pressure (160/95 mm Hg) or above. Hypertensive people have up to 10 times the normal risk of stroke, depending on the severity of the blood pressure. Hypertension is also an important cause of so-called silent cerebral infarcts, blockages in the blood vessels in the brain that may predict major stroke or progression to dementia over time.

Uncontrolled chronic high blood pressure is also associated with reduced short-term memory and mental abilities. Isolated systolic hypertension may pose a particular risk for complications in the brain. Fortunately, controlling blood pressure with medications can reduce or even prevent memory loss and mental decline due to hypertension. A 2006 study of older men indicated that anti-hypertensive treatment for at least 5 years may help prevent the development of dementia. Other studies suggest that anti-hypertensive drugs may help protect against Alzheimer's disease in people with genetic susceptibility to this disease.

High blood pressure is a major risk factor for heart disease.

Heart Attack. About half of people who suffer their first heart attack have moderate hypertension (160/95 mm Hg) or greater. High blood pressure increases the risk for a heart attack by up to five times, depending on the severity of the hypertension.

Heart Failure. Hypertension precedes heart failure in 75 - 90% of heart failure cases. High blood pressure has various effects that cause the heart to fail, including:

To compensate for increased blood pressure, the heart must work harder to pump blood, and so its muscles thicken (hypertrophy), usually on the left side (left-ventricle dysfunction). These thickened muscles pump inefficiently, and, over time, the force of their contractions weakens. The heart muscles then have difficulty relaxing and filling the heart with blood. The heart begins to fail.

Click the icon to see an image of a hypertensive heart.

The failing heart then triggers a number of hormonal and neurochemical mechanisms to correct imbalances in blood pressure and flow. This response, called remodeling, is helpful in the short run but very destructive and irreversible over time.
As part of the remodeling process, the heart muscle cells elongate. The muscular walls of the heart dilate and become thinner and inefficient. The cells themselves undergo molecular changes that result in calcium loss, a mineral crucial for healthy heart contractions.
The end-result of remodeling is a falling volume of blood pumped to the kidneys; the kidneys retain water and salt in response, increasing fluid buildup in the body.
To make matters worse, the body's arteries narrow in response to a lower blood volume. This constriction forces the heart to work even harder to pump blood through these narrowed vessels, increasing blood pressure and continuing the cycle.

A 2006 analysis of ALLHAT trial data indicated that diuretics are the best first-line high blood pressure medication for preventing heart failure.

Diabetes. High blood pressure, and the medications used to treat it, can increase the risk for developing diabetes. Studies have reported that thiazide diuretics and beta blockers carry a higher risk for causing diabetes than other anti-hypertensive drugs. However, an important 2006 ALLHAT study compared the effects of various drug classes on blood sugar levels and diabetes development. The results suggested that while diuretics may slightly increase diabetes risk more than other types of anti-hypertensive drugs, this effect does not cause worse heart problems. Most experts believe that thiazide diuretics should remain the first choice for high blood pressure treatment, and that the benefit of blood pressure reduction outweighs the risk of diabetes development.

Diabetes-Related Kidney Disease. High blood pressure is strongly associated with diabetic nephropathy (diabetes-related kidney disease). Most patients with type 2 diabetes who show early signs of nephropathy already have high blood pressure. When patients with type 1 diabetes are diagnosed with early nephropathy, on the other hand, they usually have normal blood pressure readings in the doctor's office. A 2002 study using home monitors, however, found that patients with type 1 diabetes often have high systolic blood pressure during sleep -- before development of nephropathy. Home blood pressure monitoring, then, may help identify patients who are at risk for kidney damage due to high systolic pressure.

End-Stage Kidney Disease. High blood pressure causes 30% of all cases of end-stage kidney disease (medically referred to as end-stage renal disease, or ESRD). Only diabetes leads to more cases of kidney failure.

Kidney Cancer. Men with high blood pressure may also have a higher risk of kidney cancer.

High blood pressure can injure the eyes, causing a condition called retinopathy.

Click the icon to see an image of hypertensive retinopathy.

Hypertension also increases the elimination of calcium in urine, potentially leading to loss of bone mineral density, a significant risk factor for fractures, particularly in elderly women. In one study, women with the highest levels of blood pressure lost bone density at nearly twice the rate of those in the lowest range. It is not clear whether this effect occurs in men or in non-Caucasian women.

Sexual dysfunction is more common and more severe in men with hypertension and in smokers than it is in the general population. Many of the drugs that treat hypertension are thought to cause impotence as a side effect. In these cases, it is reversible when the drugs are stopped. More recent evidence suggests, however, that the disease process that causes hypertension is itself the major cause of erectile dysfunction in these men.

Newer anti-hypertensive drugs, including angiotensin-converting enzyme (ACE) inhibitors and angiotensin-receptor blockers (ARBs), are less associated with erectile dysfunction. ARBs, such as losartan (Cozaar), may be particularly effective in restoring erectile function in men with high blood pressure. Sildenafil (Viagra) is successful in achieving erections in almost two-thirds of patients with controlled high blood pressure. Because sildenafil has a shorter half-life and is eliminated more quickly from the body than newer erectile dysfunction drugs, it may be a safer option for men with hypertension. In a 2003 review of safety data, sildenafil did not appear to pose a risk for men who had both high blood pressure and erectile dysfunction.

Severe, sudden high blood pressure in pregnant women is one component of a condition called preeclampsia (commonly called toxemia) that can be very serious for both mother and child. Preeclampsia occurs in up to 10% of all pregnancies, usually in the third trimester of a first pregnancy, and resolves immediately after delivery. Other symptoms and signs of preeclampsia include protein in the urine, severe headaches, and swollen ankles.

This condition may be caused by a failure of the placenta to embed properly in the uterus, which causes it to misconnect with the mother's blood vessels. As a result, the fetus does not receive a sufficient blood supply, and the mother's own blood pressure increases to replace it. The risk for preeclampsia is higher for first births, multiple births, and for very young women (teenagers) and those over age 35. Pre-existing high blood pressure, diabetes, and kidney disease also increase the risk for preeclampsia. There appears to be a genetic component for this condition, so women whose mothers experienced preeclampsia are also at higher risk.

