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Although diabetes and cardiovascular disease account for substantial disease prevalence among adults in the United States, their prevalence among racial and ethnic subgroups is inadequately characterized. To fill this gap, CDC described the prevalence of diagnosed cardiometabolic diseases among U.S. adults, by disaggregated racial and ethnic subgroups, among 3,970,904 respondents to the Behavioral Risk Factor Surveillance System during 2013-2021. Prevalence of each disease (diabetes, myocardial infarction, angina or coronary heart disease, and stroke), stratified by race and ethnicity, was based on self-reported diagnosis by a health care professional, adjusting for age, sex, and survey year. Overall, mean respondent age was 47.5 years, and 51.4% of respondents were women. Prevalence of cardiometabolic diseases among disaggregated race and ethnicity subgroups varied considerably. For example, diabetes prevalence within the aggregated non-Hispanic Asian category (11.5%) ranged from 6.3% in the Vietnamese subgroup to 15.2% in the Filipino subgroup. Prevalence of angina or coronary heart disease for the aggregated Hispanic or Latino category (3.8%) ranged from 3.1% in the Cuban subgroup to 6.3% in the Puerto Rican subgroup. Disaggregation of cardiometabolic disease prevalence data by race and ethnicity identified health disparities among subgroups that can be used to better help guide prevention programs and develop culturally relevant interventions. [ABSTRACT FROM AUTHOR]

Background In industrialized populations, low male testosterone is associated with higher rates of cardiovascular mortality. However, coronary risk factors like obesity impact both testosterone and cardiovascular outcomes. Here, we assess the role of endogenous testosterone on coronary artery calcium in an active subsistence population with relatively low testosterone levels, low cardiovascular risk and low coronary artery calcium scores. Methodology In this cross-sectional community-based study, 719 Tsimane forager-horticulturalists in the Bolivian Amazon aged 40+ years underwent computed tomography (49.8% male, mean age 57.6 years). Results Coronary artery calcium levels were low; 84.5% had no coronary artery calcium. Zero-inflated negative binomial models found testosterone was positively associated with coronary artery calcium for the full sample (Incidence Rate Ratio [IRR] = 1.477, 95% Confidence Interval [CI] 1.001–2.170, P = 0.031), and in a male-only subset (IRR = 1.532, 95% CI 0.993–2.360, P = 0.053). Testosterone was also positively associated with clinically relevant coronary atherosclerosis (calcium >100 Agatston units) in the full sample (Odds Ratio [OR] = 1.984, 95% CI 1.202–3.275, P = 0.007) and when limited to male-only sample (OR = 2.032, 95% CI 1.118–4.816, P = 0.024). Individuals with coronary artery calcium >100 had 20% higher levels of testosterone than those with calcium <100 (t = –3.201, P = 0.007). Conclusions and Implications Among Tsimane, testosterone is positively associated with coronary artery calcium despite generally low normal testosterone levels, minimal atherosclerosis and rare cardiovascular disease (CVD) events. Associations between low testosterone and CVD events in industrialized populations are likely confounded by obesity and other lifestyle factors. [ABSTRACT FROM AUTHOR]

The world's population is estimated to reach 10 billion by 2050 and 75% of this population will live in cities. Two-third of the European population already live in urban areas and this proportion continues to grow. Between 60% and 80% of the global energy use is consumed by urban areas, with 70% of the greenhouse gas emissions produced within urban areas. The World Health Organization states that city planning is now recognized as a critical part of a comprehensive solution to tackle adverse health outcomes. In the present review, we address non-communicable diseases with a focus on cardiovascular disease and the urbanization process in relation to environmental risk exposures including noise, air pollution, temperature, and outdoor light. The present review reports why heat islands develop in urban areas, and how greening of cities can improve public health, and address climate concerns, sustainability, and liveability. In addition, we discuss urban planning, transport interventions, and novel technologies to assess external environmental exposures, e.g. using digital technologies, to promote heart healthy cities in the future. Lastly, we highlight new paradigms of integrative thinking such as the exposome and planetary health, challenging the one-exposure-one-health-outcome association and expand our understanding of the totality of human environmental exposures. [ABSTRACT FROM AUTHOR]

Aims Little is known about the trade-off between the health benefits of physical activity (PA) and the potential harmful effects of increased exposure to air pollution during outdoor PA. We examined the association of the combined effects of air pollution and changes in PA with cardiovascular disease (CVD) in young adults. Methods and results This nationwide cohort study included 1 469 972 young adults aged 20–39 years. Air pollution exposure was estimated by the annual average cumulative level of particulate matter (PM). PA was calculated as minutes of metabolic equivalent tasks per week (MET-min/week) based on two consecutive health examinations from 2009 to 2012. Compared with the participants exposed to low-to-moderate levels of PM2.5 or PM10 who continuously engaged in ≥1000 MET-min/week of PA, those who decreased their PA from ≥1000 MET-min/week to 1–499 MET-min/week [PM10 adjusted hazard ratio (aHR) 1.22; 95% confidence interval (CI) 1.00–1.48] and to 0 MET-min/week (physically inactive; PM10 aHR 1.38; 95% CI 1.07–1.78) had an increased risk of CVD (P for trend <0.01). Among participants exposed to high levels of PM2.5 or PM10, the risk of CVD was elevated with an increase in PA above 1000 MET-min/week. Conclusion Reducing PA may lead to subsequent elevation of CVD risk in young adults exposed to low-to-moderate levels of PM2.5 or PM10, whereas a large increase in PA in a high-pollution environment may adversely affect cardiovascular health. [ABSTRACT FROM AUTHOR]

The article discusses that how Covid-19 pandemic has caused illness and mortality on a global scale. It mentions the devastating effects of air pollution on Covid-19 spread and lethality, in addition to the well-known devastating effects on cardiovascular health. It discusses the guidelines on sports cardiology and exercise in patients with cardiovascular disease.

Abstract Purpose Few previous studies have investigated the association between urban green space and cardiovascular disease (CVD) within Asian populations. We aimed to determine the relationship between amount of green space in the residential environment and CVD within a large general Asian population in this population-based longitudinal study. Methods The study population consisted of 351,409 participants aged over 20 years extracted from the National Health Insurance Service National Sample Cohort. Data on newly-occurred CVD events were collected from hospital admission records for the period 1 January 2006 to 31 December 2013. Cox proportional hazards regression analysis was used for determining the risk of developing CVD according to urban green space coverage (% area), adjusting for a number of relevant confounders. Results Compared to those within the lowest quartile of green space coverage, those within the highest quartile of urban space had a reduced risk of total CVD (hazard ratio, HR 0.85, 95% confidence interval, CI 0.81–0.89), coronary heart disease (HR 0.83, 95% CI 0.78–0.89), acute myocardial infarction (HR 0.77, 95% CI 0.68–0.88), total stroke (HR 0.87, 95% CI 0.82–0.93) and ischemic stroke (HR 0.86, 95% CI 0.80–0.94), but not hemorrhagic stroke (HR 0.98, 95% CI 0.86–1.12). The risk-reducing effect of green space coverage was preserved after stratification according to sex, household income, and Charlson comorbidity index. Conclusion Residing in urban regions with greater green space coverage may lead to a reduced risk of CVD. Urban planning intervention policies that increase urban green space coverage could help to reduce the risk of CVD. Highlights • Those living in areas with greater amounts of green space found to have lower risk of CVD. • The association was preserved regardless of income and sex groups of participants. • Residing in urban regions with greater green space coverage may lead to reduced risk of CVD. [ABSTRACT FROM AUTHOR]

Abstract Non-alcoholic fatty liver disease (NAFLD) is highly prevalent and includes a spectrum of abnormalities ranging from steatosis to cirrhosis. In this review, we address recent evidence and limitations of studies that evaluated the association of NAFLD with atherosclerotic cardiovascular disease. NAFLD is considered an ectopic fat deposit associated with metabolic (insulin resistance, hyperglycemia and dyslipidemia), inflammatory, coagulation and blood pressure disturbances. Prospective studies have associated NAFLD presence and severity, particularly steatohepatitis and fibrosis, with an increased risk of cardiovascular disease. However, these studies are limited by heterogeneity concerning NAFLD diagnostic criteria and disease severity stratification, as well as by the presence of confounding factors. In addition, genetic variants predisposing to NAFLD, such as the PNPLA3 I148M mutation, were not consistently associated with an increased risk of cardiovascular events. Therefore, currently, it is not possible to prove a causal relation between NAFLD and cardiovascular disease. Furthermore, there is presently no evidence that NAFLD diagnosis can be used as a tool to improve cardiovascular risk stratification and modify treatment. Specific treatments for NAFLD are being developed and must be tested prospectively in adequately designed trials to determine the potential of reducing both hepatic and cardiovascular diseases and to prove whether NAFLD is indeed a cause of atherosclerosis. Graphical abstract Image 1 Highlights • NAFLD is highly prevalent ranging from steatosis to cirrhosis. • NAFLD advanced forms associated with cardiovascular risk. • NAFLD studies limited by heterogeneity and confounders. • Genetic variants predisposing to NAFLD not consistently associated with cardiovascular events. • No proof that NAFLD is causal of cardiovascular disease. [ABSTRACT FROM AUTHOR]

