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Heart Attack and Acute Coronary Syndrome

* Please note that most treatment modalities listed below are based on conventional medicine. PreventDisease.com does advocate the use of any pharmaceutical drug treatments. Long-term drug therapy is detrimental to human health. All drug information is for your reference only and readers are strongly encouraged to research healthier alternatives to any drug therapies listed.

WHAT IS A HEART ATTACK (MYOCARDIAL INFARCTION) AND WHAT CAUSES IT?

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, which occurs when blood flow to the myocardium is interrupted.

In general, in patients with coronary artery disease, the presence of one of three of the following syndromes suggests different degrees of severity.

Stable Angina. Angina is the primary symptom of coronary artery disease and is typically experienced as chest pain. Stable angina is predictable chest pain and can usually be managed with life-style measures and medications, such as low-dose aspirin. [ See Box Angina.]

Acute Coronary Syndromes. Acute coronary syndromes are severe and sudden heart conditions that require aggressive treatment but have not developed into a full blown heart attack. Acute coronary syndromes include the following:

Unstable angina. Unstable angina is a much more serious situation and is often an intermediate stage between stable angina and a heart attack.
Non Q-wave myocardial infarction. (This latter condition is diagnosed when blood tests and ECGs suggest a developing heart attack. In such cases, injury in the arteries appears to be less severe than with a full-blown heart attack.)

Heart Attack. The full blown heart attack occurs when blood flow is blocked and tissue death occurs from loss of oxygen, severely damaging the heart. In such cases, an injury known as an infarct occurs, or in other words, a myocardial infarction , more commonly known as a heart attack.

The Process of Atherosclerosis

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 and some are not fully understood.

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, powdery nutrient 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.

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 over-produced.
In excess amounts, they can be very dangerous, including damaging cells and even effecting genetic material.
For example, in the case of 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.

Inflammatory Response. For the arteries to harden there must be a persistent reaction in the body that causes on-going harm. Researchers now believe that this reaction is an immune process known as the inflammatory response.

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 cells that attach 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.

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.
These narrow and inelastic arteries not only slow down blood flow but they also become vulnerable to injury and tears.

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.

(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.

WHAT ARE THE SYMPTOMS OF A HEART ATTACK?

Common Heart Attack Symptoms

Any unusual chest pain, angina, or other suspicious symptoms that do not clear up with medications is a signal to go to the hospital in people with known heart disease. (It should be noted, however, that only about 20% of heart attacks follow long-standing angina.) The sooner one is treated for a heart attack the better the outcome. ANYONE WHO BELIEVES THEY ARE HAVING A HEART ATTACK SHOULD NOT HESITATE TO CALL THE EMERGENCY MEDICAL SYSTEM. [ See Box Angina.]

Some signs to watch out for are as follows:

Pain experienced as a crushing weight against the chest, which is 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 even be numb.
Chest pain, usually precipitated by exercise or stress, that does not clear up when medications are taken or when resting.
Mild chest pain with unexplained fatigue and ill health. Depression may be present. In patients with known heart disease, such symptoms have sometimes been reported within a month of a heart attack.

It should be noted, however, that degree of pain and the specific symptoms before a heart attack vary greatly among individuals.

Some people may feel severe pain; others might feel only a tingling sensation. Some people may only have a sense of fullness, squeezing, or pressure in the chest.)
A feeling of indigestion or heartburn is common, as are nausea and vomiting.
Some people report a great fear of impending death, a phenomena known as angor animi.

Atypical Symptoms in Specific Populations

About one-third of all heart attack patients do not have chest pain at all, putting them at much higher risk for a misdiagnosis. Women and the elderly are particularly more likely to have atypical symptoms (although they can certainly have classic heart attack symptoms as well.)

A 2000 study suggested that heart attacks might go undiagnosed in people over 65 who do not have a history of angina or heart failure. Any older person with unexplained weakness, a rapid heart beat, difficulty in breathing, or a sudden drop in blood pressure should be evaluated for a heart problem.
Symptoms of angina in women are also often not typical. 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 the same symptom in men. Because of these reasons, women are less likely than men to be tested aggressively for serious heart problems when they enter the emergency room.

Actions that the Patient Should Take at the Onset of Symptoms

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 five 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. Anyone who has heart disease or risk factors for it and experiences heart attack symptoms should contact emergency services. It should be noted that only 20% of heart attacks occur in patients with long-standing angina.

The patient should chew an aspirin and be sure that emergency health providers are informed of this so an additional dose isn't given.

Chest pain sufferers should go immediately to the nearest emergency room, preferably traveling by ambulance. They should not drive themselves.

ANGINA

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 doesn't 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 conditions:

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

Angina itself is not a disease. Much evidence exists, in fact, 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:

It is often reported as a dull, heavy pressure that may resemble a crushing object on the chest.
Pain often radiates to the neck, jaw, or left shoulder and arm.
Less commonly, patients report mild burning chest discomfort, sharp chest pain, or pain that radiates to the right arm or back.
Sometimes a patient experiences shortness of breath, fatigue, or palpitations instead of 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.
Some people have also reported a higher sensitivity to heat on the skin with the onset of angina.
Angina can also be precipitated by large meals, which place an immediate demand upon the heart for more oxygen.

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 the following:

exercise,
cold weather,
emotional tension, or
large meals.

Angina attacks can occur at any time during the day, but a high proportion seems to take place between the hours of 6:00 AM and noon.

Unstable Angina. 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 two-month period, and medications are less effective in relieving its pain.

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 experience angina pain, a condition 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. In one study, people with silent ischemia experienced much higher complication and mortality rates than those with anginal pain. (Angina pain may actually protect the heart by conditioning it before a heart attack.)

HOW SERIOUS IS A HEART ATTACK?

Severity of a Heart Attack

In 2001, an estimated 650,000 Americans will suffer a first heart attack and 450,000 will have a recurrent episode. Heart attacks may be rapidly fatal, may evolve into a chronic disabling condition, or may lead to full recovery. They will be fatal in about 220,000 of patients. It should be noted, however, that 12,400,000 people who have had a heart attack, angina, or both are alive today.

The rate of hospitalization for a first heart attack has not changed significantly over the past few years. (In fact, it has increased in African American women.) On the positive side, however, improved treatments have significantly reduced mortality rates and rehospitalizations. About 88% of people under age 65 can expect to return to work.

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

Elderly (particularly those who are thinner).
Women have a higher mortality rate after a heart attack than men do.
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.

Factors 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 four 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 arrythmias.)
Signs of severe physical damage to the heart.
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 the past 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.

Long-term Outlook

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. Within six 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 at this time no tests can reliably 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. [ See Who Is At Risk for a Heart Attack and What Risk Factors Can Be Managed?, in this report. ]

WHO IS AT RISK FOR A HEART ATTACK AND WHAT RISK FACTORS CAN BE MANAGED?

About 12.4 million Americans currently have heart disease and 1.1 million people are expected to have a serious heart event this year. An estimated 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 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 US 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.

