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Cardiac magnetic resonance imaging (MRI) is widely applied fur the noninvasive assessment of cardiac structure and function, and for tissue characterization. For more than 2 decades, 1.5 T has been considered the field strength of choice for cardiac MRI. Although the number of 3-T systems significantly increased in the past 10 years and numerous new developments were made, challenges seem to remain that hamper a widespread clinical use of 3-T MR systems for cardiac applications. As the number of clinical cardiac applications is increasing, with each having their own benefits at both field strengths, no "holy grail" field strength exists fur cardiac MRI that one should ideally use. This review describes the physical differences between 1.5 and 3 T, as well as the effect of these differences on major (routine) cardiac MRI applications, including functional imaging, edema imaging. late gadolinium enhancement. first-pass stress perfusion, myocardial mapping, and phase contrast flow imaging. For each application, the advantages and limitations at both 1.5 and 3 Tare discussed. Solutions and alternatives are provided to overcome potential limitations. Finally, we briefly elaborate on the potential use of alternative field strengths (ie, below 1.5 T and above 3 T) for cardiac MRI and conclude with field strength recommendations for the future of cardiac MRI.

We thank all EPIC participants and staff for their contribution to the study. We also thank staff from the EPIC-CVD coordinating centres for sample preparation and data handling. This research has been conducted using the UK Biobank Resource (application number 29916). Data on coronary artery disease have been contributed by CARDIoGRAMplusC4D investigators and have been downloaded from www.CARDIOGRAMPLUSC4D.ORG.I Sluijswas supported by a personal Dr. Dekker postdoctoral grant (2015T019) from the Netherlands Heart Foundation. NGF and FI acknowledge core Medical Research Council Epidemiology Unit support (MC_UU_12015/5) and NGF acknowledges NIHR Biomedical Research Centre Cambridge: Nutrition, Diet, and Lifestyle Research Theme (IS-BRC-1215-20014). The InterAct project was funded by the EU FP6 programme (grant number LSHM_CT_2006_037197) and provided the biomarker data in the sub-cohort that was used in the current study. These analyses were supported by Cancer Research UK (C8221/A19170). The coordination of EPIC is financially supported by the European Commission (DG-SANCO) and the International Agency for Research on Cancer. The national cohorts are supported by Danish Cancer Society (Denmark); German Cancer Aid, German Cancer Research Center (DKFZ), Federal Ministry of Education and Research (BMBF), Deutsche Krebshilfe, Deutsches Krebsforschungszentrum and Federal Ministry of Education and Research (Germany); Associazione Italiana per la Ricerca sul Cancro-AIRC-Italy and National Research Council (Italy); Dutch Ministry of Public Health, Welfare and Sports (VWS), Netherlands Cancer Registry (NKR), LK Research Funds, Dutch Prevention Funds, Dutch ZON (Zorg Onderzoek Nederland), World Cancer Research Fund (WCRF), Statistics Netherlands (The Netherlands); Health Research Fund (FIS) PI13/00061 (EPIC-Granada) and PI13/01162 (EPIC-Murcia), Regional Governments of Andalucia, Asturias, Basque Country, Murcia and Navarra, ISCIII Health Research Funds RD12/0036/0018 (cofounded by FEDER funds/European Regional Development Fund ERDF) (Spain); Swedish Cancer Society, Swedish Research Council and County Councils of Skane and Vasterbotten (Sweden); Cancer Research UK (14136 to EPIC-Norfolk; C570/A16491 and C8221/A19170 for EPIC-Oxford), Medical Research Council (1000143 to EPIC-Norfolk, MR/M012190/1 to EPIC-Oxford) (UK). EPIC-CVD has been supported by the European Commission Framework Programme 7 (HEALTH-F2-2012-279233), the European Research Council (268834), the UK Medical Research Council (MR/L003120/1), the British Heart Foundation (RG13/13/30194 and RG/18/13/33946) and the National Institute for Health Research (Cambridge Biomedical Research Centre at the Cambridge University Hospitals NHS Foundation Trust). The MEGASTROKE project received funding from sources specified at http://www.megastroke.org/acknowledgments.html. L.E.T.V.analysed the data and drafted the manuscript. L. E. T. V., I. S. and Y. T. vdS. had access to all data for this study. L. E. T. V., I. S., Y. T. vdS., S. B., N. G. F., H. F., F. I., T. K. N., F. R., E. W., K. A., C. D., A. P. C., M. B. S., T. Y. N. T. and A. S. B. contributed to study conception, design and interpretation of data. All authors contributed to critical revision of the manuscript and approval of version to be published., Higher milk intake has been associated with a lower stroke risk, but not with risk of CHD. Residual confounding or reverse causation cannot be excluded. Therefore, we estimated the causal association of milk consumption with stroke and CHD risk through instrumental variable (IV) and gene-outcome analyses. IV analysis included 29 328 participants (4611 stroke; 9828 CHD) of the European Prospective Investigation into Cancer and Nutrition (EPIC)-CVD (eight European countries) and European Prospective Investigation into Cancer and Nutrition-Netherlands (EPIC-NL) case-cohort studies. rs4988235, a lactase persistence (LP) SNP which enables digestion of lactose in adulthood was used as genetic instrument. Intake of milk was first regressed on rs4988235 in a linear regression model. Next, associations of genetically predicted milk consumption with stroke and CHD were estimated using Prentice-weighted Cox regression. Gene-outcome analysis included 777 024 participants (50 804 cases) from MEGASTROKE (including EPIC-CVD), UK Biobank and EPIC-NL for stroke, and 483 966 participants (61 612 cases) from CARDIoGRAM, UK Biobank, EPIC-CVD and EPIC-NL for CHD. In IV analyses, each additional LP allele was associated with a higher intake of milk in EPIC-CVD (beta = 13 center dot 7 g/d; 95 % CI 8 center dot 4, 19 center dot 1) and EPIC-NL (36 center dot 8 g/d; 95 % CI 20 center dot 0, 53 center dot 5). Genetically predicted milk intake was not associated with stroke (HR per 25 g/d 1 center dot 05; 95 % CI 0 center dot 94, 1 center dot 16) or CHD (1 center dot 02; 95 % CI 0 center dot 96, 1 center dot 08). In gene-outcome analyses, there was no association of rs4988235 with risk of stroke (OR 1 center dot 02; 95 % CI 0 center dot 99, 1 center dot 05) or CHD (OR 0 center dot 99; 95 % CI 0 center dot 95, 1 center dot 03). Current Mendelian randomisation analysis does not provide evidence for a causal inverse relationship between milk consumption and stroke or CHD risk., Netherlands Heart Foundation 2015T019, UK Research & Innovation (UKRI) Medical Research Council UK (MRC), European Commission MC_UU_12015/5, NIHR Biomedical Research Centre Cambridge: Nutrition, Diet, and Lifestyle Research Theme IS-BRC-1215-20014, European Commission LSHM_CT_2006_037197, Cancer Research UK C8221/A19170, European Commission European Commission Joint Research Centre, International Agency for Research on Cancer, Danish Cancer Society, Deutsche Krebshilfe German Cancer Research Center (DKFZ) (Germany), Federal Ministry of Education & Research (BMBF), Deutsche Krebshilfe Deutsches Krebsforschungszentrum (Germany), Fondazione AIRC per la ricerca sul cancro Consiglio Nazionale delle Ricerche (CNR), Netherlands Government Netherlands Government, World Cancer Research Fund International (WCRF), Netherlands Government, Instituto de Salud Carlos III PI13/00061 PI13/01162, Junta de Andalucia Regional Government of Asturias (Spain) Regional Government of Basque Country (Spain) Regional Government of Murcia (Spain) Regional Government of Navarra (Spain), ISCIII Health Research Funds (FEDER funds/European Regional Development Fund ERDF) (Spain) RD12/0036/0018, Swedish Cancer Society Swedish Research Council County Council of Skane (Sweden) County Council of Vasterbotten (Sweden), European Commission Framework Programme 7 HEALTH-F2-2012-279233 European Research Council (ERC) European Commission 268834, UK Research & Innovation (UKRI) Medical Research Council UK (MRC) MR/L003120/1 British Heart Foundation RG13/13/30194 RG/18/13/33946 National Institute for Health Research (Cambridge Biomedical Research Centre at the Cambridge University Hospitals NHS Foundation Trust) UK Research & Innovation (UKRI) Medical Research Council UK (MRC) 1000143 MR/M012190/1 Cancer Research UK C8221/A19170 14136 C570/A16491

