Abstract 4366602: Altered Left Ventricular Hemodynamic Forces in Transposition of Great Arteries Following Arterial Switch Operation

Introduction: As patients with d-looped transposition of the great arteries (d-TGA) reach adulthood following the arterial switch operation (ASO), clinical focus has shifted toward understanding long-term ventricular function. However, the impact of surgical repair on left ventricular (LV) mechanics and intracavitary forces remains incompletely characterized. While myocardial strain has emerged as a valuable marker of regional function, the role of intraventricular hemodynamic forces (HDF) remain less established. Methods: This retrospective study included cardiac magnetic resonance (CMR) imaging from patients with d-TGA post-ASO, processed by a single core lab compared to normal controls. Feature-tracking analysis (QStrain, Medis) was performed on short- and long-axis cine images to assess LV global longitudinal strain (GLS), global circumferential strain (GCS), and conventional volumetric parameters. HDF were estimated from cine-derived velocity fields using the Navier–Stokes equations and Gauss’s divergence theorem, which permit calculation of net intracavitary force vectors from surface-integrated momentum flux across the endocardial surface. The analysis focused on the root mean square (RMS) magnitude of forces in apical-to-basal and septal-to-lateral directions during systole and diastole. All HDF values were normalized by ventricular volume and blood specific gravity to allow for inter-subject comparison. Results: Ninety-six d-TGA patients (mean age 18.6 years, mean BSA 1.59 m2) were included. LV GLS magnitude was significantly increased in the d-TGA group compared to normal controls (p =0.0005). Normalized systolic HDF values were reduced in d-TGA patients. A decrease in mean apex-to-base HDF RMS (p<0.0001), and septal-to-lateral (p=0.0001) was observed (image 1). These differences remained significant after adjusting for end-diastolic volume, strain, and aortic valve diameter (table 2), indicating an independent association with post-ASO anatomy. Conclusions: Patients with d-TGA following ASO demonstrate significantly altered left ventricular hemodynamic forces despite preserved or augmented myocardial strain. These reductions in systolic HDF may reflect a distinct biomechanical pattern related to ventricular function following ASO. The decoupling between strain and force metrics underscores the need for further investigation to determine whether alterations in HDF contribute to long-term remodeling or subclinical dysfunction in this population.