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Computational model of coarctation of the aorta in rabbits suggests persistent ascending aortic remodeling post-correction
Computational model of coarctation of the aorta in rabbits suggests persistent ascending aortic remodeling post-correction
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Computational model of coarctation of the aorta in rabbits suggests persistent ascending aortic remodeling post-correction
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Computational model of coarctation of the aorta in rabbits suggests persistent ascending aortic remodeling post-correction
Computational model of coarctation of the aorta in rabbits suggests persistent ascending aortic remodeling post-correction

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Computational model of coarctation of the aorta in rabbits suggests persistent ascending aortic remodeling post-correction
Computational model of coarctation of the aorta in rabbits suggests persistent ascending aortic remodeling post-correction
Journal Article

Computational model of coarctation of the aorta in rabbits suggests persistent ascending aortic remodeling post-correction

2025
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Overview
Coarctation of the aorta (CoA) is a common congenital cardiovascular lesion that presents as a localized narrowing of the proximal descending aorta. While improvements in surgical and catheter-based techniques have increased short-term survival, there is a high long-term risk of hypertension and a reduced average lifespan despite correction. Computational models can be used to estimate aortic remodeling and peripheral vascular compensation, potentially serving as key tools in developing a mechanistic understanding of the interplay between pre-treatment dynamics, post-treatment recovery, and long-term hypertension risk. In this study, we developed a lumped-parameter model of the heart and circulation to simulate CoA. After fitting model parameters using imaging and catheterization data from healthy rabbits, we then used the model to estimate differences in ascending aortic compliance and peripheral resistance between the healthy group and rabbits with both untreated and corrected CoA using their imaging and catheterization data. CoA was defined by the current putative clinical treatment threshold (a pressure gradient > 20 mm Hg). Model inputs were fitted such that outputs matched reported stroke volume, ejection fraction, systolic and diastolic aortic pressure, peak aortic flow, mean and peak blood pressure gradients, and upper-to-lower body flow split, with all results falling within one standard deviation of the data for all groups. In the untreated CoA and corrected simulations, a decrease in ascending aortic compliance was necessary to match reported hemodynamics. This suggests exposure to a pressure gradient > 20 mm Hg results in vascular remodeling that persists after repair, a process strongly correlated with hypertension.