Abstract
Atrial fibrillation (AF), the most common arrhythmia, is associated with increased morbidity and mortality.1,2 Although new concepts of AF pathophysiology have emerged, underlying molecular mechanisms are still poorly understood.1 Abnormal automaticity, triggered activity, and reentry are the most accepted pathophysiological mechanisms underlying AF.1 Ectopic activity, that is, electrical impulse generation outside the sinoatrial node, particularly around the pulmonary veins (PVs), can trigger reentry when a vulnerable substrate is present.
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