Publication: The hemodynamic and atrial electrophysiologic consequences of chronic left atrial volume overload in a controllable canine model
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Issued Date
2018-11-01
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1097685X
00225223
00225223
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2-s2.0-85054745629
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Mahidol University
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SCOPUS
Bibliographic Citation
Journal of Thoracic and Cardiovascular Surgery. Vol.156, No.5 (2018), 1871-1879.e1
Suggested Citation
Chawannuch Ruaengsri, Matthew R. Schill, Timothy S. Lancaster, Ali J. Khiabani, Joshua L. Manghelli, Daniel I. Carter, Jason W. Greenberg, Spencer J. Melby, Richard B. Schuessler, Ralph J. Damiano The hemodynamic and atrial electrophysiologic consequences of chronic left atrial volume overload in a controllable canine model. Journal of Thoracic and Cardiovascular Surgery. Vol.156, No.5 (2018), 1871-1879.e1. doi:10.1016/j.jtcvs.2018.05.078 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/46211
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Title
The hemodynamic and atrial electrophysiologic consequences of chronic left atrial volume overload in a controllable canine model
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Abstract
© 2018 Objective: The purpose of this study was to determine the effects of chronic left atrial volume overload on atrial anatomy, hemodynamics, and electrophysiology using a titratable left ventriculoatrial shunt in a canine model. Methods: Canines (n = 16) underwent implantation of a shunt between the left ventricle and the left atrium. Sham animals (n = 8) underwent a median sternotomy without a shunt. Atrial activation times and effective refractory periods were determined using 250-bipolar epicardial electrodes. Biatrial pressures, systemic pressures, left atrial and left ventricle diameters and volumes, atrial fibrillation inducibility, and durations were recorded at the initial and at 6-month terminal study. Results: Baseline shunt fraction was 46% ± 8%. The left atrial pressure increased from 9.7 ± 3.5 mm Hg to 13.8 ± 4 mm Hg (P <.001). At the terminal study, the left atrial diameter increased from a baseline of 2.9 ± 0.05 cm to 4.1 ± 0.6 cm (P <.001) and left ventricular ejection fraction decreased from 64% ± 1.5% to 54% ± 2.7% (P <.001). Induced atrial fibrillation duration (median, range) was 95 seconds (0-7200) compared with 0 seconds (0-40) in the sham group (P =.02). The total activation time was longer in the shunt group compared with the sham group (72 ± 11 ms vs 62 ± 3 ms, P =.003). The right atrial and not left atrial effective refractory periods were shorter in the shunt compared with the sham group (right atrial effective refractory period: 156 ± 11 ms vs 141 ± 11 ms, P =.005; left atrial effective refractory period: 142 ± 23 ms vs 133 ± 11 ms, P =.35). Conclusions: This canine model of mitral regurgitation reproduced the mechanical and electrical remodeling seen in clinical mitral regurgitation. Left atrial size increased, with a corresponding decrease in left ventricle systolic function, and an increased atrial activation times, lower effective refractory periods, and increased atrial fibrillation inducibility. This model provides a means to understand the remodeling by which mitral regurgitation causes atrial fibrillation.