What is a heart attack?
A heart attack (also known as a myocardial infarction) is the death of heart muscle
from the sudden blockage of a coronary artery by a blood clot. Coronary arteries are blood vessels that supply the heart muscle with blood and oxygen. Blockage of a coronary artery deprives the heart muscle of blood and oxygen, causing injury to the heart muscle. Injury to the heart muscle causes chest pain and pressure. If blood flow is not restored within 20 to 40 minutes, irreversible death of the heart muscle will begin to occur. Muscle continues to die for six to eight hours at which time the heart attack usually is "complete." The dead heart muscle is replaced by scar tissue.
Approximately one million Americans suffer a heart attack each year. Four hundred thousand of them die as a result of their heart attack.
What causes a heart attack? Atherosclerosis
Atherosclerosis is a gradual process in which plaques (collections) of cholesterol are deposited in the walls of arteries. Cholesterol plaques cause hardening of the arterial walls and narrowing of the inner channel (lumen) of the artery. Arteries that are narrowed by atherosclerosis cannot deliver enough blood to maintain normal function of the parts of the body they supply. For example, atherosclerosis of the arteries in the legs causes reduced blood flow to the legs. Reduced blood flow to the legs can lead to pain in the legs while walking or exercising, leg ulcers, or a delay in the healing of wounds to the legs. Atherosclerosis of the arteries that furnish blood to the brain can lead to vascular dementia (mental deterioration due to gradual death of brain tissue over many years) or stroke (sudden death of brain tissue).
In many people, atherosclerosis can remain silent (causing no symptoms or health problems) for years or decades. Atherosclerosis can begin as early as the teenage years, but symptoms or health problems usually do not arise until later in adulthood when the arterial narrowing becomes severe. Smoking cigarettes, high blood pressure, elevated cholesterol, and diabetes mellitus can accelerate atherosclerosis and lead to the earlier onset of symptoms and complications, particularly in those people who have a family history of early atherosclerosis.
Coronary atherosclerosis (or coronary artery disease) refers to the atherosclerosis that causes hardening and narrowing of the coronary arteries. Diseases caused by the reduced blood supply to the heart muscle from coronary atherosclerosis are called coronary heart diseases (CHD). Coronary heart diseases include heart attacks, sudden unexpected death, chest pain (angina), abnormal heart rhythms, and heart failure due to weakening of the heart muscle.
Atherosclerosis and angina pectoris
Angina pectoris (also referred to as angina) is chest pain or pressure that occurs when the blood and oxygen supply to the heart muscle cannot keep up with the needs of the muscle. When coronary arteries are narrowed by more than 50 to 70 percent, the arteries cannot increase the supply of blood to the heart muscle during exercise or other periods of high demand for oxygen. An insufficient supply of oxygen to the heart muscle causes angina. Angina that occurs with exercise or exertion is called exertional angina. In some patients, especially diabetics, the progressive decrease in blood flow to the heart may occur without any pain or with just shortness of breath or unusually early fatigue.
Exertional angina usually feels like a pressure, heaviness, squeezing, or aching across the chest. This pain may travel to the neck, jaw, arms, back, or even the teeth, and may be accompanied by shortness of breath, nausea, or a cold sweat. Exertional angina typically lasts from one to 15 minutes and is relieved by rest or by placing a nitroglycerin tablet under the tongue. Both resting and nitroglycerin decrease the heart muscle's demand for oxygen, thus relieving angina. Exertional angina may be the first warning sign of advanced coronary artery disease. Chest pains that just last a few seconds rarely are due to coronary artery disease.
Angina also can occur at rest. Angina at rest more commonly indicates that a coronary artery has narrowed to such a critical degree that the heart is not receiving enough oxygen even at rest. Angina at rest infrequently may be due to spasm of a coronary artery (a condition called Prinzmetal's or variant angina). Unlike a heart attack, there is no permanent muscle damage with either exertional or rest angina.
