With one fifth of the world's total population, China's prevention and control of cardiovascular disease (CVD) may affect the success of worldwide efforts to achieve sustainable CVD reduction. To understand China's current cardiovascular epidemic, requires awareness of the economic development in the past decades. The rapid economic transformations (industrialization, marketization, urbanization, globalization, and informationalization) contributed to the aging demography, unhealthy lifestyles, and environmental changes. The later have predisposed to increasing cardiovascular risk factors and the CVD pandemic. Rising CVD rates have had a major economic impact, which has challenged the health care system and the whole society. With recognition of the importance of health, initial political steps and national actions have been taken to address the CVD epidemic. Looking to the future, we recommend that four priorities should be taken: pursue multi-sectorial government and non-government strategies targeting the underlying causes of CVD (the "whole-of-government and whole-of-society" policy); give priority to prevention; reform the health care system to fit the nature of noncommunicable diseases; and conduct research for evidence-based, low-cost, simple, sustainable, and scalable interventions. By pursuing the four priorities, the pandemic of CVD and other major NCDs in China will be reversed and the global sustainable development goal achieved.
AIMS: B-type natriuretic peptide (BNP) and C-reactive protein (CRP) predict atrial fibrillation (AF) risk. However, their risk stratification abilities in the broad community remain uncertain. We sought to improve risk stratification for AF using biomarker information. METHODS AND RESULTS: We ascertained AF incidence in 18 556 Whites and African Americans from the Atherosclerosis Risk in Communities Study (ARIC, n=10 675), Cardiovascular Health Study (CHS, n = 5043), and Framingham Heart Study (FHS, n = 2838), followed for 5 years (prediction horizon). We added BNP (ARIC/CHS: N-terminal pro-B-type natriuretic peptide; FHS: BNP), CRP, or both to a previously reported AF risk score, and assessed model calibration and predictive ability [C-statistic, integrated discrimination improvement (IDI), and net reclassification improvement (NRI)]. We replicated models in two independent European cohorts: Age, Gene/Environment Susceptibility Reykjavik Study (AGES), n = 4467; Rotterdam Study (RS), n = 3203. B-type natriuretic peptide and CRP were significantly associated with AF incidence (n = 1186): hazard ratio per 1-SD ln-transformed biomarker 1.66 [95% confidence interval (CI), 1.56-1.76], P < 0.0001 and 1.18 (95% CI, 1.11-1.25), P < 0.0001, respectively. Model calibration was sufficient (BNP, chi(2) = 17.0; CRP, chi(2) = 10.5; BNP and CRP, chi(2) = 13.1). B-type natriuretic peptide improved the C-statistic from 0.765 to 0.790, yielded an IDI of 0.027 (95% CI, 0.022-0.032), a relative IDI of 41.5%, and a continuous NRI of 0.389 (95% CI, 0.322-0.455). The predictive ability of CRP was limited (C-statistic increment 0.003). B-type natriuretic peptide consistently improved prediction in AGES and RS. CONCLUSION: B-type natriuretic peptide, not CRP, substantially improved AF risk prediction beyond clinical factors in an independently replicated, heterogeneous population. B-type natriuretic peptide may serve as a benchmark to evaluate novel putative AF risk biomarkers. Cardiology 2014. This work is written by (a) US Government employee(s) and is in the public domain in the US.
Lack of social integration predicts coronary heart disease mortality in prospective studies; however, the biological pathways that may be responsible are poorly understood. The specific aims of this study were to examine whether social networks are associated with serum concentrations of the inflammatory markers interleukin-6 (IL-6), C-reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1) and monocyte chemoattractant protein-1 (MCP-1). Participants in the Framingham Study attending examinations from 1998 to 2001 (n=3267) were eligible for inclusion in the study. Social networks were assessed using the Berkman–Syme Social Network Index (SNI). Concentrations of IL-6, CRP, sICAM-1 and MCP-1 were measured in fasting serum samples. Multivariable linear regression analyses were used to assess the association of social networks with inflammatory markers adjusting for potential confounders including age, smoking, blood pressure, total:HDL cholesterol ratio, body mass index, lipid-lowering and antihypertensive medication, diabetes, cardiovascular disease, depression and socioeconomic status. Results found that the SNI was significantly inversely associated with IL-6 in men (p=0·03) after adjusting for potential confounders. In age-adjusted analyses, social networks also were significantly inversely associated with IL-6 for women (p=0·03) and were marginally to modestly associated with CRP and sICAM-1 for men (p=0·08 and 0·02, respectively), but these associations were not significant in the multivariate analyses. In conclusion, social networks were found to be inversely associated with interleukin-6 levels in men. The possibility that inflammatory markers may be potential mediators between social integration and coronary heart disease merits further investigation.
