title: Anatomically determined functional conduction delay in the posterior left atrium relationship to structural heart disease.
abstract: OBJECTIVE
  This study sought to characterize the conduction properties of the posterior left atrium (PLA) in patients with different forms of structural heart disease undergoing cardiac surgery.
  
  
  BACKGROUND
  The PLA plays an important role in the initiation and maintenance of atrial fibrillation.
  
  
  METHODS
  This study included 34 patients having elective cardiac surgery. There were 4 groups of patients: normal left ventricular (LV) function (coronary artery bypass grafting [CABG]); severe LV dysfunction (LVF/CABG); severe mitral regurgitation (MR); severe aortic stenosis (AS). Epicardial mapping of the PLA was performed in sinus rhythm and during differential pacing. Activation patterns, regional conduction velocity (CV), conduction heterogeneity, anisotropy, and total plaque activation time (TAT) were assessed.
  
  
  RESULTS
  Left atrial size in patients with LVF/CABG (47 +/- 7 mm) and MR (54 +/- 6 mm) was larger than patients with CABG (39 +/- 7 mm) and AS (42 +/- 6 mm; p < 0.05). During pacing, all patients developed a vertical line of conduction delay running between the pulmonary veins. The extent of this conduction delay was greater in patients with LVF/CABG and MR than patients with AS and CABG (p < 0.05). Conduction heterogeneity, anisotropy, and TAT were greater in patients with LVF/CABG and MR than patients with CABG (p < 0.05). These changes resulted in circuitous wave front propagation.
  
  
  CONCLUSIONS
  There is a line of functional conduction delay in a consistent anatomical location in the PLA in patients with structural heart disease. This is most marked in conditions associated with significant chronic atrial enlargement and leads to circuitous wave front propagation, suggesting a potential role in arrhythmogenesis.
authors.affiliation: Department of Cardiology, Royal Melbourne Hospital, and the University of Melbourne, Melbourne, Australia.
authors.forename: Kurt C
authors.initials: KC
authors.lastname: Roberts-Thomson
authors.forename: Irene H
authors.initials: IH
authors.lastname: Stevenson
authors.forename: Peter M
authors.initials: PM
authors.lastname: Kistler
authors.forename: Haris M
authors.initials: HM
authors.lastname: Haqqani
authors.forename: John C
authors.initials: JC
authors.lastname: Goldblatt
authors.forename: Prashanthan
authors.initials: P
authors.lastname: Sanders
authors.forename: Jonathan M
authors.initials: JM
authors.lastname: Kalman
mesh_terms: D000368:Aged; D001281:Atrial Fibrillation / Q000209:etiology*; D003324:Coronary Artery Disease / Q000150:complications* / Q000503:physiopathology* / Q000601:surgery; D004594:Electrophysiology; D005260:Female; D006325:Heart Atria / Q000503:physiopathology*; D006329:Heart Conduction System / Q000503:physiopathology*; D006349:Heart Valve Diseases / Q000150:complications* / Q000503:physiopathology* / Q000601:surgery; D006801:Humans; D008297:Male; D008875:Middle Aged; D013997:Time Factors