Distinct Purkinje electrogram phenotypes at ventricular fibrillation trigger sites in idiopathic and structural heart...

Purkinje fibers are established triggers of ventricular fibrillation (VF). In structural heart disease, septal fibrosis and border-zone remodeling may alter Purkinje electrograms at VF-triggering sites; however, classical electrogram criteria derived from structurally normal hearts have not been validated in scarred substrate.

The purpose of this study was to compare Purkinje electrogram morphology at VF-triggering sites in patients with idiopathic and structural heart disease undergoing catheter ablation.

37 consecutive patients underwent Purkinje-targeted VF ablation (12 idiopathic, 25 structural). Bipolar electrograms at mapped triggering sites were quantitatively analyzed in 12 patients with discrete trigger localization and high-quality recordings (4 idiopathic, 8 structural). Abnormal Purkinje electrograms were defined as prolonged (>25 ms), multicomponent, or fragmented signals.

Abnormal Purkinje-like electrograms were identified almost exclusively in patients with structural VF (7 of 8 [87.5%] vs 0 of 4 [0%] idiopathic VF; P = .01). Structural VF demonstrated greater electrogram complexity, with more multiphasic components (3.0 ± 1.1 vs 1.0 ± 0.0; P < .001), longer Purkinje potential duration (37.9 ± 8.3 ms vs 18.0 ± 4.0 ms; P < .001), and longer Purkinje-ventricular intervals (50.9 ± 13.6 ms vs 18.0 ± 4.0 ms; P < .001). In 2 patients with structural VF without voltage-defined scar, computed tomography identified septal substrate, with Purkinje-to-ventricular intervals of 28 and 35 ms, values intermediate between those observed in idiopathic VF and voltage scar-positive structural VF. 12-month VF-free survival was similar between groups (83.3% vs 80.0%; P = .79).

Purkinje electrogram morphology at VF-triggering sites differs between idiopathic and structural heart disease and is consistent with differences at the Purkinje-myocardial interface. These findings suggest that electrogram phenotype may inform selection of focal vs substrate-based ablation strategies, supporting a tailored approach that balances arrhythmia control with conduction system preservation.