Regression of left ventricular hypertrophy hypertension with indapamide
in
In hypertensive patients, the development of left ventricular hypertrophy seems to increase the risk of cardiovascular death. Although some antihypertensive agents have been associated with regression in left ventricular hypertrophy, diuretics, the most widely used ones, have not. lndapamlde is a new, nonthiazlde diuretic and vasodilator. To test its effects on left ventricular hypertrophy, patients with essential hypertension and left ventricular hypertrophy were studied before and at the end of 6 months of therapy with 2.5 mg of indapamide daily. Candidates had to have moderate, uncontrolled essential hypertension with echocardiographically documented left ventricular hypertrophy (left ventricular mass index 1130 gm/m* for men and L 110 gm/m* for women). Patients wlth complicated hypertension or with significant cardiovascular or metabolic diseases were excluded. Patients could remain on antihypertensive drugs other than diuretics, provided doses remained stable for 3 months before entry and there was no know regression of left ventricular hypertrophy. Of 13 patients selected, 2 dropped out. The remaining 11 patients successfully completed 6 months of therapy. The average age was 56 + 10 years. lndapamide was associated with a significant reduction of mean systolic blood pressure from 172 to 142 mm Hg (p < O.OOl), diastolic blood pressure from 101 to 63 mm Hg (p < O.OOl), and left ventricular mass index from 146 & 22 to 124 + 22 gm/m* (mean & SD) (p < 0.003). The mean serum potasslum level dropped from 4.3 to 3.6 mmol/L (p < O.OOl), and the mean serum uric acid level increased slightly from 366 to 430 Amol/L. There was no significant change in hematocrit, fastlng blood sugar, and cholesterol levels and body weight. The mechanism by which indapamide had provoked a regression In left ventricular hypertrophy is not yet known. Different theories have been proposed for other antthypertensive agents. In our study, indapamide was well tolerated and effective in reducing both blood pressure and left ventricular mass in patients with essential hypertension and left ventricular hypertrophy. (AM HEART J 1991;122:1215-6.)
Magdi Sami, MD, and Richard Haichin, MD Montreal,
Quebec, Canada
In hypertensive patients, the development of left ventricular hypertrophy seemsto increase the risk of cardiovascular death.lm4Regression of concentric left ventricular hypertrophy has been reported by a variety of investigators.5-7 Although &blockers,8Fg antiadrenergic drugs,6*lo, l1 and converting enzyme inhibitor& l3 have been associated with a decrease in left ventricular mass in patients with hypertension, diuretics, such as hydrochlorothiaxide, do not usually reduce left ventricular massexcept in isolated cases.14ll5 Similarly, arterial vasodilators such as apresoline, minoxidil, and postsynaptic a-blockers such as Praxosin, all of which lack antiadrenergic
effects, do not decrease left ventricular hypertrophy despite adequate arterial pressure control.10l 111l4 Indapamide is a nonthiazide diuretic that also has peripheral vasodilator action but no known antiadrenergic effects. Based on its chemical properties, it would not be predicted to cause a significant reduction in left ventricular mass in patients with hypertension. Preliminary studies, however, suggested that indeed it does. These intriguing findings prompted a multicenter trial that would prospectively study the effect of indapamide on left ventricular mass in patients with moderate hypertension. We present here the preliminary data from one of these centers.
From the Department of Medicine, Royal Victoria Hospital, McGill University. Supported by a grant from Institut de Recherche International Servier, France. Reprint requests: Magdi Sami, MD, Cardiology Division, Royal Victoria Hospital, 687 Pine Ave. West, Montreal, Quebec, Canada, H3A 1Al. 4/o/30537
METHODS Selection
of patients. Patients were eligible for this prospective, open-labeltrial if they werebetween30 and 75 years of ageand had essentialhypertension with a systolic blood pressureof 180 mm Hg or more or diastolic blood pressurebetween 95 to 115 mm Hg. In addition, they had
1215
12
16
LVM -13.6
Sami and Haichin
American
(gm) = l.O4[(LVID
LVMI = LVM (gm)/BSA
+ PWT + IVST)3 - (LVID)3] (m2)
Fig. 1. Devereux formula for determination of left ventricular mass by echocardiographic criteria. LVh4, Left ventricular mass;L VID, left ventricular internal diastolic diameter; PWT, posterior wall thickness; ZVST, interventricular septal thickness; LVMI, left ventricular mass index; BSA, body surface area.
