Heart attack

A heart attack also known as a myocardial infarction is the death of the 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 the blood and oxygen. Blockage of a coronary artery deprives the heart muscle of blood and oxygen causing injury of the heart muscle. Injury of the heart muscle causes chest pain and chest pressure sensation. If blood flow is not restored to the heart muscle within 20 to 40 minutes irreversible death of the heart muscle will begin to occur. Muscle continues to die for 6 to 8 hours at which time the heart attack usually is “complete”. The dead heart muscle is eventually replaced by scar tissue.

Approximately 1 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. It is a gradual process by 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 or narrowing of the coronary arteries. Diseases caused be the reduced blood supply to the heart muscle from coronary atherosclerosis are called coronary heart diseases (CHD). They 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 may not be able to 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 usually 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 1 to 15 minutes and is relieved by rest or by taking nitroglycerin by placing a 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 last a few seconds are rarely due to coronary artery disease.

Angina can also 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. 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 unless blood flow can be promptly restored usually within 1 to 6 hours.

While heart attacks can occur at any time more heart attacks occur between 4.00 A.M. and 10.00 A.M. because of higher blood levels of adrenaline released from the adrenal gland 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.

What are the symptoms of a heart attack? Although chest pain or pressure is the most common symptom of a heart attack, heart attack victims may experience a variety of symptoms including pain, fullness, and squeezing sensation of the chest; jaw pain, toothache, headache, shortness of breath, nausea, vomiting, and general epigastric (upper middle abdomen) discomfort; sweating, heartburn, and indigestion; arm pain (more commonly the left arm but may be the either arm), upper back pain, general malaise (vague feeling of illness); 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” 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 may also occur as a result of a sudden onset of arrhythmia such as ventricular fibrillation.

What are the complications of a heart attack?

Heart failure. When 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.

Ventricular fibrillation. Injury to heart muscle can also lead to ventricular fibrillation. It 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 later die frequently had suffered major damage to the heart muscle initially or additional damage at a later time.

Death 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 to pump blood. In 2008 The American Heart Association modified the mouth-to mouth instruction of CPR and recommends that chest compressions alone are effective if a bystander is reluctant to do mouth-to-mouth. When paramedics arrive medications and 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 rapid response by paramedics can improve the chances of survival from a heart attack. In addition, many public venues now have automatic external defibrillators (AEDs) that provide the electric shock needed to restore a normal heart rhythm even before the paramedics arrive. This greatly improves the chances for 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, and a family history of coronary heart disease. 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 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. Cholesterol in the blood is either combined with lipoproteins as very low-density lipoproteins (VLDL), low-density lipoproteins (LDL), or high-density lipoproteins (HDL).

Cholesterol that is combined with LDL (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.

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 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 are.

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 o heart attack. It has been shown that controlling hypertension with medications can reduce the risk of heart attack.

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.

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.

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 the age of 55 in the father or other first-degree male relative or before the age of 65 in the mother or other first-degree female relative.

How is a heart attack diagnosed? When there is a severe chest pain suspicion that a heart attack is occurring is usually high and tests can be performed quickly that will confirm the heart attack. A problem arises, however, when the symptoms of 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 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 subfractions of CPK and troponin and their levels can be measured in blood. These cardiac enzymes are typically elevated in the blood several hours after the onset of a heart attack. A series of blood tests for 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 the blood flow is reestablished, the more heart muscle that is saved.

Large and active medical centers of the 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.