title: Apoptosis in myocarditis and dilated cardiomyopathy: does enterovirus genome persistence protect from apoptosis? An endomyocardial biopsy study.
abstract: The purpose of this study was to examine the role of apoptosis in myocarditis and dilated cardiomyopathy. Apoptosis is an active energy-consuming mechanism of cell death in several cardiac diseases in different quality and quantity.
  
  
  METHODS
  Endomyocardial biopsies from 81 patients with active (1) and chronic myocarditis (10), dilated cardiomyopathy with inflammation (DCMi; 10) and without inflammation (DCM; 20), with borderline myocarditis and positive PCR for cytomegalovirus-DNA (6), adenovirus-DNA, or enterovirus-RNA (7), and controls (17) were analysed. Apoptosis was detected by using the TUNEL method. The highest rate of apoptotic cardiocytes was found in active and chronic myocarditis. One patient with severe active myocarditis demonstrated 6.15% of apoptotic cardiocytes. Mean percentage of apoptotic cardiocytes in chronic myocarditis was significantly increased (0.61+/-1.25%) when compared to controls (0.01+/-0.04%, P<.05). Particularly, patients with cytomegalovirus-DNA persistence in borderline myocarditis had an elevated rate of apoptosis (0.34+/-0.68%, P<.05). Increased rates of apoptosis were found in borderline myocarditis with adenovirus-DNA persistence (0.20+/-0.57%) and in DCM (0.06+/-0.15%). Only a nonsignificant increase of apoptotic cardiocytes was found in DCMi (0.03+/-0.08%). No apoptosis was found in patients with enteroviral genome persistence in borderline myocarditis.
  
  
  CONCLUSIONS
  Apoptosis of cardiac cells is increased in myocarditis and dilated cardiomyopathy, being highest in severe active myocarditis. Apoptosis thus contributes to cell death in active myocarditis and may play a role not to be neglected in dilated cardiomyopathy. Enteroviruses seem to have anti-apoptotic effects, because no apoptosis at all was found in the myocardium.
authors.affiliation: Department of Internal Medicine and Cardiology, Philipps-University Marburg/Lahn, Baldingerstrasse, D-35033, Marburg, Germany. alter@mailer.uni-marburg.de
authors.forename: P
authors.initials: P
authors.lastname: Alter
authors.forename: M
authors.initials: M
authors.lastname: Jobmann
authors.forename: E
authors.initials: E
authors.lastname: Meyer
authors.forename: S
authors.initials: S
authors.lastname: Pankuweit
authors.forename: B
authors.initials: B
authors.lastname: Maisch
mesh_terms: D017209:Apoptosis / Q000502:physiology; D001706:Biopsy; D002311:Cardiomyopathy, Dilated / Q000235:genetics / Q000473:pathology / Q000503:physiopathology* / Q000821:virology; D002908:Chronic Disease; D004699:Endocardium / Q000473:pathology; D004770:Enterovirus / Q000235:genetics*; D016679:Genome, Viral; D006801:Humans; D009205:Myocarditis / Q000235:genetics / Q000473:pathology / Q000503:physiopathology* / Q000821:virology; D009206:Myocardium / Q000473:pathology