(Hypertension. 2000;36:975.)
© 2000 American Heart Association, Inc.
Editorial |
From the Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, England, UK.
Correspondence to Dr Gregory Yh Lip, Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, B18 7QH England, UK. E-mail G.Y.H.LIP@bham.ac.uk
| Introduction |
|---|
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 Virchows 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
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