Author + information
- Received July 25, 1983
- Revision received September 27, 1983
- Accepted October 21, 1983
- Published online April 1, 1984.
- Richard W. Walsh, MD, FACCa,
- Charles B. Porter, MD,
- Mark R. Starling, MD, FACC and
- Robert A. O'Rourke, MD, FACC
- ↵aAddress for reprints: Richard A. Walsh, MD, Department of Medicine/Cardiology, The University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, Texas 78284.
Concern persists about the potential negative inotropic effects of calcium channel blockers in patients with severely depressed myocardial function. Therefore, intravenous diltiazem (100 to 200 ltg/kg per min infusion) was administered for 40 minutes followed by oral diltiazem (90 to 120 mg/8 hours) for 24 hours to patients with advanced congestive heart failure (New York Heart Association class III to IV, mean ejection fraction 26 ± 4 [SD]). Intravenous diltiazem (eight patients) increased cardiac index 20% (2.05 ± 0.8 to 2.47 ± 0.8 liters/min per MZ, p < 0.01), stroke volume index 50% (22 ± 9 to 33 ± 12 MI/M2, p < 0.001) and stroke work index 27% (19 ± 10 to 24 ± 10 g-m/MZ, p < 0.05); while reducing heart rate 23% (97 ± 18 to 75 ± 11 beats/min, p < 0.01), mean arterial pressure 18% (95 ± 13 to 78 ± 7 mm Hg) and pulmonary wedge pressure 34% (29 ± 9 to 19 ± 7 mm Hg), without altering maximal first derivative of left ventricular pressure (dP/dtmax). Oral diltiazem (seven patients) produced equivalent hemodynamic effects. Transient junctional arrhythmias were observed in three of eight patients with intravenous diltiazem and one of seven patients with oral diltiazem.
It is concluded that intravenous and short-term oral diltiazem improve left ventricular performance and reduce myocardial oxygen demand by heart rate and afterload reduction without significantly depressing contractile function in severe congestive heart failure. Caution should be exercised to avoid potential adverse, druginduced electrophysiologic effects in such patients.
This study was supported in part by Grants HL 07350 and IF32 HL6539 from the National Institutes of Health and the Veterans Administration, Bethesda, Maryland. The data were presented in part at the 55th Annual Scientific Sessions of the American Heart Association, Dallas, Texas, November 1982.
- Received July 25, 1983.
- Revision received September 27, 1983.
- Accepted October 21, 1983.
- American College of Cardiology Foundation