前交通动脉瘤形成、破裂和复发的危险因素及破裂的血流动力学机制研究
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摘要
第一部分前交通动脉瘤生成的危险因素研究
     背景与目的:
     颅内动脉瘤一旦破裂,就会引起蛛网膜下腔出血,其病死率和病残率都非常高。因此对动脉瘤的病因学研究意义重大。虽然对颅内动脉瘤形成的危险因素研究较多,但是对前交通动脉瘤目前还缺乏亚组分析。前交通动脉瘤是前循环中最为复杂的一个动脉瘤亚组,前交通动脉血管解剖生理非常特殊。本研究的目的是探讨前交通动脉瘤形成的独特的危险因素,从而为临床预防提供理论基础。
     资料与方法:
     本研究是一项回顾性病例对照研究。病例组收集自2006年1月至2012年10月间收治的256例前交通动脉瘤病例,均经由磁共振血管造影或数字减影血管造影证实。对照组为512例没有颅内动脉瘤的患者。我们对各种可能的危险因素都进行了数据收集,分析各临床和解剖生理因素在前交通动脉瘤形成中所起的作用。为了找出前交通动脉瘤形成的危险因素,我们对各种危险因素运用了单因素分析和多因素逻辑回归分析。
     结果:
     病例组的平均年龄大于对照组(P值=0.016)。单因素分析揭示:高血压、前交通动脉单侧优势A1段或一侧缺如A1段,与前交通动脉瘤的发生明显相关。多因素逻辑回归分析表明:年龄(比值比1.014,95%可信区间1.001到1.027)、高血压病史(比值比1.627,95%可信区间1.090到2.135)、单侧优势A1段(比值比2.845,95%可信区间2.019-04.009)或一侧缺如A1段(比值比4.301,95%可信区间2.174到8.507)都是前交通动脉瘤形成的独立危险因素。
     结论:
     年龄、高血压、单侧优势A1段或一侧缺如A1段,这些都是形成前交通动脉瘤的独立危险因素。对于具有这些危险因素的人群,应该运用磁共振血管造影定期筛查,早期发现前交通动脉瘤。当然,这种筛查需要卫生经济学上的进一步评估。
     第二部分年龄、瘤体大小和A1段血管构象预测前交通动脉瘤的破裂风险
     背景与目的:
     随着神经影像学的进步,颅内动脉瘤的发现率相应提高。预防动脉瘤破裂出血是降低病死率和病残率最有效的方式。因此,对动脉瘤破裂风险因素进行研究很有价值,有益于预测动脉瘤将来破裂风险。尽管笼统的颅内动脉瘤破裂的危险因素已有所研究,但是前交通动脉瘤这一亚组的破裂风险却鲜有研究。基于前交通动脉解剖生理的特殊性,前交通动脉瘤被认为是前循环中最为复杂的一个动脉瘤亚组。本研究旨在分析前交通动脉瘤破裂的危险因素,为临床决策提供理论依据。
     资料与方法:
     本研究收集了自2006年6月至2012年10月间在我院收治的前交通动脉瘤病例。全部病例经由磁共振血管造影(MRA)或数字减影血管造影(DSA)检查证实。前交通动脉瘤破裂的危险因素有可能为:患者临床特征、前交通动脉A1段解剖构象和动脉瘤瘤体相关特征。比较分析前交通破裂动脉瘤和前交通未破裂动脉瘤病例之间,这些危险因素方面存在哪些差异。运用单因素和多因素逻辑回归分析方法,找出能预测前交通动脉瘤破裂的独立危险因素。
     结果:
     本研究总共收集了256例前交通动脉瘤病例,其中104例患者表现为前交通破裂动脉瘤。通过单因素分析,我们发现前交通动脉瘤破裂风险与以下因素明显相关:年龄55岁以下、有吸烟史、有饮酒史、前交通动脉A1段不对称时呈现单侧优势型A1段,或者前交通动脉一侧缺如A1段、以及动脉瘤瘤径3毫米以上。通过多因素逻辑回归分析,我们发现前交通动脉瘤破裂的独立预测因素为:年龄在55岁以下(比值比5.975,95%可信区间2.739到13.032)、前交通动脉单侧优势A1段(比值比2.463,95%可信区间1.83到5.13)或前交通动脉一侧缺如A1段(比值比6.268,95%可信区间1.819到21.601)、动脉瘤瘤径在3毫米以上(比值比23.429,95%可信区间10.998到49.908)。
     结论:
     年龄在55岁以下、有吸烟史、有饮酒史、前交通动脉单侧优势A1段或前交通动脉一侧缺如A1段、以及动脉瘤瘤径在3毫米以上,以上这些因素是前交通动脉瘤破裂的独立预测因素。对于具备这些危险因素的患者,建议给予预防性治疗。
     第三部分破裂与未破裂前交通动脉瘤血流动力学数值模拟研究
     背景与目的:
     由于不同部位动脉瘤以及毗邻载瘤动脉几何学结构各不相同,别处的动脉瘤血流动力学结论不能推广到前交通动脉瘤亚组。以往,运用3D-DRA技术研究前交通动脉瘤血流动力学特点以及动脉瘤破裂的血流动力学机制,仅仅以一侧大脑前动脉A1段为流入血管,不足阐明前交通动脉瘤破裂的血流动力学特点和真正机制。本研究的目的是通过利用3D-TOF-MRA新技术,在接近真实解剖生理状态下,来探讨前交通动脉瘤独特的血流特征,找出血流动力学特征与动脉瘤破裂之间可能存在的关系。
     资料与方法:
     从同期我院诊治的前交通动脉瘤破裂病例中选取18例患者,以性别和年龄(±2岁)匹配,与未破裂前交通动脉配对。所有入选患者均行头颅3D-TOF MRA检查。将所获得的3D-TOF MRA原始DICOM数据输入计算机,采用专用的计算机辅助设计软件(MIMICS12.0)建立动脉瘤3D模型,应用ANSYS CFX12.0软件进行计算。获取血流动力学相关参数,包括壁面切应力分布、流线及流场基本特征、速度场、动脉瘤内血流方式、射入流速度及宽度、冲击域大小,并对动脉瘤的血液动力学特征进行分析。
     结果:
     在本研究中,4种血流模式类型均被发现。在未破裂的动脉瘤中,以Ⅰ型(25%)和Ⅱ型(45%)血流模式多见;但在破裂和未破裂前交通动脉瘤中,血流模式类型分布没有明显的统计学差异(P=0.175)。以Ⅰ型血流模式为参照,Ⅱ型、Ⅰ型和Ⅳ型血流模式,动脉瘤破裂的发生率虽然有增高的趋势,但这种趋势并未达到统计学意义;以II型血流模式为参照,Ⅲ型、Ⅳ型血流模式动脉瘤破裂的发生率同样有增高的趋势,但这种趋势仍未达到统计学意义。
     18个动脉瘤双侧A1段解剖结构上对称,流线分析表现为A型瞬时流线9个(50%),另外9个动脉瘤仅接受单侧大脑前动脉A1段血流。17个一侧A1段解剖结构上优势的动脉瘤,仅接受单侧大脑前动脉A1段血流。在A型瞬时流线中,66.7%为未破裂动脉瘤,在B、C、D型瞬时流线中,破裂动脉瘤比例似乎呈上升趋势,分别占44.4%、53.8%、66.7%。但这种趋势并未达到统计学意义(P=0.5343)。
     在本研究中,我们在切应力轮廓图上测得最大壁切应力范围10-1500dyne/cm2,平均196dyne/cm2.未破裂动脉瘤,最大壁切应力值范围10-230dyne/cm2(平均,124dyne/cm2),破裂动脉瘤最大壁切应力范围35-1500dyne/cm2(平均,269dyne/cm2),以P值<0.1有统计学意义,破裂和未破裂动脉瘤最大壁切应力差异有统计学意义。未破裂的、A型流线的动脉瘤壁切应力较低,平均63dyne/cm2,A型流线中破裂的动脉瘤壁平均切应力为690dyne/cm2;B型流线的动脉瘤,最大壁切应力相对较小,破裂的动脉瘤最大壁切应力80dyne/cm2,未破裂动脉瘤最大壁切应力60dyne/cm2.C型流线的动脉瘤壁切应力大,破裂和未破裂动脉瘤平均最大壁切应力分别为285和225dyne/cm2,而在D型,破裂和未破裂动脉瘤平均最大壁切应力分别为165和150dyne/cm2。
     结论:
     本研究中,我们发现动脉瘤破裂与A1段发育不良、缺如所造成的不对称血流相关,破裂动脉瘤通常伴随射入流方向改变(Ⅲ、Ⅳ型血流模式)或多个涡流(Ⅱ、Ⅳ型血流模式),冲击域的大小的与动脉瘤之前破裂相关。高的壁面切应力与动脉瘤之前的破裂相关。
     第四部分前交通动脉瘤的血管内栓塞复发的危险因素分析
     背景和目的:
     可能影响到动脉瘤弹簧圈治疗后复发的危险因素较多。其中风险较高的因素有:瘤径大、瘤颈宽、瘤腔内存在血栓、弹簧圈盘曲不致密、瘤颈残留、填塞不完全、随访周期过长、动脉瘤位于后循坏、高颈-顶比等。这些结果能否推及前交通动脉瘤的这一特别亚组中,目前不得而知。本研究旨在弄清楚接受过弹簧圈栓塞治疗的前交通动脉瘤复发的危险因素,对减少内管内治疗后复发有临床价值。
     方法:
     在本研究中,我们回顾性地分析了59例2006年1月至2012年10月间接受过弹簧圈栓塞治疗的前交通动脉瘤患者。研究其临床特点、形态学特征、原始血管造影以及3个月以上随访血管造影结果。分析患者各种临床特点、动脉瘤的形态特征、血管造影结果,通过逻辑回归模型找出能够预测动脉瘤栓塞治疗后复发的危险因素。
     结果:
     年龄、性别、吸烟史、饮酒史、糖尿病史及高血压史等临床特点在病例组和对照组间没有明显差异。]Hunter-Hess分级和血管内治疗时机在病例组和对照组间没有明显差异。瘤颈宽度在4mm以上(OR=5.570,95%CI,1.377-22.535;P=0.016)、瘤颈残留(OR=4.809,95%CI,1.015-22.792;P=0.048)以及动脉瘤腔的不完全填塞(OR=14.037,95%CI,2.683-73.447;P=0.002)是预测前交通动脉瘤血管内治疗后复发的独立危险因素。
     结论:
     瘤颈宽度在4mm以上、瘤颈残留、以及动脉瘤腔的不完全填塞是前交通动脉瘤血管内治疗后复发的独立危险因素。结果提示:1、在开发和评估宽颈动脉瘤新疗法时,要注重瘤颈的新内皮化问题。2、对前交通动脉瘤而言,血管内治疗要尽可能地做到致密填塞。3、对于瘤颈宽度在4mm以上、瘤颈残留、以及动脉瘤腔的不完全填塞的病例,必须进行严格的血管造影随访,以便早期发现早期治疗动脉瘤复发。
SECTION1Risk Factors for the Formation of Anterior Communicating Artery aneurysms
     Objectives:
     Risk factors for the formation of intracranial aneurysms (IAs) have been widely investigated; however, there is lack of subgroup analysis on risk factors for the formation of anterior communicating artery (ACoA) aneurysms. The purpose of this study was to determine risk factors for the formation of ACoA aneurysms.
     Methods:
