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Update in atherothrombotic disease
Authors:Viles-Gonzalez Juan F  Anand Sunil X  Valdiviezo Carolina  Zafar M Urooj  Hutter Randolf  Sanz Javier  Rius Teresa  Poon Michael  Fuster Valentin  Badimon Juan J
Affiliation:Cardiovascular Biology Research Laboratory, Zena and Michael A. Wiener Cardiovascular Institute, Box 1030, Mount Sinai School of Medicine, One East 100th Street, New York, NY 10029, USA.
Abstract:Crucial advances in our understanding of the pathogenesis of atherothrombosis, defined as atherosclerosis and its thrombotic complications, have been achieved during the past two decades. The historical hypothesis of pathogenesis ("lipid accumulation") has evolved to integrate several factors contributing to the initiation and evolution of this complex disease. Endothelial dysfunction is considered to be the earliest event in atherogenesis. Inflammation and apoptosis play critical roles in its progression and onset. Tissue factor is postulated to be a central actor in determining plaque thrombogenicity. A hyperreactive state of the blood ("vulnerable blood") may be responsible for one-third of all the acute coronary syndromes. This review will discuss emerging concepts in the pathogenesis of and therapeutic approaches to atherothrombotic disease.
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