title: Prostanoids but not oral therapies improve right ventricular function in pulmonary arterial hypertension.
abstract: OBJECTIVE
  This study hypothesized that right ventricular stroke work index (RVSWI) and pulmonary capacitance (PC) would increase after treatment for pulmonary arterial hypertension (PAH) and that prostanoids would have a stronger effect than oral therapy.
  
  
  BACKGROUND
  Right ventricular (RV) function is a major determinant of outcome in patients with PAH. Little is known about the response of RV function or its hemodynamic determinants to PAH-specific therapy.
  
  
  METHODS
  We reviewed hemodynamic and health data on 58 patients from an institutional registry and analyzed changes in hemodynamic status between diagnostic and first repeat catheterization after initiation of therapy for PAH.
  
  
  RESULTS
  The RVSWI and PC increased significantly after therapy (p = 0.007 and p = 0.02, respectively). Improvement in RV function was limited to patients treated with prostanoid-only therapy (p = 0.04); no improvement was found in patients treated with oral therapy (p = 0.25). Patients with the poorest baseline RV function (lowest tertile) had the greatest improvement post-therapy (p = 0.005 and p < 0.001 vs. middle and highest tertiles). The major determinant of RVSWI was change in stroke volume (r(s) = 0.54, p < 0.001), indicating RVSWI is an accurate reflection of RV function.
  
  
  CONCLUSIONS
  Right ventricular function improves after therapy with regimens including prostanoids but not oral-only regimens. Patients with the least compensated RV function at diagnosis might derive the most benefit from therapy. Larger studies are needed to determine whether changes in RVSWI after therapy are associated with outcomes.
authors.affiliation: Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee. Electronic address: evan.brittain@vanderbilt.edu.
authors.forename: Evan L
authors.initials: EL
authors.lastname: Brittain
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
authors.forename: Meredith E
authors.initials: ME
authors.lastname: Pugh
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
authors.forename: Lisa A
authors.initials: LA
authors.lastname: Wheeler
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
authors.forename: Ivan M
authors.initials: IM
authors.lastname: Robbins
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
authors.forename: James E
authors.initials: JE
authors.lastname: Loyd
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
authors.forename: John H
authors.initials: JH
authors.lastname: Newman
authors.affiliation: Department of Pediatrics, Vanderbilt Children's Hospital, Nashville, Tennessee.
authors.forename: Eric D
authors.initials: ED
authors.lastname: Austin
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, Tennessee.
authors.forename: Anna R
authors.initials: AR
authors.lastname: Hemnes
mesh_terms: D000284:Administration, Oral; D000328:Adult; D000959:Antihypertensive Agents / Q000008:administration & dosage*; D065627:Familial Primary Pulmonary Hypertension; D005260:Female; D006801:Humans; D006976:Hypertension, Pulmonary / Q000188:drug therapy* / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D011453:Prostaglandins / Q000494:pharmacology / Q000627:therapeutic use*; D012189:Retrospective Studies; D016278:Ventricular Function, Right / Q000187:drug effects*
chemical_list: D000959:Antihypertensive Agents; D011453:Prostaglandins