102 research outputs found
Association between incarceration and incident cardiovascular disease events: results from the CARDIA cohort study
BACKGROUND: Incarceration has been associated with higher cardiovascular risk, yet data evaluating its association with cardiovascular disease events are limited. The study objective was to evaluate the association between incarceration and incident fatal and non-fatal cardiovascular disease (CVD) events.
METHODS: Black and white adults from the community-based Coronary Artery Risk Development in Young Adult (CARDIA) study (baseline 1985-86, n = 5105) were followed through August 2017. Self-reported incarceration was measured at baseline (1985-1986) and Year 2 (1987-1988), and fatal and non-fatal cardiovascular disease events, including coronary heart disease, stroke, and heart failure, and all-cause mortality, were captured through 2017. Analyses were completed in September 2019. Cumulative CVD incidence rates and Cox proportional hazards were compared overall by incarceration status. An interaction between incarceration and race was identified, so results were also analyzed by sex-race groups.
RESULTS: 351 (6.9%) CARDIA participants reported a history of incarceration. Over 29.0 years mean follow-up, CVD incidence rate was 3.52 per 1000 person-years in participants with a history of incarceration versus 2.12 per 1000 person-years in participants without a history of incarceration (adjusted HR = 1.33 [95% CI, 0.90-1.95]). Among white men, incarceration was associated with higher risk of incident cardiovascular disease (adjusted HR = 3.35 [95% CI, 1.54-7.29) and all-cause mortality (adjusted HR = 2.52 [95% CI, 1.32-4.83]), but these associations were not statistically significant among other sex-race groups after adjustment.
CONCLUSIONS: Incarceration was associated with incident cardiovascular disease rates, but associations were only significant in one sex-race group after multivariable adjustment
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Estimated Impact of Achieving Optimal Cardiovascular Health Among US Adults on Cardiovascular Disease Events
Background Better cardiovascular health (CVH) scores are associated with lower risk of cardiovascular disease (CVD). However, estimates of the potential population-level impact of improving CVH on US CVD event rates are not currently available. Methods and Results Using data from the National Health and Nutrition Examination Survey 2011 to 2016 (n=11 696), we estimated the proportions of US adults in CVH groups. Levels of 7 American Heart Association CVH metrics were scored as ideal (2 points), intermediate (1 point), or poor (0 points), and summed to define overall CVH (low, 0-8 points; moderate, 9-11 points; or high, 12-14 points). Using individual-level data from 7 US community-based cohort studies (n=30 447), we estimated annual incidence rates of major CVD events by levels of CVH. Using the combined data sources, we estimated population attributable fractions of CVD and the number of CVD events that could be prevented annually if all US adults achieved high CVH. High CVH was identified in 7.3% (95% CI, 6.3%-8.3%) of US adults. We estimated that 70.0% (95% CI, 56.5%-79.9%) of CVD events were attributable to low and moderate CVH. If all US adults attained high CVH, we estimated that 2.0 (95% CI, 1.6-2.3) million CVD events could be prevented annually. If all US adults with low CVH attained moderate CVH, we estimated that 1.2 (95% CI, 1.0-1.4) million CVD events could be prevented annually. Conclusions The potential benefits of achieving high CVH in all US adults are considerable, and even a partial improvement in CVH scores would be highly beneficial
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Associations of Blood Pressure and Cholesterol Levels During Young Adulthood With Later Cardiovascular Events.
