A structural multi-mechanism damage model for cerebral arterial tissue.

Area of Science:

• Biomedical Engineering
• Computational Mechanics
• Cardiovascular Research

Background:

• Early-stage cerebral aneurysms involve internal elastic lamina disruption.
• The exact cause of this breakdown remains unclear, with theories including fatigue failure and hemodynamic stress.
• Understanding this process is crucial for predicting aneurysm formation and rupture.

Purpose of the Study:

• To model the disruption of the internal elastic lamina in early cerebral aneurysms.
• To incorporate structural damage mechanisms into a previously developed constitutive model for cerebral arteries.
• To investigate the role of elastin degradation and collagen fiber recruitment in aneurysm development.

Main Methods:

• Developed a structural damage model based on nonlinear, inelastic multi-mechanism models for cerebral arteries.
• Included subfailure damage of elastin, affecting tissue mechanical properties and reference length.
• Modeled anisotropic collagen fibers arranged in two helical families with dispersed orientations.
• Evaluated the constitutive model using experimental data and implemented it in finite element analysis software.
• Validated the model using analytical solutions.

Main Results:

• The model characterizes gradual degradation of elastin and the recruitment of anisotropic collagen fibers.
• Simulations capture changes in tissue mechanical properties due to subfailure damage.
• The model provides a framework for understanding the interplay between hemodynamics, wall tension, and tissue failure.

Conclusions:

• The proposed structural damage model offers a novel approach to simulating early cerebral aneurysm development.
• This model can elucidate the mechanisms underlying internal elastic lamina disruption.
• Further research can utilize this model for predicting aneurysm progression and informing treatment strategies.