ABSTRACT
Objectives To study the risk factors for influencing recrudescence after endovascular embolization of intracranial aneurysms and to establish a regression model to predict the risk of recrudescence in patients with specific intracranial aneurysm after endovascular embolization. Methods From May 2012 to May 2014,429 patients (a total of 441 aneurysms)with intracranial saccular aneurysm who met the inclusion criteria and treated with endovascular embolization at the Cerebrovascular Treatment Center, Changhai Hospital,the Second Military Medical University were analyzed retrospectively. Multiple aneurysms were calculated separately according to per aneurysm. The aneurysms were divided into either a recurrent group (n = 66)or an unrecurrent group (n = 375)according to whether they had recrudescence or not. The differences of 11 factors such as clinical features,treatment technology and materials,and aneurysm anatomy of both groups were compared. Logistic regression was used to analyze the risk factors for recrudescence after endovascular embolization of intracranial aneurysms,and its effectiveness of predicting recrudescence was evaluated. Results There were significant differences in the size of aneurysms (χ2 = 46. 352,P 10 -25 mm)(OR,4. 914,95% CI 2. 277 -10. 604,P 25 mm)(OR,35. 743,95% CI 3. 511 -363. 837,P = 0. 003) were the risk factors for recrudescence after aneurysm embolization. The effective test results of the regression model in predicting recrudescence showed that the area under the curve of the recrudescence predicting model was 73. 5% . Raymond grade was 56. 6%,and the non -stent embolization was 60. 1%,and the size of aneurysms was 40. 3% . Z test was used to calculate the differences of recurrent scores and non-stent embolization,Raymond grade,the area under ROC curve of aneurysm size. The Z values were 2. 662, 3. 513,and 6. 308,respectively,and the P values were 0. 007,0. 004,and 0. 001,respectively. Conclusions Large or giant aneurysms,non - stent - assisted embolization,incomplete embolization immediately after procedure were associated with the recrudescence after endovascular embolization of intracranial aneurysms. The established regression model may reflect the size of the recurrent risk.
ABSTRACT
Objective Toinvestigatethemolecularmechanismsofmitochondrialpathway-mediated apoptosisinintracranialaneurysminitiationinrabbits.Methods FifteenNewZealandwhiterabbitswere divided into 3 groups using the computer random method. After using bilateral carotid artery ligation for modeling basilar artery aneurysm,they were divided into a 2-day group (n=3),a 7-day group (n=6)(3 of them were used for real-time quantitative polymerase chain reaction [PCR]analysis),and a sham operation group (n=6)(3 of them were used for real-time quantitative PCR analysis). The tissue of apex of basilar artery was harvested and the histopathological changes in the vascular wall were observed. TUNEL staining was used to detect apoptotic cells and immunohistochemical staining,and quantitative analysis was used to analyze inflammatory cell distribution. Real-time quantitative PCR was used to detect the expression of apoptosis-related protein mRNA. Results (1 )After modeling,the apoptotic cells were found at the apex of basilar artery in rabbits (the site of internal elastic layer lesion )of the 2-day group and 7-day group. In the 2-day group after operation,the numbers of apoptotic cells (4. 02 ± 0. 21)were significantly higher than those of the basilar artery trunk (0. 40 ± 0. 13),the left posterior cerebral artery (0. 41 ± 0.22),and the right posterior cerebral artery (0. 29 ± 0. 11). The differences were statistically significant (P<0. 05). After modeling,the numbers of apoptotic cells (5. 01 ± 0. 29)of the 7-day group were significantly higher than those of the basilar artery trunk (0. 49 ± 0. 21),the left posterior cerebral artery (0. 31 ± 0. 12),and the right posterior cerebral artery (0. 41 ± 0. 19)(P<0. 05). The internal elastic layer lesions and apoptotic cells were not observed in the rabbits of the sham operation group. (2)After modeling, the expression levels of caspase 9 (1. 97 ± 0. 23)and caspase-3 mRNA (2. 31 ± 0. 40)at the apex of basilar artery in rabbits of the 7-day group were increased significantly compared with that of the sham group (P<0.01).Conclusion Apoptosisisinvolvedintheearlyprocessofaneurysmsinsimple hemodynamics-induced basilar terminus aneurysm formation. Its molecular mechanisms are activated by Bcl-2-mediated mitochondrial pathway through caspase-9.