The Basics of Coronary Artery Disease

Coronary artery disease can be defined as a condition that reduces blood flow through the coronary arteries to the heart muscle by some pathological process. The most frequent pathological process involved is coronary atherosclerosis. Disorders of the coronary arteries are the most common cause of death in affluent countries and are responsible for much disability. More than one million Americans are affected by this disease each year, a rate of one every 30 seconds. Almost half of these people die from cardiac arrest; of that number, 95% die within two hours after the onset of symptoms and before medical care is reached. This is known as sudden cardiac death.

Coronary artery disease usually exists for many years before it has any adverse effects upon the myocardium. Myocardial ischemia develops when the coronary circulation is inadequate to supply myocardial oxygen demands.

The development of ischemia depends upon the:

Location and severity of the stenosis or stenoses

Presence of collateral vessels

Demands of the myocardium

Coexistence of various risk factors

Ischemia has three major clinical manifestations: angina pectoris, myocardial infarction, and sudden cardiac death. Angina pectoris is a clinical syndrome resulting from transient and reversible ischemia (reduced blood flow).

Myocardial infarction results from total coronary occlusion and loss of blood flow. The affected area of the myocardium dies and no longer contributes to the ventricle's pumping action. Thus, a greater burden of work falls to the remaining viable myocardium.

Watch atherosclerosis develop in this animation

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The Primary Disease is Atherosclerosis

The pathologic process in the coronary arteries that leads to atherosclerosis appears to begin at birth. It is apparent in autopsies of 20- to 30-year-old patients who have small deposits of cholesterol and fatty acids (lipids) in the walls (intima) of the coronary arteries. As this process continues, portions of the intima become raised and fatty deposits accumulate in the lumen of the artery. This buildup interferes with the smooth flow of blood through the vessel, causing fibrin and platelets to be deposited, further increasing the size of the roughened area. Gradually, calcium and other substances are deposited and a plaque is formed. Plaques can be readily identified during surgery or autopsy as hard, rough, irregular areas projecting into the lumen of the vessel. So the real disease is atherosclerosis—the insidious, relentless accumulation of fatty deposits on the inside of arterial walls. Exactly how these deposits form, how they grow to become obstructive raised plaques, and their relation to the many risk factors associated with coronary artery disease are as yet incompletely answered. Despite these uncertainties, much is known about atherosclerosis, and the clinical consequences are clear.

The lesions of atherogenesis usually are classified into three types:

Fatty streaks. These yellowish deposits of fat are composed largely of cholesterol that comes from the blood. The deposits are typically long and flat, and they do not significantly obstruct the vessel. Fatty streaks are found in the arteries of every child by about the age of 10, regardless of race, sex, or cultural/geographical environment. They do not cause clinical disease—ischemic or arrhythmic. Although it is logical that fatty streaks would eventually develop into plaques, it is only speculative at this time.

Fibrous plaques. These lesions are associated with clinical disease. They are raised, protrude into the arterial lumen, and obstruct blood flow. Typically, the plaque consists of a central core of lipid covered on the lumen side by a fibrous cap, which is a fibromuscular layer of tissue that may be several times the thickness of the normal intima.

Complicated lesions. Fibrous plaques that have undergone or produced degenerative changes, such as thrombosis in the vessel wall, hemorrhage, ulceration, or calcification, are called complicated lesions. Complicated lesions are unquestionably associated with clinical disease. They cause not only obstructive disease, but may lead to aneurysm, or hemorrhage into the weakened vessel wall that causes the layers of the wall to split. In addition, blood clots, or thrombi, may form on the atheromatous plaques. These clots may further obstruct blood flow at the site of the plaque, or they may break off to form emboli that travel downstream, lodge in a distant artery and obstruct flow.

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