Objective The current study was undertaken to prospectively explore whether having low levels of von Willebrand factor (vWF) antigen and vWF activity reduce the risk for cardiovascular disease and death. Methods VWF antigen and vWF activity were measured by enzyme-linked immunosorbent assay and an immunological-based assay, respectively, in a subsample of 4857 individuals aged between 35 and 74 years old, enrolled between April 2007 and October 2008 in the population-based Gutenberg Health Study. VWF antigen and activity below the 20th percentile was set as a measure of "low vWF." Adjusted robust Poisson regression models were used to analyze the relation between low vWF and the incidence of cardiovascular disease (CVD). Consequent adjusted cox regression models as well as cumulative incidence plots were calculated to explore the relation between all-cause and cardiovascular mortality and low vWF. Results VWF activity levels

Cardiac magnetic resonance imaging (MRI) is widely applied for the noninvasive assessment of cardiac structure and function, and for tissue characterization. For more than 2 decades, 1.5 T has been considered the field strength of choice for cardiac MRI. Although the number of 3-T systems significantly increased in the past 10 years and numerous new developments were made, challenges seem to remain that hamper a widespread clinical use of 3-T MR systems for cardiac applications. As the number of clinical cardiac applications is increasing, with each having their own benefits at both field strengths, no "holy grail" field strength exists for cardiac MRI that one should ideally use. This review describes the physical differences between 1.5 and 3 T, as well as the effect of these differences on major (routine) cardiac MRI applications, including functional imaging, edema imaging, late gadolinium enhancement, first-pass stress perfusion, myocardial mapping, and phase contrast flow imaging. For each application, the advantages and limitations at both 1.5 and 3 T are discussed. Solutions and alternatives are provided to overcome potential limitations. Finally, we briefly elaborate on the potential use of alternative field strengths (ie, below 1.5 T and above 3 T) for cardiac MRI and conclude with field strength recommendations for the future of cardiac MRI.

Background Population-based levels of the chronic low-grade systemic inflammation biomarker, C-reactive protein (CRP), vary widely among traditional populations, despite their apparent absence of chronic conditions associated with chronic low-grade systemic inflammation, such as type 2 diabetes, metabolic syndrome and cardiovascular disease. We have previously reported an apparent absence of aforementioned conditions amongst the traditional Melanesian horticulturalists of Kitava, Trobriand Islands, Papua New Guinea. Our objective in this study was to clarify associations between chronic low-grade systemic inflammation and chronic cardiometabolic conditions by measuring CRP in a Kitava population sample. For comparison purposes, CRP was also measured in Swedish controls matched for age and gender. Methods Fasting levels of serum CRP were measured cross-sectionally in ≥ 40-year-old Kitavans (N = 79) and Swedish controls (N = 83). Results CRP was lower for Kitavans compared to Swedish controls (Mdn 0.5 mg/L range 0.1—48 mg/L and Mdn 1.1 mg/L range 0.1—33 mg/L, respectively, r = .18 p = .02). Among Kitavans, there were small negative associations between lnCRP for CRP values Conclusions Chronic low-grade systemic inflammation, measured as CRP, was lower among Kitavans compared to Swedish controls, indicating a lower and average cardiovascular risk, respectively, for these populations.

Chronic coronary syndromes (CCS) and stable angina are a growing clinical burden worldwide. This is of particular concern in the Gulf region given its high prevalence of cardiovascular risk factors, especially diabetes mellitus and smoking. Despite recommendations on the use of first- and second-line anti-anginal medication, management challenges remain. Current guidelines for pharmacologic treatment are not determined by the range of pathophysiological mechanisms of ischaemia and consequent angina, which may occur either in isolation or co-exist. In this article, we highlight the need to improve knowledge of the epidemiology of chronic coronary syndromes in the Middle East and Gulf region, and the need for studies of stratified pharmacologic approaches to improve symptomatic angina and quality of life in the large and growing number of patients with coronary artery disease from this region. We discuss the role of nicorandil, currently recommended as a second-line anti-anginal drug in CCS patients, and suggest that this may be a particularly useful add-on therapy for patients in the Gulf region.

BACKGROUND & AIMS: There is an ongoing debate on whether non-alcoholic fatty liver disease (NAFLD) is an active contributor or an innocent bystander in the pathogenesis of coronary artery disease (CAD). The aim of the present study was to assess the causal relationship between NAFLD and CAD.APPROACH & RESULTS: We performed two-sample Mendelian randomization (MR) analyses using summary-level data to assess the association between genetically predicted NAFLD (i.e. chronically-elevated serum alanine aminotransferase levels [cALT], imaging-based and biopsy-confirmed NAFLD) and risk of CAD. Analyses were repeated after exclusion of NAFLD susceptibility genes that are associated with impaired VLDL secretion. Inverse-variance weighted (IVW) MR analyses showed a statistically significant association between genetically predicted cALT and risk of CAD (odds ratio [OR]:1.116, 95% confidence interval [CI]:1.039,1.199), but not for the other NAFLD-related traits (OR:1.046, 95%CI:0.764,1.433 and OR:1.014, 95%CI:0.968,1.062 for imaging-based and biopsy-confirmed NAFLD, respectively). MR Egger regression revealed a statistically significant intercept, indicative of directional pleiotropy, for all traits. Repeat analyses after exclusion of genes associated with impaired VLDL secretion, showed consistent associations between genetically predicted NAFLD and CAD for all traits, i.e. cALT (OR:1.203, 95%CI:1.113,1.300), imaging-based (OR:2.149, 95%CI:1.276,3.620) and biopsy-confirmed NAFLD (OR:1.113, 95%CI:1.041,1.189), which persisted when more stringent biopsy-confirmed NAFLD criteria were used (OR:1.154, 95%CI:1.043,1.278) or when more stringent MR methods were applied. MR Egger regression did not show a statistically significant intercept.CONCLUSION: The two-sample MR analyses showed a robust association between genetically predicted NAFLD and CAD after exclusion of genetic variants that are implicated in impaired VLDL secretion.

Context Blood lipid levels are linked to the risk of cardiovascular disease and regulated by genetic factors. A low-frequency polymorphism Arg82Cys (rs72836561) in the membrane protein nepmucin, encoded by CD300LG, is associated with lower fasting concentration of high-density lipoprotein cholesterol (HDLc) and higher fasting triglycerides. However, whether the variant is linked to postprandial lipids and glycemic status remains elusive. Objective Here, we augment the genetic effect of Arg82Cys on fasting plasma concentrations of HDL subclasses, postprandial lipemia after a standardized high-fat meal, and glycemic status to further untangle its role in HDL metabolism. Methods We elucidated fasting associations with HDL subclasses in a population-based cohort study (Oxford BioBank, OBB), including 4522 healthy men and women. We investigated fasting and postprandial consequences on HDL metabolism in recall-by-genotype (RbG) studies (fasting: 20 carrier/20 noncarrier; postprandial: 7 carrier/17 noncarrier), and shed light on the synergistic interaction with glycemic status. Results A lower fasting plasma concentration of cholesterol in large HDL particles was found in healthy male carriers of the Cys82 polymorphism compared to noncarriers, both in the OBB (P = .004) and RbG studies (P = .005). In addition, the Cys82 polymorphism was associated with low fasting plasma concentrations of ApoA1 (P = .008) in the OBB cohort. On the contrary, we did not find differences in postprandial lipemia or 2-hour plasma glucose levels. Conclusion Taken together, our results indicate an association between the Arg82Cys variant and a lower concentration of HDL particles and HDLc, especially in larger HDL subclasses, suggesting a link between nepmucin and HDLc metabolism or maturation.

