onomorphic ventricular tachycardia (VT) in the presence of structural heart disease is largely attributable to anatomically bound macro-re-entry involving regions of myocardial scarring or the bundle branches. 1 In contrast; repetitive, idiopathic right and left ventricular (LV) outflow tract VTs are attributable to triggered activity or abnormal automaticity of the ventricular myocardium. 2,3 There is evidence that triggers originating from distal Purkinje arborization play an important role in the initiation of malignant arrhythmias such as polymorphic VT and ventricular fibrillation in a variety of clinical scenarios. [4][5][6][7][8] We report a patient with hypertrophic cardiomyopathy (HCM) in whom life-threatening repetitive monomorphic VTs developed. Radiofrequency (RF) ablation targeting the Purkinje-like potentials preceding the VT prevented recurrence.
Case ReportA 35-year-old man with HCM presented with recurrent episodes of palpitation and chest discomfort. Electrocardiographic monitoring during palpitation showed an incessant nonsustained, wide QRS tachycardia with a QRS duration of 130 ms at 180-200 beats/min. On admission to hospital, 12-lead ECG showed incessant nonsustained VT with right bundle branch block (RBBB) morphology and a northwest axis deviation (Fig 1). Intravenous lidocaine and verapamil were effective in terminating the VT but ineffective in preventing recurrence. A 12-lead ECG obtained during sinus rhythm after intravenous administration of verapamil showed poor R wave progression in the precordial leads (Fig 2). The signal-averaged ECG was recorded during sinus rhythm after intravenous administration of 5 mg of verapamil. Oral administration of -blocker, class I antiarrhythmic drugs (pilsicainide and cibenzoline), and amiodarone was ineffective in preventing the VT. The late potential was positive (filtered QRS duration: 139 ms, root mean square voltage of the terminal 40 ms of the filtered QRS complex: 6.6 V; the duration of low-amplitude signals <40 V of the terminal filtered QRS complex: 56 ms). Transthoracic echocardiography showed nonobstructive HCM (LV ejection fraction: 88.8%, left atrial dimension: 36.9 mm, LV end-diastolic dimension: 31.8 mm, LV enddiastolic dimension: 13.4 mm, interventricular septum thickness: 19.4 mm, LV posterior wall thickness: 10.9 mm) and 2-dimensional echocardiography showed mid-septal hypertrophy. After written informed consent was given by the patient, coronary angiography, left ventriculography and electrophysiologic study were performed in the postabsorptive state after all antiarrhythmic drugs, except amiodarone, had been discontinued for at least 5 lives. Coronary angiography was normal and left ventriculography showed there was neither obstruction in the LV nor pressure gradients within the LV or between the LV and aorta. Three diagnostic catheters were inserted via the femoral veins and placed at the high right atrium, His bundle position and right ventricular apex. A decapolar catheter was inserted into the coronary sinus via the right int...