CONGESTIVE HEART FAILLURE Elfects of milrinone on coronary hemodynamics and myocardial energetics in patients with congestive heart failure

To examine the effect of milrinone on myocardial energetics in patients with congestive heart failure, we measured systemic, pulmonary, and coronary hemodynamics in 18 patients before and after intravenous administration of milrinone (125 36 Mg/kg). There was a 45% increase in cardiac index (2.1 ± 0.5 to 3.0 0.6 liters/min/m2; p = .0001), a 39% fall in the pulmonary capillary wedge pressure (28 + 8 to 17 + 8 mm Hg; p = .0001), and a 42% increase in left ventricular external work (3758 ± 1419 to 5340 1598 g-m/min; p = .0001). Both the heart rate-blood pressure product (9624 + 2272 to 9380 2428 mm Hg-beats/min; p = NS) and regional left ventricular myocardial oxygen consumption (7.6 ± 2.9 to 8.1 ± 3.1 ml 02/min; p = NS) were unchanged after milrinone, resulting in a 45% increase in calculated left ventricular external efficiency (p = .004). Although myocardial oxygen consumption did not change, regional great cardiac venous blood flow increased significantly (73 ± 32 to 85 34 ml/min; p .02) as a result of a 30% reduction in regional coronary vascular resistance (1.32 0.99 to 0.93 0.54 mm Hg-min/ml; p = .004), a decrease comparable to the concurrent 37% and 38% falls seen in systemic and pulmonary vascular resistances, respectively. These changes were associated with an 1 1 % fall in the transcoronary arterial-venous oxygen difference (111 + 24 to 99 + 21 ml/02/liter; p = .0001), which is consistent with a primary coronary vasodilator effect of milrinone. Thus, milrinone enhances cardiac performance without a systematic increase in myocardial oxygen consumption, i.e., it increases left ventricular external efficiency. Furthermore, milrinone may improve coronary flow reserve by direct coronary vasodilation and/or reduction in left ventricular diastolic pressure. MILRINONE, a bipyridine compound, causes major hemodynamic improvement in patients with advanced congestive heart failure" 2by a combination of positive inotropic" 3-S and systemic arteriolar vasodilatorl 6 effects. Although a reduction of left ventricular systolic and diastolic pressures might be expected to improve myocardial oxygen balance through reduced myocar-dial work7-9 and improved subendocardial blood flow,'102 respectively, these potential benefits may be From the Charles A. offset by a concurrent increase in oxygen demand resulting from increases in heart rate and contractility.'3 Any net increase in myocardial oxygen demand could be deleterious in patients with limited coronary vasodi-lator reserve due to coronary artery disease or myocar-dial hypertrophy, and might constitute a major limitation to …