title: Immunosuppressive therapy for active lymphocytic myocarditis: virological and immunologic profile of responders versus nonresponders.
abstract: BACKGROUND
  The beneficial effect of immunosuppressive treatment on myocarditis is still controversial, possibly because the immunologic and virological profile of potential candidates is largely unknown.
  
  
  RESULTS
  Out of 652 biopsied patients, 112 had a histological diagnosis of active lymphocytic myocarditis; 41 of these 112 patients were characterized by progressive heart failure despite conventional therapy and were treated with prednisone and azathioprine for 6 months. All were resubmitted to cardiac catheterization, angiography, and endomyocardial biopsy at 1 and 6 months and followed-up for 1 year. A total of 21 patients responded with prompt improvement in left ventricular ejection fraction from 25.7+/-4.1% to 47.1+/-4.4% and showed evidence of healed myocarditis at control biopsy. Conversely, 20 patients failed to respond and showed a histological evolution toward dilated cardiomyopathy: 12 remained stationary, 3 underwent cardiac transplantation, and 5 died. We retrospectively performed a polymerase chain reaction on frozen endomyocardial tissue for the most common cardiotropic viruses and assessed circulating serum cardiac autoantibodies. Viral genomes were present in biopsy specimens of 17 nonresponders (85%), including enterovirus (n=5), Epstein-Barr virus (n=5) adenovirus (n=4), both adenovirus and enterovirus (n=1), influenza A virus (n=1), parvovirus-B19 (n=1), and in 3 responders, who were all positive for hepatitis C virus. Cardiac autoantibodies were present in 19 responders (90%) and in none of the nonresponders.
  
  
  CONCLUSIONS
  In patients with active lymphocytic myocarditis, those with circulating cardiac autoantibodies and no viral genome in the myocardium are the most likely to benefit from immunosuppression. The beneficial effect of immunosuppression in hepatitis C virus myocarditis suggests a relevant immunomediated component of damage.
authors.affiliation: Department of Cardiology, Catholic University, Rome, Italy. biocard@rm.unicatt.it
authors.forename: Andrea
authors.initials: A
authors.lastname: Frustaci
authors.forename: Cristina
authors.initials: C
authors.lastname: Chimenti
authors.forename: Fiorella
authors.initials: F
authors.lastname: Calabrese
authors.forename: Maurizio
authors.initials: M
authors.lastname: Pieroni
authors.forename: Gaetano
authors.initials: G
authors.lastname: Thiene
authors.forename: Attilio
authors.initials: A
authors.lastname: Maseri
mesh_terms: D000293:Adolescent; D000328:Adult; D001323:Autoantibodies / Q000097:blood; D001379:Azathioprine / Q000627:therapeutic use; D001706:Biopsy; D002316:Cardiotonic Agents / Q000627:therapeutic use; D002908:Chronic Disease; D004452:Echocardiography; D005260:Female; D005500:Follow-Up Studies; D006321:Heart / Q000187:drug effects / Q000821:virology; D006333:Heart Failure / Q000276:immunology / Q000473:pathology / Q000821:virology*; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D008214:Lymphocytes / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009205:Myocarditis / Q000150:complications / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D009206:Myocardium / Q000473:pathology; D011241:Prednisone / Q000627:therapeutic use; D012189:Retrospective Studies; D012720:Severity of Illness Index; D013318:Stroke Volume / Q000187:drug effects; D016896:Treatment Outcome
chemical_list: D001323:Autoantibodies; D002316:Cardiotonic Agents; D007166:Immunosuppressive Agents; D001379:Azathioprine; D011241:Prednisone