Background A majority of recurrent pregnancy loss cases (RPL) remains unexplained. We hypothesized that complications in vascular and metabolic status may guide towards underlying problems that also predispose to RPL and that the number of pregnancy losses is related. Methods A retrospective study in 123 women with either a history of low-order RPL (2–3 pregnancy losses) or high-order RPL (≥ 4 pregnancy losses) and 20 women with a history of uncomplicated pregnancy (controls) was performed. Vascular status was assessed by measuring hemodynamic parameters, determining abnormal parameters and analyzing their contribution to the circulatory risk profile (CRP). In a similar way, metabolic status was assessed. Metabolic parameters were measured, used to determine abnormal parameters and analyzed for their contribution to the metabolic syndrome (MetS). Results No major differences were observed in vascular or metabolic parameters between women with RPL and controls. There was no relation with the number of pregnancy losses. However, when analyzing the presence of abnormal constituents, more than 80% of women with RPL had at least one abnormal constituent of the CRP. While only 27% had one or more abnormal constituent of the MetS. Conclusions The presence of abnormal circulatory factors prior to pregnancy, and to lesser extent constituents of the metabolic syndrome, may predispose to RPL and offer new insights to its pathophysiology.

Introduction Preeclampsia is associated with adverse maternal and neonatal outcomes. It is unclear whether multivitamin use reduces the risk of preeclampsia. This systematic review and meta-analysis aimed to evaluate the association between multivitamin use and the risk of preeclampsia. Material and methods We searched PubMed, Embase and the Cochrane Library from database inception to July 2021. Randomized controlled trials (RCTs), case-control and cohort studies assessing the association between multivitamin use and risk of preeclampsia were eligible. Studies of treatment with a single micronutrient were excluded. Relative risks and 95% confidence intervals (95% CI) were calculated using random-effects models. RoB2, the Newcastle Ottawa Scale and GRADE were used to assess risk of bias and quality of evidence. The protocol was registered in PROSPERO (no. CRD42021214153). Results Six studies were included (33 356 women). Only two RCTs were found, both showing a significantly decreased risk of preeclampsia in multivitamin users. These studies were not compatible for meta-analysis due to clinical heterogeneity. A meta-analysis of observational studies using a random-effects model showed an unchanged risk of preeclampsia following multivitamin use (relative risk 0.85, 95% CI 0.69-1.03). The quality of evidence according to GRADE was very low. Conclusions Very weak evidence suggests that multivitamin use might reduce the risk of preeclampsia; however, more research is needed. Large RCTs should be prioritized. The results of this review do not allow any final conclusions to be drawn regarding a preventive effect of multivitamin use in relation to preeclampsia.

Following a request from five European Nordic countries, the EFSA Panel on Nutrition, Novel Foods and Food Allergens (NDA) was tasked to provide scientific advice on a tolerable upper intake level (UL) or a safe level of intake for dietary (total/added/free) sugars based on available data on chronic metabolic diseases, pregnancy-related endpoints and dental caries. Specific sugar types (fructose) and sources of sugars were also addressed. The intake of dietary sugars is a well-established hazard in relation to dental caries in humans. Based on a systematic review of the literature, prospective cohort studies do not support a positive relationship between the intake of dietary sugars, in isocaloric exchange with other macronutrients, and any of the chronic metabolic diseases or pregnancy-related endpoints assessed. Based on randomised control trials on surrogate disease endpoints, there is evidence for a positive and causal relationship between the intake of added/free sugars and risk of some chronic metabolic diseases: The level of certainty is moderate for obesity and dyslipidaemia (> 50-75% probability), low for non-alcoholic fatty liver disease and type 2 diabetes (> 15-50% probability) and very low for hypertension (0-15% probability). Health effects of added vs. free sugars could not be compared. A level of sugars intake at which the risk of dental caries/chronic metabolic diseases is not increased could not be identified over the range of observed intakes, and thus, a UL or a safe level of intake could not be set. Based on available data and related uncertainties, the intake of added and free sugars should be as low as possible in the context of a nutritionally adequate diet. Decreasing the intake of added and free sugars would decrease the intake of total sugars to a similar extent. This opinion can assist EU Member States in setting national goals/recommendations.

Objective To investigate associations between exposure to fetal hypoxia and indicators of metabolic health in young adult offspring of women with type 1 diabetes (OT1D). Methods 156 OT1D born between 7/1995 and 12/2000 at Helsinki University Hospital, Finland, were invited for follow-up between 3/2019 and 11/2019. A control group of 442 adults born from non-diabetic pregnancies, matched for date and place of birth, was obtained from the Finnish Medical Birth Register. In total, 58 OT1D and 86 controls agreed to participate. All OT1D had amniotic fluid (AF) sampled for erythropoietin (EPO) measurement within two days before delivery in order to diagnose fetal hypoxia. In total, 29 OTID had an AF EPO concentration

Lipid-lowering in patients with coronary artery disease (CAD) is related to a lower risk of cardiovascular events. We evaluated factors related to the management of hypercholesterolemia in patients with established CAD. Patients were interviewed 6–18 months after hospitalization for an acute coronary syndrome (ACS) or a myocardial revascularization procedure. Statins were prescribed at discharge to 94.4% of patients, while 68.1% of the patients hospitalized for an ACS were prescribed a high-dose statin. Hospitalization in a teaching hospital, percutaneous coronary intervention, cholesterol measurement during hospitalization and the male sex were related to prescription of statins at discharge. The intensity of lipid-lowering therapy in the post-discharge period increased in 17.3%, decreased in 11.7%, and did not change in 71.0% of the patients. The prescription of a lipid-lowering drug (LLD) at discharge (odds ratio 5.88 [95% confidence intervals 3.05–11.34]) and a consultation with a cardiologist (2.48 [1.51–4.08]) were related to the use of LLDs, while age (1.32 [1.10–1.59] per 10 years), loneliness (0.42 [0.19–0.94]), professional activity (1.56 [1.13–2.16]), and diabetes (1.66 [1.27–2.16]) were related to achieving an LDL cholesterol goal 6–18 months after discharge. In conclusion, health-system-related factors are associated with the LLD utilization, whereas mainly patient-related factors are related to the control of hypercholesterolemia following hospitalization for CAD.

ObjectiveTo assess whether recent declines in cardiovascular mortality have benefited all socioeconomic groups equally and whether these declines have narrowed or widened inequalities in cardiovascular mortality in Europe.MethodsIn this prospective registry-based study, we determined changes in cardiovascular mortality between the 1990s and the early 2010s in 12 European populations by gender, educational level and occupational class. In order to quantify changes in the magnitude of differences in mortality, we calculated both ratio measures of relative inequalities and difference measures of absolute inequalities.ResultsCardiovascular mortality has declined rapidly among lower and higher socioeconomic groups. Relative declines (%) were faster among higher socioeconomic groups; absolute declines (deaths per 100 000 person-years) were almost uniformly larger among lower socioeconomic groups. Therefore, although relative inequalities increased over time, absolute inequalities often declined substantially on all measures used. Similar trends were seen for ischaemic heart disease and cerebrovascular disease mortality separately. Best performer was England and Wales, which combined large declines in cardiovascular mortality with large reductions in absolute inequalities and stability in relative inequalities in both genders. In the early 2010s, inequalities in cardiovascular mortality were smallest in Southern Europe, of intermediate magnitude in Northern and Western Europe and largest in Central-Eastern European and Baltic countries.ConclusionsLower socioeconomic groups have experienced remarkable declines in cardiovascular mortality rates over the last 25 years, and trends in inequalities can be qualified as favourable overall. Nevertheless, further reducing inequalities remains an important challenge for European health systems and policies.