     This is a retrospective case-control study. Cases consisted of256patients with ACoA aneurysms confirmed by MRA and/or DSA. Controls consisted of512patients without IAs. Possible risk factors for the formation of ACoA aneurysms were collected and analyzed using univariate analysis and multivariate logistic regression.
     Results:
     The average age was significantly older in the case group than in the control group (P=0.016). Univariate analysis revealed that hypertension and a dominant or incomplete A1were significantly associated with the presence of ACoA aneurysms. Multivariate logistic regression analysis showed that age (OR1.014,95%CI1.001to1.027), history of hypertension (OR1.627,95%CI1.090to2.135), dominant (OR2.845,95%CI2.019to4.009) or incomplete A1(OR4.301,95%CI2.174to8.507) were independent risk factors for the formation of ACoA aneurysm.
     Conclusions:
     Age, hypertension, and a dominant or incomplete A1were independent risk factors for the formation of ACoA aneurysm, for those with these risk factors, a periodical screening with MR angiography might be beneficial to early detection of unruptured ACoA aneurysm. However, the cost-effective of such a screening should be further evaluated.
     SECTION2Age, aneurysm size and Al anatomic configuration predict rupture of anterior communicating artery aneurysms
     Object:
     The risk factors for the rupture of intracranial aneurysms (IAs) have been widely investigated; however, there is little subgroup analysis on the risk factors for the rupture of anterior communicating artery (ACoA) aneurysms. The purpose of this study was to determine risk factors for the rupture of ACoA aneurysms.
     Methods:
     Patients with ACoA aneurysm confirmed by MRA and/or DSA between June2006and October2012were included in this study. Possible risk factors for the rupture of ACoA aneurysms including clinical characteristics, Al anatomic configuration and aneurysm-related characteristics were compared by univariate analysis and multivariate logistic regression between those with ruptured ACoA aneurysms and those with unruptured ACoA aneurysm.
     Results:
     A total of256patients with AcomA aneurysm were included,104patients had ruptured ACoA aneurysms. Univariate analysis revealed that age<55years, cigarette smoking, alcohol consumption, a dominant or incomplete Al, and aneurysm size≥3mm were significantly associated with ACoA aneurysms rupture. Multivariate logistic regression analysis showed that only age<55years (OR5.975,95%CI2.739to13.032), a dominant (OR2.463,95%CI1.83to5.13) or incomplete Al (OR6.268,95%CI1.819to21.601) and aneurysm size≥3mm (OR23.429,95%CI10.998to49.908) were independent predictive factors for the rupture of ACoA aneurysms.
     Conclusion:
     Age<55years, a dominant or incomplete Al and aneurysm size>3mm were independent predictive factors for the rupture of ACoA aneurysms. For patients with these risk factors, prophylactic treatment should be recommended.
     SECTION3Hemodynamic Mechanism of Rupture of Anterior Communicating Artery aneurysms
     Background and Purpose:
     The anterior communicating artery (AcomA) is a predilect location of aneurysms which typically carry higher rupture risks than other locations in the anterior circulation. The purpose of this study was to characterize the different flow types present in AcomA aneurysms and to investigate possible associations with rupture.
     Materials and Methods:
     Patient-specific computational models of36AcomA aneurysms were constructed from3D-TOF-MRA images. Visualizations of flow velocity, instantaneous streamlines, and wall shear stress (WSS) were performed. These were analyzed for flow patterns, size of the impaction zone, and peak WSS and then correlations were made with prior history of rupture.
     Results:
     4types of flow patterns had been detected, type1(25%) and type2(45%) were the most common. In the18aneurysms with bilateral Al Segments,9showed type A streamlines (50%), the others received blood flow from one side. In the type A streamline,66.7%of them were unruptured aneurysms. And the ratio of ruptured aneurysms were44.4%,53.85and66.7%in typeB, type C, and type D respectively. Maximum intra-aneurysmal WSS (MWSS) in type C streamline were higher than that in type A, type B and typeD. Maximum intra-aneurysmal WSS (MWSS) for the unruptured aneurysms ranged from10to230dyne/cm2(mean,124dyne/cm2) compared with ruptured aneurysms, which ranged from35to1500dyne/cm2(mean, 269dyne/cm2). This difference in MWSS was statistically significant at90%confidence levels.
     Conclusions:
     Aneurysms with higher flow rates entering the aneurysm, small impaction zones, and elevated MWSS are associated with a clinical history of previous rupture.