BackgroundBlood pressure (BP) and cholesterol are major modifiable risk factors for cardiovascular disease (CVD), but effects of exposures during young adulthood on later life CVD risk have not been well quantified.ObjectiveThe authors sought to evaluate the independent associations between young adult exposures to risk factors and later life CVD risk, accounting for later life exposures.MethodsThe authors pooled data from 6 U.S. cohorts with observations spanning the life course from young adulthood to later life, and imputed risk factor trajectories for low-density lipoprotein (LDL) and high-density lipoprotein cholesterols, systolic and diastolic BP starting from age 18 years for every participant. Time-weighted average exposures to each risk factor during young (age 18 to 39 years) and later adulthood (age âĽ40 years) were calculated and linked to subsequent risks of coronary heart disease (CHD), heart failure (HF), or stroke.ResultsA total of 36,030 participants were included. During a median follow-up of 17 years, there were 4,570 CHD, 5,119 HF, and 2,862 stroke events. When young and later adult risk factors were considered jointly in the model, young adult LDL âĽ100 mg/dl (compared with <100 mg/dl) was associated with a 64% increased risk for CHD, independent of later adult exposures. Similarly, young adult SBP âĽ130 mm Hg (compared with <120 mm Hg) was associated with a 37% increased risk for HF, and young adult DBP âĽ80 mm Hg (compared with <80 mm Hg) was associated with a 21% increased risk.ConclusionsCumulative young adult exposures to elevated systolic BP, diastolic BP and LDL were associated with increased CVD risks in later life, independent of later adult exposures
Body mass index trajectories in young adulthood predict nonâ alcoholic fatty liver disease in middle age: The CARDIA cohort study
Background & AimsNonâ alcoholic fatty liver disease is an epidemic. Identifying modifiable risk factors for nonâ alcoholic fatty liver disease development is essential to design effective prevention programmes. We tested whether 25â year patterns of body mass index change are associated with midlife nonâ alcoholic fatty liver disease.MethodsIn all, 4423 participants from Coronary Artery Risk Development in Young Adults, a prospective populationâ based biracial cohort (age 18â 30), underwent body mass index measurement at baseline (1985â 1986) and 3 or more times over 25Ă years. At Year 25, 3115 had liver fat assessed by nonâ contrast computed tomography. Nonâ alcoholic fatty liver disease was defined as liver attenuation â ¤40 Hounsfield Units after exclusions. Latent mixture modelling identified 25â year trajectories in body mass index per cent change (%Ă ) from baseline.ResultsWe identified four distinct trajectories of BMI%Ă : stable (26.2% of cohort, 25â year BMI %Ă Ă =Ă 3.1%), moderate increase (46.0%, BMI%Ă Ă =Ă 21.7%), high increase (20.9%, BMI%Ă Ă =Ă 41.9%) and extreme increase (6.9%, BMI%Ă Ă =Ă 65.9%). Y25 nonâ alcoholic fatty liver disease prevalence was higher in groups with greater BMI %Ă : 4.1%, 9.3%, 13.0%, and 17.6%, respectively (Pâ trend <.0001). In multivariable analyses, participants with increasing BMI%Ă had increasingly greater odds of nonâ alcoholic fatty liver disease compared to the stable group: OR: 3.35 (95% CI: 2.07â 5.42), 7.80 (4.60â 13.23) and 12.68 (6.68â 24.09) for moderate, high and extreme body mass index increase, respectively. Associations were only moderately attenuated when adjusted for baseline or Y25 body mass index.ConclusionsTrajectories of weight gain during young adulthood are associated with greater nonâ alcoholic fatty liver disease prevalence in midlife independent of metabolic covariates and baseline or concurrent body mass index highlighting the importance of weight maintenance throughout adulthood as a target for primary nonâ alcoholic fatty liver disease prevention.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142937/1/liv13603.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/142937/2/liv13603_am.pd
Twentyâ fiveâ year trajectories of insulin resistance and pancreatic Ă²â cell response and diabetes risk in nonalcoholic fatty liver disease
Background & AimsInsulin resistance is a risk marker for nonâ alcoholic fatty liver disease, and a risk factor for liver disease progression. We assessed temporal trajectories of insulin resistance and Ă²â cell response to serum glucose concentration throughout adulthood and their association with diabetes risk in nonâ alcoholic fatty liver disease.MethodsThree thousand and sixty participants from Coronary Artery Risk Development in Young Adults, a prospective biâ racial cohort of adults age 18â 30Ă years at baseline (1985â 1986; Y0) who completed up to 5 exams over 25Ă years and had fasting insulin and glucose measurement were included. At Y25 (2010â 2011), nonâ alcoholic fatty liver disease was assessed by noncontrast computed tomography after exclusion of other liver fat causes. Latent mixture modelling identified 25â year trajectories in homeostatic model assessment insulin resistance and Ă²â cell response homeostatic model assessmentâ Ă².ResultsThree distinct trajectories were identified, separately, for homeostatic model assessment insulin resistance (lowâ stable [47%]; moderateâ increasing [42%]; and highâ increasing [12%]) and homeostatic model assessmentâ Ă² (lowâ decreasing [16%]; moderateâ decreasing [63%]; and highâ decreasing [21%]). Y25 nonâ alcoholic fatty liver disease prevalence was 24.5%. Among nonâ alcoholic fatty liver disease, highâ increasing homeostatic model assessment insulin resistance (referent: lowâ stable) was associated with greater prevalent (OR 95% CIĂ =Ă 8.0, 2.0â 31.9) and incident (ORĂ =Ă 10.5, 2.6â 32.8) diabetes after multivariable adjustment including Y0 or Y25 homeostatic model assessment insulin resistance. In contrast, nonâ alcoholic fatty liver disease participants with lowâ decreasing homeostatic model assessmentâ Ă² (referent: highâ decreasing) had the highest odds of prevalent (ORĂ =Ă 14.1, 3.9â 50.9) and incident (ORĂ =Ă 10.3, 2.7â 39.3) diabetes.ConclusionTrajectories of insulin resistance and Ă²â cell response during young and middle adulthood are robustly associated with diabetes risk in nonâ alcoholic fatty liver disease. Thus, how persons with nonâ alcoholic fatty liver disease develop resistance to insulin provides important information about risk of diabetes in midlife above and beyond degree of insulin resistance at the time of nonâ alcoholic fatty liver disease assessment.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/146427/1/liv13747_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/146427/2/liv13747.pd
Relative contributions of six lifestyle- and health-related exposures to epigenetic aging: The Coronary Artery Risk Development in Young Adults (CARDIA) study
BACKGROUND: DNA methylation-based GrimAge acceleration (GrimAA) is associated with a wide range of age-related health outcomes including cardiovascular disease. Since DNA methylation is modifiable by external and behavioral exposures, it is important to identify which of these exposures may have the strongest contributions to differences in GrimAA, to help guide potential intervention strategies. Here, we assessed the relative contributions of lifestyle- and health-related components, as well as their collective association, to GrimAA.
