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Published on: November 26, 2018
A systematic quantification of hemodynamic differences persisting after aortic coarctation repair
Christopher Jensen1,2, Arash Ghorbannia1, David Urick1,3
1Department of Biomedical Engineering, Duke University, Durham, NC, United States.
Insights
High shear stress in repaired aortic coarctation may cause poor outcomes. Abnormal shear stress and stenosis severity show a nonlinear relationship, potentially worsening aortic remodeling.
Area of Science:
- Cardiovascular Surgery
- Biomedical Engineering
- Medical Imaging
Background:
- Aortic coarctation (CoA) is a significant congenital heart defect, often requiring surgical repair.
- Patients with repaired CoA face high risks of long-term complications, particularly recoarctation.
Purpose of the Study:
- To investigate the relationship between hemodynamic factors and long-term outcomes in patients with repaired aortic coarctation.
- To assess wall shear stress in the aortic arch and repair site of CoA patients compared to healthy controls.
Main Methods:
- Hemodynamic simulations were conducted on six patients post-CoA repair and age/sex-matched healthy controls.
- Progressive narrowing at the CoA repair site was modeled to simulate recoarctation.
- Time-averaged wall shear stress (TAWSS) was measured in the aortic arch and at the CoA repair site.
Main Results:
- Repaired aortas exhibited significantly higher TAWSS in both the aortic arch (3.46 vs 1.24 Pa) and at the repair site (4.34 vs 1.56 Pa) compared to healthy aortas.
- A nonlinear relationship was observed between stenosis severity and TAWSS, indicating that increasing narrowing leads to disproportionately abnormal shear stress.
Conclusions:
- Elevated TAWSS in repaired aortas may contribute to poor long-term outcomes and recoarctation.
- The nonlinear relationship suggests a feedback mechanism where abnormal shear stress exacerbates pathological remodeling.
- Hemodynamic simulations show promise for clinical management of aortic coarctation patients.
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.
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