     SECTION4Endovascular Embolization of Anterior Communicating Artery Aneurysm:Frequency and Risk Factors of Recurrence
     Background and purpose:
     Possible risk factors for recurrent of a coiled aneurysm over time have been investigated widely, large aneurysm size, wide aneurysm neck, presence of intraluminal thrombus, low packing density, neck remnant, initial incomplete occlusion, duration of follow-up, ruptured aneurysms, location in the posterior circulation and a large neck-dome ratio are associated with a higher risk of recurrence after coiling. However, whether these results can be deduced to a special subgroup of intracranial aneurysm remains unclear. The purpose of this study was to determine risk factors of recurrence after endovascular embolization of ACoA aneurysm.
     Methods:
     In this study, we retrospectively analyze clinical, morphological characteristics and initial angiographic results of59patients who underwent coil embolization for ACoA aneurysm and had at least a3-month follow-up angiography between January2006and October2012. Clinical characteristics of patients, characteristics of aneurysm morphology, and immediate angiographic results were were entered into a logistic regression model for the risk factors predictive of aneurysm recurrence.
     Results:
     There was no significant difference between the groups in terms of age, gender, history of cigarette smoking, history of alcohol consumption, history of diabetic Mellitus, history of hypertension. There was no significant difference in Hunter-Hess classification and timing of EVT at the time of initial treatment between the groups. Neck size>4(0R=5.570,95%CI,1.377-22.535; P=0.016), neck remnant (OR=4.809,95%CI,1.015-22.792; P=0.048) or incomplete occlusion (OR=14.037,95%CI,2.683-73.447; P=0.002) were identified as independent risk factors for ACoA aneurysm recurrence.
     Conclusion:
     Wide neck (neck size>4), neck remnant or incomplete aneurismal embolization at the time of initial endovascular treatment were independent factors predictive for the recurrence of ACoA aneurysm. The present results suggest:1) developing and evaluating new strategies of treatment and technique, especially for wide-neck aneurysms, with a focus on reinforcement and neoendothelialization at the level of the neck as objectives;2) for ACoA aneurysms, packing aneurysm with coil as densely as possible should be performed; and3) for ACoA aneurysms with a wide neck (neck size>4), or neck remnant or incomplete aneurismal embolization at the time of initial endovascular treatment, the strict follow-up angiography should be performed to detect the potential aneurysm recanalization.
引文
[1]Rinkel GJ, Djibuti M, Algra A, van Gijn J. Prevalence and risk of rupture of intracranial aneurysms:a systematic review. Stroke.1998;29:251-256.
    [2]Juvela S, Poussa K, Porras M. Factors affecting formation and growth of intracranial aneurysms:a long-term follow-up study. Stroke.2001;32:485-491.
    [3]Juvela S. Natural history of unruptured intracranial aneurysms:risks for aneurysm formation, growth, and rupture. Acta Neurochir Suppl.2002;82:27-30.
    [4]Inagawa T. Risk factors for the formation and rupture of intracranial saccular aneurysms in Shimane, Japan. World Neurosurg.2010;73:155-164.
    [5]Nguyen TV, Chandrashekar K, Qin Z, Parent AD, Zhang J. Epidemiology of intracranial aneurysms of Mississippi:a 10-year (1997-2007) retrospective study. J Stroke Cerebrovasc Dis.2009;18:374-380.
    [6]Lindner SH, Bor AS, Rinkel GJ. Differences in risk factors according to the site of intracranial aneurysms. J Neurol Neurosurg Psychiatry.2010;81:116-118.
    [7]Inagawa T. Site of ruptured intracranial saccular aneurysms in patients in Izumo City, Japan. Cerebrovasc Dis.2010;30:72-84.
    [8]Leipzig TJ, Morgan J, Horner TG, Payner T, Redelman K, Johnson CS. Analysis of intraoperative rupture in the surgical treatment of 1694 saccular aneurysms. Neurosurgery.2005;56:455-468.
    [9]Tarulli E, Fox AJ. Potent risk factor for aneurysm formation:termination aneurysms of the anterior communicating artery and detection of A1 vessel asymmetry by flow dilution. AJNR Am J Neuroradiol.2010;31:1186-1191.
    [10]Bor AS, Velthuis BK, Majoie CB, Rinkel GJ. Configuration of intracranial arteries and development of aneurysms:a follow-up study. Neurology.2008;70: 700-705.
    [11]de Rooij NK, Velthuis BK, Algra A, Rinkel GJ. Configuration of the circle of Willis, direction of flow, and shape of the aneurysm as risk factors for rupture of intracranial aneurysms. J Neurol.2009;256:45-50.
    [12]Charbel FT, Seyfried D, Mehta B, Dujovny M, Ausman JI. Dominant A1: angiographic and clinical correlations with anterior communicating artery aneurysms. Neurol Res.1991;13:253-256.
    [13]Kayembe KN, Sasahara M, Hazama F. Cerebral aneurysms and variations in the circle of Willis. Stroke.1984;15:846-850.
    [14]Li MH, Li YD, Tan HQ, Gu BX, Chen YC, Wang W, et al. Contrast-free MRA at 3.0 T for the detection of intracranial aneurysms. Neurology.2011;77:667-676.
    [15]Fox AJ, Millar J, Raymond J, Pryor JC, Roy D, Tomlinson GA, et al. Dangerous advances in measurements from digital subtraction angiography:when is a millimeter not a millimeter? AJNR Am J Neuroradiol.2009;30:459-461.
    [16]Chuang YM, Liu CY, Pan PJ, Lin CP. Anterior cerebral artery A1 segment hypoplasia may contribute to A1 hypoplasia syndrome. Eur Neurol.2007;57:208-211.
    [17]Perlmutter D, Rhoton AL, Jr. Microsurgical anatomy of the anterior cerebral-anterior communicating-recurrent artery complex. J Neurosurg.1976;45: 259-272.
    [18]Ujiie H, Sato K, Onda H, Oikawa A, Kagawa M, Takakura K, et al. Clinical analysis of incidentally discovered unruptured aneurysms. Stroke.1993;24:1850-1856.
    [19]de la Monte SM, Moore GW, Monk MA, Hutchins GM. Risk factors for the development and rupture of intracranial berry aneurysms. Am J Med.1985;78: 957-964.
    [20]Mhurchu CN, Anderson C, Jamrozik K, Hankey G, Dunbabin D. Hormonal factors and risk of aneurysmal subarachnoid hemorrhage:an international population-based, case-control study. Stroke.2001;32:606-612.
    [21]Kongable GL, Lanzino G, Germanson TP, Truskowski LL, Alves WM, Torner JC, et al. Gender-related differences in aneurysmal subarachnoid hemorrhage. J Neurosurg.1996;84:43-48.
    [22]Lindekleiv HM, Valen-Sendstad K, Morgan MK, Mardal KA, Faulder K, Magnus JH, et al. Sex differences in intracranial arterial bifurcations. Gend Med.2010;7: 149-155.
    [23]Lindekleiv H, Sandvei MS, Njolstad I, Lochen ML, Romundstad PR, Vatten L, et al. Sex differences in risk factors for aneurysmal subarachnoid hemorrhage:a cohort study. Neurology.2011;76:637-643.
    [24]Juvela S. Risk factors for multiple intracranial aneurysms. Stroke.2000;31:392-397.
    [25]Price JF, Mowbray PI, Lee AJ, Rumley A, Lowe GD, Fowkes FG. Relationship between smoking and cardiovascular risk factors in the development of peripheral arterial disease and coronary artery disease:Edinburgh Artery Study. Eur Heart J. 1999;20:344-353.
    [26]Haass M, Kubler W. Nicotine and sympathetic neurotransmission. Cardiovasc Drugs Ther.1997;10:657-665.
    [27]Sunyer J, Munoz A, Peng Y, Margolick J, Chmiel JS, Oishi J, et al. Longitudinal relation between smoking and white blood cells. Am J Epidemiol.1996;144:734-741.
    [28]Gaetani P, Tartara F, Tancioni F, Klersy C, Forlino A, Baena RR. Activity of alpha 1-antitrypsin and cigarette smoking in subarachnoid haemorrhage from ruptured aneurysm. JNeurol Sci.1996;141:33-38.
