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Updated: May 27, 2026
Intravascular Ultrasound Image-Based Finite Element Modeling Approach for Quantifying In Vivo Mechanical Properties of Human Coronary Artery
Published on: December 6, 2024
Image-based modeling of hemodynamics in coronary artery aneurysms caused by Kawasaki disease
Dibyendu Sengupta1, Andrew M Kahn, Jane C Burns
1Department of Mechanical and Aerospace Engineering, University of California San Diego-UCSD, San Diego, CA, USA.
Insights
Kawasaki Disease (KD) causes pediatric heart disease. Patient-specific modeling reveals abnormal blood flow and reduced wall shear stress in coronary artery aneurysms, increasing thrombosis risk.
Area of Science:
- Cardiovascular Science
- Biomedical Engineering
- Pediatric Cardiology
Background:
- Kawasaki Disease (KD) is a primary cause of acquired pediatric heart disease.
- Coronary artery aneurysms in KD patients elevate risks of thrombosis and myocardial infarction.
- Hemodynamic effects of KD-induced coronary aneurysms remain poorly understood.
Observation:
- Patient-specific modeling quantified hemodynamics and wall shear stress in KD coronary artery aneurysms.
- Multi-detector computed tomography (CT) data informed models of altered coronary anatomy.
- Simulations compared hemodynamics in aneurysmal vs. normal coronary arteries.
Findings:
- KD coronary artery aneurysms cause flow recirculation and significantly reduced wall shear stress.
- Wall shear stress in KD subjects was an order of magnitude lower than in normal models.
- Particle residence times were substantially higher in aneurysmal regions, indicating sluggish flow.
Implications:
- Abnormal flow patterns in KD coronary aneurysms are linked to increased thrombosis risk.
- This modeling approach offers insights into KD aneurysm hemodynamics.
- Methodology can aid in risk stratification for KD patients requiring intervention.
Abstract:
Kawasaki Disease (KD) is the leading cause of acquired pediatric heart disease. A subset of KD patients develops aneurysms in the coronary arteries, leading to increased risk of thrombosis and myocardial infarction. Currently, there are limited clinical data to guide the management of these patients, and the hemodynamic effects of these aneurysms are unknown. We applied patient-specific modeling to systematically quantify hemodynamics and wall shear stress in coronary arteries with aneurysms caused by KD. We modeled the hemodynamics in the aneurysms using anatomic data obtained by multi-detector computed tomography (CT) in a 10-year-old male subject who suffered KD at age 3 years. The altered hemodynamics were compared to that of a reconstructed normal coronary anatomy using our subject as the model. Computer simulations using a robust finite element framework were used to quantify time-varying shear stresses and particle trajectories in the coronary arteries. We accounted for the cardiac contractility and the microcirculation using physiologic downstream boundary conditions. The presence of aneurysms in the proximal coronary artery leads to flow recirculation, reduced wall shear stress within the aneurysm, and high wall shear stress gradients at the neck of the aneurysm. The wall shear stress in the KD subject (2.95-3.81 dynes/sq cm) was an order of magnitude lower than the normal control model (17.10-27.15 dynes/sq cm). Particle residence times were significantly higher, taking 5 cardiac cycles to fully clear from the aneurysmal regions in the KD subject compared to only 1.3 cardiac cycles from the corresponding regions of the normal model. In this novel quantitative study of hemodynamics in coronary aneurysms caused by KD, we documented markedly abnormal flow patterns that are associated with increased risk of thrombosis. This methodology has the potential to provide further insights into the effects of aneurysms in KD and to help risk stratify patients for appropriate medical and surgical interventions.
