Key Points
- To identify the biomechanical, hemodynamic, and physical factors responsible for the initiation, structural enlargement, and eventual rupture of human intracranial saccular aneurysms.
- Simulated arterial bifurcation hemodynamics using glass flow models to evaluate mechanical force distributions at vessel apexes.
- Auscultated aneurysm sacs for turbulent bruits (N=19) and directly recorded intra-aneurysmal pressures (N=4) during craniotomy.
- Assessed the static elastic properties and distensibility of human intracranial aneurysm wall segments in vitro relative to normal intracranial arteries.
- Turbulent blood flow bruits were detected in 12 of 19 intraoperatively monitored aneurysms (63.2%), and direct recordings confirmed intra-aneurysmal pressure equaled systemic arterial pressure (N=4).
- Aneurysm walls exhibited severe nondistensibility compared to normal major intracranial arteries, reflecting focal destruction of the internal elastic membrane.
- Physical analysis demonstrated that rupture likelihood increases with higher intra-aneurysmal pressure, larger sac diameter, reduced minimum wall thickness, and reduced structural tissue strength.
Structured PICO
PPopulation19 clinical cases of human intracranial saccular aneurysms studied at the time of craniotomy, along with glass models and in vitro human intracranial aneurysm specimens.
OOutcomeHemodynamic forces, turbulence (bruits), intra-aneurysmal pressure, and static elastic propertiessurrogate
This biomechanical study demonstrates that hemodynamic forces, turbulence, and altered elasticity play critical roles in the initiation, growth, and rupture of intracranial saccular aneurysms.