Target organ damage and the prothrombotic state in hypertension.

Abstract

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 Evidence for the prothrombotic or hypercoagulable state in hypertension has been extensively reviewed.3 4 However, we all recognize that the presence of target organ damage makes a dramatic difference to clinical outcome in hypertension. The “target organ” effects of hypertension are particularly manifest in the heart, brain, kidney, peripheral arteries, and the eye. Indeed, hypertensive patients with evidence of target organ damage are well recognized to be at high risk of cardiovascular and cerebrovascular events, and they should be targeted for aggressive blood pressure and risk factor management. Indeed, one may postulate that the “high-risk” hypertensives with evidence of target organ damage are more likely to exhibit a greater prothrombotic or hypercoagulable state. It is therefore of little surprise that the abnormalities in the prothrombotic or …