Discussion

In this study, right ventricular function was comprehensively evaluated in patients followed after repair of tetralogy of Fallot, and the determinant effect of pulmonary regurgitation on right ventricular mechanical performance was demonstrated. Our findings show that, although conventional echocardiographic parameters remained within normal limits in most patients, right ventricular free-wall longitudinal strain more sensitively reflected functional heterogeneity and subclinical dysfunction in the postoperative period. ^{Reference Geva, Wald and Bucholz12} These results support the concept that strain analysis may serve as a complementary and more sensitive assessment tool compared with conventional measurements during follow-up after tetralogy of Fallot repair. ^{Reference Moscatelli, Pergola and Motta18}

We observed a significant deterioration in right ventricular free-wall strain values with increasing pulmonary regurgitation severity (p = 0.036). ^{Reference Gao, Li and He19} Similarly, the reduction in fractional area change with greater pulmonary regurgitation severity (p = 0.044) suggests systolic performance impairment related to chronic volume overload. ^{Reference Arroyo-Rodríguez, Fritche-Salazar and Posada-Martínez20} In contrast, traditional parameters reflecting longitudinal motion, such as tricuspid annular plane systolic excursion and right ventricular systolic velocity, did not differ significantly across pulmonary regurgitation grades, indicating that these measures may be limited in detecting early and mid-term functional deterioration. ^{Reference Gao, Li and He19,Reference Meca Aguirrezabalaga, Silva Guisasola, Díaz Méndez, Escalera Veizaga and Hernández-Vaquero Panizo21} These findings are consistent with previous studies reporting that strain measurements represent one of the earliest and most sensitive markers of right ventricular dysfunction in the post-tetralogy of Fallot repair setting. ^{Reference Moscatelli, Pergola and Motta18,Reference Meca Aguirrezabalaga, Silva Guisasola, Díaz Méndez, Escalera Veizaga and Hernández-Vaquero Panizo21}

At first glance, the observed reduction in right ventricular free-wall strain with increasing pulmonary regurgitation may appear counterintuitive, as acute volume loading has been shown to increase myocardial strain in conditions such as ventricular septal defect or valvular regurgitation. However, this apparent discrepancy likely reflects differences between early compensatory and late maladaptive remodelling. In the setting of chronic pulmonary regurgitation after tetralogy of Fallot repair, prolonged volume overload leads to progressive right ventricular dilatation, increased wall stress, myocardial fibrosis, and reduced contractile efficiency. As a result, right ventricular strain may decline despite ongoing volume loading, representing a transition from compensatory hyperfunction to mechanical dysfunction. ^{Reference Geva, Wald and Bucholz12,Reference Leonardi, Perrone and Calcaterra16,Reference Moscatelli, Pergola and Motta18}

Although previous studies have reported an association between increasing pulmonary regurgitation severity, right ventricular dilatation, and QRS prolongation, such a relationship was not observed in the present cohort. ^{Reference Krieger, Zeppenfeld and DeWitt9,Reference Geva, Wald and Bucholz12} This discrepancy may be explained by the relatively mid-term duration of follow-up and the heterogeneity of postoperative right ventricular remodelling patterns. Electrical remodelling, as reflected by QRS prolongation, may lag behind mechanical impairment detected by strain analysis, particularly in younger patients or during earlier stages of chronic pulmonary regurgitation. In this context, right ventricular free-wall longitudinal strain may represent a more sensitive marker of early right ventricular dysfunction than QRS duration. ^{Reference Krieger, Zeppenfeld and DeWitt9,Reference Gao, Li and He19,Reference Bitterman, Hui and Fan22}

Repaired tetralogy of Fallot is characterised by a spectrum of residual right ventricular outflow tract pathologies, including isolated pulmonary regurgitation, residual stenosis, mixed valve disease, or minimal valve dysfunction. Rather than stratifying patients by these phenotypes, the present study focused on the hemodynamic impact of pulmonary regurgitation severity itself. This approach reflects real-world clinical follow-up, where mixed valve physiology is common, and suggests that the association between pulmonary regurgitation burden and right ventricular mechanical impairment may remain relevant even in the presence of coexisting residual lesions. ^{Reference Ammash, Dearani, Burkhart and Connolly2}

Given that the majority of patients in our cohort underwent transannular patch repair, a broad pulmonary regurgitation jet was frequently observed. Nevertheless, despite this relative homogeneity in surgical technique, pulmonary regurgitation severity—expressed as jet width relative to the pulmonary annulus—remained the strongest correlate of right ventricular free-wall strain impairment. Although age and duration of exposure to pulmonary regurgitation may contribute to right ventricular remodelling, our findings suggest that the hemodynamic burden of pulmonary regurgitation itself plays a dominant role in determining right ventricular mechanical performance during mid-term follow-up. ^{Reference Ammash, Dearani, Burkhart and Connolly2,Reference Geva, Wald and Bucholz12}