Atherosclerosis and heart attack
Occasionally the surface of a cholesterol plaque in a coronary artery may rupture, and a blood clot forms on the surface of the plaque. The clot blocks the flow of blood through the artery and results in a heart attack (see diagram below). The cause of rupture that leads to the formation of a clot is largely unknown, but contributing factors may include cigarette smoking or other nicotine exposure, elevated LDL cholesterol, elevated levels of blood catecholamines (adrenaline), high blood pressure, and other mechanical and biochemical forces.
Unlike exertional or rest angina, heart muscle dies during a heart attack, and loss of the muscle is permanent.
While heart attacks can occur at any time, more heart attacks occur between 4:00 A.M. and 10:00 A.M. because of the higher blood levels of adrenaline released from the adrenal glands during the morning hours. Increased adrenaline, as previously discussed, may contribute to rupture of cholesterol plaques.
Approximately 50% of patients who develop heart attacks have warning symptoms such as exertional angina or rest angina prior to their heart attacks, but these symptoms may be mild and discounted.
No symptoms (Approximately one quarter of all heart attacks are silent, without chest pain or new symptoms. Silent heart attacks are especially common among patients with diabetes mellitus.)
Even though the symptoms of a heart attack at times can be vague and mild, it is important to remember that heart attacks producing no symptoms or only mild symptoms can be just as serious and life–threatening as heart attacks that cause severe chest pain. Too often patients attribute heart attack symptoms to "indigestion," "fatigue," or "stress" and consequently delay seeking prompt medical attention. One cannot overemphasize the importance of seeking prompt medical attention in the presence of symptoms that suggest a heart attack. Early diagnosis and treatment saves lives, and delays in reaching medical assistance can be fatal. A delay in treatment can lead to permanently reduced function of the heart due to more extensive damage to the heart muscle. Death also may occur as a result of the sudden onset of arrhythmias such as ventricular fibrillation.
What are the complications of a heart attack? Heart failure
If a large amount of heart muscle dies, the ability of the heart to pump blood to the rest of the body is diminished, and this can result in heart failure. The body retains fluid, and organs, for example, the kidneys, begin to fail
Injury to heart muscle also can lead to ventricular fibrillation. Ventricular fibrillation occurs when the normal, regular, electrical activation of heart muscle contraction is replaced by chaotic electrical activity that causes the heart to stop beating and pumping blood to the brain and other parts of the body. Permanent brain damage and death can occur unless the flow of blood to the brain is restored within five minutes.
Most of the deaths from heart attacks are caused by ventricular fibrillation of the heart that occurs before the victim of the heart attack can reach an emergency room. Those who reach the emergency room have an excellent prognosis; survival from a heart attack with modern treatment should exceed 90%. The 1% to 10% of heart attack victims who die later include those victims who suffer major damage to the heart muscle initially or who suffer additional damage at a later time.
Deaths from ventricular fibrillation can be avoided by cardiopulmonary resuscitation (CPR) started within five minutes of the onset of ventricular fibrillation. CPR requires breathing for the victim and applying external compression to the chest to squeeze the heart and force it to pump blood. When paramedics arrive, medications and/or an electrical shock (cardioversion) can be administered to convert ventricular fibrillation back to a normal heart rhythm and allow the heart to pump blood normally. Therefore, prompt CPR and a rapid response by paramedics can improve the chances of survival from a heart attack. In addition, many public venues now have defibrillators that provide the electrical shock needed to restore a normal heart rhythm even before the paramedics arrive. This greatly improves the chances of survival.
What are the risk factors for atherosclerosis and heart attack?
Factors that increase the risk of developing atherosclerosis and heart attacks include increased blood cholesterol, high blood pressure, use of tobacco, diabetes mellitus, male gender, obesity, and a family history of coronary heart disease amongst other . While family history and male gender are genetically determined, the other risk factors can be modified through changes in lifestyle and medications.
