Left ventricular hypertrophy is a common consequence of chronic hypertension. Although the hypertrophic response can be considered an adaptive mechanism in the initial stages, its progression is associated with increased cardiovascular morbidity and mortality rates. Therefore, reversal of left ventricular hypertrophy may provide considerable clinical benefits to hypertensive patients. Although treatment of hypertension per se is important, blood pressure alone may not explain the course of the hypertrophic process. Not all antihypertensive drugs cause a reversal of hypertrophy, though they may produce equal effects on blood pressure. Factors other than the severity of blood pressure may play a role in the genesis of left ventricular hypertrophy. Adrenergic inhibitors cause its regression, whereas direct vasodilators may promote progression. In this study, therapy with the alpha-adrenergic inhibitor prazosin resulted in significant regression of left ventricular hypertrophy in a group of patients with moderate-to-severe hypertension. This study utilized a new technique-[123I]phenylpen-tadecanoic acid myocardioscintigraphy-to measure the left ventricular mass. In this study, it was shown that monotherapy with prazosin produced significant relative reductions in systolic and diastolic blood pressure, along with significant reductions in left ventricular mass.
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