Reducing Multiple Risk Factors. The risk for heart disease increases with multiple risk factors, importantly unhealthy cholesterol or lipid levels, diabetes, obesity, smoking, and hypertension. Conversely, risk plummets in the absence of multiple risk factors. For example, a 1999 study found that men and women of all ages who had none of these risk factors had a risk of dying from heart attack that was between 77% and 92% lower than those with one or more of them. (The people with no risk factors also had a lower risk for stroke and cancer.) Conversely, a 2000 study reported that patients who aggressively pursued a healthy lifestyle (low-fat diet, stress management, smoking cessation, moderate aerobic exercise) significantly reduced their risk for heart attack, cardiac surgery, and death.

Nonmodifiable Risk Factors

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, ten to fifteen 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 are. The American Heart Association reported in 2001 that four million women had angina compared to 2.3 million men. Younger women with heart disease often do not have the same symptoms as their male counterparts do and may be less likely to be diagnose correctly. Studies are now suggesting, however, that the overall higher mortality rates and the less aggressive treatments in women with heart disease appear to be due to their older agent and sicker condition than their male peers at the time of a heart event. (Interestingly, one 1999 study found that although, indeed, women with unstable angina were treated less aggressively than men, when their risk factors were compared head to head, men actually had a worse long-term outcome.)

Genetic Factors . Genetics are involved in increasing the likelihood of developing important risk factors (eg, diabetes, obesity, and high blood pressure). One genetic variant called apolipoprotein E4 (ApoE4) affects cholesterol levels, particularly those associated with heart disease. A 1999 study suggests that it may be a significant risk factor for coronary artery disease in early middle age. (The presence of this variant may also be associated with increased risk for Alzheimer's disease.)

Genetic factors that increase the risk for blood clots are also associated with high risk for heart disease and heart attack. Of particular importance are those called factor VII genes that affect the way blood coagulates.

Ethnicity

African Americans. In a 1998 analysis, although mortality rates from coronary artery disease declined between 1987 and 1994 in both Caucasians and African Americans, they did not decline significantly in African Americans. 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.) 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 lack of access to health care.
All African Americans face discrimination, 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 US population, African Americans have comprised only 2% to 9% of subjects in most of the major research trials, and 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 in women.
One study found that African Americans produce less nitric oxide in response to stress; this substance is critical for opening blood vessels and increasing blood flow.

Other Groups. 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.

Cholesterol and Other Lipids

Cholesterol. High cholesterol levels are strong risk factors for heart disease, particularly when the harmful type known as low-density lipoprotein (LDL) cholesterol is elevated. The higher the cholesterol, the greater the risk. For example, according to a 2000 study, men with cholesterol levels over 240 mg/dl have a risk that is 2.15 to 3.63 times higher than those whose cholesterol is below 200.

Triglycerides. Triglycerides are made up of fatty acid molecules and are the basic chemicals in animal and plant fats. Evidence now suggests that these molecules may be major trouble-makers for the heart. Some evidence also suggests that high triglycerides are risk factors for heart disease on their own regardless of cholesterol levels.

Cholesterol Goals
Total Cholesterol Goals	LDL Goals	HDL Goals	Triglyceride Goals
200 mg/dl or less. (One study suggested that the ideal cholesterol goal for older people is between 200 and 220. There is a heart risk below and above these levels.)	160 mg/dL or less. (People with two or more risk factors for heart disease should aim for LDL levels of 130 mg/dl or below. People with existing heart disease should aim for LDL levels of below 100 mg/dl.*)	35 mg/dL or more. (Some experts suggest higher goals, 45 for men and 50 for women, with everyone aiming for about 60.)	200 mg/dL or less. (Evidence is suggesting that levels over only 100 may predict an increased risk for heart disease.)
*Risk factors for heart disease include a family history of heart problems, smoking, high blood pressure, diabetes, being older (over 45 for men and 55 for women), and having HDL levels below 35 mg/dl.

Other Lipids. Elevated levels of other fatty molecules (lipids) are also now thought to be important indicators of heart disease risk. They include lipoprotein (a) and apolipoprotein A-1 and B. Apolipoprotein B, for example, may actually turn out to be a very accurate indicator of heart disease risk in women. ApoE4, a genetic form of another apolipoprotein, is associated with Alzheimer's disease and is also under investigation for a role in heart disease. [For more information, see the Reports #23, Cholesterol and #43, Heart Healthy Diet .]

High Blood Pressure

High blood pressure, or hypertension, has long been a proven cause of coronary artery disease. Blood pressure is categorized as:

Optimal (below 120/80 mm Hg).
Normal (between 120/80 and 130/85 mm Hg).
High normal (between 130/85 and 139/89). (Some studies indicate that high normal puts one at higher risk for heart events and stroke, although others suggest this risk exists primarily in people with diabetes.)
Hypertension, or high blood pressure (140/90). [For more information, see the Report #14, High Blood Pressure .]

Obesity and Overweight

Obesity is related to hypertension, diabetes, abnormal cholesterol levels, and lack of exercise, all conditions contributing to heart attack risk. Obesity in children is a greater risk for future heart trouble than a family history of heart disease. People who are overweight in middle age may still not completely reduce their risk for coronary artery disease later in life, even if they lose excess weight. Abdominal obesity (the "beer belly") poses a particular risk. Obesity is determined by measurement of body fat, not merely body weight.

People might be over the weight limit for normal standards, but if they are very muscular with low body fat, they are not obese. Others might be normal or underweight, but still have excessive body fat. The current best single gauge for body fat is a measurement called body mass index (BMI). It is derived by a series of calculations:

Multiply one's weight in pounds by 703.
Divide that answer by one's height in inches.
Divide that answer once again by height in inches. The resulting number is the BMI.

Current federal and WHO guidelines define overweight as a BMI of 25 to 29.9 and obesity as a BMI of 30 or greater.

[For more information, see the Report #53, Weight Control and Diet .]

Sedentary Lifestyle and Exercise

People who are sedentary are almost twice as likely to suffer heart attacks as are people who exercise regularly. Regular moderate aerobic exercise benefits the heart in many ways. For instance, brisk walking has the following advantages:

Lowers the heart rate and blood pressure.
Raises HDL ("good") cholesterol.
Lowers blood sugar levels.
Opens up the blood vessels and, in combination with a healthy diet, may improve blood clotting factors.
Reduces stress and improves mood.

Some studies suggest that for the greatest heart protection, it is not the duration of the exercise 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. Even elderly people with unstable angina or who had a previous heart attack can benefit from a structured exercise program. Exercises that train and strengthen the chest muscles may also prove to be very important for patients with angina.

It should be noted that sudden strenuous exercise (such as snow shoveling and mowing lawns) puts such 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 the Report #29 Exercise.]

Diabetes and Insulin Resistance

Heart attacks account for 60% and strokes for 25% of deaths in all diabetics. A 1998 study reported that people with type 2 diabetes and no history of heart disease have the same seven-year risk for a heart attack as nondiabetics with heart disease.

Long-term insulin resistance, even without type 2 diabetes, appears to have significant damaging effects on the heart. This condition occurs when insulin levels are normal to high but the body is unable to use the insulin to regulate metabolism of blood sugar and to store it for energy. In such cases, the body compensates by increasing insulin levels (hyperinsulinemia), which in turn increases triglyceride levels and reduces HDL cholesterol. Normally, insulin stimulates the release of two substances, endothelin and nitric oxide, that are important in keeping arteries elastic and open. Insulin resistance may cause an imbalance in these substances. [For more information, see the Reports #9, Diabetes: Type I or #60, Diabetes: Type II .]

