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VF Ablation in Early Repolarization Syndrome
Study Questions:
What is the arrhythmogenic substrate and mechanism behind early repolarization syndrome (ERS) associated with recurrent ventricular fibrillation (VF), and what role may ablation play in management of this syndrome?
Methods:
A total of 51 ERS patients (four females; median age, 35 years) with recurrent VF episodes underwent body-surface electrocardiographic imaging (ECGI) along with endocardial and epicardial electroanatomic mapping of both ventricles during sinus rhythm and VF for localization of triggers, substrates, and drivers. Ablations were performed on: 1) VF substrates defined as areas that had late depolarization abnormalities characterized by low voltage fractionated late potentials, and 2) VF triggers.
Results:
Detailed three-dimensional mapping revealed two phenotypes: 1) Group 1 with late depolarization abnormalities predominantly at the right ventricular (RV) epicardium (n = 40), and 2) Group 2 with no depolarization abnormalities (n = 11). Group 1 can be subcategorized into two groups: Group 1A included 33 ERS patients with Brugada ECG pattern, and Group 1B included 7 ERS patients without Brugada ECG pattern. Late depolarization areas were found to co-localize with VF driver areas. The anterior RV outflow tract (RVOT)/RV epicardium and the RV inferior epicardium were the major substrate sites for Group 1. The Purkinje network was the leading underlying VF trigger in Group 2 that had no substrates.
Ablations were performed in 43 patients: 33 Group 1 patients had only VF substrate ablation, while 5 patients in Group 1 had both VF substrates and VF trigger; 5 Group 2 patients and 1 without group classification had only Purkinje VF trigger ablation. Ablations were successful in reducing VF recurrences (p < 0.0001). After follow-up of 31 ± 26 months, 39 (91%) had no VF recurrences.
Conclusions:
There are two phenotypes of ERS: 1) one with late depolarization abnormality as the underlying mechanism of high amplitude J-wave elevation that predominantly resides in the RVOT and RV inferolateral epicardium, and 2) the other with pure ERS devoid of VF substrates, but with VF triggers that are associated with Purkinje sites. Ablation is effective in treating symptomatic patients with ERS and frequent VF.
Perspective:
Early repolarization syndrome has been thought of as benign, but when exhibiting inferolateral repolarization abnormality, it may be associated with greater risk of sudden death. The prevalent explanation behind early repolarization syndrome and Brugada syndrome is that they are caused by voltage gradients during repolarization. The present study, however, raises the possibility that alternative mechanisms may play a role in the pathophysiology of the ERS, including conduction abnormalities (e.g., local depolarization abnormality or a combination of both repolarization and depolarization abnormalities). The authors showed that late depolarization abnormalities, predominantly in the RV epicardium, contribute to the underlying mechanism of the syndrome and that the Purkinje network plays an important role in giving rise to VF triggers and initiators.
Keywords: Arrhythmias, Cardiac, Brugada Syndrome, Death, Sudden, Electrocardiography, Endocardium, Epicardial Mapping, Heart Defects, Congenital, Heart Failure, Pericardium, Phenotype, Ventricular Fibrillation
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