title: Transient left ventricular failure following bilateral lung transplantation for pulmonary hypertension.
abstract: BACKGROUND
  Bilateral lung transplantation is an established therapy for end-stage pulmonary hypertension. Its early postoperative outcome may be biased by various complications resulting in unexpected deterioration of the patient in terms of hemodynamics and blood gases.
  
  
  METHODS
  We have reviewed the early postoperative course of patients who underwent bilateral lung transplantation for pulmonary hypertension at our institution and analyzed all available data, especially hemodynamic measurements, echocardiographic documentation and therapeutical strategies, in those cases where cardiac dysfunction was found to be responsible for clinical deterioration.
  
  
  RESULTS
  Three out of 20 lung transplant recipients operated for pulmonary hypertension experienced severe respiratory insufficiency accompanied by hemodynamic decompensation during the first days after surgery. Clinical and laboratory findings together with results of echocardiography and pulmonary artery catheterism helped establish the diagnosis of left ventricular failure. This proved to be transitory, but the response to therapy (inotropic drugs, afterload reduction and eventually prostaglandins) was very variable. Adequately treated, this complication did not preclude the outcome of transplantation by itself.
  
  
  CONCLUSIONS
  Left ventricular failure is a possible complication after lung transplantation for pulmonary hypertension. Echocardiography and pulmonary artery catheterism may be useful adjuvant diagnostic tools, beside routine physical examination, chest X-ray, and laboratory analysis. Therapy of this complication must be adapted individually and may be complex.
authors.affiliation: Department of Cardiothoracic Surgery, University of Vienna, Austria.
authors.forename: T
authors.initials: T
authors.lastname: Bîrsan
authors.forename: A
authors.initials: A
authors.lastname: Kranz
authors.forename: P
authors.initials: P
authors.lastname: Mares
authors.forename: O
authors.initials: O
authors.lastname: Artemiou
authors.forename: S
authors.initials: S
authors.lastname: Taghavi
authors.forename: A
authors.initials: A
authors.lastname: Zuckermann
authors.forename: W
authors.initials: W
authors.lastname: Klepetko
mesh_terms: D000328:Adult; D000527:Alprostadil / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000627:therapeutic use; D002303:Cardiac Output, Low / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000209:etiology*; D002316:Cardiotonic Agents / Q000627:therapeutic use; D002407:Catheterization, Swan-Ganz; D003000:Clonidine / Q000627:therapeutic use; D004280:Dobutamine / Q000627:therapeutic use; D004452:Echocardiography; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000601:surgery*; D016040:Lung Transplantation / Q000009:adverse effects*; D008297:Male; D009543:Nifedipine / Q000627:therapeutic use; D012131:Respiratory Insufficiency / Q000209:etiology; D016896:Treatment Outcome; D014665:Vasodilator Agents / Q000627:therapeutic use; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000209:etiology*
chemical_list: D000959:Antihypertensive Agents; D002316:Cardiotonic Agents; D014665:Vasodilator Agents; D004280:Dobutamine; D000527:Alprostadil; D009543:Nifedipine; D003000:Clonidine