TY - JOUR
T1 - The hemodynamic and atrial electrophysiologic consequences of chronic left atrial volume overload in a controllable canine model
AU - Ruaengsri, Chawannuch
AU - Schill, Matthew R.
AU - Lancaster, Timothy S.
AU - Khiabani, Ali J.
AU - Manghelli, Joshua L.
AU - Carter, Daniel I.
AU - Greenberg, Jason W.
AU - Melby, Spencer J.
AU - Schuessler, Richard B.
AU - Damiano, Ralph J.
N1 - Funding Information:
R.J.D. is a speaker for AtriCure, Inc, LivaNova, Inc, CryoLife, Inc, and Edwards Lifesciences, Inc, and a consultant for Medtronic, Inc. He has received research funding and educational grants from AtriCure, Inc, and Edwards Lifesciences, Inc. All other authors have nothing to disclose with regard to commercial support.
Funding Information:
Sources of Funding: M.R.S., T.S.L., A.J.K., and J.L.M. are supported by T32-HL007776. R.L.D. Jr, and R.B.S. are supported by R01-HL032257 and the Barnes Jewish Foundation. S.J.M. is supported by Veterans Administrations Merit I01 CX001526.
Publisher Copyright:
© 2018
PY - 2018/11
Y1 - 2018/11
N2 - 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.
AB - 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.
KW - atrial fibrillation
KW - mitral regurgitation
UR - http://www.scopus.com/inward/record.url?scp=85054745629&partnerID=8YFLogxK
U2 - 10.1016/j.jtcvs.2018.05.078
DO - 10.1016/j.jtcvs.2018.05.078
M3 - Article
C2 - 30336917
AN - SCOPUS:85054745629
VL - 156
SP - 1871-1879.e1
JO - Journal of Thoracic and Cardiovascular Surgery
JF - Journal of Thoracic and Cardiovascular Surgery
SN - 0022-5223
IS - 5
ER -