High Blood Cholesterol (Hyperlipidemia). A high level of cholesterol in the blood is associated with an increased risk of heart attack because cholesterol is the major component of the plaques deposited in arterial walls. Cholesterol, like oil, cannot dissolve in the blood unless it is combined with special proteins called lipoproteins. (Without combining with lipoproteins, cholesterol in the blood would turn into a solid substance.) The cholesterol in blood is either combined with lipoproteins as very low–density lipoproteins (VLDL), low–density lipoproteins (LDL) or high–density lipoproteins (HDL).
The cholesterol that is combined with low–density lipoproteins (LDL cholesterol) is the "bad" cholesterol that deposits cholesterol in arterial plaques. Thus, elevated levels of LDL cholesterol are associated with an increased risk of heart attack.
The cholesterol that is combined with HDL (HDL cholesterol) is the "good" cholesterol that removes cholesterol from arterial plaques. Thus, low levels of HDL cholesterol are associated with an increased risk of heart attacks.
Measures that lower LDL cholesterol and/or increase HDL cholesterol (losing excess weight, diets low in saturated fats, regular exercise, and medications) have been shown to lower the risk of heart attack. One important class of medications for treating elevated cholesterol levels (the statins) have actions in addition to lowering LDL cholesterol which also protect against heart attack. Most patients at "high risk" for a heart attack should be on a statin no matter what the levels of their cholesterol. For more, please see the Cholesterol and Your Heart article.
High Blood Pressure (Hypertension). High blood pressure is a risk factor for developing atherosclerosis and heart attack. Both high systolic pressure (when the heart beats) and high diastolic pressure (when the heart is at rest) increase the risk of heart attack. It has been shown that controlling hypertension with medications can reduce the risk of heart attack. For more, please see the High Blood Pressure article.
Tobacco Use (Smoking). Tobacco and tobacco smoke contain chemicals that cause damage to blood vessel walls, accelerate the development of atherosclerosis, and increase the risk of heart attack. For more, please see the Smoking and Quitting Smoking article.
Diabetes (Diabetes Mellitus). Both insulin dependent and non–insulin dependent diabetes mellitus (type 1 and 2, respectively) are associated with accelerated atherosclerosis throughout the body. Therefore, patients with diabetes mellitus are at risk for reduced blood flow to the legs, coronary heart disease, erectile dysfunction, and strokes at an earlier age than non–diabetic subjects. Patients with diabetes can lower their risk through rigorous control of their blood sugar levels, regular exercise, weight control, and proper diets. For more, please see the Diabetes article.
Male Gender. At all ages, men are more likely than women to develop atherosclerosis and coronary heart disease. Some scientists believe that this difference is partly due to the higher blood levels of HDL cholesterol in women than in men. However, this gender difference narrows as men and women grow older.
Family History of Heart Disease. Individuals with a family history of coronary heart diseases have an increased risk of heart attack. Specifically, the risk is higher if there is a family history of early coronary heart disease, including a heart attack or sudden death before age 55 in the father or other first–degree male relative, or before age 65 in the mother or other female first–degree female relative.
How is a heart attack diagnosed?
When there is severe chest pain, suspicion that a heart attack is occurring usually is high, and tests can be performed quickly that will confirm the heart attack. A problem arises, however, when the symptoms of a heart attack do not include chest pain. A heart attack may not be suspected, and the appropriate tests may not be performed. Therefore, the initial step in diagnosing a heart attack is to be suspicious that one has occurred.
Electrocardiogram. An electrocardiogram (ECG) is a recording of the electrical activity of the heart. Abnormalities in the electrical activity usually occur with heart attacks and can identify the areas of heart muscle that are deprived of oxygen and/or areas of muscle that have died. In a patient with typical symptoms of heart attack (such as crushing chest pain) and characteristic changes of heart attack on the ECG, a secure diagnosis of heart attack can be made quickly in the emergency room and treatment can be started immediately. If a patient's symptoms are vague or atypical and if there are pre–existing ECG abnormalities, for example, from old heart attacks or abnormal electrical patterns that make interpretation of the ECG difficult, the diagnosis of a heart attack may be less secure. In these patients, the diagnosis can be made only hours later through detection of elevated cardiac enzymes in the blood.
