Progressive Myocardial Metabolic Dysfunction After Stereotactic Arrhythmia Radioablation for Ventricular Tachycardia in Hypertrophic Cardiomyopathy: A Serial Multimodality Imaging Case Report

Background Stereotactic arrhythmia radioablation (STAR) for ventricular tachycardia (VT) has emerged as a promising treatment for patients in whom catheter ablation is challenging or unsuccessful; however, its underlying mechanisms remain unclear, particularly with respect to early antiarrhythmic effects. Case Summary A 51-year-old man with hypertrophic cardiomyopathy exhibited extensive mid-septal scar on contrast-enhanced cardiac magnetic resonance imaging (CE-MRI) and suffered from refractory VT. The VT was presumed to originate from the mid-septal scar with preferential conduction toward the outflow region. STAR was performed, delivering 25 Gy to the core scar and 20 Gy to the surrounding wall and outflow region. VT episodes decreased immediately after STAR and disappeared within three months, but recurred 24 months later. Serial multimodality imaging provided novel insight into the mechanism: progressive metabolic dysfunction (reduced iodine-123-beta-methyl-p-iodophenyl-pentadecanoic acid uptake) and wall motion deterioration began soon after irradiation. The progressive decline in R-wave amplitude in the shock lead also suggested ongoing myocardial injury. These changes occurred without corresponding alterations in perfusion (thallium-201 chloride) or fibrosis (CE-MRI). Motion-phase analysis revealed a septal contraction delay before STAR that resolved at 1 month but evolved into a heterogeneous pattern by 1 year, and further deteriorated by 2 years. Discussion Myocardial irradiation with 20 to 25 Gy can induce progressive, non-ischemic myocardial injury with limited fibrotic change over a prolonged period. This injury may exert short-term antiarrhythmic effects but could potentially create new arrhythmogenic substrates in the long term. Careful consideration is required when irradiating normal myocardium.