title: Compensatory mechanisms for cardiac dysfunction in myocardial infarction.
abstract: Loss of contractile myocardial tissue by myocardial infarction would result in depressed cardiac output if compensatory mechanisms would not be operative. Frank-Straub-Starling-mechanism and increased heart rate and contractility due to sympathetic stimulation are unlikely to chronically compensate for cardiac dysfunction. Structural left ventricular dilatation may be compensatory, but results in increased wall stress and, ultimately, in progressive dilatation and heart failure. In patients with myocardial infarction, we have shown left-ventricular dilatation in dependence of infarct size and time after infarction. Dilatation is compensatory first and normalizes stroke volume. However, left ventricular dilatation progresses without further hemodynamic profit and, thus, may participate in development of heart failure.
authors.affiliation: Medizinische Klinik, Universität Würzburg, FRG.
authors.forename: G
authors.initials: G
authors.lastname: Ertl
authors.forename: P
authors.initials: P
authors.lastname: Gaudron
authors.forename: C
authors.initials: C
authors.lastname: Eilles
authors.forename: W
authors.initials: W
authors.lastname: Schorb
authors.forename: K
authors.initials: K
authors.lastname: Kochsiek
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000209:etiology*; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology; D009203:Myocardial Infarction / Q000150:complications*; D013318:Stroke Volume / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*