## 4 Discussion
Previous research suggests patients with PHT demonstrate lower wall shear stress [5; 7]. Although these studies were conducted using an adult PHT population, the findings possess relevance to the broader definition of PHT. For vorticity, a recent study conducted by [PERSON] et al. found that vortices are observed in healthy controls and patients with PHT [19]. Similarly, [PERSON] et al. identified reduced vorticity but increased helicity in patients with PHT [6]. For EL, [PERSON] et al. demonstrated greater total energy losses over the cardiac cycle throughout the entirety of the PA [20] in PHT patients. PHT patients may also demonstrate greater retrograde flow and lower peak velocity [21; 22]. In contrast, anatomical changes are more well-studied using CT, identifying dilation of the main pulmonary artery in various stages of the disease [23; 24]. These findings have been replicated using MRI and appear to be prevalent in the later stages [25]. Our findings generally corroborate results of previous studies and provide insight into novel biomarkers. We observed lower WSS, maximum energy attained, and regurgitation fractions in the LPA and RPA in patients with PHT. Maximum EL at peak systole remained lower in patients than in controls in all PA sections. Mean EL tended to be also lower, except for the LPA. EL reported in our study was quantified at peak systole, which provides further support in addition of previous findings reported over the cardiac cycle. Contrary to other studies, we found that vorticity tended to increase in PHT patients. For anatomical changes, we observed dilation in the MPA and part of the RPA. Of note, we are the first study to our knowledge to identify greater bifurcation distances associated with PHT. We speculate this could be an additional form of anatomical remodeling associated with disease progression. However, the exact significance is unknown. Further studies investigating changes in bifurcation geometry at various disease stages are needed to better understand their significance. The difference between the RPA and LPA characterization may be influenced by the patient's anatomy and the hemodynamic resistance from the lungs. However, the latter requires additional investigation. Furthermore, sex-matching analysis confirmed the impact of advanced hemodynamic parameters in PHT patients and highlighted the importance of subject matching in future studies. This study has a few limitations. First, our study was limited by the spatiotemporal resolution constraints of MRI. For example, while we could visualize larger vortex networks, smaller vortices occurring at faster speeds exceeding the available resolution could be missed. Second, as a single centre study, the addition of multiple centres would improve the generalization of results. Furthermore, due to its retrospective nature, the sample size and power is limited. Third, our control patients were not age and sex-normalized to the patient cohort, which suggests normal cardiac aging and sex differences could have impacted results. Fourth, PHT is a progressive multi-factorial condition with diverse underlying etiology. Clinical protocols did not mandate further characterization of the disease into smaller subgroups such as pulmonary arterial hypertension, or patients at varying stages of the disease, limiting the characterization of disease progression. The relatively small cohort size did not allow one to explore the effect of medical therapy in 4D-flow derived parameters. The latter remains an important aspect to assess in future studies. Finally, we did not explore the right ventriculo-pulmonary arterial coupling in the present cohort. This coupling analysis may produce a better understanding of the bidirectional effects between the RV and the pulmonary artery tree.