The reduced supply of blood to the placenta can cause low birth weight and eye or brain damage in the fetus. Severe cases of preeclampsia can cause kidney damage, convulsion, and coma in the mother and can be lethal to both mother and child. Evidence also suggests that preeclampsia can lead to increased risks later in life for coronary heart disease and other heart problems.

Women at risk for preeclampsia (particularly those with existing hypertension) may benefit from having an ultrasound of uterine arteries at 20 - 24 weeks of pregnancy, followed (if abnormal) by 24-hour blood pressure monitoring. Blood pressure medications may be required. Delivery is the main cure for preeclampsia. In severe cases, the obstetrician will need to induce pre-term birth.

High blood pressure may increase the risk of developing fibroids, according to data from the Nurses’ Health Study. Tracking women for 10 years, the prospective epidemiologic study found that for every 10 mm/Hg increase in diastolic blood pressure, the risk for developing fibroids increased by 8 - 10%.

Children with high blood pressure should first be treated with lifestyle changes, including weight reduction, increased physical activity, and diet modification. If blood pressure is not controlled with lifestyle changes, drug treatment may be required. Although there are few clinical trials conducted in children, a 2005 study found that the angiotensin receptor blocker losartan was safe and effective in children. Results of studies evaluating outcomes of children with hypertension suggest that early abnormalities, including enlarged heart and abnormalities in the kidney and eyes, may occur even in children with mild hypertension. Children and adolescents with hypertension should be monitored and evaluated for any early organ damage. Secondary hypertension (high blood pressure due to another disease or drug) is more common in children than adults.

Symptoms

Hypertension has aptly been called the "silent killer" because it usually produces no symptoms. Untreated hypertension increases slowly over the years. It is important for anyone with risk factors to have their blood pressure checked regularly and to make appropriate lifestyle changes. Such recommendations are especially important for individuals who have prehypertension or hypertension, a family history of hypertension, are overweight, or are over age 40.

In rare cases (fewer than 1% of all patients with hypertension), the blood pressure rises quickly (with diastolic pressure usually rising to 130 mm Hg or higher), resulting in malignant or accelerated hypertension. This is a life-threatening condition and must be treated immediately. People with uncontrolled hypertension or a history of heart failure are at increased risk for this crisis.

People should call a doctor immediately if these symptoms occur:

Drowsiness
Confusion
Headache
Nausea
Loss of vision

Treatment

Patients with hypertension should work with their doctors to set blood pressure goals based on individual risk factors. Lifestyle and medication programs need to be planned on an individual basis.

Healthy lifestyle changes are imperative for anyone, and are critical for people with even normal blood pressure (120/80 mm Hg) and above. In appropriate patients, aggressive drug treatment of long-term high blood pressure can significantly reduce the incidence of mental decline and death from heart disease and other serious physical effects of hypertension. In people with diabetes, controlling both blood pressure and blood glucose levels prevents serious complications of that disease. Anti-hypertensive drugs may even prevent mental decline, including in people genetically susceptible to Alzheimer's disease. Nevertheless, only slightly over half of patients with hypertension are treated at all, and only a quarter have adequately controlled pressure.

It is not clear when drugs should be started, particularly for people with prehypertension or mild high blood pressure. To help make treatment choices, the U.S. National Heart, Lung, and Blood Institute has created categories (denoted as groups A, B, and C) according to a patient's risk factors for heart disease. Applying these categories to the severity of hypertension helps determine whether lifestyle changes alone or medications are needed.


Risk Groups	Blood Pressure Stages (Systolic/Diastolic)
	Prehypertension (120 - 139/80 - 89)	Mild (Stage 1) Blood Pressure (140 - 159/90 - 99)	Moderate-to-Severe (Stage 2) Blood Pressure (Systolic pressure over 160 or diastolic pressure over 100)
Risk Group A Have no risk factors for heart disease.	Lifestyle changes only. (Exercise and dietary program with regular monitoring.)	Year trial of lifestyle changes only. If blood pressure is not lower at 1 year, add drug treatments.	Lifestyle changes and medications.
Risk Group B Have at least one risk factor for heart disease* (excluding diabetes) but have no target organ damage (such as in the kidneys, eyes, or heart, or existing heart disease).	Lifestyle changes only.	6-month trial of lifestyle changes only. If blood pressure is not lower at 6 months, add drug treatments. Medications considered for patients with multiple risk factors.	Lifestyle changes and medications.
Risk Group C Have diabetes with or without target organ damage and existing heart disease (with or without risk factors for heart disease).	Lifestyle changes and medications.	Lifestyle changes and medications.	Lifestyle changes and medications.

* Risk factors for heart disease include the following: family history of heart disease, smoking, unhealthy cholesterol and lipid levels, diabetes, being over 60 years old.

Lifestyle Changes

Healthy lifestyle changes are an important first step for lowering blood pressure. Current guidelines recommend that people should:

Exercise at least 30 minutes a day
Maintain normal weight
Reduce salt intake
Increase potassium intake
Limit alcohol consumption; however, moderate alcohol consumption (1 – 2 glasses a day) may actually lower the risk for heart attack among men with high blood pressure
Consume a diet rich in fruits, vegetables, and low-fat dairy products while reducing total and saturated fat intake. (The DASH diet is one way of achieving such a dietary plan.)

The DASH diet (Dietary Approaches to Stop Hypertension) is proven to help lower blood pressure. Results are sometimes seen within a few weeks. Restricting sodium improves results. The diet appears to have antioxidant effects and may help lower LDL cholesterol levels, although beneficial HDL levels also decline. This diet is not only rich in important nutrients and fiber but also includes foods that contain far more electrolytes, potassium (4,700 mg/day), calcium (1,250 mg/day), and magnesium (500 mg/day) than are found in the average American diet.

A diet that is effective in lowering blood pressure is called Dietary Approaches to Stop Hypertension (DASH).

DASH diet recommendations:

Limit salt intake to no more than 2,300 mg a day (a maximum intake of 1,500 mg a day is an even better goal).
Reduce saturated fat to no more than 6% of daily calories and total fat to 27% of daily calories. (But, include dairy products that are non- or low-fat. Low-fat dairy products appear to be especially beneficial for lowering systolic blood pressure).
When choosing fats, select monounsaturated oils, such as olive or canola oils.
Choose whole grains over white flour or pasta products.
Choose fresh fruits and vegetables every day. In one study, people who increased their intake of fruits and vegetables experienced a drop in blood pressure after 6 months. Many of these foods are rich in potassium, fiber, or both, possibly helping lower blood pressure.
Include nuts, seeds, or legumes (dried beans or peas) daily.
Choose modest amounts of protein (no more than 18% of total daily calories). Fish, skinless poultry, and soy products are the best protein sources.
Other daily nutrient goals in the DASH diet include limiting carbohydrates to 55% of daily calories and dietary cholesterol to 150 mg. Patients should try to get at least 30 g of daily fiber.

