How does a plaque contribute to coronary artery disease (CAD)?

A plaque contributes to coronary artery disease (CAD) primarily through the mechanism of forming a lesion within the arterial wall that undergoes oxidation and inflammation. As plaques develop, they consist of lipids, cholesterol, calcium, and cellular debris that accumulate in the arteries. Over time, this buildup leads to a process known as atherosclerosis, which is characterized by the thickening and hardening of arterial walls.

When the plaque becomes oxidized, it triggers an inflammatory response. This inflammation is critical because it destabilizes the plaque, making it more likely to rupture. A ruptured plaque can lead to the formation of a thrombosis (blood clot) that can partially or completely occlude the artery, significantly decreasing blood flow to the heart muscle. This blockage is a direct cause of angina or myocardial infarction (heart attack), highlighting the lethal potential of plaque in the context of CAD.

Understanding the inflammatory component and the oxidative changes of plaques helps illuminate the disease process in CAD, making clear why the progression of plaque formation is detrimental to cardiovascular health. Other options, such as increasing blood pressure, reducing lipid levels, or decreasing heart rate, do not directly relate to the role of plaques in the pathophysiology of coronary artery disease.