(Hypertension. 2006;48:541.)
© 2006 American Heart Association, Inc.
Editorial Commentaries |
From the Hospital S. Maria della Misericordia (P.V., F.A.), Clinical Research UnitPreventive Cardiology, Perugia, Italy; and the Department of Internal Medicine (S.T.), University of Pisa, Pisa, Italy.
Correspondence to Paolo Verdecchia, Hospital S. Maria della Misericordia, University of Perugia, Clinical Research UnitPreventive Cardiology, Piazzale G. Menghini, 1, 06100 Perugia, Italy. E-mail verdec@tin.it
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Brachial cuff blood pressure (BP) continues to guide almost every decision related to the clinical management of the hypertensive patient. However, the BP within the central aorta (ie, aortic pressure) is receiving growing attention for 2 main reasons. First, brachial BP does not necessarily predict aortic pressure, and subjects with equal values of brachial cuff pressure may differ markedly in their aortic pressure.1 Second, aortic pressure may be superior to brachial BP for the prediction of several vascular complications, including the degree of carotid atherosclerosis,2 the extent of coronary artery disease,3 the likelihood of reocclusion after angioplasty,4 and, more important, the risk of major cardiovascular events.1,5
Aortic BP may be estimated noninvasively from analysis of peripheral radial artery waveforms with applanation tonometry. Although the reliability of derived aortic BP is crucially dependent on the validity of the transfer function used to generate the central aortic waveforms, the correspondence between estimated central aortic and intra-arterial systolic BP and pulse pressure (PP) seems to be quite close.6 In addition to central PP, pulse wave velocity (PWV) is another good marker of arterial wall stiffness and predictor of cardiovascular events in different clinical settings.7
Initial data suggest that endothelial dysfunction may play a role in the pathogenesis of arterial stiffening. An impaired endothelial function detected at the peripheral8 and coronary9 level has been associated with a wide peripheral PP. Through a decreased production of NO, endothelial dysfunction may increase arterial stiffness by promoting atherosclerosis or even inducing contraction of the surrounding vascular muscle
Related Article:
Hypertension 2006 48: 602-608.
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