Orthotopic heart transplantation (OHT) creates a surgically altered electrophysiologic substrate defined by the suture-line scar, residual recipient atrial tissue, and autonomic denervation, that fundamentally alters the mechanisms, presentation, and management of atrial tachyarrhythmias. This narrative review synthesizes current evidence on the mechanisms, mapping strategies, procedural safety considerations, and outcomes of catheter ablation (CA) for atrial arrhythmias after OHT, based on a structured search of PubMed and Embase (1995-2025). Atrial flutter (AFL), particularly cavotricuspid isthmus (CTI)-dependent macro-reentry, is the dominant arrhythmia in stable OHT recipients. The ablation isthmus is anatomically redefined by suture lines rather than the native inferior vena cava, and CA achieves acute success rates exceeding 90% for CTI-dependent flutter, with a significant survival benefit over medical management alone (median 11.3 vs. 5.8 years; p = 0.026). Atrial fibrillation (AF) is uncommon in stable recipients and, when present, most often arises from residual recipient atrial tissue or donor-recipient conduction bridges; ablation requires individualized electroanatomic mapping rather than routine pulmonary vein isolation. Atrioatrial conduction (AAC) develops in approximately 20-30% of patients presenting with arrhythmias, with a mean onset of 10.1 years post-transplant. Procedural considerations unique to OHT include protamine hypersensitivity risk, rhythm misclassification due to dual atrial physiology, anticoagulation complexity, and drug-immunosuppressant interactions, which collectively strengthen the rationale for ablation over pharmacologic therapy. CA is feasible, effective, and associated with improved survival in appropriately selected OHT recipients. Prospective multicenter registries with standardized reporting are needed to advance evidence-based practice in this population.
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