Introduction
Idiopathic ventricular arrhythmias (VA) are frequently encountered in arrhythmia clinics and treatment options include anti-arrhythmic drugs (AAD) and catheter ablation. Limited efficacy and potential side effects restrict the long-term use of AAD’s. On the other hand, catheter ablation is effective with relatively low complications rates and recommended as the first-line therapy by current guidelines1. However, despite the technologic advances in mapping techniques and ablation tools, catheter ablation fails to suppress VA in some patients. In this regard, VA’s originating from the left ventricular summit (LVS) pose a particular challenge in the laboratory and are associated with lower procedural and long-term success rate due to its proximity to the bifurcation of left main coronary artery (LMCA), anatomical difficulties for advancing catheters and the necessity of epicardial approach in high proportion of cases.
Ivabradine is an inhibitor of funny current (If) in cardiac pacemaker cells by binding to hyperpolarization-activated cyclic nucleotide-gated (HCN) channels2. Ivabradine is currently indicated in the treatment of heart failure and stable coronary artery disease after being tested in large randomized clinical trials3,4. In addition, it is frequently used for treating patients with inappropriate sinus tachycardia and postural orthostatic tachycardia syndrome5.
Previous case reports suggested promising role of ivabradin in the in pediatric population for treating junctional and atrial ectopic tachycardias in which increased automaticity were considered as the primary underlying mechanism6-8. Ivabradine offers a plausible treatment choice by effectively inhibiting If current and having relatively better safety profile compared to other anti-arrhythmic drugs (AAD) and catheter ablation.
Here we reported the use of ivabradine in the treatment of idiopathic VA which was originated from the LVS and resistant to multiple AAD’s and catheter ablation.