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Medical repair of hypertensive left ventricular remodeling
W H Motz1, S Scheler, B E Strauer
1Department of Medicine-Cardiology, Pneumology, and Angiology, Heinrich-Heine University, Düsseldorf, Germany.
Insights
Antihypertensive treatments targeting left ventricular hypertrophy should reverse myocyte changes, reduce fibrosis, and improve coronary flow. Certain medications effectively reverse these structural changes, offering a causal treatment for hypertensive heart disease.
Area of Science:
- Cardiology
- Hypertension Research
- Cardiovascular Pharmacology
Background:
- Hypertensive left ventricular (LV) hypertrophy causes myocyte hypertrophy, fibrosis, and coronary microcirculation alterations.
- These structural changes impair LV diastolic function and coronary flow reserve, even with normal epicardial arteries.
Purpose of the Study:
- To evaluate antihypertensive treatments for their ability to reverse structural myocardial changes and improve coronary microcirculation.
- To identify therapeutic strategies that address the root causes of hypertensive heart disease beyond blood pressure reduction.
Main Methods:
- Review of clinical studies on long-term antihypertensive therapies.
- Analysis of drug classes including ACE inhibitors, calcium-channel blockers, beta-blockers, and vasodilators/diuretics.
- Assessment of effects on myocyte hypertrophy, interstitial fibrosis, and coronary flow reserve.
Main Results:
- Long-term treatment with ACE inhibitors, calcium-channel blockers, and beta-blockers can induce regression of hypertensive LV hypertrophy.
- Vasodilators and diuretics were less effective, potentially due to increased angiotensin II and catecholamine activity.
- ACE inhibitors show promise in reversing interstitial fibrosis, linked to angiotensin II's role in fibroblast growth.
- Long-term antihypertensive therapy can improve impaired coronary vasodilator reserve.
Conclusions:
- Effective antihypertensive treatment must aim to reverse myocyte hypertrophy, regress fibrosis, and improve coronary flow reserve.
- ACE inhibitors, calcium-channel blockers, and beta-blockers demonstrate efficacy in reversing structural changes associated with hypertensive heart disease.
- A comprehensive antihypertensive strategy restoring myocardial structure and coronary microcirculation offers causative treatment for hypertensive heart disease.
Abstract:
Hypertensive left ventricular (LV) hypertrophy leads to myocytic hypertrophy, interstitial fibrosis, and structural alterations of the coronary microcirculation. This structural remodeling of the myocardium results in an impairment of diastolic function of the left ventricle and of coronary flow reserve despite normal epicardial arteries. Consequently, an antihypertensive treatment should aim at (a) reversing myocytic hypertrophy, (b) regression of myocardial fibrosis, and (c) improvement of coronary flow reserve apart from blood pressure lowering. In recent years many clinical studies have shown that regression of hypertensive hypertrophy can be induced by long-term treatment with angiotensin-converting enzyme (ACE) inhibitors, calcium-channel blockers, beta-receptor blockers, and antisympathonic drugs. However, vasodilators and diuretics, which stimulate adrenoceptor activity and increase angiotensin II levels, were found to be less effective in reversing LV hypertrophy. The trophic influence of catecholamines and angiotensin II on the myocardium counteracts the effect of systolic wall stress reduction due to blood pressure lowering. In respect of reversal of interstitial fibrosis, ACE inhibitors seem to be effective because the growth of fibroblasts was found to be stimulated by angiotensin II. Recently, clinical studies have confirmed previous experimental data that an improvement of the impaired coronary vasodilator reserve can be realized by long-term antihypertensive therapy. An antihypertensive treatment strategy which fully restores myocardial structure and completely repairs coronary microcirculation has to be considered as a causative treatment of hypertensive heart disease.