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Background: Cardiac magnetic resonance (CMR)-guided catheter ablation of the cavotricuspid isthmus (CTI) has been proven feasible, but determinants of local electrogram (EGM) voltage drops during radiofrequency (RF) applications are unknown. Objective: The purpose of this study was to investigate local atrial bipolar EGM voltage drops and the association with delivered RF energy and anatomical information derived from peri-procedural CMR imaging. Methods: In consecutive patients undergoing CMR-guided CTI ablation procedures, relative EGM voltage drops for RF applications ≥20 seconds were calculated. Pre- and post-ablation CMR imaging was performed. Associations of relative EGM voltage drops with patient characteristics, delivered RF energy, and CTI anatomy were analyzed. Results: In total, 216 RF applications were evaluated from 12 patients (18 ± 5 applications/patient). EGM voltage amplitude at baseline was significantly higher in the group with the strongest relative EGM voltage drop (P < .05), whereas RF ablation settings (duration, power, temperature) and lesion characteristics (impedance drop, slope of impedance drop) did not differ. The EGM voltage amplitude at baseline (P < .001), left ventricular ejection fraction (LVEF) (P = .020), right atrium volume index (RAVI) (P = .027), and CTI line length (P = .026) showed the strongest association with relative EGM voltage drop. Four of 12 patients (33%) underwent a re-do procedure, 2 patients showed a regional late reconnection, which could be visually identified in the T2-weighted images (T2WI) of the index procedure. Conclusion: Local EGM voltage amplitude, LVEF, RAVI, and CTI length are associated with relative EGM voltage drop during CMR-guided CTI ablation. Post-ablation CMR imaging during the index procedure may help to identify areas of late reconnection.

Summary: After myocardial infarction, remote ventricular remodeling and atrial cardiomyopathy progress despite successful revascularization. In a rat model of ventricular ischemia/reperfusion, pharmacological inhibition of the protease activity of cathepsin A initiated at the time point of reperfusion prevented extracellular matrix remodeling in the atrium and the ventricle remote from the infarcted area. This scenario was associated with preservation of more viable ventricular myocardium and the prevention of an arrhythmogenic and functional substrate for atrial fibrillation. Remote ventricular extracellular matrix remodeling and atrial cardiomyopathy may represent a promising target for pharmacological atrial fibrillation upstream therapy following myocardial infarction. Key Words: atrial cardiomyopathy, atrial fibrillation, ischemia/reperfusion, myocardial infarction, remote remodeling