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In This Report

•	Highlights
•	Introduction
•	Symptoms
•	Prognosis
•	Risk Factors
•	Diagnosis
•	Treatment
•	Secondary Prevention
•	Rehabilitation
•	Resources
•	References

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Heart attack and acute coronary syndrome

Highlights

Updated Guidelines for Heart Attack Management

In December 2007, the American Heart Association and American College of Cardiology released updated guidelines for treating patients who have had a type of heart attack known as ST elevation myocardial infarction (STEMI). STEMI heart attacks occur when a heart’s artery is completely blocked. This type of heart attack is very severe, but quick treatment can help to minimize damage. The new guidelines also include recommendations for secondary prevention measures that patients should follow to reduce their risk of a second heart attack.

Immediate Treatment of a Heart Attack

The new guidelines recommend:

• Percutaneous coronary intervention (PCI), also called angiography, is a procedure that should be performed within 90 minutes of a heart attack.
• Fibronolytic (“clot-busting”) therapy should be given within 30 minutes of a heart attack if a center that performs PCI is not available.
• Patients who routinely use nonsteroidal anti-inflammatory drugs (NSAIDs), including COX-2 inhibitors but NOT aspirin, should stop them while being treated for a heart attack. (In general, patients with heart disease or heart disease risk factors should use NSAIDs as a last resort for pain management.)

Secondary Prevention of Heart Attack

The new guidelines emphasize the importance of secondary prevention measures, including blood pressure and cholesterol control, weight management, smoking cessation, and regular exercise. Most patients will need to take aspirin and clopidogrel (Plavix) on an ongoing basis, and they may need an ACE inhibitors or beta-blocker. Do not leave the hospital without discussing secondary prevention steps with your doctor.

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 tissues of the body. To perform this strenuous task, the heart muscle itself needs a plentiful supply of oxygen-rich blood, 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. [For more information, 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:

• If the artery becomes completely blocked and ischemia becomes so extensive that oxygen-bearing tissues around the heart die.
• 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 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, the primary symptom of coronary artery disease, is typically experienced as chest pain. There are two kinds of angina:

• Stable Angina. This is predictable chest pain that can usually be managed with lifestyle changes and medications, such as low-dose aspirin.
• Unstable Angina. This situation is much more serious than stable angina, and 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, although needing aggressive treatment, has not developed into a full blown heart attack. Acute coronary syndrome includes:

• Unstable Angina.
• 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

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:

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

Click the icon to see an image about angina.

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.

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.

Stable Angina. Stable angina is predictable chest pain. Although less serious than unstable angina, it can be extremely painful or uncomfortable. 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.

Specific symptoms that are more likely to indicate angina include:

• Angina pain or discomfort is typically described by patients as fullness or tingling, squeezing, pressure, 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.
• A typical angina attack lasts minutes. If it is more fleeting or lasts for hours, it is probably not angina.
• 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, or even to the upper abdomen.
• Stable angina is usually relieved by rest or by taking nitroglycerine under the tongue.

Other symptoms that may indicate angina or accompany the pain or pressure in the chest include:

• Shortness of breath
• Nausea, vomiting, and cold sweats
• A feeling of indigestion or heartburn
• Unexplained fatigue after activity (more common in women)
• Dizziness or lightheadedness
• Palpitations

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.
• Fainting episode.

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, 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. [For more information, see In-Depth Report #12: Heart attack and acute coronary syndrome.]

Doctors use a number of factors to help predict which patients with unstable angina or acute coronary syndrome 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, and peripheral artery disease) or other complicating conditions (such as lung disease and 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
• A history of severe chronic angina
• Abnormal lung sounds called rales (a bubbling or crackling sound) on examination
• ST-segment deviation on the electrocardiogram
• Either very slow or very fast heat beats
• Very low blood pressure

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

People with known heart disease and any unusual chest pain or other symptoms described above that do not clear up with medications should call 911. The degree of pain and the specific symptoms before a heart attack vary greatly among individuals. Symptoms can be abrupt, gradual, or intermittent. Some studies suggest that nearly half of patients with heart attack do not have chest pain as the primary symptom. Patients most likely to have atypical symptoms are women and the very elderly (although they can certainly have classic heart attack symptoms as well).

