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Background In the past two decades, the built environment emerged as a conceptually important determinant of obesity. As a result, an abundance of studies aiming to link environmental characteristics to weight-related outcomes have been published, and multiple reviews have attempted to summarise these studies under different scopes and domains. We set out to summarise the accumulated evidence across domains by conducting a review of systematic reviews on associations between any aspect of the built environment and overweight or obesity. Methods Seven databases were searched for eligible publications from the year 2000 onwards. We included systematic literature reviews, meta-analyses and pooled analyses of observational studies in the form of cross-sectional, case–control, longitudinal cohort, ecological, descriptive, intervention studies and natural experiments. We assessed risk of bias and summarised results structured by built environmental themes such as food environment, physical activity environment, urban–rural disparity, socioeconomic status and air pollution. Results From 1850 initial hits, 32 systematic reviews were included, most of which reported equivocal evidence for associations. For food- and physical activity environments, associations were generally very small or absent, although some characteristics within these domains were consistently associated with weight status such as fast-food exposure, urbanisation, land use mix and urban sprawl. Risks of bias were predominantly high. Conclusions Thus far, while most studies have not been able to confirm the assumed influence of built environments on weight, there is evidence for some obesogenic environmental characteristics. Registration : This umbrella review was registered on PROSPERO under ID CRD42019135857.

Cardiovascular diseases (CVDs) are the most common cause of non-communicable disease mortality in sub-Saharan African (SSA) countries. Gaps in knowledge of CVD conditions and their risk factors are important barriers in effective prevention and treatment. Yet, evidence on the awareness and knowledge level of CVD and associated risk factors among populations of SSA is scarce. This review aimed to synthesize available evidence of the level of knowledge of and perceptions towards CVDs and risk factors in the SSA region. Five databases were searched for publications up to December 2016. Narrative synthesis was conducted for knowledge level of CVDs, knowledge of risk factors and clinical signs, factors influencing knowledge of CVDs and source of health information on CVDs. The review was registered with Prospero (CRD42016049165). Of 2212 titles and abstracts screened, 45 full-text papers were retrieved and reviewed and 20 were included: eighteen quantitative and two qualitative studies. Levels of knowledge and awareness for CVD and risk factors were generally low, coupled with poor perception. Most studies reported less than half of their study participants having good knowledge of CVDs and/or risk factors. Proportion of participants who were unable to identify a single risk factor and clinical symptom for CVDs ranged from 1.8% in a study among hospital staff in Nigeria to a high of 73% in a population-based survey in Uganda and 7% among University staff in Nigeria to 75.1% in a general population in Uganda respectively. High educational attainment and place of residence had a significant influence on the levels of knowledge for CVDs among SSA populations. Low knowledge of CVDs, risk factors and clinical symptoms is strongly associated with the low levels of educational attainment and rural residency in the region. These findings provide useful information for implementers of interventions targeted at the prevention and control of CVDs, and encourages them to incorporate health promotion and awareness campaigns in order to enhance knowledge and awareness of CVDs in the region.

Prediction models for gestational hypertension and preeclampsia have been developed with data and assumptions from developed countries. Their suitability and application for low resource settings have not been tested. This review aimed to identify and assess the methodological quality of prediction models for gestational hypertension and pre-eclampsia with reference to their application in low resource settings. Using combinations of keywords for gestational hypertension, preeclampsia and prediction models seven databases were searched to identify prediction models developed with maternal data obtained before 20 weeks of pregnancy and including at least three predictors (Prospero registration CRD 42017078786). Prediction model characteristics and performance measures were extracted using the CHARMS, STROBE and TRIPOD checklists. The National Institute of Health quality assessment tools for observational cohort and cross-sectional studies were used for study quality appraisal. We retrieved 8,309 articles out of which 40 articles were eligible for review. Seventy-seven percent of all the prediction models combined biomarkers with maternal clinical characteristics. Biomarkers used as predictors in most models were pregnancy associated plasma protein-A (PAPP-A) and placental growth factor (PlGF). Only five studies were conducted in a low-and middle income country. Most of the studies evaluated did not completely follow the CHARMS, TRIPOD and STROBE guidelines in prediction model development and reporting. Adherence to these guidelines will improve prediction modelling studies and subsequent application of prediction models in clinical practice. Prediction models using maternal characteristics, with good discrimination and calibration, should be externally validated for use in low and middle income countries where biomarker assays are not routinely available.