Slight changes to the DASH diet might help further lower blood pressure, as well as improve cholesterol and lipid levels. Researchers reporting in the Journal of the American Medical Association and at the 2005 American Heart Association meeting said that replacing some carbohydrates in the DASH diet with more protein (from plant sources) or monounsaturated fats may help further reduce heart disease risk factors.

A combination of the DASH diet and salt restriction is extremely effective in reducing blood pressure. Reducing sodium may also help protect against heart failure. People with normal blood pressure should consume no more than 2,400 milligrams (about one teaspoon) of sodium each day. People with blood pressure should consume much less. (Patients should consult their doctor on individual recommendations for salt intake.) The following higher-risk groups should take particular measures to restrict salt:

People at Risk for Salt-Sensitivity. About half of people with hypertension have blood pressure that reacts significantly to salt. Such people are known to be salt-sensitive. Groups at particularly high risk for salt-sensitivity include African-Americans, the elderly, and people with diabetes. Even people with normal blood pressure can be salt-sensitive. High-salt diets in anyone who is salt-sensitive may harm the heart, kidneys, and brain and increase the risk for death, regardless of blood pressure. Because testing for salt-sensitivity is not easy, experts recommend that everyone proactively restrict their daily salt-intake.
Overweight People. Overweight individuals may absorb and retain sodium differently from people with normal weights. Reducing sodium can also help lower the risk of heart disease and stroke in people who are overweight. Unfortunately, because overweight people generally consume more calories, they are also likely take in more sodium.
People on Anti-Hypertensive Drugs. Restricting salt also enhances the benefits of many standard anti-hypertensive drugs by reducing potassium loss, and may help protect against kidney disease in patients who are also taking calcium-blocker drugs. A low-salt diet can also increase the chances for being able to stop such medications.

Simply eliminating table and cooking salt can be beneficial. Salt substitutes, such as Cardia, (containing mixtures of potassium, sodium, and magnesium) are available, but they are expensive. In any case, about 75% of the salt in the typical American diet comes from processed or commercial foods, not from food cooked at home, so the benefits of table-salt substitutes are likely to be very modest. Some sodium is essential to protect the heart, but most experts agree that the amount is significantly less than that found in the average American diet. If people cannot significantly reduce the amount of salt in their diets, adding potassium-rich foods might help to restore a healthy balance.

Evidence strongly indicates that a potassium-rich diet can help achieve healthy blood pressure levels, and that potassium supplements can lower systolic blood pressure by 1.8 m Hg and diastolic blood pressure by 1 mm Hg. Some evidence suggests that a potassium-rich diet can reduce the risk of stroke by 22 - 40%. Current expert guidelines support the use of potassium supplements or enough dietary potassium to achieve 3,500 mg per day for people with normal or high blood pressure (who have no risk factors for excess potassium levels). This goal is particularly important in people who have high sodium intake.

The best source of potassium is the fruits and vegetables that contain them. Some potassium-rich foods include bananas, oranges, pears, prunes, cantaloupes, tomatoes, dried peas and beans, nuts, potatoes, and avocados.

Excess potassium can cause abdominal distress, muscle weakness, and, in rare cases, dangerous heart events. Some people should be particularly cautious about excess potassium, including those with conditions, such as diabetes or kidney disease, that increase potassium levels. People who take medications, such as ACE inhibitors or potassium-sparing diuretics that limit the kidney's ability to excrete potassium, should not take potassium supplements.

Smoking. Everyone should quit smoking.

Alcohol. People who drink alcohol should do so in moderation. Men with hypertension should limit their intake to no more than one or two drinks a day, and women and lighter people should drink less.

Caffeine Drinks. Coffee drinking is associated with small increases in blood pressure, but the risk is very small in people with normal blood pressure. People with existing hypertension should avoid caffeine altogether.

Fiber. Fiber supplementation can help reduce blood pressure levels. It may take up to 8 weeks to achieve the maximum benefit.

Folate. Increasing folate (a B vitamin) intake to more than 800 mcg/day can help reduce blood pressure, particularly for younger women (under age 46). Dietary sources of folate include citrus fruits, leafy green vegetables, beans, and grain products. Folate helps to reduce homocysteine levels.

Fish Oil and Omega 3 Fatty Acids. Omega 3 fatty acids (docosahexaenoic and eicosapentaneoic acids) are found in oily fish. Studies indicate that they may have specific benefits for many medical conditions, including hypertension. They appear to help keep blood vessels flexible and may help protect the nervous system. Fatty acids are also available in supplements, but their long-term effects on blood pressure are unknown.

Click the icon to see an image of omega-3 fatty acids

Calcium. Calcium regulates the tone of the smooth muscles lining blood vessels. Studies have found that people who have sufficient dietary calcium have lower blood pressure than those who do not. Hypertension itself increases calcium loss from the body. The effects of extra calcium on blood pressure, however, are mixed, with some even showing higher pressure.

Click the icon to see an image of the sources of calcium.

Magnesium. Some studies reported that magnesium supplements may induce small but significant reductions in blood pressure. No major studies, however, have been done on long-term benefits or risks of magnesium supplements. A major 2001 study on diet found no effect on blood pressure from magnesium intake from foods.

Antioxidant Supplements. Antioxidants are substances that help the body eliminate oxidants, (also called oxygen-free radicals), which are damaging particles produced as part of the body's chemical processes. Some antioxidant supplements, including vitamins C and E and alpha-lipoic acid, are being studied for possible benefits in protecting against hypertension by preventing injury in the blood vessels. Vitamin C may have specific benefits for hypertension by preventing dangerous effects on nitric acid, the substance that keeps arteries flexible.

Click the icon to see an image of vitamin C sources.

Click the icon to see an image of vitamin E sources.