    [29]Schievink WI, Prakash UB, Piepgras DQ Mokri B. Alpha 1-antitrypsin deficiency in intracranial aneurysms and cervical artery dissection. Lancet.1994;343:452-453.
    [30]St Jean P, Hart B, Webster M, Steed D, Adamson J, Powell J, et al. Alpha-1-antitrypsin deficiency in aneurysmal disease. Hum Hered.1996;46:92-97.
    [31]Teunissen LL, Rinkel GJ, Algra A, van Gijn J. Risk factors for subarachnoid hemorrhage:a systematic review. Stroke.1996;27:544-549.
    [32]Gu YX, Chen XC, Song DL, Leng B, Zhao F. Risk factors for intracranial aneurysm in a Chinese ethnic population. Chin Med J (Engl).2006;119:1359-1364.
    [33]Qureshi AI, Suarez JI, Parekh PD, Sung G, Geocadin R, Bhardwaj A, et al. Risk factors for multiple intracranial aneurysms. Neurosurgery.1998;43;22-26.
    [34]Puddey IB, Beilin LJ, Vandongen R, Rouse IL, Rogers P. Evidence for a direct effect of alcohol consumption on blood pressure in normotensive men. A randomized controlled trial. Hypertension.1985;7:707-713.
    [35]Taylor CL, Yuan Z, Selman WR, Ratcheson RA, Rimm AA. Cerebral arterial aneurysm formation and rupture in 20,767 elderly patients:hypertension and other risk factors. J Neurosurg.1995;83:812-819.
    [36]Ellamushi HE, Grieve JP, Jager HR, Kitchen ND. Risk factors for the formation of multiple intracranial aneurysms. J Neurosurg.2001;94:728-732.
    [37]Morimoto M, Miyamoto S, Mizoguchi A, Kume N, Kita T, Hashimoto N. Mouse model of cerebral aneurysm:experimental induction by renal hypertension and local hemodynamic changes. Stroke.2002;33:1911-1915.
    [38]Castro MA, Putman CM, Sheridan MJ, Cebral JR. Hemodynamic patterns of anterior communicating artery aneurysms:a possible association with rupture. AJNR Am J Neuroradiol.2009;30:297-302.
    [39]Kasuya H, Shimizu T, Nakaya K, Sasahara A, Hori T, Takakura K. Angeles between Al and A2 segments of the anterior cerebral artery visualized by three-dimensional computed tomographic angiography and association of anterior communicating artery aneurysms. Neurosurgery.1999;45:89-93.
    [40]Alnaes MS, Isaksen J, Mardal KA, Romner B, Morgan MK, Ingebrigtsen T. Computation of hemodynamics in the circle of Willis. Stroke.2007;38:2500-2505.
    [1]Unruptured intracranial aneurysms--risk of rupture and risks of surgical intervention. International Study of Unruptured Intracranial Aneurysms Investigators. N Engl J Med 339:1725-1733,1998
    [2]Adamson J, Humphries SE, Ostergaard JR, Voldby B, Richards P, Powell JT, et al: Are cerebral aneurysms atherosclerotic? Stroke 25:963-966,1994
    [3]Castro MA, Putman CM, Sheridan MJ, Cebral JR:Hemodynamic patterns of anterior communicating artery aneurysms:a possible association with rupture. AJNR Am J Neuroradiol 30:297-302,2009.
    [4]Charbel FT, Seyfried D, Mehta B, Dujovny M, Ausman JI:Dominant Al: angiographic and clinical correlations with anterior communicating artery aneurysms. Neurol Res 13:253-256,1991
    [5]de la Monte SM, Moore GW, Monk MA, Hutchins GM:Risk factors for the development and rupture of intracranial berry aneurysms. Am J Med 78:957-964, 1985
    [6]de Rooij NK, Velthuis BK, Algra A, Rinkel GJ:Configuration of the circle of Willis, direction of flow, and shape of the aneurysm as risk factors for rupture of intracranial aneurysms. J Neurol 256:45-50,2009
    [7]Etminan N, Beseoglu K, Steiger HJ, Hanggi D:The impact of hypertension and nicotine on the size of ruptured intracranial aneurysms. J Neurol Neurosurg Psychiatry 82:4-7,2011
    [8]Feigin VL, Rinkel GJ, Lawes CM, Algra A, Bennett DA, van Gijn J, et al:Risk factors for subarachnoid hemorrhage:an updated systematic review of epidemiological studies. Stroke 36:2773-2780,2005
    [9]Forget TR Jr, Benitez R, Veznedaroglu E, Sharan A, Mitchell W, Silva M, et al:A review of size and location of ruptured intracranial aneurysms. Neurosurgery 49: 1322-1325; discussion 1325-1326,2001
    [10]Fox AJ, Millar J, Raymond J, Pryor JC, Roy D, Tomlinson GA, et al:Dangerous advances in measurements from digital subtraction angiography:when is a millimeter not a millimeter? AJNR Am J Neuroradiol 30:459-461,2009
    [11]Gaetani P, Tartara F, Tancioni F, Klersy C, Forlino A, Baena RR:Activity of alpha 1-antitrypsin and cigarette smoking in subarachnoid haemorrhage from ruptured aneurysm. J Neurol Sci 141:33-38,1996
    [12]Hassan T, Hassan AA, Ahmed YM:Influence of parent vessel dominancy on fluid dynamics of anterior communicating artery aneurysms. Acta Neurochir (Wien) 153:305-310,2011.
    [13]Horikoshi T, Akiyama I, Yamagata Z, Sugita M, Nukui H:Magnetic resonance angiographic evidence of sex-linked variations in the circle of willis and the occurrence of cerebral aneurysms. J Neurosurg 96:697-703,2002
    [14]Inagawa, T:Risk factors for aneurysmal subarachnoid hemorrhage in patients in Izumo City, Japan. J Neurosurg 102:60-67,2005
    [15]Inagawa, T:Risk factors for the formation and rupture of intracranial saccular aneurysms in Shimane, Japan. World Neurosurg 73:155-164,2010
    [16]Inagawa, T:Site of ruptured intracranial saccular aneurysms in patients in Izumo City, Japan. Cerebrovasc Dis 30:72-84,2010
    [17]Ishibashi T, Murayama Y, Urashima M, Saguchi T, Ebara M, Arakawa H, et al: Unruptured intracranial aneurysms:incidence of rupture and risk factors. Stroke 40:313-316,2009
    [18]Jimenez-Yepes CM, Londono-Fernandez JL:Risk of aneurysmal subarachnoid hemorrhage:the role of confirmed hypertension. Stroke 39:1344-1346,2008
    [19]Juvela S:Natural history of unruptured intracranial aneurysms:risks for aneurysm formation, growth, and rupture. Acta Neurochir Suppl 82:27-30,2002
    [20]Juvela S, Hillbom M, Numminen H, Koskinen P:Cigarette smoking and alcohol consumption as risk factors for aneurysmai subarachnoid hemorrhage. Stroke 24: 639-646,1993
    [21]Juvela S, Porras M, Heiskanen O:Natural history of unruptured intracranial aneurysms:a long-term follow-up study. J Neurosurg 79:174-182,1993
    [22]Juvela S, Porras M, Poussa K:Natural history of unruptured intracranial aneurysms:probability of and risk factors for aneurysm rupture. J Neurosurg 108: 1052-1060,2008
    [23]Juvela S, Poussa K, Porras M:Factors affecting formation and growth of intracranial aneurysms:a long-term follow-up study. Stroke 32:485-491,2001
    [24]Karmonik C, Yen C, Grossman RG, Klucznik R, Benndorf G:Intra-aneurysmal flow patterns and wall shear stresses calculated with computational flow dynamics in an anterior communicating artery aneurysm depend on knowledge of patient-specific inflow rates. Acta Neurochir (Wien) 151:479-485,2009
    [25]Kayembe KN, Sasahara M, Hazama F:Cerebral aneurysms and variations in the circle of Willis. Stroke 15:846-850,1984
