Effect of Pacemaker Current Inhibitor (Ivabradine) on Sinoatrial Node Function and Pulmonary Vein Arrhythmogenesis

Atrial fibrillation (AF) is the most common cardiac arrhythmia seen in clinical practice, which can induce cardiac dysfunction and strokes. However, the mechanism of AF is not fully elucidated. One of the main mechanism of AF initiation is one or more triggering foci from pulmonary veins (PVs). Circumferential PV ablation is the main therapy for the catheter ablation of AF with a success rate of around 50-88%. PVs contain a mixture of working myocardium and pacemaker cells, which can induce atrial arrhythmias. Because the risk factors (inflammatory cytokines, stretching, and angiotensin II) for AF have all been shown to increase PV and atrial arrhythmogenesis. Ivabradine, a unique specific If current inhibitor, may exert direct effect on sinoatrial node as well as PVs, which may in turn reduce the chance of arrhythmia induction. Therefore, the purpose of the present study was to evaluate the electrophysiological effects of ivabradine on PVs and the sinoatrial node, and to investigate whether ivabradine can alter the PVs arrhythmogenesis and to study the detailed mechanisms.