Purpose: The main purpose of this study was to test the hypothesis that incidental cardiac irradiation is associated with changes in cardiac function in breast cancer (BC) survivors treated with radiation therapy (RT).Methods and Materials: We conducted a cross-sectional study consisting of 109 BC survivors treated with RT between 2005 and 2011. The endpoint was cardiac function, assessed by echocardiography. Systolic function was assessed with the left ventricular ejection fraction (LVEF) (n = 107) and the global longitudinal strain (GLS) of the left ventricle (LV) (n = 52). LV diastolic dysfunction (n = 109) was defined by e' at the lateral and septal region, which represents the relaxation velocity of the myocardium. The individual calculated RT dose parameters of the LV and coronary arteries were collected from 3-dimensional computed tomographyebased planning data. Univariable and multivariable analysis using forward selection was performed to identify the best predictors of cardiac function. Robustness of selection was assessed using bootstrapping. The resulting multivariable linear regression model was presented for the endpoints of systolic and diastolic function.Results: The median time between BC diagnosis and echocardiography was 7 years. No relation between RT dose parameters and LVEF was found. In the multivariable analysis for the endpoint GLS of the LV, the maximum dose to the left main coronary artery was most often selected across bootstrap samples. For decreased diastolic function, the most often selected model across bootstrap samples included age at time of BC diagnosis and hypertension at baseline. Cardiac dose-volume histogram parameters were less frequently selected for this endpoint.Conclusions: This study shows an association between individual cardiac dose distributions and GLS of the LV after RT for BC. No relation between RT dose parameters and LVEF was found. Diastolic function was most associated with age and hypertension at time of BC diagnosis. Further research is needed to make definitive conclusions. (C) 2019 Elsevier Inc. All rights reserved.

Radiotherapy is an effective treatment for breast cancer and other thoracic tumors. However, while high-energy radiotherapy treatment successfully kills cancer cells, radiation exposure of the heart and large arteries cannot always be avoided, resulting in secondary cardiovascular disease in cancer survivors. Radiation-induced changes in the cardiac vasculature may thereby lead to coronary artery atherosclerosis, which is a major cardiovascular complication nowadays in thoracic radiotherapy-treated patients. The underlying biological and molecular mechanisms of radiation-induced atherosclerosis are complex and still not fully understood, resulting in potentially improper radiation protection. Ionizing radiation (IR) exposure may damage the vascular endothelium by inducing DNA damage, oxidative stress, premature cellular senescence, cell death and inflammation, which act to promote the atherosclerotic process. Intercellular communication mediated by connexin (Cx)-based gap junctions and hemichannels may modulate IR-induced responses and thereby the atherosclerotic process. However, the role of endothelial Cxs and their channels in atherosclerotic development after IR exposure is still poorly defined. A better understanding of the underlying biological pathways involved in secondary cardiovascular toxicity after radiotherapy would facilitate the development of effective strategies that prevent or mitigate these adverse effects. Here, we review the possible roles of intercellular Cx driven signaling and communication in radiation-induced atherosclerosis. ispartof: CELLULAR AND MOLECULAR LIFE SCIENCES vol:78 issue:7 pages:3087-3103 ispartof: location:Switzerland status: published

Contains fulltext : 232373.pdf (Publisher’s version ) (Closed access) AIMS: Adherence to statins ranges from 32% to 79%. Patients' beliefs about medication are associated with adherence. There is lack of insight into the possible association between beliefs of healthcare practitioners (HCPs) about statins and patients' beliefs and adherence. This study aims to examine whether HCPs' beliefs about statins are associated with patients' beliefs and adherence about/to statins. METHODS: Cross-sectional study in 48 pharmacies and affiliated physicians' practices between 3 September 2014 and 20 March 2015. HCPs' (prescribers and pharmacy staff) and patients' beliefs about statins were assessed with the Beliefs about Medicine Questionnaire (BMQ) specific. Adherence to statins was assessed with the MARS-5 questionnaire. Multilevel regression analysis was performed to assess the association between HCPs' beliefs and patients' beliefs and adherence. RESULTS: 1504 patients (mean age 66.8 [s.d. ± 9.9] years, 46.5% female) and 734 HCPs (209 physicians, 118 pharmacists and 366 pharmacy technicians) participated in this study. Patients have higher BMQ necessity (16.9 [s.d. ± 4.3]) and BMQ concern (12.3 [s.d. ± 3.9]) scores than HCPs (15.0 [s.d. ± 3.0] and 11.5 [s.d. ± 2.9], P < 0.001). No associations were found between any of the HCPs' BMQ and patients' BMQ scores and adherence to statins. Patients' BMQ necessity, concern and necessity-concerns (NC)-differential scores were associated with patients' adherence (MARS-5) scores. B (95% CI) coefficients were 0.057 (0.035-0.079), -0.040 (-0.064 to -0.016) and.061 (0.043-0.079). CONCLUSIONS: Patients have stronger beliefs about medication compared to HCPs. No associations were found between HCPs' BMQ scores on the one hand and patients' BMQ scores and adherence to statins on the other hand.

When acute myocardial injury is found in a clinical setting suggestive of myocardial ischemia, the event is labeled as acute myocardial infarction (MI), and the absence of ≥50% coronary stenosis at angiography or greater leads to the working diagnosis of myocardial infarction with non-obstructed coronary arteries (MINOCA). Determining the mechanism of MINOCA and excluding other possible causes for cardiac troponin elevation has notable implications for tailoring secondary prevention measures aimed at improving the overall prognosis of acute MI. The aim of this review is to increase the awareness that establishing the underlying cause of a MINOCA is possible in the vast majority of cases, and that the proper classification of any MI should be pursued. The initial diagnosis of MINOCA can be confirmed or ruled out based on the results of subsequent investigations. Indeed, a comprehensive clinical evaluation at the time of presentation, followed by a dedicated diagnostic work-up, might lead to the identification of the pathophysiologic abnormality leading to MI in almost all cases initially labeled as MINOCA. When a specific cause of acute MI is identified, cardiologists are urged to transition from the “all-inclusive” term “MINOCA” to the proper classification of any MI, as evidence now exists that MINOCA does not provide conceptual clarity for actionable decision-making in MI with angiographically normal coronary arteries.

Background BRCA1/2 mutation carriers are recommended to undergo risk-reducing salpingo-oophorectomy (RRSO) at 35 to 45 years of age. RRSO substantially decreases ovarian cancer risk, but at the cost of immediate menopause. Knowledge about the potential adverse effects of premenopausal RRSO, such as increased risk of cardiovascular disease, osteoporosis, cognitive dysfunction, and reduced health-related quality of life (HRQoL), is limited. Objective The aim of this study is to assess the long-term health effects of premenopausal RRSO on cardiovascular disease, bone health, cognitive functioning, urological complaints, sexual functioning, and HRQoL in women with high familial risk of breast or ovarian cancer. Methods We will conduct a multicenter cross-sectional study with prospective follow-up, nested in a nationwide cohort of women at high familial risk of breast or ovarian cancer. A total of 500 women who have undergone RRSO before 45 years of age, with a follow-up period of at least 10 years, will be compared with 250 women (frequency matched on current age) who have not undergone RRSO or who have undergone RRSO at over 55 years of age. Participants will complete an online questionnaire on lifestyle, medical history, cardiovascular risk factors, osteoporosis, cognitive function, urological complaints, and HRQoL. A full cardiovascular assessment and assessment of bone mineral density will be performed. Blood samples will be obtained for marker analysis. Cognitive functioning will be assessed objectively with an online neuropsychological test battery. Results This study was approved by the institutional review board in July 2018. In February 2019, we included our first participant. As of November 2020, we had enrolled 364 participants in our study. Conclusions Knowledge from this study will contribute to counseling women with a high familial risk of breast/ovarian cancer about the long-term health effects of premenopausal RRSO. The results can also be used to offer health recommendations after RRSO. Trial Registration ClinicalTrials.gov NCT03835793; https://clinicaltrials.gov/ct2/show/NCT03835793. International Registered Report Identifier (IRRID) DERR1-10.2196/24414