In people who are overweight, even modest reductions in weight, particularly in the abdominal area, can immediately reduce blood pressure. Weight loss, particularly accompanied by salt restriction, may allow patients with mild hypertension, even older people, to safely reduce or go off medications. The benefits of weight loss on blood pressure are long-lasting.

Positive Effects on Blood Pressure. Regular exercise helps keep arteries elastic, even in older people, which in turn ensures blood flow and normal blood pressure. Sedentary people have a 35% greater risk of developing hypertension than athletes.

Experts recommend at least 30 minutes of exercise on most -- if not all-days. In one study, moderate exercise (jogging two miles per day) controlled hypertension so well that more than half the patients who had been taking drugs for high blood pressure were able to discontinue their medication.

Studies have also indicated that yoga and Tai Chi, an ancient Chinese exercise involving slow, relaxing movements, may lower blood pressure almost as well as moderate-intensity aerobic exercises.

High-intensity exercise may not lower blood pressure as effectively as moderate intensity exercise and may be dangerous in people with hypertension.

Negative Effects. Each year an estimated 75,000 heart attacks (5% of all heart attacks) occur after heavy exertion, leading to 25,000 deaths. Older people and those with uncontrolled hypertension or other serious medical conditions should be cautious when exercising. Studies report that older people who begin vigorous exercise are at a slightly higher than average risk for a heart attack during the first year, but over time, regular exercise is likely to be protective.

The following activities may pose particular dangers for high-risk individuals:

Intense workouts (snow shoveling, slow jogging, speed walking, tennis, heavy lifting, heavy gardening). They tend to stress the heart, raise blood pressure for a brief period, and may cause spasms in the arteries leading to the heart.
Competitive sports, which couple intense activity with aggressive emotions.

Effects of Anti-Hypertensive Drugs on Exercise. Certain anti-hypertensive medications, including diuretics and beta-blockers, can interfere with exercise capacity. ACE inhibitors or calcium-channel blockers are the best drugs for active individuals. However, patients who take drugs that interfere somewhat with exercise capability should still adhere to an exercise program and consult a doctor on how best to balance medications with exercise.

Click the icon to see an image about lifestyle changes for hypertension.

Certain sleep disorders, especially sleep apnea, are associated with hypertension. Even chronic, insufficient sleep may raise blood pressure in patients with hypertension, placing them at increased risk of heart disease and death. Stress hormone levels increase with sleeplessness, which can activate the sympathetic nervous system, a strong player in hypertension. Patients who have chronic insomnia or other severe sleep disturbances, (particularly sleep apnea), may want to consult a sleep expert. Patients with hypertension who are habitually poor sleepers should consider long-acting blood pressure medications to help counteract the increase in blood pressure that occurs in the early morning hours.

Improving mood or relieving stress may be helpful. The following studies suggested possible benefits:

Stress reduction programs that use cognitive-behavioral therapy may reduce blood pressure.
Active religious faith was associated with healthy blood pressure levels, possibly indicating the combined benefits of a strong social network and reduced stress from spiritual activities.
A simple relaxation technique called transcendental meditation (TM), which involves silent repetition of a single sound, was associated with lower blood pressure.

Treating stress cannot cure medical problems. Stress management programs are not a substitute for standard medical treatments, but can be a very important component of a lifestyle plan.

Medications

Dozens of anti-hypertensive drugs are available. Most fall into the following categories:

Diuretics rid the body of extra water and salt. Diuretics are usually the first-line treatment for high blood pressure.
Beta-blockers block the effects of adrenaline and ease the heart's pumping action.
Angiotensin converting enzyme (ACE) inhibitorsreduce the production of angiotensin, a chemical that causes arteries to narrow.
Calcium-channel blockers (CCBs) decrease the contractions of the heart and widen blood vessels.
Angiotensin-receptor blockers (ARBs) block angiotensin, another chemical that constricts the arteries.
Vasodilators expand blood vessels.

In about half of patients a single-drug regimen can control mild to moderate hypertension. More severe hypertension often requires a combination of two or more drugs. Each drug has specific benefits, but their effects may vary depending on the individual patient.

One of the most difficult issues that patients face, particularly those with primary hypertension, is that the treatment may make them feel worse than the disease, which usually has no symptoms. Whatever the difficulties, compliance with a drug and lifestyle program is worth the effort. It is very important that patients discuss medication concerns with their doctors. If current blood pressure drugs are causing uncomfortable side effects, the doctor may adjust dosages or combinations.

Patients whose blood pressure has been well-controlled and who are able to maintain a healthy life style may choose to withdraw from medications. They should do so in a step-down manner (gradual reduction) and be monitored regularly. Stopping too quickly can have adverse effects, including serious effects on the heart. The highest success rates are more likely in those who lose weight and reduce sodium intake, in patients who have been treated with a single drug, and in those who have maintained lower systolic blood pressure during treatment. People over 75 years old may have more trouble than younger adults in maintaining normal blood pressure after withdrawal.

Classes of Medications

There are several classes of drugs used to treat hypertension.

Diuretics help the kidneys get rid of excess salt and water. They are the mainstays of anti-hypertensive therapy and are the first drug of choice for most people with hypertension. They are especially helpful for treating the elderly and African-American patients. (African-Americans are more likely to be salt-sensitive, so they respond well to these drugs.) They also work well for patients with diabetes.

Results from the long-term Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), published in the Journal of the American Medical Association in 2005, confirm that thiazide-type diuretics should be the first treatment option for most patients with hypertension. The landmark trial included over 33,000 patients (35% black) with hypertension and at least one other cardiovascular risk factor. Patients were randomized to receive a calcium channel blocker, an ACE inhibitor, or a thiazide-type diuretic.

Results suggested that the diuretic worked just as well as the newer drugs in lowering blood pressure and was more effective in preventing heart failure, heart attack, and stroke. The benefits for the diuretic were even more significant for African-American patients. Other trial results indicated that patients taking the calcium channel blocker had the greatest risk for heart failure, and that the ACE inhibitor was much less effective than the diuretic in lowering blood pressure and preventing stroke in African-American patients.

Diuretic Types and Brands. There are many brands of diuretics. They are generally inexpensive. Some need to be taken once a day, some twice a day. Low doses are usually as effective for lowering blood pressure as higher doses. Diuretics are usually used in combination with other drugs, especially ACE inhibitors and beta blockers.