Several clinical trials have reported inconsistent findings for the effect of fibrates on cardiovascular risk. We undertook a systematic review and meta-analysis to investigate the effects of fibrates on major clinical outcomes. We systematically searched Medline, Embase, and the Cochrane Library for trials published between 1950 and March, 2010. We included prospective randomised controlled trials assessing the effects of fibrates on cardiovascular outcomes compared with placebo. Summary estimates of relative risk (RR) reductions were calculated with a random effects model. Outcomes analysed were major cardiovascular events, coronary events, stroke, heart failure, coronary revascularisation, all-cause mortality, cardiovascular death, non-vascular death, sudden death, new onset albuminuria, and drug-related adverse events. We identified 18 trials providing data for 45 058 participants, including 2870 major cardiovascular events, 4552 coronary events, and 3880 deaths. Fibrate therapy produced a 10% RR reduction (95% CI 0–18) for major cardiovascular events (p=0·048) and a 13% RR reduction (7–19) for coronary events (p<0·0001), but had no benefit on stroke (−3%, −16 to 9; p=0·69). We noted no effect of fibrate therapy on the risk of all-cause mortality (0%, −8 to 7; p=0·92), cardiovascular mortality (3%, −7 to 12; p=0·59), sudden death (11%, −6 to 26; p=0·19), or non-vascular mortality (−10%, −21 to 0·5; p=0·063). Fibrates reduced the risk of albuminuria progression by 14% (2–25; p=0·028). Serious drug-related adverse events were not significantly increased by fibrates (17 413 participants, 225 events; RR 1·21, 0·91–1·61; p=0·19), although increases in serum creatinine concentrations were common (1·99, 1·46–2·70; p<0·0001). Fibrates can reduce the risk of major cardiovascular events predominantly by prevention of coronary events, and might have a role in individuals at high risk of cardiovascular events and in those with combined dyslipidaemia. National Health and Medical Research Council of Australia.

This is the introductory paper in a series of eight papers. In this series, we integrate the theoretical design options with the practice of conducting pragmatic trials. For most new market-approved treatments, the clinical evidence is insufficient to fully guide physicians and policy makers in choosing the optimal treatment for their patients. Pragmatic trials can fill this gap, by providing evidence on the relative effectiveness of a treatment strategy in routine clinical practice, already in an early phase of development, while maintaining the strength of randomized controlled trials. Selecting the setting, study population, mode of intervention, comparator, and outcome are crucial in designing pragmatic trials. In combination with monitoring and data collection that does not change routine care, this will enable appropriate generalization to the target patient group in clinical practice. To benefit from the full potential of pragmatic trials, there is a need for guidance and tools in designing these studies while ensuring operational feasibility. This paper introduces the concept of pragmatic trial design. The complex interplay between pragmatic design options, feasibility, stakeholder acceptability, validity, precision, and generalizability will be clarified. In this way, balanced design choices can be made in pragmatic trials with an optimal chance of success in practice.

In the past years many inflammatory markers have been studied in association with clinically manifest cardiovascular disease (CVD) and carotid intima-media thickness (CIMT) in HIV-infected patients, to obtain insights in the increased cardiovascular risk observed in HIV infection. This systematic review provides an oversight of the current knowledge. A search was performed in PubMed, Embase and Cochrane in July 2014, identifying all articles from 1996 onwards addressing the relation between inflammatory markers and CVD or CIMT in HIV-positive adults. Two authors, using predefined criteria, independently conducted the selection of articles, critical appraisal and extraction of the data. Analysis was focused on the immune markers that were most frequently assessed. The review protocol was registered in the PROSPERO database at 11 July 2014 (registration number CRD42014010516). This review was performed according to the PRISMA guideline. Forty articles were selected; eight addressing cardiovascular disease (CVD) and thirty-two addressing CIMT. C-reactive protein (CRP), interleukin-6 (IL-6) and d-dimer were assessed most frequently in relation to the occurrence of CVD; in four out of eight studies. All three markers were positively related to CVD in three out of four studies. Studies addressing CIMT were too heterogeneous with respect to patient populations, inflammatory markers, CIMT measurement protocols and statistical methods to allow for a formal meta-analysis to obtain summary statistics. CRP, IL-6 and soluble vascular cell adhesion molecule (sVCAM-1) were the most studied markers in relation to CIMT. None of the inflammatory markers showed an association with CIMT. This review showed a relation between some inflammatory markers and CVD, however, no consistent relation is observed for CIMT. Statistical approaches that yields effect estimates and standardized CIMT protocols should be chosen. Further research should focus on prospective studies and a selected set of inflammatory markers.

