Hemodynamic and Angiocardiographic Studies on Cardiodynamics Experimental Mitral Insufficiency

Mitral regurgitation was produced in experimental dogs by cutting the chorda tendinea. The biplane angiography was applied to follow up the geometrical response of the left ventricle to the increased volume overload. The left ventricular cavity volume had continued increasing since the onset of cardiac defects to make up for the diminished effective stroke volume by increasing the total stroke volume which had been achieved without any significant change in the ejection fraction. The end-diastolic pressure which had been elevated soon after the beginning of mitral regurgitation, was shown to be reduced after a sufficient time had elapsed as a consequence of the increased compliance of the left ventricular wall with the development of a muscular hypertrophy. The hypertrophy was evidenced by the regain in the thickness of the left ventricular wall, and the initial stress was shown to be de-creased in consequence. The peak stress was not changed in any consistent fashion but it revealed the tendency to be more elevated when the distension was more marked. These observation suggested that the distension of the ventricular wall should be the primary stimulus for cardiac hypertrophy. The inotropic intervension of the cardiac performance was almost the same in both the normal and diseased hearts. The more rapid velocity of contraction and greater extent of shortening was attained by the contraction originating from the smaller end-diastolic volume with the smaller mural force. These findings form a striking contrast with those observed following the rupture of chorda tendinea and it was indicated that the regulation of the cardiac function following the onset of the acute volume overload depended primarily on the mechanical factor rather than neurohumoral. The augmentation of cardiac output was attained by the increase in the heart rate with an almost unchanged stroke volume. In those with mitral incompetence, the regurgitation was significantly suppressed by isoproterenol. These data suggest the clinical usefulness of this drug in the treatment of acute heart failure due to mitral regurgitation.