[Ischemic heart disease].

During the progression of early atherosclerotic lesions, atherosclerotic plaque rupture, with intraluminal thrombosis superimposed, which is one of the principle mechanisms of evolving atherosclerosis, may lead to thrombotic occlusion and ischemic coronary syndrome. Pathologic studies suggest that plaque rupture and overlying thrombi, which are dynamic and repetitive may frequently occur. In most cases, healed ruptures and incorporation of thrombi produce plaque progression without manifestation of clinical symptoms. However, acute mural occlusive thrombi, overlying plaque ruptures, cause unstable angina and acute myocardial infarction. The different pathogenesis between unstable angina and acute myocardial infarction might depend on the composition and stability of the thrombus resulting from the degree of vessel injury and blood flow. Soft lipid-rich plaques appear more prone to rupture, particularly when the lipid pool is localized eccentrically within the intima. Macrophages in the plaque may also facilitate plaque rupture by releasing proteases.