Objective: Smoking is a well-known cardiovascular risk factor associated with weight loss. We aimed to evaluate the association between smoking, serum leptin levels, and abdominal fat.Design: Cross-sectionalSetting: Data from examinations 2 or 3 (2002-2005) of the Multi-Ethnic Study of Atherosclerosis (MESA)Participants: 1,875 asymptomatic, community-dwelling adultsMain Outcomes Measures: We used multivariable linear regression models to assess the race/ethnicity-specific associations between smoking, serum loge-leptin levels, and computed tomography ascertained abdominal fat. Results were adjusted for demographic and relevant clinical covariates.Results: Participants (mean age 64.5±9.6 years; 50.6% women; 42.2% former, 11.4% current smokers) were White (40.1%), Hispanic (25.8%), African American (21.1%), and Chinese (13.0%). Overall, median (25th – 75th percentile) leptin levels were significantly lower among current (11.14 ng/mL; 4.13 – 26.18) and former smokers (11.68 ng/mL; 4.72 – 27.57), as compared with never smokers (15.61 ng/mL; 3.05 – 30.12) (P<.001). The difference in median leptin levels between current and never smokers were significantly higher for Hispanics (Δ9.64 ng/mL) and African Americans (Δ8.81 ng/mL) than Whites (Δ2.10 ng/mL) and Chinese (Δ4.70 ng/mL) (P<.001). After adjustment for total abdominal fat, loge- leptin levels remained lower for former (-.14 [-.22 – -.07]) and current (-.17 [-.28 – -.05]) smokers, compared with never smokers. Results differed by race/ethnicity, with significantly lower loge-leptin levels observed only among current and former African Americans and Hispanic smokers, compared with their never smoker counterparts. (Ps for interaction <.05)Conclusions: Among smokers, leptin levels significantly vary by race/ethnicity. Former and current smoking are associated with lower leptin levels, although this may be restricted to Hispanics and African Americans. Ethn Dis. 2018;28(4):531-538; doi:10.18865/ed.28.4.531
Importance Understanding the major health problems in the United States and how they are changing over time is critical for informing national health policy. Objectives To measure the burden of diseases, injuries, and leading risk factors in the United States from 1990 to 2010 and to compare these measurements with those of the 34 countries in the Organisation for Economic Co-operation and Development (OECD) countries. Design We used the systematic analysis of descriptive epidemiology of 291 diseases and injuries, 1160 sequelae of these diseases and injuries, and 67 risk factors or clusters of risk factors from 1990 to 2010 for 187 countries developed for the Global Burden of Disease 2010 Study to describe the health status of the United States and to compare US health outcomes with those of 34 OECD countries. Years of life lost due to premature mortality (YLLs) were computed by multiplying the number of deaths at each age by a reference life expectancy at that age. Years lived with disability (YLDs) were calculated by multiplying prevalence (based on systematic reviews) by the disability weight (based on population-based surveys) for each sequela; disability in this study refers to any short- or long-term loss of health. Disability-adjusted life-years (DALYs) were estimated as the sum of YLDs and YLLs. Deaths and DALYs related to risk factors were based on systematic reviews and meta-analyses of exposure data and relative risks for risk-outcome pairs. Healthy life expectancy (HALE) was used to summarize overall population health, accounting for both length of life and levels of ill health experienced at different ages. Results US life expectancy for both sexes combined increased from 75.2 years in 1990 to 78.2 years in 2010; during the same period, HALE increased from 65.8 years to 68.1 years. The diseases and injuries with the largest number of YLLs in 2010 were ischemic heart disease, lung cancer, stroke, chronic obstructive pulmonary disease, and road injury. Age-standardized YLL rates increased for Alzheimer disease, drug use disorders, chronic kidney disease, kidney cancer, and falls. The diseases with the largest number of YLDs in 2010 were low back pain, major depressive disorder, other musculoskeletal disorders, neck pain, and anxiety disorders. As the US population has aged, YLDs have comprised a larger share of DALYs than have YLLs. The leading risk factors related to DALYs were dietary risks, tobacco