Blood tests. Cardiac enzymes are proteins that are released into the blood by dying heart muscles. These cardiac enzymes are creatine phosphokinase (CPK), special sub–fractions of CPK (specifically, the MB fraction of CPK), and troponin, and their levels can be measured in blood. These cardiac enzymes typically are elevated in the blood several hours after the onset of a heart attack. A series of blood tests for the enzymes performed over a 24 hour period are useful not only in confirming the diagnosis of heart attack, but the changes in their levels over time also correlates with the amount of heart muscle that has died.
The most important factor in diagnosing and treating a heart attack is prompt medical attention. Rapid evaluation allows early treatment of potentially life–threatening abnormal rhythms such as ventricular fibrillation and allows early reperfusion (return of blood flow to the heart muscle) by procedures that unclog the blocked coronary arteries. The more rapidly blood flow is reestablished, the more heart muscle that is saved.
Large and active medical centers often have a "chest pain unit" where patients suspected of having heart attacks are rapidly evaluated. If a heart attack is diagnosed, prompt therapy is initiated. If the diagnosis of heart attack is initially unclear, the patient is placed under continuous monitoring until the results of further testing are available.
Treatment of heart attacks include:
The primary goal of treatment is to quickly open the blocked artery and restore blood
flow to the heart muscle, a process called reperfusion. Once the artery is open, damage to heart muscle ceases, and the patient becomes pain free. By minimizing the extent of heart muscle damage, early reperfusion preserves the pumping function of the heart. Optimal benefit is obtained if reperfusion can be established within the first four to six hours of a heart attack. Delay in establishing reperfusion can result in more widespread damage to heart muscle and a greater reduction in the ability of the heart to pump blood. Patients with hearts that are unable to pump sufficient blood develop heart failure, decreased ability to exercise, and abnormal heart rhythms. Thus, the amount of healthy heart muscle remaining after a heart attack is the most important determinant of the future quality of life and longevity.
What can a patient expect during recovery from a heart attack?
Heart attack patients are monitored in the hospital for three or more days prior to discharge home. Rhythm disturbances, shortness of breath due to heart failure, or recurrent chest pain are reasons for further therapy such as balloon angioplasty or coronary stenting, additional medications, or bypass surgery.
Patients gradually increase their activity under observation. Before discharge, a low–level exercise stress test may be performed to detect important residual narrowing in the coronary arteries, exercise–induced cardiac rhythm abnormalities, and heart muscle failure, and to help guide the doctor in prescribing an activity regimen after hospitalization. An abnormal stress test prior to hospital discharge following a heart attack predicts a high risk for subsequent cardiac events; if the patient has not yet had a coronary angiogram, an abnormal pre–discharge stress test is a strong reason for doing angiography. Since most patients usually receive angiography early, the use of pre–discharge stress testing has declined.
Before resuming full activity or work, several weeks may be needed for the heart muscle to heal. After a small heart attack (little damage to heart muscle), patients usually can resume normal activities after two weeks. These activities include returning to work as well as normal sexual activity. A moderate heart attack (moderate damage to heart muscle) requires limited, gradually increasing activity for up to four weeks, while a large heart attack (much damage to heart muscle) may result in a recovery period of six weeks or longer. These time frames are necessary in order for the dead heart muscle to substantially complete the scarring process. During this healing period, patients should avoid vigorous exertion and heavy lifting (over 20 pounds) or any strenuous activity that causes shortness of breath or undue fatigue.
Cardiac rehabilitation typically begins during hospitalization and continues during the months following a heart attack. Cardiac rehabilitation programs provide a helpful transition to a safe and full return to a normal lifestyle. In addition, cardiac rehabilitation allows the prescription of a long–term exercise program tailored to each patient and helps patients and their families adjust to lifestyle changes and the difficult and conflicting emotions that often follow a heart attack
Follow a diet that is low in cholesterol (less than 200 mg daily) and saturated fat (less than seven percent of total calories). For more, please see the Therapeutic Lifestyle Changes (TLC) Daily Food Guide, Eating Heart Healthy.