There are three main types of diuretics:

Potassium-sparing diuretics. These include amiloride (Midamor), spironolactone (Aldactone), and triamterene (Dyrenium).
Thiazide diuretics. These include chlorothiazide (Diuril), chlorthalidone (Hygroton), indapamide (Lozol), hydrochlorothiazide (Esidrix, HydroDiuril), and metolazone (Mykrox, Zaroxolyn).
Loop diuretics. Because loop diuretics act faster than other diuretics it is important to avoid dehydration and potassium loss. Loop diuretics include bumetanide (Bumex), furosemide (Lasix), and torsemide (Demadex).

Benefits of Diuretics. Diuretics can:

Reduce the risk for stroke
Reduce the risk for heart attack and heart failure
Protect against blood clots.

Problems with Diuretics. Loop and thiazide diuretics reduce the body's supply of potassium, which, if left untreated, increases the risk for arrhythmias. Arrhythmias are heart rhythm disturbances that can, in rare instances, lead to cardiac arrest. In such cases, doctors will prescribe lower doses of the current diuretic, recommend potassium supplements, or use potassium-sparing diuretics either alone or in combination with a thiazide. Potassium-sparing drugs have their own risks, which include dangerously high levels of potassium in people with existing elevated levels of potassium or in those with damaged kidneys. However, all diuretics are generally more beneficial than harmful.

Common Diuretic Side Effects:

Fatigue
Depression and irritability
Urinary incontinence
Reduced sexual drive

Beta-blockers help slow heart rate and lower blood pressure. They are usually used in combination with other drugs such as ACE inhibitors and diuretics.

Brands. Propranolol (Inderal), acebutolol (Sectral), atenolol (Tenormin), betaxolol (Kerlone), carteolol (Cartrol), metoprolol (Lopressor), nadolol (Corgard), penbutolol (Levatol), pindolol (Visken), carvedilol (Coreg), and timolol (Blocadren). The drugs may differ in their effects and benefits.

Problems with Beta-Blockers. Evidence presented at the 2005 meeting of the American College of Cardiology suggested that an ACE-inhibitor combined with a calcium channel blocker works just as well as a beta-blocker-diuretic combination in treating hypertension, and poses less risk of diabetes. Other recent studies suggest that beta-blockers may increase the risk of stroke, and should not be a first-line choice for high blood pressure treatment.

Do not abruptly stop taking these drugs. The sudden withdrawal of beta blockers can rapidly increase heart rate and blood pressure. The doctor may want the patient to slowly decrease the dose before stopping completely.
Beta blockers are categorized as non-selective or selective. Non-selective beta blockers such as carvedilol and propranolol may sometimes narrow bronchial airways. These beta blockers should not be used by patients with asthma, emphysema, or chronic bronchitis.
Beta blockers can lower HDL (“good”) cholesterol.
These drugs can hide warning signs of low blood sugar (hypoglycemia) in patients with diabetes. When combined with a diuretic, the risk of diabetes may be increased.

Common Side Effects

Fatigue and lethargy
Vivid dreams and nightmares
Depression
Memory loss
Dizziness and lightheadedness
Reduced ability to exercise
Coldness in extremities (legs, toes, arms, hands)

Check with your doctor about any side effects. Do not stop taking these drugs on your own..

Angiotensin-converting enzyme (ACE) inhibitors open blood vessels and decrease the workload of the heart. They are used to treat high blood pressure but can also help improve heart and lung muscle function.

These drugs are particularly important for patients with diabetes. A large study reported that patients with diabetes who took these drugs had fewer heart attacks and lower overall mortality rates than patients who took other types of high blood pressure medications. ACE inhibitors may also help slow progression of kidney disease, in addition to controlling blood pressure. They may also be better at preventing the development of diabetes in patients with kidney disease than other types of blood pressure medication. In a 2006 study of African-American patients with high blood pressure and kidney disease, patients who took an ACE inhibitor had a lower risk of developing diabetes than those who took a calcium channel blocker or beta-blocker drug.

Brands. ACE inhibitors include captopril (Capoten), enalapril (Vasotec), quinapril (Accupril), benazepril (Lotensin), ramipril (Altace), perindopril (Aceon), and lisinopril (Prinivil, Zestril).

Common Side Effects of ACE Inhibitors:

Low blood pressure is the main side effect of ACE inhibitors. This can be severe in some patients, especially at the start of therapy.
Irritating cough is a common side effect, which some people find intolerable. Although all ACE inhibitors can have this side effect, sometimes switching to another brand will reduce this symptom.
ACE inhibitors can harm a developing fetus and should not be used during pregnancy. While it has long been known that these drugs can cause problems in the second and third trimester, an important 2006 study indicated that ACE inhibitors can also cause major heart birth defects when taken during the first trimester. The FDA and the American Heart Association recommend that women who become pregnant should change from ACE inhibitors to another type of blood pressure drug as soon as possible. Women of child-bearing age who are considering becoming pregnant should also discuss alternative drugs with their doctors.

Uncommon Side Effects of ACE Inhibitors:

ACE inhibitors protect against kidney disease, but they may also increase potassium retention by the kidneys. If potassium levels become extremely high, they can cause the heart to stop beating (cardiac arrest). This side effect is rare, except in patients with significant kidney disease. Because of this risk, ACE inhibitors are not usually used in combination with potassium-sparing diuretics or potassium supplements.
A rare but severe side effect is granulocytopenia, an extreme reduction in infection-fighting white blood cells.
In very rare cases, patients suffer a sudden and severe allergic reaction, called angioedema that causes swelling in the eyes and mouth and may close off the throat.

Patients who have difficulty tolerating ACE inhibitor side effects are usually switched to an angiotensin-receptor blocker (ARB).

ARBs, also known as angiotensin II receptor antagonists, are similar to ACE inhibitors in their ability to open blood vessels and lower blood pressure. They may have fewer or less-severe side effects than ACE inhibitors, especially coughing, and are sometimes prescribed as an alternative to ACE inhibitors. ARBs are particularly important drugs for patients with diabetes. They may help protect against kidney disease and kidney failure.

A 2006 study in the New England Journal of Medicine suggested that some patients with prehypertension may benefit from treatment with an ARB drug. Patients in the study received candesartan (Atacand).

