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Regression of left ventricular hypertrophy in hypertension: comparative effects of three different drugs
Insights
Three antihypertensive drugs effectively lowered blood pressure and reduced left ventricular mass. However, effects on heart rate and plasma renin activity varied, suggesting the sympathetic nervous system isn't solely responsible for left ventricular hypertrophy.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Left ventricular hypertrophy (LVH) is a significant risk factor for cardiovascular events.
- Antihypertensive agents are crucial for managing hypertension and its sequelae.
- The role of the sympathetic nervous system in LVH is not fully elucidated.
Purpose of the Study:
- To compare the effects of nifedipine, timolol, and indapamide on blood pressure, heart rate, plasma catecholamines, plasma renin activity, and left ventricular mass.
- To investigate the relationship between antihypertensive drug action and left ventricular hypertrophy.
Main Methods:
- A study involving 26 hypertensive patients.
- Treatment groups: nifedipine (calcium antagonist), timolol (beta-blocker), and indapamide (diuretic).
- Measurements included blood pressure, heart rate, plasma catecholamines, plasma renin activity, and echocardiographic left ventricular mass.
Main Results:
- All three drugs effectively reduced blood pressure and left ventricular mass.
- Timolol showed a greater reduction in diastolic blood pressure and heart rate compared to the other agents.
- Plasma renin activity decreased with timolol, remained unchanged with nifedipine, and increased with indapamide.
- No significant changes in plasma adrenaline or noradrenaline were observed with any drug.
Conclusions:
- The findings do not support the hypothesis that the sympathetic nervous system is the primary driver of left ventricular hypertrophy.
- Reduction of left ventricular mass by antihypertensive agents is achievable across different drug classes.
- Further research is needed to fully understand the mechanisms underlying antihypertensive-induced changes in cardiac structure.
Abstract:
We examined the effect of three antihypertensive agents with differing modes of action on blood pressure, heart rate, plasma catecholamines, plasma renin activity, and echocardiographic left ventricular mass. Twenty-six patients were studied; nine were treated with nifedipine, a calcium antagonist, nine were treated with timolol, a nonselective beta-blocker, and eight were treated with indapamide, a diuretic with some probable calcium antagonist properties. All drugs reduced blood pressure satisfactorily; the reduction of systolic blood pressure was not significantly different among the three drugs, but timolol reduced diastolic blood pressure by a greater amount than did either indapamide or nifedipine. Left ventricular (LV) mass was reduced equally by all three drugs. However, there were markedly different effects on the other parameters measured. Heart rate was reduced to a greater extent by timolol than by the other two drugs. Plasma renin activity was reduced by timolol, unchanged by nifedipine, and increased by indapamide. There were no significant changes in either adrenaline or noradrenaline with any of the three drugs. We conclude that these data do not support the hypothesis that the sympathetic nervous system is primarily responsible for left ventricular hypertrophy, and suggest that reduction of left ventricular mass with antihypertensive agents is not the property of any one class of drug.