A systematic quantification of hemodynamic differences persisting after aortic coarctation repair

Abstract

Introduction: Aortic coarctation (CoA) comprises 6%-8% of all congenital heart diseases and is the second most common cardiovascular disease requiring neonatal surgical correction. However, patients remain at high risk for long-term complications, notably recoarctation.

Methods: Hemodynamic simulations were performed in a group of six patients following CoA repair, as compared to a group of age and sex-matched healthy controls. Progressive narrowing at the CoA repair site was modeled to simulate the recoarctation process. Key measurements included time-averaged wall shear stress (TAWSS) in the aortic arch and CoA repair site.

Results: Repaired aortas demonstrated significantly higher TAWSS compared to healthy aortas in the aortic arch (3.46 vs 1.24 Pa, p $<$ 0.05) and CoA repair site (4.34 vs 1.56 Pa, p $<$ 0.05). A pronounced nonlinear relationship between stenosis severity and TAWSS was observed suggesting that increasing stenosis corresponds to progressively abnormal shear stress.

Discussion: The persistent high TAWSS in CoA-repaired aortas may underlie the poor long-term outcomes observed in this population. The identified nonlinear relationship between stenosis severity and TAWSS magnitude suggests a potential positive feedback mechanism, where abnormal shear stress exacerbates pathologic remodeling in the repaired aorta, highlighting the potential role of hemodynamic simulations in the clinical management of CoA patients.

Keywords: aortic coarctation; computational fluid dynamics; late aneurysmal degeneration; long-term complications of coarctation; restenosis.

FIGURE 1

Baseline aortic geometries of repaired coarctation patients (top row) and healthy control patients (middle row.) Each geometry is paired with its matched control (e.g., R0 with C0, R1 with C1, etc. Bottom row, from left: Representative geometry with stenosis $\sigma =0$ % (unmodified baseline), 10%, 50%, and 80%.

FIGURE 2

Top panel, from left: Peak systolic wall shear stress (WSS) in the aorta of a patient with repaired CoA. The repair site is clearly visible as a band of elevated WSS. Middle: a vessel wall section demonstrating the cylindrical coordinate re-parameterization: r is the distance from the aortic wall to the vessel centerline (dashed line); $\theta =0$ corresponds to the inner curve of the aorta, while $\theta =\pm \pi$ corresponds to the outside curve; finally, the vessel centerline is normalized to have length 1, ranging from l = 1 (aortic inlet) to l = 0 (distal aortic outlet). Right: This normalized cylindrical coordinate system allows any aortic vessel wall to be “unwrapped” into a 2D plot of l and $\theta$ , with the repair site now seen as a horizontal band of elevated WSS.

FIGURE 3

Top: TAWSS following CoA repair is significantly elevated in the aortic arch and lesion repair site (bold line = median TAWSS, shaded region = IQR). Bottom left: TAWSS is smoothly and uniformly distributed across the aortic endothelium of the control cohort, but is notably elevated around the aortic arch and the outer curvature of the repair site (bottom middle), which is further highlighted by the repaired/control TAWSS ratio (bottom right).

FIGURE 4

By contrast, oscillatory shear index (OSI) is higher in the aortic arch but lower in the CoA region and pDA. Shear metrics are plotted as median (bold line) with IQR (shaded region).

FIGURE 5

Circumferentially-averaged time-averaged wall shear stress (TAWSS) plotted along the aortic centerline for control (top left) and repaired patient cohorts (bottom left). Cohort data summarized as median (line) and interquartile range (shaded region). Right: Both cohorts demonstrate a sharp, nonlinear relationship between stenosis severity $\sigma$ and peak TAWSS (dashed lines), as well as peak systolic WSS (solid lines).

FIGURE 6

Circumferentially-averaged oscillatory shear index (OSI) plotted along the aortic centerline for repaired (top left) and control cohorts (bottom left). Cohort data summarized as median (line) and interquartile range (shaded region). Right: OSI sharply increases from $\sigma =10$ % to 50%, but then decreases.

FIGURE 7

Left: oscillatory shear index (OSI) heatmaps for all control geometries (top) and repair geometries (bottom), stratified by CoA severity $\sigma$ . Right, from top: histograms of OSI distribution across $\theta$ at the aortic arch (top), coarctation region (middle), and proximal descending aorta (bottom) can better show OSI variation within aortic regions of interest.

FIGURE 8

L2 norms of TAWSS (top row) and OSI (bottom row) for healthy controls (left) and repaired patients (right). Comparisons are calculated by taking the L2 norm of the difference in TAWSS/OSI between two geometry heatmaps, then normalizing by the maximum L2 norm value. The rightmost column shows the median L2 norm value for each geometry, as compared to all other geometries in the cohort.

FIGURE 9

TAWSS maps of three different hemodynamic phenotypes following coarctation repair: residual stenosis (left), arch angulation (middle), and normal/uniform (right). Velocity field streamlines in the thoracic aortic section at three synthetically generated stenosis degrees (10%, 50%, and 80%), showing progressive complexity of ascending and arch flow regimes by increasing degree of residual and/or re-coarctation.

FIGURE 10

Unwrapped distribution of significant (dark gray) differences in TAWSS and OSI between Repaired and Control groups. A linear mixed effect approach was used to model hemodynamic metrics of interest with designed main effects, i.e., Group, Severity, and the interaction term Group:Severity as fixed effects whereas other patient-specific predictors not included in the current study were lumped into a random effect with one categorical outcome per case. This way, the patient-specific baseline variability in TAWSS and OSI were incorporated into the random effect and accounted for in the statistical analysis. Statistical inferences are made based on a 0.05 level of significance.