Purpose: Radiation-induced acute coronary events (ACEs) may occur as a treatment-related late adverse effect of breast cancer (BC) radiation. However, the underlying mechanisms behind this radiation-induced cardiac disease remain to be determined. The objective of this study was to test the hypothesis that radiation dose to calcified atherosclerotic plaques in the left anterior descending coronary artery (LAD) is a better predictor for ACEs than radiation dose to the whole heart or left ventricle in patients with BC treated with radiation therapy. Methods and Materials: The study cohort consisted of 910 patients with BC treated with postoperative radiation therapy after breast-conserving surgery. In total, 163 patients had an atherosclerotic plaque in the LAD. The endpoint was the occurrence of an ACE after treatment. For each individual patient, the mean heart dose, volume of the left ventricle receiving >= 5 Gy (LV-V5), mean LAD dose, and mean dose to calcified atherosclerotic plaques in the LAD, if present, were acquired based on planning computed tomography scans. Cox regression analysis was used to analyze the effects on the cumulative incidence of ACEs. Results: The median follow-up time was 9.2 years (range, 0.1-14.3 years). In total, 38 patients (4.2%) developed an ACE during follow-up. For patients with an atherosclerotic plaque (n = 163), the mean dose to the atherosclerotic plaque was the strongest predictor for ACEs, even after correction for cardiovascular risk factors (hazard ratio [HR], 1.269; 95% CI, 1.090-1.477; P =.002). The LV-V5 was associated with ACEs in patients without atherosclerotic plaques in the LAD (n = 680) (HR, 1.021; 95% CI, 1.003-1.039; P =.023). Conclusions: The results of this study suggest that radiation dose to pre-existing calcified atherosclerotic plaques in the LAD is strongly associated with the development of ACEs in patients with BC. (C) 2021 The Authors. Published by Elsevier Inc.

Aims Little is known about usual care by physicians and pharmacy teams to support adherence to statins and whether the extent of this care is associated with adherence to statins. Objective of the study was to examine the relationship between the extent of adherence supporting activities of healthcare practitioners (HCPs) and patients’ adherence to statins. Methods Cross-sectional study in 48 pharmacies and affiliated physicians’ practices, between September 3, 2014 and March 20, 2015. Patients visiting the pharmacy with a statin prescription from participating prescribers were invited to participate. Usual care to support adherence was assessed among HCPs with the Quality of Standard Care questionnaire about usual care activities to support adherence. Adherence to statins was assessed among patients with the MARS-5 questionnaire. The association between the extent of HCPs’ adherence supporting activities and patients’ adherence was examined by means of multilevel regression analysis. Results 1,504 patients and 692 HCPs (209 physicians, 118 pharmacists and 365 pharmacy technicians) participated. No association was found between the extent of physicians’ adherence supporting activities and patients’ adherence to statins. The extent of adherence supporting activities by pharmacy teams in usual care was negatively associated with patients’ adherence to statins (B coefficient -0.057 (95%CI: -0.112- -0.002). Conclusions This study suggests that there is no positive relationship between the extent of HCPs’ adherence supporting activities in usual care and patients’ adherence to statins. Other methods than questionnaires (e.g. electronic monitors (to assess adherence) and observations (to assess usual care) should be applied to confirm the results of this study.

AIMTo assess the functionality of congenital coronary artery fistulas (CAFs) using adenosine stress N-13-ammonia positron emission tomography computed tomography (PET-CT).METHODSCongenital CAFs were incidentally detected during coronary angiography (CAG) procedures in 11 adult patients (six males and five females) with a mean age of 64.3 years (range 41-81). Patients were collected from three institutes in the Netherlands. The characteristics of the fistulas (origin, pathway and termination), multiplicity of the origins and pathways of the fistulous vessels were assessed by CAG. Five patients underwent adenosine pharmacologic stress N-13-ammonia PET-CT to assess myocardial perfusion and the functional behavior of the fistula.RESULTSEleven patients with 12 CAFs, 10 unilateral and one bilateral, originating from the left anterior descending coronary artery (n = 8), right coronary artery (n = 2) and circumflex (n = 2). All fistulas were of the vascular type, terminating into either the pulmonary artery (n = 11) or coronary sinus (n = 1). The CAG delineated the characteristics of the fistula (origin, pathway and termination). Multiplicity of the origins and pathways of the fistulous vessels were common in most fistulas (8/12, 67% and 9/12, 75%, respectively). Multiplicity was common among the different fistula components (23/36, 64%). Adenosine pharmacologic stress N-13-ammonia PET-CT revealed normal myocardial perfusion and ejection fraction in all but one patient, who showed a reduced ejection fraction.CONCLUSIONPET-CT may be helpful for assessing the functional status of congenital CAFs in selected patients regarding clinical decision-making. Studies with a larger patient series are warranted.

Activation of the immune system in heart failure (HF) has been recognized for over 20 years. Initially, experimental studies demonstrated a maladaptive role of the immune system. However, several phase III trials failed to show beneficial effects in HF with therapies directed against an immune activation. Preclinical studies today describe positive and negative effects of immune activation in HF. These different effects depend on timing and aetiology of HF. Therefore, herein we give a detailed review on immune mechanisms and their importance for the development of HF with a special focus on commonalities and differences between different forms of cardiomyopathies. The role of the immune system in ischaemic, hypertensive, diabetic, toxic, viral, genetic, peripartum, and autoimmune cardiomyopathy is discussed in depth. Overall, initial damage to the heart leads to disease specific activation of the immune system whereas in the chronic phase of HF overlapping mechanisms occur in different aetiologies.

Purpose To summarize the physical principles, imaging method, available tools for and the clinical value of quantitative perfusion evaluation with cardiac PET as well as future aims in the field in a narrative review. Results Cardiac positron-emission tomography (PET) currently constitutes the reference standard for non-invasive quantitative evaluation of myocardial blood flow. This added modality provides useful information beyond standard semi-quantitative myocardial perfusion evaluation. A description of how the different phases of PET studies are interpreted is provided, as well as a short depiction of the most commonly used radiotracers and the main characteristics affecting their clinical utility. The diagnostic and prognostic utility concerning myocardial perfusion quantified in absolute terms is discussed and the additional contribution of the increasingly spread hybrid equipment is summarized. Conclusion PET myocardial perfusion represents an excellent noninvasive technique for the evaluation of known or suspected ischemic heart disease, and its clinical application should widen in the near future. The clinical value of PET quantitative perfusion is expected to improve patient outcomes and optimize therapeutic decisions, which constitute key elements for the future of cardiovascular medicine.

Purpose To summarize the physical principles, imaging method, available tools for and the clinical value of quantitative perfusion evaluation with cardiac PET as well as future aims in the field in a narrative review.Results Cardiac positron-emission tomography (PET) currently constitutes the reference standard for non-invasive quantitative evaluation of myocardial blood flow. This added modality provides useful information beyond standard semi-quantitative myocardial perfusion evaluation. A description of how the different phases of PET studies are interpreted is provided, as well as a short depiction of the most commonly used radiotracers and the main characteristics affecting their clinical utility. The diagnostic and prognostic utility concerning myocardial perfusion quantified in absolute terms is discussed and the additional contribution of the increasingly spread hybrid equipment is summarized.Conclusion PET myocardial perfusion represents an excellent noninvasive technique for the evaluation of known or suspected ischemic heart disease, and its clinical application should widen in the near future. The clinical value of PET quantitative perfusion is expected to improve patient outcomes and optimize therapeutic decisions, which constitute key elements for the future of cardiovascular medicine.

