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Impact of Ischemic and Valvular Heart Disease on Atrial Excitation:A High‐Resolution Epicardial Mapping Study
Author(s) -
Mouws Elisabeth M. J. P.,
Lanters Eva A. H.,
Teuwen Christophe P.,
Does Lisette J. M. E.,
Kik Charles,
Knops Paul,
Yaksh Ameeta,
Bekkers Jos A.,
Bogers Ad J. J. C.,
Groot Natasja M. S.
Publication year - 2018
Publication title -
journal of the american heart association
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.494
H-Index - 85
ISSN - 2047-9980
DOI - 10.1161/jaha.117.008331
Subject(s) - medicine , cardiology , atrial fibrillation , interatrial septum , pulmonary vein , coronary sinus , sinus rhythm , heart disease , atrium (architecture) , valvular heart disease , left atrium
Background The influence of underlying heart disease or presence of atrial fibrillation ( AF ) on atrial excitation during sinus rhythm ( SR ) is unknown. We investigated atrial activation patterns and total activation times of the entire atrial epicardial surface during SR in patients with ischemic and/or valvular heart disease with or without AF . Methods and Results Intraoperative epicardial mapping (N=128/192 electrodes, interelectrode distances: 2 mm) of the right atrium, Bachmann's bundle ( BB ), left atrioventricular groove, and pulmonary vein area was performed during SR in 253 patients (186 male [74%], age 66±11 years) with ischemic heart disease (N=132, 52%) or ischemic valvular heart disease (N=121, 48%). As expected, SR origin was located at the superior intercaval region of the right atrium in 232 patients (92%). BB activation occurred via 1 wavefront from right‐to‐left (N=163, 64%), from the central part (N=18, 7%), or via multiple wavefronts (N=72, 28%). Left atrioventricular groove activation occurred via (1) BB : N=108, 43%; (2) pulmonary vein area: N=9, 3%; or (3) BB and pulmonary vein area: N=136, 54%; depending on which route had the shortest interatrial conduction time ( P <0.001). Ischemic valvular heart disease patients more often had central BB activation and left atrioventricular groove activation via pulmonary vein area compared with ischemic heart disease patients (N=16 [13%] versus N=2 [2%]; P =0.009 and N=86 [71%] versus N=59 [45%]; P <0.001, respectively). Total activation times were longer in patients with AF ( AF : 136±20 [92–186] ms; no AF : 114±17 [74–156] ms; P <0.001), because of prolongation of right atrium ( P =0.018) and BB conduction times ( P <0.001). Conclusions Atrial excitation during SR is affected by underlying heart disease and AF , resulting in alternative routes for BB and left atrioventricular groove activation and prolongation of total activation times. Knowledge of atrial excitation patterns during  SR and its electropathological variations, as demonstrated in this study, is essential to further unravel the pathogenesis of AF .

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