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. To compare Purkinje electrogram morphology at VF-triggering sites in patients with idiopathic versus structural heart disease undergoing catheter ablation. Thirty-seven 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 structural patients (7/8 [87.5%] vs. 0/4 idiopathic; p=0.01). Structural VF demonstrated greater electrogram complexity, with more multiphasic components (3.0±1.1 vs. 1.0±0.0; p<0.001), longer Purkinje potential duration (37.9±8.3 vs. 18.0±4.0 ms; p<0.001), and longer Purkinje-ventricular intervals (50.9±13.6 vs. 18.0±4.0 ms; p<0.001). In two structural patients without voltage-defined scar, CT identified septal substrate, with P-V intervals of 28 and 35 ms-intermediate between idiopathic and scar-positive patients. Twelve-month VF-free survival was similar between groups (83.3% vs. 80.0%; p=0.79). 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 versus substrate-based ablation strategies, supporting a tailored approach that balances arrhythmia control with conduction system preservation.