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[Regression of left ventricular hypertrophy with antihypertensive treatment]
1Service de Cardiologie Clinique et Expérimentale, CHU Rangueil, Toulouse.
Insights
Left ventricular hypertrophy (LVH) in hypertension can regress with specific antihypertensive drugs, improving cardiac function and reducing cardiovascular risk. This regression does not negatively impact myocardial structure or coronary hemodynamics.
Area of Science:
- Cardiology
- Pharmacology
- Hypertension Research
Context:
- Left ventricular hypertrophy (LVH) is a significant predictor of poor outcomes in patients with essential arterial hypertension.
- Regression of LVH under antihypertensive therapy is achievable and clinically relevant.
Purpose:
- To evaluate the impact of different antihypertensive drug classes on left ventricular mass.
- To assess the effects of LVH regression on myocardial structure, function, and cardiovascular risk.
Summary:
- Angiotensin-converting enzyme inhibitors, calcium antagonists, centrally acting agents, and beta-blockers effectively reduce left ventricular mass.
- Diuretics and vasodilators generally do not affect LVH due to sympathetic and renin-angiotensin system stimulation.
- Animal studies confirm that LVH regression is safe for myocardial changes and improves coronary hemodynamics.
Impact:
- LVH regression preserves left ventricular systolic function, enhances diastolic function, and may reduce ventricular hyperexcitability.
- Antihypertensive treatments promoting LVH regression are expected to lower cardiovascular risk in hypertensive individuals.
- Understanding drug-specific effects on LVH is crucial for optimizing hypertension management and patient prognosis.
Abstract:
The presence of left ventricular hypertrophy (LVH) is of poor prognosis in essential arterial hypertension, but it may regress under antihypertensive treatment. Angiotensin-converting enzyme inhibitors, calcium antagonists, centrally acting antihypertensive agents and beta-blockers with low intrinsic sympathomimetic activity constantly reduce the left ventricular mass. This stands in contrast with diuretics and vasodilators which induce stimulation of the sympathetic and/or renin-angiotensin systems and usually have no effect on LVH. Animal experiments have shown that regression of LHV has no adverse effect on the myocardial changes aimed at correcting the LVH-associated abnormalities (collagen content, changes in isomyosins, density of beta-adrenergic receptors, etc.) and that it improves the coronary haemodynamics disturbed by LVH. In clinical practice, reducing the ventricular mass does not modify the left ventricular systolic function, usually improves the diastolic function precociously altered by LVH and seems to reduce the LVH-induced ventricular hyperexcitability. The regression of LVH under antihypertensive treatment should result in a lesser cardiovascular risk in hypertensive patients.