BACKGROUND: It is well known that superior vena cava (SVC) is one of the important non-pulmonary vein (PV) foci of atrial fibrillation (AF). However, little is known regarding the role of arrhythmogenic SVC in AF. METHODS AND RESULTS: Among 1,425 patients who underwent AF ablation in 2 centers, PV antrum isolation was performed in all and SVC isolation was added in 74 (5.2%) patients with arrhythmogenic SVC (58 ± 10 years; 54 males) when the latter was identified as an AF source. The arrhythmogenicity was identified at the 1st, 2nd, and 3rd procedures in 62 (83.8%), 7 (9.5%), and 5 (6.7%) patients, respectively. In 7 (9.5%), 26 (35.1%), and 14 (18.9%) patients, it was identified following adenosine injection, isoproterenol infusion, and electrical cardioversion, respectively. SVC triggering AF was identified in 58 out of 74 (78.4%) patients. In this subset, AF initiated from SVC; however, AF cycle length was longer in SVC than in the right atrium once AF persisted, which suggested its role as an initiator. In 24 (32.4%) patients following the isolation of SVC, AF terminated or converted to atrial flutter and/or confined SVC tachycardia/fibrillation was observed, which suggested its role as a perpetuator. Sixty-four (86.5%) of 74 patients were free from any atrial tachyarrhythmias without antiarrhythmic drugs mean 12.1 ± 9.4 months after the last ablation procedure (mean 1.38 procedures/patient). CONCLUSIONS: In a subset of patients, SVC plays a role in AF not only as an initiator/trigger but also as a driver/perpetuator.
BACKGROUND: It is well known that superior vena cava (SVC) is one of the important non-pulmonary vein (PV) foci of atrial fibrillation (AF). However, little is known regarding the role of arrhythmogenic SVC in AF. METHODS AND RESULTS: Among 1,425 patients who underwent AF ablation in 2 centers, PV antrum isolation was performed in all and SVC isolation was added in 74 (5.2%) patients with arrhythmogenic SVC (58 ± 10 years; 54 males) when the latter was identified as an AF source. The arrhythmogenicity was identified at the 1st, 2nd, and 3rd procedures in 62 (83.8%), 7 (9.5%), and 5 (6.7%) patients, respectively. In 7 (9.5%), 26 (35.1%), and 14 (18.9%) patients, it was identified following adenosine injection, isoproterenol infusion, and electrical cardioversion, respectively. SVC triggering AF was identified in 58 out of 74 (78.4%) patients. In this subset, AF initiated from SVC; however, AF cycle length was longer in SVC than in the right atrium once AF persisted, which suggested its role as an initiator. In 24 (32.4%) patients following the isolation of SVC, AF terminated or converted to atrial flutter and/or confined SVC tachycardia/fibrillation was observed, which suggested its role as a perpetuator. Sixty-four (86.5%) of 74 patients were free from any atrial tachyarrhythmias without antiarrhythmic drugs mean 12.1 ± 9.4 months after the last ablation procedure (mean 1.38 procedures/patient). CONCLUSIONS: In a subset of patients, SVC plays a role in AF not only as an initiator/trigger but also as a driver/perpetuator.