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Evaluation of the Vasodilator vs Inotropic Effect of Milrinone Using an Animal Model of Left Ventricular Failure: Reversal of Disopyramide Depression of the Myocardium with Milrinone

Division of Cardiology, Department of Medicine, Beth Israel Medical Center, Mount Sinai School of Medicine, City University of New York, New York, New York

Russell Berdoff

Division of Cardiology, Department of Medicine, Beth Israel Medical Center, Mount Sinai School of Medicine, City University of New York, New York, New York

George Spivack

Division of Cardiology, Department of Medicine, Beth Israel Medical Center, Mount Sinai School of Medicine, City University of New York, New York, New York

Azriel Haimowitz

Division of Cardiology, Department of Medicine, Beth Israel Medical Center, Mount Sinai School of Medicine, City University of New York, New York, New York

Steven Tay

Division of Cardiology, Department of Medicine, Beth Israel Medical Center, Mount Sinai School of Medicine, City University of New York, New York, New York

Milrinone (M) has been shown to improve left ventricular (LV) performance in animal and human studies. M has strong vasodilator action, and whether increased LV performance is due primarily to vasodilation or to a direct positive inotropic effect is unclear.

Ten mongrel dogs were studied. Disopyramide caused a significant and sus tained decrease in LV function and was a good model for myocardial depres sion. At equal reduction in systemic vascular resistance (SVR), M reversed this LV depression to a significantly greater degree than nitroprusside (NP) did.

At equal levels of vasodilation, M produced significantly greater improve ment in indices of LV function than NP did in our model of disopyramide- induced LV failure. This suggests that its effect on LV function is not due entirely to afterload reduction, or to reflex sympathetic stimulation, but has a substantial component of direct inotropic stimulation. This study also demon strated a reversal of disopyramide-induced LV dysfunction by M, which may be clinically useful since, as in many antiarrhythmics, myocardial depression may be a limiting factor in its use.

Angiology, Vol. 38, No. 9, 657-662 (1987)
DOI: 10.1177/000331978703800902


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