Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited 
arrhythmogenic disease that can cause sudden cardiac death due to ventricular 
fibrillation (VF). While pharmacological therapy with beta-blockers and/or 
Ca(2)(+) antagonists is often unreliable, a recent study has demonstrated that 
flecainide can effectively suppress arrhythmia in a murine model of CPVT as well 
as clinically in two human subjects suffering from CPVT. We here present the 
case of an 11-year-old boy suffering from CPVT-1 as well as a review of the 
current relevant literature. After resuscitation due to VF at age 9, an 
automated implantable cardioverter-defibrillator (ICD) was implanted in 2007. 
Under beta-blocker therapy, repeated shocks were delivered due to either fast 
ventricular tachycardia (VT) or VF. This persisted under additional therapy with 
verapamil. Implantable cardioverter-defibrillator routine interrogations showed 
frequent non-sustained VT with an average of 8.8 per day. Additionally, the 
patient suffered from impaired physical performance due to decreased 
chronotropic competence. In July 2009, flecainide was added to the 
beta-blocker/verapamil regimen, resulting in a plasma level of 0.20 mg/L. No ICD 
shock or sustained VT occurred until December 2010. Genetic testing revealed an 
RyR2 receptor mutation. The case demonstrates the challenge of diagnosis and 
management of CPVT. It furthermore supports recent experimental evidence that 
the class 1 antiarrhythmic drug flecainide can suppress CPVT. The presented case 
supports a novel strategy in treating CPVT with the class I antiarrhythmic agent 
flecainide.