Tetralogy of Fallot: Impact of the Excursion of the Interventricular Septum on Left Ventricular Systolic Function and Fibrosis after Surgical Repair

Purpose: To quantify the excursion of interventricular septum (IVS) in patients after repair of tetralogy of Fallot (TOF), a marker of interventricular interaction, and assess its association with left ventricular (LV) ejection fraction, LV septal wall thickening, and LV fibrosis. Materials and Methods: The HIPAA-compliant protocol received institutional board review approval. IVS excursion was measured at cardiovascular magnetic resonance (MR) imaging in 82 patients after repair of TOF and in 10 healthy volunteers. IVS excursion was correlated with LV ejection fraction, LV septal wall thickening, and LV delayed gadolinium enhancement. Independent predictors of reduced LV ejection fraction were identified, including significant univariable predictors with use of a multivariable logistic regression model. Results: IVS excursion was greater in patients than in healthy volunteers (5.3 mm +/- 3.1 vs 1.2 mm +/- 0.4, P < .01). Patients (n = 68) with abnormal excursion of the IVS had reduced LV ejection fraction (57% +/- 7 vs 61% +/- 4, P < .01) and reduced LV septal wall thickening (24% +/- 10 vs 29% +/- 5, P = .01) compared with patients with normal IVS excursion. Maximal IVS excursion (odds ratio = 1.27 per millimeter, P = .03) and right ventricular (RV) ejection fraction (odds ratio = 0.92 per percentage, P = .031) were independent predictors of reduced LV ejection fraction (< 55%). Among the 44 patients with delayed enhancement images, those with abnormal excursion of the IVS had higher LV delayed enhancement scores (median, 1.5 [interquartile range, 0-2] vs 0 [interquartile range, 0-0]; P < .01] than patients with normal IVS excursion. Notably, in all but one patient the delayed enhancement was located at the RV-LV hinge points. Conclusion: Abnormal IVS excursion after repair of TOF is associated with reduced global and septal LV systolic function and LV fibrosis at the RV-LV hinge points, suggesting a mechanism of adverse interventricular interaction. (C) RSNA, 2011