Enhanced platelet biosynthesis of thromboxane A(2) is associated with several cardiovascular risk factors, as a consequence of a direct effect on platelet biochemistry and/or some form of endothelial dysfunction. Moreover, episodic increases in thromboxane biosynthesis occur in acute coronary and cerebral ischemic syndromes. Thromboxane-dependent platelet activation represents an important mechanism that amplifies the consequences of acute vascular lesions as well as those of longstanding metabolic or hemodynamic disturbances, and results in increased risk of vascular occlusive events.
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