RESUMEN
Background: Understanding the risk factors leading to intracranial aneurysm (IA) rupture have still not been fully clarified. They are vital for proper medical guidance of patients harboring unruptured IAs. Clarifying the hemodynamics associated with the point of rupture could help could provide useful information about some of the risk factors. Thus far, few studies have studied this issue with often diverging conclusions. Methods: We identified a point of rupture in patients operated for an IAs during surgery, using a combination of preoperative computed tomography (CT) and computed tomography angiography (CTA). Hemodynamic parameters were calculated both for the aneurysm sac as a whole and the point of rupture. In two cases, the results of CFD were compared with those of the experiment using particle image velocimetry (PIV). Results: We were able to identify 6 aneurysms with a well-demarcated point of rupture. In four aneurysms, the rupture point was near the vortex with low wall shear stress (WSS) and high oscillatory shear index (OSI). In one case, the rupture point was in the flow jet with high WSS. In the last case, the rupture point was in the significant bleb and no specific hemodynamic parameters were found. The CFD results were verified in the PIV part of the study. Conclusion: Our study shows that different hemodynamic scenarios are associated with the site of IA rupture. The numerical simulations were confirmed by laboratory models. This study further supports the hypothesis that various pathological pathways may lead to aneurysm wall damage resulting in its rupture.
RESUMEN
PURPOSE: Intracranial aneurysm (IA) rupture results in one of the most severe forms of stroke, with severe neurological sequelae. Inflammation appears to drive aneurysm formation and progression with macrophages playing a key role in this process. However, less is known about their involvement in aneurysm rupture. This study is aimed at demonstrating how relationship between the M1 (pro-inflammatory) and M2 (reparative) macrophage subtypes affect an aneurysm's structure resulting in its rupture. METHODS: Forty-one saccular aneurysm wall samples were collected during surgery including 13 ruptured and 28 unruptured aneurysm sacs. Structural changes were evaluated using histological staining. Macrophages in the aneurysm wall were quantified and defined as M1 and M2 using HLA-DR and CD163 antibodies. Aneurysm samples were divided into four groups according to the structural changes and the M2/1 ratio. Data were analyzed using the Mann-Whitney U test. RESULTS: This study has demonstrated an association between the severity of structural changes of an aneurysm with inflammatory cell infiltration within its wall and subsequent aneurysm rupture. More severe morphological changes and a significantly higher number of inflammatory cells were observed in ruptured IAs (p < 0.001). There was a prevalence of M2 macrophage subtypes within the wall of ruptured aneurysms (p < 0.001). A subgroup of unruptured IAs with morphological and inflammatory changes similar to ruptured IAs was observed. The common feature of this subgroup was the presence of an intraluminal thrombus. CONCLUSIONS: The degree of inflammatory cell infiltration associated with a shift in macrophage phenotype towards M2 macrophages could play an important role in structural changes of the aneurysm wall leading to its rupture.
