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Bachmann's Bundle and Coronary Sinus Ostial Pacing Accentuate Left Atrial Electrical Dyssynchrony in an Acute Canine Model
Author(s) -
CHOUDHURI INDRAJIT,
KRUM DAVID,
AGARWAL ANUJ,
HARE JOHN,
BELOHLAVEK MAREK,
AHMAD ABDUR,
PINNINTI MAMATHA,
KHANDHERIA BIJOY K.
Publication year - 2014
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/jce.12511
Subject(s) - medicine , cardiology , coronary sinus
Activation Sequence During Atrial Pacing Introduction In patients with intraatrial conduction delay and sinus node (SN) dysfunction, pacing Bachmann's bundle (BBR) and coronary sinus ostium (CSO) has been suggested to achieve atrial resynchronization with potential beneficial impact on atrial fibrillation and diastolic heart failure. Clinical studies have not shown superiority of one approach. Methods and Results We studied electrical activation sequence in an open‐chest acute canine model of normal atrial function in 8 mongrel dogs under general anesthesia. Bipolar plunge electrodes were distributed over the surface of the atria during unifocal pacing, and intracardiac activation sequence was observed. SN pacing resulted in near‐simultaneous activation at midline sites (BBR and CSO); the left atrium (LA) was activated by anterior and posterior wavefronts simultaneously propagating septally to laterally and meeting at the low‐lateral perimitral LA. Right atrial appendage (RAA) pacing created intra‐RA conduction delay and delayed onset of LA activation. Pacing from RAA, CSO, and BBR resulted in nonsimultaneous activation at midline sites and produced an anteroposterior gradient of LA activation. This phenomenon was seen to the greatest degree with midline pacing and shifted the site of latest activation away from the low‐lateral perimitral LA in all pacing configurations except SN pacing. Conclusion Pacing‐induced intra‐LA activation dispersion is enhanced with midline atrial pacing, and secondarily shifts the site of latest activation away from the lateral mitral annulus. Measuring atrial activation times to the low‐lateral perimitral LA can underestimate the degree of atrial dyssynchrony and be misinterpreted as atrial synchrony. Establishing clinical impact requires evaluation of human data.