Correspondence on "Tetralogy of Fallot: management of residual hemodynamic and electrophysiological abnormalities" by Zaidi

To the Editor In clinical practice, tetralogy of Fallot (TOF) has been a specific form of cyanotic congenital heart disease particularly requiring a lifelong followup. The recently published article by Zaidi has focused on residual abnormalities in the setting of repaired tetralogy of Fallot (rTOF). In this context, functional tricuspid regurgitation (TR) and its management might also have important implications in patients with rTOF requiring pulmonary valve replacement (PVR). It is well known that functional TR might potentially follow a progressive course after cardiac surgeries performed for leftsided valvular pathologies with pulmonary hypertension (despite a transient postoperative improvement in TR severity) largely due to the ongoing structural changes of tricuspid annulus. 3 As expected, this most likely occurs in patients with significant degrees of preoperative TR and/or tricuspid annular dilatation potentially mandating concomitant tricuspid and leftsided valve interventions in these patients. 3 These notions 3 might also apply to the setting of rTOF with a significant pulmonary infundibular or valvular pathology (associated with right ventricular (RV) pressure or volume overload) requiring reintervention. In the recently reported largest study comprising 542 subjects with rTOF or pulmonary stenosis requiring PVR, concomitant tricuspid valve intervention (TVI) led to an additional 2.3fold decrease in TR severity without any significant increases in length of hospital stay and early adverse outcomes. The authors particularly suggested concomitant TVI as an efficient and safe option that might further improve TR grade beyond the favourable impact of RV offloading obtained with PVR in isolation. In this context, patients with preoperative significant TR or tricuspid annulus diameter of >40 mm or those with structural leaflet pathologies including leaflet entrapment, leadrelated injury and congenital anomalies have been suggested to be particularly eligible for combined TVI and PVR. Based on the abovementioned notions, functional TR with highrisk features (including increased annulus diameter) might also be labelled as an important residual haemodynamic abnormality usually emerging in association with pulmonary regurgitation and/or infundibular restenosis in patients with rTOF. Importantly, this form of TR might have the potential to hamper RV reverse remodelling, and might even lead to endstage right heart failure (even after successful PVR) potentially mandating TVI at the time of PVR in this specific group of relatively young patients.