Adaptations of the Left Ventricle to Chronic Volume Overload

Physiological and structural adaptations to experimental chronic volume overloading have been examined. Serial studies were performed in dogs subjected to a large aortocaval fistula which resulted in progressive left ventricular (LV) dilatation and moderate left ventricular hypertrophy. Analysis of force-velocity curves from single, induced left ventricular (LV) isovolumic beats showed no detectable depression of contractility despite markedly elevated LV end-diastolic (ED) pressures and hypertrophy (average LV weight increase 20%). With cineradiographic techniques LVED volume was shown to increase from an average of 70 ml at one week to 100 ml at between eight to ten weeks after creation of the shunt, a change that was accompanied by a further increase in stroke volume (average 30%). Mean velocity of wall shortening during ejection normalized for end-diastolic circumference (mean V_CF) and per cent shortening of the minor equator were within normal limits and showed no detectable change between early and late studies; however, in one animal with severe cardiac failure, these values were markedly reduced. The shift to the right and increased stiffness of the diastolic pressure-circumference relation after chronic volume overloading were similar to changes observed previously in some patients with severe aortic regurgitation. After closure of the arteriovenous fistula, a reversal of this abnormal pressure-circumference curve toward normal occurred, a finding similar to that in patients demonstrated to have normal contractility before and after surgical treatment of aortic regurgitation.

When these results are coupled with other experimental observations which showed no increase in midwall sarcomere lengths between acutely volume overloaded and chronically dilated left ventricles, it is proposed that by a change in geometry and increased number of sarcomeres, the left ventricle is able to augment its performance during chronic progressive dilatation without further use of the Frank-Starling mechanism (at the ultrastructural level) and at an unchanged, normal contractile state. Therefore, the enhancement of overall cardiac performance during chronic volume overloading appears to be mediated through normal performance of each unit of an enlarged circumference operating at an optimal sarcomere length.