Vascular Injury And Thrombosis

Rupture or erosion of an atherosclerotic plaque with subsequent platelet aggregation and coronary artery thrombosis is a central pathophysiologic event across the entire

From: Contemporary Cardiology: Management of Acute Coronary Syndromes, Second Edition Edited by: C. P. Cannon © Humana Press Inc., Totowa, NJ

spectrum of acute ACS (1-3). As the plaque matures and increases in size, macrophages and foam cells preferentially infiltrate its shoulder regions (4,5) and are capable of releasing several enzymes and inflammatory mediators that play a crucial role in the degradation of the extracellular matrix and weakening of the fibrous cap (6). In addition, contraction, bending, flexing and shear stress fluctuations of the cap during the cardiac cycle can weaken the plaque and render it prone to rupture (1).

The resulting discontinuity in the fibrous cap leads to exposure of the highly throm-bogenic fatty gruel contained within the plaque to flowing arterial blood (7), with subsequent thrombosis on the luminal surface of the plaque. Endothelial denudation, exposure of subendothelial collagen and other matrix proteins, the initiation of the extrinsic pathway of coagulation by the high content of tissue factor (TF) present in the fatty gruel (8), together with a turbulent flow around a swollen plaque, are all potent stimuli for platelet activation and thrombus formation. It is, therefore, not surprising that antiplatelet and antithrombin therapies are the cornerstones in the treatment of ACS.

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