Pathophysiology of Thrombosis in Peripheral Artery Disease

Under physiological conditions, peripheral arteries release endogenous vascular-protective and\r\nantithrombotic agents. Endothelial cells actively synthesize vasoactive mediators, which regulate\r\nvascular tone and platelet reactivity thus preventing thrombosis. Atherosclerosis disrupts homeostasis\r\nand favours thrombosis by triggering pro-thrombotic responses in the vessels, platelet activation,\r\naggregation as well as vasoconstriction, phenomena that ultimately lead to symptomatic lumen\r\nrestriction or complete occlusion. In the present review, we will discuss the homeostatic role of arterial\r\nvessels in releasing vascular-protective agents, such as nitric oxide and prostacyclin, the role of proand anti-thrombotic vascular receptors as well as the contribution of circulating platelets and\r\ncoagulation factors in triggering the pro-thrombotic response(s). We will discuss the pathological\r\nconsequences of disrupting the protective pathways in the arteries and the pharmacological\r\ninterventions along these pathways.