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Changes in left ventricular mass during a double-blind study with chlorthalidone and slow-release nifedipine
Insights
This study investigated the link between blood pressure reduction and left ventricular mass changes in hypertensive patients. Results indicate that while some antihypertensives lower blood pressure, only chlorthalidone significantly altered ventricular mass, suggesting other factors are involved.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Hypertension is a major risk factor for left ventricular hypertrophy (LVH).
- The relationship between blood pressure reduction and regression of LVH by antihypertensive drugs requires further elucidation.
Purpose of the Study:
- To investigate the correlation between changes in left ventricular mass and the degree of blood pressure reduction in hypertensive patients treated with different antihypertensive drugs.
Main Methods:
- 40 outpatients with hypertension were studied using M-mode echocardiography.
- Patients were divided into groups receiving chlorthalidone, slow-release nifedipine, or placebo, with varying treatment durations and run-in periods.
Main Results:
- Chlorthalidone and nifedipine significantly reduced both systolic and diastolic blood pressure.
- Only patients treated with chlorthalidone showed a significant change in left ventricular mass.
- No significant changes in blood pressure or left ventricular mass were observed in the placebo group.
Conclusions:
- Blood pressure reduction alone does not fully explain the regression of left ventricular hypertrophy.
- Factors beyond the decrease in systolic wall tension may influence the reversal of LVH in hypertensive patients.
Abstract:
The presence of a possible correlation between changes in left ventricular mass of hypertensive patients and the degree of blood pressure reduction with different antihypertensive drugs has been investigated in 40 outpatients by M-mode echocardiography. Ten of these, with blood pressure in normal limits with different antihypertensive treatment had their therapy changed in chlorthalidone 25 mg/day without any run-in (Group A); other 30 patients, with a previously uncontrolled blood pressure, after a 14 day run-in, were randomly allocated to chlorthalidone 25 mg/day (Group B), slow release nifedipine 20 mg/day (Group C) or placebo (Group D). At the end of the eight week treatment period a further decrease in systolic blood pressure was observed in Group A without changes in ventricular mass; an highly significant decrease in both systolic and diastolic blood pressure was observed in B and C but only patients on chlorthalidone changed their ventricular mass; no change in both blood pressure and ventricular mass was observed on placebo. As changes in ventricular mass are not correlated with blood pressure reduction, we conclude that other, not well defined factors, apart from the decrease in duration and degree of left ventricular systolic wall tension, may be responsible for reversal of left ventricular hypertrophy.