Competing pathways of intracranial aneurysm growth: linking regional growth distribution and hemodynamics

OBJECTIVE The complex mix of factors, including hemodynamic forces and wall remodeling mechanisms, that drive intracranial aneurysm growth is unclear. This study focuses on the specific regions within aneurysm walls where growth occurs and their relationship to the prevalent hemodynamic conditions to reveal critical mechanisms leading to enlargement. METHODS The authors examined hemodynamic models of 67 longitudinally followed aneurysms, identifying 88 growth regions. These regions (of enlargement) were pinpointed through alignment and distance mapping between baseline and follow-up models. Aneurysm wall subdivisions were created based on saccular anatomy and flow-related characteristics, which were used to assess local hemodynamics. The distribution of growing regions across these subdivisions was then studied and stratified by aneurysm location and morphology to reveal distinct growth patterns. Statistical significance was evaluated using the Kruskal-Wallis and Mann-Whitney tests. RESULTS Growth predominantly occurred in the body (p < 0.0001) of aneurysms, with anterior communicating artery (ACom) (p < 0.0001) and lateral (p = 0.002) aneurysms showing a significantly greater tendency for growth in this region. In comparison, middle cerebral artery (MCA) (p < 0.0001) and bifurcation (p = 0.0001) aneurysms demonstrated growth in both the dome and the body. Notable differences in growth distribution across saccular regions included ACom versus MCA (neck, p = 0.038), bifurcation versus lateral (neck, p = 0.008), and so forth. The central flow region saw the most growth (p < 0.0001); although not significant, ACom (p = 0.196) and lateral (p = 0.218) aneurysms showed a tendency for growth in inflow and central zones, while MCA (p = 0.001) and bifurcation (p < 0.0001) aneurysms were more likely to grow in the central flow region. CONCLUSIONS Two primary mechanisms seem to influence aneurysm growth: high-flow impingement jets in the neck, body, and inflow zones leading to wall degeneration/thinning, mainly in ACom aneurysms; and slow, oscillatory flow conditions in the dome and central flow zones promoting wall remodeling/thickening, mainly in MCA aneurysms. This latter mechanism is also observed as secondary flows in ACom aneurysms. These findings emphasize the need to understand the distinct and sometimes concurrent mechanisms of aneurysm growth, advocating for targeted monitoring and interventions that mitigate rupture risks by considering the unique hemodynamic environments within different aneurysm regions and locations.