Flow alterations in the pulmonary artery (PA) of patients with repaired tetralogy of Fallot (rTOF) may be link with the expending of kinetic energy (KE)¹. Furthermore, complex flow patterns (vortical and helical) may be associated with the energy dissipation within the PA² and can be evaluated by the mean of flow vorticity³. Three-dimensional time-resolved phase contrast MRI (4D flow) allows for the non-invasive volumetric assessment of flow hemodynamics, vorticity, and KE in patients with rTOF in the PA. Thus, the aim was to investigate the impact of flow alterations in the PA and its association with KE and vorticity.15 pediatric patients with rTF (age=9±6 yrs, 6 females) underwent aortic 4D flow MRI as part of an IRB-approved protocol. 4D flow MRI⁴ was performed at 1.5T (Philips, Achieva, Best, The Netherlands) with full 3D coverage of the thoracic aorta and PA (spatial resolution=2.5×2.1×3.2 mm³; temporal resolution=40-50 ms) using prospective PPU and respiratory navigator gating. Pulse sequence parameters were as follows: 1.5 T scan parameters ranged from TE/TR=2.3–3.4/4.8–6.6 ms, flip angle α=15°, Venc= 1.5-5 m/s, and a field of view of 340–400×200–300 mm. 4D flow dataset pre-processing⁵ include: eddy-current correction, flow aliasing, and calculation of 3D phase contrast angiography (3D PC-MRA). A 3D segmentation of the PA (Figure 1B) was obtained from the 3D PC-MRA using Matlab (The Mathworks, Natick, MA, USA) and was used to mask the PA velocity field and for flow pattern visualization in the PA. Masked velocity field was used to calculate KE (KE=1/2×rho×v², were rho is the blood density = 1.06 g/mL and v the velocity field), and vorticity (ω= curl (v)). Maximum intensity projections (MIPs) were calculated for flow velocity, KE, and vorticity. Flow measurements were perform the main pulmonary artery (MPA), right pulmonary artery (RPA), and left pulmonary artery (LPA) using manually located analysis planes (Figure 1C). From each plane (MPA, RPA, LPA) the pulmonic lumen was segmented and used to extract following flow hemodynamic parameters: peak velocity (PV), maximal flow (Qmax), mean flow (Qmean). Volumetric median of KE was used to divide the evaluated cohort in two groups: 1) low KE and 2) elevated KE. The association of kinetic energy at MPA, RPA, and LPA with other flow parameters were assessed by Pearson’s correlation. Comparison between low and elevated KE groups was performed by Mann-Whiteney test.Maximal, mean KE in the pulmonary artery showed a global correlation with PV (r=0.47, p=0.008; r=0.38, p<0.037), Qmax (r=0.49, p<0.005; r=0.45, p<0.014), and Qmean (r=0.49, p<0.006; r=0.44, p<0.015). Both maximal and mean KE were mainly originated from the RPA where associations with PV (r=0.87, p=0.001; r=0.84, p<0.002), Qmax (r=0.77, p<0.01; r=0.75, p<0.013), and Qmean (r=0.69, p=0.028; r=0.69, p=0.027) were more important. Maximal KE was 59% higher in the MPA than in the RPA, as well as mean KE with 33% increment. Flow distribution was the major contributor to these correlations and increment in the RPA for KE. Velocity, KE, and vorticity MIPs (Figure 1E) allowed to identify regions proximal to pulmonary bifurcation with elevated KE, and vortical flow in the dominant direction of the flow. PA volumetric mean and median KE were associated with volumetric mean vorticity, r=0.78 (p<0.001) and r=0.44 (p<0.001) respectively. When comparing low and elevated KE significant differences were found for volumetric mean KE (0.029±0.019 mJ vs. 0.047±0.022 mJ, p=0.02), median KE (0.041±0.012 mJ vs. 0.07±0.02 mJ, p<0.001), and mean vorticity (0.032±0.008 1/s vs. 0.037±0.006 1/s, p<0.04).In this pilot study, maximal and mean KE in the RPA was associated with flow hemodynamic parameters, whereas KE in the MPA and LPA were not. This observation was explain by flow distribution within the PA and the regions (proximal PA bifurcation) where elevated energy dissipation occurs. A large cohort study is needed to evaluate the clinical usefulness of KE to survey patients with rTOF.