title: Reversal of left ventricular hypertrophy: a desirable therapeutic goal?
abstract: It is controversial whether myocardial hypertrophy in essential hypertension represents an adaptive physiologic or pathological response to increased pressure load imposed on the heart. Cardiac structural adaptations in endurance athletes fulfill the criteria of physiologic hypertrophy: maintained cardiac performance and full reversibility of cardiac structural changes following cessation of endurance training. In contrast, there is some evidence that cardiac hypertrophy in arterial hypertension is a pathological process. Diastolic function of the left ventricle is impaired; systolic function, although maintained in the early stages of myocardial hypertrophy, becomes reduced beyond a critical mass; and cardiac structural changes are not fully reversible. An increasing number of prospective studies document that left ventricular hypertrophy in essential hypertension represents an independent risk factor for cardiovascular mortality and morbidity, in particular for sudden cardiac death. Ventricular arrhythmias were regarded as the pathophysiologic link between cardiac structural adaptation and the increased risk of sudden death due to left ventricular hypertrophy. Structural changes of the coronary circulation may represent one confounding factor in the relationship between left ventricular hypertrophy and its cardiovascular risk. As a consequence, optimal antihypertensive therapy should aim at reducing both arterial hypertension and left ventricular hypertrophy. Whether regression of myocardial hypertrophy indeed reduces cardiovascular risk cannot be definitively answered from the available data.
authors.affiliation: Department of Medicine, Universität Erlangen-Nürnberg, F.R.G.
authors.forename: R E
authors.initials: RE
authors.lastname: Schmieder
authors.forename: F H
authors.initials: FH
authors.lastname: Messerli
mesh_terms: D006332:Cardiomegaly / Q000188:drug therapy* / Q000209:etiology; D003326:Coronary Circulation / Q000502:physiology; D003645:Death, Sudden / Q000209:etiology; D004562:Electrocardiography; D006801:Humans; D006973:Hypertension / Q000150:complications*; D012307:Risk Factors