No abstract

Treatment of non-saccular aneurysms of the posterior circulation poses a great challenge with unpredictable outcomes due to the absence of a true aneurysm neck and the presence of perforating vessels. In this article, we aim to compare endovascular treatment of unruptured posterior circulation non-saccular aneurysms with stent-assisted coiling (SAC) and flow diversion (FD) in terms of occlusion rate and clinical outcomes. A systematic search of electronic databases from inception to August 2019 identified 484 articles for screening. After proper inclusion/exclusion criteria, 15 articles were included and data were extracted and analyzed using meta-analysis of proportions. The pooled cohort consisted of 430 aneurysms: 128 (29.7%) treated with SAC in 5 studies and 302 (70.3%) treated with FD in 11 studies. Complete/near-complete occlusion was achieved in 83% after FD (95% CI 0.75 to 0.90; I2=45%) and 84% after SAC (95% CI 0.72 to 0.91; I2=22%), with no significant difference between techniques (p=0.95). Periprocedural complications were observed in 18% after FD (95% CI 0.14 to 0.23; I2=0%) and 6% after SAC (95% CI 0.02 to 0.13; I2=0%); the subgroup analysis was statistically significant (p=0.008). Furthermore, no statistically significant difference was observed in favorable clinical outcomes between groups. These results suggest similar efficacy in occlusion rate and favorable clinical outcome for posterior circulation non-saccular aneurysms treated with SAC and FD. Stroke was the most common complication regardless of treatment modality, and a lower periprocedural complication rate was noted with SAC. Further studies are needed with the primary focus of reducing the risk of stroke with either modality.

Elevated levels of serum homocysteine (Hcy) resulting in hyperhomocysteinemia (HHcy) have been implicated in cardiac pathological conditions including: coronary heart disease (CHD), acute myocardial infarction, arrhythmogenesis and sudden cardiac death (SCD). The mechanisms by which HHcy leads to arrhythmogenesis and SCD are unknown. Novel findings indicate that Hcy is an agonist of the N-methyl-D-aspartate receptor (NMDA-R), known to be present in cardiac tissue, and when activated, increases intracellular calcium leading to increased cell excitability. Also, HHcy induces oxidative stress in cardiac cells and activates matrix metalloproteinases (MMPs) that degrade cell membranes and proteins. Here we review the literature relevant to HHcy-induced oxidative stress leading to cardiac tissue remodelling that may adversely affect cell-to-cell impulse conduction, in particular on the heart's specialized conduction system, and may provide substrate for arrhythmogenesis and SCD. Efficacy of B vitamin supplementation in patient populations with HHcy and CHD is also reviewed.

Background Excessive complement activation is an integral part of ischemia and reperfusion (IR) injury (IRI) of organs. In kidney transplantation the pathological consequence of IRI and complement activation can lead to delayed graft function which in turn is associated with acute rejection. Previous strategies to reduce complement induced IRI required systemic administration of agents, which can lead to increased susceptibility to infections/immune diseases. The objective of this study was to determine whether an increase in complement control defenses of rat kidney endothelium reduces IRI. We hypothesized that increased complement control on the endothelial barrier reduces IR-mediated complement activation and reduces kidney dysfunction. Materials and methods Fisher 344 rats underwent left kidney ischemia for 45 min. and treatment with a novel fusogenic lipid vesicle (FLVs) delivery system to decorate endothelial cells with Vaccinia virus complement control protein (VCP), followed by reperfusion for 24h. Assessment included renal function by serum creatinine and urea, myeloperoxidase assay for neutrophil infiltration, histopathology, and quantification of C3 production in kidneys. Results Animals in which the kidney endothelium was bolstered by FLVs+VCP treatment had better renal function with a significant reduction in serum creatinine as compared to vehicle controls. C3 production was significantly reduced (p<0.05) in treated animals compared to vehicle controls. Conclusion Increasing complement control at the endothelial barrier with FLVs+VCP modulates complement activation/production during the first 24h, reducing renal dysfunction following IRI.