Target organ damage and the prothrombotic state in hypertension.

Hypertension causes target organ damage by the direct physical effect of increased blood pressure, as well as the active promotion of atherosclerosis and thrombogenesis. More importantly, the processes of thrombogenesis and atherogenesis are intimately related, and many of the basic concepts of thrombogenesis can be applied to atherogenesis. Over 150 years ago, Virchow1 postulated that a triad of conditions are needed to predispose to thrombus formation, that is, abnormalities in blood flow, blood constituents, and the vessel wall. Although Virchow was referring to venous thrombosis, the same concepts could essentially be applied to arterial thrombosis. A modern viewpoint of Virchow’s triad includes abnormalities of hemorheology and turbulence at bifurcations and stenotic regions (that is, “abnormal blood flow”), abnormalities in platelets and the coagulation and fibrinolytic pathways (“abnormal blood constituents”), and, finally, abnormalities in the endothelium (“abnormal vessel wall”). This may explain an important pathophysiological paradox in hypertension, in which despite the blood vessels being exposed to high pressures, the main complications of hypertension are generally thrombotic in nature rather than hemorrhagic.2