Symptoms That Are Less Likely to Indicate Angina or a Heart Attack. The following symptoms are less likely to be due to coronary artery disease:

• Sharp pain brought on by breathing in and or when 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.

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.

Silent Ischemia. Some people with severe coronary artery disease do not have angina pain. This condition is known as silent ischemia, which some experts attribute to the brain abnormally processing of heart pain. 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.

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 is unclear what causes this condition, imaging tests suggest that Syndrome X may also be caused by ischemia, as is angina.

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

Other causes of chest pain or discomfort include:

• Problems affecting the ribs and chest muscles include injured muscles, fractures, arthritis, muscle spasms, and infections
• Anxiety attacks
• Gastrointestinal disorders (gallstone attacks, peptic ulcer disease, hiatal hernia, heartburn)
• Asthma
• Rupture of the aorta
• Collapsed lung
• Acute inflammation of the heart
• Blood clot in the lung (pulmonary embolism)
• High thyroid levels (hyperthyroidism)
• Anemia
• Vasculitis (a group of disorders that cause inflammation of the blood vessels)

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 with heart disease or risk factors for it and has heart attack symptoms should contact emergency services.
• The patient should chew an aspirin (250 - 500 mg) and be sure to tell emergency health providers 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.

Prognosis

Each year, an estimated 650,000 Americans will suffer a first heart attack, and 450,000 will have a recurrent episode. Half of the men and 63% of the women who died of heart disease have 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 have 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 another heart 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, including:

• 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 dying from a first heart attack). 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 have 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

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.

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

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, in fact, are more likely to have angina than men. 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 to die after a heart attack.

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.

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. For instance:

• 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.
• 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.

Click the icon to see an image about serum 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.

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.

[For more information, see In-Depth Report #23: Cholesterol and In-Depth Report #43: Heart-healthy diet.]

Estrogen therapy, either alone or in combination with a progesterone drug, is no longer recommended as a strategy for preventing heart disease. Studies published over the last 5 - 8 years have identified a potential increased risk for stroke and heart disease with chronic estrogen replacement therapy. Estrogen replacement therapy still probably has a role for treatment of severe perimenopausal and postmenopausal symptoms.

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 Table: Blood Pressure Ranges.]

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.)

Click the icon to see an image about hypertension.

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. Over 20% of the population is estimated to have this condition. Obesity is highly linked with type 2 diabetes, and diabetes itself poses a significant risk for high cholesterol levels and heart disease. Insulin resistance alone is also probably a risk factor for heart disease.

[For more information, 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.

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 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. [For more information, 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.) Even though signs of heart disease are often not evident in the majority of patients with PAD, most of these patients also have coronary artery disease present. [See In-Depth Report #102: Peripheral artery disease.]

Smoking is the most important risk factor for heart disease. Smoking can cause elevated blood pressure, worsen lipids, and make platelets very sticky, raising the risk of clots. 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, 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. [For more information, see In-Depth Report #41: Smoking.]

Diet plays an important role in the health of the heart. [For more information, 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 active 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. [For more information, see In-Depth Report #31: Stress.]

Depression. Noticeable depression is present in around 50% of patients after a heart attack, and one third or more of these patients have what is called a major depression. Many patients with chronic heart disease, even when stable, also suffer from depression. People with depression feel more severe cardiac symptoms. Depression also may have a negative effect on patients' ability and willingness to follow their treatment plans. The risk of heart attacks and even death from heart disease is increased in patients with chronic angina and depression.

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. [For more information, 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. However, this benefit must be considered against all the risks of patients who are unable to limit their alcohol intake.

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.

However, studies have shown that while B vitamin supplements do help lower homocysteine levels, they have no effect on heart disease outcomes. Results of these studies have shown 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. However, treatment with appropriate antibiotics is not found to reduce the risk of future heart problems for patients infected with this organism.

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.

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. About 50% of patients with high blood pressure (hypertension) also have obstructive sleep apnea. The relationship between sleep apnea and hypertension has been thought to be largely due to obesity, but studies are finding a higher rate of hypertension in people with sleep apnea regardless of their weight. The use of a device known as nasal continuous positive airway pressure (CPAP) to treat patients with both sleep apnea and hypertension has been found to have only a small benefit for high blood pressure.

