Pulmonary artery hemodynamic assessment of blood flow characteristics in repaired tetralogy of Fallot patients versus healthy child volunteers

Background: This study aimed to assess the severity of helix and vortex flow in pulmonary artery hemodynamic using 4-dimensional flow cardiac magnetic resonance (4D flow CMR) in patients with repaired tetralogy of Fallot (rTOF) and healthy child volunteers and to explore the relationship between pulmonary hemodynamic changes and right heart function. Methods: CMR studies were performed in 25 rTOF patients (15 M/10 F; 8.44 +/- 4.52 years) and 10 normal child volunteers (7 M/3 F; 8.2 +/- 1.22 years) on 3.0T MR scanners. Cardiac function was calculated in the patient and control groups. Systolic diameter, peak velocity, net flow, and regurgitation was quantified in the main pulmonary artery ( MPA) plane, left pulmonary artery (LPA) plane, and right pulmonary artery (RPA) plane. The relationship between the hemodynamic parameters and quantitative flow indices and right ventricular (RV) function were analyzed through simple linear regression analysis using Pearson R-values. We analyzed differences in flow patterns between the 2 groups for the same slice. According to the severity of the helix and vortex flow in the 4D flow CMR, we categorized rTOF patients into the following groups: group 1, severe flow grading; group 2, mild flow grading; group 3, no flow grading; the control cases with no flow grade were included in group 4. We compared RV cardiac function, wall shear stress (WSS), and viscous energy loss (EL) between group 1+2 and group 3+4 using unpaired t-test analysis for normally distributed data and the Mann-Whitney test for non-normally distributed continuous variables. Results: RV end- diastolic volume index (EDVi) (127.8 +/- 36.13 vs. 83.11 +/- 6.18, respectively; P<0.001), RV end- systolic volume index (ESVi) (65.14 +/- 27.02 vs. 36.13 +/- 5.95, respectively; P<0.001), and ejection fraction (EF) (49.97 +/- 6.39 vs. 56.71 +/- 4.56, respectively; P= 0.006,) were significantly different between the groups. The rTOF diameters of the MPA and RPA were significantly larger than those of the control group (19.74 +/- 4.01 vs. 14.97 +/- 2.37 for MPA, P= 0.001; 12.04 +/- 3.28 vs. 8.99 +/- 1.23 for RPA, P=0.004, respectively). There were correlations between peak WSS and pulmonary regurgitation ( PR) in the MPA (R=0.48, P=0.014), correlations between peak systolic EL and RVEDV (R=0.51, P=0.008), and between peak systolic EL and RVESV (R=0.51, P=0.009). The peak systole and diastole WSS of group 1+2 were significantly different compared to group 3+4 in the MPA (P<0.05). The peak systole and diastole EL of group 1+2 was significantly different from group 3+4 in the MPA (P<0.05). The peak systole EL of group 1+ 2 was significantly different from group 3+4 in the RPA (P<0.01). Conclusions: Increased peak WSS and EL were associated with pulmonary hemodynamic changes in the MPA and RPA. There might be an earlier marker of evolving hemodynamic inefficiency than that in traditional parameters. The better understanding of pulmonary artery hemodynamic assessment in rTOF may lead to a greater insight into pulmonary artery (PA)-RV interactions and how they ultimately impact RV function.