90 Catheter Ablation of Frequently Recurring Ventricular Fibrillation in a Patient after Aortic Valve Repair YI-GANG LI, M.D., GERIAN GR ¨ ONEFELD, M.D., CARSTEN ISRAEL, M.D., and STEFAN H. HOHNLOSER, M.D. From the Department of Medicine, Division of Cardiology, J.W. Goethe-University, Frankfurt, Germany Ablation of Ventricular Fibrillation. It has been demonstrated that idiopathic ventricular fibrillation (VF) can be triggered by ventricular premature beats (VPBs) arising from the Purkinje fibers. Eliminating these VPBs by radiofrequency catheter ablation prevented VF recurrences. Whether the same pathophys- iology and the same treatment option exist in patients with structural heart disease is unknown. Recurrent VF was observed in a 17-year-old patient after aortic valve repair of a perforated noncoronary cusp with resulting severe aortic regurgitation. VF recurred despite therapy with various antiarrhythmic drugs. A maximum of 14 external defibrillations was necessary during a 24-hour period to stabilize the patient. Due to increasing hemodynamic instability as a result of this electrical storm, the patient was referred for inva- sive diagnostics. During electrophysiologic study, frequent short runs of VF initiated by VPB with a narrow QRS complex were observed. After extensive mapping of the right and left ventricles, two distinct sources of VPBs originating from anteroseptal and inferoseptal areas of the left ventricle could be successfully ablated. VPBs were preceded by distinct Purkinje potentials with intervals from the Purkinje potential to QRS onset of VPB of 68 ms and 30 ms at effective sites, respectively. During short-term follow-up of 2 months, there was no VF recurrence. VPB originating from the Purkinje system may be one possibility for VF initiation in patients with structural heart disease. Eliminating these sources of VPBs by catheter ablation can prevent recurrent VF in such patients. (J Cardiovasc Electrophysiol, Vol. 15, pp. 90-93, January 2004) ventricular fibrillation, radiofrequency catheter ablation Introduction Recent evidence obtained from patients without structural heart disease indicates that ventricular fibrillation (VF) can be initiated by ventricular premature beats (VPBs) originating from the Purkinje system. 1,2 These triggers of life-threatening ventricular tachyarrhythmias could be eliminated by focal energy delivery during catheter ablation. Whether VF can be similarly initiated by VPBs arising from Purkinje fibers in patients with underlying structural heart disease still is un- known. This report describes findings in a patient with aor- tic valve disease in whom VPBs from the Purkinje system triggered recurrent VF that could be eliminated by radiofre- quency catheter ablation of these triggers. Case Report A 17-year-old male had undergone aortic valve repair follow- ing endocarditis-mediated perforation of the noncoronary cusp of the aortic valve with resulting severe aortic regurgitation. There was significant impairment of left ventricular function with left ventricular dilation (left ventricular end-diastolic di- mension 56 mm; left ventricular ejection fraction 35%). Past medical history was free of any palpitations or syncope. There were no documented arrhythmias before cardiac surgery, and there was no family history of sudden cardiac death. Three Address for correspondence: Stefan H. Hohnloser, M.D., Department of Medicine, Division of Cardiology, J.W. Goethe University, Theodor Stern Kai 7, 60590 Frankfurt, Germany. Fax: 49-6173-950290; E-mail: Hohnloser@em.uni-frankfurt.de Manuscript received 23 July 2003; Accepted for publication 16 September 2003. doi: 10.1046/j.1540-8167.2004.03386.x days after surgery, recurrent episodes of VF occurred that ne- cessitated repeated external defibrillation. During the postop- erative period, electrolytes and cardiac enzymes were closely monitored, and 12-lead ECG recordings were performed twice daily. There were no signs of perioperative ischemia secondary to cardioplegia. There was no change in QRS duration, and QT and QTc interval were within normal limits. No other non- cardiac medications that could cause ventricular tachyarrhyth- mias were used. VF could not be suppressed by successive in- travenous administration of beta-blockers, quinidine, and amio- darone. Hemodynamics deteriorated as a result of rhythm in- stability, and the patient had to be intubated and placed on a respirator. Continuous ECG monitoring in the cardiac care unit demonstrated frequent nonsustained or sustained episodes of polymorphic ventricular tachycardia or VF (Fig. 1). These episodes were always initiated by VPBs showing two distinct morphologies with narrow QRS complexes (Fig. 1). Due to con- tinued hemodynamic and electrical instability, the patient was referred for electrophysiologic study and catheter ablation. Electrophysiologic Study and Radiofrequency Ablation Three quadripolar electrode catheters were inserted via the femoral vein and positioned in the right atrium, the His-bundle position, and the right ventricle. A 7-French deflectable ablation catheter with a 4-mm tip electrode and 2-5-2 mm interelectrode spacing (temperature-guided; Cordis Webster Inc., Miami, FL, USA) was used for mapping and radiofrequency current appli- cation. The surface ECG and intracardiac electrograms were recorded using a computerized multichannel system (BARD Labsystem 2.56). At the beginning of the study, short episodes of frequent polymorphic ventricular tachycardia/VFs were ob- served. Detailed mapping was performed in the right and left ventricles. For mapping of the left ventricle, the catheter was advanced retrogradely over the aortic valve. Particular care was taken not to damage the repaired valve. VPBs with two different QRS morphologies triggering short episodes of poly- morphic ventricular tachycardias/VF were identified. One VPB