Abstract

See related article, pages 2860–2865. Antihypertensive treatment is accepted as the most effective means for preventing stroke, and its effectiveness is solidly founded on a series of large randomized controlled trials.1,2 Hypertension experts can be proud that antihypertensive therapy has been the first among cardiovascular therapies that has been tested by randomized controlled trials using so-called hard end points (ie, fatal and nonfatal stroke, fatal and nonfatal myocardial infarction, cardiovascular death, and death by any cause), all verified by independent blind clinical event committees.3 Trials are intended to be examples of treatment in everyday life, and hard end point trials measure and compare results (or outcomes) of different interventions by simply counting dead bodies or wounded bodies on the battlefield. This is what is rightly considered solid evidence. Although trials generally cannot explore mechanisms, unavoidably (and, up to a given extent, usefully), investigators try to understand, and more often to figure out, the reasons and the mechanisms that may have led to differences in the measured outcomes. The same is the case in history: there is no uncertainty in the outcome of the battle of Waterloo, but historians take delight in interpreting (post hoc) the reasons and may conclude that Napoleon matched Wellington alone but lost to the combination Wellington plus Blucher, whereas Grouchy arrived too late to make a successful combination with Napoleon. Subtler interpretations may call on Napoleon's bad health, on excessive raining, and the lot of mud that hampered the advantage of the French army, quick movement of troops, and the like. However, these exercises look like war games rather than real wars. Like the outcomes of Napoleon's wars, the benefits of antihypertensive therapy shown by randomized controlled trials have also stimulated post hoc interpretations and debates about the hypothesis that all …

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