    [26]Kongable GL, Lanzino G, Germanson TP, Truskowski LL, Alves WM, Torner JC, et al:Gender-related differences in aneurysmal subarachnoid hemorrhage. J Neurosurg 84:43-48,1996
    [27]Lazzaro MA, Ouyang B, Chen M:The role of circle of Willis anomalies in cerebral aneurysm rupture. J Neurointerv Surg 4:22-26,2012
    [28]Lindekleiv H, Sandvei MS, Nj(?)lstad I, L(?)chen ML, Romundstad PR, Vatten L, et al:Sex differences in risk factors for aneurysmal subarachnoid hemorrhage:a cohort study. Neurology 76:637-643,2011
    [29]Lindekleiv HM, Valen-Sendstad K, Morgan MK, Mardal KA, Faulder K, Magnus JH, et al:Sex differences in intracranial arterial bifurcations. Gend Med 7: 149-155,2010
    [30]Lindner SH, Bor AS, Rinkel GJ:Differences in risk factors according to the site of intracranial aneurysms. J Neurol Neurosurg Psychiatry 81:116-118,2010
    [31]Mhurchu CN, Anderson C, Jamrozik K, Hankey G, Dunbabin D; Australasian Cooperative Research on Subarachnoid Hemorrhage Study (ACROSS) Group: Hormonal factors and risk of aneurysmal subarachnoid hemorrhage:an international population-based, case-control study. Stroke 32:606-612,2001
    [32]Mira JM, Costa FA, Horta BL, Fabiao OM:Risk of rupture in unruptured anterior communicating artery aneurysms:meta-analysis of natural history studies. Surg Neurol 66 Suppl 3:S12-19,2006
    [33]Nahed BV, DiLuna ML, Morgan T, Ocal E, Hawkins AA, Ozduman K, et al: Hypertension, age, and location predict rupture of small intracranial aneurysms. Neurosurgery 57:676-683,2005
    [34]Ohkuma H, Tabata H, Suzuki S, Islam MS:Risk factors for aneurysmal subarachnoid hemorrhage in Aomori, Japan. Stroke 34:96-100,2003
    [35]Okamoto K, Horisawa R, Ohno Y:The relationships of gender, cigarette smoking, and hypertension with the risk of aneurysmal subarachnoid hemorrhage:a case-control study in Nagoya, Japan. Ann Epidemiol 15:744-748,2005
    [36]Price JF, Mowbray PI, Lee AJ, Rumley A, Lowe GD, Fowkes FG:Relationship between smoking and cardiovascular risk factors in the development of peripheral arterial disease and coronary artery disease:Edinburgh Artery Study. Eur Heart J 20:344-353,1999
    [37]Puddey IB, Beilin LJ, Vandongen R, Rouse IL, Rogers P:Evidence for a direct effect of alcohol consumption on blood pressure in normotensive men. A randomized controlled trial. Hypertension 7:707-713,1985
    [38]Rinkel GJ, Djibuti M, Algra A, van Gijn J:Prevalence and risk of rupture of intracranial aneurysms:a systematic review. Stroke 29:251-256,1998
    [39]Sandvei MS, Romundstad PR, Muller TB, Vatten L, Vik A:Risk factors for aneurysmal subarachnoid hemorrhage in a prospective population study:the HUNT study in Norway. Stroke 40:1958-1962,2009
    [40]Schievink WI, Prakash UB, Piepgras DG, Mokri B:Alpha 1-antitrypsin deficiency in intracranial aneurysms and cervical artery dissection. Lancet 343:452-453, 1994
    [41]Sonobe M, Yamazaki T, Yonekura M, Kikuchi H:Small unruptured intracranial aneurysm verification study:SUAVe study, Japan. Stroke 41:1969-1977,2010
    [42]St Jean P, Hart B, Webster M, Steed D, Adamson J, Powell J, et al: Alpha-1-antitrypsin deficiency in aneurysmal disease. Hum Hered 46:92-97, 1996
    [43]Sunyer J, Munoz A, Peng Y, Margolick J, Chmiel JS, Oishi J, et al:Longitudinal relation between smoking and white blood cells. Am J Epidemiol 144: 734-741,1996
    [44]Tarulli E, Fox AJ:Potent risk factor for aneurysm formation:termination aneurysms of the anterior communicating artery and detection of Al vessel asymmetry by flow dilution. AJNR Am J Neuroradiol 31:1186-1191,2010
    [45]Taylor CL, Yuan Z, Selman WR, Ratcheson RA, Rimm AA:Cerebral arterial aneurysm formation and rupture in 20,767 elderly patients:hypertension and other risk factors. J Neurosurg 83:812-819,1995
    [46]Teunissen LL, Rinkel GJ, Algra A, van Gijn J:Risk factors for subarachnoid hemorrhage:a systematic review. Stroke 27:544-549,1996
    [47]Tsutsumi K, Ueki K, Morita A, Kirino T:Risk of rupture from incidental cerebral aneurysms. J Neurosurg 93:550-553,2000.
    [48]Ujiie H, Sato K, Onda H, Oikawa A, Kagawa M, Takakura K, Kobayashi N, et al: Clinical analysis of incidentally discovered unruptured aneurysms. Stroke 24: 1850-1856,1993
    [49]Wermer MJ, van der Schaaf IC, Algra A, Rinkel GJ:Risk of rupture of unruptured intracranial aneurysms in relation to patient and aneurysm characteristics:an updated meta-analysis. Stroke 38:1404-1410,2007
    [50]Wiebers DO, Whisnant JP, Huston J 3rd, Meissner I, Brown RD Jr, Piepgras DG, et al:Unruptured intracranial aneurysms:natural history, clinical outcome, and risks of surgical and endovascular treatment. Lancet 362:103-111,2003
    [1]Horiuchi T, Tanaka Y, Hongo K. Surgical treatment for aneurysmal subarachnoid hemorrhage in the 8th and 9th decades of life. Neurosurgery 2005;56:469-75; discussion-75.
    [2]Leipzig TJ, Morgan J, Homer TG, Payner T, Redelman K, Johnson CS. Analysis of intraoperative rupture in the surgical treatment of 1694 saccular aneurysms. Neurosurgery 2005;56:455-68; discussion-68.
    [3]Brilstra EH, Rinkel GJ, van der Graaf Y, van Rooij WJ, Algra A. Treatment of intracranial aneurysms by embolization with coils:a systematic review. Stroke 1999;30:470-6.
    [4]Mira JM, Costa FA, Horta BL, Fabiao OM. Risk of rupture in unruptured anterior communicating artery aneurysms:meta-analysis of natural history studies. Surg Neurol 2006;66 Suppl 3:S12-9; discussion S9.
    [5]Matsukawa H, Uemura A, Fujii M, Kamo M, Takahashi O, Sumiyoshi S. Morphological and clinical risk factors for the rupture of anterior communicating artery aneurysms. J Neurosurg 2012.
    [6]Cebral JR, Castro MA, Appanaboyina S, Putman CM, Millan D, Frangi AF. Efficient pipeline for image-based patient-specific analysis of cerebral aneurysm hemodynamics:technique and sensitivity. IEEE Trans Med Imaging 2005;24: 457-67.
    [7]Cebral JR, Castro MA, Burgess JE, Pergolizzi RS, Sheridan MJ, Putman CM. Characterization of cerebral aneurysms for assessing risk of rupture by using patient-specific computational hemodynamics models. AJNR Am J Neuroradiol 2005;26:2550-9.
    [8]Castro MA, Putman CM, Sheridan MJ, Cebral JR. Hemodynamic patterns of anterior communicating artery aneurysms:a possible association with rupture. AJNR Am J Neuroradiol 2009;30:297-302.
    [9]Cebral JR, Mut F, Weir J, Putman CM. Association of hemodynamic characteristics and cerebral aneurysm rupture. AJNR Am J Neuroradiol 2011;32: 264-70.
    [10]Kerber CW, Imbesi SG, Knox K. Flow dynamics in a lethal anterior communicating artery aneurysm. AJNR Am J Neuroradiol 1999;20:2000-3.