Brands. Losartan (Cozaar, Hyzaar), olmesartan (Benicar) candesartan (Atacand), telmisartan (Micardis), eprosartan (Teveten), irbesartan (Avapro), and valsartan (Diovan). A combination medication containing candesartan and the diuretic hydrochlorothiazide (Diovan HCT, Atacand HCT) is also available.

Side Effects:

Low blood pressure
Dizziness and lightheadedness
Raised potassium levels
Drowsiness
Nasal congestion
Should not be used during pregnancy

Calcium-channel blockers (CCBs), or calcium antagonists, help relax blood vessels. Along with diuretics, CCBs may work better than other drug classes for lowering blood pressure in African-Americans. Recent research indicates that newer types of drugs (CCBs, ACE inhibitors) may be a better treatment option for some patients than older drugs (especially beta blockers).

Brands. Diltiazem (Cardizem, Dilacor), amlodipine (Norvasc), felodipine (Plendil), isradipine (DynaCirc), verapamil (Calan, Isoptin, Verelan), nisoldipine (Sular), nicardipine (Cardene), nifedipine (Adalat, Procardia), lercanidipine (Zanidip), lacidipine (Motens), and nitrendipine (Nitrepin). In 2004, a dual-therapy calcium channel blocker-statin combination drug (Caduet) was approved to treat high blood pressure and high cholesterol. Caduet is a fixed-dose combination of amlodipine and atorvastatin.

Side Effects:

Swelling in the feet
Constipation
Fatigue
Erectile dysfunction
Gingivitis
Rash
Food interactions (do not take CCBs with grapefruit or Seville orange products)

Alpha blockers such as doxazosin (Cardura), prazosin (Minipress), and terazosin (Hytrin) help widen small blood vessels. They are generally not used as first-line drugs for high blood pressure, but are prescribed if other drugs do not work or as add-on medication.

Vasodilators, which help open blood vessels by relaxing muscles in the blood vessel walls. These drugs are usually used in combination with a diuretic or a beta-blocker. They are rarely used by themselves. Vasodilators include hydralazine (Apresoline), clonidine (Catapres), available in tablets or as a skin patch), and Minoxidil (Loniten). Some of these drugs should be used with caution or not at all in people who have angina or who have had a heart attack.

Aliskiren (Tekturna). In 2007, the FDA approved aliskiren for treatment of high blood pressure. Aliskiren can be taken either alone or in combination with other blood pressure medication. It should not be used during pregnancy as it can cause injury or death to the fetus. Aliskiren is the first hypertension drug that inhibits renin, a kidney enzyme that is associated with the regulation of blood pressure.

Statins. Statins, common drugs used to lower cholesterol, are proving to have many other health benefits. They include lovastatin (Mevacor), pravastatin (Pravachol), simvastatin (Zocor), fluvastatin (Lescol), atorvastatin (Lipitor), and rosuvastatin (Crestor). In an important 2002 study, patients with high blood pressure but normal or slightly high cholesterol levels had fewer heart attacks and strokes when they took the a statin drug. In 2004, a calcium channel blocker-statin combination drug (Caduet) was approved to treat simultaneously high blood pressure and high cholesterol. Caduet is a fixed-dose combination of amlodipine and atorvastatin.

Resources

www.acc.org -- American College of Cardiology
www.americanheart.org -- American Heart Association
www.ash-us.org -- American Society of Hypertension
www.nhlbi.nih.gov/hbp -- National Heart, Lung, and Blood Institute
www.nhlbi.nih.gov/health/public/heart/hbp/dash -- DASH diet
www.ishib.org -- International Society on Hypertension in Blacks
www.eatright.org -- American Dietetic Association

References

Barzilay JI, Davis BR, Cutler JA, Pressel SL, Whelton PK, Basile J, et al. Fasting glucose levels and incident diabetes mellitus in older nondiabetic adults randomized to receive 3 different classes of antihypertensive treatment: a report from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). Arch Intern Med. 2006 Nov 13;166(20):2191-201.

Beulens JW, Rimm EB, Ascherio A, Spiegelman D, Hendriks HF, Mukamal KJ. Alcohol consumption and risk for coronary heart disease among men with hypertension. Ann Intern Med. 2007 Jan 2;146(1):10-9.

Cooper WO, Hernandez-Diaz S, Arbogast PG, Dudley JA, Dyer S, Gideon PS, et al. Major congenital malformations after first-trimester exposure to ACE inhibitors. N Engl J Med. 2006 Jun 8;354(23):2443-51.

Davis BR, Piller LB, Cutler JA, Furberg C, Dunn K, Franklin S, et al. Role of diuretics in the prevention of heart failure: the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial. Circulation. 2006 May 9;113(18):2201-10.

Djousse L, Pankow JS, Hunt SC, Heiss G, Province MA, Kabagambe EK, et al. Influence of saturated fat and linolenic acid on the association between intake of dairy products and blood pressure. Hypertension. 2006 Aug;48(2):335-41.

Forman JP, Rimm EB, Curhan GC. Frequency of analgesic use and risk of hypertension among men. Arch Intern Med. 2007 Feb 26;167(4):394-9.

Peila R, White LR, Masaki K, Petrovitch H, Launer LJ. Reducing the risk of dementia: efficacy of long-term treatment of hypertension. Stroke. 2006 May;37(5):1165-70.

Taylor EN, Hu FB, Curhan GC. Antihypertensive medications and the risk of incident type 2 diabetes. Diabetes Care. 2006 May;29(5):1065-70.

Thornley-Brown D, Wang X, Wright JT Jr, Randall OS, Miller ER, Lash JP, et al. Differing effects of antihypertensive drugs on the incidence of diabetes mellitus among patients with hypertensive kidney disease. Arch Intern Med. 2006 Apr 10;166(7):797-805.

Review Date:
4/12/2007
Reviewed By:
Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital.

A.D.A.M. Copyright

adam.com

Heart failure

FitSugar — Wed, 08 Oct 2008 17:34:55 -0700

Overview

Signs and Symptoms
Causes
Risk Factors
Diagnosis
Treatment Approach
Supporting Research

HEALTH GUIDE REFERENCE FROM A.D.A.M

Heart failure (or congestive heart failure) doesn’t mean your heart has failed or stopped beating. It means that your heart, which is a muscle that pumps blood to all parts of your body, is not working as well as it should be and can’t pump as much blood as your body needs. As your heart's pumping action lessens, blood may back up in your lungs, liver, or legs. This can cause shortness of breath, leg swelling (called edema), and other problems. In addition, organs in your body may not get the oxygen and nutrients they need, meaning that they also can’t function properly.