Hypertension is a major cause of cardiovascular disease morbidity and mortality in Ghana. This study examines the prevalence, awareness, treatment and control of hypertension among Ghanaian aged 15–49 years. This cross-sectional study retrieved data from the 2014 Ghana Demographic and Health Survey (GDHS). The sample, comprising of 13,247 respondents aged 15–49 years, was analysed using descriptive statistics, Chi-Square tests, independent sample t-tests and binary logistic regressions. The overall prevalence of hypertension was 13.0% (12.1% for males and 13.4% for females). Among respondents who had hypertension, 45.6% were aware of their hypertension status; 40.5% were treating the condition while 23.8% had their blood pressure controlled (BP <140/90 mmHg). Socio-economic and demographic factors, health insurance coverage and recent visit to health facilities played significant roles in hypertension prevalence and awareness. While region of residence and health facility visits were predictors of hypertension treatment, age and region of residence predicted hypertension control in this population. This study suggests that in order to address the increasing burden of hypertension in Ghana, there should be an expansion of the National Health Insurance Scheme and development of measures to reduce health inequities. Also, some of the determining factors such as age, gender, marital status are similar to other cultures; therefore, existing interventions from those cultures could be adapted in addressing hypertension prevalence, awareness, treatment and control in Ghana. [ABSTRACT FROM AUTHOR]

Abstract Background Epidemiologic evidence indicates common risk factors, including air pollution exposure, for respiratory and cardiovascular diseases, suggesting the involvement of common altered molecular pathways. Objectives The goal was to find intermediate metabolites or metabolic pathways that could be associated with both air pollutants and health outcomes (“meeting-in-the-middle”), thus shedding light on mechanisms and reinforcing causality. Methods We applied a statistical approach named ‘meet-in-the-middle’ to untargeted metabolomics in two independent case-control studies nested in cohorts on adult-onset asthma (AOA) and cardio-cerebrovascular diseases (CCVD). We compared the results to identify both common and disease-specific altered metabolic pathways. Results A novel finding was a strong association of AOA with ultrafine particles (UFP; odds ratio 1.80 [1.26, 2.55] per increase by 5000 particles/cm3). Further, we have identified several metabolic pathways that potentially mediate the effect of air pollution on health outcomes. Among those, perturbation of Linoleate metabolism pathway was associated with air pollution exposure, AOA and CCVD. Conclusions Our results suggest common pathway perturbations may occur as a consequence of chronic exposure to air pollution leading to increased risk for both AOA and CCVD. Highlights • Strong association of long-term ultrafine particle exposure with adult-onset asthma • Linoleate metabolism and carnitine shuttle as “meeting-in-the-middle” pathways. • Metabolic pathways mediate the air pollution effects on health outcomes. [ABSTRACT FROM AUTHOR]

Objective: The etiology of cardiovascular disease (CVD) is complex owing to the interactions of genetic variance with environmental factors. Inflammatory processes are now being increasingly implicated in the pathogenesis of CVD. This meta-analysis investigated the potential role of interleukin-6 (IL-6) as a risk factor for CVD development in healthy individuals. Methods: Literature search was carried out in multiple electronic databases, and study selection followed a priori eligibility criteria. Meta-analyses of standardized mean differences were carried out to determine an overall effect size of the difference in IL-6 levels between CVD cases and non-CVD matched controls. Meta-regression analyses were performed to examine the relationship between the IL-6 levels in CVD cases and several explanatory variables. Results: Seventeen studies enrolling 288738 healthy individuals with an average follow-up duration of 7.4 ± 4.1 years were found eligible. Overall, data of 5400 CVD cases and 14607 matched non-CVD controls are used in the present meta-analysis. Baseline IL-6 levels were significantly higher in CVD cases than in non-CVD controls (standardized mean difference [95% confidence interval]) of 0.14 [0.09, 0.20]/mean difference of 0.36 [0.28, 0.44] picogram per milliliter). Total cholesterol, LDL-cholesterol, and triglyceride levels were also significantly higher, and HDL-cholesterol levels were significantly lower in CVD cases in comparison with the controls. Systolic blood pressure and total cholesterol levels had a significantly positive relationship, whereas triglyceride levels had a significantly inverse relationship with the levels of IL-6. Conclusion: Higher IL-6 levels in healthy individuals are associated with CVD risk, which is co-associated with hypertension and hypercholesterolemia. [ABSTRACT FROM AUTHOR]

Background and Aims Atherosclerosis as an inflammatory disease involved in the etiology of cardiovascular disease worldwide, in our days demands an array of different therapeutic approaches in order to soon be able to visualize an effective prevention. Based on an immunotherapeutic approach, we designed a non-invasive vaccine (HB-ATV-8), contained in a micellar nanoparticle composed of lipids and a peptide segment derived from the C-terminus of the cholesterol-ester transfer protein (CETP). Now we extend our successful proof of concept from the rabbit to a porcine model and investigated its effect in an attempt to undoubtedly establish the efficacy of vaccination in a model closer to the human. Methods A preclinical trial was designed to study the efficacy of vaccine HB-ATV-8 in pigs (Large White × Landrace). Male experimental animals were fed with standard diet (control), high fat diet (HFD) or the same HFD but treated with HB-ATV-8 (HFD + Vaccine) applied nasally for up to 7 months. All biochemical and enzymatic analyses were performed in peripheral venous blood and thoracic aorta and liver samples examined using conventional, two-photon excitation and second harmonic generation microscopy to identify atherosclerotic and hepatic lesions. mRNA concentrations for KLF2 , ACTA2 , SOD1, COL1A1 genes and protein levels for PPARα and ABCA1 were quantified in aorta and liver respectively using qPCR and Western blot analysis. Results The administration of vaccine HB-ATV-8 induced anti-CETP IgG antibodies and reduced atherosclerotic and hepatic lesions promoted by the high fat diet. In addition, plasma triglyceride levels of vaccine treated pigs fed the HFD were similar to those of control group, in contrast to high concentrations reached with animals exclusively fed with HFD. Moreover, HFD promotes a tendency to decrease hepatic PPARα levels and increase in aorta gene expression of KLF2 , ACTA2 , SOD1 and COL1A1 , while vaccine application promotes recovery close to control values. Conclusions Vaccine HB-ATV-8 administration constitutes a promissory preventive approach useful in the control of atherogenesis and fatty liver disease. The positive results obtained, the non-invasive characteristics of the vaccine, the simple design employed in its conception and its low production cost, support the novelty of this therapeutic strategy designed to prevent the process of atherogenesis and control the development of fatty liver disease. [ABSTRACT FROM AUTHOR]

Background: The effects of skeletal muscle mass on depressive symptoms remain poorly understood, especially in the middle-aged population. We examined the relationship between skeletal muscle mass and depressive symptoms according to sex and menopausal status in the middle-aged Korean population.Methods: Herein, 1,151 men and 2,176 women aged 30-64 years completed questionnaires and underwent health examinations in the Cardiovascular and Metabolic Disease Etiology Research Center study. Appendicular skeletal muscle mass (ASM) was measured via bioelectrical impedance analysis and adjusted for height squared (ASM/Ht2). Both continuous values and tertile groups of ASM/Ht2 were used for analysis. Depressive symptoms were assessed using the Beck Depressive Inventory-II (BDI), and the prevalence of depressive symptoms was determined as a BDI score ≥ 20.Results: Multiple logistic regression analysis using a fully adjusted model showed that depressive symptoms were more frequently observed among men in the lower ASM/Ht2 tertile and middle ASM/Ht2 tertile than among those in the higher ASM/Ht2 tertile. Each 1-kg/m2 decrease in ASM/Ht2 was significantly associated with the presence of depressive symptoms in men. Such significant association was not observed among premenopausal and postmenopausal women.Limitations: The cross-sectional nature of the study design, measurement of skeletal muscle mass and depressive symptoms only once, estimation of skeletal muscle mass using bioelectrical impedance analysis, assessing depressive symptoms by self-reported questionnaire, and potential unknown confounding variables constitute the limitations of our study.Conclusions: The independent association between low skeletal muscle mass and depressive symptoms was observed in men but not in women. [ABSTRACT FROM AUTHOR]

