Yazarlar : Kumar A, Kar S, Fay WP.

Yayın : J Appl Physiol.

Yayın Yılı : 2011

Pubmed Linki : http://www.ncbi.nlm.nih.gov/pubmed/21596926

Konu : Tromboz

Literatür İçeriği :  

Abstract

Acute coronary syndromes (ACS) are common, life-threatening cardiac disorders that typically are triggered by rupture or erosion of an atherosclerotic plaque. Platelet deposition and activation of the blood coagulation cascade in response to plaque disruption lead to the formation of a platelet-fibrin thrombus, which can grow rapidly, obstruct coronary blood flow, and cause myocardial ischemia and/or infarction. Several clinical studies have examined the relationship between physical activity and ACS, and numerous preclinical studies have identified specific mechanisms by which physical activity regulates the susceptibility of atherosclerotic plaques to rupture. In addition, physical activity regulates the function of blood platelets, the coagulation cascade, and the fibrinolytic (clot-dissolving) system. This article reviews the available literature regarding the role of physical activity in determining the incidence of atherosclerotic plaque rupture and the pace and extent of thrombus formation after plaque rupture.

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