smoking, high body mass index, high blood pressure, high fasting plasma glucose, physical inactivity, and alcohol use. Among 34 OECD countries between 1990 and 2010, the US rank for the age-standardized death rate changed from 18th to 27th, for the age-standardized YLL rate from 23rd to 28th, for the age-standardized YLD rate from 5th to 6th, for life expectancy at birth from 20th to 27th, and for HALE from 14th to 26th. Conclusions and Relevance From 1990 to 2010, the United States made substantial progress in improving health. Life expectancy at birth and HALE increased, all-cause death rates at all ages decreased, and age-specific rates of years lived with disability remained stable. However, morbidity and chronic disability now account for nearly half of the US health burden, and improvements in population health in the United States have not kept pace with advances in population health in other wealthy nations. The United States spends the most per capita on health care across all countries,1,2 lacks universal health coverage, and lags behind other high-income countries for life expectancy3and many other health outcome measures.4 High costs with mediocre population health outcomes at the national level are compounded by marked disparities across communities, socioeconomic groups, and race and ethnicity groups.5,6 Although overall life expectancy has slowly risen, the increase has been slower than for many other high-income countries.3In addition, in some US counties, life expectancy has decreased in the past 2 decades, particularly for women.7,8 Decades of health policy and legislative initiatives have been directed at these challenges; a recent example is the Patient Protection and Affordable Care Act, which is intended to address issues of access, efficiency, and quality of care and to bring greater emphasis to population health outcomes.9 There have also been calls for initiatives to address determinants of poor health outside the health sector including enhanced tobacco control initiatives,10-12 the food supply,13-15 physical environment,16,17 and socioeconomic inequalities.18 With increasing focus on population health outcomes that can be achieved through better public health, multisectoral action, and medical care, it is critical to determine which diseases, injuries, and risk factors are related to the greatest losses of health and how these risk factors and health outcomes are changing over time. The Global Burden of Disease (GBD) framework19 provides a coherent set of concepts, definitions, and methods to do this. The GBD uses multiple metrics to quantify the relationship of diseases, injuries, and risk factors with health outcomes, each providing different perspectives. Burden of disease studies using earlier variants of this approach have been published for the United States for 199620-22 and for Los Angeles County, California.23 In addition, 12 major risk factors have also been compared for 2005.24 In this report, we use the GBD Study 2010 to identify the leading diseases, injuries, and risk factors associated with the burden of disease in the United States, to determine how these health burdens have changed over the last 2 decades, and to compare the United States with other Organisation for Economic Co-operation and Development (OECD) countries.
Background Dysfunction in blood vessel dynamics may contribute to changes in muscle measures. Therefore, we examined associations of vascular health measures with grip strength and gait speed in adults from the Framingham Heart Study.
Methods The cross-sectional study (1998–2001) included participants with 1 measure of grip strength (kg, dynamometer) or gait speed (4-m walk, m/s) and at least 1 measure of aortic stiffness (carotid–femoral pulse wave velocity, brachial pulse pressure, and brachial flow pulsatility index) or brachial artery structure and function (resting flow velocity, resting brachial artery diameter, flow-mediated dilation %, hyperemic brachial blood flow velocity, and mean arterial pressure [MAP]) assessed by tonometry and brachial artery ultrasound. The longitudinal study included participants with ≥1 follow-up measurement of gait speed or grip strength. Multivariable linear regression estimated the association of 1 standard deviation (SD) higher level of each vascular measure with annualized percent change in grip strength and gait speed, adjusting for covariates.
