ABSTRACT
Thrombosis is best defined as pathological hemostasis. Classically, the etiology of thrombosis was first elucidated by Virchow in 1856 as dependent upon the presence of either blood stasis, endothelial injury, and/or hypercoagulability. While stasis and injury are self-explanatory, hypercoagulability is a vague term that refers to a congenital or acquired pathological state favoring thrombus formation. The regulation of coagulation is a carefully orchestrated balance between pro-and antithrombotic factors derived from the vascular endothelium and circulating blood. Thrombosis results when a shift in that hemostatic equilibrium occurs that favors coagulation, and a “hypercoagulable state” refers to this bias on a continual basis. Interestingly, the initiating mechanisms that elicit thromboses in the venous and arterial system appear to be different. Venous thrombosis is principally predicated upon blood stasis and is influenced by the presence of a hypercoagulable state. Clinically, venous thromboses are manifest as lower extremity deep venous thrombosis (DVT) and pulmonary embolism (PE) or in situ thromboses of the hepatic, renal, mesenteric, pulmonary, or cerebral venous systems. Conversely, arterial thromboses most commonly occur in the setting of endothelial injury resulting from a preexisting atherosclerotic lesion. Arterial thrombotic events are also influenced by the presence of a hypercoagulable state; however, there appears an intriguing segregation among the hypercoagulable factors that favor arterial and venous thrombosis. The clinical manifestations of atherothrombosis include peripheral vascular disease (infrainguinal, aortic/mesenteric, subclavian, or carotid systems), cerebrovascular disease, and coronary artery disease.