Heart failure is a chronic (ongoing) condition that usually develops over time. It is usually caused by underlying conditions such as high blood pressure or heart disease. These conditions damage your heart, making the heart muscle stiff or thick. The damaged muscle either can’t relax properly to let the pumping chambers of the heart – the ventricles – fill with enough blood, or it can’t contract properly to let the ventricles pump out enough blood. The left ventricle is the main pumping chamber, and heart failure usually starts on the left side. When the left ventricle can’t contract enough, it’s called systolic heart failure. When the left ventricle can’t fill with enough blood, it’s called diastolic heart failure. You can have a combination of both types of heart failure.

Although some conditions that cause heart failure are irreversible, you can manage the condition and improve your health and quality of life with a combination of lifestyle changes and medications.

Signs and Symptoms

You may experience one or more of the following symptoms of chronic heart failure:

Swollen feet, ankles, and sometimes abdomen
Weight gain from fluid retention
Shortness of breath and cough
Racing or skipping heart beat (palpitations)
Stomach upset, nausea and vomiting, and loss of appetite
Difficulty sleeping
Fatigue, weakness, and a reduced ability to exercise
Lightheadedness
Difficulty concentrating or staying alert

The more advanced your heart failure, the more likely you are to have symptoms.

Acute heart failure occurs when something suddenly damages your heart (such as a heart attack, blood clot in the lungs, allergic reaction, or severe infection). Symptoms are similar to those for chronic heart failure, but are more serious and get worse quickly. Acute heart failure is life-threatening and you should seek immediate emergency medical attention.

Causes

The most common causes of heart failure are high blood pressure and coronary artery (heart) disease. Other causes of heart failure include:

Heart attack
Damaged heart valves (valves separate the chambers of the heart and keep blood flowing in the right direction)
Cardiomyopathy (weakening of the heart muscle, which may be from infection, diseases such as rheumatoid arthritis or lupus, alcohol or drug abuse, or sometimes for unknown reasons)
Congenital heart disease (heart defects at birth)
Myocarditis (inflammation of the heart from a virus)
Abnormal heart rhythms (arrhythmias)

Risk Factors

You are at risk for developing heart failure if you:

Have high blood pressure
Have diabetes
Have had a heart attack or have heart disease of any kind.
Have high blood pressure or diabetes.
Are overweight.
Have sleep apnea
Take certain medications
Abuse alcohol, smoke cigarettes, or use cocaine.

Diagnosis

Your doctor will take a detailed medical history and do a physical exam. He or she will examine your heart and lungs, checking for enlargement of the heart and fluid in the lungs. Other signs of heart failure that your doctor will look for include enlarged neck veins, swelling in your legs or abdomen, and tenderness of the liver. A chest x-ray can help to see if there is fluid on your lungs or enlargement of your heart – two factors that often go along with heart failure.

After the initial diagnosis, your doctor will look for the underlying cause of heart failure. He or she may order these tests:

Blood tests, to check kidney or thyroid function
Echocardiogram, to determine systolic heart failure or diastolic heart failure
Ejection fraction, to see how much blood you heart is pumping out
Electrocardiogram (ECG), to look for heart rhythm problems
Coronary catheterization (angiogram), to look for narrowed arteries

Treatment Approach

With proper treatment, you can control symptoms of heart failure and improve your health. Many lifestyle changes, such as losing weight, cutting down on salt, and getting regular exercise can make a difference in your condition. Medications are also available to help your heart better pump blood. Some complementary and alternative therapies can be helpful, too, when used along with standard medical treatment. However, heart failure is a serious condition and you should always seek medical care; do not take any herbs or supplements without your doctor’s supervision.

Lifestyle

Carefully monitoring your health and helping to manage your condition makes a big difference in keeping heart failure under control. To do this, track your weight on a daily basis. Weight gain can be a sign that you are retaining fluid and that the pump function of your heart is getting worse. Make sure you weigh yourself at the same time each day and on the same scale.

Other important measures include:

Take your medications as directed. Carry a list of medications with you wherever you go.
Cut down on salt. People with heart failure should consume no more than 2,000 mg per day. Keep in mind that most salt in your diet doesn’t come from the salt shaker, but from processed foods that already contains high levels of sodium. (See “Tips to lower your sodium intake” below.)
If you smoke, quit.
Exercise and stay active. Walk or ride a stationary bicycle, for example. One study showed that a walking program was safe for people with heart failure and helped improve symptoms. Talk to your doctor before starting any new exercise program; he or she can help you find one that’s right for you.
Lose weight if you are overweight.
Get enough rest, including after exercise, eating, or other activities. This allows your heart to rest, too. Keep your feet elevated to decrease swelling.

Tips to lower your sodium intake

Look for foods labeled "low-sodium," "sodium-free," "no salt added," or "unsalted." Check the total sodium content on food labels. Be especially careful of canned, packaged, and frozen foods.
Don't cook with salt or add salt to what you are eating. Try pepper, garlic, lemon, or other spices for flavor instead. Be careful of packaged spice blends as these often contain salt or salt products (like monosodium glutamate, MSG).
Avoid foods that are naturally high in sodium, like anchovies, meats (particularly cured meats, bacon, hot dogs, sausage, bologna, ham, and salami), olives, pickles, sauerkraut, soy and Worcestershire sauces, and cheese.
Take care when eating out. Stick to steamed, grilled, baked, boiled, and broiled foods with no added salt, sauce, or cheese.
Use oil and vinegar instead of bottled dressings on salads.
Eat fresh fruit or sorbet when having dessert.

Medications

ACE inhibitors - widen blood vessels and make it easier on your heart to pump blood. Side effects can include chronic cough. ACE inhibitors include

Benazepril (Lotensin)
Captopril (Capoten)
Fosinopril (Monopril)
Lisinopril (Zestril)
Enlapril (Vasotec)

ARBs - also dilate blood vessels and may be used in people who can’t take ACE inhibitors. They include

Irbesartan (Avapro)
Candesartan (Atacand)
Losartan (Cozaar)
Valsartan (Diovan)

Digoxin (Lanoxin) - helps your heart pump more blood by increasing the strength of its contractions.

