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    The prognostic effects of hemodynamic parameters on rupture of intracranial aneurysm: A systematic review and meta-analysis. Han Peng,Jin Dianshi,Wei Wei,Song Chong,Leng Xiaolei,Liu Le,Yu Jun,Li Xuqin International journal of surgery (London, England) BACKGROUND:Many risk factors are associated with rupture of intracranial aneurysm. However, the prognostic effects hemodynamic factors on intracranial aneurysm rupture remains poorly understood. A meta-analysis was performed based on contemporary studies to evaluate the prognostic effect of hemodynamic parameters on rupture of intracranial aneurysm. METHODS:The Cochrane Library, PubMed, Embase, and Web of Science were searched for cohort studies that analyzed hemodynamic parameters for intracranial aneurysm rupture prior to May 1, 2020. The standardized mean difference (SMD) and odds ratio (OR) with 95% confidence interval (CI) were calculated to assess the effect of individual hemodynamic parameters on intracranial aneurysm rupture. The primary outcomes were difference in wall shear stress (WSS), oscillatory shear index (OSI) and low shear index (LSA) between ruptured and unruptured intracranial aneurysm. Two reviewers independently assessed the quality of the trials and the associated data. All statistical analyses were performed using standard statistical procedures in Review Manager 5.2. RESULTS:A total of 15 studies including 779 patients with 900 aneurysms were identified for this meta-analysis. The pooled results indicated that the average WSS, OSI and LSA% had significant associations with rupture of intracranial aneurysm, with pooled SMDs of -0.36 (95% CI -0.57 to -0.15; P = 0.001), 0.37 (95% CI 0.19 to 0.55; P < 0.0001) and 0.57% (95% CI 0.18 to 0.95; P = 0.004), respectively. In addition, other hemodynamic parameters, including aneurysm size, aspect ratio, mean volume, undulation index, ellipticity index, nonsphericity index, number of vorticies, and relative residence time significant associations with intracranial aneurysm rupture. Multivariate analysis indicated that circumferential wall tension, angle btwn, irregular shape and size of aneurysms were independent risk factors of intracranial aneurysm rupture. CONCLUSIONS:This meta-analysis identified WSS, OSI and LSA% as influential hemodynamic parameters on rupture of intracranial aneurysm. The roles of other hemodynamic parameters and risk factors for intracranial aneurysm rupture need further assessments in future. 10.1016/j.ijsu.2020.12.012
    Saccular intracranial aneurysm: pathology and mechanisms. Frösen Juhana,Tulamo Riikka,Paetau Anders,Laaksamo Elisa,Korja Miikka,Laakso Aki,Niemelä Mika,Hernesniemi Juha Acta neuropathologica Saccular intracranial aneurysms (sIA) are pouch-like pathological dilatations of intracranial arteries that develop when the cerebral artery wall becomes too weak to resist hemodynamic pressure and distends. Some sIAs remain stable over time, but in others mural cells die, the matrix degenerates, and eventually the wall ruptures, causing life-threatening hemorrhage. The wall of unruptured sIAs is characterized by myointimal hyperplasia and organizing thrombus, whereas that of ruptured sIAs is characterized by a decellularized, degenerated matrix and a poorly organized luminal thrombus. Cell-mediated and humoral inflammatory reaction is seen in both, but inflammation is clearly associated with degenerated and ruptured walls. Inflammation, however, seems to be a reaction to the ongoing degenerative processes, rather than the cause. Current data suggest that the loss of mural cells and wall degeneration are related to impaired endothelial function and high oxidative stress, caused in part by luminal thrombosis. The aberrant flow conditions caused by sIA geometry are the likely cause of the endothelial dysfunction, which results in accumulation of cytotoxic and pro-inflammatory substances into the sIA wall, as well as thrombus formation. This may start the processes that eventually can lead to the decellularized and degenerated sIA wall that is prone to rupture. 10.1007/s00401-011-0939-3