Chapters authored
Pathology and Pathophysiology of Atherothrombosis: Virchow's Triad Revisited
Part of the book: Traditional and Novel Risk Factors in Atherothrombosis
Pathophysiology of Atherothrombosis — Thrombus Growth, Vascular Thrombogenicity, and Plaque Metabolism
Atherosclerotic plaque disruption does not always result in acute symptomatic events. Therefore, the formation of a large thrombus is a critical step in the development of atherothrombosis. However, little is known about the mechanisms involved in thrombus growth processes after plaque disruption. Studies in vivo have demonstrated that the tissue factor (TF) derived from the vascular wall contributes to the formation of thrombin-dependent platelet–fibrin thrombus on atherosclerotic arteries but not on normal arteries, and that altered blood flow in disrupted atherosclerotic arteries promotes platelet recruitment mediated by von Willebrand factor (VWF) on the thrombus surface and augmented blood coagulation resulting in thrombus growth. The thrombogenic potential of plaques is a fundamental factor in atherothrombosis. We recently found that the arterial glucose uptake reflects vascular thrombogenicity, which might be partly explained by metabolic adaptation and enhanced procoagulant activity in a hypoxic microenvironment. Hypoxic responses might link atherometabolism to vascular thrombogenicity.
Part of the book: Thrombosis, Atherosclerosis and Atherothrombosis