title: The Electrophysiologic Effects of Acute Mitral Regurgitation in a Canine Model.
abstract: BACKGROUND
  Atrial fibrillation (AF) occurs in 30% of patients with mitral regurgitation referred for surgical intervention. However, the underlying mechanisms in this population are poorly understood. This study examined the effects of acute left atrial volume overload on atrial electrophysiology and the inducibility of AF.
  
  
  METHODS
  Ten canines underwent insertion of an atrioventricular shunt between the left ventricle and left atrium. Shunt and aortic flows were calculated, and the shunt was titrated to a shunt fraction to 40% to 50% of cardiac output. An epicardial plaque with 250 bipolar electrodes was used to determine activation and refractory periods. Biatrial pressures and volumes, conduction times, and atrial fibrillation inducibility were recorded. Data were collected at baseline and 20 minutes after shunt opening and closure.
  
  
  RESULTS
  Mean shunt flow was 1.3 ± 0.5 L/min with a shunt fraction of 43% ± 6% simulating moderate to severe mitral regurgitation. Compared with baseline, left atrial volumes and maximum pressures increased by 27% and 29%, respectively, after shunt opening. Biatrial effective refractory periods did not change significantly after shunt opening or closure. Conduction times increased by 9% with shunt opening and returned to baseline after closure. AF duration or inducibility did not change with shunt opening.
  
  
  CONCLUSIONS
  This canine model of mitral regurgitation demonstrated that acute left atrial volume overload did not increase the inducibility of atrial arrhythmias in contrast with experimental and clinical findings of chronic left atrial volume overload. This suggests that the substrates for AF in patients with mitral regurgitation are a result of chronic remodeling.
authors.affiliation: Division of Cardiothoracic Surgery, Washington University School of Medicine in St. Louis, Barnes-Jewish Hospital, St. Louis, Missouri.
authors.forename: Christopher P
authors.initials: CP
authors.lastname: Lawrance
authors.affiliation: Division of Cardiothoracic Surgery, Washington University School of Medicine in St. Louis, Barnes-Jewish Hospital, St. Louis, Missouri.
authors.forename: Matthew C
authors.initials: MC
authors.lastname: Henn
authors.affiliation: Division of Cardiothoracic Surgery, Washington University School of Medicine in St. Louis, Barnes-Jewish Hospital, St. Louis, Missouri.
authors.forename: Jacob R
authors.initials: JR
authors.lastname: Miller
authors.affiliation: Division of Cardiothoracic Anesthesia, Washington University School of Medicine in St. Louis, Barnes-Jewish Hospital, St. Louis, Missouri.
authors.forename: Michael A
authors.initials: MA
authors.lastname: Kopek
authors.affiliation: Division of Cardiothoracic Surgery, Washington University School of Medicine in St. Louis, Barnes-Jewish Hospital, St. Louis, Missouri.
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Zhang
authors.affiliation: Division of Cardiothoracic Surgery, Washington University School of Medicine in St. Louis, Barnes-Jewish Hospital, St. Louis, Missouri.
authors.forename: Richard B
authors.initials: RB
authors.lastname: Schuessler
authors.affiliation: Division of Cardiothoracic Surgery, Washington University School of Medicine in St. Louis, Barnes-Jewish Hospital, St. Louis, Missouri. Electronic address: damianor@wustl.edu.
authors.forename: Ralph J
authors.initials: RJ
authors.lastname: Damiano
mesh_terms: D000208:Acute Disease; D000818:Animals; D001281:Atrial Fibrillation / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D062185:Atrial Pressure; D004195:Disease Models, Animal; D004285:Dogs; D006329:Heart Conduction System / Q000503:physiopathology; D008944:Mitral Valve Insufficiency / Q000150:complications* / Q000503:physiopathology*