    [11]Ferguson GG. Physical factors in the initiation, growth, and rupture of human intracranial saccular aneurysms. J Neurosurg 1972;37:666-77.
    [12]Cebral JR, Sheridan M, Putman CM. Hemodynamics and bleb formation in intracranial aneurysms. AJNR Am J Neuroradiol 2010;31:304-10.
    [13]Zhang Y, Mu S, Chen J, et al. Hemodynamic analysis of intracranial aneurysms with daughter blebs. Eur Neurol 2011;66:359-67.
    [14]Shojima M, Oshima M, Takagi K, et al. Magnitude and role of wall shear stress on cerebral aneurysm:computational fluid dynamic study of 20 middle cerebral artery aneurysms. Stroke 2004;35:2500-5.
    [15]Castro MA, Putman CM, Cebral JR. Computational fluid dynamics modeling of intracranial aneurysms:effects of parent artery segmentation on intra-aneurysmal hemodynamics. AJNR Am J Neuroradiol 2006;27:1703-9.
    [16]Lu G, Huang L, Zhang XL, et al. Influence of hemodynamic factors on rupture of intracranial aneurysms:patient-specific 3D mirror aneurysms model computational fluid dynamics simulation. AJNR Am J Neuroradiol 2011;32: 1255-61.
    [17]Acevedo-Bolton G, Jou LD, Dispensa BP, et al. Estimating the hemodynamic impact of interventional treatments of aneurysms:numerical simulation with experimental validation:technical case report. Neurosurgery 2006;59:E429-30; author reply E-30.
    [18]Omodaka S, Sugiyama S, Inoue T, et al. Local hemodynamics at the rupture point of cerebral aneurysms determined by computational fluid dynamics analysis. Cerebrovasc Dis 2012;34:121-9.
    [19]Kawaguchi T, Nishimura S, Kanamori M, et al. Distinctive flow pattern of wall shear stress and oscillatory shear index:similarity and dissimilarity in ruptured and unruptured cerebral aneurysm blebs. J Neurosurg 2012;117:774-80.
    [20]Jou LD, Lee DH, Morsi H, Mawad ME. Wall shear stress on ruptured and unruptured intracranial aneurysms at the internal carotid artery. AJNR Am J Neuroradiol 2008;29:1761-7.
    [21]Castro MA, Putman CM, Cebral JR. Patient-specific computational fluid dynamics modeling of anterior communicating artery aneurysms:a study of the sensitivity of intra-aneurysmal flow patterns to flow conditions in the carotid arteries. AJNR Am J Neuroradiol 2006;27:2061-8.
    [22]San Millan Ruiz D, Yilmaz H, Dehdashti AR, Alimenti A, de Tribolet N, Rufenacht DA. The perianeurysmal environment:influence on saccular aneurysm shape and rupture. AJNR Am J Neuroradiol 2006;27:504-12.
    [1]Molyneux AJ, Kerr RS, Yu LM, et al. International subarachnoid aneurysm trial (IS AT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms:a randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion. Lancet 2005;366:809-17.
    [2]Brilstra EH, Rinkel GJ, van der Graaf Y, van Rooij WJ, Algra A. Treatment of intracranial aneurysms by embolization with coils:a systematic review. Stroke 1999;30:470-6.
    [3]Campi A, Ramzi N, Molyneux AJ, et al. Retreatment of ruptured cerebral aneurysms in patients randomized by coiling or clipping in the International Subarachnoid Aneurysm Trial (ISAT). Stroke 2007;38:1538-44.
    [4]Cognard C, Weill A, Spelle L, et al. Long-term angiographic follow-up of 169 intracranial berry aneurysms occluded with detachable coils. Radiology 1999;212:348-56.
    [5]Piotin M, Spelle L, Mounayer C, et al. Intracranial aneurysms:treatment with bare platinum coils--aneurysm packing, complex coils, and angiographic recurrence. Radiology 2007;243:500-8.
    [6]Raymond J, Guilbert F, Weill A, et al. Long-term angiographic recurrences after selective endovascular treatment of aneurysms with detachable coils. Stroke 2003;34:1398-403.
    [7]Sluzewski M, Menovsky T, van Rooij WJ, Wijnalda D. Coiling of very large or giant cerebral aneurysms:long-term clinical and serial angiographic results. AJNR Am J Neuroradiol 2003;24:257-62.
    [8]Sluzewski M, van Rooij WJ, Slob MJ, Bescos JO, Slump CH, Wijnalda D. Relation between aneurysm volume, packing, and compaction in 145 cerebral aneurysms treated with coils. Radiology 2004;231:653-8.
    [9]Murayama Y, Nien YL, Duckwiler G, et al. Guglielmi detachable coil embolization of cerebral aneurysms:11 years' experience. J Neurosurg 2003;98: 959-66.
    [10]Vallee JN, Aymard A, Vicaut E, Reis M, Merland JJ. Endovascular treatment of basilar tip aneurysms with Guglielmi detachable coils:predictors of immediate and long-term results with multivariate analysis 6-year experience. Radiology 2003;226:867-79.
    [11]Peluso JP, van Rooij WJ, Sluzewski M, Beute GN. Coiling of basilar tip aneurysms:results in 154 consecutive patients with emphasis on recurrent haemorrhage and re-treatment during mid-and long-term follow-up. J Neurol Neurosurg Psychiatry 2008;79:706-11.
    [12]Standhardt H, Boecher-Schwarz H, Gruber A, Benesch T, Knosp E, Bavinzski G Endovascular treatment of unruptured intracranial aneurysms with Guglielmi detachable coils:short-and long-term results of a single-centre series. Stroke 2008;39:899-904.
    [13]Birknes JK, Hwang SK, Pandey AS, et al. Feasibility and limitations of endovascular coil embolization of anterior communicating artery aneurysms: morphological considerations. Neurosurgery 2006;59:43-52; discussion 43-52.
    [14]van Rooij WJ, Sprengers ME, Sluzewski M, Beute GN. Intracranial aneurysms that repeatedly reopen over time after coiling:imaging characteristics and treatment outcome. Neuroradiology 2007;49:343-9.
    [15]Kawanabe Y, Sadato A, Taki W, Hashimoto N. Endovascular occlusion of intracranial aneurysms with Guglielmi detachable coils:correlation between coil packing density and coil compaction. Acta Neurochir (Wien) 2001; 143:451-5.
    [16]Li MH, Gao BL, Fang C, et al. Angiographic follow-up of cerebral aneurysms treated with Guglielmi detachable coils:an analysis of 162 cases with 173 aneurysms. AJNR Am J Neuroradiol 2006;27:1107-12.
    [17]Grunwald IQ, Papanagiotou P, Struffert T, et al. Recanalization after endovascular treatment of intracerebral aneurysms. Neuroradiology 2007;49:41-7.
    [18]Ries T, Siemonsen S, Thomalla G, Grzyska U, Zeumer H, Fiehler J. Long-term follow-up of cerebral aneurysms after endovascular therapy prediction and outcome of retreatment. AJNR Am J Neuroradiol 2007;28:1755-61.
    [19]Kai Y, Hamada J, Morioka M, Yano S, Kuratsu J. Evaluation of the stability of small ruptured aneurysms with a small neck after embolization with Guglielmi detachable coils:correlation between coil packing ratio and coil compaction. Neurosurgery 2005;56:785-92; discussion-92.
    [20]Leipzig TJ, Morgan J, Homer TG, Payner T, Redelman K, Johnson CS. Analysis of intraoperative rupture in the surgical treatment of 1694 saccular aneurysms. Neurosurgery 2005;56:455-68; discussion-68.
    [21]Kassell NF, Torner JC. The International Cooperative Study on Timing of Aneurysm Surgery--an update. Stroke 1984; 15:566-70.
    [22]Moret J, Pierot L, Boulin A, Castaings L, Rey A. Endovascular treatment of anterior communicating artery aneurysms using Guglielmi detachable coils. Neuroradiology 1996;38:800-5.
