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      Testing bioresorbable stent feasibility in a rat aneurysm model

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          Abstract

          Background

          Advances in stent-assisted coiling have incrementally expanded endovascular treatment options for complex cerebral aneurysms. After successful coil consolidation and aneurysm occlusion, endovascular scaffolds are no longer needed. Thus, bioresorbable stents that disappear after aneurysm healing could avoid future risks of in-stent thrombosis and the need for lifelong antiplatelet therapy.

          Objective

          To assess the applicability and compatibility of a bioresorbable magnesium- alloy stent (brMAS) for assisted coiling.

          Methods

          Saccular sidewall aneurysms were created in 84 male Wistar rats and treated with brMAS alone, brMAS + aspirin, or brMAS + coils + aspirin. Control groups included no treatment (natural course), solely aspirin treatment, or conventional cobalt–chromium stent + coils + aspirin treatment. After 1 and 4 weeks, aneurysm specimens were harvested and macroscopically, histologically, and molecularly examined for healing, parent artery perfusion status, and inflammatory reactions. Stent degradation was monitored for up to 6 months with micro-computed and optical coherence tomography.

          Results

          Aneurysms treated with brMAS showed advanced healing, neointima formation, and subsequent stent degradation. Additional administration of aspirin sustained aneurysm healing while reducing stent-induced intraluminal and periadventitial inflammatory responses. No negative interaction was detected between platinum coils and brMAS. Progressive brMAS degradation was confirmed.

          Conclusions

          brMAS induced appropriate healing in this sidewall aneurysm model. The concept of using bioresorbable materials to promote complete aneurysm healing and subsequent stent degradation seems promising. These results should encourage further device refinements and clinical evaluation of this treatment strategy for cerebrovascular aneurysms.

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          Most cited references 28

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          Changes in case fatality of aneurysmal subarachnoid haemorrhage over time, according to age, sex, and region: a meta-analysis.

          In a systematic review, published in 1997, we found that the case fatality of aneurysmal subarachnoid haemorrhage (SAH) decreased during the period 1960-95. Because diagnostic and treatment strategies have improved and new studies from previously non-studied regions have been published since 1995, we did an updated meta-analysis to assess changes in case fatality and morbidity and differences according to age, sex, and region. A new search of PubMed with predefined inclusion criteria for case finding and diagnosis identified reports on prospective population-based studies published between January, 1995, and July, 2007. The studies included in the previous systematic review were reassessed with the new inclusion criteria. Changes in case fatality over time and the effect of age and sex were quantified with weighted linear regression. Regional differences were analysed with linear regression analysis, and the regions of interest were subsequently defined as reference regions and compared with the other regions. 33 studies (23 of which were published in 1995 or later) were included that described 39 study periods. These studies reported on 8739 patients, of whom 7659 [88%] were reported on after 1995. 11 of the studies that were included in the previous review did not meet the current, more stringent, inclusion criteria. The mean age of patients had increased in the period 1973 to 2002 from 52 to 62 years. Case fatality varied from 8.3% to 66.7% between studies and decreased 0.8% per year (95% CI 0.2 to 1.3). The decrease was unchanged after adjustment for sex, but the decrease per year was 0.4% (-0.5 to 1.2) after adjustment for age. Case fatality was 11.8% (3.8 to 19.9) lower in Japan than it was in Europe, the USA, Australia, and New Zealand. The unadjusted decrease in case fatality excluding the data for Japan was 0.6% per year (0.0 to 1.1), a 17% decrease over the three decades. Six studies reported data on case morbidity, but these were insufficient to assess changes over time. Despite an increase in the mean age of patients with SAH, case-fatality rates have decreased by 17% between 1973 and 2002 and show potentially important regional differences. This decrease coincides with the introduction of improved management strategies. Netherlands Organisation for Scientific Research; ZonMw.
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            Biology of intracranial aneurysms: role of inflammation.

            Intracranial aneurysms (IAs) linger as a potentially devastating clinical problem. Despite intense investigation, our understanding of the mechanisms leading to aneurysm development, progression and rupture remain incompletely defined. An accumulating body of evidence implicates inflammation as a critical contributor to aneurysm pathogenesis. Intracranial aneurysm formation and progression appear to result from endothelial dysfunction, a mounting inflammatory response, and vascular smooth muscle cell phenotypic modulation producing a pro-inflammatory phenotype. A later final common pathway appears to involve apoptosis of cellular constituents of the vessel wall. These changes result in degradation of the integrity of the vascular wall leading to aneurysmal dilation, progression and eventual rupture in certain aneurysms. Various aspects of the inflammatory response have been investigated as contributors to IA pathogenesis including leukocytes, complement, immunoglobulins, cytokines, and other humoral mediators. Furthermore, gene expression profiling of IA compared with control arteries has prominently featured differential expression of genes involved with immune response/inflammation. Preliminary data suggest that therapies targeting the inflammatory response may have efficacy in the future treatment of IA. Further investigation, however, is necessary to elucidate the precise role of inflammation in IA pathogenesis, which can be exploited to improve the prognosis of patients harboring IA.
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              Saccular intracranial aneurysm: pathology and mechanisms.

              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.
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                Author and article information

                Journal
                Journal of NeuroInterventional Surgery
                J NeuroIntervent Surg
                BMJ
                1759-8478
                1759-8486
                September 12 2019
                October 2019
                October 2019
                March 09 2019
                : 11
                : 10
                : 1050-1054
                Article
                10.1136/neurintsurg-2018-014697
                © 2019

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