The most common cause of coronary artery disease is atherosclerosis. Atherosclerosis is a chronic, progressive disease of the arteries in which “plaques” made up of cholesterol deposits, calcium, and abnormal cells develop on the inner lining of the arteries.
Figure 1 - Atherosclerosis The top artery shows a normal lumen, or opening ("L"). The bottom artery illustrates what happens to the lumen when atherosclerotic plaques form in the arterial wall.
These plaques cause a gradual, progressive narrowing of the the lumen of the artery, and thus make blood flow through the artery progressively more difficult. In addition, these plaques are subject to sudden rupture. When the plaques rupture, they trigger a clotting event within the artery that can cause acute obstruction of the lumen.
“Angina” refers to the symptoms a patient experiences any time the heart muscle is not getting enough blood flow through the coronary arteries. Angina is usually perceived as a discomfort (often a pressure-like pain) in or around the chest, shoulders, neck or arms.
“Stable angina” is angina that occurs in a nearly predictable fashion, that is, with exertion or after a big meal. Stable angina generally indicates that a stable atherosclerotic plaque is present in one of the coronary arteries, causing a partial obstruction of that artery. When the patient is at rest, the partially obstructed artery is able to meet the needs of the cardiac muscle. But when exertion occurs (or some other stress that causes increased cardiac work,) the obstruction prevents an adequate increase in blood flow to the muscle, and angina is experienced. Thus, stable angina implies a fixed, stable atherosclerotic plaque.
“Unstable angina” is angina that occurs sporadically, or unpredictably, or at rest. There is no particular pattern to unstable angina. Unstable angina implies the existence of an unstable plaque, one that has partially ruptured, or in which blood clots may be forming and breaking off, so that the lumen of the artery is not fixed, but is changing. Patients with unstable angina have a high incidence of total occlusion of the coronary artery, and thus a high incidence of heart attacks. A myocardial infarction, or heart attack, occurs when a coronary artery becomes completely occluded, so that the heart muscle supplied by that artery dies. A heart attack, therefore, is death of heart muscle. The consequences of a myocardial infarction depend largely on how much heart muscle has died. A small heart attack is one in which only a small portion of the heart muscle dies. A large heart attack is one in which a large portion of heart muscle dies.
Figure 2 - Blockages in the coronary arteries In this figure, arterial narrowings in the LAD and circumflex arteries threaten to cause myocardial infarctions with substantial muscle loss.
Most heart attacks are now felt to be due to a sudden rupture of an atherosclerotic plaque, and subsequent clotting off of the artery. If patients come under medical attention within a few hours of the onset of a heart attack, the size of the heart attack can be greatly reduced by administering “clot-busting” drugs, or by performing an immediate angioplasty to open up the occluded blood vessel.
After a heart attack, the remaining heart muscle “remodels” itself. The damaged heart tends to dilate, and can lead to a dilated cardiomyopathy. If the heart attack is relatively large, heart failure can develop immediately, or over the next several months. Heart muscle that has been damaged due to coronary artery disease can become quite prone to developing ventricular tachycardia or ventricular fibrillation. In fact, sudden death is extremely common in people who have survived heart attacks, and all these patients should be assessed for the propensity to develop lethal arrhythmias.
Preventing heart attacks is largely a matter of retarding the development of atherosclerotic plaques in the coronary arteries. This is done thorough smoking cessation, weight control, maintaining an active lifestyle, and cholesterol control.
After atherosclerotic heart disease has set in, the blood flow to the heart muscle can be improved by means of angioplasty, stenting, or coronary artery bypass surgery. Drugs used for coronary artery disease – beta blockers and nitrates – do not appreciably increase blood flow to the heart muscle. Instead, these drugs reduce the oxygen demand of the heart muscle.
Much research is being conducted to find non-invasive ways to halt the progression of coronary artery disease, or even to reverse it. The use of statin drugs and of antioxidants has attracted the most attention.
