title: Atrial septopulmonary bundle of the posterior left atrium provides a substrate for atrial fibrillation initiation in a model of vagally mediated pulmonary vein tachycardia of the structurally normal heart.
abstract: BACKGROUND
  The posterior left atrium (PLA) and pulmonary veins (PVs) have been shown to be critical for atrial fibrillation (AF) initiation. However, the detailed mechanisms of reentry and AF initiation by PV impulses are poorly understood. We hypothesized that PV impulses trigger reentry and AF by undergoing wavebreaks as a result of sink-to-source mismatch at specific PV-PLA transitions along the septopulmonary bundle, where there are changes in thickness and fiber direction.
  
  
  RESULTS
  In 7 Langendorff-perfused sheep hearts AF was initiated by a burst of 6 pulses (CL 80 to 150ms) delivered to the left inferior or right superior PV ostium 100 to 150 ms after the sinus impulse in the presence of 0.5 micromol/L acetylcholine. The exposed septal-PLA endocardial area was mapped with high spatio-temporal resolution (DI-4-ANEPPS, 1000-fr/s) during AF initiation. Isochronal maps for each paced beat preceding AF onset were constructed to localize areas of conduction delay and block. Phase movies allowed the determination of the wavebreak sites at the onset of AF. Thereafter, the PLA myocardial wall thickness was quantified by echocardiography, and the fiber direction in the optical field of view was determined after peeling off the endocardium. Finally, isochrone, phase and conduction velocity maps were superimposed on the corresponding anatomic pictures for each of the 28 episodes of AF initiation. The longest delays of the paced PV impulses, as well as the first wavebreak, occurred at those boundaries along the septopulmonary bundle that showed sharp changes in fiber direction and the largest and most abrupt increase in myocardial thickness.
  
  
  CONCLUSIONS
  Waves propagating from the PVs into the PLA originating from a simulated PV tachycardia triggered reentry and vagally mediated AF by breaking at boundaries along the septopulmonary bundle where abrupt changes in thickness and fiber direction resulted in sink-to-source mismatch and low safety for propagation.
authors.affiliation: SUNY Upstate Medical University (M.K.), Syracuse, NY, USA.
authors.forename: Matthew
authors.initials: M
authors.lastname: Klos
authors.forename: David
authors.initials: D
authors.lastname: Calvo
authors.forename: Masatoshi
authors.initials: M
authors.lastname: Yamazaki
authors.forename: Sharon
authors.initials: S
authors.lastname: Zlochiver
authors.forename: Sergey
authors.initials: S
authors.lastname: Mironov
authors.forename: José-Angel
authors.initials: JA
authors.lastname: Cabrera
authors.forename: Damian
authors.initials: D
authors.lastname: Sanchez-Quintana
authors.forename: José
authors.initials: J
authors.lastname: Jalife
authors.forename: Omer
authors.initials: O
authors.lastname: Berenfeld
authors.forename: Jérôme
authors.initials: J
authors.lastname: Kalifa
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D022062:Electrophysiologic Techniques, Cardiac / Q000379:methods; D006325:Heart Atria / Q000294:innervation*; D006329:Heart Conduction System / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D009412:Nerve Fibers / Q000473:pathology*; D011667:Pulmonary Veins / Q000294:innervation* / Q000473:pathology; D012756:Sheep; D014630:Vagus Nerve / Q000503:physiopathology*