Smoking

Smokers in their thirties and forties 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.

Specific Effects on the Heart. Its damaging effects on the heart are multifold:

Smoking lowers HDL levels (the so-called good cholesterol) even in adolescents.
It causes deterioration of elastic properties in the aorta, the largest blood vessel in the body, and increases the risk for blood clots.
It increases the activity of the sympathetic nervous system (which regulates the heart and blood vessels).
Tobacco smoke may increase cardiovascular disease in women through an effect that reduces estrogen levels.

Effects of Second-Hand Smoke. Studies continue to confirm the dangers of second-hand smoke. Regular exposure to passive smoke is now estimated to increase the risk of heart disease in the nonsmoker by between 25% and 91%, causing 30,000 to 60,000 deaths each year. [For more information, see the Report Smoking.]

Eating Habits

Eating habits can be protective or dangerous to the heart. Although the best diet is not clear for each individual, avoiding saturated fats and trans-fatty acids is recommended for everyone. [ See Box Dietary Factors and Heart Disease.]

Dietary Factors and Heart Disease

Diet plays an important role in the health of the heart. There is no single diet that suits everyone, but a few general observations can be made. [ For detailed dietary information, see the report Heart Healthy Diet .]

Fats

Experts now believe that fats can have both harmful and beneficial effects. Whether harmful or beneficial they are still high in calories:

Harmful Fats. Reducing consumption of saturated fats and trans-fatty acids is the first essential step in managing cholesterol levels through diet.

Saturated Fats. Saturated fats are found predominantly in animal products, including meat and dairy products. They are strongly associated with higher cholesterol levels. Although certain fatty acids in saturated fats called stearic acids may have some benefits, there is no simple method for defining foods that contain them, so, in general, saturated fats should be avoided. (The so-called tropical oils (palm, coconut, and cocoa butter) are [also high in saturated fats. Evidence] is lacking, however, about their effects on the heart. The countries with the highest palm-oil intake, Costa Rica and Malaysia also have much lower heart disease rates and cholesterol levels than Western nations.)
Trans-fatty Acids. Trans-fatty acids are manufactured fats created during a process called hydrogenation, which is aimed at stabilizing polyunsaturated oils to prevent them from becoming rancid and to keep them solid at room temperature. They may be particularly dangerous for the heart and may pose a risk for certain cancers. Some experts believe that these partially hydrogenated fats are even worse than saturated fats because they both increase LDL and reduce HDL cholesterol levels and may have harmful effects on the linings of the arteries. One study of 80,000 nurses reported that women whose total fat consumption was 46% of total caloric intake had no greater risk in general for a heart attack than did those for whom fat represented 30% of calories consumed. Women whose diets were high in trans-fatty acids, however, had a 53% increased risk for heart attack compared to those who consumed the least of those fats. Hydrogenated fats are used in stick margarine and in many fast foods and baked goods, including most commercially produced white breads. (Liquid margarine is not hydrogenated and is recommended.) The FDA has now required that food labels include information on trans-fatty acids.

Beneficial oils: Public attention has mainly focused on the possible benefits of small amounts of monounsaturated and polyunsaturated fats found in vegetable oils. Researchers are most interested, however, in the smaller fatty-acid building blocks contained in these oils called essential fatty acids. Three important fatty acids are the essential fatty acids omega-3, omega-6, and omega-9.

Omega-3 fatty acids: They are further categorized as alpha-linolenic acid and docosahexaenoic and eicosapentaenoic acids.

Docosahexaenoic (DHA) and Eicosapentaenoic (EPA) Acids. Fish oils, which contain docosahexaenoic (DHA) and eicosapentaenoic acids (EPA), have anti-inflammatory and anti-blood clotting effects and may be significantly beneficial to the heart. DHA is the most unsaturated of all fatty acids. These fatty acids may reduce triglyceride levels and have modest positive effects on HDL. In patients with high triglyceride levels, but not in others, omega 3 fatty acids may increase LDL. Overall cholesterol levels are not affected. DHA appears to have specific benefits on blood pressure. The International Society for the Study of Fatty Acids and Lipids, in fact, recommends fish oil supplements for heart protection. Omega-3 fatty acids in fish may reduce risks for other disorders, including stroke, rheumatoid arthritis, asthma, ulcerative colitis, and some types of cancers.

Alpha-linolenic Acid . Alpha-linolenic acid is a plant precursor of DHA, which means the body can convert it to DHA. Sources include canola oil, soybeans, flaxseed, and certain nuts and seeds (walnut, flax, chia and sometimes pumpkin seed). Studies have been positive about the effects on the heart of these oils or foods containing these oils.

Omega-6 polyunsaturated fatty acids. Sources are corn, safflower, soybean, and sunflower oil. PUFA oils containing omega-6 fatty acids constitute most of the oils consumed in the US. Some omega-6 fatty acids are important for health. There is some association with a higher risk for certain cancer and some chronic diseases with diets high in omega-6 fatty acids, however.
Omega-9 monounsaturated fatty acids: Sources are canola and olive oil. Extra virgin olive oil has been associated with lower blood pressure and a 2000 study reported that it may have specific benefits for people with diabetes type 2. Of concern is a small study reporting higher concentrations of LDL in subjects consuming an olive-oil rich diet compared to those on a sunflower or rapeseed oil rich diet.

Research suggests that our current Western diet contains an unhealthy high ratio (10 to 1) of omega-6 to omega-3 fatty acid. Omega-9 fatty acids may also contain chemicals that block harmful factors found in omega-6 fatty acids. Researchers are finding then that the most benefits may be found in mixture of all three fatty acids found in both poly- and monounsaturated oils, but in modest amounts that do not add too many calories.

Carbohydrates

Meals overly rich in carbohydrates tend to set off angina attacks, possibly because they raise insulin levels. One study suggested, in fact, that in women, sugar may pose an even higher risk for heart disease than fats do. Whole grains and fresh fruits and vegetables (particularly dark-colored ones), however, are very important. They are rich in fiber, vitamins, and other important nutrients that are heart-protective. Natural chemicals in cooked tomatoes, garlic, nuts, apples, onions, wine, and tea also appear to offer protection for the heart.

Protein

Meat and Fish. For heart protection, one 1999 study suggested that it didn't matter if you chose fish, poultry, beef, or pork as long as the meat was lean. (Saturated fat in meat is the primary danger to the heart.) The fat content of meat varies depending on the type and cut. It is best to eat skinless chicken or turkey; the leanest cuts of pork (loin and tenderloin), veal, and beef are nearly comparable to chicken in calories and fat and their effect on LDL and HDL levels. It should be noted, however, that even chicken and lean meat do not improve cholesterol levels, and, in terms of cardiac health, fish is a more desirable choice. Much evidence suggests that eating fish two or three times a week, particularly oily fish (such as salmon, halibut, swordfish, and tuna) is protective.

Soy. Soy is proving to be a particularly excellent source of protein. It is rich in both soluble and insoluble fiber, omega-3 fatty acids, and provides all essential proteins. A number of studies have indicated that subjects that consume about 40 grams of soy protein each day reduce LDL and triglycerides and increase HDL. Powdered soy protein that contains at least 60 mg of isoflavones may provide similar benefits. (Tablets of individual isoflavones found in soy, however, do not appear to offer any advantages.)

