Author + information
- Received October 28, 1991
- Revision received January 6, 1992
- Accepted January 30, 1992
- Published online July 1, 1992.
- Marc J. Semigran, MD,
- Constantine N. Aroney, MBBS,
- Howard C. Herrmann, MD, FACC,
- G.William Dec Jr., MD, FACC,
- Charles A. Boucher, MD, FACC and
- Michael A. Fifer, MD, FACC∗,1
- ↵∗Address for correspondence: Michael A. Fifer, MD, Cardiac Unit, Massachusetts General Hospital, WACC 478, 15 Farkman Street, Boston, Massachusetts 02114.
Atrial natriuretic peptide alters left ventricular performance in patients with heart failure. To assess the direct effects of this hormone on myocardial function, its actions were compared with those of the pure vasodilator nitroprusside in 10 patients with heart failure. Simultaneous left ventricular micromanometer pressure and radionuclide volume were obtained during a baseline period, during nitroprusside infusion, during a second baseline period and during atrial natriuretic peptide infusion. The baseline end-systolic pressure-volume relation was generated in nine patients from pressure-volume loops obtained during the two baseline periods and during afterload reduction with nitroprusside.
Mean arterial pressure decreased with atrial natriuretic peptide (89 ± 3 to 80 ± 2 mm Hg, p < 0.05) and by a greater amount with nitroprusside (90 ± 4 to 73 ± 3 mm Hg, p < 0.05). Left ventricular end-diastolic pressure also decreased with atrial natriuretic peptide (24 ± 2 to 16 ± 3 mm Hg, p < 0.05) and by a greater amount with nitroprusside (24 ± 2 to 13 ± 3 mm Hg, p < 0.05). Cardiac index increased during infusion of each agent from 2.0 ± 0.2 to 2.4 ± 0.2 liters/min per m2(p < 0.01). Heart rate increased slightly with nitroprusside but did not change with atrial natriuretic peptide. Peak positive first derivative of left ventricular pressure (dP/dt), ejection fraction and stroke work index were unchanged by either agent. The relation between end-systolic pressure and volume during atrial natriuretic peptide infusion was shifted slightly leftward from the baseline value in four patients, slightly rightward in four and not at all in one patient, indicating no consistent inotropic effect. Both agents shortened the time constant of isovolumetric relaxation calculated by the logarithmic method, but only nitroprusside shortened the time constant calculated by the derivative method. Peak filling rate was unchanged from baseline with either agent. Atrial natriuretic peptide did not shift the end-diastolic pressure-volume point away from the relation constructed from baseline and nitroprusside points.
It is concluded that atrial natriuretic peptide has no direct effect on myocardial contractile or diastolic function in patients with heart failure.
↵1 Dr. Fifer's tenure as a Clinician-Scientist of the American Heart Association, Dallas, Texas.
☆ This study was performed during Dr. Aroney's tenure as an Overseas Clinical Fellow of the National Heart Foundation of Australia, Canberra, ACT, Australia.
☆☆ This work was supported in part by a grant from Wyeth-Ayerst Laboratories, Philadelphia, Pennsylvania.
- Received October 28, 1991.
- Revision received January 6, 1992.
- Accepted January 30, 1992.