Author + information
- Received December 13, 1983
- Revision received February 6, 1984
- Accepted February 28, 1984
- Published online August 1, 1984.
- ↵*Address for reprints: T. Barry Levine, MD, University of Minnesota Hospitals, Box 79, Mayo Memorial Building, Minneapolis, Minnesota 55455.
The hemodynamic and neurohumoral effects of cummulative intravenous doses of piroximone (MDL 19205), a noncatecholamine, nonglycoside, imidazole derivative with positive inotropic and vasodilating properties, were studied in eight patients with severe congestive heart failure. A dose of 1.25 mg/kg in seven patients and 1.75 mg/kg in one patient increased cardiac index by 75% from 1.96 to 3.41 liters/min per m2 and decreased systemic vascular resistance (−41%), right atrial (−66%) and pulmonary wedge pressure (−35%) (all p < 0.005). Mean arterial pressure was slightly reduced from 78 to 71 mm Hg (p < 0.05) and forearm blood flow increased by 42%. Plasma norepinephrine decreased from 830 to 542 pg/ml (p < 0.05) and plasma renin activity tended to increase. In four patients, dobutamine (15 μg/kg per min) produced a comparable increase in cardiac index (+100%), but less decrease in pulmonary wedge pressure (−21 versus −41%, p < 0.05 versus piroximone) and, unlike piroximone, significantly increased heart rate (+22%, p < 0.05 versus piroximone) and heart rate-blood pressure product (+30%, p < 0.01 versus piroximone). In four other patients, a single intravenous dose of piroximone (1 mg/kg) resulted in a 35% increase in the first derivative of left ventricular pressure (dP/dt) from 796 to 1,068 mm Hg/s (p < 0.01). Thus, piroximone is a potent inotropic agent with an acute hemodynamic profile that may be more favorable than that of dobutamine. Because the drug is orally absorbed, clinical trials of chronic efficacy are indicated.
- Received December 13, 1983.
- Revision received February 6, 1984.
- Accepted February 28, 1984.
- American College of Cardiology Foundation