Background: Identifying unrecognizedmyocardial infarction (MI) is important for secondary prevention. The aim of this study is to determine the prevalence and correlates of unrecognizedMI and the associationwithmortality in the general population.Methods: All participants >= 18 years participating in the Lifelines population, a three- generation Cohort Study and Biobank, were included (n= 152,180). Participants with unrecognized MI were matched with controls without MI (1: 2) based on age and gender. Unrecognized MI was defined when no history of MI was reported in combinationwith electrocardiographic (ECG) signs corresponding to MI. A history ofMIwas defined as a reported history of MI in combination with ECG signs and/ or the use of antithrombotic medication.Results: MI was present in 1881(1.2%) of participants and was unrecognized in 431 (22.9%) participants. Under the age of 50 years, percentages of unrecognized MI relative to the total amount of MI were 34% and 55% in men and women respectively. Compared to recognized MI, classical cardiovascular risk factors were less prevalent in participants with unrecognized MI. During a median follow- up time of 5, 4 and 4 years, 4.4%, 6.4% and 2.2% of participants with unrecognizedMI, recognized MI and without MI died, respectively. In a multivariable logistic regression unrecognized MI was an independent predictor of death.Conclusions: The prevalence of unrecognized MI is substantial and classical cardiovascular risk factors are less prevalent in participants with unrecognized MI. Nevertheless, unrecognized MI is associated with mortality. Risk stratification and early diagnosis is necessary to reduce the morbidity and mortality after MI. (C) 2017 Elsevier B. V. All rights reserved.

Chronic obstructive pulmonary disease (COPD) describes a predominantly smoking-induced small airway and/or emphysematous disease associated with airflow limitation. Considered progressive, irreversible, and responsible for substantial morbidity and mortality worldwide, COPD remains the subject of vigorous study, and advances made during 2016 are already reflected in the Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2017 guidelines (1). Researchers continue to explore strategies, pharmacological or otherwise, to improve the lives of those who have developed this condition; and it is hoped, by improving phenotyping of this heterogeneous disease, that we might ultimately deliver personalized medicine. Debate remains over how to identify undiagnosed COPD in individuals who would benefit from intervention, while avoiding overdiagnosis, and these controversies perhaps highlight shortcomings in accepted disease definitions. Not unrelatedly, renewed interest has emerged in explaining why some individuals develop COPD and identifying the formative stages of COPD development.

Background and aims High-density lipoprotein cholesterol (HDL-C), an established risk marker for atherosclerotic cardiovascular disease (CVD), has been shown to be inversely and independently associated with incident hypertension. Paraoxonase-1 (PON-1) is an HDL-bound esterase enzyme associated with CVD, but its relationship with incident hypertension has not been previously investigated. We aimed at evaluating the prospective association between PON-1 and hypertension risk. Methods PON-1 arylesterase activity was measured in serum at baseline in 3988 participants without pre-existing hypertension in the Prevention of Renal and Vascular End-stage Disease (PREVEND) prospective population-based study. During a median follow-up of 10.7 years, 1206 participants developed hypertension. Results In age- and sex-adjusted analysis, the hazard ratio (95% CI) for incident hypertension per 1 standard deviation increase in PON-1 was 1.01 (0.96–1.07; p = 0.656), which remained non-significant after adjustment for several established hypertension risk factors and other potential confounders (0.99, 0.93 to 1.05; p = 0.764). The association was also non-existent on further adjustment for HDL-C (1.00 (0.94–1.06; p = 0.936)) and did not importantly vary across several clinical subgroups. In analyses in the same set of participants, HDL-C was continuously inversely and independently associated with hypertension risk; the association persisted after further adjustment for PON-1 activity and was not modified by PON-1 activity. Conclusions In this Caucasian cohort of men and women, HDL-C, but not its anti-oxidant constituent - PON-1, is inversely, continuously and independently associated with future risk of hypertension. The association is independent of and not modified by PON-1.

We examined the validity of the social inhibition component of Type D, its distinctiveness from negative affectivity, and value regarding emotional distress as measured with the DS14 in 173 coronary artery disease patients. In dimensional analysis, social inhibition and negative affectivity emerged as distinct traits. Analysis of continuous negative affectivity and social inhibition measures showed main effects for several emotional and inhibition markers and an interaction effect for social anxiety. Categorical analysis indicated that Type D patients reported more depression, negative mood, social anxiety, and less positive mood. Social inhibition is not a redundant trait, but has additional conceptual value.

Monocytes are heterogeneous effector cells involved in the maintenance and restoration of tissue integrity. Monocytes and macrophages are involved in cardiovascular disease progression, and are associated with the development of unstable atherosclerotic plaques. Hyperlipidaemia can accelerate cardiovascular disease progression. However, monocyte responses to hyperlipidaemia are poorly understood. In the past decade, accumulating data describe the relationship between the dynamic blood lipid environment and the heterogeneous circulating monocyte pool, which might have profound consequences for cardiovascular disease. In this Review, we explore the updated view of monocytes in cardiovascular disease and their relationship with macrophages in promoting the homeostatic and inflammatory responses related to atherosclerosis. We describe the different definitions of dyslipidaemia, highlight current theories on the ontogeny of monocyte heterogeneity, discuss how dyslipidaemia might alter monocyte production, and explore the mechanistic interface linking dyslipidaemia with monocyte effector functions, such as migration and the inflammatory response. Finally, we discuss the role of dietary and endogenous lipid species in mediating dyslipidaemic responses, and the role of these lipids in promoting the risk of cardiovascular disease through modulation of monocyte behaviour.

The aim of this review is to provide clinicians with an overview of the role of coronary artery calcium (CAC) scoring across the spectrum ranging from asymptomatic individuals to chronic chest pain patients. We will briefly introduce the technical background of CAC scoring, summarize the major guidelines per type of patient at risk and discuss latest research with respect to CAC. Finally, the reader should be able to determine when CAC scoring is indicated or may be of added value.

BACKGROUND: Epidemiological research on effects of transportation noise on incident hypertension is inconsistent. OBJECTIVES: We aimed to investigate whether residential road traffic noise increases the risk for hypertension. METHODS: In a population-based cohort of 57,053 individuals 50-64 years of age at enrollment, we identified 21,241 individuals who fulfilled our case definition of filling formula presented prescriptions and formula presented defined daily doses of antihypertensive drugs (AHTs) within a year, during a mean follow-up time of 14.0 y. Residential addresses from 1987 to 2016 were obtained from national registers, and road traffic noise at the most exposed façade as well as the least exposed façade was modeled for all addresses. Analyses were conducted using Cox proportional hazards models. RESULTS: We found no associations between the 10-y mean exposure to road traffic noise and filled prescriptions for AHTs, with incidence rate ratios (IRRs) of 0.999 [95% confidence intervals (CI): 0.980, 1.019)] per 10-dB increase in road traffic noise at the most exposed façade and of 1.001 (95% CI: 0.977, 1.026) at the least exposed façade. Interaction analyses suggested an association with road traffic noise at the least exposed façade among subpopulations of current smokers and obese individuals. CONCLUSION: The present study does not support an association between road traffic noise and filled prescriptions for AHTs. https://doi.org/10.1289/EHP6273.

The aim of this review is to provide clinicians with an overview of the role of coronary artery calcium (CAC) scoring across the spectrum ranging from asymptomatic individuals to chronic chest pain patients. We will briefly introduce the technical background of CAC scoring, summarize the major guidelines per type of patient at risk and discuss latest research with respect to CAC. Finally, the reader should be able to determine when CAC scoring is indicated or may be of added value.

