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2000
Volume 3, Issue 2
  • ISSN: 1573-4021
  • E-ISSN: 1875-6506

Abstract

Hypertensive heart disease (HHD) encompasses a spectrum of abnormalities resulting from structural and functional adaptations to chronic pressure overload. The clinical manifestations of HHD range from asymptomatic left ventricular hypertrophy (LVH) to symptomatic heart failure. HHD has been associated with increased risk of cardiovascular morbidity and all cause mortality. However, regression of LVH by antihypertensive therapy has been associated with improved outcome. The pathogenesis of HHD involves various hemodynamic and nonhemodynamic factors including neurohormone, aldosterone. Aldosterone enhances myocardial fibrosis through its direct effect on mineralocorticoid and angiotensin II receptors leading to excessive collagen deposition within the myocardium. Increased myocardial fibrosis is a major determinant of hypertensive remodeling and the transition to heart failure. Aldosterone antagonists are effective antihypertensive agents. Additionally, they have been shown to improve LV structural remodeling, systolic and diastolic function in patients with HHD independent of its effect on blood pressure. Data on long-term benefit of these agents have thus far been limited to patients with advanced systolic heart failure and post-acute myocardial infarction LV systolic dysfunction. The potential benefit of aldosterone antagonists in patients with heart failure and preserved LV systolic function is currently being investigated in large scale clinical trials.

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/content/journals/chyr/10.2174/157340207780598482
2007-05-01
2025-09-04
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