# Progressive myocardial metabolic dysfunction after stereotactic arrhythmia radioablation for ventricular tachycardia in hypertrophic cardiomyopathy: a serial multimodality imaging case report

## TL;DR

A patient with heart disease showed improved arrhythmia after radiation treatment, but later developed new heart issues, suggesting radiation can have both short-term benefits and long-term risks.

## Contribution

This case report provides novel insights into the progressive myocardial injury caused by stereotactic arrhythmia radioablation.

## Key findings

- Progressive metabolic dysfunction and wall motion deterioration occurred after irradiation without changes in perfusion or fibrosis.
- Short-term antiarrhythmic effects were observed, but new arrhythmogenic substrates developed over time.
- Septal contraction patterns changed progressively over two years following treatment.

## Abstract

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.

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 towards the outflow region. Stereotactic arrhythmia radioablation was performed, delivering 25 Gy to the core scar and 20 Gy to the surrounding wall and outflow region. Ventricular tachycardia episodes decreased immediately after STAR and disappeared within 3 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.

Myocardial irradiation with 20–25 Gy can induce progressive, non-ischaemic 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.