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Published ahead of print on September 8, 2005, doi:10.1164/rccm.200505-766OC
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American Journal of Respiratory and Critical Care Medicine Vol 172. pp. 1586-1589, (2005)
© 2005 American Thoracic Society
doi: 10.1164/rccm.200505-766OC

Original Article

Transition from Intravenous Epoprostenol to Intravenous Treprostinil in Pulmonary Hypertension

Mardi Gomberg-Maitland, Victor F. Tapson, Raymond L. Benza, Vallerie V. McLaughlin, Abigail Krichman, Allison C. Widlitz and Robyn J. Barst

University of Chicago Hospitals, Chicago, Illinois; Duke University Medical Center, Durham, North Carolina; University of Alabama, Birmingham, Alabama; University of Michigan, Ann Arbor, Michigan; and Columbia University College of Physicians and Surgeons, New York, New York

Correspondence and requests for reprints should be addressed to Mardi Gomberg-Maitland, M.D., M.Sc., Pulmonary Hypertension Center, University of Chicago Hospitals, 5841 South Maryland Avenue, MC 2016, Chicago, IL 60637. E-mail: mgomberg{at}medicine.bsd.uchicago.edu

Rationale: Intravenous epoprostenol improves exercise capacity and survival in patients with pulmonary arterial hypertension. The prostacyclin analog treprostinil is also efficacious by subcutaneous infusion, is easier to administer, and has a longer half-life. With the demonstration of bioequivalence between subcutaneous and intravenous treprostinil, intravenous treprostinil may have an overall better risk–benefit profile than intravenous epoprostenol.

Objective: To evaluate the safety and efficacy of transitioning patients with pulmonary arterial hypertension from intravenous epoprostenol to intravenous treprostinil.

Methods: Patients enrolled in a 12-wk prospective open label study were switched from intravenous epoprostenol to intravenous treprostinil over 24 to 48 h. The intravenous treprostinil dose was adjusted to minimize symptoms/side effects.

Results: Thirty-one patients (mean age, 43 yr; 22 women) were enrolled. Twenty-seven patients completed the protocol; 4 patients transitioned back to epoprostenol. Six-minute walk distance (n = 27; baseline, 438 ± 16 m; Week 12, 439 ± 16 m), Naughton-Balke treadmill test time (n = 26; baseline, 582 ± 50 s; Week 12, 622 ± 48 s), functional class, and Borg score were maintained with intravenous treprostinil at Week 12 versus intravenous epoprostenol before transition. At Week 12, mean pulmonary artery pressure increased 4 ± 1 mm Hg (n = 27, p < 0.01), cardiac index decreased 0.4 ± 0.1 L/min/m2 (n = 27, p = 0.01), and pulmonary vascular resistance increased 3 ± 1 Wood units · m2 (n = 26, p < 0.01). No serious adverse events were attributed to treprostinil.

Conclusions: These data suggest that transition from intravenous epoprostenol to intravenous treprostinil is safe and effective; whether the hemodynamic differences associated with intravenous treprostinil are clinically important requires longer follow-up.

Key Words: epoprostenol • intravenous treprostinil • pulmonary arterial hypertension




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