Results In cross-sectional analyses (n = 2 498, age 61 ± 10 years; 56% women), higher resting brachial artery diameter (β ± standard error [SE] per 1 SD: 0.59 ± 0.24, p = .01) and MAP (β ± SE: 0.39 ± 0.17, p = .02) were associated with higher grip strength. Higher brachial pulse pressure (β ± SE: −0.02 ± 0.01, p = .07) was marginally associated with slower gait speed. In longitudinal analyses (n = 2 157), higher brachial pulse pressure (β ± SE: −0.19 ± 0.07, p = .005), was associated with slowing of gait speed but not with grip strength.
Conclusions Higher brachial artery pulse pressure (measure of aortic stiffness) was associated with loss of physical function over ~11 years, although we found no evidence that microvascular function contributed to the relation.
BACKGROUND: A high circulating concentration of interleukin 6 is associated with increased risk of coronary heart disease. Blockade of the interleukin-6 receptor (IL6R) with a monoclonal antibody (tocilizumab) licensed for treatment of rheumatoid arthritis reduces systemic and articular inflammation. However, whether IL6R blockade also reduces risk of coronary heart disease is unknown. METHODS: Applying the mendelian randomisation principle, we used single nucleotide polymorphisms (SNPs) in the gene IL6R to evaluate the likely efficacy and safety of IL6R inhibition for primary prevention of coronary heart disease. We compared genetic findings with the effects of tocilizumab reported in randomised trials in patients with rheumatoid arthritis. FINDINGS: In 40 studies including up to 133,449 individuals, an IL6R SNP (rs7529229) marking a non-synonymous IL6R variant (rs8192284; p.Asp358Ala) was associated with increased circulating log interleukin-6 concentration (increase per allele 9·45%, 95% CI 8·34-10·57) as well as reduced C-reactive protein (decrease per allele 8·35%, 95% CI 7·31-9·38) and fibrinogen concentrations (decrease per allele 0·85%, 95% CI 0·60-1·10). This pattern of effects was consistent with IL6R blockade from infusions of tocilizumab (4-8 mg/kg every 4 weeks) in patients with rheumatoid arthritis studied in randomised trials. In 25,458 coronary heart disease cases and 100,740 controls, the IL6R rs7529229 SNP was associated with a decreased odds of coronary heart disease events (per allele odds ratio 0·95, 95% CI 0·93-0·97, p=1·53×10(-5)). INTERPRETATION: On the basis of genetic evidence in human beings, IL6R signalling seems to have a causal role in development of coronary heart disease. IL6R blockade could provide a novel therapeutic approach to prevention of coronary heart disease that warrants testing in suitably powered randomised trials. Genetic studies in populations could be used more widely to help to validate and prioritise novel drug targets or to repurpose existing agents and targets for new therapeutic uses. FUNDING: UK Medical Research Council; British Heart Foundation; Rosetrees Trust; US National Heart, Lung, and Blood Institute; Du Pont Pharma; Chest, Heart and Stroke Scotland; Wellcome Trust; Coronary Thrombosis Trust; Northwick Park Institute for Medical Research; UCLH/UCL Comprehensive Medical Research Centre; US National Institute on Aging; Academy of Finland; Netherlands Organisation for Health Research and Development; SANCO; Dutch Ministry of Public Health, Welfare and Sports; World Cancer Research Fund; Agentschap NL; European Commission; Swedish Heart-Lung Foundation; Swedish Research Council; Strategic Cardiovascular Programme of the Karolinska Institutet; Stockholm County Council; US National Institute of Neurological Disorders and Stroke; MedStar Health Research Institute; GlaxoSmithKline; Dutch Kidney Foundation; US National Institutes of Health; Netherlands Interuniversity Cardiology Institute of the Netherlands; Diabetes UK; European Union Seventh Framework Programme; National Institute for Healthy Ageing; Cancer Research UK; MacArthur Foundation.