In the era of precision medicine, treatments that target specific modifiable characteristics of high-risk patients have the potential to lower further the residual risk of atherosclerotic cardiovascular events. Correction of atherogenic dyslipidemia, however, remains a major unmet clinical need. Elevated plasma triglycerides, with or without low levels of high-density lipoprotein cholesterol (HDL-C), offer a key modifiable component of this common dyslipidemia, especially in insulin resistant conditions such as type 2 diabetes mellitus. The development of selective peroxisome proliferator-activated receptor alpha modulators (SPPARM) offers an approach to address this treatment gap. This Joint Consensus Panel appraised evidence for the first SPPARM agonist and concluded that this agent represents a novel therapeutic class, distinct from fibrates, based on pharmacological activity, and, importantly, a safe hepatic and renal profile. The ongoing PROMINENT cardiovascular outcomes trial is testing in 10,000 patients with type 2 diabetes mellitus, elevated triglycerides, and low levels of HDL-C whether treatment with this SPPARM agonist safely reduces residual cardiovascular risk.

Purpose We developed a job exposure matrix (JEM) to study the association between long-term exposure to heavy physical effort or heavy lifting and carrying at work with disability pension due to musculoskeletal disorders and premature all-cause mortality. Methods Exposure to heavy physical effort at work during 1996–2005 was estimated with JEM developed for this study population, where the exposure was based on occupational titles of the participants. We included all employees of the City of Helsinki, Finland, who had annual data of exposure for 8–10 years (1996–2005, n = 18387). The outcome variables were register-based, and the follow-up was from 2006 until 2015. The risk estimates were evaluated using competing risk survival analysis. Results There were 530 (3%) disability pension events due to musculoskeletal disorders during the 10-year follow-up. After adjustment for sex, age, education and chronic diseases, employees in the second (SHR = 1.46, 95% CI 1.05–2.05), third (SHR = 2.73, 95% CI 2.00–2.29), and the highest exposure quartile (SHR = 2.56, 95% CI 1.88–3.50) had a higher risk of musculoskeletal disability pension than employees in the lowest quartile. A total of 110 (4%) men and 266 (2%) women died during the follow-up. Men in the third quartile (SHR = 2.29, 95% CI 1.23–4.24), and women in the highest exposure quartile (SHR = 1.54, 95% CI 0.99–2.41) had a higher risk of premature mortality than those in the lowest quartile. Conclusions Eight to ten years of exposure to heavy physical effort at work is strongly associated with disability pension due to musculoskeletal disorders. This exposure also increases the risk of premature mortality, particularly among men. Electronic supplementary material The online version of this article (10.1007/s00420-018-1393-5) contains supplementary material, which is available to authorized users.

Previous cross-sectional studies examining whether John Henryism (JH), or high-effort coping with socioeconomic adversity, potentiates the inverse association between socioeconomic position (SEP) and cardiovascular health have focused mainly on hypertension in African Americans. We conducted the first longitudinal test of this hypothesis on incident acute myocardial infarction (AMI) using data from the Kuopio Ischemic Heart Disease Risk Factor Study in Finland (N = 1405 men, 42-60 years). We hypothesized that the expected inverse gradient between SEP and AMI risk would be stronger for men scoring high on JH than for those scoring low. John Henryism was measured by a Finnish version of the JH Scale for Active Coping. Four different measures of SEP were used: childhood SEP, education, income, and occupation. AMI hazard ratios (HR) by SEP and JH were estimated using COX proportional hazard models, before and after adjustment for study covariates. 205 cases of AMI occurred over a median of 14.9 years. Men employed in lower rank (farmer, blue-collar) occupations who scored high on JH had significantly higher age-adjusted risks of AMI than men in higher rank (white-collar) occupations (HR = 3.14, 95% CI: 1.65-5.98 for blue collar; HR = 2.33, 95% Cl: 1.04-5.22 for farmers) who also scored high on JH. No socioeconomic differences in AMI were observed for men who scored low on JH (HR = 136, 95% CI: 0.74 2.47 for blue collar; HR = 0.93, 95% CI: 0.59-1.48 for farmers; p = 0.002 for the SEP x JH interaction). These findings persisted after adjustment for sociodemographic, behavioral, and biological factors. Results for other SEP measures were in the same direction, but did not reach statistical significance. Repetitive high-effort coping with adversity (John Henryism) was independently associated with increased risk for AMI in Finnish men, underscoring the potential relevance of the John Henryism hypothesis to CVD outcomes other than hypertension and to populations other than African Americans. (C) 2016 Published by Elsevier Ltd.

Background The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context.Methods We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors-the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. We characterised risk exposure in relation to a Socio-demographic Index (SDI).Findings Between 1990 and 2015, global exposure to unsafe sanitation, household air pollution, childhood underweight, childhood stunting, and smoking each decreased by more than 25%. Global exposure for several occupational risks, high body-mass index (BMI), and drug use increased by more than 25% over the same period. All risks jointly evaluated in 2015 accounted for 57.8% (95% CI 56.6-58.8) of global deaths and 41.2% (39.8-42.8) of DALYs. In 2015, the ten largest contributors to global DALYs among Level 3 risks were high systolic blood pressure (211.8 million [192.7 million to 231.1 million] global DALYs), smoking (148.6 million [134.2 million to 163.1 million]), high fasting plasma glucose (143.1 million [125.1 million to 163.5 million]), high BMI (120.1 million [83.8 million to 158.4 million]), childhood undernutrition (113.3 million [103.9 million to 123.4 million]), ambient particulate matter (103.1 million [90.8 million to 115.1 million]), high total cholesterol (88.7 million [74.6 million to 105.7 million]), household air pollution (85.6 million [66.7 million to 106.1 million]), alcohol use (85.0 million [77.2 million to 93.0 million]), and diets high in sodium (83.0 million [49.3 million to 127.5 million]). From 1990 to 2015, attributable DALYs declined for micronutrient deficiencies, childhood undernutrition, unsafe sanitation and water, and household air pollution; reductions in risk-deleted DALY rates rather than reductions in exposure drove these declines. Rising exposure contributed to notable increases in attributable DALYs from high BMI, high fasting plasma glucose, occupational carcinogens, and drug use. Environmental risks and childhood undernutrition declined steadily with SDI; low physical activity, high BMI, and high fasting plasma glucose increased with SDI. In 119 countries, metabolic risks, such as high BMI and fasting plasma glucose, contributed the most attributable DALYs in 2015. Regionally, smoking still ranked among the leading five risk factors for attributable DALYs in 109 countries; childhood underweight and unsafe sex remained primary drivers of early death and disability in much of sub-Saharan Africa.Interpretation Declines in some key environmental risks have contributed to declines in critical infectious diseases. Some risks appear to be invariant to SDI. Increasing risks, including high BMI, high fasting plasma glucose, drug use, and some occupational exposures, contribute to rising burden from some conditions, but also provide opportunities for intervention. Some highly preventable risks, such as smoking, remain major causes of attributable DALYs, even as exposure is declining. Public policy makers need to pay attention to the risks that are increasingly major contributors to global burden. Copyright (C) The Author(s). Published by Elsevier Ltd.

