Diastolic myocardial wall stiffness of the left ventricle in chronic pressure overload*.

Five dogs were instrumented with a left ventricular (LV) micromanometer, pairs of ultrasonic crystals to measure L V short axis and L V wall thickness and an inflatable cuff around the ascending aorta. Wall stress, midwall strain and strain rate were calculated at rest, after acute pressure elevation, and one, two and three weeks as well as 24 h after release of aortic constriction. Myocardial wall stiffness and viscosity were determined from a viscoelastic stress-strain model. Reference values at zero pressure were determined in all five dogs. LV end-diastolic pressure increased from 7 mm Hg at rest to 25 mm Hg after acute pressure elevation, to 18 mm Hg after two weeks and decreased to 16 mm Hg after three weeks of pressure elevation, and 11 mm Hg at release of aortic constriction. L V peak systolic pressure increased from 140 mm Hg at rest to 218 mm Hg after acute pressure elevation, to 227 mm Hg after three weeks of pressure elevation and returned to normal (143 mm Hg) after cuff release. Diastolic myocardial wall stiffness showed no change from 23 at rest to 19 after acute pressure elevation, but increased to 47 after one and 81 after two weeks, and it decreased to 50 after three weeks and 45 after cuff release. Myocardial viscosity increased from 0.1 at rest to 3.0 after acute pressure elevation and remained elevated during chronic pressure elevation. The reference values at zero filling pressure showed an increase in LV short axis (creep) from 25.6 mm at rest to a maximum of 28.9 mm after one and two weeks of pressure elevation and then decreased to 27.0 mm after three weeks. LV wall thickness at zero pressure increased from 12.8 mm at rest to 13.7 mm after three weeks of pressure elevation and remained elevated after cuff release (13.8 mm). Thus, diastolic myocardial wall stiffness increased during the initial stages of chronic pressure overload during ventricular dilatation, but decreased when dilatation regressed and concentric hypertrophy developed. Myocardial viscosity was increased during both acute and chronic pressure overload. It is suggested that the early increase in myocardial stiffness may be more importantly related to ventricular dilatation with creep than to wall hypertrophy per se. [ABSTRACT FROM PUBLISHER]