title: Weaning from mechanical cardiac support in patients with idiopathic dilated cardiomyopathy.
abstract: BACKGROUND
  Implantation of mechanical cardiac support systems (MCSS) in patients with idiopathic dilated cardiomyopathy (IDC) may improve cardiac function and allow explantation of the device. We report of long-term effects of ventricular unloading on cardiac function, humoral anti-beta1-adrenoceptor autoantibodies (A-beta1-AABs), and myocardial fibrosis.
  
  
  RESULTS
  Seventeen patients in New York Heart Association functional class IV with nonischemic IDC received MCSS. All had a cardiac index of < 1.6 L x min(-1) x m(-2) of body surface area, a left ventricular ejection fraction (LVEF) of <16%, and a left ventricular internal diameter in diastole (LVIDd) of >68 mm and tested positive for A-beta1-AABs. Echocardiographic evaluation, serum tests for A-beta1-AABs, and histological assessment of myocardial fibrosis were performed before and after MCSS implantation. The mean support duration was 230+/-201 days. Six patients died, four were transplanted, and two are still on MCSS. Five patients with significant cardiac recovery (mean LVIDd, 54+/-2.3 mm; LVEF, 47+/-3.7%) were weaned after 160 to 794 days and are now device free for 51 to 592 days. A-beta1-AABs disappeared gradually during MCSS without increase after weaning; cardiac function and volume density of fibrosis remained normal. Nine patients' cardiac function hardly improved during ventricular unloading.
  
  
  CONCLUSIONS
  Cardiac function can be normalized in selected patients with end-stage IDC by MCSS. The degree of preoperative myocardial fibrosis may be an indicator for outcome; A-beta1-AABs can be used to monitor myocyte recovery. Weaning from MCSS offers an alternative to cardiac transplantation in certain patients.
authors.affiliation: German Heart Institute Berlin, Department of Cardiac and Vascular Surgery, and the Max-Delbrück-Center.
authors.forename: J
authors.initials: J
authors.lastname: Müller
authors.forename: G
authors.initials: G
authors.lastname: Wallukat
authors.forename: Y G
authors.initials: YG
authors.lastname: Weng
authors.forename: M
authors.initials: M
authors.lastname: Dandel
authors.forename: S
authors.initials: S
authors.lastname: Spiegelsberger
authors.forename: S
authors.initials: S
authors.lastname: Semrau
authors.forename: K
authors.initials: K
authors.lastname: Brandes
authors.forename: V
authors.initials: V
authors.lastname: Theodoridis
authors.forename: M
authors.initials: M
authors.lastname: Loebe
authors.forename: R
authors.initials: R
authors.lastname: Meyer
authors.forename: R
authors.initials: R
authors.lastname: Hetzer
mesh_terms: D000328:Adult; D000368:Aged; D001323:Autoantibodies / Q000097:blood; D002311:Cardiomyopathy, Dilated / Q000097:blood / Q000276:immunology / Q000503:physiopathology / Q000628:therapy*; D005500:Follow-Up Studies; D006353:Heart-Assist Devices; D006801:Humans; D008297:Male; D008875:Middle Aged; D018342:Receptors, Adrenergic, beta-1 / Q000097:blood; D013997:Time Factors; D016277:Ventricular Function, Left
chemical_list: D001323:Autoantibodies; D018342:Receptors, Adrenergic, beta-1