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An Acute Model for Atrial Fibrillation Arising from a Peripheral Atrial Site: Evidence for Primary and Secondary Triggers
Author(s) -
SCHERLAG BENJAMIN J.,
HOU YINGLONG,
LIN JIAXIONG,
LU ZHIBING,
ZACHARIAS SONI,
DASARI TARUN,
NIU GUODONG,
GHIAS MUHAMMAD,
PATTERSON EUGENE,
JACKMAN WARREN M.,
LAZZARA RALPH,
PO SUNNY S.
Publication year - 2008
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.2007.01087.x
Subject(s) - medicine , atrial fibrillation , pulmonary vein , acetylcholine , cardiology , clamp , atrial appendage , anesthesia , atrium (architecture) , thoracotomy , clamping , sinus rhythm , mechanical engineering , engineering
Background: We previously demonstrated that acetylcholine (Ach) injected into cardiac ganglionated plexi (GP) causes pulmonary vein (PV) ectopy initiating atrial fibrillation (AF). Objective: To determine the effects of Ach applied at non‐PV sites. Methods: Overall, 54 dogs were anesthetized with Na‐pentobarbital. A right and left thoracotomy allowed the placement of multielectrode catheters to record from the superior PVs, mid portion of the atrium and the atrial appendages (AA). A monophasic action potential (MAP) was recorded from the AA. Ach (1, 10, 100 mM) was applied sequentially to the AA. Results: In 19 of 26 animals, Ach 100 mM on the right (n = 15) or left (n = 4) AA induced focal, sustained AF (≥10 minutes) with rapid regular firing (cycle length = 37 ± 7 ms) at the AA. A clamp with teeth placed across the AA caused arrest in the AA. However, AF was sustained only when PV sites adjacent to the GP manifested complex fractionated atrial electrograms (CFAE). Clamping the AA prior to Ach (100 mM) application resulted in focal AF arising at the PVs but not at the AA. When a clamp without teeth was applied prior to Ach application, no AF at either AA or PV site could be induced. Conclusion: Isolation of the focal AF at the AA (primary trigger) by clamping caused cessation of activity in the AA, but AF continued due to secondary triggers arising from PVs. The possible mechanism(s) responsible for these findings are discussed, and various ancillary experiments (n = 28) were added to help elucidate mechanisms.