Safety and efficacy of high-dose adenosine-induced asystole during endovascular AAA repair.
Computational and Mathematical Methods in Medicine
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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.
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Hemodynamics of Cerebral Aneurysms: Computational Analyses of Aneurysm Progress and Treatment
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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
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