Abstract

One of the great successes of modern medicine is the development of effective pharmacological treatments to lower blood pressure (BP). Of the modifiable risk factors for cardiovascular disease, elevated BP or hypertension has the highest population attributable risk,1 and a near continuous relationship with rates of stroke and coronary heart disease from levels of 115 mm Hg systolic and 75 mm Hg diastolic BP.2 Overviews of randomized trials are consistent in showing that lowering systolic BP by 5 to 10 mm Hg reduces the risk of stroke by one third, irrespective of disease history, initial BP level, or type of agent used.3–5 Moreover, more intensive long-term BP lowering can result in additional benefits proportional to the size of fall in BP.4–6 Despite this body of evidence, there has been longstanding controversy (and consternation) over the levels to which BP should be brought down by treatment for the prevention of cardiovascular disease. Because there has been limited randomized evidence, guideline committees have been challenged in defining BP targets below 130 to 140 mm Hg to manage individual patients.7 Concerns over diminishing net benefit being overtaking by excessive harm with increasing reductions in BP is supported by a physiological argument over critical thresholds for organ perfusion and secondary analysis of randomized trials suggesting a J-shaped relationship with cardiovascular events.8 Moreover, recent trials of more intensive BP lowering, including the Action to Control Cardiovascular Risk on Type 2 Diabetes (ACCORD)9 and Secondary Prevention of Small Subcortical Strokes (SPS3),10 failed to show significant reductions in rates of ischemic stroke with systolic BP reductions below 120 and 130 mm Hg, respectively. The main result of the Systolic …

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