Introduction: In the last decades, consistent data derived from experimental, epidemiological, and clinical studies pointed obstructive sleep apnea (OSA), the most common sleep disordered breathing worldwide, as a potential risk factor for incidence and recurrence of atrial fibrillation (AF). Areas covered: This review article describes the impact of OSA on AF and discusses potential strategies for managing OSA in the AF scenario. Expert commentary: Untreated OSA seems to be one important predictor of AF treatment failure after chemical or electrical cardioversion as well as after a successful AF ablation. There is biological plausibility for this association including the effects of intermittent hypoxia and sleep fragmentation promoting sympathetic activation, blood pressure instability, inflammation, and oxidative stress. The negative swings derived from the obstructive events also increases left ventricle afterload contributing to cardiac remodeling. Altogether, these factors provide a structural and electrical substrate for AF. Despite this evidence, however, OSA remains still poorly recognized and consequently undertreated in clinical practice. Therefore, active programs to incorporate valid screening for cardiologists to work in partnership to sleep medicine experts may ultimately contribute to decreasing the burden of AF. [ABSTRACT FROM AUTHOR]

Introduction: Certain frail patients fail to achieve adequate functional or mortality benefit despite successful transcatheter aortic valve replacement (TAVR). Therefore, frailty assessment methods are becoming an important tool to identify and intervene on this high-risk patient subset for improving clinical outcomes. Areas covered: The authors provide an overview of frailty and frailty assessment tools being used in clinical practice and discuss the impact of frailty on the cardiac patients, particularly among the TAVR population. Expert commentary: Available evidence suggests that frailty assessment is critical for identifying patients at high risk of morbidity and mortality after TAVR procedures. However, there is lack of consensus for the best methodology to determine frailty and its optimal management in TAVR populations. Although, physical exercise is a commonly employed intervention to reduce frailty, a greater attention towards improving nutrition may convey more benefit than either intervention alone. Ongoing studies are investigating the benefits of a multicomponent approach to improve clinical outcomes in frail patients undergoing TAVR. [ABSTRACT FROM AUTHOR]

Introduction: We evaluated cardiovascular disease (CVD) risk associated with darunavir treatment and examined the demographic/clinical characteristics of darunavir users based on data from Janssen-sponsored clinical trials, post-marketing pharmacovigilance databases, and administrative claims databases.Methods: First, selected CVD events [myocardial infarction, stroke, sudden death, invasive cardiovascular procedures (coronary artery angioplasty or bypass, or carotid endarterectomy)] were analyzed in 19 Janssen-sponsored phase 2-4 studies (incidence rates estimated from pooled data; 95% confidence intervals derived from Poisson distribution). Second, analyses were conducted to identify spontaneously reported CVD events in post-marketing pharmacovigilance databases and evaluate disproportional reporting of CVD events for darunavir (using Empirical Bayesian Geometric Mean scores). Third, baseline demographic/clinical characteristics of human immunodeficiency virus-1 (HIV-1)-infected patients in general and new users of darunavir and atazanavir were explored using three US administrative claims databases.Results: Among 19 Janssen-sponsored clinical trials (treatment durations ≤ 6 years), the CVD event rate (95% CI) per 1000 person-years (pooled population; n = 5713) was 6.15 (2.91-11.89), and was lower for patients who used once-daily darunavir/ritonavir 800/100 mg [0.71 (0.16-3.05); n = 1326] versus twice-daily darunavir/ritonavir 600/100 mg [9.21 (4.94-16.04); n = 3058]. Trend analysis of post-marketing pharmacovigilance data showed that cumulative CVD event reporting rates for darunavir users (any dose) generally declined over time. Spontaneously reported CVD events were not disproportionately reported with darunavir versus other protease inhibitors. Compared with the general HIV-1-infected population and atazanavir users, higher proportions of darunavir users were male, older, and had comorbidities associated with CVD risk based on results from US administrative claims databases.Conclusions: This comprehensive review of Janssen-sponsored clinical trial, post-marketing, and epidemiological data does not suggest that CVD should be considered an important risk for users of darunavir. [ABSTRACT FROM AUTHOR]

Systemic inflammation induced by bacterial infection is one of several causative agents for cardiovascular disorders in patients with periodontal disease. Experimental results indicate that miRNAs play important roles in systemic inflammation induced by endotoxins. Further evidence states that stem cell based therapy shows potential in the treatment of inflammatory responses induced by sepsis. This study investigates if stem cells show protective effects on cardiomyocyte damage induced by porphyromonas gingivalis‐LPS (Pg‐LPS) through regulating miRNAs. H9c2 cardiomyoblasts and neonatal rat cardiomyocytes (NRCMs) were damaged using Pg‐LPS in this study. Pg‐LPS damaged H9c2 or NRCMs were then rescued using adipose‐derived stem cells (ADSC). The experimental results reveal that Pg‐LPS treatment is capable of inducing TLR4/NFκB axis activation, cell death signaling and IGF1R/PI3 K/Akt axis suppression. miR181b was downregulated in Pg‐LPS damaged H9c2/NRCMs. All markers were improved in H9c2/NRCMs cocultured with ADSC. miR181b mimic and inhibitor confirmed that miR181b plays a central role in regulating the cardio protective effect on Pg‐LPS damaged H9c2/NRCMs cocultured with ADSC. miR181b acts as potential therapeutic marker in cardiomyopathy induced by Pg‐LPS. Transplantation of adipose‐derived stem cells show potential in the treatment of cardiomyopathy induced by porphyromonas gingivalis endotoxin via regulation of miR181b. [ABSTRACT FROM AUTHOR]

Objective: To verify the association between the caspase recruitment domain-containing protein 8 (CARD8) single nucleotide polymorphism rs2043211 in the CARD8 gene and cardiovascular diseases. Methods: A comprehensive search was conducted for related literature in the PubMed, Embase, Cochrane Library, Web of Science, Wanfang Data, and China National Knowledge Infrastructure databases. At last, Six eligible case-control studies were included in this meta-analysis. Crude odds ratios (ORs) and 95% confidence intervals (CI) were calculated to estimate the strength of the association between CARD8 rs2043211 polymorphisms and the susceptibility of cardiovascular diseases. Results: For the homozygous model, OR was 1.21 (1.08-1.36, I² =0.0%, Pheterogeneity=0.542). For the heterozygous model (AT vs. AA), OR was 1.20 (1.04-1.38, I² =57.2%, Pheterogeneity=0.039). For the dominant model, OR was 1.24 (1.14-1.34, I²=38.5%, Pheterogeneity=0.149). For the allele model, OR was 0.96 (0.77-1.20, I² =92.7%, Pheterogeneity=0.000). For the recessive model, OR was 1.00 (0.91-1.10, I² =48.4%, Pheterogeneity=0.085). Conclusion: The present study showed that CARD8 rs2043211 polymorphism is associated with cardiovascular diseases. (Anatol J Cardiol 2018; 20: 70-6) [ABSTRACT FROM AUTHOR]

Deprivation indices constitute a valuable tool for assessing health inequalities. A key issue when analyzing deprivation is the choice of the geographical scale and spatial unit of analysis. Our objective was to evaluate statistical and geographical stability of an Area Based Deprivation Index (ABDI) computed at different spatial scales and to study their relation with cardiovascular disease. The present study has been conducted in the city of Madrid, Spain. Madrid divides its territory in three different administrative units nested within each other: census section, neighborhoods and districts. For each unit a deprivation index was calculated through Principal Component Analysis (PCA). The data source was the 2011 national census from where a range of socioeconomic and demographic indicators were selected. To study statistical and geographical stability of deprivation we used an Exploratory Spatial Data Analysis and bivariate Local Indicators of Spatial Association analysis. We also conducted Pearson correlation analyses to study the change in the relationship between deprivation and the prevalence of cardiovascular disease (CVD) across the three scales. At census section and neighborhood level, first component showed four and five factors loading higher than 0.6, respectively. These factors loading related to occupancy/labor market and education. However at district level, first component showed seven factors loading higher than 0.6 and related to occupancy/labor market, education and immigration. With indicators of these factors loading, deprivation indices were calculated for each administrative unit by extracting a single PCA axis. Variance explained for each index was 65%, 86% and 79%, respectively. Bivariate local autocorrelation analyses showed aggregated areas of low and high stability with variable degree of significance in the three scales. The ABDIs calculated at census section level, neighborhood level and district level presented different significant correlations with CVD prevalence (r = 0.328; r = 0.635; and r = 0.739 respectively). These results show that the deprivation index did not remain stable across the three scales, neither were the correlations between deprivation and age-adjusted CVD prevalence. Understanding the stability of a spatial phenomenon across different scales is essential to determine the best unit of aggregation of data when studying an important process such as socioeconomic deprivation and its possible health impacts. [ABSTRACT FROM AUTHOR]

