Nature of enhanced performance of the dilated left ventricle in the dog during chronic volume overloading.

The size and the performance of the left ventricle were examined in six conscious dogs early (within 1 week) and late (average 7 weeks) after the production of a large infrarenal arteriovenous fistula. Radiopaque beads were implanted near the endocardium of the left ventricle, and in each study the end-diastolic pressure was adjusted to 22 mm Hg by transfusion or bleeding. The shortening of the minor equator of the left ventricle and its mean velocity of shortening were compared in each dog before and after chronic left ventricular dilatation (ventricular end-diastolic volumes of 71 ml early and 101 ml late, P<0.05) . In five dogs the stroke volume increased by an average of 42% (P < 0.05) between early and late studies, but the percent change in circumference and the mean velocity of shortening remained unchanged (24.2 ± 2% (SE) and 23.6 ± 2%, 1.43 ± 0.12 circumferences/sec and 1.44 ± 0.09 circumferences/sec, respectively) at comparable heart rates. In one animal with congestive heart failure, the percent change in circumference and the mean velocity of shortening fell progressively to 19% and 0.74 circumferences/sec. It is concluded that in the absence of myocardial failure the enhanced performances of the chronically dilated left ventricle is mediated by normal performance of each unit of circumference of the enlarged chamber. The nature of this adaptation supports the application of several measures of contractility used for the assessment of chronic variations of inotropic state. Previously, diastolic sarcomere lengths were shown to be maximal and essentially the same after acute over-transfusion as they were during chronic volume overloading, and the present studies provide physiological support for the view that the chronic adaptation to volume overload need not involve the FrankStarling mechanism at the sarcomere level. The observed adaptation provides a reserve mechanism, in addition to the usual factors regulating cardiac performance, by which chronic alterations in ventricular geometry allow the delivery of more external work.