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Objective: To provide an updated estimate of the global prevalence of CVD and to comprehensively evaluate risk factors associated with this condition. Background: CVD is an important cause of morbidity internationally, but the global burden of this condition is poorly characterized. The burden of CVD must be better characterized to optimize service provision and permit workforce planning to care for patients with different stages of CVD. Methods: A systematic search in Ovid MEDLINE and Embase (1946-2019) identified 1271 articles. Full-text, English language articles reporting on the epidemiology of CVD in a general adult population were included. Data extraction was performed by 2 independent reviewers, in accordance with a preregistered protocol (PROSPERO: CRD42019153656). STATA and Review Manager were used for quantitative analysis. A crude, unadjusted pooled prevalence was calculated for each Clinical (C) stage in the Clinical, Etiologic, Anatomic, Pathophysiologic classification and across different geographical regions. Qualitative analysis was performed to evaluate associated risk factors in CVD. Results: Thirty-two articles across 6 continents were identified. Nineteen studies were included in the overall pooled prevalence for each Clinical (C) stage; pooled estimates were:

BackgroundEpigenetic variations in peripheral blood have potential as biomarkers for disease. This systematic review assesses the association of lung function and chronic obstructive pulmonary disease (COPD) with DNA methylation profiles in peripheral blood from population-based studies.MethodsOnline databases Medline, Embase, and Web of Science were searched. Google Scholar was searched to identify grey literature. After removing duplicate articles, 1155 articles were independently screened by two investigators. Peer reviewed reports on population-based studies that examined peripheral blood DNA methylation in participants with measured lung function (FEV1, FEV1/FVC ratio) or known COPD status were selected for full-text review. Six articles were suitable for inclusion. Information regarding study characteristics, designs, methodologies and conclusions was extracted. A narrative synthesis was performed based on published results.ResultsThree of the six articles assessed the association of COPD with DNA methylation, and two of these also included associations with lung function. Overall, five reports examined the association of lung function with DNA methylation profiles. Five of the six articles reported ‘significant’ results. However, no consistent CpG sites were identified across studies for COPD status or lung function values.ConclusionsDNA methylation patterns in peripheral blood from individuals with reduced lung function or COPD may be different to those in people with normal lung function. However, this systematic review did not find any consistent associations of lung function or COPD with differentially methylated CpG sites. Large studies with a longitudinal design to address reverse causality may prove a more fruitful area of research.Trial registrationPROSPERO 2016: CRD42016037352.Electronic supplementary materialThe online version of this article (doi:10.1186/s12890-017-0397-3) contains supplementary material, which is available to authorized users.

We investigated changes in gene expression that occur in chronic obstructive pulmonary disease (COPD) after corticosteroid treatment and sought to identify the mechanisms that regulate these changes. Biopsy samples were taken from patients with COPD (Global Initiative for Chronic Obstructive Lung Disease stage I to II) before and after treatment with fluticasone propionate (FP)/salmeterol (SM) (50/500, 4 wk). Gene expression was measured by microarray and was confirmed by real-time reverse transcription-quantitative PCR (RTqPCR). The effect of FP on IgG expression and B-cell proliferation in the presence of oxidative stress was also studied. FP/SM significantly increased the expression of 180 genes while repressing 343 genes. The top 5 downregulated genes were associated with immunoglobulin production, whereas the immunomodulatory FK506 binding protein (FK506BP) was up-regulated. Genes including IL6, IL8, and TBET-encoding TBX21 were unaffected. FP reduced IgG protein and mRNA expression and proliferation of human B cells through the dephosphorylation of ERK-1/2 via increased DUSP1 (dual-specificity protein phosphatase 1) expression. Consistent with in vivo data, oxidative stress did not prevent FP-induced suppression of IgG expression in human B cells in vitro. Changes in expression were validated by RT-qPCR and by gene set enrichment analysis in distinct COPD cohorts. FP may reduce the adaptive immune response in COPD and may be more effective in patients with an increased B-cell/antibody response indicated by high autoantibody