Reduce LDL (bad) cholesterol and increase HDL (good) cholesterol. Reduction of LDL cholesterol to a value below 100 mg/dl, particularly with the statin group of medications, has been demonstrated to prevent further heart attacks. Patients with low HDL (less than 35 mg/dl) are encouraged to exercise regularly and to take medications to increase HDL. For more in–depth information about cholesterol, LDL, and HDL, please see the Cholesterol article.
Undergo further testing. In the months following a heart attack, further cardiac stress testing, with or without nuclear or echocardiographic imaging, may be prescribed to determine if additional therapy will be necessary to prevent future heart attacks. In addition, special testing may be required to evaluate the risk of developing cardiac arrhythmias. All such testing should be discussed with the doctor.
What about heart attacks in women?Risk of heart attacks in women
Coronary artery disease (CAD) and heart attacks are erroneously believed to occur primarily in men. Although it is true that the prevalence of CAD among women is lower before menopause, the risk of CAD rises in women after menopause. At age 75, a woman's risk for CAD is equal to that of a man's. CAD is the leading cause of death and disability in women after menopause. In fact, a 50–year–old woman faces a 46% risk of developing CAD and a 31% risk of dying from coronary artery disease. In contrast, her probability of contracting and dying from breast cancer is 10% and 3%, respectively.
The risk factors for developing CAD in women are the same as in men; they are increased blood cholesterol, high blood pressure, smoking cigarettes, diabetes mellitus, and a family history of coronary heart disease at a young age.
Even "light" smoking raises the risk of CAD. In one study, middle–aged women who smoked 1 to 14 cigarettes per day had a twofold increase in strokes (caused by atherosclerosis of the arteries to the brain) whereas those who smoked more than 25 cigarettes per day had a risk of stroke 3.7 fold higher than that of nonsmoking women. Furthermore, the combination of smoking and the use of birth control pills increase the risk of heart attacks even further, especially in women over 35.
Quitting smoking immediately begins to reduce the risk of heart attacks. The risk gradually decreases back down to the same risk of nonsmoking women after several years of not smoking.
Cholesterol treatment guidelines in women
Current NCEP (National Cholesterol Education Program) treatment guidelines for undesirable cholesterol levels are the same for women as for men.
Diagnosis of heart attacks in women
Women are more likely to encounter delays in establishing the diagnosis of heart attack than men. This is in part because women tend to seek medical care later than men, and in part because diagnosing heart attacks in women can sometimes be more difficult than diagnosing heart attacks in men. The reasons are:
Women are more likely than men to have atypical heart attack symptoms such as neck and shoulder pain, abdominal pain, nausea, vomiting, fatigue, and shortness of breath.
Silent heart attacks (heart attacks with little or no symptoms) are more common among women than among men.
Women have a higher occurrence than men of chest pain that is not caused by heart disease, for example chest pain from spasm of the esophagus.
Women are less likely than men to have the typical findings on the ECG that are necessary to diagnose a heart attack quickly.
Women are more likely than men to have angina (chest pain due to lack of blood supply to the heart muscle) that is caused by spasm of the coronary arteries or caused by disease of the smallest blood vessels (microvasculature disease). Cardiac catheterization with coronary angiograms (x–ray studies of the coronary arteries that are considered most reliable tests for CAD) will reveal normal coronary arteries and therefore cannot be used to diagnose either of these two conditions.
Women are more likely to have misleading, or "false positive" noninvasive tests for CAD then men.
Because of the atypical nature of symptoms and the occasional difficulties in diagnosing heart attacks in women, women are less likely to receive aggressive thrombolytic therapy or coronary angioplasty, and are more likely to receive it later than men. Women also are less likely to be admitted to a coronary care unit.