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 LV wall thickness and an inflatable cuff around the ascendingaorta. Wall stress, midwall strain and strain rate were calculatedat rest, after acute pressure elevation, and one, two and threeweeks as well as 24 h after release of aortic constriction.Myocardial wall stiffness and viscosity were determined froma viscoelastic stress-strain model. Reference values at zeropressure were determined in all five dogs. LV end-diastolic pressure increased from 7 mm Hg at rest to25 mm Hg after acute pressure elevation, to 18 mm Hg after twoweeks and decreased to 16 mm Hg after three weeks of pressureelevation, and 11 mm Hg at release of aortic constriction. LV peak systolic pressure increased from 140 mm Hg at rest to218 mm Hg after acute pressure elevation, to 227 mm Hg afterthree weeks of pressure elevation and returned to normal (143mm Hg) after cuff release. Diastolic myocardial wall stiffnessshowed no change from 23 at rest to 19 after acute pressureelevation, 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 afteracute pressure elevation and remained elevated during chronicpressure elevation. The reference values at zero filling pressureshowed an increase in LV short axis (creep) from 25.6 mm atrest to a maximum of 28.9 mm after one and two weeks of pressureelevation and then decreased to 27.0 mm after three weeks. LVwall thickness at zero pressure increased from 12.8 mm at restto 13.7 mm after three weeks of pressure elevation and remainedelevated after cuff release (13.8 mm). Thus, diastolic myocardial wall stiffness increased during theinitial stages of chronic pressure overload during ventriculardilatation, but decreased when dilatation regressed and concentrichypertrophy developed. Myocardial viscosity was increased duringboth acute and chronic pressure overload. It is suggested thatthe early increase in myocardial stiffness may be more importantlyrelated to ventricular dilatation with creep than to wall hypertrophyper se.