Antioxidant Vitamins and Supplements

Vitamin E. Vitamin E may prevent blood clots and the formation of fatty plaques and cell proliferation on the walls of the arteries. Experts have hoped that supplements of this vitamin prove to be protective. However, few studies have offered any strong support for these hopes. One major 2000 study, for example, reported that patients who took a natural vitamin E at 400 IU for four to six years did not gain any protection against cardiovascular disease. Different vitamin E compounds, such as gamma tocopherol or tocotrienol, may prove to have benefits that the standard synthetic supplements (dl alpha tocopherol) do not, but more research is needed.

Vitamin C. Although in the laboratory, vitamin C has positive effects on blood vessels, there is no proof that supplements of vitamin C offer any actual protection against heart disease. And there is some evidence that high doses may even speed up existing damaging processes in the arteries.

B Vitamins. Several important studies have demonstrated a link between deficiencies in the B vitamins folic acid (folate), B6, and B12 and elevated blood levels of an amino acid homocysteine, a possible risk factor for atherosclerosis. Folic acid is particularly potent in reducing homocysteine levels, and folate deficiencies are associated with a higher risk from heart disease. (Green vegetables and legumes, enriched cereals and grains, and orange juice are rich in folate.) It is not clear yet if taking folate supplements and reducing homocysteine levels will actually protect against heart disease. Major studies are under way and small studies are promising. [ See Homocysteine under Emerging Risk Factors .]

Another important B vitamin is niacin (Vitamin B3), which improves cholesterol and triglyceride levels.

Note: Studies are continuing to indicate that high doses of antioxidants supplements, such as vitamins C, E, and beta carotene, may have pro-oxidant effects that can actually harm the arteries and incur other damage. [For more information, see the Report, Vitamins, Carotenoids, and Phytochemicals .]

Stress and Psychologic Factors

Stress. Incidents of acute stress have been associated with a higher risk for serious cardiac events, such as heart rhythm abnormalities and heart attacks, and even death from such events in people with heart disease. Most studies have focused on the negative effects of stress on the hearts of men, particularly from work, but a 2000 study reported that marital stress (but not work stress) also hurts women's hearts. Stress may have actual negative physical effects on the heart. [ See the Report #31, Stress .]

Depression. In one 30-year study, men who were clinically depressed had a greater risk for heart disease and heart attack than men who were not depressed. This higher risk lasted for decades. The more severe the depression, the more dangerous to the health. Some studies have indicated that even mild depression, including feelings of hopelessness, experienced over many years, may harm the hearts in people with no early signs of heart disease. A number of studies have suggested that depression has biologic effects on the heart, including blood clotting and heart rate. Depression may also impair a patient's response to medication for heart disease. (On the other hand hardening of the arteries in the brain may cause depression, so depression may simply be a marker of severe cardiovascular disease.)

Anger and Hostility. There have been some reports of an association between angry temperaments and heart disease. According to a 2000 study on Army personnel, however, psychologic factors (including depression, anxiety, hostility, and stress) did not appear to have any effect on hardening of the arteries, the primary cause of coronary artery disease. And, another 2000 study suggested that anger itself posed no higher risk to the heart, although outwardly expressed anger plus low social support did appear to predict progression of heart disease. [ See the Report #8, Depression.]

Alcohol

The effects of alcohol on heart disease varies depending on consumption. Evidence strongly suggests that light to moderate alcohol consumption (one or two drinks a day) protects the heart, even in people with type 2 diabetes. The benefits are strongest in people at high risk for heart disease and may be fairly small in those at low risk. No one recommends that nondrinkers start using alcohol for health reasons or that regular drinkers increase their intake. Large amounts of alcohol can raise blood pressure, trigger irregular heartbeats, and damage the heart muscle. Binge drinkers have a significantly higher risk for a cardiac emergency.

Emerging or Possible Risk Factors for Heart Disease

Homocysteine. Abnormally high blood levels of the amino acid homocysteine are strongly linked to an increased risk of coronary artery disease and stroke. Homocysteine may harm the lining of the arteries and reduce blood flow. Excessive levels occur with deficiencies of vitamins B6, B12, and folic acid.

Infectious Agents. Some microorganisms and viruses have been under suspicion for triggering the inflammation and damage in the arteries that contributes to heart disease. The primary suspect has been Chlamydia pneumoniae (a non-bacterial organism that causes mild pneumonia in young adults). Other organisms under investigation include H. pylori (the bacteria responsible for peptic ulcers), and the viruses herpesvirus and cytomegalovirus.

Iron Overload. Iron overload (high levels of iron in the blood) has been associated with coronary artery disease in animals. Results of studies on high iron levels in people, however, have been mixed. In a 2000 study of people with high iron levels, for example, Caucasian men had no higher mortality risk, but women had a higher death rate from heart disease and African American men had higher mortality rates from all causes. And a 2001 study reported that blood donations (which reduce iron levels) had no protective effect on heart disease. Most studies have been conducted on Caucasian men, and none have provided clear proof one way or the other on the effects of iron on the heart in any group.

Inflammatory Factors. An immune response that produces inflammation and damage in the arteries (possibly triggered by infection or other factors) is now strongly associated with heart disease. Specific inflammatory factors involved in the process may include those called C reactive protein and fibrinogen.

Elevated levels of C-reactive protein strongly predict future heart attacks in patients with existing heart disease, particularly unstable angina. Some studies have even suggested that the protein itself may directly play a role in damage to heart muscles. Nevertheless, high levels of C-reactive protein may simply be a by-product of processes involved in heart disease, such as obesity or smoking, rather than an independent predictor or cause of heart disease.
High levels of fibrinogen, a protein that is a central participant in the clotting process, is also a potential indicator of heart disease.

Periodontal (Gum) Disease. Some studies have reported a 1.5- to four-fold risk for heart disease in people with peridontal disease. In one, 85% of heart attack patients had periodontal disease compared to 29% of people who were free of heart disease. The bacteria that cause periodontitis may stimulate inflammatory factors that cause blood clots and other proteins that contribute to this higher risk. On the other hand, gum disease may simply be a common risk factor among other known risk factors for stroke, including being poor, African American, older, and overweight.

Oral Contraceptives. Some women who took early forms of oral contraceptives (OCs), particularly if they smoked, had high blood pressure, or both, have a higher risk for heart attack and stroke. Newer forms pose a much lower risk. And, in fact, a 2001 study found no higher risk for a heart attack in women using newer, low-dose OCs.

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 is often accompanied by snoring and short, gasping wakefulness. Many risk factors are associated with both stroke and sleep apnea (obesity, high blood pressure, a risk for blood clots, and narrowing of the arteries). These factors may also increase the risk for heart attacks. In one 2001 study, researchers observed that the higher the number of apneas a patient had, the higher his risk for heart attack.

Cocaine Use. A 2001 study suggested that one fourth of all non-fatal heart attacks in people under age 45 were due to regular cocaine use.

Conditions Associated with 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. A 2000 British study reinforced the idea that pre-birth or other early events have little significant effect on heart disease risk in later life.
Seasonal Differences. More deaths from heart disease occur in December and January and 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 white males. (Interestingly, in African American men, of these factors, only creased earlobes were associated with a higher risk in one study.)
Air Pollution. A 2000 study suggested that air pollution is linked to a higher risk of sudden death in patients with heart problems. It is possible that small particles can affect heart rhythms, which may be dangerous for people with heart conditions.

