(Circulation. 2000;101:218.)
© 2000 American Heart Association, Inc.
Editorial |
From the Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, England.
Correspondence to Dr G.Y.H. Lip, Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham B18 7QH, England. E-mail g.y.h.lip@bham.ac.uk
Key Words: Editorials hypertension thrombosis coagulation
Despite advances in pharmacology that have led to increasingly effective antihypertensive drug treatments, the precise pathophysiological mechanisms of hypertension and its complications are still poorly understood. Increasing clinical and laboratory evidence suggests that hypertension per se may confer a prothrombotic or hypercoagulable state.1 This may explain in part why, despite exposure of the blood vessels to high pressures, the main complications of hypertension (that is, heart attacks and strokes) are paradoxically thrombotic in nature rather than hemorrhagic.
See p 264
In recent years, it has become increasingly evident that components of the coagulation and fibrinolytic pathways are primary and secondary predictors of cardiovascular events.2 The close association of these markers with cardiac outcome and the common cardiovascular risks factors raises the possibility that such indices are not merely markers or consequences of thrombosis but rather may significantly contribute to the pathogenesis of arterial thrombotic disease. Indeed, the processes of thrombogenesis and atherogenesis are intimately related.3
As long as 150 years ago, Virchow suggested 3 components that should be
fulfilled for thrombus formation (thrombogenesis). These are now
referred to as Virchows triad: abnormalities of the vessel wall
(which we today recognize as endothelial dysfunction or
damage), blood constituents (with abnormal levels of hemostatic and
fibrinolytic factors and platelet activation), and blood flow
(focusing on rheology and flow reserve). For hypertension to confer a
hypercoagulable or prothrombotic state, each of these components must
be adequately fulfilled. These components also need to be related to
hypertensive target organ damage, long-term prognosis, and alteration
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