Measures of interaction on an additive scale (relative excess risk due to interaction [RERI], attributable proportion [AP], synergy index [S]), were developed for risk factors rather than preventive factors. It has been suggested that preventive factors should be recoded to risk factors before calculating these measures. We aimed to show that these measures are problematic with preventive factors prior to recoding, and to clarify the recoding method to be used to circumvent these problems. Recoding of preventive factors should be done such that the stratum with the lowest risk becomes the reference category when both factors are considered jointly (rather than one at a time). We used data from a case-control study on the interaction between ACE inhibitors and the ACE gene on incident diabetes. Use of ACE inhibitors was a preventive factor and DD ACE genotype was a risk factor. Before recoding, the RERI, AP and S showed inconsistent results (RERI = 0.26 [95% CI: -0.30; 0.82], AP = 0.30 [95% CI: -0.28; 0.88], S = 0.35 [95% CI: 0.02; 7.38]), with the first two measures suggesting positive interaction and the third negative interaction. After recoding the use of ACE inhibitors, they showed consistent results (RERI = -0.37 [95% CI: -1.23; 0.49], AP = -0.29 [95% CI: -0.98; 0.40], S = 0.43 [95% CI: 0.07; 2.60]), all indicating negative interaction. Preventive factors should not be used to calculate measures of interaction on an additive scale without recoding.

Background Air pollution is a major risk factor for cardiovascular diseases and contributes to health disparities, particularly among minority ethnic groups, who often face higher exposure levels. Knowledge on whether the effect of air pollution on cardiovascular diseases differs between ethnic groups is crucial for identifying mechanisms underlying health disparities, ultimately informing targeted public health strategies and interventions. We explored differences in associations between air pollution and ischemic stroke and ischemic heart disease (IHD) for the six largest ethnic groups in the Netherlands. Methods This nationwide analysis (2014–2019), linked residential-address concentrations of NO 2 and PM 2.5 to individual-level hospital and mortality data. To evaluate incident ischemic stroke, we created a cohort of residents ≥30 years and free of ischemic stroke at baseline and for incident IHD we created a cohort free of IHD. We performed Cox proportional hazard survival analyses in each cohort with 2014 average concentrations of PM 2.5 or NO 2 as determinants, stratified by ethnicity (Dutch, German, Indonesian, Surinamese, Moroccan, Turkish) and adjusted for age, sex, socioeconomic indicators and region. Results Both cohorts included > 9.5 million people. During follow-up, 127,673 (1.3%) developed ischemic stroke and 156,517 (1.6%) developed IHD. For ischemic stroke, the p-values for the interaction between air pollution and ethnicity were 0.057 for NO 2 and 0.055 for PM 2.5 . The HR of 1 IQR increase (6.42 µg/m 3 ) of NO 2 for ischemic stroke was lowest for Moroccans (0.92 [0.84–1.02], p-value = 0.032 difference with Dutch) and highest for Turks (1.09 [1.00-1.18], p-value = 0.157 difference with Dutch). PM 2.5 results were similar. For IHD, higher exposure was unexpectedly associated with lower incidence. The p-values for the interaction with ethnicity were 1.75*10 − 5 for NO 2 and 1.06*10 − 3 for PM 2.5 . The HRs for IHD were lowest for Turks (NO 2 : 0.88 [0.83–0.92], p-value = 2.0*10 − 4 difference with Dutch, PM 2.5 : 0.86 [0.82–0.91], p-value = 1.3*10 − 4 difference with Dutch) and highest for Surinamese (NO 2 : 1.02 [0.97–1.07], p-value = 0.014 difference with Dutch) and Dutch (PM 2.5 : 0.96 [0.94–0.98]). Conclusions Associations between air pollutants and ischemic stroke or IHD differ notably between ethnic groups in the Netherlands. Policies to reduce air pollution and prevent ischemic stroke should target populations vulnerable to air pollution with a high cardiovascular disease risk.

Patients with large abdominal aortic aneurysms were assigned to undergo open surgical repair or endovascular repair. At 6 years, the cumulative survival rates did not differ significantly between groups. The rate of secondary intervention was significantly higher with endovascular repair. Patients with large abdominal aortic aneurysms were assigned to undergo open surgical repair or endovascular repair. At 6 years, the cumulative survival rates did not differ significantly between groups. Randomized trials have shown that endovascular repair offers a perioperative survival benefit over open repair for patients with a large abdominal aortic aneurysm. However, this advantage is not sustained beyond 2 years after surgery. 1 – 4 There is concern that endovascular repair lacks durability, with the possibility of an increased risk of late rupture, 5 and that more reinterventions are required in patients undergoing this technique. Long-term outcome data from these trials are considered to be of crucial importance in deciding which treatment option a patient should be offered. 6 , 7 To date, only limited data beyond 2 years after randomization have been . . .