Until recently, PET was regarded as a luxurious way of performing myocardial perfusion scintigraphy, with excellent image quality and diagnostic capabilities that hardly justified the additional cost and procedural effort. Quantitative perfusion PET was considered a major improvement over standard qualitative imaging, because it allows the measurement of parameters not otherwise available, but for many years its use was confined to academic and research settings. In recent years, however, several factors have contributed to the renewal of interest in quantitative perfusion PET, which has become a much more readily accessible technique due to progress in hardware and the availability of dedicated and user-friendly platforms and programs. In spite of this evolution and of the growing evidence that quantitative perfusion PET can play a role in the clinical setting, there are not yet clear indications for its clinical use. Therefore, the Cardiovascular Committee of the European Association of Nuclear Medicine, starting from the experience of its members, decided to examine the current literature on quantitative perfusion PET to (1) evaluate the rationale for its clinical use, (2) identify the main methodological requirements, (3) identify the remaining technical difficulties, (4) define the most reliable interpretation criteria, and finally (5) tentatively delineate currently acceptable and possibly appropriate clinical indications. The present position paper must be considered as a starting point aiming to promote a wider use of quantitative perfusion PET and to encourage the conception and execution of the studies needed to definitely establish its role in clinical practice.

Background Increasing evidence suggests a relation between having had spontaneous preterm delivery and cardiovascular disease in the future. We performed a systematic review and meta-analysis to assess the relation between a history of spontaneous preterm delivery and risk of ischaemic heart disease (IHD), stroke or overall cardiovascular disease (CVD).Methods We carried out a systematic search in Medline (from 1966 to 17 July 2014) and Embase (from 1980 to 17 July 2014). We included studies with a cohort design assessing the relation between spontaneous preterm delivery and fatal or nonfatal IHD, stroke, or overall CVD. IHD, stroke and CVD were assessed through linkage with national registries. Hazard ratios (HRs) were pooled using a random-effects model.Results Of the 10 cohort studies included; sample sizes ranged from 3706 to 923,686 women and follow-up ranged from 12-35 years. Spontaneous preterm delivery was related to an increased risk of developing or dying from IHD (HR 1.38, 95% confidence interval (CI) 1.22-1.57), stroke (HR 1.71, 95% CI 1.53-1.91) and overall CVD (relative risk (HR) 2.01, 95% CI 1.52-2.65). All studies found a positive effect, although substantial between-study heterogeneity was found for IHD and CVD.Conclusion Spontaneous preterm delivery is an independent risk factor for the development of IHD, stroke and overall CVD.

Background and aims: Non-LDL dyslipidemia (NLD) confers cardiovascular risk, and prevalence rates appear to be high in elderly populations. Small cohorts have identified several lifestyle, anthropometric, and medical factors associated with NLD. We aimed to assess sex-and age-specific prevalence of NLD in a contemporary population cohort (n = 167 729), and to identify independent determinants of NLD, focusing on lifestyle, anthropometric, and medical factors.Methods: The prevalence of NLD was assessed per 10-year age intervals in adults without cardiovascular disease not using lipid-modifying drugs from the Dutch LifeLines cohort. NLD was defined as low HDL-cholesterol or high triglycerides or high remnant cholesterol as per guideline cut-off values. Multivariable regression was used to identify factors independently associated with NLD. Determinants included age, smoking, alcohol use, physical activity, diet, BMI, diabetes mellitus (DM), chronic kidney disease, and in women, menopausal state and oral contraceptive use.Results: NLD occurred in 15-19% of women and 13-30% of men in this cohort, with the highest prevalence of 30% in 35-55 year old men. In most age groups, the prevalence in women was lower than in men. Obesity (both sexes: Odds ratio (OR) 5.3, 95% confidence interval (95% CI) 5.0-5.7), current smoking (men: OR 1.8, 95% CI 1.7-1.9; women OR 2.2, 95% CI 2.1-2.3), and DM (men: OR 2.2, 95% CI 1.8-2.6; women: OR 2.7, 95% CI 2.3-3.1) were strongly associated with NLD.Conclusions: NLD already occurs frequently at an early age. Modifiable lifestyle choices, obesity, and DM were strong determinants of NLD. Public health efforts could substantially contribute to decrease NLD. (C) 2018 Elsevier B.V. All rights reserved.

Modern work life is characterized by constant change, reorganizations, and requirements of efficiency, which make the distribution of resources and obligations, as well as justice in decisionmaking, highly important. In the work life context, it is a question not only of distributing resources and obligations, but also of the procedures and rules that guide the decisionmaking in the organization. Studies of these rules and procedures have provided the basis for a new line of research that evaluates leadership and social relationships in working communities; that is, distributive, procedural, and relational justice. This review follows the development of research on organizational justice from its origins in early social and motivational psychological theories to its establishment as a major line of research in modern work and organizational psychology. The adverse consequences of injustice include poor team climate, reduced productivity and well-being, and work-related illnesses.

Background—Mendelian randomization data suggest genetic determinants of lifetime higher triglyceride-rich lipoprotein-cholesterol (TRL-C) are causally related to cardiovascular disease and therefore a potential therapeutic target. The relevance of TRL-C among patients receiving statins is unknown. We assessed the relationship between TRL-C and cardiovascular risk, and whether this risk was modifiable among patients receiving statins in the TNT trial. Methods—Patients with coronary heart disease [CHD] and LDL-C 130-250mg/dL entered an 8-week run-in phase with atorvastatin 10mg/day (ATV10). After this period, participants with LDL-C

The purpose of this review was to assess the relationship between premature ovarian insufficiency (POI), defined as natural menopause40 years, and risk of ischaemic heart disease (IHD), stroke and overall cardiovascular disease (CVD).We performed a systematic search in PubMed (1966-2012), EMBASE (1980-2012). Studies were included if they were prospective, follow-up3 years, assessment of age menopause40 years, and incident cases of fatal or nonfatal IHD, stroke, or overall CVD. Relative risks (RRs) and 95% confidence interval (CI) were pooled using a random-effect model. Overall, 10 observational studies were identified, comprising 190,588 women (follow-up 4-37 years) with 9440 events (2026 events for IHD (seven studies) and 6438 events for stroke (seven studies) and 976 for total CVD (two studies). POI was assessed by questionnaire and incident cases through certification and event registers. POI was related to an increased risk of developing or dying from IHD (hazard ratio (HR) 1.69, 95% CI 1.29-2.21, p = 0.0001) and total CVD (HR 1.61, 95% CI 1.22-2.12, p = 0.0007). No relation was found for stroke (HR 1.03, 0.88-1.19, p = 0.74). We found no evidence for heterogeneity.POI is an independent though modest risk factor of IHD and overall CVD but not of stroke. Because of the limited impact of POI on CVD risk compared to classical cardiovascular risk factors, it is unlikely that POI will be implemented as modifier of cardiovascular risk classification.

Context: The currently applied reference ranges for thyroid function are under debate. Despite evidence that thyroid function within the reference range is related with several cardiovascular disorders, its association with the risk of stroke has not been evaluated previously.Design and Setting: We identified studies through a systematic literature search and the Thyroid Studies Collaboration, a collaboration of prospective cohort studies. Studies measuring baseline TSH, free T-4, and stroke outcomes were included, and we collected individual participant data from each study, including thyroid function measurements and incident all stroke (combined fatal and nonfatal) and fatal stroke. The applied reference range for TSH levels was between 0.45 and 4.49 mIU/L.Results: We collected individual participant data on 43 598 adults with TSH within the reference range from 17 cohorts, with a median follow-up of 11.6 years (interquartile range 5.1-13.9), including 449 908 person-years. Age- and sex-adjusted pooled hazard ratio for TSH was 0.78 (95% confidence interval [CI] 0.65-0.95 across the reference range of TSH) for all stroke and 0.83 (95% CI 0.62-1.09) for fatal stroke. For the free T4 analyses, the hazard ratio was 1.08 (95% CI 0.99-1.15 per SD increase) for all stroke and 1.10 (95% CI 1.04-1.19) for fatal stroke. This was independent of cardiovascular risk factors including systolic blood pressure, total cholesterol, smoking, and prevalent diabetes.Conclusion: Higher levels of TSH within the reference range may decrease the risk of stroke, highlighting the need for further research focusing on the clinical consequences associated with differences within the reference range of thyroid function.