title: Transition from intravenous epoprostenol to intravenous treprostinil in pulmonary hypertension.
abstract: BACKGROUND
  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 x 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.
authors.affiliation: Pulmonary Hypertension Center, University of Chicago Hospitals, 5841 South Maryland Avenue, MC 2016, Chicago, IL 60637, USA. mgomberg@medicine.bsd.uchicago.edu
authors.forename: Mardi
authors.initials: M
authors.lastname: Gomberg-Maitland
authors.forename: Victor F
authors.initials: VF
authors.lastname: Tapson
authors.forename: Raymond L
authors.initials: RL
authors.lastname: Benza
authors.forename: Vallerie V
authors.initials: VV
authors.lastname: McLaughlin
authors.forename: Abigail
authors.initials: A
authors.lastname: Krichman
authors.forename: Allison C
authors.initials: AC
authors.lastname: Widlitz
authors.forename: Robyn J
authors.initials: RJ
authors.lastname: Barst
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000959:Antihypertensive Agents / Q000008:administration & dosage*; D002648:Child; D018592:Cross-Over Studies; D011464:Epoprostenol / Q000008:administration & dosage* / Q000031:analogs & derivatives*; D017079:Exercise Tolerance / Q000502:physiology; D005260:Female; D006801:Humans; D006976:Hypertension, Pulmonary / Q000188:drug therapy* / Q000503:physiopathology; D007262:Infusions, Intravenous; D008297:Male; D008875:Middle Aged; D016896:Treatment Outcome
chemical_list: D000959:Antihypertensive Agents; D011464:Epoprostenol; C427248:treprostinil