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Possible regression of left ventricular hypertrophy during antihypertensive treatment with diuretics and/or beta
Insights
Diuretics and beta blockers can regress left ventricular hypertrophy (LVH) in hypertensive patients. However, acebutolol showed no effect on LV mass, unlike other treatments.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Left ventricular hypertrophy (LVH) is a common complication of hypertension.
- Regression of LVH is a therapeutic goal in managing hypertension.
Purpose of the Study:
- To assess the regression of left ventricular hypertrophy (LVH) in hypertensive patients treated with diuretics and/or beta blockers.
- To compare the efficacy of different antihypertensive treatments on LV mass reduction.
Main Methods:
- Echocardiography was used to assess LV mass in 78 hypertensive patients.
- Patients were divided into five groups receiving different treatments: diuretics alone, chlorthalidone plus SR oxprenolol, acebutolol followed by atenolol, timolol alone, or atenolol alone.
Main Results:
- All treatments except acebutolol significantly reduced LV mass within 12 months.
- Acebutolol did not modify LV mass even after 24 months, despite its antihypertensive effect.
- LV mass reduction was linked to decreased wall thickness (beta blockers) or LV dimension (chlorthalidone).
- Only 31% of patients achieved normalized LV mass; no significant change was observed in patients with normal pretreatment LV mass.
- LV mass decrease correlated with reduced cardiac output but not blood pressure reduction.
Conclusions:
- Long-term antihypertensive therapy, particularly with certain beta blockers and diuretics, can lead to LVH regression.
- Acebutolol appears ineffective in reducing LV mass despite blood pressure control.
- LV systolic function showed a trend towards improvement with long-term antihypertensive treatment.
Abstract:
The possible regression of left ventricular hypertrophy (LVH) during treatment with diuretics and/or beta blockers was assessed in 78 hypertensive patients by echocardiography. Five groups of patients were treated, respectively, with diuretics alone, chlorthalidone plus SR oxprenolol, acebutolol followed by atenolol, timolol alone, or atenolol alone. All patients, except those receiving acebutolol had a significantly reduced LV mass within 12 months. Acebutolol did not modify LV mass even after 24 months, in spite of its antihypertensive efficacy. The reduction of LV mass was due to a decrease in wall thickness after administration of beta blockers and a decrease in LV dimension after chlorthalidone. Normalization of LV mass (less than 130 g/m2) occurred only in 31% of patients. LV mass was not significantly modified in patients with normal mass in pretreatment condition. The decrease of LV mass correlated with a decrease in cardiac output but not with the reduction in blood pressure. In conclusion, LV systolic function showed a tendency toward improvement after long-term antihypertensive therapy.