Carotid Endarterectomy After Intracranial Endovascular Thrombectomy for Acute Ischaemic Stroke in Patients with Carotid Artery Stenosis

Objective: Recent randomised controlled trials demonstrated the benefit of intracranial endovascular thrombectomy (EVT) in acute ischaemic stroke. There is no consensus, however, on how to treat concomitant extracranial carotid artery stenosis after EVT. The aim of this study was to evaluate the outcome in patients treated with carotid endarterectomy (CEA) after EVT, comparing complication rates among patients undergoing CEA for stroke without previous EVT. Methods: This was a registry study of all patients (n = 3 780) treated with CEA after stroke in Sweden and the capital Helsinki region, Finland, from January 2011 to September 2020. Sixty three patients (1.7%; 0.5% 2011, 4.3% 2019) underwent EVT prior to CEA. The primary outcome was 30 day stroke and death rate. Results: The EVT+CEA group had major stroke as the qualifying neurological event (QNE) in 79%, but just 5.9% had this in the CEA only group (p < .001). Intravenous thrombolysis was administered before EVT in 54% of patients in the EVT+CEA group, but in just 12% in those receiving CEA only (p < .001). The combined stroke and death rate at 30 days for EVT+CEA was 0.0% (95% confidence interval [CI] 0.0 - 5.7). One patient had a post-operative TIA, none had post-operative intracerebral or surgical site haemorrhage. CEA was performed within a median of seven days (interquartile range 4, 15) after QNE, and 75% had CEA Conclusion: These results indicate that CEA is safe to perform after previous successful EVT for acute ischaemic stroke. Results were comparable with those undergoing CEA only, despite the EVT+CEA patients having more severe stroke symptoms prior to surgery, and timing was similar.Peer reviewe

The sac evolution imaging follow-up after endovascular aortic repair:An international expert opinion-based Delphi consensus study

Objective: Management of follow-up protocols after endovascular aortic repair (EVAR) varies significantly between centers and is not standardized according to sac regression. By designing an international expert-based Delphi consensus, the study aimed to create recommendations on follow-up after EVAR according to sac evolution. Methods: Eight facilitators created appropriate statements regarding the study topic that were voted, using a 4-point Likert scale, by a selected panel of international experts using a three-round modified Delphi consensus process. Based on the experts' responses, only those statements reaching a grade A (full agreement ≥75%) or B (overall agreement ≥80% and full disagreement &lt;5%) were included in the final document. Results: One-hundred and seventy-four participants were included in the final analysis, and each voted the initial 29 statements related to the definition of sac regression (Q1-Q9), EVAR follow-up (Q10-Q14), and the assessment and role of sac regression during follow-up (Q15-Q29). At the end of the process, 2 statements (6.9%) were rejected, 9 statements (31%) received a grade B consensus strength, and 18 (62.1%) reached a grade A consensus strength. Of 27 final statements, 15 (55.6%) were classified as grade I, whereas 12 (44.4%) were classified as grade II. Experts agreed that sac regression should be considered an important indicator of EVAR success and always be assessed during follow-up after EVAR. Conclusions: Based on the elevated strength and high consistency of this international expert-based Delphi consensus, most of the statements might guide the current clinical management of follow-up after EVAR according to the sac regression. Future studies are needed to clarify debated issues.</p

Global Expression Profiling in Atopic Eczema Reveals Reciprocal Expression of Inflammatory and Lipid Genes

Atopic eczema (AE) is a common chronic inflammatory skin disorder. In order to dissect the genetic background several linkage and genetic association studies have been performed. Yet very little is known about specific genes involved in this complex skin disease, and the underlying molecular mechanisms are not fully understood.We used human DNA microarrays to identify a molecular picture of the programmed responses of the human genome to AE. The transcriptional program was analyzed in skin biopsy samples from lesional and patch-tested skin from AE patients sensitized to Malassezia sympodialis (M. sympodialis), and corresponding biopsies from healthy individuals. The most notable feature of the global gene-expression pattern observed in AE skin was a reciprocal expression of induced inflammatory genes and repressed lipid metabolism genes. The overall transcriptional response in M. sympodialis patch-tested AE skin was similar to the gene-expression signature identified in lesional AE skin. In the constellation of genes differentially expressed in AE skin compared to healthy control skin, we have identified several potential susceptibility genes that may play a critical role in the pathological condition of AE. Many of these genes, including genes with a role in immune responses, lipid homeostasis, and epidermal differentiation, are localized on chromosomal regions previously linked to AE.Through genome-wide expression profiling, we were able to discover a distinct reciprocal expression pattern of induced inflammatory genes and repressed lipid metabolism genes in skin from AE patients. We found a significant enrichment of differentially expressed genes in AE with cytobands associated to the disease, and furthermore new chromosomal regions were found that could potentially guide future region-specific linkage mapping in AE. The full data set is available at http://microarray-pubs.stanford.edu/eczema

