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Published ahead of print on September 8, 2005, doi:10.1164/rccm.200505-766OC

Am. J. Respir. Crit. Care Med., Volume 172, Number 12, December 2005, 1586-1589

A more recent version of this article appeared on December 15, 2005
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Submitted on May 16, 2005
Accepted on September 6, 2005

Transition from Intravenous Epoprostenol to Intravenous Treprostinil in Pulmonary Hypertension

Mardi Gomberg-Maitland1*, Victor F Tapson2, Raymond L Benza3, Vallerie V McLaughlin4, Abigail Krichman2, Allison C Widlitz5, and Robyn J Barst5

1 Department of Cardiology, The University of Chicago Hospitals, Chicago, Illinois, USA, 2 Department of Pulmonary Medicine, Duke University Medical Center, Durham, North Carolina, USA, 3 Department of Cardiology, The University of Alabama, Birmingham, Alabama, USA, 4 Department of Cardiology, The University of Michigan, Ann Arbor, Michigan, USA, 5 Department of Pediatric Cardiology, Columbia University College of Physicians and Surgeons, New York, New York, USA

* To whom correspondence should be addressed. E-mail: mgomberg{at}medicine.bsd.uchicago.edu.

Rationale: Intravenous epoprostenol improves exercise capacity and survival in pulmonary arterial hypertension patients. The prostacyclin analogue treprostinil is also efficacious by subcutaneous infusion, is easier to administer, and has a longer half-life. With recent 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 pulmonary arterial hypertension patients from intravenous epoprostenol to intravenous treprostinil. Methods: Patients enrolled in a 12 week prospective open label study were switched from intravenous epoprostenol to intravenous treprostinil over 24-48 hours. The intravenous treprostinil dose was adjusted to minimize symptoms/side effects. Results: 31 patients (mean age 43 yrs; 22 women) were enrolled. 27 patients completed the protocol; four patients transitioned back to epoprostenol. Six-minute walk distance (n=27; baseline: 438+/-16m; week 12: 439 +/-16m), Naughton-Balke treadmill test time (n=26; baseline:658+/-75 sec; week 12: 707+/-54 sec), functional class, and Borg score were maintained with intravenous treprostinil at week 12 vs. intravenous epoprostenol before transition. At week 12, mean pulmonary artery pressure increased 4 +/- 1 mmHg (n=27, p <0.01), cardiac index decreased 0.4 +/- 0.1 L/m/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 of intravenous treprostinil are clinically important requires longer follow-up.
Key words: pulmonary arterial hypertension, intravenous treprostinil, epoprostenol




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