    [23]Proust F, Debono B, Hannequin D, et al. Treatment of anterior communicating artery aneurysms:complementary aspects of microsurgical and endovascular procedures. J Neurosurg 2003;99:3-14.
    [24]Molyneux A, Kerr R, Stratton I, et al. International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms:a randomised trial. Lancet 2002;360: 1267-74.
    [25]Wiebers DO, Whisnant JP, Huston J,3rd, et al. Unruptured intracranial aneurysms: natural history, clinical outcome, and risks of surgical and endovascular treatment. Lancet 2003;362:103-10.
    [26]Songsaeng D, Geibprasert S, Willinsky R, Tymianski M, TerBrugge KG, Krings T. Impact of anatomical variations of the circle of Willis on the incidence of aneurysms and their recurrence rate following endovascular treatment. Clin Radiol2010;65:895-901.
    [27]Songsaeng D, Geibprasert S, ter Brugge KG, Willinsky R, Tymianski M, Krings T. Impact of individual intracranial arterial aneurysm morphology on initial obliteration and recurrence rates of endovascular treatments:a multivariate analysis. J Neurosurg 2011;114:994-1002.
    [28]Gonzalez N, Sedrak M, Martin N, Vinuela F. Impact of anatomic features in the endovascular embolization of 181 anterior communicating artery aneurysms. Stroke 2008;39:2776-82.
    [29]Tarulli E, Fox AJ. Potent risk factor for aneurysm formation:termination aneurysms of the anterior communicating artery and detection of A1 vessel asymmetry by flow dilution. AJNR Am J Neuroradiol 2010;31:1186-91.
    [30]Kole MK, Pelz DM, Kalapos P, Lee DH, Gulka IB, Lownie SP. Endovascular coil embolization of intracranial aneurysms:important factors related to rates and outcomes of incomplete occlusion. J Neurosurg 2005; 102:607-15.
    [31]Hayakawa M, Murayama Y, Duckwiler GR, Gobin YP, Guglielmi G, Vinuela F. Natural history of the neck remnant of a cerebral aneurysm treated with the Guglielmi detachable coil system. J Neurosurg 2000;93:561-8.
    [32]Pierot L, Cognard C, Anxionnat R, Ricolfi F. Endovascular treatment of ruptured intracranial aneurysms:factors affecting midterm quality anatomic results: analysis in a prospective, multicenter series of patients (CLARITY). AJNR Am J Neuroradiol 2012;33:1475-80.
    [33]Ortiz R, Stefanski M, Rosenwasser R, Veznedaroglu E. Cigarette smoking as a risk factor for recurrence of aneurysms treated by endosaccular occlusion. J Neurosurg 2008; 108:672-5.
    [34]Meyers PM, Schumacher HC, Higashida RT, et al. Reporting standards for endovascular repair of saccular intracranial cerebral aneurysms. Stroke 2009;40: e366-79.
    [35]Weir B, Macdonald RL, Stoodley M. Etiology of cerebral vasospasm. Acta Neurochir Suppl 1999;72:27-46.
    [36]Ferns SP, Sprengers ME, van Rooij WJ, et al. Coiling of intracranial aneurysms:a systematic review on initial occlusion and reopening and retreatment rates. Stroke 2009;40:e523-9.
    [37]Goddard JK, Moran CJ, Cross DT,3rd, Derdeyn CP. Absent relationship between the coil-embolization ratio in small aneurysms treated with a single detachable coil and outcomes. AJNR Am J Neuroradiol 2005;26:1916-20.
    [38]Hope JK, Byrne JV, Molyneux AJ. Factors influencing successful angiographic occlusion of aneurysms treated by coil embolization. AJNR Am J Neuroradiol 1999;20:391-9.
    [39]Choi DS, Kim MC, Lee SK, Willinsky RA, Terbrugge KG. Clinical and angiographic long-term follow-up of completely coiled intracranial aneurysms using endovascular technique. J Neurosurg 2010; 112:575-81.
    [40]Dhar S, Tremmel M, Mocco J, et al. Morphology parameters for intracranial aneurysm rupture risk assessment. Neurosurgery 2008;63:185-96; discussion 96-7.
    [41]Meng H, Wang Z, Hoi Y, et al. Complex hemodynamics at the apex of an arterial bifurcation induces vascular remodeling resembling cerebral aneurysm initiation. Stroke 2007;38:1924-31.
    [42]Geyik S, Ertugrul O, Yavuz K, Geyik P, Saatci I, Cekirge HS. Comparison of bioactive coils and bare platinum coils for treatment of intracranial aneurysms:a matched-pair analysis. J Neurosurg 2010;112:709-13.
    [43]Linfante I, DeLeo MJ,3rd, Gounis MJ, Brooks CS, Wakhloo AK. Cerecyte versus platinum coils in the treatment of intracranial aneurysms:packing attenuation and clinical and angiographic midterm results. AJNR Am J Neuroradiol 2009;30: 1496-501.
    [44]Wakhloo AK, Mandell J, Gounis MJ, et al. Stent-assisted reconstructive endovascular repair of cranial fusiform atherosclerotic and dissecting aneurysms: long-term clinical and angiographic follow-up. Stroke 2008;39:3288-96.
    [45]Luo B, Yang X, Wang S, et al. High shear stress and flow velocity in partially occluded aneurysms prone to recanalization. Stroke 2011;42:745-53.
    [46]Ortega J, Hartman J, Rodriguez J, Maitland D. Post-treatment hemodynamics of a basilar aneurysm and bifurcation. Ann Biomed Eng 2008;36:1531-46.
    [47]Chatziprodromou I, Tricoli A, Poulikakos D, Ventikos Y. Haemodynamics and wall remodelling of a growing cerebral aneurysm:a computational model. J Biomech 2007;40:412-26.
    [48]Rayz VL, Boussel L, Lawton MT, et al. Numerical modeling of the flow in intracranial aneurysms:prediction of regions prone to thrombus formation. Ann Biomed Eng 2008;36:1793-804.
    [49]Byun HS, Rhee K. CFD modeling of blood flow following coil embolization of aneurysms. Med Eng Phys 2004;26:755-61.
    [50]Renowden SA, Benes V, Bradley M, Molyneux AJ. Detachable coil embolisation of ruptured intracranial aneurysms:a single center study, a decade experience. Clin Neurol Neurosurg 2009;111:179-88.
    [1]Yoneyama T,Kasuya H, Onda H, at al. Collagen type I alpha2 (COL1A2)is the susceptible gene for intracranial aneurysm. Stroke 2004;35:443-448
    [2]Hofer A,Ozkan S,Hermans M, etal. Mutations in the lysyl oxidase gene not associated with intracranial aneurysm in central European families. Cerebrovasc Dis2004;18:189-193
    [3]Yoneyama T,Kasuya H,Onda H,et al. Association of positional and functional candidate genes FGF1,FBN2,and LOX on 5q31 with intracranial aneurysm. J Hum Genet,2003;48:309-314
    [4]Krex D, Kotteck Kt Konig IR. et al. Matrix metalloproteinase-9 coding sequence single-nucleotide polymorphisms in Caucasians with intracranial aneurysms. Neurosurgery 2004;55:207
    [5]Krex D, Rohl H, Konig IR. et al. Tissue inhibitor of metalloproteinases-1,-2, and-3 polymorphisms in a white population with intracranial aneurysms. Stroke 2003;34:2817-2821
    [6]Bruno G, Todor R, Lewis I, et al. Vascular extracellular matrix remodeling in cerebral aneurysms. J Neurosurg 1998;89(3):431-40.
