Influence of acute mechanical overload on dimension and dynamics of interventricular septal thickness in dogs

Abstract

To evaluate directly septal thickness and related dynamic changes, miniature ultrasonic crystals were Implanted across the Interventricular septum and left ventricular free wall and In the circumferential endocanNal segments of the left and right ventricles In 12 open chest dogs. In the control resting state, end-dlastollc wall thickness of the septum and the left ventricular free wall was 9.4 ± 2.1 and 9.6 ± 2.6 mm, respectively (mean ± standard deviation). Wall thickness Increased during systole by 15 percent In the septum and by 17 percent in the free wall. With constriction of the ascending aorta, left ventricular end-dlastollc segment Increased by 13 percent with reciprocal thinning In the end-dlaslollc thickness of the septum (by −8.5 percent) and the left ventricular free wall (by −5.2 percent); there were decreases in percent shortening of the left ventricular segment (from 21.0 to 15.5 percent) and In percent thickening of both the septum (from 14.6 to 11.8 percent) and the free wall (from 16.9 to 13.1 percent). Pulmonary arterial constriction resulted In significant right ventricular chamber enlargement; however, there was no direct change In dimension and dynamics of the septum. When mitral regurgitation was produced by sectioning the chordae tendlneae, left ventricular end-dlastollc segment length Increased (by 23.5 percent) with reciprocal thinning of the enddlastollc thickness of the septum (by −8.6 percent) and the free wall (by −6.9 percent). The left ventricular segment shortening and wall thickening of the septum and the free wall were equally augmented (from 18.6 to 37.5, from 16.1 to 31.0 and from 19.8 to 29.3 percent, respectively). Wtth the onset of acute tricuspld regurgitation, right ventricular end-dlastollc segment and its shortening Increased markedly, but there were no direct changes in the septum. Thus, the interventrlcular septum can be regarded as a functional part of the left ventricle, and any form of mechanical loading on the left ventricle will ultimately Induce proportionate changes in the septum and left ventricular free wall.