ABSTRACT
Coronary stenoses that contain plaques with ruptured fibrous caps and superimposed thromboses often produce distinctive patterns on contrast angiography characterized as complex lesions. Several investigators have demonstrated increased smooth muscle cell death by apoptosis in human plaques, and several key players of the death-signaling pathway have been identified in atherosclerotic lesions. Thrombosis is triggered following plaque rupture when thrombogenic components of the plaque are exposed to circulating blood. The extracellular lipid core is composed of free cholesterol, cholesterol crystals, and cholesterol esters derived from lipids that have infiltrated the arterial wall and also lipids derived from the deaths of foam cells, mostly macrophages. Several angiographic studies have shown that risk factor modification leads to reduced new lesion formation, less lesion progression and, in some cases, actual regression. The prevalence of inflammation is also lower than that in plaque rupture.