Mechanisms of thrombosis and restenosis after vascular injury

Atherosclerosis is the underlying cause of about 50% of all deaths in the western world. Peripheral vascular disease commonly affects the arteries supplying the leg and is mostly caused by atherosclerosis. When medical treatment of lower extremity ischemia has failed, percutaneous transluminal angioplasty (PTA) and bypass surgery are two major therapeutic options. The advances in vascular surgery and endovascular techniques over the past half-century have greatly expanded the number of arterial lesions that can be treated. The major limitations of a successful revascularisation are thrombosis and the later development of restenosis. This thesis has explored the mechanisms of thrombosis and restenosis after vascular injury, focusing on the interaction between coagulation, inflammation, and oxidative stress. The long-term outcome of infrainguinal PTA was evaluated in 77 patients. Cumulative primary and secondary patency rates, respectively, were 81% and 86% at 1 year, 65% and 73% at 5 years, and 12% and 17% at 10 years. Patency rates were better for patients with claudication than critical ischemia. Stenoses had better primary patency than occlusions. Generalised femoral artery disease and diabetes mellitus predicted poor survival. Although the overall long-term patency of infrainguinal PTA is poor, the technique has a low morbidity and can be performed in selected patients with a reasonable long-term result. If conservative treatment has failed infrainguinal PTA should be considered, when lesions and patients are suitable, because of its minimal invasive nature. It is also important when treating patients with peripheral arterial disease to give attention to their general cardiovascular condition. In an experimental study a specific direct thrombin inhibitor, inogatran, reduced neointimal hyperplasia after arterial injury in rats. A more prolonged administration of the thrombin inhibitor gave a further reduction of the neointimal hyperplasia. It seems that inhibition of thrombin activity is not only important early after injury, but also later. This could have clinical implications in the treatment of restenosis. Inflammation and oxidative stress in the vessel wall may play important roles in the development of restenosis after angioplasty. In patients with peripheral arterial disease, a much more prolonged inflammatory response than previously noted was observed after angioplasty, but only minor changes in coagulation activity. C-reactive protein was elevated the day after angioplasty and peaked after one week. Coagulation and inflammatory markers were not significantly related to restenosis. The redox-active protein, thioredoxin, was significantly elevated 4 hours after angioplasty and returned to baseline within 24 hours. Circulating thioredoxin could theoretically impair the chemotactic response at local sites of inflammation. An association in patients with elevated levels of thioredoxin after angioplasty and reduced restenosis needs to be further evaluated. This thesis has discussed the intimate relation between thrombosis, inflammation, oxidative stress, and restenosis. Further studies are needed to delineate the molecular mechanisms behind these observations and their involvement in thrombosis and restenosis. It is not only important to be able to understand the individual pathways of these processes, but also the ways they intersect and interact. If these pathways are further defined, improved treatment strategies, including antithrombotic treatments, statins, and thioredoxin, to modulate postprocedure inflammation could be tailored

A systematic review of hemorrhage and vascular injuries in civilian public mass shootings

Abstract Background Civilian public mass shootings (CPMSs) are a major public health issue and in recent years several events have occurred worldwide. The aim of this systematic review was to characterize injuries and mortality after CPMSs focusing on in-hospital management of hemorrhage and vascular injuries. Method A systematic review of all published literature was undertaken in Medline, Embase and Web of Science January 1st, 1968, to February 22nd, 2021, according to the PRISMA guidelines. Literature was eligible for inclusion if the CPMS included three or more people shot, injured or killed, had vascular injuries or hemorrhage. Results The search identified 2884 studies; 34 were eligible for inclusion in the analysis. There were 2039 wounded in 45 CPMS events. The dominating anatomic injury location per event was the extremity followed by abdomen and chest. The median number of operations and operated patients per event was 22 (5–101) and 10.5 (4–138), respectively. A total of 899 deaths were reported with a median mortality rate of 36.1% per event (15.9–71.4%) Thirty-eight percent (13/34) of all studies reported on vascular injuries. Vascular injuries ranged from 8 to 29%; extremity vascular injury the most frequent. Specific vascular injuries included thoracic aorta 18% (42/232), carotid arteries 6% (14/232), and abdominal aorta 5% (12/232). Vascular injuries were involved in 8.3%-10% of all deaths. Conclusion This systematic review showed an overall high mortality after CPMS with injuries mainly located to the extremities, thorax and abdomen. About one quarter of deaths was related to hemorrhage involving central large vessel injuries. Further understanding of these injuries, and structured and uniform reporting of injuries and treatment protocols may help improve evaluation and management in the future. Level of Evidence Systematic review and meta-analysis, level III