RT Book, Section A1 Weitz, Jeffrey I. A2 Longo, Dan L. SR Print(0) ID 1128355212 T1 ANTIPLATELET, ANTICOAGULANT, AND FIBRINOLYTIC DRUGS T2 Harrison's Hematology and Oncology, 2e YR 2013 FD 2013 PB McGraw-Hill Education PP New York, NY SN 9780071814904 LK hemonc.mhmedical.com/content.aspx?aid=1128355212 RD 2024/03/28 AB Arterial and venous thromboses are major causes of morbidity and mortality rates. Arterial thrombosis is the most common cause of acute myocardial infarction (MI), ischemic stroke, and limb gangrene, whereas deep-vein thrombosis (DVT) leads to pulmonary embolism (Pulmonary Embolism), which can be fatal, and to the postphlebitic syndrome. Most arterial thrombi are superimposed on disrupted atherosclerotic plaque because plaque rupture exposes thrombogenic material in the plaque core to the blood. This material then triggers platelet aggregation and fibrin formation, which results in the generation of a platelet-rich thrombus that can temporarily or permanently occlude blood flow. In contrast to arterial thrombi, venous thrombi rarely form at sites of obvious vascular disruption. Although they can develop after surgical trauma to veins or secondary to indwelling venous catheters, venous thrombi usually originate in the valve cusps of the deep veins of the calf or in the muscular sinuses, where they are triggered by stasis. Sluggish blood flow in these veins reduces the oxygen supply to the avascular valve cusps. Endothelial cells lining these valve cusps become activated and express adhesion molecules on their surface. Tissue factor–bearing leukocytes and microparticles adhere to these activated cells and induce coagulation. Local thrombus formation is exacerbated by reduced clearance of activated clotting factors as a result of impaired blood flow. If the thrombi extend into more proximal veins of the leg, thrombus fragments can dislodge, travel to the lungs, and produce a Pulmonary Embolism.