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(Hypertension. 2008;52:218.)
© 2008 American Heart Association, Inc.

Editorial Commentaries

Endothelium and Fibrinolysis in Hypertension

Important Facets of a Prothrombotic State?

Gregory Y.H. Lip; Andrew D. Blann

From the Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, United Kingdom.

Correspondence to Gregory 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

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Despite the blood vessels in hypertension being exposed to high pressure, the main complications of hypertension (ie, heart attacks and stroke) are paradoxically thrombotic in nature rather than hemorrhagic. Increasing clinical and laboratory evidence is consistent with the concept that hypertension, per se, may confer a prothrombotic or hypercoagulable state, with abnormalities of coagulation, platelets, and the endothelium.¹ Indeed, it has long been suggested that the latter organ, with roles in hemostasis and in regulating the NO/endothelin-mediated relaxation and contraction of the blood vessel wall, may be both a target and/or promoter of hypertension and a promoter of thrombosis and, thus, atherosclerosis.²

Other evidence linking the endothelium to atherogenesis is the presence of vasa vasorum in the adventitia and media at a higher density in atherosclerotic tissue, as well as neovascularization and collateral growth bypassing stenotic vascular disease. Such neovascularization reflects the process of angiogenesis, and given these close links, it is no surprise that angiogenesis is yet another important aspect of the pathophysiology of vascular disease, intimately linked with both thrombogenesis and atherogenesis, in a new "vascular triad."³ For example, the major angiogenic growth factor, vascular endothelial growth factor, is linked with both NO and with a major proinflammatory cytokine, interleukin-6.³ However, skeptics would argue that the clinical (ie, human) evidence does not conclusively show evidence of overt angiogenesis, per se, in conditions such as hypertension, despite (eg) the presence of high levels of factors associated with angiogenesis, such as vascular endothelial growth factor. Thus, we have even proposed . . . [Full Text of this Article]

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