Mr. David C. Wendell Profile

David C. Wendell

at Marquette Univ

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Proceedings Article | 9 March 2010 Paper

A new image-based process for quantifying hemodynamic contributions to long-term morbidity in a rabbit model of aortic coarctation

David Wendell, Ronak Dholakia, Paul Larsen, Arjun Menon, John LaDisa

Proceedings Volume 7626, 76260J (2010) https://doi.org/10.1117/12.846373

KEYWORDS: Hemodynamics, Data modeling, Magnetic resonance imaging, Arteries, Blood circulation, Heart, Blood pressure, Image segmentation, Computational fluid dynamics, Cardiovascular magnetic resonance imaging

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Coarctation of the aorta (CoA) is associated with reduced life expectancy despite successful surgical treatment. Interestingly, much of the related long-term morbidity can be explained by abnormal hemodynamics, vascular biomechanics and cardiac function. MRI has played an important role in assessing coarctation severity, but the heterogeneity and small number of patients at each center presents an obstacle for determining causality. This work describes optimized imaging parameters to create computational fluid dynamics (CFD) models revealing changes in hemodynamics and vascular biomechanics from a rabbit model. CoA was induced surgically at 10 weeks using silk or dissolvable ligatures to replicate native and end-to-end treatment cases, respectively. Cardiac function was evaluated at 32 weeks using a fastcard SPGR sequence in 6-8 two-chamber short-axis views. Left ventricular (LV) volume, ejection fraction, and mass were quantified and compared to control rabbits. Phase contrast (PC) and angiographic MRI were used to create CFD models. Ascending aortic PCMRI data were mapped to the model inflow and outflow boundary conditions replicated measured pressure (BP) and flow. CFD simulations were performed using a stabilized finite element method to calculate indices including velocity, BP and wall shear stress (WSS). CoA models displayed higher velocity through the coarctation region and decreased velocity elsewhere, leading to decreased WSS above and below the stenosis. Pronounced wall displacement was associated with CoA-induced changes in BP. CoA caused reversible LV hypertrophy. Cardiac function was maintained, but caused a persistent hyperdynamic state. This model may now be used to investigate potential mechanisms of long-term morbidity.

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