title: Ventricular/vascular interaction in health and heart failure.
abstract: In summary, the concept of aortic input impedance, which has been examined in detail, requires evaluation of the flow and pressure pulsations within the ascending aorta to determine an input impedance spectrum. This function describes the load imposed on the ejecting left ventricle by the systemic vasculature in terms of pulsatile and steady-flow components and is independent of changes in ventricular performance. The components contain information about the mechanical properties of the large vessels (elastance), arteriolar bed (resistance), and waves reflected (reflectance) within the arterial system. Our investigations indicate that in health the mechanical characteristics of the vasculature appear to minimize pulsatile and steady-flow loading components. The optimal loading pattern is influenced by aging and hypertension so that elastance is increased. This alteration increases the pulsatile flow component of loading, which has the potential to limit left ventricular responses to exercise. In patients with heart failure, the vascular system presents an increase in pulsatile and steady-flow load to the diseased left ventricle. Here the altered loading pattern is due to increased resistance, elastance, and reflectance. The left ventricle has a markedly diminished response to power output in the face of this altered vascular load. With vasorelaxation, all components of vascular loading decrease and result in markedly improved generation of left ventricular power and cardiac output. Recent evidence suggests that agents inducing vasorelaxation can influence various regions of the aorta and large vascular beds in a different manner. This would result in the ability to alter elastance, resistance, and reflectance selectively to affect pulsatile and steady-flow components of load.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Division of Cardiovascular Medicine, College of Medicine, University of Florida, Gainesville 32610.
authors.forename: W W
authors.initials: WW
authors.lastname: Nichols
authors.forename: C J
authors.initials: CJ
authors.lastname: Pepine
mesh_terms: D001011:Aorta / Q000503:physiopathology; D004548:Elasticity; D006333:Heart Failure / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D014655:Vascular Resistance; D016277:Ventricular Function, Left / Q000502:physiology