Pathophysiology Basics of Acute Myocardial Infarction

The earliest recognizable lesion of atherosclerosis is the intimal thickening (type I lesion), an aggregation of lipid-rich macrophages and T lymphocytes within the innermost layer of the artery wall, the intima. Early lesions mature into others with smooth muscle cell infil- tration and lipid (type II, “fatty streak”) and connective tissue deposition (type III) (7). The ubiquity and precocity of the atherosclerotic process are attested by the finding of fatty streak in the coronary arteries of half of the autopsy specimens from children aged 10 to 14 years. The early lesions develop within the first three decades of life in areas of localized turbulent flow within the coronary arteries (7). Their development is accelerated by condi- tions such as hypercholesterolemia, diabetes mellitus, hypertension, and smoking. As these early lesions grow into softer plaques with a high extracellular lipid and cholesteryl ester content and progressively thinner fibrous cap (types IV-Va, “atheroma”), they become more vul- nerable to disruption (8). Ruptured plaques with overlying thrombus (type VI) are described as “complicated lesions.” These lesions contain a great number of cell types, including inflammatory cells and smooth muscle cells. When they achieve a significant degree of stenosis to decrease flow without sufficient collateral circulation, these lesions result in ACSs. In the period after the plaque rupture, thrombus over the complicated disrupted lesion organizes and the lesion calcifies (type Vb) or fibroses (type Vc) into chronic stenotic lesions (8). However, the advanced, stenotic plaques are not the only types prone to disruption. In fact, plaque disruption occurs independently of lesion size and degree of stenosis, and the relationship is complicated by vascular remodeling (3). Most AMIs actually result from disruption of lesions that are not initially flow limiting, with rapid progression to occlusion.