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(Hypertension. 2003;41:199.)
© 2003 American Heart Association, Inc.

Editorial Commentary

Hypertension, Platelets, and the Endothelium

The "Thrombotic Paradox" of Hypertension (or "Birmingham Paradox") Revisited

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

Correspondence to Professor 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

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

Platelets are the smallest of the blood cells, yet they are one of the main players during the process of thrombus formation (thrombogenesis). Furthermore, the traditional belief that the endothelium exists simply to provide an inert interface between the blood and the vessel wall is no longer accurate. Indeed, the endothelium produces a large number of substances that affect blood flow and in turn are affected by changes in the blood and the pressure of blood flow.

Despite many therapeutic advances that have lead to increasingly effective antihypertensive drug treatments, the precise pathophysiological mechanisms of hypertension and its complications are still poorly understood. In hypertension, the delicate balance between the vasodilators and the vasoconstrictors is upset, leading to changes that then take place in the vascular beds, setting up a vicious cycle that further maintains the high blood pressure. There is also increasing evidence that platelets and the endothelium, which both get activated in hypertension, have a crucial role in the increased thrombotic tendency seen in hypertension. Indeed, despite exposure of the blood vessels to high pressures, the main complications of hypertension (that is, myocardial infarction and stroke) are paradoxically thrombotic in nature rather than hemorrhagic—"the thrombotic paradox of hypertension" or "Birmingham paradox." Certainly, increasing clinical and laboratory evidence suggests that hypertension per se may confer a prothrombotic or hypercoagulable state, with abnormalities of coagulation, platelets, and the endothelium—in fulfillment of Virchow’s triad for thrombogenesis.¹

The processes of thrombogenesis and atherogenesis are also intimately related. Many components of the coagulation . . . [Full Text of this Article]

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