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.