WHAT ARE THE TESTS USED TO DETERMINE A HEART ATTACK?

Electrocardiogram

An electrocardiogram (ECG or EKG) measures and records the electrical activity of the heart. Between 25% and 50% of people who suffer from angina or have silent ischemia, however, have normal ECG readings, and experts estimate that it may fail to detect 60% of heart attacks.

Recording the Heart Beats. ECGs record wave patterns that correspond to the contraction and relaxation pattern of the different parts of the heart. Specific waves seen on an ECG are named with letters as follows:

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.

Physicians will 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. Elevated ST segments indicate that the artery to an area of the heart is blocked and that the full thickness of the heart muscle is damaged. In most cases patients go on to develop a full-blown heart attack, medically referred to as a Q-wave myocardial infarction. ST-elevations are good indicators for aggressive treatments (thrombolytic drugs or angioplasty) to reopen blood vessels. In some cases, however, patients with elevated ST-segments turn out to actually have only non-Q-wave myocardial infarctions, which are generally less serious conditions [see below].

Non-Elevated ST Segments. Non-elevated ST segments indicate less complete blockage and occur in about half of patients with other signs of a heart event. In such cases, laboratory tests are needed to determine the extent, if any, of heart damage. In general, one of three following conditions may be present:

Angina (blood test results or other tests show no serious problems and chest pain resolves). Most patients with angina can go home.
Unstable angina (blood tests do not show markers for heart attack but chest pain is persistent). Unstable angina is potentially serious.
Non Q-wave myocardial infarction (blood tests suggest a developing heart attack, but most likely, injury in the arteries is less serious than with a full-blown heart attack).

Acute coronary syndrome refers to both unstable angina and non Q-wave myocardial infarction, because they are treated differently then full-blown heart attacks. [ See Box Managing Acute Coronary Syndromes.]

Angiography

Angiography is an invasive test that may be performed on patients who have very incapacitating angina that does not respond to medical therapy. It may be useful in certain cases following a heart attack to assess treatment success.

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.

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.

Imaging Tests

Echocardiograms. Echocardiograms are useful in patients who are suspected of having a heart attack but whose EKGs are normal. They are particularly important to diagnose the extent of damage to the heart muscle and to diagnose congestive heart failure.

Magnetic Resonance Imaging (MRI). A very promising investigative approach using magnetic resonance imaging (MRI) and a contrast material (an injected dye) can provide images of the entire thickness of the heart muscle instead of just the surface. It is proving to be accurate enough to allow prediction of which patients might benefit most from surgical procedures. This approach is unlikely to be widely available for some time.

Radionuclide Imaging. 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 the following situations:

Diagnosing or determining the severity of unstable angina when less expensive diagnostic approaches are unavailable or unreliable.
Determining the severity of chronic coronary artery disease.
To assess the success of surgeries for coronary artery disease.
To diagnose a heart attack.

Blood and Urine Markers

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. Some of these factors include the following:

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.
Creatine kinase myocardial band (CK-MB). CK-MB has been a standard marker but the MB fraction is not very accurate, since elevated levels can appear in people without heart injury. Certain forms of CK-MB, however, may improve its ability to specifically target 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.
Fibrinogen. Fibrinogen is a protein involved in blood clotting, but it is not routinely measured at this time.
Brain (B-type) natriuretic peptide. This is a hormone that is synthesized in the heart. High levels may identify patients at higher risk for a poor outcome from heart attack or acute coronary syndromes.
C-Reactive Protein. C-reactive protein is a product of the inflammatory process. Elevated levels may be important indicators for aggressive treatment in patients with unstable angina. At this time, it is not routinely measured.

Ruling out Other Causes of Symptoms

Other Conditions that Cause Chest Pain. Many conditions may cause chest pain. High on the list are the following:

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

Determining Treatments and Severity

Patients with chest pain and ECG showing elevated ST segments or other obvious signs of dangerous blockage usually have heart attacks and are immediately treated accordingly. Patients with chest pain and ECGs showing non-elevated ST-segments, however, may have angina, unstable angina, or pending heart attack. [ See Electrocardiogram above.] Unstable angina and non-Q-wave myocardial infarction are collectively referred to as acute coronary syndromes.

In order to predict which patients with non-elevated ST segments are most at risk for developing a more serious condition with two weeks of admission, some experts developed a very promising and easy scoring system based on the following criteria:

Age 65 years or older.
Three or more risk factors for heart disease (family history, hypertension, diabetes, current smoking, or unhealthy cholesterol levels).
Previous blockage of an artery of at least 50%.
ST-segment deviation.
Severe angina symptoms.
Aspirin use within the previous week.
Elevated creatine kinase or its MB fraction. [ See Blood and Urine Tests above.]

In one 2000 study, the lowest score (having 1 or none of these risk factors) suggested a 5% risk for a so-called triple endpoint: death from any cause, nonfatal heart attack, and arteries that are so blocked that they require an urgent operation to open them within two weeks. The highest score (6 or 7) suggested a 40% risk.

WHAT ARE THE GENERAL PROCEDURES IN THE EMERGENCY ROOM AND GUIDELINES FOR TREATING A HEART ATTACK?

Diagnosing a Heart Attack and Determining Treatment Options

Patients with heart disease or those with risk factors should seek emergency medical help if they have any signs or symptoms of an attack. Early treatment is critical for recovery. (A 2000 study has warned that patients at highest risk for late arrivals are those who are poor, female, and African American.)

When a patient arrives at the hospital with a possible heart attack the patient is given an electrocardiogram within 10 minutes and put on constant monitoring. Blood and other tests are taken to determine the condition. [ See What Are the Tests used to Determine a Heart Attack?]

Treatment options will depend on whether the patient has angina, acute coronary syndromes, or a full-blown heart attack. [For information on acute coronary syndromes, see Box Guidelines for Managing Acute Coronary Syndromes.]

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.

Drugs Used to Relieve Pain and Produce Comfort

Nitroglycerin. Most heart attack patients will usually receive nitroglycerin, 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 (eg, those with recurrent angina, congestive heart failure, or high blood pressure). There is some evidence suggesting 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 it also dilates blood vessels, thereby aiding the circulation of blood and oxygen to the heart. Morphine can decrease blood pressure and slow down the heart. In certain patients where such conditions can worsen their heart attacks, other drugs such as meperidine (Demerol) or nalbuphine (Nubain) may be used.

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.

Antianxiety Agents. Select patients may be given medications to reduce anxiety, such as haloperidol, although they are not routinely administered unless the patients are agitated or delirious.

Opening the Arteries: Clot Busting Drugs Versus Surgery

After a heart attack, clots form in the injured artery within four to six hours in 90% of heart attack victims. Opening a clotted artery as quickly as possible is the best approach to improving survival. (One study reported that very early treatment may even help reduce the long-term risk for heart failure.)

Specific medical and surgical solutions to this problem are now available. Primarily, they involve the following.

Thrombolytics are known as blood-clot-busting drugs. They are now the standard medications used to open the arteries. [ See What Are Thrombolytic Drugs Used To Restore Blood Flow After a Heart Attack?]
Angioplasty is the major surgical procedure for opening the arteries. [ See What Are the Surgical Procedures for Restoring Blood Flow After Heart Attack?]