Table I. Clinical and biochemicalchangesafter 6 months of
therapy with indapamide Baseline Parameter
SBP DBP Serum
potassium Serum uric acid Serum cholesterol Random SBG Serum sodium Hematocrit
Weight (kg)
(mean
+ SD)
172 + 24 101 + 7
After indapamide (mean t SD)
p value
4.3 k 0.5
142 zk 21 83 + 12 3.6 + 0.5
in
In hypertensive patients, the development of left ventricular hypertrophy seems to increase the risk of cardiovascular death. Although some antihypertensive agents have been associated with regression in left ventricular hypertrophy, diuretics, the most widely used ones, have not. lndapamlde is a new, nonthiazlde diuretic and vasodilator. To test its effects on left ventricular hypertrophy, patients with essential hypertension and left ventricular hypertrophy were studied before and at the end of 6 months of therapy with 2.5 mg of indapamide daily. Candidates had to have moderate, uncontrolled essential hypertension with echocardiographically documented left ventricular hypertrophy (left ventricular mass index 1130 gm/m* for men and L 110 gm/m* for women). Patients wlth complicated hypertension or with significant cardiovascular or metabolic diseases were excluded. Patients could remain on antihypertensive drugs other than diuretics, provided doses remained stable for 3 months before entry and there was no know regression of left ventricular hypertrophy. Of 13 patients selected, 2 dropped out. The remaining 11 patients successfully completed 6 months of therapy. The average age was 56 + 10 years. lndapamide was associated with a significant reduction of mean systolic blood pressure from 172 to 142 mm Hg (p < O.OOl), diastolic blood pressure from 101 to 63 mm Hg (p < O.OOl), and left ventricular mass index from 146 & 22 to 124 + 22 gm/m* (mean & SD) (p < 0.003). The mean serum potasslum level dropped from 4.3 to 3.6 mmol/L (p < O.OOl), and the mean serum uric acid level increased slightly from 366 to 430 Amol/L. There was no significant change in hematocrit, fastlng blood sugar, and cholesterol levels and body weight. The mechanism by which indapamide had provoked a regression In left ventricular hypertrophy is not yet known. Different theories have been proposed for other antthypertensive agents. In our study, indapamide was well tolerated and effective in reducing both blood pressure and left ventricular mass in patients with essential hypertension and left ventricular hypertrophy. (AM HEART J 1991;122:1215-6.)
Magdi Sami, MD, and Richard Haichin, MD Montreal,
Quebec, Canada
In hypertensive patients, the development of left ventricular hypertrophy seemsto increase the risk of cardiovascular death.lm4Regression of concentric left ventricular hypertrophy has been reported by a variety of investigators.5-7 Although &blockers,8Fg antiadrenergic drugs,6*lo, l1 and converting enzyme inhibitor& l3 have been associated with a decrease in left ventricular mass in patients with hypertension, diuretics, such as hydrochlorothiaxide, do not usually reduce left ventricular massexcept in isolated cases.14ll5 Similarly, arterial vasodilators such as apresoline, minoxidil, and postsynaptic a-blockers such as Praxosin, all of which lack antiadrenergic
effects, do not decrease left ventricular hypertrophy despite adequate arterial pressure control.10l 111l4 Indapamide is a nonthiazide diuretic that also has peripheral vasodilator action but no known antiadrenergic effects. Based on its chemical properties, it would not be predicted to cause a significant reduction in left ventricular mass in patients with hypertension. Preliminary studies, however, suggested that indeed it does. These intriguing findings prompted a multicenter trial that would prospectively study the effect of indapamide on left ventricular mass in patients with moderate hypertension. We present here the preliminary data from one of these centers.
From the Department of Medicine, Royal Victoria Hospital, McGill University. Supported by a grant from Institut de Recherche International Servier, France. Reprint requests: Magdi Sami, MD, Cardiology Division, Royal Victoria Hospital, 687 Pine Ave. West, Montreal, Quebec, Canada, H3A 1Al. 4/o/30537
METHODS Selection
of patients. Patients were eligible for this prospective, open-labeltrial if they werebetween30 and 75 years of ageand had essentialhypertension with a systolic blood pressureof 180 mm Hg or more or diastolic blood pressurebetween 95 to 115 mm Hg. In addition, they had
1215
12
16
LVM -13.6
Sami and Haichin
American
(gm) = l.O4[(LVID
LVMI = LVM (gm)/BSA
+ PWT + IVST)3 - (LVID)3] (m2)
Fig. 1. Devereux formula for determination of left ventricular mass by echocardiographic criteria. LVh4, Left ventricular mass;L VID, left ventricular internal diastolic diameter; PWT, posterior wall thickness; ZVST, interventricular septal thickness; LVMI, left ventricular mass index; BSA, body surface area.
Table I. Clinical and biochemicalchangesafter 6 months of
therapy with indapamide Baseline Parameter
SBP DBP Serum
potassium Serum uric acid Serum cholesterol Random SBG Serum sodium Hematocrit
Weight (kg)
(mean
+ SD)
172 + 24 101 + 7
After indapamide (mean t SD)
p value
4.3 k 0.5
142 zk 21 83 + 12 3.6 + 0.5
