SCG, using a Micro-Infusion Device for transmural drug delivery. Methods Eight SCGs in four Yorkshire swine were surgically identified. After confirming appropriate sympathetic-mediated intracranial vasoconstriction response with SCG stimulation, an endovascular Micro-Infusion Device was used for transmural targeting of the SCG and delivery of 1.5-2mL of 1% lidocaine-contrast mixture to the perivascular space. (figure 1) Digital subtraction angiography was obtained at: 1) baseline; 2) with SCG stimulation; and 3) after lidocaine delivery to the SCG using the Micro-Infusion Device with concurrent SCG stimulation. Vessel diameters were measured and compared.Results Stimulation of the SCG resulted in significant ipsilateral vasoconstriction response in the cervico-cranial vasculature. Endovascular transmural delivery of lidocaine to the SCG and carotid perivascular tissue using the Micro-Infusion Device successfully inhibited sympathetic-mediated vasoconstriction despite subsequent SCG stimulation in all eight cervico-cranial vasculatures. All measured vessel diameter means were within 13% of, and non-statistically different from baseline measurements. Conclusions We demonstrate a novel endovascular technique of transmural delivery of lidocaine to the SCG and carotid artery perivascular tissues to inhibit sympathetic mediated cerebral vasospasm. These results suggest promising translation to humans for clinical use in patients suffering from cerebral vasospasm.
posterior circulation intracranial aneurysms. Previous studies demonstrated high rates of successful aneurysm occlusion and a favorable safety profile. Location specific results are needed to guide treatment decision making. However, it is unclear whether there are specific differences in safety and efficacy outcomes between carotid and more distal anterior circulation aneurysms. Methods The ATLAS IDE trial was a prospective, single arm, independently adjudicated, multicenter study that evaluated the safety and efficacy of the Neuroform Atlas Stent System. We compare differences in efficacy and safety outcomes of proximal internal carotid artery (ICA) versus distal and bifurcation anterior circulation aneurysms. Primary effectiveness endpoint: complete aneurysm occlusion without clinically significant stenosis or retreatment. Primary safety endpoint: rate of major ipsilateral stroke (increase in NIHSS score !4) or neurological death.Results Of the 202 anterior circulation participants enrolled, 182 patients composed the modified intention to treat cohort and were included in the analysis. Proximal subgroup included 70 (38.5%) aneurysms located at the internal carotid artery (ICA) and 112 (61.5%) at the distal anterior circulation (including ICA terminus/bifurcation). Patients from proximal aneurysm subgroup were more likely to be younger (57.4 vs. 62.1, p=.03), female (85.7% vs. 65.2%, p=.006), and to have larger parent vessel diameters (p<.0001). At one-year follow-up, there were no significant differences in the primary efficacy endpoint (85.5% vs. 83.9%, p=0.78), complete aneurysm occlusion rates (88.7% vs. 87.9%, p=0.78), recanalization rates (6.5% vs. 5.4%, p=0.76), and incidence of retreatment (2.9% vs. 4.5%, p=.55) between proximal ICA aneurysms and distal aneurysms, respectively. While it appeared that the distal group had a higher complication rate, the result was not statistically significant (6.3% vs. 1.4%, p=0.14). Conclusion Based on these findings of the ATLAS IDE trial, the Neuroform Atlas Stent System is a safe and efficacious treatment modality for unruptured anterior circulation intracranial aneurysms in both proximal and distal, bifurcation aneurysms. Additional, studies are needed to assess complication rates in larger populations. This may have important implications for the selection of treatment modalities for intracranial aneurysms.
hemorrhagic stroke. In this study, we analyzed protein expression signature in human CCM tissue samples by using highly specific and sensitive multiplexing technique, proximity extension assay (PEA) in Olink platform. Methods Relative expression of 184 biomarkers were analyzed from fresh-frozen CCM lesion samples (n=6; age 3-66 years; male:female ratio 2:4) and brain tissue controls from normal cerebral cortex (n=3; age 34-69 years; male:female ratio 2:1; Amsbio, Abington, UK) using Olink Target 96 Cardiovascular III and Inflammation panels. In addition, in 2 CCMs, protein extraction was done by separating tissue from the lesion area and the surrounding brain tissue representing normal caliber brain vasculature; thus, allowing analysis of biomarkers in a spatially resolving manner. Results Data analysis revealed 76 biomarkers with significantly higher expression in CCM lesion than control brain tissue. These biomarkers belong to pathways previously connected to CCM pathogenesis (e.g. endothelial-to-mesenchymal transition, toll-like receptor signaling); in addition, novel pathways (neutrophil-extracellular-trap formation, coagulation cascade and NFkB signaling) were defined. Biomarker expression profiles were in-line with disease severity, representing higher level of especially inflammatory markers in ruptured (n=3) than nonruptured (n=3) samples. Furthermore, biomarkers involved in compensatory mechanisms were defined from the CCM border area (n=2). Conclusions Here, we present a novel technique for proteomics analysis on human CCMs, offering a possibility for highthroughput screening from small amount of fresh-frozen tissue. Biomarkers detected here will advance our understanding of the causes and mechanisms of CCM and help later development of new, targeted treatment strategies.
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