A heart attack (also known as a myocardial infarction or MI) is the damage and death of heart muscle from a coronary artery’s sudden blockage by a blood clot. Coronary arteries are blood vessels that supply the heart muscle with blood and oxygen. The blockage of a coronary artery deprives the heart muscle of blood and oxygen, injuring the heart muscle. Injury to 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 six to eight hours, at which time the heart attack usually is complete. The dead heart muscle is eventually replaced by scar tissue.
Plaque can occur in coronary and other arteries. Cholesterol plaques cause the hardening of the arterial walls and narrow the artery’s inner channel (lumen).
Atherosclerosis is a gradual process by which plaques (collections) of cholesterol are deposited in arteries’ walls. Cholesterol plaques cause the hardening of the arterial walls and narrow the artery’s inner channel (lumen). Arteries that are limited by atherosclerosis cannot deliver enough blood to maintain the 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 brain tissue’s gradual death over many years) or stroke (sudden damage and death of brain tissue).
Atherosclerosis can remain silent (causing no symptoms or health problems) for years or decades. Atherosclerosis can begin as early as the teenage years. Still, signs of 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 who have a family history of early atherosclerosis.
Coronary atherosclerosis (or coronary artery disease) refers to atherosclerosis that causes hardening and narrowing of the coronary arteries. Illnesses 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 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 muscle’s needs. When coronary arteries are narrowed by more than 50 to 70 percent, the arteries may not increase blood supply to the heart muscle during exercise or other periods of high oxygen demand. 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 in people with diabetes, 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. Usually, it is relieved by rest or by placing a tablet of nitroglycerin under the tongue. Both resting and nitroglycerin decrease the heart muscle’s demand for oxygen, thus reducing angina. Exertional angina may be the first warning sign of advanced coronary artery disease. Chest pains that 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 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. However, angina is a warning sign that there is an increased chance of a heart attack in the future.
Atherosclerosis and heart attack
Occasionally, the surface of a cholesterol plaque in a coronary artery may rupture—a blood clot forms on the plaque’s surface. The clot blocks blood flow through the artery and results in a heart attack (see picture below). The cause of rupture that leads to the formation of a clot is mostly unknown. Still, contributing factors may include cigarette smoking or other nicotine exposure, elevated low-density lipoprotein (LDL) cholesterol, elevated levels of blood catecholamines (adrenaline), high blood pressure, and other mechanical and biochemical stimuli.
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 one to six hours.
While heart attacks can occur at any time, more heart attacks occur between 4 A.M. and 10 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 the rupture of cholesterol plaques.
Only half of the patients who develop heart attacks have warning signs such as exertional angina or rest angina before their heart attacks. Still, these signs may be mild and ignored as unimportant.
When there is severe chest pain, a suspicion that a heart attack is occurring usually is high. Tests can be performed quickly to 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 so that the proper tests can be done.
Electrocardiogram. An electrocardiogram (ECG) is a recording of the electrical activity of the heart. Abnormalities in electrical activity usually occur with heart attacks. They can identify the heart muscle areas deprived of oxygen and or areas of muscle that have died. In a patient with a typical heart attack (such as crushing chest pain) and characteristic changes of a heart attack on the ECG, a secure diagnosis of heart attack can be made quickly in the emergency room. Treatment can be started immediately. If a patient’s symptoms are vague or atypical and if there are pre-existing ECG abnormalities, such as 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 blood tests.
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 (precisely, 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. Currently, troponin levels are considered the preferred lab tests to diagnose a heart attack, as they are cardiac muscle injury or death indicators. A series of blood tests for the enzymes performed over 24 hours are useful not only in confirming the diagnosis of a heart attack but in their levels over time also correlates with the amount of heart muscle that has died.
The most critical 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. It will enable 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. At this time, mechanical reperfusion with angioplasty and or stenting to increase the flow of blood to the heart is the preferred way to preserve heart muscle if it can be performed within 90 minutes of arrival to the hospital; if there will be a delay, thrombolytic agents (clot busters) are preferred.
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. Suppose the diagnosis of a heart attack is initially unclear. In that case, the patient is placed under continuous monitoring until further testing results are available.
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If you are interested in finding out more, please contact our Multi-Specialty Facility. Avoid worrisome self-diagnosis; the best cardiology doctors will properly diagnose your problem and refer you to a specialist if necessary. No information on this site should be used to diagnose, treat, prevent, or cure any disease or condition.