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A Prospective, Randomized, Crossover Study of Inhaled Nitric Oxide and Inhaled Prostacyclin in Heart and Lung Transplant Patients
T. A. Khan, D. Ross, G. Schnickel, S. Bastani, H. Laks*, F. Esmailian*, D. Marelli*, R. Beygui, L. Watson, I. Vartapetian, A. Ardehali*. UCLA, Los Angeles, CA,
BACKGROUND: Inhaled nitric oxide (NO) has been shown to reduce pulmonary vascular resistance in cardiothoracic surgery patients, but is limited by toxicity, the need for special monitoring, and excessive cost. Inhaled prostacyclin (PGI2) also decreases pulmonary hypertension and improves oxygenation, and is relatively free of toxicity, requires no specific monitoring, and is significantly less expensive. Our purpose is to compare NO and PGI2 in a prospective, randomized study of the treatment of pulmonary hypertension and refractory hypoxemia in thoracic transplant patients.
METHODS: Heart and lung transplant patients were randomized to NO or PGI2 as initial treatment, followed by a crossover to the other agent after 6 hrs. Pulmonary vasodilators were initiated in the OR for pulmonary hypertension or refractory hypoxemia. NO was administered at 20ppm, and PGI2 at 20,000ng/mL. Pulmonary artery (PA) pressures, central venous pressure (CVP), PaO2/FiO2 (P/F) ratio, cardiac index (CI), mixed venous blood O2 saturation (SvO2), and systemic blood pressures were recorded at baseline (prior to any therapy) and after 60 min of treatment. After 6 hrs, the drug was stopped for 30 min and parameters were measured in the absence of drug treatment. PGI2 then was started as the crossover drug after NO, or NO as the crossover agent following PGI2. Hemodynamic and oxygenation parameters were recorded 60 min after crossover.
RESULTS: Heart and lung transplant patients (n=17) were randomized by initial treatment (NO, n=10 and PGI2, n=7). The mean age was 58±13 yrs. The study included 12 lung (2 double and 10 single) and 5 heart transplants. NO reduced PA pressures (PA systolic 31±1.1 vs. 45±2.9 mmHg, p=0.0003 vs. baseline; PA diastolic 17±1.1 vs. 24±1.8 mmHg, p=0.0004 vs. baseline; and PA mean 22±1.1 vs. 33±2.2 mmHg, p=0.0001 vs. baseline). PGI2 similarly decreased PA pressures (PA systolic 30±0.97 vs. 45±2.9 mmHg, p=0.0001 vs. baseline; PA diastolic 17±1.1 vs. 24±1.8 mmHg, p=0.0002 vs. baseline; and PA mean 23±0.96 vs. 33±2.2 mmHg, p=0.0002 vs. baseline). Both NO and PGI2 reduced CVP (NO: 10±0.73 vs. 13±0.91 mmHg, p=0.001 vs. baseline; PGI2: 9.2±0.76 vs. 13±0.91 mmHg, p=0.0004 vs. baseline). NO and PGI2 also improved the P/F ratio (NO: 302±28 vs. 206±20, p=0.003 vs. baseline; PGI2: 330±45 vs. 206±20, p=0.007 vs. baseline). There were no significant differences between NO and PGI2 in the reduction of PA pressures and CVP or improvement in P/F ratio. NO increased the CI (3.2±0.19 vs. 2.8±0.15 L/min/m2, p=0.04 vs. baseline) and SvO2 (73±2.0 vs. 68±1.9%, p=0.01 vs. baseline). PGI2 also increased the SvO2 (74±2.6 vs. 68±1.9%, p=0.006 vs. baseline), but the trend toward an increased CI was not significant (3.1±0.22 vs. 2.8±0.15 L/min/m2, p=0.14 vs. baseline). There were no differences in systemic blood pressure with NO or PGI2 (data not shown). No complications of PGI2 delivery or NO toxicity were observed.
CONCLUSIONS: In heart and lung transplant patients, NO and PGI2 similarly reduce PA pressures and CVP as well as improve P/F ratio and SvO2. Overall, PGI2 may offer an alternative to NO in the treatment of pulmonary hypertension and refractory hypoxemia in thoracic transplantation.
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