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(Hypertension. 2008;51:1272.)
© 2008 American Heart Association, Inc.
Editorial Commentaries |
From the Departments of Clinical Neurological Sciences (Neurology) and Internal Medicine (Clinical Pharmacology), Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada; and the Stroke Prevention and Atherosclerosis Prevention Centre, Robarts Research Institute, London, Ontario, Canada.
Correspondence to David Spence, Stroke Prevention and Atherosclerosis Research Centre, 1400 Western Rd, London, Ontario, Canada N6G 2V2. E-mail dspence@robarts.ca
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The article in this issue from Puato et al1 in Padova, Italy, is important because it was prospective, with 5 years of follow-up, and the hypertensive patients were never treated. They showed that carotid intima-media thickness was greater at baseline in white-coat hypertensive subjects (WCHs), increased more during follow-up than in normotensive subjects, and was not different in WCHs with sustained hypertension.
There is a widespread tendency, which I characterize as wishful thinking,2 to believe that it is a kindness to withhold therapy in patients with white-coat hypertension. Withholding therapy avoids labeling, the cost of therapy, and the adverse effects of antihypertensive drugs, so is thought to be desirable if therapy does not reduce cardiovascular events. This is justified by the important prospective findings of Verdecchia et al,3 who showed that when ambulatory blood pressure was consistently <130/80 mm Hg, there was no excess of cardiovascular events. It is seldom remembered that this definition was very strict and that even ambulatory blood pressure between 130/80 mm Hg and 131/86 mm Hg (for women) or 136/87 mm Hg (for men) was as strongly associated with cardiovascular events as were higher pressures.
Several cross-sectional studies have shown that white-coat hypertension is a form of hypertension that is intermediate between normotension and sustained hypertension.4,5 Glen et al4 found that left ventricular function and arterial compliance, elasticity, and stiffness were similarly adversely affected compared with normotensive subjects, in WCHs, and in patients with sustained hypertension. Cerasola et al5 showed that left ventricular mass, carotid
Related Article:
Hypertension 2008 51: 1300-1305.
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