Abstract
Catheter ablation is an established treatment method for atrial fibrillation. In most cases, the arrhythmia substrate is located within the pulmonary veins and their isolation has become the cornerstone of catheter ablation therapy. However, it is estimated that in 10-20% of patients, the trigger and/or sustaining factors for the arrhythmia are located outside the pulmonary veins. This is particularly relevant in patients with significant disease progression and persistent forms of AF, where these sites are likely responsible for treatment failure and arrhythmia recurrence. Identifying non-pulmonary vein triggers of AF and understanding their impact on disease progression is crucial but remains insufficiently explored. Gaining such insights offers hope for optimizing treatment strategies and improving outcomes for patients. The most commonly mentioned ectopic arrhythmogenic focus include the superior vena cava (SVC). Despite its clinical significance in arrhythmogenesis, the detailed electrophysiological properties of the SVC have received relatively limited research attention compared to other cardiac structures. Moreover, scientific papers that present extensive knowledge on SVC- from its embryology to the electrophysiology scarce. Therefore we would like to offer a comprehensive analysis of existing literature concerning SVC as an arrhythmogenic substrate for AF.