Author + information
- Received January 28, 1994
- Revision received April 14, 1994
- Accepted April 26, 1994
- Published online October 1, 1994.
- Marc J. Semigran, MD,
- Barbara A. Cockrill, MD,
- Robert Kacmarek, PhD,
- B.Taylor Thompson, MD,
- Warren M. Zapol, MD,
- G.William Dec, MD, FACC and
- Michael A. Fifer, MD, FACC∗
- ↵∗Address for correspondence: Dr. Michael A. Fifer, Cardiac Unit, Massachusetts General Hospital, WACC 478, 15 Parkman Street, Boston, Massachusetts 02114.
Objectives. This study was performed to assess the utility of inhaled nitric oxide as a selective pulmonary vasodilator in patients with seven chronic heart failure and to compare its hemodynamic effects with those of nitroprusside, a nonselective vasodilator.
Background. Preoperative pulmonary vascular resistance is a predictor of right heart failure after heart transplantation. Nonselective vasodilators administered preoperatively to assess the reversibility of pulmonary vasoconstriction cause systemic hypotension, limiting their utility.
Methods. Systemic and pulmonary hemodynamic measurements were made at baseline, during oxygen inhalation and with the addition of graded doses of inhaled nitric oxide or intravenous nitroprusside in 16 patients with New York Heart Association class III or IV heart failure referred for heart transplantation.
Results. Pulmonary vascular resistance decreased to a greater extent with 80 ppm nitric oxide (mean ± SEM 256 ± 41 to 139 ± 14 dynes · s · cm−5) than with the maximally tolerated dose of nitroprasside (264 ± 49 to 169 ± 30 dynes · s · cm−5, p < 0.05, nitric oxide vs. nitroprusside). Pulmonary capillary wedge pressure increased with 80 ppm nitric oxide (26 ± 2 to 32 ± 2 mm Hg, p < 0.05). Mean arterial pressure did not change with nitric oxide but decreased with nitroprusside. Seven of the 16 patients, including 1 patient who did not have an adequate decrease in pulmonary vascular resistance with nitroprasside but did with nitric oxide, have undergone successful heart transplantation.
Conclusions. Inhaled nitric oxide is a selective pulmonary vasodilator in patients with pulmonary hypertension due to left heart failure and may identify patients with reversible pulmonary vasoconstriction in whom agents such as nitroprusside cause systemic hypotension. Inhaled nitric oxide causes an increase in left ventricular filling pressure by an unknown mechanism.
☆ This study was supported in part by Grant HL43297 to Dr. Zapol from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. It was presented in part at the 42nd Annual Scientific Session of the American College of Cardiology, Anaheim, California, March, 1993.
- Received January 28, 1994.
- Revision received April 14, 1994.
- Accepted April 26, 1994.