A number of studies indicated that in centers experienced with emergency angioplasty, the surgical procedure is more effective than thrombolytic therapy in many patients, particularly those who have risk factors for bleeding or stroke. It should be noted, however, that angioplasty has better results than thrombolytic agents only in centers that have performed many of these procedures. Nevertheless, as more and more centers become experienced in angioplasty, it is becoming an increasingly advantageous option.

Combinations of Thrombolytics and Angioplasty. Some studies suggest that a combination of early administration of a thrombolytic followed by angioplasty may prove to have significant benefits for many patients. Although adverse effects are of concern, one 2001 study reported that after two years, 90% of patients with this combined approach were alive and had not suffered a recurrent heart attack.

It should be noted not all are candidates for both and that specific patient groups may do better with one treatment or the other. [Individual discussions of each approach are covered in detail in other sections.]

Other Heart Supportive Agents

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

Anti-clotting agents are used to prevent further blood clots. They include anti-platelet drugs (aspirin, glycoprotein IIb/IIIa receptor antagonists, clopidogrel) or anticoagulants (eg, heparin, warfarin). They may be used alone or in combinations.
Beta-blockers reduce the oxygen demand of the heart by slowing the heart rate and lowering arterial pressure. Intravenous administration of beta-blockers (metoprolol or esmolol) within the first few hours of a heart attack can reduce the destruction of heart tissue.
Cholesterol lowering agents. Agents called statins are particularly beneficial for heart attack patients and may have heart-protective properties that go beyond lowering cholesterol.
Angiotensin converting enzyme (ACE) inhibitors are becoming important after a heart attack, particularly in patients at risk for heart failure.

[For details, see What Are Other Agents Used for Heart Attacks and for Treating Acute Coronary Syndrome?]

Treatment for Patients in Shock or with Congestive Heart Failure

Severely ill patients, particularly those in shock (a dangerous condition that includes a drop in blood pressure and other abnormalities) or with congestive heart failure, will be monitored closely and stabilized. Fluids are administered or replaced when it is appropriate to either increase or reduce blood pressure. In patients with shock, pressure in the arteries may be measured using a catheter that is inserted into a major artery. A procedure called intra-aortic balloon counterpulsation is used to treat shock, which involves coordinating the inflation and deflation of a balloon within the artery to boost blood pressure.

Treatment and Prevention of Arrhythmias

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 heart attack patients 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 Arrythmias. People who develop ventricular fibrillation do not always experience warning arrhythmias, and to date, there are no effective agents for preventing arrhythmias.

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.
Implantable cardioverter-defibrillators are being investigated for select groups of high-risk patients. These are devices that administer electrical shocks that are timed to counteract the abnormal rhythms.

Treating Arrhythmias.

Patients who develop ventricular arrhythmias are given electrical shocks with defibrillators to restore normal rhythms.
Antiarrhythmic Agents. Antiarrhythmic drugs include lidocaine, procainamide, or amiodarone. People with an arrhythmia called atrial fibrillation have a higher risk for stroke after a heart attack and should be treated very aggressively. Other rhythm disturbances called bradyarrythmias (very slow rhythm disturbances) frequently develop in association with a heart attack and may be treated with atropine or pacemakers.

GUIDELINES FOR MANAGING ACUTE CORONARY SYNDROMES

An acute coronary syndrome is either unstable angina or a non-Q wave heart attack, they are less severe than heart attacks but may develop into full-blown attacks without aggressive treatment. The generally recommended initial approach is as follows:

Perform Diagnostic Tests. Using the results of electrocardiograms and blood tests, including those for the protein troponin T, the physician determines which patients need the most aggressive treatments.

Administer Medications. Appropriate anti-clotting medications are started immediately in all patients.

Aspirin is given to low-risk patients.
Heparin is generally used in moderate to high-risk patients. Low-molecular weight heparin, such as enoxaparin, may prove to be more effective in reducing mortality rates than standard heparin.
Specific anti-clotting agents called glycoprotein IIb/IIIa inhibitors are also now being used alone or with heparin in higher-risk patients.

Other medications may be appropriate depending on coinciding conditions. For example, studies are suggesting that aggressive use of statins (important cholesterol-lowering agents) can reduce the risk for a heart event in patients with high cholesterol levels and acute coronary syndromes. Whether they have the same impact on patients with normal cholesterol levels is less clear.

Determine More Aggressive Therapies. The best candidates for aggressive procedures appear to be those who are at high- or intermediate risk for a heart attack and who have blood tests that show elevated levels of the protein troponin T.

In general, a combination of surgery and anti-clotting medications may be the best approach for such patients. For example, specific glycoprotein IIb/IIIa inhibitors, such as abciximab, are proving to be very effective when used along with angioplasty and coronary stenting, especially for high-risk patients. [ See Also Box Anti-Clotting Agents.]

WHAT ARE THROMBOLYTIC DRUGS USED TO RESTORE BLOOD FLOW AFTER A HEART ATTACK?

Thrombolytic, or clot-busting, drugs are now a mainstay in the early treatment of heart attacks. These drugs dissolve the clot, or thrombus, responsible for causing artery blockage and heart-muscle tissue death.

Specific Thrombolytics

The current standard thrombolytic drug is t-PA or alteplase (Activase). Others used include reteplase (Retavase), urokinase (Abbokinase), and finally streptokinase (Kabikinase, Streptase). Reteplase and alteplase are equally effective, and the other two are somewhat less effective. Tenectaplase, a newer agent can be delivered more rapidly than alteplase, and to date, survival rates are similar. Others include lanoteplase and anistreplase (Eminase).

Thrombolytic Administration

The earlier thrombolytic drugs are administered, the better. The advantages of thrombolytics are highest in the first 90 minutes and are still considerable at three hours. In fact, administering thrombolytics in the ambulance may reduce the risk for death by over 15%. (Not all chest pain victims have heart attacks, however, and not all heart attack patients are candidates for thrombolytics. Such administration should be done only by an experienced health professional.) Administering these drugs more than 6 hours after symptoms have started adds little or no benefit.

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

Other anti-clotting agents are being tested in combination with thrombolytic agents. Of particular interest are studies on combinations of thrombolytics with the glycoprotein IIb/IIIa receptor antagonists. Results to date, however, are mixed, and it is not clear which patients might benefit from this approach.

Complications

Hemorrhagic stroke, usually occuring 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 three in every 1,000 patients treated with thrombolytics, whereas 39 patients out of 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.

Candidates

The best candidates for thrombolytic therapy are the following:

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). Symptoms occurred within 12 hours. The benefits extend to people fitting this description who have diabetes, systolic blood pressure less than 180 mm Hg, any heart rate, or a history of heart attack.

The use of thrombolytics in the following patients should be avoided or used with great caution:

People older than 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.
Patients with nonelevated ST-segment heart attacks. (More studies are needed to confirm this, however.)
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 depressed ST segments.
Patients with a history of stroke. (Selected patients whose strokes were not recent may benefit from these drugs, but more research is needed to confirm this.)
Patients with uncontrolled high blood pressure.

A number of studies report that women do worse after thrombolytic therapy. Evidence indicates, however, that they are generally older with 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.

