title: Atrial remodeling is directly related to end-diastolic left ventricular pressure in a mouse model of ventricular pressure overload.
abstract: BACKGROUND
  Atrial fibrillation (AF) is often preceded by underlying cardiac diseases causing ventricular pressure overload.
  
  
  OBJECTIVE
  It was our aim to investigate the progression of atrial remodeling in a small animal model of ventricular pressure overload and its association with induction of AF.
  
  
  METHODS
  Male mice were subjected to transverse aortic constriction (TAC) or sham operation. After four or eight weeks, echocardiographic measurements and hemodynamic measurements were made and AF induction was tested. The hearts were either fixed in formalin or ventricles and atria were separated, weighed and snap-frozen for RNA analysis.
  
  
  RESULTS
  Four weeks of pressure overload induced ventricular hypertrophy and minor changes in the atria. After eight weeks a significant reduction in left ventricular function occurred, associated with significant atrial remodeling including increased atrial weight, a trend towards an increased left atrial cell diameter, atrial dilatation and increased expression of markers of hypertrophy and inflammation. Histologically, no fibrosis was found in the left atrium. But atrial gene expression related to fibrosis was increased. Minor changes related to electrical remodeling were observed. AF inducibility was not different between the groups. Left ventricular end diastolic pressures were increased and correlated with the severity of atrial remodeling but not with AF induction.
  
  
  CONCLUSIONS
  Permanent ventricular pressure overload by TAC induced atrial remodeling, including hypertrophy, dilatation and inflammation. The extent of atrial remodeling was directly related to LVEDP and not duration of TAC per se.
authors.affiliation: Department of Cardiology, University of Groningen, University Medical Center Groningen, The Netherlands ; The Interuniversity Cardiology Institute Netherlands, Utrecht, The Netherlands.
authors.forename: Anne Margreet
authors.initials: AM
authors.lastname: De Jong
authors.forename: Isabelle C
authors.initials: IC
authors.lastname: Van Gelder
authors.forename: Inge
authors.initials: I
authors.lastname: Vreeswijk-Baudoin
authors.forename: Megan V
authors.initials: MV
authors.lastname: Cannon
authors.forename: Wiek H
authors.initials: WH
authors.lastname: Van Gilst
authors.forename: Alexander H
authors.initials: AH
authors.lastname: Maass
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000209:etiology / Q000503:physiopathology*; D064752:Atrial Remodeling; D003971:Diastole; D005355:Fibrosis; D015870:Gene Expression; D006325:Heart Atria / Q000378:metabolism; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism; D051672:Shal Potassium Channels / Q000378:metabolism; D016277:Ventricular Function, Left; D017725:Ventricular Pressure; D020257:Ventricular Remodeling
chemical_list: D024661:Potassium Channels, Inwardly Rectifying; D051672:Shal Potassium Channels
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