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Articles

  1. Computational and Mathematical Methods in Medicine
  2. 1 Introduction
  3. Hemodynamics of Cerebral Aneurysms: Computational Analyses of Aneurysm Progress and Treatment
  4. Cerebral aneurysms and inflammation

Safety and efficacy of high-dose adenosine-induced asystole during endovascular AAA repair.

Computational and Mathematical Methods in Medicine

J Endovasc Ther ; Adenosine-induced cardiac arrest and EEG changes in patients with thoracic aorta endovascular repair. Br J Anaesth ; Adenosine-induced ventricular asystole to induce transient profound systemic hypotension in patients undergoing endovascular therapy. Dose-response characteristics. Adenosine-induced cardiac pause for endovascular embolization of cerebral arteriovenous malformations: Technical case report. Neurosurgery ; Adenosine-induced transient asystole for management of a basilar artery aneurysm.

Case report. J Neurosurg ; Transient cardiac standstill induced by adenosine in the management of intraoperative aneurysmal rupture: Technical case report. Basilar tip aneurysm-Adenosine induced asystole for the treatment of a basilar tip aneurysm following failure of temporary clipping.

Acta Neurochir Wien ; Surgical management of proximal carotid artery aneurysms. Clin Neurosurg ; Large and giant paraclinoid aneurysms: Surgical techniques, complications, and results. Endovascular retrograde suction decompression as an adjunct to surgical treatment of ophthalmic aneurysms: Analysis of risks and clinical outcomes. Neurosurgery ;64 3 Suppl:ons Retrograde suction decompression of giant paraclinoid aneurysms using a No. Technical note. Anesthetic management of deep hypothermic circulatory arrest for cerebral aneurysm clipping.

Cerebral blood flow and metabolism during adenosine-induced hypotension in patients undergoing cerebral aneurysm surgery. Acta Anaesthesiol Scand ; Clinical experience with adenosine for controlled hypotension during cerebral aneurysm surgery.

1 Introduction

Thus, considering both hemodynamic and morphological factors can thoroughly understand the mechanism of IAs rupture. Yet recent many studies propose other parameters including LSAR, which RSS was not involved, could also suggest the abnormal characteristics Zhang et al. However, the ruptured rate in high risk group was Meanwhile, if a tool can effectively help clinical work, it should be easy to understand and simple operation.

Our study developed a score system to simplify and visualize the morphological-hemodynamic analysis of aneurysm. The proposed model is meant to help physicians who are contemplating timely intervention in face of IA patients. There are some limitations in our study. First and foremost, as this study is a retrospective study, small sample and short-time follow-up, the conclusion is limited and needs further study to provide more evidences to confirm value of the IARS.

Second, although we used the image before rupture to avoid the effect from the event of the rupture, which might not completely reflect the rupture condition. However, the considered statue was nearly close to rupture condition. It may need further prospective study to explore that. Third, we just balanced the risk factors based on previous studies here. However, there may be potential risk factors which may affect the hemodynamic condition in aneurysm. Thus, it was difficult to avoid selection bias because of high selection we selected from patients with ruptured aneurysm.

Fourth, all morphological parameters were calculated from 3D CTA which is suitable for clinical visiting and can exclude the effect from thrombus, but do not give essentially image like 3D angiography. Meanwhile, all hemodynamic models were established from 3D CTA that may affect the accuracy of our simulation.

Correlation with angiogram can improve the result, but we did not routinely perform angiogram in clinical visiting. Fifth, our threshold of some parameters was different with previous study. However, all aneurysms in our series came from a single center. The real threshold may require pooling of data from multiple centers. Sixth, some clinical characteristics were not considered, such as multi-IAs and IAs with vascular stenosis.

There are also several limitations related to our CFD analysis. We used the similar modeling and simulating method from Meng et al. The limitations that Meng have given will also exist in our study, such as the traction-free boundary condition at the outlet and definition of low WSS.

In our study, differently from Meng, we used the velocity inlet boundary from a representative patient. However, the velocity boundary does not match with the CTA which was scanned before aneurysm rupture. Thus, the pulsatile wave may not be a good representation of the ruptured condition. Considering the CFD is sensitive to the velocity condition, it may affect our result. In the other hand, the effects from magnitude of wave form and so on will also limit our result. In the future study, we may invite reliable ultrasonic expert to join our study.

However, strict convergence in traditional sense is difficult to reach. Our effort was done to reach the better result. All those questions will be solved in the further study. However, multiple research groups are trying to use CFD analysis to assess aneurysm rupture risk. We believe that CFD may help physicians to make decision-making in the future.


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The study was approved by the institutional review board. Written informed consents were obtained from all participants or their legally authorized representatives and privacy of patients was effectively protected. SW and YC were in charge of supervising the whole study. PJ and QL were responsible for the design of the article and drafting. QL was responsible for revising, responding to reviewer and statistical analysis. PJ and JW were also responsible for statistical analysis and confirmed the final article. BG and YC provided a reliable technical support. D, Principal Investigator: YC. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Castro, M. Understanding the role of hemodynamics in the initiation, progression, rupture, and treatment outcome of cerebral aneurysm from medical image-based computational studies. ISRN Radiol. Cebral, J. Wall mechanical properties and hemodynamics of unruptured intracranial aneurysms.

