Plaque in the Arteries

What is Atherosclerotic Plaque?

Atherosclerotic plaque is complex material, and physicians and scientists have only recently begun to understand its composition and how it leads to certain complications, such as heart attacks (often referred to as myocardial infarction, or MI) or heart failure. The development of atherosclerotic plaque is a prolonged process, which begins very early in life and evolves throughout adulthood.

Early coronary artery atherosclerosis, called fatty streaks, is usually detectable in people by the age of 20. Fatty streaks are mostly composed of fat, or lipid, accumulating within inflammatory cells called macrophages associated with other inflammatory cells and cells lining the muscular wall of the coronary arteries, known as smooth muscle cells.

As more lipid, inflammatory cells, and smooth muscle cells accumulate, fatty streaks may progress to atherosclerotic plaque formation. The outer surface of plaque usually has a fibrous cap. Although the composition and evolution of atherosclerotic plaque are complex processes, it is known that inflammation and vessel injury are critical components of the formation and progression of atherosclerotic plaque. In some patients, the plaque may continue to enlarge but may eventually undergo a healing response; as a result of this healing, the plaque may become calcified.

These calcified plaques are relatively stable and are often referred to as hard plaques. If the plaque became large enough to narrow the coronary artery lumen, angina may result; if not, the plaque may only be detected by imaging studies (see below). In other instances, the plaque does not undergo a healing response, and instead the internal portion of the plaque remains soft and fatty, and the outer portion of the plaque, in contact with the blood flowing within the coronary artery, consists of a fibrous covering- often referred to as soft plaque. Soft plaque may remain stable, enlarge, or may rupture. When rupture occurs, the outer fibrous cap is torn, and blood flow gains access to the internal fatty portion of the atherosclerotic plaque.

The internal portion of atherosclerotic plaque tends to promote clot, or thrombus, formation. If the clot that forms is large, it may block the coronary artery blood flow completely. When this occurs, heart muscle supplied by the affected artery is deprived of oxygen and dies - this process is called myocardial infarction, or heart attack. It is thought that this process is responsible for many heart attacks. In fact, a soft atherosclerotic plaque that does not cause much coronary artery narrowing is potentially dangerous because it may undergo rupture and the affected artery goes from minimally or mildly narrowed to completely blocked in a matter of minutes.

Cardiac catheterization studies have shown that atherosclerotic plaques that cause heart attacks usually occupy less than 50% of the coronary artery cross sectional area. This mechanism is one of the reasons CAD is a silent killer - for many Americans, sudden cardiac death is the first, and only, sign of CAD.