George Comas, Steve Xydas, Kyle Glithero, Jonathan Chang, Alexandra Stylianos, Christina Lesch, Eileen Barnwell, Amy Dzierba, Ervant Nishanian, Robert Sladen, Mehmet Oz; Columbia University Medical Center, New York, NY
Objective: To evaluate the acute hemodynamic effects of inhaled prostacyclin (iPGI2) in patients with pulmonary hypertension, right ventricular failure, and/or life-threatening hypoxemia in comparison to patients that were crossed-over to inhaled nitric oxide (iNO) therapy.Methods: A prospective study was conducted on adult patients (> 18 years) with pulmonary hypertension, right heart failure, or hypoxemia who received iPGI2 and iNO therapy between July 1, 2003 to March 1, 2004. Patients were generally started on iPGI2 therapy, with crossover therapy using iNO in patients deemed to non-responders to iPGI2 therapy. Response was defined as 20% improvement in mean pulmonary artery pressure for pulmonary hypertension patients and PaO2/FiO2 for life-threatening hypoxemia patients.
Results: : The participants (n=113) in the study were divided into four categories based on observed clinical outcomes: (1) patients that received iPGI2, experienced a positive clinical response and were continued on iPGI2 therapy for the course of their treatment (n=41); (2) patients who did not respond to iPGI2 and were subsequently crossed over to iNO therapy (n=26); (3) patients who did not respond to iPGI2, were weaned off iPGI2, and whose subsequent course of treatment did not include iNO2 (n=27); (4) patients presenting with pulmonary hypertension, right ventricular failure, amd/or life threatening hypoxemia whose primary treatment was iNO2 therapy (n=19). In patients receiving iPGI2, the ratio of mean pulmonary artery pressure (mPAP) to mean arterial pressure (MAP) decreased from 0.47 (baseline) to 0.38 (6 hours) (P=0.001). In patients receiving iNO, the ratio of mPAP to MAP decreased from 0.46 (baseline) to 0.34 (6 hours) (P=0.16). There were no differences in likelihood of improvement in hemodynamic or respiratory parameters between the subgroups of patients who presented with life threateninghypoxemia versus right heart failure/pulmonary hypertension. Seven patients in the iPGI2 group were weaned off iPGI2 because of systemic hypotension.
Conclusion: Overall, iPGI2 therapy leads to a decrease in mPAP with no overall change in MAP. There seemed to be no benefit to starting patients on iNO2 in the event that they did not respond to iPGI2 as crossover patients generally did not show a positive clinical response when transitioned from iPGI2 to iNO therapy. Hypotension is a potential concern because of the systemic absorption of iPGI2.
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