Effect of congestive heart failure on in vivo canine aortic elastic properties.

Abstract

The aim of this study was to characterize fully in vivo aortic compliance over a wide range of passive distending pressures, and to study pharmacologically induced alterations in compliance using an intravascular ultrasound-based technique in the canine model of heart failure. Altered aortic compliance may influence considerably the function of the failing heart. Although some studies demonstrate that patients with heart failure have decreased aortic compliance, data from other studies are conflicting. Aortic pressures and dimensions in seven dogs were determined both before and after pacing-induced congestive heart failure (CHF) using simultaneous micromanometer and intravascular ultrasound transducers. Decreases in aortic pressure were produced at baseline and after nitroprusside and dobutamine infusions. Inner and outer aortic circumferences were drawn at the lumen-intimal and media-adventitial borders. Aortic pressure-dimension (chamber) stiffness constants were greater after heart failure was produced (10.0+/-1.5 vs. 6.7+/-1.5, p < 0.05), but stress-strain stiffness (material) constants were similar (11.4+/-1.8 vs. 11.3+/-1.0, p=NS). Equivasodilating doses of nitroprusside and 10 microg/kg/min dobutamine decreased pressure-dimension stiffness constants after pacing-induced heart failure but not beforehand. The aortic wall thickness to diameter ratio was significantly greater in CHF than in the control condition (0.30+/-0.08 vs. 0.16+/-0.03, p < 0.01). Aortic compliance is decreased in this model of CHF, and this change is attributable primarily to vessel geometry rather than material properties. Equivasodilating doses of nitroprusside and equivalent doses of dobutamine increase aortic chamber compliance in dogs with CHF, but not in normal dogs. These data suggest that the beneficial effects of nitroprusside and dobutamine in CHF occur in part from improvement in aortic compliance.