Regression of left ventricular hypertrophy in patients with essential hypertension: Results of 6 month treatment with indapamide

Left ventricular hypertrophy (LVH) is a major risk factor for cardiovascular morbidity in hypertensive patients. The effects of diuretics on LVH have raised controversies, but recent studies suggest that diuretics are able to reduce LVH in hypertensive patients, mainly through a reduction in ventric...

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Published inAmerican journal of hypertension Vol. 9; no. 8; pp. 828 - 832
Main Authors Curry, C.L., Robinson, H., Brown, R., Olivan, J., Sami, M., Honos, G., Ruddy, T.D., Balazovjech, I., Touzek, F., Galinier, F., Mariani, M., de Cordoüe, A., Barrandon, S., Brault, Y., Guez, D.
Format Journal Article Conference Proceeding
LanguageEnglish
Published New York, NY Elsevier Inc 01.08.1996
Elsevier Science
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Summary:Left ventricular hypertrophy (LVH) is a major risk factor for cardiovascular morbidity in hypertensive patients. The effects of diuretics on LVH have raised controversies, but recent studies suggest that diuretics are able to reduce LVH in hypertensive patients, mainly through a reduction in ventricular diameter. The present multicenter open study was designed to test the effects of indapamide, a widely used nonthiazide diuretic, on LVH in patients with essential hypertension. Patients had to have mild-to-moderate essential hypertension (supine diastolic blood pressure [sDBP] 95 to 115 mm Hg) with echocardiagraphic evidence of LVH (left ventricular mass index [LVMI] > 130 g/m 2 for men and > 110 g/m 2 for women). After a 2 week placebo run-in period, eligible patients underwent a 6 month treatment with 2.5 mg indapamide daily. All echograms were performed by the same investigator before and after 6 months of indapamide. Clinical and biological acceptability and quality of life (visual analog scale) were also studied. One hundred and thirty patients were included in the study and 112 completed the trial. Indapamide induced a significant reduction in systolic and diastolic blood pressures. Indapamide induced a marked reduction in posterior wall thickness (from 12.1 ± 2.0 to 11.2 ± 1.6 mm) and in interventricular wall thickness (from 12.7 ± 1.7 to 11.8 ± 1.9 mm; each P < .001) and a slight decrease in left ventricular diameter ( P = .049). This resulted in a 13% reduction in LVMI (from 161.9 ± 37.9 to 140.7 ± 33.8 g/m 2, P < .001). Left ventricular fractional shortening remained unchanged. There was no significant relation between changes in LVMI and changes in systolic, diastolic, or mean blood pressure. No significant adverse clinical or biological effects were reported during the study. The increased score of the visual analog scale indicated that overall well-being was improved ( P < .001). Our study indicates that indapamide, in addition to blood pressure control, is able to reduce LVH. This effect was achieved mainly through a reduction in wall thicknesses rather than in internal cavity diameter.
ISSN:0895-7061
1879-1905
DOI:10.1016/0895-7061(96)00105-7