title: Hemodynamic stability after transitioning between endothelin receptor antagonists in patients with pulmonary arterial hypertension.
abstract: BACKGROUND
  Maintenance of a favourable hemodynamic profile is central to therapeutic success in pulmonary arterial hypertension (PAH). There is little information about the safety of transitioning patients between oral therapies for PAH. Endothelin receptor antagonists (ERAs) have been a therapeutic mainstay in PAH, providing benefit to many patients. Three ERAs, bosentan, sitaxsentan, and ambrisentan have been approved for clinical use. Sitaxsentan was voluntarily withdrawn from the market in late 2010 resulting in the need to quickly transition a large number of stable patients.
  
  
  METHODS
  We transitioned 30 clinically stable patients to either ambrisentan or bosentan. Patients underwent a right heart catheterization, measurement of serum N-terminal pro-brain natriuretic peptide (NT-proBNP), and assessment of functional class before changing ERA and again 4 months later. We present a retrospective analysis of those data.
  
  
  RESULTS
  Of the 30 patients transitioned (15 to ambrisentan, 15 to bosentan), 23 had complete hemodynamic data. No significant change was observed in the groups in right atrial, mean pulmonary artery, and pulmonary artery wedge pressures, or in cardiac output, pulmonary vascular resistance, or NT-proBNP levels. There was no change in World Health Organization functional class. Four ambrisentan and 2 bosentan-treated patients reported fluid retention, and 3 bosentan-treated patients had elevation of hepatic transaminases. Two of the patients had a right atrial pressure increase of ≥5 mm Hg, and 4 had pulmonary artery wedge pressure increase of ≥5 mm Hg.
  
  
  CONCLUSIONS
  Transitioning between ERAs in stable PAH patients does not result in hemodynamic or clinical deterioration during the first 4 months posttransition. A minority of patients have developed increased cardiac filling pressures.
authors: Center for Pulmonary Vascular Disease, Jewish General Hospital and McGill University, Montreal, Québec, Canada.
authors: Benjamin
authors: B
authors: Fox
authors: David
authors: D
authors: Langleben
authors: Andrew M
authors: AM
authors: Hirsch
authors: Robert D
authors: RD
authors: Schlesinger
authors: Mark J
authors: MJ
authors: Eisenberg
authors: Dominique
authors: D
authors: Joyal
authors: Fay
authors: F
authors: Blenkhorn
authors: Lyda
authors: L
authors: Lesenko
mesh_terms: D000284:Administration, Oral; D000368:Aged; D000959:Antihypertensive Agents / Q000008:administration & dosage / Q000627:therapeutic use; D000077300:Bosentan; D065128:Endothelin Receptor Antagonists; D065627:Familial Primary Pulmonary Hypertension; D005260:Female; D006801:Humans; D006976:Hypertension, Pulmonary / Q000188:drug therapy* / Q000503:physiopathology; D007555:Isoxazoles / Q000008:administration & dosage / Q000627:therapeutic use*; D008875:Middle Aged; D010666:Phenylpropionates / Q000008:administration & dosage / Q000627:therapeutic use*; D011669:Pulmonary Wedge Pressure / Q000187:drug effects*; D011724:Pyridazines / Q000008:administration & dosage / Q000627:therapeutic use*; D012189:Retrospective Studies; D013449:Sulfonamides / Q000008:administration & dosage / Q000627:therapeutic use*; D013876:Thiophenes / Q000008:administration & dosage / Q000627:therapeutic use*; D016896:Treatment Outcome; D014655:Vascular Resistance / Q000187:drug effects*
chemical_list: D000959:Antihypertensive Agents; D065128:Endothelin Receptor Antagonists; D007555:Isoxazoles; D010666:Phenylpropionates; D011724:Pyridazines; D013449:Sulfonamides; D013876:Thiophenes; C467894:ambrisentan; C106276:sitaxsentan; D000077300:Bosentan