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.