Abstract: Background and Objective: Several studies have shown an association between periodontitis and cardiovascular disease (CVD). Atherosclerosis is the major cause of CVD, and a key event in the development of atherosclerosis is accumulation of lipoproteins within the arterial wall. Bacteria are the primary etiologic agents in periodontitis and Porphyromonas gingivalis is the major pathogen in the disease. Several studies support a role of modified low‐density lipoprotein (LDL) in atherogenesis; however, the pathogenic stimuli that induce the changes and the mechanisms by which this occur are unknown. This study aims to identify alterations in plasma lipoproteins induced by the periodontopathic species of bacterium, P. gingivalis, in vitro. Material and Methods: Plasma lipoproteins were isolated from whole blood treated with wild‐type and gingipain‐mutant (lacking either the Rgp‐ or Kgp gingipains) P. gingivalis by density/gradient‐ultracentrifugation and were studied using 2‐dimensional gel electrophoresis followed by matrix‐assisted laser desorption/ionization mass spectrometry. Porphyromonas gingivalis‐induced lipid peroxidation and antioxidant levels were measured by thiobarbituric acid‐reactive substances and antioxidant assay kits, respectively, and lumiaggregometry was used for measurement of reactive oxygen species (ROS) and aggregation. Results: Porphyromonas gingivalis exerted substantial proteolytic effects on the lipoproteins. The Rgp gingipains were responsible for producing 2 apoE fragments, as well as 2 apoB‐100 fragments, in LDL, and the Kgp gingipain produced an unidentified fragment in high‐density lipoproteins. Porphyromonas gingivalis and its different gingipain variants induced ROS and consumed antioxidants. Both the Rgp and Kgp gingipains were involved in inducing lipid peroxidation. Conclusion: Porphyromonas gingivalis has the potential to change the expression of lipoproteins in blood, which may represent a crucial link between periodontitis and CVD. [ABSTRACT FROM AUTHOR]

Angiotensin II (Ang II) is implicated in the development of cardiovascular disorders including hypertension and atherosclerosis. However, the role of Ang II in the interaction between apurinic/apyrimidinic endonuclease/redox factor-1 (APE/Ref-1) and sphingosine-1-phosphate (S1P) signals in relation to vascular disorders remains to be clarified. This study aimed to determine whether APE/Ref-1 plays a role in epigenetic regulation of the S1P receptor (S1PR) in response to Ang II in vascular smooth muscle cell (VSMC) migration and vascular neointima formation. Ang II augmented the expression of S1PR1 in aortic smooth muscle cells of Sprague Dawley rats (RASMCs), which was attenuated by Ang II receptor (AT) 1 inhibitors, antioxidants, and APE/Ref-1 knockdown with small interference RNA. Ang II stimulation produced H 2 O 2 , and exogenous H 2 O 2 elevated S1PR1 expression in RASMCs. Moreover, Ang II caused translocation of cytoplasmic APE/Ref-1 into the nucleus in RASMCs. H3 histone acetylation and APE/Ref-1 binding at the S1PR1 promoter were increased in RASMCs treated with Ang II. In addition, Ang II induced migration in RASMCs, which was suppressed by AT1 and S1PR1 inhibitors. The expression of S1PR1, and colocalization of APE/Ref-1 and acetylated histone H3 in vascular neointima, were greater in Ang II-infused rats compared with a control group. These findings demonstrate that Ang II stimulates the epigenetic regulation of S1PR1 expression via H 2 O 2 -mediated APE/Ref-1 translocation, which may consequently be involved in Ang II-induced VSMC migration and vascular neointima formation. Therefore, APE/Ref-1-mediated overexpression of S1PR1 may be implicated in the vascular dysfunction evoked by Ang II. [ABSTRACT FROM AUTHOR]

Objectives Plasma branched-chain amino acid (BCAA) levels, measured on nuclear magnetic resonance (NMR) metabolomics research platforms or by mass spectrometry, have been shown to be associated with type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD). We developed a new test for quantification of BCAA on a clinical NMR analyzer and used this test to determine the clinical correlates of BCAA in 2 independent cohorts. Design and methods The performance of the NMR-based BCAA assay was evaluated. A method comparison study was performed with mass spectrometry (LC-MS/MS). Plasma BCAA were measured in the Insulin Resistance Atherosclerosis Study (IRAS, n = 1209; 376 T2DM subjects) and in a Groningen cohort (n = 123; 67 T2DM subjects). In addition, carotid intima media thickness (cIMT) was measured successfully in 119 subjects from the Groningen cohort. Results NMR-based BCAA assay results were linear over a range of concentrations. Coefficients of variation for inter- and intra-assay precision ranged from 1.8–6.0, 1.7–5.4, 4.4–9.1, and 8.8–21.3%, for total BCAA, valine, leucine, and isoleucine, respectively. BCAA quantified from the same samples using NMR and LC-MS/MS were highly correlated (R 2  = 0.97, 0.95 and 0.90 for valine, leucine and isoleucine). In both cohorts total and individual BCAA were elevated in T2DM ( P  = 0.01 to ≤0.001). Moreover, cIMT was associated with BCAA independent of age, sex, T2DM and metabolic syndrome (MetS) categorization or alternatively of individual MetS components. Conclusions BCAA levels, measured by NMR in the clinical laboratory, are elevated in T2DM and may be associated with cIMT, a proxy of subclinical atherosclerosis. [ABSTRACT FROM AUTHOR]

Abstract: Aims/Introduction: To investigate whether the ratio of visceral fat area (VFA) to subcutaneous fat area (SFA; V/S ratio) could be predictive of cardiovascular disease (CVD) as compared with VFA or SFA in patients with diabetes. Materials and Methods: A total of 682 patients with type 2 diabetes (mean age 64 ± 13 years; 41% women) were enrolled. VFA (cm2) and SFA (cm2) were assessed by a dual bioelectrical impedance analyzer. The patients were divided into four groups according to the quartiles of the V/S ratio. The study end‐point was the first occurrence or recurrence of CVD. Results: Over a median follow up of 2.5 years, 21 patients reached the end‐point. The number of patients who reached the end‐point was increased along with the increasing of the V/S ratio quartiles. The V/S ratio was significantly associated with incident or recurrent CVD (hazard ratio [HR] 1.82, 95% CI: 1.09–3.04, P = 0.021) after adjusting for estimated glomerular filtration rate (HR 0.98, 95% CI: 0.96–1.00), brain‐type natriuretic peptide (HR 1.00, 95% CI: 1.00–1.01), use of antiplatelet agents (HR 4.26, 95% CI: 1.63–11.13), coefficient of variation of R‐R intervals (HR 0.85, 95% CI: 0.69–1.10) and glycated hemoglobin (HR 1.37, 95% CI: 1.05–1.79). The addition of the V/S ratio to age, estimated glomerular filtration rate, brain‐type natriuretic peptide, antiplatelet agents and glycated hemoglobin significantly improved classification performance for CVD using net reclassification improvement (0.60, 95% CI: 0.21–1.00) and the integrated discrimination improvement (0.02, 95% CI: 0.00–0.05). Conclusions: The V/S ratio measured by dual bioelectrical impedance analyzer is an independent predictor of CVD in patients with type 2 diabetes. [ABSTRACT FROM AUTHOR]

