Comparison of the effects on arterial-ventricular coupling between phosphodiesterase inhibitor and dobutamine in the diseased human heart

AbstractObjectives. The aim of this study was to compare the effects of a phosphodiesterase inhibitor and catecholamine on arterial-ventricular coupling and myocardial energetics in the diseased human heart.Background. Recent experimental studies have indicated that the arterial-ventricular coupling analysis using the time-varying elastance model could discriminate between inotropic and vasoactive effects of the two agents.Methods. With the use of a conductance catheter, left ventricular contractility and arterial afterload were measured from the slope of the end-systolic pressure-volume relation, Emax, and the slope of the end-systolic pressure-stroke volume relation, Ea. Arterial-ventricular coupling was assessed by Ea/Emaxbefore and after administration of a new phosphodiesterase inhibitor, E-1020 (0.3 μg/kg per min), and a beta1-stimulant, dobutamine (5 μg/kg per min), in 20 patients with heart disease. Left ventricular mechanical efficiency was assessed as the ratio of stroke work to myocardial oxygen consumption per beat measured by the thermodilution method.Results. The slope of the end-systolic pressure-volume relation increased comparably with both E-1020 (39%, p < 0.01) and dobutamine (47%, p < 0.01), but Ea/Emaxdecreased with E-1020 (1.25 to 0.78, −37%, p < 0.01) more than with dobutamine (1.23 to 0.99, −16%, p < 0.05). Although stroke work index increased with both agents, myocardial oxygen consumption remained unchanged with E-1020 but increased with dobutamine (p < 0.05). Consequently, left ventricular mechanical efficiency increased with E-1020 (0.30 to 0.36, p < 0.05) but remained unchanged with dobutamine (0.27 to 0.29, p = NS).Conclusions. The phosphodiesterase inhibitor E-1020 improved arterial-ventricular coupling more than did dobutamine, with a resultant increase in mechanical efficiency. These data were in accordance with the theoretic prediction of the coupling analysis in the diseased human heart