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Figure 4 The thrombotic complications of atherosclerosis. Thrombi complicating atheroma arise by 2 major mechanisms. The first, depicted in the left panel of this diagram, involves a through-and-through rupture of the plaque’s fibrous cap, which has been weakened by the mechanisms described in the text and in the legend to Figure 3. The rent in the fibrous cap permits blood and its coagulation factors to contact tissue factor expressed by macrophages and smooth muscle cell (SMC) and on microparticles elaborated by these cells and endothelial cells (EC). Moreover, the activated cells in the local environment of the plaque, including ECs and SMCs, elaborate large amounts of plasminogen activator inhibitor-1, a potent inhibitor of the endogenous fibrinolytic enzymes also found in the plaque such as urokinase and tissue-type plasminogen activator. A second common mechanism of coronary thrombus formation involves a superficial erosion of the endothelial cells (right panel), perhaps caused by endothelial apoptosis or desquamation.
