title: Acute improved hemodynamics following inhaled iloprost in chronic thromboembolic pulmonary hypertension.
abstract: BACKGROUND
  Chronic thromboembolic pulmonary hypertension (CTEPH) is a potential consequence to pulmonary embolism. The histologic picture is similar to idiopathic pulmonary hypertension (IPAH) suggesting that vascular remodeling also contributes to CTEPH. The treatment of choice is pulmonary endarterectomy. However, this treatment option is not adequate for all patients with CTEPH. Currently, no data exist on standard vasodilative therapy for CTEPH. Intravenous and oral prostanoids, both well-known vasodilators in IPAH, have been used with promising results, whereas the same has not been consistently observed for inhaled iloprost.
  
  
  OBJECTIVE
  In this study, we examined acute hemodynamic effects of inhaled iloprost in patients with CTEPH.
  
  
  METHODS
  In a prospective study, right heart catheterization was performed in 20 patients (mean age 56 years, New York Heart Association class II-IV) at the time of diagnosis of CTEPH. Pulmonary vascular resistance (PVR), mean pulmonary arterial pressure (mPAP), cardiac output (CO), mean systemic arterial pressure (MAP) and oxygen partial pressure (PaO(2)) were obtained before and 20 min after inhaling 5 mug iloprost. Subsequently, all patients were evaluated for pulmonary endarterectomy. Six patients were eligible for surgery.
  
  
  RESULTS
  Significant changes in pulmonary and systemic hemodynamics were observed following the inhalation of iloprost (before to after inhalation): PVR: 1,057 +/- 404.3 to 821.3 +/- 294.3 dyn.s.cm(-5), p < 0.0001; mPAP: 50.55 +/- 8.43 to 45.75 +/- 8.09 mm Hg, p = 0.0002; CO: 3.66 +/- 1.05 to 4.05 +/- 0.91 l/min, p < 0.0106. MAP and PaO(2) decreased significantly (MAP: 94.15 +/- 11.58 to 89.45 +/- 14.29 mm Hg, p = 0.0111; PaO(2): 7.33 +/- 1.17 to 6.64 +/- 1.25 kPa, p = 0.0260).
  
  
  CONCLUSIONS
  Hemodynamic changes directly following inhalation of iloprost suggest a significant contribution of a reversible component of vasoconstriction to pulmonary arterial hypertension in patients with CTEPH.
authors.affiliation: Department of Respiratory Medicine, University of Leipzig, Leipzig, Germany.
authors.forename: Sabine
authors.initials: S
authors.lastname: Krug
authors.forename: Stefan
authors.initials: S
authors.lastname: Hammerschmidt
authors.forename: Hans
authors.initials: H
authors.lastname: Pankau
authors.forename: Hubert
authors.initials: H
authors.lastname: Wirtz
authors.forename: Hans-Jürgen
authors.initials: HJ
authors.lastname: Seyfarth
mesh_terms: D000280:Administration, Inhalation; D000328:Adult; D000368:Aged; D005260:Female; D006439:Hemodynamics; D006801:Humans; D006976:Hypertension, Pulmonary / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D016285:Iloprost / Q000627:therapeutic use*; D008168:Lung / Q000098:blood supply; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011655:Pulmonary Embolism / Q000150:complications*; D014661:Vasoconstriction; D014665:Vasodilator Agents / Q000627:therapeutic use*