About a third of patients with coronary artery disease also have obstructive sleep apnea. Patients with severe, untreated apnea have been found to have an increased incidence of stroke and cardiac events (such as heart attack). However, there is no evidence to date that identifies obstructive sleep apnea as an independent cause of cardiac events or stroke.

Factors before Birth and in Infancy. Low birth weight, particularly in girls, has been associated with high blood pressure in both childhood and adulthood.

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.

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.

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.

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.

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 care provider can rule out either a non-heart problem or possible other serious accompanying conditions.
• An electrocardiogram (ECG) reading is taken, recording the waves made by 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 the 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 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 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.

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 an exercise stress test, to detect the location and extent of heart muscle damage.

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

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. In the procedure:

• 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 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.

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 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.

Treatment

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

Patients 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, 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.

Treatment options for acute coronary syndrome or heart attack include:

• Oxygen therapy
• Relieving pain and discomfort using nitroglycerin or morphine
• Controlling any arrhythmias (abnormal heart rhythms)
• Blocking further clotting (if possible), using aspirin and other anti-platelet drugs, as well as possibly anticoagulant drugs
• Opening up the artery that is blocked as soon as possible, by using medicines that open up the clot or by performing angioplasty
• Giving the patient beta-blockers, calcium channel blockers, or angiotensin converting enzyme inhibitor drugs to help the heart muscle and arteries work better

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, 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 whom such effects may worsen their heart attacks, other drugs such as meperidine (Demerol) or nalbuphine (Nubain) may be used.

With a heart attack, clots form in the coronary arteries that supply oxygen to the heart muscle. Opening a clotted artery as quickly as possible is the best approach to improving survival and limiting the amount of heart muscle that is permanently damaged.

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 preferably within 90 minutes of arriving at the hospital and no later than 12 hours after a heart attack.
• Thrombolytics, known as blood-clot-busting drugs, are the standard medications used to open the arteries.

Factors considered in choosing a strategy include:

• How likely it is the patient is having a heart attack
• Patient's age (preferably fewer than 75 years)
• Presence of risk factors for bleeding or history of recent bleeding
• Elapsed time since symptoms began (preferably fewer than 12 hours)
• Whether a patient needs to be transported in order to have PCI
• Blood pressure level
• History of stroke or cancer
• Which and how many coronary arteries are blocked

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. Generally speaking, thrombolysis is considered a good option for patients with heart attacks when symptoms have been present for fewer than 3 hours. Ideally, they should be given within 30 minutes of arriving at the hospital if a PCI is not a viable option. Other situations where it may be used include when:

• Prolonged transport will be required
• Too long of a time will pass before a catheterization lab is available
• PCI procedure is not successful or anatomically too difficult

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

• Patients older than 75 years
• When 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
• 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, especially when systolic is higher than 180 mm Hg

Specific Thrombolytics. 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.

Thrombolytic Administration. 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).

Complications. 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.

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/PCI is the standard procedure for heart attacks. 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, recent studies have shown that balloon angioplasty and stenting fails to prevent heart complications in patients who receive the procedure 3 - 28 days after a heart attack.
• Coronary bypass surgery is typically used as elective surgery for patients with blocked arteries. It may occasionally be used after a heart attack if angioplasty or thrombolytics fail or are not appropriate. It is usually not performed for several days to allow recovery of the heart muscles.

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).

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.

Situations where percutaneous interventions may be recommended include:

• Patients with unstable angina who are considered high-risk for continued symptoms or for developing a heart attack, or who continued to be unstable
• Patients who have a heart attack, within 12 hours of symptom onset
• Patients who have a heart attack or heart failure or other high-risk findings
• Patients who continue to show signs of ischemia after receiving a thrombolytic drug
• Patients with a heart attack who are not considered safe candidates for thrombolysis or for whom thrombolysis has been delayed
• Patients with ACS who have findings on angiography indicating PCI is necessary

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.

Angioplasty/PCI 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.

