Chawannuch Ruaengsri1, Matthew R Schill2, Timothy S Lancaster2, Ali J Khiabani2, Joshua L Manghelli2, Daniel I Carter2, Jason W Greenberg2, Spencer J Melby2, Richard B Schuessler2, Ralph J Damiano3. 1. Division of Cardiothoracic Surgery, Department of Surgery, Washington University School of Medicine, Barnes-Jewish Hospital, St Louis, Mo; Division of Cardiothoracic Surgery, Department of Surgery, Mahidol University, Ramathibodi Hospital, Bangkok, Thailand. 2. Division of Cardiothoracic Surgery, Department of Surgery, Washington University School of Medicine, Barnes-Jewish Hospital, St Louis, Mo. 3. Division of Cardiothoracic Surgery, Department of Surgery, Washington University School of Medicine, Barnes-Jewish Hospital, St Louis, Mo. Electronic address: damianor@wustl.edu.
Abstract
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.
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.
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Authors: J L Cox; T E Canavan; R B Schuessler; M E Cain; B D Lindsay; C Stone; P K Smith; P B Corr; J P Boineau Journal: J Thorac Cardiovasc Surg Date: 1991-03 Impact factor: 5.209
Authors: Matthew R Schill; Phillip S Cuculich; Christopher M Andrews; Ramya Vijayakumar; Chawannuch Ruaengsri; Matthew C Henn; Timothy S Lancaster; Spencer J Melby; Richard B Schuessler; Yoram Rudy; Ralph J Damiano Journal: J Atr Fibrillation Date: 2020-08-31