S-EPMC5129303 - Arsenic Exposure and Predicted 10-Year Atherosclerotic Cardiovascular Risk Using the Pooled Cohort Equations in U.S. Hypertensive Adults. - OmicsDI

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Arsenic Exposure and Predicted 10-Year Atherosclerotic Cardiovascular Risk Using the Pooled Cohort Equations in U.S. Hypertensive Adults.

ABSTRACT: This study was to evaluate the association of urine arsenic with predicted 10-year atherosclerotic cardiovascular disease (ASCVD) risk in U.S. adults with hypertension. Cross-sectional analysis was conducted in 1570 hypertensive adults aged 40-79 years in the 2003-2012 National Health and Nutrition Examination Survey (NHANES) with determinations of urine arsenic. Predicted 10-year ASCVD risk was estimated by the Pooled Cohort Equations, developed by the American College of Cardiology/American Heart Association in 2013. For men, after adjustment for sociodemographic factors, urine dilution, ASCVD risk factors and organic arsenic intake from seafood, participants in the highest quartiles of urine arsenic had higher 10-year predicted ASCVD risk than in the lowest quartiles; the increases were 24% (95% confidence interval (CI): 2%, 53%) for total arsenic, 13% (95% CI: 2%, 25%) for dimethylarsinate and 22% (95% CI: 5%, 40%) for total arsenic minus arsenobetaine separately. For women, the corresponding increases were 5% (95% CI: -15%, 29%), 10% (95% CI: -8%, 30%) and 0% (95% CI: -15%, 19%), respectively. Arsenic exposure, even at low levels, may contribute to increased ASCVD risk in men with hypertension. Furthermore, our findings suggest that particular circumstances need urgently to be considered while elucidating cardiovascular effects of low inorganic arsenic levels.

SUBMITTER: Nong Q

PROVIDER: S-EPMC5129303 | biostudies-other | 2016 Nov

REPOSITORIES: biostudies-other

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Arsenic Exposure and Predicted 10-Year Atherosclerotic Cardiovascular Risk Using the Pooled Cohort Equations in U.S. Hypertensive Adults.

Nong Qingjiao Q Zhang Yiyi Y Guallar Eliseo E Zhong Qiuan Q

International journal of environmental research and public health 20161107 11

This study was to evaluate the association of urine arsenic with predicted 10-year atherosclerotic cardiovascular disease (ASCVD) risk in U.S. adults with hypertension. Cross-sectional analysis was conducted in 1570 hypertensive adults aged 40-79 years in the 2003-2012 National Health and Nutrition Examination Survey (NHANES) with determinations of urine arsenic. Predicted 10-year ASCVD risk was estimated by the Pooled Cohort Equations, developed by the American College of Cardiology/American He ...[more]

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Project description:ImportanceThe American College of Cardiology/American Heart Association (ACC/AHA) Pooled Cohort risk equations were developed to estimate atherosclerotic cardiovascular disease (CVD) risk and guide statin initiation.ObjectiveTo assess calibration and discrimination of the Pooled Cohort risk equations in a contemporary US population.Design, setting, and participantsAdults aged 45 to 79 years enrolled in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study between January 2003 and October 2007 and followed up through December 2010. We studied participants for whom atherosclerotic CVD risk may trigger a discussion of statin initiation (those without clinical atherosclerotic CVD or diabetes, low-density lipoprotein cholesterol level between 70 and 189 mg/dL, and not taking statins; n = 10,997).Main outcomes and measuresPredicted risk and observed adjudicated atherosclerotic CVD incidence (nonfatal myocardial infarction, coronary heart disease [CHD] death, nonfatal or fatal stroke) at 5 years because REGARDS participants have not been followed up for 10 years. Additional analyses, limited to Medicare beneficiaries (n = 3333), added atherosclerotic CVD events identified in Medicare claims data.ResultsThere were 338 adjudicated events (192 CHD events, 146 strokes). The observed and predicted 5-year atherosclerotic CVD incidence per 1000 person-years for participants with a 10-year predicted atherosclerotic CVD risk of less than 5% was 1.9 (95% CI, 1.3-2.7) and 1.9, respectively, risk of 5% to less than 7.5% was 4.8 (95% CI, 3.4-6.7) and 4.8, risk of 7.5% to less than 10% was 6.1 (95% CI, 4.4-8.6) and 6.9, and risk of 10% or greater was 12.0 (95% CI, 10.6-13.6) and 15.1 (Hosmer-Lemeshow χ2 = 19.9, P = .01). The C index was 0.72 (95% CI, 0.70-0.75). There were 234 atherosclerotic CVD events (120 CHD events, 114 strokes) among Medicare-linked participants and the observed and predicted 5-year atherosclerotic CVD incidence per 1000 person-years for participants with a predicted risk of less than 7.5% was 5.3 (95% CI, 2.8-10.1) and 4.0, respectively, risk of 7.5% to less than 10% was 7.9 (95% CI, 4.6-13.5) and 6.4, and risk of 10% or greater was 17.4 (95% CI, 15.3-19.8) and 16.4 (Hosmer-Lemeshow χ2 = 5.4, P = .71). The C index was 0.67 (95% CI, 0.64-0.71).Conclusions and relevanceIn this cohort of US adults for whom statin initiation is considered based on the ACC/AHA Pooled Cohort risk equations, observed and predicted 5-year atherosclerotic CVD risks were similar, indicating that these risk equations were well calibrated in the population for which they were designed to be used, and demonstrated moderate to good discrimination.

