Case report
Twelve years ago, a 33-year-old man (now 45 years old) with no significant family history and a medical history of syncope when playing golf developed sudden cardiac arrest (SCA) after drinking alcohol. His heartbeat was restored by an automated external defibrillator, and a fast ventricular tachycardia (VT) with a short cycle length (CL), including a partially polymorphic waveform, was recorded at another hospital (Figure 1A). Thus, cardiologists at the previous hospital judged that this patient had VT or ventricular fibrillation (VF) at that time. Although various examinations including cardiac magnetic resonance imaging (MRI), coronary angiography, echocardiogram, and a pilsicainide provocation test were performed, the underlying heart disease was not clear. Also, the electrocardiogram (ECG) at rest showed no specific findings except a complete right bundle branch block (Figure 1B). The patient was diagnosed with idiopathic ventricular fibrillation (IVF) by the cardiologists at the previous hospital. An implantable cardioverter defibrillator (ICD) was not implanted because of his rejection. Amiodarone was also recommended, but he refused the prescription because of the possible side effects. Thus, he began oral medication with bisoprolol 2.5 mg per day for the arrhythmia. However, 5 years later, a second SCA occurred due to the same ventricular arrhythmia, and he received an ICD (Dual chamber ICD, mode DDI) implantation after successful resuscitation.
Twelve years later, the patient was admitted to our hospital for frequent ICD shocks. His ICD record showed rapid monomorphic VT (mean CL, 185 ms), which was always triggered by the same premature ventricular contraction (PVC) (Figure 2A). The morphology of the PVC was a left bundle branch block configuration with an inferior axis; catheter ablation of the trigger PVC was performed (Figure 2B). A three-dimensional (3D) voltage map of the right ventricle was constructed, and a low-voltage area (LVA) on the free wall of the right ventricular outflow tract (RVOT) was detected. However, only a few PVCs were observed during the catheter ablation, and we performed a pacemap-guided ablation of the PVC. A good pacemap was obtained at the border zone of the LVA, and the target PVC was ablated at the site. Shortly after discharge, he experienced a recurrence of ICD shocks and underwent a second ablation session the following month. However, the second ablation failed again because very few PVCs were observed, and he revisited our hospital a month after the second session for frequent ICD shocks. Monomorphic VT originating from the RVOT was recorded on an ECG (Figure 3A), and a third ablation session for recurrent VT was performed. The morphology of the VT was the same as the trigger PVC, which was frequently observed during his sessions. An almost perfect pacemap (score, 96) with PVC was obtained near the LVA, slightly posterior to the prior ablation site. The ventricular potential of the PVC on the ablation catheter showed up earlier than the QRS onset in any leads on the ECG at this site (Figure 3B–C). Both VT and PVC were successfully eliminated and not inducible after ablation. There were no ICD shocks one-and-a-half years after the last session.