Abstract

Purpose The current study was performed to assess the functional sequelae of reducing left ventricular hypertrophy in patients with essential hypertension. Patients and methods To analyze left ventricular function and contractility in patients with essential hypertension after reduction of left ventricular hypertrophy, 14 patients with essential hypertension and left ventricular hypertrophy were studied prospectively by echocardiogram (1) before, (2) during, and (3) after left ventricular mass had been reduced by antihypertensive therapy of 19 ± 3 months' duration. All drugs were discontinued four weeks before the first and the third study. Results At the time of the third study, arterial pressure had returned to pretreatment values, and mean, peak, and isovolumetric (but not end-systolic) wall stress increased, whereas left ventricular mass remained diminished. Despite the increased pressure load to the heart, myocardial contractility was maintained or improved after reduction of left ventricular hypertrophy, as indicated by the ratio of end-systolic wall stress to end-systolic volume index (p <0.02) and by the relation of fractional shortening to end-systolic wall stress (p <0.06). End-diastolic volume, an indicator of preload, remained reduced after therapy (p <0.05). As a result, pump function of the left ventricle improved as shown by an increase in the ejection fraction (p <0.05), fractional fiber shortening (p <0.05), and velocity of circumferential fiber shortening (p <0.01). Conclusion Thus, in patients with essential hypertension, reduction of myocardial hypertrophy by antihypertensive therapy appears to be beneficial rather than detrimental to cardiac pump performance. The current study was performed to assess the functional sequelae of reducing left ventricular hypertrophy in patients with essential hypertension. To analyze left ventricular function and contractility in patients with essential hypertension after reduction of left ventricular hypertrophy, 14 patients with essential hypertension and left ventricular hypertrophy were studied prospectively by echocardiogram (1) before, (2) during, and (3) after left ventricular mass had been reduced by antihypertensive therapy of 19 ± 3 months' duration. All drugs were discontinued four weeks before the first and the third study. At the time of the third study, arterial pressure had returned to pretreatment values, and mean, peak, and isovolumetric (but not end-systolic) wall stress increased, whereas left ventricular mass remained diminished. Despite the increased pressure load to the heart, myocardial contractility was maintained or improved after reduction of left ventricular hypertrophy, as indicated by the ratio of end-systolic wall stress to end-systolic volume index (p <0.02) and by the relation of fractional shortening to end-systolic wall stress (p <0.06). End-diastolic volume, an indicator of preload, remained reduced after therapy (p <0.05). As a result, pump function of the left ventricle improved as shown by an increase in the ejection fraction (p <0.05), fractional fiber shortening (p <0.05), and velocity of circumferential fiber shortening (p <0.01). Thus, in patients with essential hypertension, reduction of myocardial hypertrophy by antihypertensive therapy appears to be beneficial rather than detrimental to cardiac pump performance.

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