Complications occur in about 10% of patients (about 80% of complications occur 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. [For more information, 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). 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 is controversial.

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

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 receive 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.]

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. Appropriate anticlotting medications are started immediately in all patients. Such drugs are sometimes used along with thrombolytics, and also as on-going maintenance to prevent a heart attack. All anti-clotting therapies carry the risk of bleeding, which can lead to dangerous situations, including stroke.

Anti-Platelet Drugs. These drugs inhibit blood platelets from sticking together, and therefore help to prevent clots. Platelets are very small disc-shaped blood cells that are important for blood-clotting.

• Aspirin. Aspirin is an antiplatelet drug. An aspirin should be taken immediately after a heart attack begins. 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. It is then continued afterwards. Using aspirin for heart attack patients has been shown to reduce mortality. It is the most common anti-clotting drug, and most people with heart disease are advised to take it daily in low dose on an ongoing basis.
• Clopidogrel (Plavix), a thienopyridine, is another type of anti-platelet drug. Clopidogrel is started either immediately or right after percutaneous intervention is performed for patients with heart attacks. It is also begun after thrombolytic therapy. Patients who receive a drug-eluting stent should take clopidogrel along with aspirin for at least 1 year to reduce the risk of clots. Patients admitted for unstable angina should receive clopidogrel if they are unable to take aspirin. Clopidogrel should also be given to patients with unstable angina for whom an invasive procedure is planned. Even for conservatively treated patients, Clopidogrel should be started and continued for up to 1 year.
• 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), particularly when invasive procedure is planned or patients are still unstable after receiving aspirin and clopidogrel.

Anticoagulant Drugs. Anticoagulants thin blood. They include:

• Heparin is usually begun during or at the end of treatment with thrombolytic drugs and continued for at least 2 days if not the whole time in the hospital.
• Fondaparinux (Arixtra) is a newer blood thinner that may be used, but its exact role remains unclear.
• Warfarin (Coumadin).
• Direct thrombin inhibitors, such as argatroban (Novastan), danaparoid (Orgaran), lepirudin (Refludan), and bivalirudin (Angiomax). A clear benefit for these drugs over heparin has not been shown. They also carry an increased risk for bleeding.

All of these drugs pose a risk for bleeding. [For more informaiton, 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. Beta-blockers are often given to patients early in their hospitalization, sometimes intravenously. Patients with heart failure or who are at risk of going into cardiogenic shock should not receive intravenous beta-blockers. Long-term oral beta-blocker therapy for patients with symptomatic coronary artery disease, particularly after heart attacks, is recommended in most patients. [For more information, see In-Depth Report #03: Coronary artery 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 (as 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. Patients with asthma, emphysema, or chronic bronchitis, should not take these beta-blockers.

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.

After being admitted to the hospital for acute coronary syndrome or a heart attack, patients should not be discharged without statins or other cholesterol medicine unless their LDL ("bad") cholesterol is below 100 mg/dL. Some doctors recommend that LDL should be below 70 mg/dL. [For more information, see In-Depth Report #23: Cholesterol.]

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. ACE inhibitors should be given on the first day to all patients with a heart attack, unless there are medical reasons for not taking them. Patients admitted for unstable angina or acute coronary syndrome should receive ACE inhibitors if they have symptoms of heart failure or evidence of reduced left ventricular fraction echocardiogram. 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).

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 inhibitor together is safe.

Calcium channel blockers may provide relief in patients with unstable angina whose symptoms do not respond to nitrates and beta-blockers, or for patients who are unable to take beta-blockers. They are also useful for patients with Prinzmetal's angina.

Stem Cell Therapy. Researchers are investigating whether infusions of adult stem cells can benefit 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. The procedure is considered experimental at this time.

Secondary Prevention

Patients can reduce the risk for a second heart attack by following secondary prevention measures. No one should be discharged from the hospital with these issues being addressed and appropriate medications prescribed.

Blood Pressure. Aim for a blood pressure goal of less than 130/80 mm Hg.

