Coronary Artery Disease Pathophysiology

Coronary artery disease is usually caused by a build up cholesterol rich deposits or plaques on the lining inside the artery. These plaques are also called atheromatous plaques or simply atheromas and they cause a thickening of the arterial wall and a narrowing of the arterial space through which blood flows to reach the heart. The amount of blood reaching and supplying the heart muscles (myocardium) with oxygen and nutrients can therefore be reduced in the presence of atheromas.

An atheroma usually starts to develop as a result of damage or injury to the inner lining of the artery called the endothelium. Once the endothelium is damaged, cholesterol, fats, lipoproteins

and other debris start to accumulate at the site of injury in the wall or intima of the artery.

High concentrations of low density lipoprotein (LDL) penetrate the damaged endothelium and undergo a chemical process called oxidation. This altered LDL acts as a beacon that attracts white blood cells or leukocytes to migrate towards the vessel wall. As macrophages appear, they engulf the lipoproteins and become foam cells. These foam cells give rise to the earliest visible form of an atheromatous lesion called the fatty streak.

Once the fatty streak is formed, it then attracts the smooth muscle cells to the site, where they multiply and start to produce extracellular matrix comprising of collagen and proteoglycan. It is this extracellular matrix that forms a large portion of the atherosclerotic plaque. This turns the fatty streak into a fibrous plaque. The lesion then starts to bulge into the inner wall of the blood vessel causing a significant narrowing of the luminal space.

Next, the fibrous plaque starts to support itself. It develops its own small vessels to provide it with a supply of blood in a process called angiogenesis. Thereafter, the plaques begin to calcify as calcium starts to deposit. The final plaque is made up of a cap of fibrous tissue covering a core that is rich in lipids as well as necrotic or dead cells. The edge of this cap is key in acute coronary disease. This region is prone to rupture, which exposes the underlying core of lipids and necrotic material to thrombogenic factors in the blood. This can cause the aggregation of platelets that form a clot across the plaque and further narrow the artery.

Arteries that have become narrowed due to the presence of plaques may lead to angina or chest pain as the muscles of the heart are deprived of oxygen. As the deposits on the plaques grow in size and dimension, the blood vessels become further narrowed and there may be obstruction leading to a heart attack or a myocardial infarction.

Further Reading

Last Updated: Aug 23, 2018



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