BACKGROUND: Methylmercury (MeHg) exposure is associated with adverse effects on neurodevelopment and cardiovascular health. Previous work indicates most MeHg is from marine fish sold in the commercial market, but does not fully resolve supply regions globally. This information is critical for linking changes in environmental MeHg levels to human exposure in the U.S. population. OBJECTIVES: We used available data to estimate the geographic origins of seafood consumed in the United States (major ocean basins, coastal fisheries, aquaculture, freshwater) and how shifts in edible supply affected MeHg exposures between 2000-2002 and 2010-2012. METHODS: Source regions for edible seafood and MeHg exposure in the United States were characterized from national and international landing, export and import data from the Food and Agricultural Organization of the United Nations and the U.S. National Marine Fisheries Service. RESULTS: Our analysis suggests 37% of U.S. population-wide MeHg exposure is from mainly domestic coastal systems and 45% from open ocean ecosystems. We estimate that the Pacific Ocean alone supplies more than half of total MeHg exposure. Aquaculture and freshwater fisheries together account for an estimated 18% of total MeHg intake. Shifts in seafood types and supply regions between 2000-2002 and 2010-2012 reflect changes in consumer preferences (e.g., away from canned light meat tuna), global ecosystem shifts (e.g., northern migration of cod stocks), and increasing supply from aquaculture (e.g., shrimp and salmon). CONCLUSION: Our findings indicate global actions that reduce anthropogenic Hg emissions will be beneficial for U.S. seafood consumers because open ocean ecosystems supply a large fraction of their MeHg exposure. However, our estimates suggest that domestic actions can provide the greatest benefit for coastal seafood consumers. [ABSTRACT FROM AUTHOR]

Conotruncal heart defects (CTDs) represent a group of severe and complicated congenital cardiovascular malformations and require opportune clinical interventions once diagnosed. Occurrence of CTD is related to the functional abnormality of the second heart field (SHF), and variants of genes which regulate the development of the second heart field have been recognized as the main genetic factors leading to CTDs. Previous studies indicated that transcriptional complex SIX1/EYA1 may contribute to SHF development, and SIX1/EYA1 knockout mice exhibited a series of conotruncal malformations. Here, we recruited and sequenced 600 Chinese conotruncal heart defect patients and 300 controls. We screened out one novel SIX1 mutation (SIX1-K134R) and four EYA1 rare mutations (EYA1-A227T, EYA1-R296H, EYA1-Q397R, EYA1-G426S), all variants were present only in the case cohort, and the mutated sites were highly conserved. We then analyzed mutations by software including Sift, PolyPhen-2, PROVEAN, Mutation Taster, HOPE, and SWISS-PdbViewer. The results showed that the mutations had varying degrees of pathogenic risk, protein properties, spatial conformations, and domain functions which might be altered or influenced. Through biological and in silico analyses, our study suggests an association between SIX1/EYA1 mutations and cardiovascular malformations, SIX1/EYA1 mutations might be partially responsible for CTDs. [ABSTRACT FROM AUTHOR]

The effect of occupational exposure to industrial air pollution on myocardial enzymes of workers of textile, sugar and fertilizer industry and oil refinery was studied. A total of 500 male volunteers of industrial workers and non-industrial individuals with and without the history of cardiovascular disease (CVD) were included in the study. The pollutants released in working areas of selected industries and the levels of myocardial enzymes of the study groups were analyzed. The levels of particulate matter, nitrogen oxide, sulfur dioxide, and carbon monoxide were found to be higher than National Environmental Quality Standards. A significant increase (2-10 folds; P<0.05) was observed in the levels of creatine phosphokinase, creatine kinase-MB, lactate dehydrogenase and serum glutamate oxaloacetate transaminase of workers with and without CVD and non-industrial individuals with CVD. The observed variation in studied parameters of industrial groups without CVD may be attributed to the elevated levels of industrial air pollutants in the industrial area. However, the variation in levels of studied parameters of industrial groups with CVD may be the cumulative effect of cardiovascular abnormalities and industrial pollutants. [ABSTRACT FROM AUTHOR]

Transmembrane 6 superfamily 2 ( TM6SF2 ), a gene identified at the locus 19p12, has been recognized to regulate plasma lipids. Here, we provide an overview of the roles of TM6SF2 as a novel target for plasma lipid regulation. We first review the association of TM6SF2 variant with plasma lipid traits, cardiovascular disease (CVD) and non-alcoholic fatty liver disease (NAFLD). Then, we present an overview about the in vivo validation of TM6SF2 as a regulator of plasma lipid levels using mice, with overexpression or knockdown/knockout of TM6SF2. Thereafter, we discuss the mechanisms underlying TM6SF2 regulation of lipid metabolism involving intestinal cholesterol absorption and hepatic cholesterol biosynthesis and transport. In conclusion, increasing evidence suggests that TM6SF2 may be a major regulator of plasma lipid levels and become a therapeutic target in cardiovascular disease. [ABSTRACT FROM AUTHOR]

In 2008 the Food and Drug Administration introduced a guidance for industry that requires the investigation of cardiovascular outcomes of glucose-lowering medications. Since then, an increasing number of cardiovascular outcome trials have been completed in diabetes patients with high cardiovascular risk for members of the SGLT-2 and DPP4 inhibitors and GLP-1 receptor agonist classes. The trials confirmed cardiovascular safety for all tested anti-hyperglycaemic drugs and, in addition empagliflozin, semaglutide and liraglutide could even reduce cardiovascular risk. The present review summarizes the results of the DEVOTE, CANVAS, EXSCEL and ACE trials that tested cardiovascular safety of Insulin degludec, canagliflozin, once-weekly exenatide and acarbose and were published in 2017. We provide context on these results by comparing them with earlier trials of glucose-lowering drugs and give an outlook on what to expect in coming years. [ABSTRACT FROM AUTHOR]

Numerous studies have evaluated the effects of long-term exposure to ambient air pollution on hypertension. However, little information exists regarding its effects on prehypertension, a very common, but understudied cardiovascular indicator. We evaluated data from 24,845 adults (ages 18–74 years) living in three Northeastern Chinese cities in 2009. Blood pressure (BP) was measured by trained observers using a standardized mercuric-column sphygmomanometer. Three-year (from 2006 to 2008) average concentrations of particles with an aerodynamic diameter ≤10 μm (PM 10 ), sulfur dioxide (SO 2 ), nitrogen dioxides (NO 2 ), and ozone (O 3 ) were calculated using data from monitoring stations. Effects were analyzed using generalized additive models and two-level regression analyses, controlling for covariates. We found positive associations of all pollutants with prehypertension (e.g. odds ratio (OR) was 1.17 (95% confidence interval (CI), 1.09–1.25) per interquartile range (IQR) of PM 10 ) in a fully adjusted model, as compared to normotensive participants. These associations were stronger than associations with hypertension (e.g. OR was 1.03 (95% CI, 1.00, 1.07) per IQR of PM 10 ). We have also found positive associations of all studied pollutants with systolic and diastolic BP: e.g., associations with PM 10 per IQR were 1.24 mmHg (95% CI, 1.03–1.45) for systolic BP and 0.47 mmHg (95% CI, 0.33–0.61) for diastolic BP. Further, we observed that associations with BP were stronger in women and in older participants (systolic BP only). In conclusion, long-term exposure to ambient air pollution was more strongly associated with prehypertension than with hypertension, especially among females and the elderly. Thus, interventions to reduce air pollution are of great significance for preventing future cardiovascular events, particularly among individuals with prehypertension. [ABSTRACT FROM AUTHOR]

Background and Objective Matrix metalloproteinase-8 ( MMP-8) is involved in a wide range of pathologies including periodontitis and cardiovascular diseases ( CVD). The association between periodontitis and CVD has been repeatedly recognized. The aim of the study was to analyze to what extent circulating active MMP-8 ( aMMP-8) is associated with periodontal disease status and oral fluid aMMP-8 levels in otherwise healthy subjects. Material and Methods In a cross-sectional study, aMMP-8 was measured in serum of 59 volunteers, comprising 19 periodontally healthy subjects, 20 patients with gingivitis as well as 20 with periodontitis. All study subjects were characterized regarding aMMP-8 concentrations in different oral fluids as well as clinically and microbiologically with respect to periodontal disease. aMMP-8 levels in gingival crevicular fluid were measured using the enzyme-linked immunosorbent assay. Saliva enzyme levels as well as circulating aMMP-8 were determined by a time-resolved immunofluorometric assay. Both methods utilized the same monoclonal antibodies. Correlation and regression analyses were performed to study the potential association between serum aMMP-8 and oral parameters. Results Oral aMMP-8 levels were significantly higher in patients with periodontitis compared to periodontally healthy or gingivitis subjects. Highest serum aMMP-8 concentration was also found in the periodontitis group. The serum levels correlated significantly with oral aMMP-8 as well as with clinical parameters in a dose-dependent manner. These results were confirmed in a multivariate regression analysis. After adjusting for potential confounders, saliva aMMP-8 concentrations as well as periodontitis severity were significant predictors of serum aMMP-8. Conclusion The associations between circulating aMMP-8 and oral aMMP-8 as well as periodontal findings in a dose-dependent manner may contribute to linking periodontal disease with increased CVDsusceptibility. [ABSTRACT FROM AUTHOR]

