BACKGROUND: This study was undertaken to identify whether diabetes mellitus (DM) accelerates the development of left ventricular hypertrophy (LVH) in hypertensive patients. METHODS: Cardiac structure, systolic function, and hemodynamics were evaluated by two-dimensional M-mode echocardiography in diabetic and nondiabetic patients with essential hypertension. RESULTS: Patients with hypertension with and without DM had the same end-systolic and end-diastolic dimensions, cardiac output, total peripheral resistance, and ejection fraction. Diabetic hypertensive patients had greater interventricular septum (1.32 +/- 0.20 vs 1.07 +/- 0.20 cm) and posterior wall (1.20 +/- 0.20 vs 1.00 +/- 0.10 cm) thickness than did nondiabetic hypertensive patients. Consequently, left ventricular mass index was greater in patients with hypertension and DM than in those without DM (158 +/- 45 vs 113 +/- 20 g/m2). With the use of Devereux criteria for recognition of LVH (left ventricular mass index above 134 g/m2 in men and above 110 g/m2 in women), 72% of the diabetic patients had LVH, whereas only 32% of the nondiabetic patients had LVH. Left ventricular contractility, as reflected by the ratio of end-systolic wall stress to end-systolic volume index, was decreased in diabetic compared with nondiabetic hypertensive patients. CONCLUSIONS: The data suggest that DM accelerates the development of LVH in patients with essential hypertension independent of arterial pressure and, therefore, may contribute to the increased cardiovascular morbidity and mortality in patients with hypertension.
BACKGROUND: This study was undertaken to identify whether diabetes mellitus (DM) accelerates the development of left ventricular hypertrophy (LVH) in hypertensivepatients. METHODS: Cardiac structure, systolic function, and hemodynamics were evaluated by two-dimensional M-mode echocardiography in diabetic and nondiabeticpatients with essential hypertension. RESULTS:Patients with hypertension with and without DM had the same end-systolic and end-diastolic dimensions, cardiac output, total peripheral resistance, and ejection fraction. Diabetic hypertensivepatients had greater interventricular septum (1.32 +/- 0.20 vs 1.07 +/- 0.20 cm) and posterior wall (1.20 +/- 0.20 vs 1.00 +/- 0.10 cm) thickness than did nondiabetic hypertensivepatients. Consequently, left ventricular mass index was greater in patients with hypertension and DM than in those without DM (158 +/- 45 vs 113 +/- 20 g/m2). With the use of Devereux criteria for recognition of LVH (left ventricular mass index above 134 g/m2 in men and above 110 g/m2 in women), 72% of the diabeticpatients had LVH, whereas only 32% of the nondiabeticpatients had LVH. Left ventricular contractility, as reflected by the ratio of end-systolic wall stress to end-systolic volume index, was decreased in diabetic compared with nondiabetic hypertensivepatients. CONCLUSIONS: The data suggest that DM accelerates the development of LVH in patients with essential hypertension independent of arterial pressure and, therefore, may contribute to the increased cardiovascular morbidity and mortality in patients with hypertension.
Authors: João S Felício; Flávia M Santos; Ana Carolina Cb de Souza; Karem M Felício; Arthur B Ribeiro; Maria T Zanella Journal: Exp Clin Cardiol Date: 2010