Abstract

Elevated blood pressure (BP), along with tobacco use and dyslipidemia, is 1 of the 3 most important modifiable risk factors for cardiovascular disease (CVD).1 Over the last 4 decades there have been a series of epidemiological studies, clinical trials, and pathophysiologic investigations that have substantially enhanced our knowledge of the relationship of elevated BP to outcomes.2,3. In brief, the risk associated with elevated BP and coronary heart disease or stroke is continuous starting at ≈110 mm Hg systolic in individuals with no previous CVD. BP lowering, per se, reduces CVD events, especially in those with systolic BP (SBP) >160 mm Hg. A reduction in SBP by 10 mm Hg can lead to an ≈25% relative risk reduction in coronary heart disease and a 35% to 40% relative risk reduction in stroke in trials of 5 years (which generally translates into ≈2.5 years of intervention before an event).3 Reducing dietary sodium, increasing potassium, and reducing weight and alcohol intake each lower SBP by 2 to 3 mm Hg depending on the degree of change in the above factors.4 The effects of these interventions on BP lowering appear to be more marked in those with elevated BP than in those with “average” BP levels. Collectively, the dual approach of lowering BP using antihypertensive drugs in those with elevated BP combined with a population-based approach to lifestyle modification, which shifts the BP distribution in a population, can lead to the greatest clinical and public health benefits. Yet, despite the widespread availability of inexpensive and safe antihypertensive agents and knowledge of nonpharmacological approaches to lowering, the burden of CVD from elevated BP in most countries remains high, and the rates of BP “control” are low. The reasons are summarized below. Most trials of hypertension that have reported clear reductions …

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