title: Medical repair of hypertensive left ventricular remodeling.
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.
authors.affiliation: Department of Medicine-Cardiology, Pneumology, and Angiology, Heinrich-Heine University, Düsseldorf, Germany.
authors.forename: W H
authors.initials: WH
authors.lastname: Motz
authors.forename: S
authors.initials: S
authors.lastname: Scheler
authors.forename: B E
authors.initials: BE
authors.lastname: Strauer
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D006332:Cardiomegaly / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology; D012084:Renin-Angiotensin System / Q000502:physiology; D013564:Sympathetic Nervous System / Q000503:physiopathology
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers