Modelling intracranial aneurysm stability/enlargement: a patient-specific mechanobiological framework

We model the enlargement of clinically detected intracranial aneurysms. The tissue is modelled as a fibre-reinforced constrained mixture and represents the collagen fibre attachment stretch distribution and its remodelling. Tissue growth and remodelling is linked to pulsatile hemodynamic stimuli and cyclic deformation. The collagenous adventitia of the parent artery is modelled as a protective mechanical sheath whereas collagen is modelled as the dominant load bearer in the aneurysm sac. Initially, we assume that the collagen fabric is in homeostasis throughout the domain. Subsequent localised collagen degradation associated with a dysfunctional endothelium drives the formation of secondary blebs on the aneurysm dome.