Background: Central arterial stiffness has been shown to play a key role in cardiovascular disease. However, evidence regarding such arterial stiffness from various arterial segments in relation to B-type natriuretic peptide (BNP) remains elusive. Methods: A total of 1255 participants (47.8% men; mean age: 62.6 ± 12.3 [SD] years) with preserved left ventricular function (ejection fraction ≥50%) and ≥1 risk factors were consecutively studied. Arterial pulse wave velocity (PWV) by automatic device (VP-2000; Omron Healthcare) for heart-femoral (hf-PWV), brachial-ankle (ba-PWV), and heart-carotid (hc-PWV) segments were obtained and related to BNP concentrations (Abbott Diagnostics, Abbott Park, IL, USA). Results: Subjects in the highest hf-PWV quartile were older and had worse renal function and higher blood pressure (all P < 0.05). Elevated PWV (m/s) was correlated with elevated BNP (pg/ml) (beta coefficient = 19.3, 12.4, 5.9 for hf-PWV, ba-PWV, hc-PWV respectively, all p < 0.05). After accounting for clinical co-variates and left ventricle mass index (LVMI), both hf-PWV and ba-PWV were correlated with higher BNP (beta coefficient = 8.3, 6.4 respectively, P < 0.01 for each). Adding both hf-PWV and ba-PWV to LVMI significantly expanded ROC in predicting abnormal BNP>100 pg/ml (both P < 0.01), but only hf-PWV presented significant integrated discrimination improvement to predict risk for BNP concentrations (0.7%, P = 0.029). Conclusion: A significant segmental PWV associated with biomarker BNP concentrations suggests that arterial stiffness is associated with myocardial damage. [ABSTRACT FROM AUTHOR]

INTRODUCTION Cardiovascular disease risk markers have become more prevalent in childhood. To provide increased understanding of the etiology of this public health issue, we investigated associations between family characteristics with cardiovascular disease risk markers in adolescents from a developing nation. METHODS In this cross-sectional study data for fasting glucose, lipoproteins (LDL-C and HDL-C), triglycerides, and total cholesterol were collected from 991 adolescents aged 10-17 who were recruited from public schools in Londrina city, Southern Brazil. Family history of cardiovascular disease and parental engagement in risk behavior (alcohol consumption and tobacco smoking) were collected using a self-reported parental questionnaire. Socioeconomic status, adolescent physical activity (estimated by Baecke questionnaire), self-reported tobacco and alcohol intake, and somatic maturation (age at peak height velocity) were used as covariates. Logistic regression was used for the main analyses. RESULTS Independent of adolescent lifestyle behaviors, associations (ORadj [95% CI]) were found between: (1) paternal family history of cardiovascular disease with increased likelihood of high adolescent offspring BMI (1.53 [1.01 to 2.32]) and high triglycerides (2.93 [1.04 to 8.27]); (2) maternal family history of cardiovascular disease with heightened odds of high adolescent offspring triglycerides (2.84 [1.02 to 7.91]); (3) maternal cardiovascular disease with higher odds of high fasting glucose (2.16 [1.13 to 4.14]), and (4) maternal smoking with increased odds of high LDL-C (1.78 [1.14 to 2.79]) and high total cholesterol (1.77 [1.01 to 3.10]) in adolescent offspring. CONCLUSION Family history of cardiovascular disease and maternal tobacco smoking are related to increased cardiovascular risk in adolescents, potentially independent of their own lifestyle behaviors. [ABSTRACT FROM AUTHOR]

A systematic review was conducted to assess the association between apical periodontitis ( AP) and cardiovascular disease ( CVD). Studies published from the earliest date available until September 2015 were retrieved from the Medline, PubMed and Embase databases. The included studies reported the results from observational studies and assessed the link between AP and CVD as confirmed by one of the following criteria: diagnosed coronary artery disease, angina pectoris, acute myocardial infarction, stroke or mortality caused by cardiac pathology. The study characteristics were abstracted by independent researchers following the PRISMA standard protocol. NOS criteria were used to rate the quality of the studies, and the GRADE was used for level of evidence evaluation. Nineteen epidemiological studies fulfilled the predetermined inclusion criteria: 10 case-control studies, five cross-sectional studies and four cohort studies. There was considerable heterogeneity amongst the included studies in terms of their study design, population, outcomes of interest and AP evaluation methods. Considering the limited availability and the heterogeneity amongst the studies, meta-analysis was not attempted. Thirteen of the 19 included studies found a significant positive association between apical periodontitis and cardiovascular disease, although in two of them, the significance was present only in univariate analysis. Five studies failed to reveal positive significance, and one study reported a negative association. In conclusion, although most of the published studies found a positive association between apical periodontitis and cardiovascular disease, the quality of the existing evidence is moderate-low and a causal relationship cannot be established. [ABSTRACT FROM AUTHOR]

Background: Apolipoprotein B (apoB) is known to be a more powerful predictor of cardiovascular disease than conventional lipids. We aimed to determine the clinical relevance of a newly developed equation to estimate serum apoB levels based on total cholesterol, HDL cholesterol and triglycerides in patients with high cardiovascular risk. Methods: The occurrence of a major cardiovascular event (MCVE) was assessed using the data from the Treating to New Targets (TNT) and Incremental Decrease in End points through Aggressive Lipid lowering (IDEAL) trials. Results: Pooled analysis of these two data sets showed that both directly-measured apoB (HR per 1-SD (95% CI): 1.16 (1.11--1.21), P < 0.001) and apoB estimated from the eq. (HR per 1-SD (95% CI): 1.14 (1.09--1.19), P < 0.001) were significantly associated with the development of a future MCVE. Prediction of MCVEs by the apoB eq. (C statistic 0.650) was nearly identical to that of directly-measured apoB (0.651). In addition, the net reclassification indices indicated no difference in the prediction of MCVEs between models including the apoB equation and directlymeasured apoB (1% (--1.3--4.0), P = 0.31). Conclusions: Our equation to predict apoB levels showed MCVE risk prediction comparable to directly-measured apoB in high risk patients with previous coronary heart disease. [ABSTRACT FROM AUTHOR]

Several regulators of programmed cell death (PCD) have been identified in plants which encode proteins with putative lipid-binding domains. Among them, VAD1 (Vascular Associated Death) contains a novel protein domain called VASt (VAD1 analog StAR-related lipid transfer) still uncharacterized. The Arabidopsis mutant vad1-1 has been shown to exhibit a lesion mimic phenotype with light-conditional appearance of propagative hypersensitive response-like lesions along the vascular system, associated with defense gene expression and increased resistance to Pseudomonas strains. To test the potential of ectopic expression of VAD1 to influence HR cell death and to elucidate the role of the VASt domain in this function, we performed a structure-function analysis of VAD1 by transient over-expression in Nicotiana benthamiana and by complementation of the mutant vad1-1. We found that (i) overexpression of VAD1 controls negatively the HR cell death and defense expression either transiently in Nicotiana benthamania or in Arabidopsis plants in response to avirulent strains of Pseudomonas syringae, (ii) VAD1 is expressed in multiple subcellular compartments, including the nucleus, and (iii) while the GRAM domain does not modify neither the subcellular localization of VAD1 nor its immunorepressor activity, the domain VASt plays an essential role in both processes. In conclusion, VAD1 acts as a negative regulator of cell death associated with the plant immune response and the VASt domain of this unknown protein plays an essential role in this function, opening the way for the functional analysis of VASt-containing proteins and the characterization of novel mechanisms regulating PCD. [ABSTRACT FROM AUTHOR]

