Basic/Translational Science -> Computer Modeling/Simulation D-PO03 - Poster Session III (ID 48) Poster

D-PO03-018 - Immuno-electrophysiological Mechanisms Of Atrial Arrhythmias Originating In Recipient Tissue In Patients After Orthotopic Heart Transplantation (ID 272)


Background: Functional inter-atrial connections (IACs) between recipient and donor atria after orthotopic heart transplantation (OHT) are poorly understood.
Objective: To determine if immune mismatch is predictive of IACs and whether computational simulation of IACs predicts the behavior of conduction paths for recipient to donor arrhythmic propagation.
Methods: We reviewed the charts of 40 OHT recipients who underwent catheter ablation for atrial tachyarrhythmias from 2005 to 2019. The Courtemanche-Ramirez-Nattel formalism was used to simulate the human atrial action potential. Mild remodeling was applied to the recipient atrial tissue. Bicaval and biatrial anastomosis (AST) with IACs widths of 1 to 6 mm were simulated in a realistic 3D model of the human atria with a conduction delay of 100 ms across the IAC.
Results: Functional IACs were found in 9/40 patients (21%) (right sided in 5, left sided in 4). In patients with IACs, tachycardia originated in recipient atrium with propagation to donor atrium. Three patients with left sided IACs had AF. In patients without IACs, tachycardia originated in the donor atrium. Time from OHT to IAC ablation was 10.4±6.6 (range 0.25-19) years. Donor specific antibodies (DSAB) were not present in patients with IACs, but were present in 45% of patients without IACs, p=0.03. In simulations, IAC width of <2 mm resulted in conduction failure. When the cycle length (CL) of a recipient tachycardia exceeded the donor’s tissue refractory period, stable 1:1 and unstable 2:1 recipient to donor conduction occurred, depending on IAC location. When the tachycardia’s CL was close to the refractory period of the recipient tissue (150 ms), reentrant activity arose with 2:1 to 3:1 recipient to donor conduction.
Conclusion: IACs are found in 21% of OHT patients presenting with atrial tachyarrhythmias and can manifest early after OHT. Patients with IAC frequently present with focal atrial tachycardias or AF originating from the recipient atria with propagation to the donor atria via IACs. Immune privilege characterized by absence of DSAB may facilitate the formation of electrically functional, and dynamic IACs.