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(Hypertension. 2006;48:1.)
© 2006 American Heart Association, Inc.
Brief Reviews |
From the Institute for Quality and Efficiency in Health Care, Cologne, Germany.
Correspondence to Peter T. Sawicki, Institute for Quality and Efficiency in Health Care, Dillenburger Str 27, D-51105 Cologne, Germany. E-mail annette.ress@iqwig.de
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
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There were 2 major reasons for this failure to transform sound scientific evidence into practice. Firstly, potential thiazide-induced metabolic effects (eg, a transient increase in serum cholesterol and a serum potassiumdependent slight increase in blood glucose levels) were thought to be responsible for the so-called shortfall in the reduction in cardiovascular events (the gap between the epidemiologically estimated decrease in the risk of hypertension-related events and the magnitude of the decrease actually achieved in intervention trials).9 Second, protective effects beyond the blood pressurelowering effect were attributed to newer agents, which include
-blockers, calcium channel blockers (CCBs), angiotensin-converting enzyme inhibitors (ACEIs), and, more recently, angiotensin receptor blockers. Despite the fact that this theory was not confirmed in head-to-head trials, the vigorous marketing of these agents, combined with a campaign against the use of diuretics, changed prescription habits worldwide.10 This controversy was the reason for the largest
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