Incessant ventricular tachycardia from a surviving Purkinje network years after myocardial infarction: A case report

Ventricular tachycardia (VT) in the setting of chronic myocardial infarction (MI) is overwhelmingly attributed to macro-reentry. We report an extremely rare case of late-onset, incessant monomorphic VT driven by abnormal Purkinje automaticity. A 77-year-old male, two years post-inferoposterior MI, presented with symptomatic VT and an exceptionally high premature ventricular contraction (PVC) burden of 29.1 %. The VT's mostly regular rhythm with occasional irregularity, combined with a reduced left ventricular ejection fraction (LVEF) of 48 %, suggested a continuous focal driver with intermittent exit block causing tachycardia-induced cardiomyopathy. High-density mapping revealed a centrifugal activation pattern, with the earliest site showing long, fractionated diastolic potentials adjacent to Purkinje potentials. A targeted regional substrate ablation strategy ("de-networking") of the arrhythmogenic substrate successfully terminated the arrhythmia. Consequently, the PVC burden was reduced to 1.5 % and the LVEF recovered to 54 % at one-month follow-up. This case demonstrates that late-onset, incessant VT from a surviving Purkinje network is a curable cause of cardiomyopathy, with targeted ablation leading to arrhythmia suppression and significant ventricular function recovery.