title: Interferon-beta treatment eliminates cardiotropic viruses and improves left ventricular function in patients with myocardial persistence of viral genomes and left ventricular dysfunction.
abstract: BACKGROUND
  Viral infections are important causes of myocarditis and may induce cardiac dysfunction and finally lead to dilated cardiomyopathy. We investigated whether interferon (IFN)-beta therapy is safe and may achieve virus clearance and prevent deterioration of left ventricular (LV) function in patients with myocardial virus persistence.
  
  
  RESULTS
  In this phase II study, 22 consecutive patients with persistence of LV dysfunction (history of symptoms, 44+/-27 months) and polymerase chain reaction-proven enteroviral or adenoviral genomes were treated with 18x10(6) IU/week IFN-beta (Beneferon) subcutaneously for 24 weeks. Histological and immunohistological analysis of endomyocardial biopsies was used to characterize myocardial inflammation. LV diameters and ejection fraction were assessed by echocardiography and angiography, respectively. During the treatment period, IFN-beta was well tolerated by all patients. No patient deteriorated. Clearance of viral genomes was observed in 22 of 22 of patients after antiviral therapy. Virus clearance was paralleled by a significant decrease of LV end diastolic and end systolic diameters, decreasing from 59.7+/-11.1 to 56.5+/-10.0 mm (P<0.001) and 43.2+/-13.6 to 39.4+/-12.1 mm (P<0.001), respectively. LV ejection fraction increased from 44.6+/-15.5% to 53.1+/-16.8% (P<0.001).
  
  
  CONCLUSIONS
  A 6 months, IFN-beta treatment was safe in patients with myocardial enteroviral or adenoviral persistence and LV dysfunction and resulted in elimination of viral genomes (22 of 22 patients) and improved LV function (15 of 22 patients).
authors.affiliation: Department of Cardiology and Pneumology, University Hospital Benjamin-Franklin, Freie Universität Berlin, Germany. dcmkuehl@zedat.fu-berlin.de
authors.forename: Uwe
authors.initials: U
authors.lastname: Kühl
authors.forename: Matthias
authors.initials: M
authors.lastname: Pauschinger
authors.forename: Peter Lothar
authors.initials: PL
authors.lastname: Schwimmbeck
authors.forename: Bettina
authors.initials: B
authors.lastname: Seeberg
authors.forename: Conny
authors.initials: C
authors.lastname: Lober
authors.forename: Michel
authors.initials: M
authors.lastname: Noutsias
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Poller
authors.forename: Heinz-Peter
authors.initials: HP
authors.lastname: Schultheiss
mesh_terms: D000256:Adenoviridae / Q000187:drug effects / Q000235:genetics / Q000302:isolation & purification; D000998:Antiviral Agents / Q000627:therapeutic use; D001706:Biopsy; D002306:Cardiac Volume / Q000187:drug effects; D002311:Cardiomyopathy, Dilated / Q000150:complications / Q000188:drug therapy* / Q000821:virology; D002452:Cell Count; D018450:Disease Progression; D004562:Electrocardiography; D004770:Enterovirus / Q000187:drug effects / Q000235:genetics / Q000302:isolation & purification; D005260:Female; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology / Q000821:virology*; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D016899:Interferon-beta / Q000009:adverse effects / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology; D016133:Polymerase Chain Reaction; D013318:Stroke Volume / Q000187:drug effects; D013601:T-Lymphocytes / Q000473:pathology; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000188:drug therapy* / Q000821:virology
chemical_list: D000998:Antiviral Agents; D016899:Interferon-beta