Background: Excess dietary sodium is associated with increased blood pressure (BP). Some drugs are associated with high sodium intake (in particular effervescent tablets), but the cardiovascular risk associated with such high sodium-containing drugs (HSCD) is largely underevaluated. Objectives: To summarize the evidence for a potential cardiovascular risk associated with exposure to HSCD, and to highlight possible risk factors associated with this iatrogenic issue; in general and/or specific populations. Methods: We conducted a systematic review, by searching electronic databases including MEDLINE, EMBASE, Web of Science, CENTRAL and grey literature between 1960 and 2015. We included studies that reported modification of cardiovascular parameters or incidence/prevalence of cardiovascular outcomes, between a group of subjects exposed to HSCD relative to a non-exposed group. The threshold used to identify HSCD was 391 mg/day. We did not consider studies evaluating exposure to sodium as an active ingredient or those focusing on dialysis solutions or enteral/parenteral nutrition. Study quality was assessed using the EPHPP tool. Results: A total of eight studies met our inclusion criteria. Four reported results for short-term exposure to HSCD (≤ 7 days) on BP fluctuations. One study reported an elevation of BP (associated sodium intake: 1,656 mg/day). Four studies evaluated a long-term exposure (≥ 2 years or discontinuation of a chronic treatment). Two studies reported iatrogenic risk. For these studies, drug associated sodium intake was high (> 1,500 mg/day) in patients with comorbidities (in particular, diabetes mellitus and hypertension). Conclusion: Despite numerous study limitations, this systematic review suggests three potential synergistic risk factors for cardiovascular complications after exposure to HSCD: a high sodium intake (≥ 1,500 mg/day), a long duration of exposure, and the presence of comorbidities. Further studies are required to characterize this iatrogenic risk. Trial registration: PROSPERO . [ABSTRACT FROM AUTHOR]

Vitamin D deficiency is typically caused by inadequate cutaneous synthesis secondary to decreased exposure to sunlight. Serum levels of 25-hydroxyvitamin D l <20 ng/ml are diagnostic of vitamin D deficiency. Vitamin D has various cardiovascular pleiotropic effects by activating its nuclear receptor in cardiomyocytes and vascular endothelial cells and by regulating the renin-angiotensin-aldosterone system, adiposity, energy expenditure, and pancreatic cell activity. In humans, vitamin D deficiency is associated with the following: vascular dysfunction; arterial stiffening; left ventricular hypertrophy; and worsened metrics of diabetes, hypertension, and hyperlipidemia. It is also linked with worse cardiovascular morbidity and mortality. However, meta-analyses of vitamin D supplementation trials have failed to show clear improvements in blood pressure, insulin sensitivity, or lipid parameters, thus suggesting that the link between vitamin D deficiency and cardiovascular disease may be an epiphenomenon. Ongoing larger randomized trials will clarify whether monitoring and supplementation of vitamin D play roles in cardiovascular protection. [ABSTRACT FROM AUTHOR]

Calcific disease of the cardiovascular system, including atherosclerotic calcification, medial calcification in diabetes and calcific aortic valve disease, is an important risk factor for many adverse cardiovascular events such as ischemic cardiac events and subsequent mortality. Although cardiovascular calcification has long been considered to be a passive degenerative occurrence, it is now recognized as an active and highly regulated process that involves osteochondrogenic differentiation, apoptosis and extracellular vesicle release. Nonetheless, despite numerous studies on the pathogenesis of cardiovascular calcification, the underlying mechanisms remain poorly understood. High mobility group box 1 (HMGB1), a nuclear protein bound to chromatin in almost all eukaryotic cells, acts as a damage-associated molecular pattern (DAMP) when released into the extracellular space upon cell activation, injury or death. Moreover, HMGB1 also functions as a bone-active cytokine participating in bone remodeling and ectopic calcification pathogenesis. However, studies on the roles of HMGB1 in promoting cardiovascular calcification are limited to date, and the mechanisms involved are still unclear. In this review, we summarize recent studies investigating the mechanism of cardiovascular calcification and discuss multiple roles of HMGB1 in its development. [ABSTRACT FROM AUTHOR]

Background: Although high-density lipoprotein-cholesterol (HDL) level is inversely correlated with cardiovascular events, HDL is also reported to be positively associated with hypertension, which is a known endothelial impairment factor. Since HDL mediates important protective actions on the vascular endothelium by increasing the number of circulating endothelial progenitor cells (CD34-positive cells), the level of circulating CD34-positive cells should influence the association between HDL and hypertension. Methods: To investigate the association between HDL and hypertension in relation to the level of circulating CD34-positive cells, we conducted a cross-sectional study of 477 elderly men aged 60-69 years who participated in general health checkup. Results: HDL was found to be significantly positively associated with hypertension in subjects with a high level of circulating CD34-positive cells, while no significant association was observed for subjects with low circulating CD34- positive cells. Known cardiovascular risk factors adjusted odds (ORs) and 95% confidence intervals (CIs) of hypertension for increments of one standard deviation (SD) in HDL (13.8 mg/dL) were 1.44 (1.06, 1.96) for subjects with a high level of circulating CD34-positive cells and 0.87 (0.63, 1.19) for subjects with low circulating CD34- positive cells. We also revealed a significant association between HDL level and CD34-positive cell level on hypertension, with fully adjusted p values for the effect of this interaction on hypertension at 0.022. Conclusions: Independent of known cardiovascular risk factors, HDL was found to be positively associated with hypertension in subjects with a high level of circulating CD34-positive cells but not for subjects with low circulating CD34-positive cells. [ABSTRACT FROM AUTHOR]

Background: Dietary habits are major contributors to coronary heart disease, stroke, and diabetes. However, comprehensive evaluation of etiologic effects of dietary factors on cardiometabolic outcomes, their quantitative effects, and corresponding optimal intakes are not well-established. Objective: To systematically review the evidence for effects of dietary factors on cardiometabolic diseases, including comprehensively assess evidence for causality; estimate magnitudes of etiologic effects; evaluate heterogeneity and potential for bias in these etiologic effects; and determine optimal population intake levels. Methods: We utilized Bradford-Hill criteria to assess probable or convincing evidence for causal effects of multiple diet-cardiometabolic disease relationships. Etiologic effects were quantified from published or de novo meta-analyses of prospective studies or randomized clinical trials, incorporating standardized units, dose-response estimates, and heterogeneity by age and other characteristics. Potential for bias was assessed in validity analyses. Optimal intakes were determined by levels associated with lowest disease risk. Results: We identified 10 foods and 7 nutrients with evidence for causal cardiometabolic effects, including protective effects of fruits, vegetables, beans/legumes, nuts/seeds, whole grains, fish, yogurt, fiber, seafood omega-3s, polyunsaturated fats, and potassium; and harms of unprocessed red meats, processed meats, sugar-sweetened beverages, glycemic load, trans-fats, and sodium. Proportional etiologic effects declined with age, but did not generally vary by sex. Established optimal population intakes were generally consistent with observed national intakes and major dietary guidelines. In validity analyses, the identified effects of individual dietary components were similar to quantified effects of dietary patterns on cardiovascular risk factors and hard endpoints. Conclusions: These novel findings provide a comprehensive summary of causal evidence, quantitative etiologic effects, heterogeneity, and optimal intakes of major dietary factors for cardiometabolic diseases, informing disease impact estimation and policy planning and priorities. [ABSTRACT FROM AUTHOR]

Major aetiologies of atherosclerotic cardiovascular diseases begin in childhood and atherosclerotic vascular abnormalities can be observed among children and adolescents. Adolescent cohort studies have important advantages because they can observe earlier changes in vascular structure and function. The purpose of the JS High School study (JSHS) is to identify biomarkers predicting or indicating early structural and functional vascular change in adolescents. The JSHS is a prospective cohort study of a Korean adolescent population. The target population of the JSHS was first-graders (aged 14 to17 years) at a high school of South Korea. Enrolment and baseline examinations were conducted in years 2007, 2010, 2011 and 2012. Among the total eligible population of 1115 students, 1071 (96.1%) participated in the study and completed all baseline examinations. Informed consent forms were obtained from each participant and his/her parent or guardian. Baseline examinations include: questionnaires on demographics, health behaviours, medical history, and depression symptoms; fasting blood analysis; anthropometric measurement; body impedance analysis; blood pressure measurement; radial artery tonometry; bone densitometry; pulmonary function tests; and carotid ultrasonography. Participants enrolled from 2007 through 2012 were re-examined after 30 months of follow-up, and those who enrolled in 2012 were re-examined after 24 months of follow-up. The corresponding author may be contacted for potential collaboration and data access. [ABSTRACT FROM AUTHOR]

