Why the study?
Timely pulmonary valve replacement alone does not appear to abort sudden cardiac death risk in repaired Tetralogy of Fallot with chronic pulmonary regurgitation, as myocardial fibrosis remains an arrhythmic substrate.
Highlights the need for comprehensive arrhythmia risk stratification beyond pulmonary valve replacement in patients with repaired Tetralogy of Fallot due to residual myocardial fibrosis.
Residual fibrosis may sustain SCD risk after timely PVR in repaired TOF; leaves open need for fibrosis-inclusive risk stratification in prospective cohorts.
Among the most feared sequelae of repaired Tetralogy of Fallot (TOF) are ventricular arrhythmias and sudden cardiac death (SCD) [1]. The presence of pulmonary regurgitation as a potential risk factor for arrhythmias has sparked interest in a more aggressive strategy for reoperation in TOF patients and chronic pulmonary regurgitation. Although this strategy was initially suggested to be protective against the development of ventricular arrhythmias, timely pulmonary valve replacement (PVR) alone, does not appear to abort the SCD risk as myocardial fibrosis, a clear arrhythmic substrate remains. In this case, we present arrhythmia risk stratification and management of a patient with repaired ToF and concomitant pulmonary regurgitation.
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Drakopoulou et al. (2022) studied this question.
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