Role of cardiac contractility in hypertrophy from chronic volume loading.
In an experimental model of chronic cardiac volume overloading, ie chronic A-V block, evaluations of cardiac function were performed during the phase of the development of hypertrophy (one and two weeks of A-V block) and at stable hypertrophy (ten weeks of A-V block). During a time period of ten weeks of volume overload left ventricular muscle mass increased to 1.41 of normal hearts. Cardiac performance measured from cardiac index, stroke volume, and left ventricular ejection fraction was not depressed at any evaluated state of hypertrophy. Normal cardiac performance was also demonstrated when the heart was stressed by high ventricular pacing rates. The contractile state of the intact heart was expressed as the velocity of the isometric left ventricular pressure rise (dP/dt) at comparable loading conditions. Increased dP/dtmax at a stage before stable hypertrophy was reached, even when preload is normalised by ventricular pacing (70/min) implies that the volume overloaded heart during the development of hypertrophy mobilises part of its contractile reserve. It is assumed that increased contractility is a functional cause of an increase in oxygen demand; and that an adequate energy availability is covered by the enlargement of the mitochondrial mass. At stable hypertrophy when the contractile material has also increased, a new steady state is reached and an again normal contractility indicates an also stable dynamic situation.
D000818:Animals; D002302:Cardiac Output; D002306:Cardiac Volume; D006332:Cardiomegaly / Q000209:etiology / Q000503:physiopathology*; D004285:Dogs; D005260:Female; D006327:Heart Block / Q000150:complications; D006439:Hemodynamics; D008297:Male; D009200:Myocardial Contraction; D013997:Time Factors