The impact of pulmonary regurgitation on right ventricular geometry was also clearly demonstrated in our study. The significant increase in right ventricular long-axis measurements with higher pulmonary regurgitation severity (p = 0.011), together with the positive correlation between pulmonary regurgitation jet width and right ventricular long-axis length (r = 0.43), indicates that chronic pulmonary regurgitation-related volume loading leads to right ventricular dilatation and geometric remodelling. ^{Reference Geva, Wald and Bucholz12} The parallel deterioration of strain values with these geometric changes suggests that mechanical dysfunction arises not only from reduced contractility but also from alterations in ventricular shape and dimensions. ^{Reference Bitterman, Hui and Fan22}

Electrocardiographic assessment revealed only a weak association between QRS duration and right ventricular free-wall strain, and QRS duration did not emerge as an independent determinant of strain impairment in multivariable analysis. This finding suggests that QRS prolongation in the post-tetralogy of Fallot repair period may represent an indirect marker of electrical remodelling and ventricular geometric changes rather than a direct indicator of mechanical dysfunction. Although a trend towards worsening strain values with increasing QRS duration was observed, the absence of a clear linear relationship supports the concept that pulmonary regurgitation-related volume overload exerts a more dominant influence on right ventricular mechanical function. ^{Reference Bitterman, Hui and Fan22,Reference Bowen, Kauling and Loff Barreto23} These results are in line with the literature indicating that QRS duration, when interpreted within a multimodal framework rather than in isolation, is more closely associated with arrhythmogenic risk and late clinical outcomes. ^{Reference Krieger, Zeppenfeld and DeWitt9,Reference Bowen, Kauling and Loff Barreto23}

One of the key findings of this study is the identification of pulmonary regurgitation jet width as the sole independent determinant of right ventricular free-wall strain impairment in multivariable linear regression analysis (β = 0.132; p = 0.038). ^{Reference Geva, Wald and Bucholz12,Reference Gao, Li and He19} The loss of statistical significance of QRS duration, right ventricular dimensions, and conventional functional parameters in the multivariable model further emphasises the dominant role of hemodynamic volume overload in determining right ventricular mechanical performance. ^{Reference Bitterman, Hui and Fan22} Nevertheless, the moderate explanatory power of the model (R ² = 0.17) highlights the multifactorial nature of right ventricular dysfunction and underscores that no single parameter can fully capture right ventricular functional impairment. ^{Reference Geva, Wald and Bucholz12,Reference Moscatelli, Pergola and Motta18} Although the overall model showed borderline significance, the identified association of pulmonary regurgitation jet width with right ventricular strain remained clinically meaningful.

The moderate discriminatory ability of pulmonary regurgitation jet width for predicting impaired strain (area under the curve = 0.67) suggests that this parameter should not be used as a stand-alone decision-making tool in clinical practice, but rather interpreted in conjunction with functional measures such as strain. ^{Reference Geva, Wald and Bucholz12} Furthermore, the observation that patients who developed late arrhythmias or required rehospitalization exhibited more impaired strain values and longer QRS durations indicates a potential association between combined electrical and mechanical remodelling and adverse clinical outcomes. However, these relationships should be interpreted cautiously, as causality cannot be inferred from the present data.

Overall, this study underscores the central role of pulmonary regurgitation in shaping right ventricular function and geometry following tetralogy of Fallot repair and demonstrates that right ventricular free-wall strain provides a more sensitive assessment of right ventricular performance compared with conventional echocardiographic parameters. Our findings suggest that strain analysis may contribute to earlier and more detailed evaluation of right ventricular function during postoperative follow-up. Nevertheless, larger prospective studies with longer follow-up durations are required to better define the role of this approach in clinical decision-making and outcome prediction.

From a clinical perspective, the present findings suggest that right ventricular free-wall longitudinal strain may provide complementary information to conventional echocardiographic parameters in patients with repaired tetralogy of Fallot. In our cohort, strain impairment was observed despite relatively preserved conventional indices of right ventricular systolic function, indicating that strain may detect early mechanical dysfunction before overt deterioration becomes apparent. While the present study was not designed to guide the timing of pulmonary valve replacement, these findings support the incorporation of right ventricular strain assessment into routine echocardiographic follow-up as an adjunctive tool for risk stratification during mid-term surveillance.