Cholesterol. LDL (“bad”) cholesterol should be substantially less than 100 mg/dL. If triglycerides are greater than or equal to 200 mg/dL, then non-HDL-C should be less than 130 mg/dL. {Non-HDL-C is the difference between total cholesterol and HDL (“good") cholesterol levels.} Patients who do not meet these goals should be prescribed medications, with statin drugs being the first choice.

It is also important to control dietary cholesterol by reducing intake of saturated fats to less than 7% of total calories. Adding plant stanol/sterols (through dietary supplements or certain types of margarine-like spreads) may also be helpful for reducing LDL cholesterol. Increased omega-3 fatty acid consumption (by eating more fish or taking fish oil supplements) can help reduce triglyceride levels. [For more information, see In-Depth Report #43: Heart-healthy diet.]

Exercise. Exercise for 30 - 60 minutes 7 days a week (or at least a minimum of 5 days a week.)

Weight Management. Combine exercise with a healthy diet rich in fresh fruits, vegetables and low-fat dairy products. Your body mass index (BMI) should be 18.5 - 24.8. Waist circumference is also an important measure of heart attack risk. Men’s waist circumferences should be fewer than 40 inches (102 centimeters) and women’s should be fewer than 35 inches (89 centimeters).

Smoking. It is essential to stop smoking. Also, avoid exposure to second-hand smoke.

Antiplatelet Drugs. Your doctor may recommend you take aspirin (75 - 162 mg) on a daily basis. If you have had a stent inserted, you must take clopidogrel (Plavix) along with aspirin for at least 1 year following surgery. Clopidogrel (Plavix) may also be prescribed as maintenance therapy for other patients as well.

Other Drugs. Your doctor may recommend that you take an ACE inhibitor or beta-blocker drug on an ongoing basis. It is also important to have an annual influenza (“flu”) vaccination.

Rehabilitation

Lifestyle choices, 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. Patients with recent episodes of acute coronary syndrome also generally need some sort of supervised exercise training. 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 suggested 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 care providers should give the patient 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. In general, 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 has 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 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

Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, Casey DE Jr, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-Elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction) developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine. J Am Coll Cardiol. 2007 Aug 14;50(7):e1-e157.

Antman EM. ST-Elevation myocardial infarcation: management. In: Libby P, Bonow RO, Mann DL, Zipes DP, eds. Libby: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. Saunders; 2007:chap 51.

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.

Antman EM, Hand M, Armstrong PW, Bates ER, Green LA, Halasyamani LK, Hochman JS, et al. 2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: developed in collaboration With the Canadian Cardiovascular Society endorsed by the American Academy of Family Physicians: 2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, Writing on Behalf of the 2004 Writing Committee. Circulation. 2008 Jan 15;117(2):296-329. Epub 2007 Dec 10.

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.

Cannon CP and Braunwald E. Unstable angina and non-ST elevation myocardial infarction. In: Libby P, Bonow RO, Mann DL, Zipes DP, eds. Libby: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. Saunders; 2007:chap 53.

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.

Di Mario C, Dudek D, Piscione F, Mielecki W, Savonitto S, Murena E, et al. Immediate angioplasty versus standard therapy with rescue angioplasty after thrombolysis in the Combined Abciximab REteplase Stent Study in Acute Myocardial Infarction (CARESS-in-AMI): an open, prospective, randomised, multicentre trial. Lancet. 2008 Feb 16;371(9612):559-68.

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.

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.

Hirsch A, Windhausen F, Tijssen JG, Verheugt FW, Cornel JH, de Winter RJ; Invasive versus Conservative Treatment in Unstable coronary Syndromes (ICTUS) investigators. Long-term outcome after an early invasive versus selective invasive treatment strategy in patients with non-ST-elevation acute coronary syndrome and elevated cardiac troponin T (the ICTUS trial): a follow-up study. Lancet. 2007 Mar 10;369(9564):827-35.

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.

King SB 3rd, Smith SC Jr, Hirshfeld JW Jr, Jacobs AK, Morrison DA, Williams DO;et al. 2007 Focused Update of the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: 2007 Writing Group to Review New Evidence and Update the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention, Writing on Behalf of the 2005 Writing Committee. Circulation. 2008 Jan 15;117(2):261-95. Epub 2007 Dec 13.

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.

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.

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.

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.

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