title: Dedifferentiation of atrial cardiomyocytes in cardiac valve disease: unrelated to atrial fibrillation.
abstract: BACKGROUND
  Valvular heart disease has become an important public health concern. The increased wall stress and underlying disease entity associated with mitral valve disease provide unfavorable circumstances for atrial cardiomyocytes. The expression of the alpha-smooth muscle actin isoform is considered characteristic of cardiomyocyte dedifferentiation (embryonic cardiomyocyte), and cardiomyocyte dedifferentiation may indicate an adaptive state, enabling cardiomyocytes to survive despite unfavorable circumstances.
  
  
  METHODS
  This study comprised 20 adult patients with symptomatic severe mitral valve disease and moderate to severe tricuspid valve disease and without coronary artery disease undergoing valve operations for congestive heart failure. Ten patients had persistent atrial fibrillation and 10 patients had never been in atrial fibrillation by history and electrocardiograms before surgery. Atrial tissues of the right atrial appendage were obtained during surgery.
  
  
  RESULTS
  Immunohistochemical study demonstrated that alpha-smooth muscle actin protein expression was not altered by atrial fibrillation, and alpha-smooth muscle actin protein expression in atrial tissues was higher in patients with sinus rhythm than in those with atrial fibrillation (the percentage of cells that were alpha-smooth muscle actin-positive was 51.5+/-34.9% for right atria from patients in sinus rhythm vs. 16.2+/-15.0% for right atria from patients with atrial fibrillation) (P<.03). Semiquantitation of alpha-smooth muscle actin by immunoblotting of extracts from atrial tissues showed similar findings as in the immunohistochemical observations: that is, atrial fibrillation did not influence the expression of alpha-smooth muscle actin protein. Interstitial fibrosis represented 43.2+/-13.9% of the right atrial tissue in the sinus group, whereas interstitial fibrosis comprised 49.8+/-8.2% of the right atrial tissue in the atrial fibrillation group (P=.320).
  
  
  CONCLUSIONS
  Dedifferentiation of atrial cardiomyocytes occurs in patients with cardiac valve disease, even without atrial fibrillation.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan, ROC. chenmien@ms76.hinet.net <chenmien@ms76.hinet.net>
authors.forename: Mien-Cheng
authors.initials: MC
authors.lastname: Chen
authors.forename: Jen-Ping
authors.initials: JP
authors.lastname: Chang
authors.forename: Shun-Chen
authors.initials: SC
authors.lastname: Huang
authors.forename: Hsueh-Wen
authors.initials: HW
authors.lastname: Chang
authors.forename: Chien-Jen
authors.initials: CJ
authors.lastname: Chen
authors.forename: Cheng-Hsu
authors.initials: CH
authors.lastname: Yang
authors.forename: Wen-Hao
authors.initials: WH
authors.lastname: Liu
mesh_terms: D000199:Actins / Q000378:metabolism*; D000328:Adult; D000368:Aged; D001281:Atrial Fibrillation / Q000378:metabolism / Q000473:pathology*; D015153:Blotting, Western; D004452:Echocardiography; D005260:Female; D006325:Heart Atria / Q000378:metabolism / Q000473:pathology*; D006349:Heart Valve Diseases / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology*
chemical_list: C541116:ACTA2 protein, human; D000199:Actins