Myocardial apoptosis play a vital role in pathogenesis of cardiovascular diseases. The intrinsic pathway of apoptosis (mitochondrial apoptosis pathway) and abnormal mitochondrial fission and fusion have a detrimental effect on cells under a variety of intracellular stresses including hypoxia, oxidative stress, drug toxicity or DNA damage and contributes to the development of heart failure ( HF), myocardial infarction ( MI), diabetic cardiomyopathy and ischaemia/reperfusion injury (I/R). Micro RNAs (mi RNAs) are endogenous short non-coding RNAs, which target 3′-untranslated region of mRNA to switch off gene expression. They play crucial roles in regulating complicated cardiac signalling and transcriptional events during cardiac development as well as in diseased condition. In this review, we summarize the molecular mechanism of mitochondrial apoptosis in cardiac cells and influence of mi RNAs on them. Mi RNAs regulate cardiac mitochondrial apoptosis by exert their effects on mitochondrial fission and fusion, reactive oxygen species ( ROS) generation and Ca2+ homeostasis, Bcl-2 family members, and other mitochondrial function proteins. This advancement in understanding mechanism of cardiac cells death provides us new therapy targets for cardiovascular diseases associated with mitochondrial dysfunctions. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases are widely distributed throughout the world. Human parasitic infections are ubiquitous. Tropical parasites are increasingly recognized as causes of cardiovascular diseases. In this review, we address the most frequently reported parasites that directly infect the myocardium, including Trypanosoma cruzi, the protozoal causative agent of American trypanosomiasis (Chagas disease), and Taenia solium, the cestode causative agent of taeniasis and cysticercosis. We also discuss tropical endomyocardial fibrosis, trichinellosis and schistosomiasis. Health systems, attitudes, the perceptions of both patients and physicians as well as socioeconomic factors should all be explored and recognized as crucial factors for improving the control of cardiovascular diseases in the tropics. Clinicians throughout the world must remain aware of imported parasites as potential causes of cardiac diseases. [ABSTRACT FROM AUTHOR]

The mineral bone disorder of CKD, called Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD), has a major role in the etiology and progression of cardiovascular disease in CKD patients. Since the main emphasis in CKD-MBD is on three categories (bone abnormalities, laboratory abnormalities, and vascular calcifications), we have routinely accepted ectopic cardiovascular calcifications as a central risk factor in the pathophysiology of CKD-MBD for cardiac events. However, recent compelling evidence suggests that some CKD-MBD-specific factors other than vascular calcification might contribute to the onset of cardiovascular disease. Most notable is fibroblast growth factor-23 (FGF23), which is thought to be independently associated with cardiac remodeling. Slow progression of cardiac disorders, such as vascular calcification and cardiac remodeling, characterizes cardiac disease due to CKD-MBD. In contrast, fatal arrhythmia may be induced when QT prolongation occurs with CKD-MBD treatment, such as with lower Ca dialysate or the use of calcimimetics. Sudden onset of fatal cardiac events, such as heart failure and sudden cardiac death, due to fatal arrhythmia would be another distinctive phenomenon of CKD-MBD. This may be defined as CKD-MBD-specific cardiac complex syndrome. [ABSTRACT FROM AUTHOR]

Human aging is associated with an increased frequency of somatic mutations in hematopoietic cells. Several of these recurrent mutations, including those in the gene encoding the epigenetic modifier enzyme TET2, promote expansion of the mutant blood cells. This clonal hematopoiesis correlates with an increased risk of atherosclerotic cardiovascular disease. We studied the effects of the expansion of Tet2-mutant cells in atherosclerosis-prone, low-density lipoprotein receptor–deficient (Ldlr–/–) mice. We found that partial bone marrow reconstitution with TET2-deficient cells was sufficient for their clonal expansion and led to a marked increase in atherosclerotic plaque size. TET2-deficient macrophages exhibited an increase in NLRP3 inflammasome–mediated interleukin-1b secretion. An NLRP3 inhibitor showed greater atheroprotective activity in chimeric mice reconstituted with TET2-deficient cells than in nonchimeric mice. These results support the hypothesis that somatic TET2 mutations in blood cells play a causal role in atherosclerosis. [ABSTRACT FROM AUTHOR]

Importance: Based on data from the 1990s, estimated prevalence of obstructive sleep apnea (OSA) in the United States is 10% for mild OSA and 3.8% to 6.5% for moderate to severe OSA; current prevalence may be higher, given the increasing prevalence of obesity. Severe OSA is associated with increased all-cause mortality, cardiovascular disease and cerebrovascular events, diabetes, cognitive impairment, decreased quality of life, and motor vehicle crashes.Objective: To issue a new US Preventive Services Task Force (USPSTF) recommendation on screening for OSA in asymptomatic adults.Evidence Review: The USPSTF reviewed the evidence on the accuracy, benefits, and potential harms of screening for OSA in asymptomatic adults seen in primary care, including those with unrecognized symptoms. The USPSTF also evaluated the evidence on the benefits and harms of treatment of OSA on intermediate and final health outcomes.Findings: The USPSTF found insufficient evidence on screening for or treatment of OSA in asymptomatic adults or adults with unrecognized symptoms. Therefore, the USPSTF was unable to determine the magnitude of the benefits or harms of screening for OSA or whether there is a net benefit or harm to screening.Conclusions and Recommendation: The USPSTF concludes that the current evidence is insufficient to assess the balance of benefits and harms of screening for OSA in asymptomatic adults. (I statement). [ABSTRACT FROM AUTHOR]

Background Hypertension is a major cause of cardiovascular disease. Periodic nationwide surveys are essential for monitoring secular trend of hypertension and its control in population. We assessed prevalence of hypertension and related awareness, treatment and control rates in Chinese adults in 2013–14. Methods A nationally representative survey recruited 174,621 adults aged > 18 years from 31 provinces in mainland China between 2013 and 2014. Population-weighted prevalence of hypertension and related rates of awareness, treatment and control were calculated and compared by age, sex, region and other factors of interest. Results Overall, 27.8% of Chinese adults were hypertensive, with the adjusted prevalence higher in men than in women and increasing steeply with rising age. Of those with hypertension, 31.9% were previously diagnosed, of those diagnosed, 82.9% were treated, and of those treated, 34.6% had their blood pressure properly controlled, resulting in an overall control rates of 9.7% among those with hypertension. Despite similar prevalence, the awareness, treatment and control were much better in urban areas than in rural areas. Among hypertensive individuals, older age, higher levels of education or household income tended to be associated with better awareness, treatment and control rates. During 2013–14, 292 million adults in China had hypertension, representing an absolute increase of 139 million individuals since year 2002. Conclusions Among Chinese adults, more than one forth had hypertension and the prevalence has increased significantly during recent decades. Despite huge efforts, the levels of awareness, treatment and control rates of hypertension remain extremely low, foreshadowing substantial unnecessary disease burden. [ABSTRACT FROM AUTHOR]

The oral microbiome is established within a few minutes after birth and consists of stable multi-species communities that engage in a dynamic equilibrium with the host immune system. Dental caries, endodontic infections and periodontal diseases are bacterially driven diseases that are caused by dysbiotic microbiomes. Over a century ago, the focal infection theory implicated these infections in the aetiology of several systemic diseases, ranging from arthritis to neurodegenerative diseases. However, a lack of concrete evidence, combined with the urgency with which clinicians embraced this approach without regard for appropriate case selection, led to its demise within 30 years. In the last decade of the 20th century, the concept of periodontal medicine was introduced to explain the correlations that were being observed between periodontitis and cardiovascular disease, rheumatoid arthritis, Alzheimer's disease, pulmonary disease, pre-term delivery of low birth weight infants and metabolic disease. It was proposed that periodontal pathobionts played a causal role in the initiating or exacerbating certain diseases either by direct invasion or by stimulating a florid immune-inflammatory response that extended into the systemic circulation. This review will examine the strength of current evidence in establishing a causal link between oral pathobionts and systemic disease. [ABSTRACT FROM AUTHOR]

Infiltrative hepatocellular carcinoma (HCC) can be overlooked on imaging. Radiologists should have a high index of suspicion for this entity in patients with chronic liver disease. Careful evaluation of the portal vein may help the radiologist diagnose infiltrative HCC, due to the high association (68%-100%) of portal vein tumor thrombus with this condition. This article will review the imaging findings of infiltrative HCC, particularly its association with portal vein thrombus, and describe imaging pitfalls and mimickers. [ABSTRACT FROM AUTHOR]