    [7]Kim SC, Singh M, Huang J, el al. Matrix metalloproteinase-9 in cerebralaneurysms. Neurosurgery 1997;41:642-647
    [8]Aoki T, Kataoka H, Morimoto M,et al. Macrophage-derived matrix metalloproteinase-2 and-9 promote the progression of cerebral aneurysms in rats. Stroke 2007;38:162-9
    [9]Jin D, Sheng J, Yang X, et al.Matrix metalloproteinases and tissue inhibitors of metalloproteinases expression in human cerebral ruptured and unruptured aneurysm. Surg Neurol.2007;68 Suppl 2:S11-6
    [10]Chyatte D, Bruno G, Desai S, et al.Inflammation and intracranial aneurysms. Neurosurgery.1999 Nov;45(5):1137-46
    [11]Kataoka K, Taneda M, Asai T, et al.Structural fragility and inflammatory response of ruptured cerebral aneurysms. A comparative study between ruptured and unruptured cerebral aneurysms. Stroke.1999;30(7):1396-401
    [12]Frosen J, Piippo A, Paetau A, et al.Remodeling of saccular cerebral artery aneurysm wall is associated with rupture:histological analysis of 24 unruptured and 42 ruptured cases. Stroke.200;35(10):2287-93
    [13]Kondo S, Hashimoto N, Kikuchi H, et al. Apoptosis of medial smooth muscle cell in the development of saccular cerebral aneurysms in rats. Stroke 1998;29: 181-189
    [14]Sakaki T,Kohmura E,Kishiguchi T,et al. Loss and apoptosisof smoot h muscle cells in int racranial aneurysms. Studies with in situ DNA end labeling and antibody against single-strand DNA. Acta Neurochir,1997,139:469-474
    [15]Hara A,Yoshimi N,Moil H. Evidence for apoptosis in human intracranial aneurysms. Neurol Res 1998;20:1127-1130
    [16]Gao L, Hoi Y, Swartz DD, et al.Nascent Aneurysm Formation at the Basilar Terminus Induced by Hemodynamics. Stroke 2008;39:2085-2090
    [17]刘兵,高永中,浦佩玉.大鼠实验性囊状动脉瘤生长塑形模型的建立中华临床神经外科杂志2004;9:444-446
    [18]Meng H, Wang ZJ, Hoi Y, et al.Complex Hemodynamics at the Apex of an arterial bifurcation induces vascular remodeling resembling cerebral aneurysm initiation. Stroke 2007;38:1924-1931
    [19]Meng H, Swartz DD, Wang Z, et al. A model system for mapping vascular responses to complex hemodynamics at arterial bifurcations invivo. Neurosurgery. 2006;59:1094-1100.
    [20]Wang Z, Kolega J, Hoi Y, et al. Molecular alterations associated with aneurismal remodeling are localized in the high hemodynamics stress region of a created carotid bifurcation. Neurosugery 2009;65:169-178
    [1]Unruptured intracranial aneurysms--risk of rupture and risks of surgical intervention. International Study of Unruptured Intracranial Aneurysms Investigators. N Engl J Med 1998;339(24):1725-33
    [2]Wiebers DO, Whisnant JP, Huston J 3rd, Meissner I, Brown RD Jr, Piepgras DG,Forbes GS, Thielen K, Nichols D, O'Fallon WM, Peacock J, Jaeger L, Kassell NF,Kongable-Beckman GL, Torner JC; International Study of Unruptured Intracranial Aneurysms Investigators.Unruptured intracranial aneurysms:natural history, clinical outcome, and risks of surgical and endovascular treatment. Lancet 2003;362(9378):103-10.
    [3]Bruno G, Todor R, Lewis I, et al. Vascular extracellular matrix remodeling in cerebral aneurysms. J Neurosurg 1998:89(3):431-40.
    [4]Kim SC, Singh M, Huang J, Prestigiacomo CJ, Winfree CJ, Solomon RA, Connolly ES Jr.Matrix metalloproteinase-9 in cerebral aneurysms. Neurosurgery 1997;41(3):642-66; discussion 646-7.
    [5]Aoki T, Kataoka H, Morimoto M, Nozaki K, Hashimoto N.Macrophage-derived matrix metalloproteinase-2 and-9 promote the progression ofcerebral aneurysms in rats. Stroke 2007;38(1):162-9.
    [6]Jin D, Sheng J, Yang X, Gao B.Matrix metalloproteinases and tissue inhibitors of metalloproteinases expression in human cerebral ruptured and unruptured aneurysm. Surg Neurol 2007;68 Suppl 2:S11-6; discussion S16.
    [7]Chyatte D, Bruno G, Desai S, Todor DR.Inflammation and intracranial aneurysms. Neurosurgery 1999;45(5):1137-46
    [8]Kataoka K, Taneda M, Asai T, Kinoshita A, Ito M, Kuroda R.Structural fragility and inflammatory response of ruptured cerebral aneurysms. A comparative study between ruptured and unruptured cerebral aneurysms. Stroke 1999;30(7): 1396-401
    [9]Frosen J, Piippo A, Paetau A, Kangasniemi M, Niemela M, Hernesniemi J,Jaaskelainen J.Remodeling of saccular cerebral artery aneurysm wall is associated with rupture:histological analysis of 24 unruptured and 42 ruptured cases. Stroke 200;35(10):2287-93
    [10]Tulamo R, Frosen J, Hernesniemi J, Niemela M.Inflammatory changes in the aneurysm wall:a review. J neurointervent Surg 2010; 2:120-130.
    [11]Zhang J, Nie L, Razavian M, Ahmed M, Dobrucki LW, Asadi A, Edwards DS, Azure M,Sinusas AJ, Sadeghi MM. Molecular imaging of activated matrix metalloproteinases in vascular remodeling. Circulation 2008;118(19):1953-60.
    [12]Razavian M, Zhang J, Nie L, Tavakoli S, Razavian N, Dobrucki LW, Sinusas AJ,Edwards DS, Azure M, Sadeghi MM.Molecular imaging of matrix metalloproteinase activation to predict murine aneurysm expansion in vivo. J Nucl Med 2010;51(7):1107-15.
    [13]Su H, Spinale FQ Dobrucki LW, Song J, Hua J, Sweterlitsch S, Dione DP, Cavaliere P, Chow C, Bourke BN, Hu XY, Azure M, Yalamanchili P, Liu R, Cheesman EH,Robinson S, Edwards DS, Sinusas AJ.Noninvasive targeted imaging of matrix metalloproteinase activation in a murine model of postinfarction remodeling. Circulation 2005; 112(20):3157-67.
    [14]Lancelot E, Amirbekian V, Brigger I, Raynaud JS, Ballet S, David C, Rousseaux O, Le Greneur S, Port M, Lijnen HR, Bruneval P, Michel JB, Ouimet T, Roques B,Amirbekian S, Hyafil F, Vucic E, Aguinaldo JQ Corot C, Fayad ZA.Evaluation of matrix metalloproteinases in atherosclerosis using a novel noninvasive imaging approach. Arterioscler Thromb Vasc Biol 2008;28(3):425-32.
    [15]Amirbekian V, Aguinaldo JG, Amirbekian S, Hyafil F, Vucic E, Sirol M, Weinreb DB,Le Greneur S, Lancelot E, Corot C, Fisher EA, Galis ZS, Fayad ZA.Atherosclerosis and matrix metalloproteinases:experimental molecular MR imaging in vivo. Radiology 2009;251(2):429-38.
    [16]Bazeli R, Coutard M, Duport BD, Lancelot E, Corot C, Laissy JP, Letourneur D,Michel JB, Serfaty JM.In vivo evaluation of a new magnetic resonance imaging contrast agent (P947) to target matrix metalloproteinases in expanding experimental abdominal aortic aneurysms. Invest Radiol 2010;45(10):662-8.
    [17]DeLeo MJ 3rd, Gounis MJ, Hong B, Ford JC, Wakhloo AK, Bogdanov AA Jr.Carotid artery brain aneurysm model:in vivo molecular enzyme-specific MR imaging of active inflammation in a pilot study. Radiology 2009;252(3):696-703.
    [18]Korosoglou G, Weiss RG, Kedziorek DA, Walczak P, Gilson WD, Schar M, Sosnovik DE,Kraitchman DL, Boston RC, Bulte JW, Weissleder R, Stuber M. Noninvasive detection of macrophage-rich atherosclerotic plaque in hyperlipidemic rabbits using "positive contrast" magnetic resonance imaging. J Am Coll Cardiol 2008;52(6):483-91.

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