Key result
VT isthmus ablation in repaired tetralogy of Fallot abolishes PVCs and normalizes LV systolic function.
Why the study?
Data are limited regarding the potential of arrhythmogenic isthmuses to generate frequent PVCs and PVC-mediated LV systolic dysfunction in repaired tetralogy of Fallot.
Case Report (n=1)
Substrate ablation of VT isthmuses in a patient with repaired Tetralogy of Fallot successfully eliminated PVCs and normalized LV systolic function.
Hypothesis-generating for VT isthmus ablation in repaired tetralogy of Fallot with PVCs; larger prospective studies needed before practice change.
Frequent premature ventricular complexes (PVCs) are associated with deleterious effects on left ventricular (LV) function in various clinical scenarios. Repaired tetralogy of Fallot (rTOF) is frequently affected by sustained ventricular arrhythmias dependent on complex post-surgical substrates. However, there is limited data regarding the potential of arrhythmogenic isthmuses to generate frequent PVCs and PVC-mediated LV systolic dysfunction development in rTOF. We present a case of rTOF experiencing relatively infrequent episodes of internal shocks for episodes of sustained monomorphic ventricular tachycardia and a high burden of PVCs associated with left ventricular systolic function deterioration, in which the successful substrate ablation of the anatomical VT isthmuses also led to PVC abolition and consequently to LV systolic function normalization. In such cases, understanding the pathogenic mechanisms that lead to LV dysfunction is only possible by rigorous clinical reasoning, which leads to a tailored specific treatment.
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Cojocaru et al. (2024) conducted a case report in Repaired tetralogy of Fallot with PVC-mediated systolic dysfunction and sustained monomorphic VT (n=1). Substrate ablation of anatomical VT isthmuses was evaluated on PVC abolition and LV systolic function normalization. Substrate ablation of anatomical VT isthmuses in a patient with repaired tetralogy of Fallot led to PVC abolition and subsequent normalization of left ventricular systolic function.
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