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Surgical site infection (SSI) is associated with increased morbidity, length of stay, and cost. Cyanoacrylate glue is a low‐cost, fluid‐proof, antimicrobial barrier. The aim of this systematic review is to assess the use of cyanoacrylate glue after standard wound closure versus dressings in the reduction of SSI. Medline, Embase, Cochrane Library, and clinical trial registries were searched with no restrictions in accordance with PRISMA guidelines. Eligibility criteria were prospective studies comparing glue versus dressings after standardised wound closure. Two reviewers independently screened articles and utilised GRADE for quality assessment. Meta‐analysis was not performed because of the heterogeneity of the data. Three articles were included in the review. Study quality was uniformly low. Incidence of SSI was low, between 0% and 4%. No significant differences were reported in the single randomised controlled trial. A single non‐randomised parallel group trial reported a significant reduction in the incidence of SSI in the cyanoacrylate group. There was no consistent evidence demonstrating reduction in SSI as a result of the use of cyanoacrylate glue. Future studies should assess the use of cyanoacrylate in procedures with a higher rate of SSI, for example, lower limb bypass.

Objective: The primary objective of this systematic review and meta-analysis was to elucidate the rate of venous thromboembolism (VTE) after endovenous interventions for varicose veins in the presence of pharmacological and mechanical thromboprophylaxis versus mechanical thromboprophylaxis alone. Background: The VTE rate after endovenous procedures for varicose veins is higher than other day-case procedures and could be reduced with pharmacological thromboprophylaxis. Methods: The review followed Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines with a registered protocol (PROSPERO: CRD42021274963). Studies of endovenous intervention for superficial venous incompetence reporting the predefined outcomes with at least 30 patients were eligible. Data were pooled with a fixed effects model. Results: There were 221 trials included in the review (47 randomized trial arms, 105 prospective cohort studies, and 69 retrospective studies). In randomized trial arms, the rate of deep venous thrombosis with additional pharmacological thromboprophylaxis was 0.52% (95% CI, 0.23%–1.19%) (9 studies, 1095 patients, 2 events) versus 2.26% (95% CI, 1.81%–2.82%) (38 studies, 6951 patients, 69 events) with mechanical thromboprophylaxis alone. The rate of pulmonary embolism in randomized trial arms with additional pharmacological thromboprophylaxis was 0.45% (95% CI, 0.09–2.35) (5 studies, 460 participants, 1 event) versus 0.23% (95% CI, 0.1%–0.52%) (28 studies, 4834 participants, 3 events) for mechanical measures alone. The rate of EHIT grade III to IV was 0.35% (95% CI, 0.09–1.40) versus 0.88% (95% CI, 0.28%–2.70%). There was 1 VTE-related mortality and 1 instance of major bleeding, with low rates of minor bleeding. Conclusions: There is a significant reduction in the rate of DVT with additional pharmacological thromboprophylaxis and routine prescription of anticoagulation after endovenous varicose vein intervention should be considered. VTE risk for individual study participants is heterogeneous and risk stratification in future randomized interventional studies is critical to establish the clinical effectiveness and safety of additional pharmacological thromboprophylaxis.

Penetrating aortic ulceration (PAU) is part of the spectrum of acute aortic syndromes (AAS), and is defined as an ulcerated intimal disruption due to atherosclerotic disease. PAU may be simple, isolated and asymptomatic, or it may be symptomatic, aneurysmal and extensive; these may progress and lead to rupture. This review aims to evaluate the treatment options for PAU. Treatment options range from radiological surveillance, risk factor modification, best medical therapy and open or endovascular surgical repair. Patients with PAU are frequently older and comorbid with relatively damaged aortic tissue; this can make open surgical repair more challenging. Endovascular repairs for larger, symptomatic, aneurysmal PAU may be performed with acceptable outcomes. Complex endovascular repairs may be required depending on the pathology. Patients with small, asymptomatic, uncomplicated PAU may be safely followed up with surveillance. PAU with concomitant intramural haematoma (IMH) should be closely monitored to observe for resolution or progression following conservative and medical management strategies. PAU is a unique entity and its natural history should be studied independently to better understand appropriate management strategies. This research is currently lacking, and larger studies or registries may be helpful in optimising PAU management.