Project description:ImportanceObesity is a global health challenge and a risk factor for atherosclerotic cardiovascular disease (ASVCD). Performance of the pooled cohort equations (PCE) for ASCVD risk by body mass index (BMI; calculated as weight in kilograms divided by height in meters squared) is unknown.ObjectiveTo assess performance of the PCE across clinical BMI categories.Design, setting, and participantsThis cohort study used pooled individual-level data from 8 community-based, prospective, longitudinal cohort studies with 10-year ASCVD event follow-up from 1996 to 2016. We included all adults ages 40 to 79 years without baseline ASCVD or statin use, resulting in a sample size of 37 311 participants. Data were analyzed from August 2017 to July 2020.ExposuresParticipant BMI category: underweight (<18.5), normal weight (18.5 to <25), overweight (25 to <30), mild obesity (30 to <35), and moderate to severe obesity (≥35).Main outcomes and measuresDiscrimination (Harrell C statistic) and calibration (Nam-D'Agostino χ2 goodness-of-fit test) of the PCE across BMI categories. Improvement in discrimination and net reclassification with addition of BMI, waist circumference, and high-sensitivity C-reactive protein (hsCRP) to the PCE.ResultsAmong 37 311 participants (mean [SD] age, 58.6 [11.8] years; 21 897 [58.7%] women), 380 604 person-years of follow-up were conducted. Mean (SD) baseline BMI was 29.0 (6.2), and 360 individuals (1.0%) were in the underweight category, 9937 individuals (26.6%) were in the normal weight category, 13 601 individuals (36.4%) were in the overweight category, 7783 individuals (20.9%) were in the mild obesity category, and 5630 individuals (15.1%) were in the moderate to severe obesity category. Median (interquartile range [IQR]) 10-year estimated ASCVD risk was 7.1% (2.5%-15.4%), and 3709 individuals (9.9%) developed ASCVD over a median (IQR) 10.8 [8.5-12.6] years. The PCE overestimated ASCVD risk in the overall cohort (estimated/observed [E/O] risk ratio, 1.22; 95% CI, 1.18-1.26) and across all BMI categories except the underweight category. Calibration was better near the clinical decision threshold in all BMI groups but worse among individuals with moderate or severe obesity (E/O risk ratio, 1.36; 95% CI, 1.25-1.47) and among those with the highest estimated ASCVD risk ≥20%. The PCE C statistic overall was 0.760 (95% CI, 0.753-0.767), with lower discrimination in the moderate or severe obesity group (C statistic, 0.742; 95% CI, 0.721-0.763) compared with the normal-range BMI group (C statistic, 0.785; 95% CI, 0.772-0.798). Waist circumference (hazard ratio, 1.07 per 1-SD increase; 95% CI, 1.03-1.11) and hsCRP (hazard ratio, 1.07 per 1-SD increase; 95% CI, 1.05-1.09), but not BMI, were associated with increased ASCVD risk when added to the PCE. However, these factors did not improve model performance (C statistic, 0.760; 95% CI, 0.753-0.767) with or without added metrics.Conclusions and relevanceThese findings suggest that the PCE had acceptable model discrimination and were well calibrated at clinical decision thresholds but overestimated risk of ASCVD for individuals in overweight and obese categories, particularly individuals with high estimated risk. Incorporation of the usual clinical measures of obesity did not improve risk estimation of the PCE. Future research is needed to determine whether incorporation of alternative high-risk obesity markers (eg, weight trajectory or measures of visceral or ectopic fat) into the PCE may improve risk prediction.

