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Comparison of Inhaled Nitric Oxide and Inhaled Aerosolized Prostacyclin in the Evaluation of Heart Transplant Candidates With Elevated Pulmonary Vascular Resistance

Åsa Haraldsson; Niels Kieler-Jensen; Ulla Nathorst-Westfelt; Claes-Håkan Bergh; Sven-Erik Ricksten
Author and Funding Information

Affiliations: From the Department of Anesthesia and Intensive Care, Sahlgrenska University Hospital, Göteborg, Sweden,  From the Department of Cardiology, Sahlgrenska University Hospital, Göteborg, Sweden

Sven-Erik Ricksten, MD, PhD, Department for Anesthesia and Intensive Care, Sahlgrenska University Hospital, S-413 45 Göteborg, Sweden


1998 by the American College of Chest Physicians


Chest. 1998;114(3):780-786. doi:10.1378/chest.114.3.780
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Abstract

Study objective: Elevated pulmonary vascular resistance is a risk factor in heart transplantation and reversibility of high pulmonary vascular resistance is evaluated preoperatively in potential recipients using IV vasodilators or inhaled nitric oxide. Prostacyclin is a potent vasodilator, which when inhaled, has selective pulmonary vasodilatory properties. The aim of this study was to compare the central hemodynamic effects of inhaled prostacyclin with those of inhaled nitric oxide in heart transplant candidates.

Design: A pharmacodynamic comparative study.

Setting: Cardiothoracic ICU or laboratory for diagnostic heart catheterization at a university hospital.

Patients: Ten heart transplant candidates with elevated pulmonary vascular resistance (>200 dynes·s·cm5 and/or a transpulmonary pressure gradient > 10 mm Hg) were included in the study.

Interventions: Nitric oxide (40 ppm) and aerosolized prostacyclin (10 µg/mL) were administered by inhalation in two subsequent 10-min periods. Hemodynamic measurements preceeded and followed inhalation of each agent.

Measurements and results: Both inhaled nitric oxide and inhaled prostacyclin reduced mean pulmonary artery pressure (−7% vs−7%), pulmonary vascular resistance (−43% vs −49%), and the transpulmonary gradient (−44% vs −38%). With inhaled prostacyclin, an 11% increase in cardiac output was observed. Other hemodynamic variables, including the systemic BP, remained unaffected by each of the agents.

Conclusions: Inhaled prostacyclin induces a selective pulmonary vasodilation that is comparable to the effect of inhaled nitric oxide. Major advantages with inhaled prostacyclin are its lack of toxic reactions and easy administration as compared with the potentially toxic nitric oxide requiring more complicated delivery systems.


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