Left ventricular diastolic function and the mechanics of the remodeled myocardium in dogs with pacing-induced heart failure

Abstract

This thesis analyzes the passive diastolic properties of the remodeled canine ventricle in a Ventricular tachycardia (VT) model of congestive heart failure. A study to investigate the hemodynamic and echocardiographic changes that occur during the development of VT heart failure was performed. A second study examined the diastolic pressure-volume relation in heart failure using two methods; (1) inflation of a balloon catheter occluding the superior and inferior vena cava, and (2) implantation of an artificial mitral valve to prevent filling of the left ventricle. The heart failure model was produced by pacing the left ventricle of a dog at a rate of 240 bpm for a period of four to six weeks. VT model produces heart failure similar to that seen clinically.;This model of heart failure resulted in biventricular dilatation, significantly increased left atrial pressure, decreased ejection fraction and ascites. E{dollar}\sb{lcub}\rm max{rcub}{dollar} and preload recruitable stroke volume, two indexes of systolic performance decreased showing the ability of the heart to contract was severely impaired in this model of heart failure. A "restrictive pattern" of diastolic filling resulted from a large atrioventricular pressure gradient, which at the time of mitral valve opening, sees a stiff ventricle increasing the peak early flow rate.;The passive diastolic filling parameters were determined using the logarithmic approach which determines material properties of the myocardium and the ventricular chamber, whereas the exponential approach, a widely used approach, is limited to information about the ventricular chamber only. This and other limitations of the exponential approach were overcome by the logarithmic approach leading to a more physiologically meaningful analysis of diastolic properties.;The equilibrium volume, an index of passive diastolic function and maximum volume increases showing the ventricle dilated. When chamber stiffness is plotted against pressure, the ventricular chamber of the heart failure group is more compliant than control until pressure exceeds 14.1 mmHg when it becomes stiffer. The heart failure hearts would be more compliant if they functioned in the lower operating range; but, they are functionally stiffer because they operate at a stiffer portion of the curve chronically calling upon the Frank-Starling mechanism to maintain cardiac output.