Project description:IntroductionCardiovascular disease is a leading cause of mortality in the U.S. Although the risk of cardiovascular disease can be mitigated substantially by following a healthy lifestyle, adhering to a healthy diet and other healthy behaviors are limited by reduced food security. This study aims to determine the association between food security and cardiovascular disease risk.MethodsThree samples from the 2007-2014 National Health and Nutrition Examination Survey were examined: (1) 7,340 non-fasting adults (aged 40-79 years); (2) 13,518 non-fasting adults (aged 20-64 years); and (3) 6,494 fasting adults (aged 20-64 years). Food security was assessed using the U.S. Household Food Security Survey Module, with households categorized as having full, marginal, low, or very low food security. Regressions were conducted in 2018 to test the associations between food security status and odds of ≥20% 10-year cardiovascular disease risk among middle-aged to older adults (OR, 95% CI) and cardiovascular disease risk factors among all adults (β, 95% CI).ResultsCompared with adults with full food security, those with very low food security had higher odds of ≥20% 10-year cardiovascular disease risk (OR=2.36, 95% CI=1.25, 4.46), whereas those with marginal food security had higher systolic blood pressure (β=0.94 mmHg, 95% CI=0.09, 1.80). Compared with adults with full food security, adults with different levels of food security had higher BMIs (marginal: 0.76, 95% CI=0.26, 1.26; low: 0.97, 95% CI=0.34, 1.60; and very low: 1.03, 95% CI=0.44, 1.63) and higher odds of current smoking (marginal: OR=1.43, 95% CI=1.17, 1.75; low: OR=1.47, 95% CI=1.22, 1.77; and very low: OR=1.95, 95% CI=1.60, 2.37).ConclusionsAdults with food insecurity have elevated cardiovascular disease risk factors and excess predicted 10-year cardiovascular disease risk. Substantially improving food security may be an important public health intervention to reduce future cardiovascular disease in the U.S.Population

Project description:BackgroundThe Framingham risk models and pooled cohort equations (PCE) are widely used and advocated in guidelines for predicting 10-year risk of developing coronary heart disease (CHD) and cardiovascular disease (CVD) in the general population. Over the past few decades, these models have been extensively validated within different populations, which provided mounting evidence that local tailoring is often necessary to obtain accurate predictions. The objective is to systematically review and summarize the predictive performance of three widely advocated cardiovascular risk prediction models (Framingham Wilson 1998, Framingham ATP III 2002 and PCE 2013) in men and women separately, to assess the generalizability of performance across different subgroups and geographical regions, and to determine sources of heterogeneity in the findings across studies.MethodsA search was performed in October 2017 to identify studies investigating the predictive performance of the aforementioned models. Studies were included if they externally validated one or more of the original models in the general population for the same outcome as the original model. We assessed risk of bias for each validation and extracted data on population characteristics and model performance. Performance estimates (observed versus expected (OE) ratio and c-statistic) were summarized using a random effects models and sources of heterogeneity were explored with meta-regression.ResultsThe search identified 1585 studies, of which 38 were included, describing a total of 112 external validations. Results indicate that, on average, all models overestimate the 10-year risk of CHD and CVD (pooled OE ratio ranged from 0.58 (95% CI 0.43-0.73; Wilson men) to 0.79 (95% CI 0.60-0.97; ATP III women)). Overestimation was most pronounced for high-risk individuals and European populations. Further, discriminative performance was better in women for all models. There was considerable heterogeneity in the c-statistic between studies, likely due to differences in population characteristics.ConclusionsThe Framingham Wilson, ATP III and PCE discriminate comparably well but all overestimate the risk of developing CVD, especially in higher risk populations. Because the extent of miscalibration substantially varied across settings, we highly recommend that researchers further explore reasons for overprediction and that the models be updated for specific populations.

