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Introduction

  • Suzanne Oparil
    Correspondence
    Address for reprints: Suzanne Oparil, MD, University of Alabama, Birmingham, Ziegler Research Building, Room 1032, Birmingham, Alabama 35294
    Affiliations
    Vascular Biology and Hypertension Program of the Division of Cardiovascular Disease, University of Alabama School of Medicine, Birmingham, Alabama, USA
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      The pharmacologic treatment of hypertension has been revolutionized by the realization that the vast majority (95% in the Framingham cohort) of hypertensive subjects have concomitant cardiovascular disease risk factors and/or target-organ damage. It has been shown that lowering blood pressure per se, even to generally recommended treatment goals, does not reduce cardiovascular disease risk to levels seen in normotensive persons. This is particularly true for coronary artery disease endpoints, which are not reduced by conventional (diuretics or β-blockers) antihypertensive treatment to the extent predicted by epidemiologic data. A possible explanation for these findings is that vascular pathology (ie, endothelial dysfunction, reduced arterial compliance, and hyperplasia/hypertrophy of resistance vessels) may antedate the development of hypertension and contribute to its pathogenesis. Broad acceptance that multiple cardiovascular disease risk factors and cardiovascular remodeling contribute to the hypertension syndrome has spawned a search for antihypertensive therapies that address these physiologic mechanisms. A class of antihypertensive drugs, the angiotensin-converting enzyme (ACE) inhibitors, has clearly been shown to produce benefits beyond blood pressure lowering.
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