AJNR Am. Flow conditions in the intracranial aneurysm lumen are associated with inflammation and degenerative changes of the aneurysm wall. Analysis of hemodynamics and wall mechanics at sites of cerebral aneurysm rupture. Chen, C. Infundibular dilations of the posterior communicating arteries: pathogenesis, anatomical variants, aneurysm formation, and subarachnoid hemorrhage. Chien, A. Quantitative hemodynamic analysis of brain aneurysms at different locations.

Cross, D. Mortality rates after subarachnoid hemorrhage: variations according to hospital case volume in 18 states. Dhar, S. Morphology parameters for intracranial aneurysm rupture risk assessment. Neurosurgery 63, — Evju, O. Robustness of common hemodynamic indicators with respect to numerical resolution in 38 middle cerebral artery aneurysms.

Hemodynamics of Cerebral Aneurysms: Computational Analyses of Aneurysm Progress and Treatment

PLoS One e Fan, J. Morphological-hemodynamic characteristics of intracranial bifurcation mirror aneurysms. World Neurosurg. Greving, J. Development of the PHASES score for prediction of risk of rupture of intracranial aneurysms: a pooled analysis of six prospective cohort studies.

Lancet Neurol. Hashimoto, T. Intracranial aneurysms: links among inflammation, hemodynamics and vascular remodeling.


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  • References.

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The role of hemodynamics in intracranial aneurysm initiation. Google Scholar. Miura, Y. Low wall shear stress is independently associated with the rupture status of middle cerebral artery aneurysms. Stroke 44, — Neurosurgery 73, — Omodaka, S. Local hemodynamics at the rupture point of cerebral aneurysms determined by computational fluid dynamics analysis. Paliwal, N. Association between hemodynamic modifications and clinical outcome of intracranial aneurysms treated using flow diverters.

SPIE Int. Qiu, T. Association between hemodynamics, morphology, and rupture risk of intracranial aneurysms: a computational fluid modeling study. Sano, T. Hemodynamic differences between ruptured and unruptured cerebral aneurysms simultaneously existing in the same location: 2 case reports and proposal of a novel parameter oscillatory velocity index. Skodvin, T. A comparative study between ruptured and unruptured cerebral aneurysms. Aminoterminal propeptide of type III procollagen in the follow-up of patients with abdominal aortic aneurysms.

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Brain Aneurysms: The Basics - Dr. Geoffrey Colby - UCLA Neurosurgery

Circulation ; Role of matrix metalloproteinases in abdominal aortic aneurysms. Ann N Y Acad Sci ; Arterioscler Thromb Vasc Biol ; Inflammation and cellular immune responses in abdominal aortic aneurysms. Intracranial aneurysms: links among inflammation, hemodynamics and vascular remodeling. Neurol Res ; Inflammation and intracranial aneurysms. Neurosurgery ; Abnormalities of collagen cross-linkage in posterior communicating artery aneurysms: a preliminary study.


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  • Angiotomography of intracranial aneurysms.
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  • Cerebral aneurysms and inflammation.

Metalloproteases and intracranial vascular lesions. NF-kappaB is a key mediator of cerebral aneurysm formation. Impact of monocyte chemoattractant protein-1 deficiency on cerebral aneurysm formation. Apoptosis of medial smooth muscle cells in the development of saccular cerebral aneurysms in rats. Disruption of gene for inducible nitric oxide synthase reduces progression of cerebral aneurysms. Impaired progression of cerebral aneurysms in interleukin-1beta-deficient mice. Tumor necrosis factor alpha is a key modulator of inflammation in cerebral aneurysms.

Cerebral aneurysms and inflammation

Genes involved in the transforming growth factor beta signalling pathway and the risk of intracranial aneurysms. J Neurol Neurosurg Psychiatry ; Suppression of cerebral aneurysm formation in rats by a tumor necrosis factor-a inhibitor. J Neurosurg ; TNF-alpha-mediated inflammation in cerebral aneurysms: a potential link to growth and rupture. Vasc Health Risk Manag ; TNF-alpha reduces cerebral blood volume and disrupts tissue homeostasis via an endothelin- and TNFR2-dependent pathway.

Brain ; Altered neuronal and microglial responses to excitotoxic and ischemic brain injury in mice lacking TNF receptors. Nat Med ; Tumor necrosis factor alpha but not interleukin 1 beta mediates neuroprotection in response to acute nitric oxide excitotoxicity. J Neurosci ; Dual role of tumor necrosis factor alpha in brain injury. Cytokine Growth Factor Rev ; A comparison of genetic chromosomal loci for intracranial, thoracic aortic, and abdominal aortic aneurysms in search of common genetic risk factors.

Cardiovasc Pathol ;