Project description:Although modern risk estimators, such as the American College of Cardiology/American Heart Association Pooled Cohort Equation, play a central role in the decisions of patients to start pharmacologic therapy to prevent atherosclerotic cardiovascular disease (ASCVD), there is limited evidence to inform expectations for 10-year ASCVD risk reduction from established lifestyle interventions. Using data from the original DASH (Dietary Approaches to Stop Hypertension) trial, we determined the effects of adopting the DASH diet on 10-year ASCVD risk compared with adopting a control or a fruits and vegetables (F/V) diet. The DASH trial included 459 adults aged 22 to 75 years without CVD and not taking antihypertensive or diabetes mellitus medications, who were randomized to controlled feeding of a control diet, an F/V diet, or the DASH diet for 8 weeks. We determined 10-year ASCVD risk with the American College of Cardiology/American Heart Association Pooled Cohort Equation based on blood pressure and lipids measured before and after the 8-week intervention. Compared with the control diet, the DASH and F/V diets changed 10-year ASCVD risk by -10.3% (95% confidence interval [CI] -14.4 to -5.9) and -9.9% (95% CI -14.0 to -5.5) respectively; these effects were more pronounced in women and Black adults. There was no difference between the DASH and F/V diets (-0.4%, 95% CI -6.9 to 6.5). ASCVD reductions attributable to the difference in systolic blood pressure alone were -14.6% (-17.3 to -11.7) with the DASH diet and -7.9% (-10.9 to -4.8) with the F/V diet, a net relative advantage of 7.2% greater relative reduction from DASH compared with F/V. This was offset by the effects on high-density lipoprotein of the DASH diet, which increased 10-year ASCVD by 8.8% (5.5 to 12.3) compared with the more neutral effect of the F/V diet of -1.9% (-5.0 to 1.2). In conclusion, compared with a typical American diet, the DASH and F/V diets reduced 10-year ASCVD risk scores by about 10% over 8 weeks. These findings are informative for counseling patients on both choices of diet and expectations for 10-year ASCVD risk reduction.

Project description:BackgroundSex-specific and race-specific pooled cohort equations (PCEs) are recommended for estimating the 10-year risk of cardiovascular disease, with an absolute risk of more than 7·5% indicating a clinical decision threshold. We compared differences between Black and White individuals in PCE-estimated absolute cardiovascular disease risk across various plausible risk factor combinations with the aim of evaluating if using the PCE might result in different clinical decisions in Black versus White individuals with identical risk profiles.MethodsWe generated in silico patient risk profiles by combining numerical risk factors (age [5-year intervals], total cholesterol [20-mg/dl intervals], HDL cholesterol [5-mg/dl intervals], systolic blood pressure [10-mm Hg intervals]) and binary risk factors (smoking, diabetes, and antihypertensive treatment). We compared PCE-estimated 10-year cardiovascular disease risk in Black versus White individuals with identical risk profiles. We did similar comparisons using eligible participants in the Framingham Heart Study (FHS) third generation cohort and the National Health and Nutrition Examination Survey (NHANES) 2017-18.FindingsFor our in silico analysis, we evaluated 29 515 risk factor combinations for women and 30 565 for men, after excluding profiles that generated 10-year cardiovascular disease risk estimates below 1% or above 30%. There were 6357 risk profiles associated with 10-year cardiovascular disease risk above 7·5% for Black men but not for White men (median risk difference [RD] 6·25%, range 0·15-22·8; median relative risk [RR] 2·40, range 1·02-12·6). There were 391 profiles with 10-year cardiovascular disease risk above 7·5% for White men but not Black men (median RD 2·68%, range 0·07-16·9%; median RR 1·42, range 1·01-3·57). There were 6543 risk profiles associated with 10-year estimated cardiovascular disease risk above 7·5% for Black women but not for White women (median RD 6·14%, range 0·35-26·8%; median RR 2·29, range 1·05-12·6). There were 318 profiles with 10-year cardiovascular disease risk above 7·5% for White women but not Black women (median RD 3·71%, range 0·22-20·1%; median RR 1·66, range 1·03-5·46). For the population-based samples, we calculated the PCE-based 10-year cardiovascular disease risk for 1272 eligible participants (378 women; median age 48 years [IQR 44-52]; 100% White) in the FHS third generation cohort and 550 participants (223 women [36·8% Black] and 327 men [40·4% Black]; median age 61 years [IQR 52-67]) in the NHANES cohort. The population-based samples showed similar risk differences to that of the in silico analyses.InterpretationThe PCE might generate substantially divergent cardiovascular disease risk estimates for Black versus White individuals with identical risk profiles, which could introduce race-related variations in clinical recommendations for cardiovascular disease prevention.FundingUS National Institutes of Health.