Catheter ablation of arrhythmic storm triggered by monomorphic ectopic beats in patients with coronary artery disease

Ventricular fibrillation is the main mechanism of sudden cardiac death. The feasibility of eliminating recurrent episodes by catheter ablation has not been reported. Twenty-seven patients without known heart disease (13 men, 14 women, 41+/-14 years of age) were studied after being resuscitated from recurrent (10+/-12) episodes of primary idiopathic ventricular fibrillation; 23 had received a defibrillator. The first initiating beat of ventricular fibrillation had an identical electrocardiographic morphology and coupling interval (297+/-41 ms) to preceding isolated premature beats typically noted in the aftermath of resuscitation. These triggers were localized by mapping the earliest electrical activity and ablated by local radiofrequency delivery. Outcome was assessed by Holter and defibrillator memory interrogation. Premature beats were elicited from the Purkinje conducting system in 23 patients: from the left ventricular septum in 10, from the anterior right ventricle in 9, and from both in 4. The interval from the Purkinje potential to the following myocardial activation varied from 10 to 150 ms during premature beat but was 11+/-5 ms during sinus rhythm, indicating location at peripheral Purkinje arborization. The premature beats originated from the right ventricular outflow tract muscle in 4 patients. The accuracy of mapping was confirmed by acute elimination of premature beats during local radiofrequency delivery. During a follow-up of 24+/-28 months, 24 patients (89%) had no recurrence of ventricular fibrillation without drug. Primary idiopathic ventricular fibrillation is a syndrome characterized by dominant triggers from the distal Purkinje system. These sources can be eliminated by focal energy delivery.

Electrical storm (ES) caused by recurrent episodes of ventricular tachycardia (VT) can cause sudden death in patients with implantable cardioverter-defibrillators and adversely affects prognosis in survivors. Catheter ablation has been proposed for treating ES, but its long-term effect in a large population has never been verified. Ninety-five consecutive patients with coronary artery disease (72 patients), idiopathic dilated cardiomyopathy (10 patients), and arrhythmogenic right ventricular dysplasia/cardiomyopathy (13 patients) undergoing catheter ablation for drug-refractory ES were prospectively evaluated. Short-term efficacy was defined by a complete protocol of programmed electric stimulation and by in-hospital outcome; long-term analysis addressed ES recurrence, cardiac mortality, and VT recurrence. Pleomorphic/nontolerated VTs required electroanatomic and noncontact mapping in 48 and 22 patients, respectively, and percutaneous cardiopulmonary support in 10 patients. An epicardial approach was used in 10 patients. After 1 to 3 procedures, induction of any clinical VT(s) by programmed electrical stimulation was prevented in 85 patients (89%). ES was acutely suppressed in all patients; a minimum period of 7 days with stable rhythm was required before hospital discharge. At a median follow-up of 22 months (range, 1 to 43 months), 87 patients (92%) were free of ES and 63 patients (66%) were free of VT recurrence. Eight of 10 patients with persistent inducibility of clinical VT(s) had ES recurrence; 4 of them died suddenly despite appropriate implantable cardioverter-defibrillator intervention. All together, 11 of 95 patients (12%) died of cardiac-related reasons. In the group of patients presenting with all clinical VTs acutely abolished, no ES recurrence was documented, and cardiac mortality was significantly lower compared with the group of patients showing > or = 1 clinical VT still inducible after catheter ablation. Advanced strategies of catheter ablation applied to a large population of patients are effective in the short-term treatment of ES. By preventing ES recurrence, catheter ablation may play a protective role over the long term and, together with long-term pharmacological therapy, may favorably affect cardiac mortality.

We report on 4 patients (aged 57 to 77 years; 3 men) who developed drug-refractory, repetitive ventricular tachyarrhythmias after acute myocardial infarction (MI). All episodes of ventricular arrhythmias were triggered by monomorphic ventricular premature beats (VPBs) with a right bundle-branch block morphology (RBBB). Left ventricular (LV) mapping was performed to attempt radiofrequency (RF) ablation of the triggering VPBs. Activation mapping of the clinical VPBs demonstrated the earliest activation in the anteromedial LV in 1 patient and in the inferomedial LV in 2 patients. Short, high-frequency, low-amplitude potentials were recorded that preceded the onset of each extrasystole by a maximum of 126 to 160 ms. At the same site, a Purkinje potential was documented that preceded the onset of the QRS complex by 23 to 26 ms during sinus rhythm. In 1 patient, only pace mapping was attempted to identify areas of interest in the LV. Six to 30 RF applications abolished all local Purkinje potentials at the site of earliest activation and/or perfect pace mapping and suppressed VPBs in all patients. No episode of ventricular tachycardia or fibrillation has recurred for 33, 14, 6, and 5 months in patients 1, 2, 3, and 4, respectively. Incessant ventricular tachyarrhythmias after MI may be triggered by VPBs. RF ablation of the triggering VPBs is feasible and can prevent drug-resistant electrical storm, even after acute MI. Catheter ablation of the triggering VPBs may be used as a bailout therapy in these patients.