Beta blockers - slow heart rate and lower blood pressure. Beta blockers include

Acebutolol (Sectral)
Atenolol (Tenormin)
Bisoprolol (Zebeta)
Carvedilol (Coreg)
Propanolol (Inderal)
Metoprolol (Lopressor, Toprol-XL)

Diuretics (water pills) - keep fluid from building up in your body by making you urinate more. There are different types of diuretics that can affect potassium and magnesium levels in your body, so your doctor will check your levels frequently.

Isosorbide dinitrate and hydralazine hydrochloride (BiDil) - BiDil combines two drugs that dilate blood vessels. It is approved for use in African-Americans who have heart failure, as an addition to standard therapy.

Nutrition and Dietary Supplements

Magnesium - Magnesium is essential to heart health. This mineral is particularly important for maintaining a normal heart rhythm and is often used by physicians to treat irregular heartbeat (arrhythmia). People with heart failure are often at risk for developing an arrhythmia. In addition, some diuretics (water pills) may cause your body to lose too much magnesium. For this reason, your doctor may recommend a supplement. Always ask your doctor before taking a magnesium supplement on your own if you have heart failure.
Carnitine (500 mg two times per day) - Some early studies suggest that L-carnitine supplements may reduce your chances of developing heart failure after a heart attack and improve exercise capacity if you already have heart failure. Carnitine is a nutrient that helps the body convert fatty acids into energy. This energy is used primarily for muscular activities throughout the body. Most studies used a special form of carnitine called propionyl-L-carnitine.
Coenzyme Q-10 (CoQ10, 100 to 200 mg per day) - Levels of CoQ10 are low in people with heart failure. Several research studies suggest that CoQ10 supplements can help reduce swelling in the legs, enhance breathing by reducing fluid in the lungs, and increase exercise capacity in people with heart failure. Not all studies agree, however. More research is needed to see if CoQ10 has any real benefit. In the meantime, talk to your doctor about whether this supplement would be good as well as safe for you.
Creatine - Creatine is a naturally occurring amino acid (protein building block) found mainly in muscles. In a few studies of people with congestive heart failure, injections of creatine (in addition to standard medical care) provided improvement in heart function and ability to exercise compared to those who received placebo. Taking creatine orally improved muscle function and endurance. More studies are needed to determine whether oral creatine has any benefit for people with heart failure.
Vitamin B1 (Thiamine) - Thiamine may be related to heart failure in several ways. First, low levels of thiamine can contribute to the development of congestive heart failure. On the flip side, people with severe heart failure can lose a significant amount of weight including muscle mass (called cachexia) and become deficient in many nutrients including thiamine. In addition, diuretics (water pills) can cause your body to lose too much thiamine. Talk to your doctor about measuring your level of vitamin B1 and whether you should take thiamine.
Amino acids - A few small studies suggest these amino acids might be helpful for heart failure, but more research is needed:
- Arginine (needed for the body to make nitric oxide, which helps blood flow)
- Taurine (helps heart muscle contract)

Herbs

The use of herbs is a time-honored approach to strengthening the body and treating disease. Herbs, however, can trigger side effects and can interact with other herbs, supplements, or medications. For these reasons, herbs should be taken with care, under the supervision of a healthcare practitioner.

Hawthorn - Hawthorn (Crataegus spp.), a member of the rose family, was used by physicians in the early 1800s to treat circulation and respiration (breathing) problems. The flowers and berries have been used traditionally to treat irregular heartbeat, high blood pressure, chest pain, atherosclerosis (hardening of the arteries), and heart failure. Several scientific studies suggest that hawthorn improves the heart’s ability to pump blood in people with heart failure. It also significantly improved symptoms (like reduced shortness of breath and fatigue) and helped people exercise longer. No studies have examined whether hawthorn can work safely with other medications, or how it compares to drugs such as ACE inhibitors. Talk to your doctor to see if hawthorn is right for you.
Berberine (300 to 500 mg four times per day) – Berberine, an active ingredient of goldenseal (Hydrastis canadensis) and other herbs, can dilate blood vessels. In one study, people who took berberine for eight weeks had better heart function and were more able to exercise than those who took placebo. A few other studies suggest that when berberine is combined with standard medicines for heart failure, it can improve heart function and quality of life. Talk to your doctor about whether it is safe and appropriate for you to take berberine in addition to your usual care.

Prognosis and Complications

Heart failure is a serious disorder that leads to a lower life expectancy. It is generally a chronic illness, but many forms of heart failure can be controlled by treating the underlying causes, making lifestyle changes, and taking medication.

Potential complications include:

Pulmonary edema (fluid buildup in the lungs)
Total failure of the heart to function (circulatory collapse or shock)
Arrhythmias (irregular heart rhythm) including fatal arrhythmias

Supporting Research

Al-Hasso. Coenzyme Q10: a review. Hosp Pharm. 2001;36(1):51-66.

Andrews R, Greenhaff P, Curtis S, Perry A, Cowley AJ. The effect of dietary creatine supplementation on skeletal muscle metabolism in congestive heart failure. Eur Heart J. 1998;19(4):617-622.

Arsenian, MA. Carnitine and its derivatives in cardiovascular disease. Progr Cardiovasc Dis. 1997;40:3:265-286.

Azuma J. Long-term effect of taurine in congestive heart failure: Preliminary report. Adv Exp Med Biol. 1994;359:425-33.

Baggio E, Gandini R, Plancher AC, Passeri M, Carmosino G. Italian multicenter study on the safety and efficacy of coenzyme Q10 as adjunctive therapy in heart failure. CoQ10 Drug Surveillance Investigators. Mol Aspects Med. 1994;15(Suppl):s287-294.

Bleske BE, Zineh I, Hwang HS, Welder GJ, Ghannam MM, Boluyt MO. Evaluation of hawthorn extract on immunomodulatory biomarkers in a pressure overload model of heart failure. Med Sci Monit. 2007 Dec;13(12):BR255-258.

Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic Guide to Herbal Medicines. Boston, Mass: Integrative Medicine Communications; 1998:120,142-144,162-163,171-172,197.

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Review Date:
12/27/2007
Reviewed By:
Steven D. Ehrlich, N.M.D., private practice specializing in complementary and alternative medicine, Phoenix, AZ. Review provided by VeriMed Healthcare Network.

A.D.A.M. Copyright

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