WHAT ARE THE SURGICAL PROCEDURES FOR RESTORING BLOOD FLOW AFTER A HEART ATTACK?

Revascularization Procedures for Opening Blocked Arteries

Percutaneous transluminal coronary angioplasty and coronary artery bypass graft surgery, known as revascularization procedures, are the standard operations for opening narrowed or blocked arteries. Emergency angioplasty is the more common procedure for heart attack patients. Coronary bypass surgery is used 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. In a 2000 Swedish study, heart-attack patients who underwent either angioplasty or bypass surgery within fourteen days of being admitted to the hospital reduced their one-year risk of death by more than 40%.

Candidates for Emergency Angioplasty

As with thrombolytic treatments, angioplasty is most effective when performed within 12 hours of symptoms, and the sooner the better. The best candidates are the following:

Most patients who are also good candidates for thrombolytic therapy.
Women who meet the criteria for both approaches may be better candidates for angioplasty than thrombolytic therapy.
Elderly patients who meet the criteria for both approaches may be better candidates for angioplasty than thrombolytic therapy.
Patients with diabetes who meet the criteria for both approaches.
Patients under age 75 who go into shock and when angioplasty can be performed within 18 hours of shock. (There is no advantage for patients over 75 who are in shock.)
Although revascularization is not effective in most patients with non-ST elevation heart attacks, it might benefit certain subsets of these patients, such as those who show reduced blood flow in the damaged artery and when angioplasty can be performed within 12 hours.
Two 1999 studies have suggested that angioplasty may be better for older people than thrombolytic therapy. In one five-year study, mortality rates after angioplasty were 13% compared to 24% with thrombolytics. Not all hospitals are equipped for emergency angioplasty, however. In such cases, thrombolysis is still a good option, and other treatments are being investigated.

It should be strongly noted that 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 and Coronary Stents

Percutaneous transluminal coronary angioplasty (PTCA), usually simply called angioplasty, involves opening the blocked artery. A typical angioplasty procedure follows the following steps:

The surgeon threads a narrow catheter (a tube) containing a fiber optic camera directly to the blocked vessel.
The physician 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 now often employ a device called a coronary stent, which is 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. There has been some concern that a metal stent might increase the risk for blood clot formations, but the use of anti-clotting medications and improvements in the stent have improved restenosis (reclosure) rates compared to angioplasty alone. (Stenting is also now being investigated as a primary treatment with good results in certain patients.)
Complications occur in about 10% of patients (about 80% within the first day). Serious ones include heart attack and the need for additional surgery. Outcomes are better in hospital settings with experienced teams and backup.

Studies report high survival rates with the use of stents, including their use with multiple blood vessels. Most, but not all, patients are suitable candidates for stents.

Reclosure and Blockage During or Shortly after Angioplasty and Prevention. Reclosure of the artery during or shortly after angioplasty often occurs. A number of anti-clotting agents are used to help prevent this, although they are not wholly protective because reclosure in some cases is due to other, unknown causes.

Prevention of Restenosis. Narrowing or reclosing of the artery (restenosis) occurs within a year of angioplasty in a large minority of angioplasty patients, often requiring a repeat operation. The narrowing of the artery in this case is not due to blood clots and so anti-clotting agents are not useful. A number of approaches have been developed to prevent restenosis after angioplasty. Most are still investigative. [For more information, see Report #3 Coronary Artery Disease and Angina.]

Other Procedures

In certain cases, other surgical procedures may be required to repair injuries to the heart or blood vessel.

WHAT ARE OTHER AGENTS USED FOR HEART ATTACKS AND FOR TREATING ACUTE CORONARY SYNDROMES?

In addition to thrombolytics, a number of agents are now available for use during a heart attack and for treating acute coronary syndrome. Some of these and other medications are also important for preventing either a first or a second heart attack.

Aspirin and Other Anti-Clotting Agents

Blood clots are a major factor in heart attacks. Anti-clotting agents that inhibit or break up blood clots are used at every stage of heart disease. They are generally either anti-platelet agents or anticoagulants. Investigators are also studying combinations of anti-clotting agents, which may be useful in patients with severe heart disease. All anti-clotting therapies carry the risk of bleeding, which can lead to dangerous situations, including stroke. [ See Table Anti-Clotting Agents.]

Anti-Platelet Agents . Anti-platelet agents prevent formation of blood platelets. Platelets are very small disc-shaped blood cells that are important for blood-clotting.

Aspirin. Aspirin is an antiplatelet agent. It is the most common anti-clotting drug and nearly anyone with heart disease is advised to take it daily in low dose. Aspirin alone has been reported to reduce risk of death from heart attack or stroke by 25% to 50% and to cut risk of non-fatal heart attacks by 34%.
Glycoprotein IIb/IIIa Inhibitors. These potent blood-thinning agents include abciximab (ReoPro, Centocor), eptifibatide (Integrilin), tirofiban (Aggrastat), and lamifiban. They are administered intravenously in the hospital and are being used after surgery angioplasty and stent placement. [ See Angioplasty and Coronary Stents , below. ] Other benefits are not yet clear.
Thienopyrindines. Clopidogrel (Plavix) and ticlopidine (Ticlid) are potent oral platelet inhibitors.

Anticoagulants. Anticoagulants help thin blood and include the following:

Heparin. Standard and low-molecular weight heparin (enoxaparin, dalteparin, tinzaparin).
Warfarin (Coumadin).

How Anti-Clotting Agents are Used. Such agents may be used immediately after a heart attack and also as on-going maintenance to prevent a heart attack in patients with acute coronary syndromes (unstable angina and non-ST elevation heart attacks).

The following anti-clotting agents are used during a heart attack:

The physician usually gives the patient heparin or aspirin, either alone or in combination with thrombolytic therapy. Unlike the thrombolytic (clot-busting ) agents, anti-clotting agents do not dissolve clots that have already formed, but they do help prevent new ones from forming. Aspirin should be given immediately, and heparin is usually started during or at the end of the thrombolytic infusion.
Other agents, such as glycoprotein IIb/IIIa receptor antagonists, are being tested in combination with thrombolytic agents.

All these drugs pose a risk for hemorrhage.

Beta-Blockers

Beta-blockers reduce the oxygen demand of the heart by slowing the heart rate and lowering pressure in the arteries. They are now well known for reducing deaths from heart disease. They 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. Intravenous administration of beta-blockers (metoprolol or esmolol) within the first few hours of a heart attack can reduce the destruction of heart tissue. Evidence strongly supports a lower incidence of complications and better survival rates after a heart attack in patients who had been treated with a beta-blocker.

Prevention after a Heart Attack. Beta-blockers are also important after a heart attack in preventing another heart attack. In fact, among elderly heart attack patients, those who do not use these agents afterward have a much poorer outcome.

Side Effects. Side effect include the following:

Some beta-blockers lower HDL cholesterol (the beneficial cholesterol) by about 10%. The effect is most marked in smokers.
Fatigue and lethargy are the most common neurologic side effects. Some people experience vivid dreams and nightmares, depression, and memory loss.
Exercise capacity may be reduced.
Other side effects may include cold extremities, asthma, decreased heart function, gastrointestinal problems (eg, heartburn, gas, diarrhea, or constipation), and sexual dysfunction.
Dizziness and lightheadedness, especially when getting up from a lying down position.

