Coronary Sinus-Triggered Atrial Fibrillation

Abstract Atrial fibrillation (AF) is one of the mostly encountered sustained arrhythmias. AF not only substantially reduces patients’ exercise tolerance and quality of life but also notably increases the risk of heart failure, stroke, and mortality. A proposed pathophysiology suggests a final common pathway that includes electrophysiological changes in atrial tissues. These changes include alterations in the regulation of membrane channels and proteins, resulting in abnormal electrical activity, that is, responsible for AF. The abnormal electrical activity typically originates from the musculature of the pulmonary veins as well as from other ectopic regions known as non-pulmonary vein triggers. These include muscular tissue sleeves within superior vena cava, the coronary sinus (CS), and remnants of the vein of Marshall. Non-pulmonary vein triggers, particularly those from the CS, have been identified as significant contributors to AF. Identifying CS triggers is crucial for achieving long-term success in radiofrequency ablation for paroxysmal AF. However, these triggers are particularly challenging to address due to the complex anatomy of the CS and the presence of muscular sleeves capable of generating ectopic activity. Studies have shown that patients with CS triggers often require more extensive ablation, longer procedural times, and higher total radiofrequency energy delivery compared to those without CS triggers. Consequently, these patients experience higher recurrence rates post-ablation. This review article examines the effect of CS triggers on the success rate of radiofrequency ablation for paroxysmal AF, evaluating procedural characteristics, outcomes, and strategies for managing CS triggers to enhance the efficacy of ablation.