The immune system in atherosclerosis and in acute myocardial infarction

Abstract

Acute myocardial infarction (AMI) occurs when the atheromatous process prevents total blood flow through the coronary artery. It was previously thought that progressive luminal narrowing from the continued growth of smooth muscle cells (SMCs) in the plaque was the main cause of infarction, however, angiographic studies, have identified culprit lesions that do not cause marked stenosis. Is now evident that plaque activation, rather than stenosis, precipitates ischemia and infarction. Coronary spasm could be involved to some extent, but most cases of AMI are due to the formation of an occluding thrombus on the surface of the plaque; the two major causes of coronary thrombosis are plaque rupture and endothelial erosion. Plaque rupture is detectable in 60- 70% of cases and preferentially occurs when the fibrous cap is thin and partly destroyed. One of the major challenges in modern cardiology is the knowledge of the factors that induce a silent atherosclerotic plaque shifting from a stable to a vulnerable form.