If side effects occur, the patient should call a physician, but it is extremely important not to stop the drug abruptly. Angina, heart attack, and even sudden death have occurred in patients who discontinued treatment without gradual withdrawal.

Statins and Other Cholesterol and Lipid-Lower Agents

A number of agents are available for lowering cholesterol and other dangerous fat molecules (lipids). They include the following:

Statins, resins, and the drug probucol target LDL cholesterol. Statins and are now the first choice for most people who require lipid-lowering therapy.
Fibrates and niacin (also known as vitamin B3 and nicotinic acid) reduce triglycerides and increase HDL. (In one report, for example, the use of niacin plus a statin stopped progression of coronary artery disease completely.)

In spite of the obvious benefits of many of these agents, according to one study, only 37% of patients with recent heart attacks and high cholesterol levels were given any drugs to lower cholesterol. [For information on other cholesterol-lowering agents see the Report, Cholesterol, Other Lipids, and Lipoproteins .]

Statin Drugs. Statins may have significant benefits for heart patients. Statins are proving to reduce the risk for heart attacks even in some people with normal or below-normal cholesterol. Researchers are studying these agents early in the course of a heart attack to determine if they may improve survival, particularly in high-risk patients. Of particular importance was a 2001 study that reported significantly better survival rates in heart attack patients who took statins at or before discharge from the hospital compared to those who did not take them. These better survival rates occurred regardless of any other risk factors. Studies in 2000 and 2001 suggest that patients with normal cholesterol but signs of inflammation in the arteries (as indicated by blood tests showing high levels of C-reactive protein) may specifically benefit from statins.

The statins include two groups:

So-called natural statins, including lovastatin (Mevacor), pravastatin (Pravachol), and simvastatin (Zocor).
Newer statins are fluvastatin (Lescol), atorvastatin (Lipitor), and rosuvastatin (Crestor). The newer agents may reduce LDL more effectively at equal doses to the natural statins.

Adverse Effects. Side effects include gastrointestinal discomfort, headaches, skin rashes, sexual dysfunction, drowsiness, dizziness, nausea, constipation, and peripheral neuropathy (numbness or tingling in the hands and feet). Statins can affect the liver, so periodic liver function tests should be administered. Statins should never be taken by anyone with liver problems or by women during pregnancy or breast-feeding. [See also Note on Withdrawal of Cerivastatin (Baycor).]

Withdrawal of Cerivastatin (Baycol)

One statin, Baycol, was withdrawn from the market because of reports of death from rhabdomyolysis, severe muscle damage that can lead to kidney failure. People at highest risk were those who were taking high doses and who also took gemfibrozil. Rhabdomyolysis has occurred rarely with other statins but has never before been associated with deaths.

Combinations and Interactions with Other Drugs and Substances. Statins can be used in combinations with other cholesterol lowering agents, including bile acid-binding resins, nicotinic acid, and fibrates, for a more wide-spread effect on other lipids. Use with certain other drugs, however, including nicotinic acid and fibrate, may increase the risk for muscle weakness or pain. (Other drugs that may have the same effect are cyclosporin, macrolide antibiotics, or certain antifungals.) Grapefruit juice may increase their potency.

Angiotensin Converting Enzyme Inhibitors

Angiotensin converting enzyme (ACE) inhibitors are important agents. In treating heart attack patients, there are commonly administered soon after an attack, particularly in patients at risk for heart failure. ACE inhibitors are important agents in hypertension and are recommended as first-line treatment for people with diabetes and kidney damage, for some heart attack survivors, and for patients with heart failure. A 2001 study, in fact, suggested that taking an ACE inhibitor at the onset of a heart attack may reduce the damage.

Side Effects. Side effects of ACE inhibitors are uncommon but may include an irritating cough, excessive drops in blood pressure, and allergic reactions. Of great concern is research suggesting that aspirin (and other so-called NSAIDs) increases the risk for heart failure in patients taking ACE inhibitors. [See Anti-Clotting Agents below.]

Magnesium

Magnesium has blood-thinning properties and may help open blood vessels. It is important to correct any magnesium deficiencies in heart attack patients (such as those who were on diuretics). For certain patients who cannot be given thrombolytic therapy, intravenous magnesium may be helpful. It must be administered within six hours for it to have any effect. A study that started in 1999 is investigating whether magnesium is beneficial when used before thrombolytic therapy or angioplasty.

Infection-Fighting Agents

Antibiotics. The antibiotics prescribed for Chlamydia pneumoniae are being investigated for prevention of heart attacks in patients with heart disease and evidence of infection. A two-year 2000 study found no significant effect for these treatments. A 2001 study on heart attack patients, however, reported that antibiotics were associated with a lower risk for a second heart attack.

Flu Vaccines. Also interesting was a study reporting that influenza vaccinations might protect heart attack patients against another attack during flu season.

WHAT IS REHABILITATION AFTER A HEART ATTACK?

Physical Rehabilitation

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

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 three days after a relatively minor attack may allow patients to go home earlier.
After eight to 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, in one survey cardiac arrest was 1 per 112,000 patient-hours and nonfatal heart attack rates were 1 per 294,000 patient-hours.
Patients generally return to work in about two months, although timing can vary depending on the severity of the condition.

Lifestyle measures, particularly dietary factors, are equally important in preventing heart attacks and must be strenuously adhered to. [ See How Can a Heart Attack be Prevented?, above.]

Emotional Rehabilitation

Many studies are showing that depression is a major predictor for increased mortality in both women and men. Depressed patients are less likely to comply with their heart medications. Physical rehabilitation itself has significant and positive emotional effects, that, according to a 2001 study, are important for long-term survival. Antidepressants, psychologic therapy, or both, are strongly recommended if a patient becomes severely depressed after a heart attack. There is some evidence to suggest that the use of antidepressants, which increase serotonin, may help protect the hearts of people who have both heart disease and depression.

Sexual activity right 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.

WHERE ELSE CAN INFORMATION ABOUT HEART ATTACKS BE OBTAINED?

National Heart, Lung, and Blood Institute, Information Center, P.O. Box 30105, Bethesda, MD 20824-0105. Call (301-592-8573) or on the Internet (http://www.nhlbi.nih.gov/nhlbi/nhlbi.htm)

Associated with the National Institute of Health, this organization offers excellent free printed information.

American College of Cardiology, Heart House, 9111 Old Georgetown Rd., Bethesda, MD 20814-1699. Call (800-253-4636) or (301-897-5400) or on the Internet (http://www.acc.org/)

American Heart Association, National Center, 7272 Greenville Ave., Dallas, Texas 75231-4596. Call (1-800-AHA-USA1) or on the Internet (http://www.americanheart.org/)

This is a primary source of information for heart problems. They are very responsible and will send free pamphlets and reading material, including useful diet information and locations of local representatives.

Medic Alert, 2323 Colorado Ave., Turlock, CA 95382. Call (888-633-4298) or on the Internet (http://www.medicalert.org).

This organization provides bracelets or neck chain emblems with critical personal medical information. Also keeps computerized medical records

Offers a useful heart risk evaluation test. (http://www.heartriskevaluations.com/)

Professional website for news on treating heart attack (http://www.thrombosisconnect.com/)

American Heart Association Guidelines (http://www.americanheart.org/Scientific/statements/)