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      Mechanisms of coronary thrombosis in cigarette smoke exposure.

      Arteriosclerosis, Thrombosis, and Vascular Biology

      pathology, mortality, complications, blood, Tobacco Use Disorder, adverse effects, Tobacco Smoke Pollution, metabolism, Thromboplastin, Smoking, Risk Factors, Risk Assessment, Prognosis, Platelet Activation, Plaque, Atherosclerotic, Oxidative Stress, Inflammation Mediators, Humans, Hemostasis, Fibrinogen, Endothelium, Vascular, Disease Progression, Coronary Vessels, etiology, Coronary Thrombosis, Animals

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          Abstract

          Acute rupture or erosion of a coronary atheromatous plaque and subsequent coronary artery thrombosis cause the majority of sudden cardiac deaths and myocardial infarctions. Cigarette smoking is a major risk factor for acute coronary thrombosis. Indeed, a majority of sudden cardiac deaths attributable to acute thrombosis are in cigarette smokers. Both active and passive cigarette smoke exposure seem to increase the risk of coronary thrombosis and myocardial infarctions. Cigarette smoke exposure seems to alter the hemostatic process via multiple mechanisms, which include alteration of the function of endothelial cells, platelets, fibrinogen, and coagulation factors. This creates an imbalance of antithrombotic/prothrombotic factors and profibrinolytic/antifibrinolytic factors that support the initiation and propagation of thrombosis.

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          Journal
          23685556
          10.1161/ATVBAHA.112.300154

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