ACE inhibitors captopril and enalapril induce regression of left ventricular hypertrophy in hypertensive patients with chronic renal failure.

BACKGROUND: Left ventricular hypertrophy is frequently noted in patients with moderate to severe chronic renal failure not requiring dialysis. Recently, several studies have shown reversal of myocardial hypertrophy in end-stage renal disease with long-term pharmacological control of blood pressure, but it is unclear whether left ventricular mass regresses or normalizes with antihypertensive treatment of patients with earlier stages of chronic renal failure. METHODS: Seventy-two undialysed patients with chronic renal failure, chronic mild-to-moderate hypertension, and left ventricular hypertrophy were randomly assigned in a prospective study to either the captopril (n = 36) or enalapril group (n = 36). Blood pressure measurements, echocardiographic and Doppler parameters were evaluated before treatment and at 6 and 12 months of therapy. RESULTS: During follow-up, six patients developed side-effects including dry cough, taste disturbances, skin rash and gastric intolerance. In the captopril group there was a decrease in mean left ventricular mass index by 12% after 6 months of treatment, which decreased by 20% after 12 months treatment. For enalapril, the average reduction of myocardial mass after 6 months treatment was 14% and after 12 months treatment, the decrease was 19%. In both treatment groups there was significant improvement of left ventricular filling dynamics. No deterioration of left ventricular systolic function was observed. CONCLUSIONS: Our results confirm that antihypertensive monotherapy with the ACE inhibitors, captopril and enalapril, in patients with chronic renal failure results in regression of left ventricular mass index associated with a significant improvement in the diastolic function of the left ventricle without a demonstrable deterioration in left ventricular systolic performance.

[The effect of angiotensin-converting enzyme inhibitors on left ventricular hypertrophy in patients with chronic glomerulonephritis and pronounced kidney failure]. / Vliianie ingibitorov angiotenzinprevrashchaiushchego fermenta na gipertrofiiu levogo zheludochka serdtsa u bol'nykh khronicheskim glomerulonefritom s vyrazhennoi pochechnoi nedostatochnost'iu.

This study compared the effects of angiotensin converting enzyme (ACE) inhibitors captopril versus enalapril on left ventricular (LV) muscle mass and LV systolic and diastolic function in 58 patients with primary glomerulonephritis and moderate chronic renal failure. The design was a 6-8 week titration phase and 6-month maintenance phase. Mean myocardial mass calculated by M-mode echocardiography in the captopril group was 153 +/- 26 g/m2 before, and 130 +/- 14 g/m2 after 6 months of treatment, in enalapril group 147 +/- 22 g/m2 before, and 126 +/- 23 g/m2 after 6 months of treatment (p < 0.05). LV ejection fraction, early and late transmitral flow velocities and early to late LV inflow velocities ratio were not significantly affected by both ACE inhibitors.

[Left ventricular hypertrophy in patients with nephrogenic arterial hypertension]. / Gipertrofiia levogo zheludochka serdtsa u bol'nykh s nefrogennoi arterial'noi gipertenziei.

Incidence and geometric peculiarities of hypertrophy of the left ventricle of the heart (HLVH) were studied on the basis of findings from the echocardiographic investigation done in 86 patients with chronic glomerulonephritis (ChGN) with arterial hypertension (AH), with the renal function being preserved and at the early stages of renal insufficiency. HLVH was detected in 30.2% of the patients, in 80.8% of whom it was concentric, and in 19.2% eccentric, in 76%--symmetric and in 23.1%--asymmetric. Incidence of HLVH did not correlate with sex, clinical variant of ChGN, renal function status, and increased with the degree and duration of AH. There was no difference in geometric peculiarities between sexes, clinical variants of ChGN, and no association with degree and duration of AH as well as with functional state of the kidneys.