Antitachycardia Pacing for Fast Scar-Mediated Ventricular Tachycardia Across Non-Ischemic Cardiomyopathies: A Case Series.

Background: Fast monomorphic ventricular tachycardia (VT) in non-ischemic and inherited cardiomyopathies is frequently treated as an imminently shock-requiring rhythm. Yet ventricular rate is an imperfect surrogate for tachycardia mechanism. When VT remains regular, monomorphic, and sustained by an organized reentrant circuit with an accessible excitable gap, antitachycardia pacing (ATP) may terminate even very rapid episodes without high-energy shock delivery. Case Series: We report five patients with distinct non-ischemic arrhythmogenic substrates in whom fast sustained monomorphic VT (≥188 beats/min; tachycardia cycle length ≤320 ms), including very fast/VF-zone events >250 beats/min, was successfully terminated by ATP. The phenotypes comprised LMNA cardiomyopathy with conduction disease and septal fibrosis; TTN truncating variant-associated dilated cardiomyopathy with VT at approximately 260 beats/min; δ-sarcoglycan-associated dilated cardiomyopathy with clustered VT/electrical storm; severe non-ischemic cardiomyopathy with left bundle branch block, CRT-D implantation, and circumferential ring-like fibrosis, followed by 27 early post-implant VT episodes all terminated by ATP; and hypertrophic cardiomyopathy with an apical left ventricular aneurysm and diffuse late gadolinium enhancement, complicated by shock-free electrical storm. Several episodes were asymptomatic or initially attributed to atrial arrhythmia, whereas device interrogation documented sustained VT requiring therapy. Discussion: Across these heterogeneous non-ischemic substrates, the unifying electrophysiological phenotype was fast, regular, monomorphic VT that remained susceptible to termination by ATP. The series illustrates how ATP response reflects the interaction among circuit organization, scar architecture, tachycardia cycle length, pacing-vector access, detection-zone design, and ATP programming. These observations complement randomized evidence supporting ATP for fast VT and contemporary shock-minimizing ICD programming, including PainFREE Rx II, PITAGORA ICD, MADIT-RIT, ADVANCE III, and APPRAISE ATP. Conclusion: Fast VT in non-ischemic cardiomyopathy should not be considered intrinsically shock-dependent. When the tachycardia is sustained, regular, monomorphic, and electrophysiologically organized, ATP may successfully terminate even very rapid episodes while preserving defibrillation as back-up therapy. The key clinical implication is that ventricular rate, although relevant to risk assessment and therapy, is an imperfect surrogate for ATP susceptibility and should not alone dictate device-programming strategy.