Particle-based computational modelling of arterial disease.

Area of Science:

• Biomedical Engineering
• Computational Biology
• Cardiovascular Research

Background:

• Accumulated glycosaminoglycans (GAGs) sequester water, causing arterial wall swelling.
• Focal swelling-induced stress concentrations are implicated in thoracic aortic disease damage and delamination.

Purpose of the Study:

• To computationally examine the role of pooled GAGs in initiating and propagating intra-lamellar delaminations in the aorta.
• To investigate how GAG accumulation affects aortic wall mechanics and stress distributions.

Main Methods:

• Utilized an extended smoothed particle hydrodynamics (SPH) approach for computational simulations.
• Modeled the murine descending thoracic aorta, calculating stress distributions in healthy and GAG-affected regions.

Main Results:

• Simulations revealed increased mechanical stress around GAG pools.
• Smooth muscle activation offered partial protection, but delamination occurred with smooth muscle dysfunction or absence.
• Nearby GAG pools were shown to coalesce, propagating delamination.

Conclusions:

• Localized GAG swelling can significantly alter aortic mechanics, potentially causing catastrophic wall damage.
• GAGs play a critical role in aortic pathology, necessitating their consideration in disease mechanisms.
• Smooth muscle function is crucial in mitigating GAG-induced swelling damage.