RESULTS: We included 744 participants (391 men and 353 women) from the Coronary Artery Risk Development in Young Adults (CARDIA) study with blood DNA methylation information at CARDIA Exam Year (Y) 20 (2005-2006, mean age 45.9 years). Six cumulative exposures by Y20 were included in the analysis: total packs of cigarettes, total alcohol consumption, education years, healthy diet score, sleep hours, and physical activity. We used quantile-based g-computation (QGC) and Bayesian kernel machine regression (BKMR) methods to assess the relative contribution of each exposure to a single overall association with GrimAA. We also assessed the collective association of the six components combined with GrimAA. Smoking showed the greatest positive contribution to GrimAA, accounting for 83.5% of overall positive associations of the six exposures with GrimAA (QGC weightâ=â0.835). The posterior inclusion probability (PIP) of smoking also achieved the highest score of 1.0 from BKMR analysis. Healthy diet and education years showed inverse contributions to GrimAA. We observed a U-shaped pattern in the contribution of alcohol consumption to GrimAA. While smoking was the greatest contributor across sex and race subgroups, the relative contributions of other components varied by subgroups.
CONCLUSIONS: Smoking, alcohol consumption, and education showed the highest contributions to GrimAA in our study. Higher amounts of smoking and alcohol consumption were likely to contribute to greater GrimAA, whereas achieved education was likely to contribute to lower GrimAA. Identifying pertinent lifestyle- and health-related exposures in a context of collective components can provide direction for intervention strategies and suggests which components should be the primary focus for promoting younger GrimAA
Association of body mass index in midlife with morbidity burden in older adulthood and longevity
Importance: Abundant evidence links obesity with adverse health consequences. However, controversies persist regarding whether overweight status compared with normal body mass index (BMI; calculated as weight in kilograms divided by height in meters squared) is associated with longer survival and whether this occurs at the expense of greater long-term morbidity and health care expenditures.
Objective: To examine the association of BMI in midlife with morbidity burden, longevity, and health care expenditures in adults 65 years and older.
Design, Setting, and Participants: Prospective cohort study at the Chicago Heart Association Detection Project in Industry, with baseline in-person examination between November 1967 and January 1973 linked with Medicare follow-up between January 1985 and December 2015. Participants included 29âŻ621 adults who were at least age 65 years in follow-up and enrolled in Medicare. Data were analyzed from January 2020 to December 2021.
Exposures: Standard BMI categories.
Main Outcomes and Measures: (1) Morbidity burden at 65 years and older assessed with the Gagne combined comorbidity score (ranging from -2 to 26, with higher score associated with higher mortality), which is a well-validated index based on International Classification of Diseases, Ninth Revision codes for use in administrative data sets; (2) longevity (age at death); and (3) health care costs based on Medicare linkage in older adulthood (aged âĽ65 years).
Results: Among 29âŻ621 participants, mean (SD) age was 40â(12) years, 57.1% were men, and 9.1% were Black; 46.0% had normal BMI, 39.6% were overweight, and 11.9% had classes I and II obesity at baseline. Higher cumulative morbidity burden in older adulthood was observed among those who were overweight (7.22 morbidity-years) and those with classes I and II obesity (9.80) compared with those with a normal BMI (6.10) in midlife (Pâ\u3câ.001). Mean age at death was similar between those who were overweight (82.1 years [95% CI, 81.9-82.2 years]) and those who had normal BMI (82.3 years [95% CI, 82.1-82.5 years]) but shorter in those who with classes I and II obesity (80.8 years [95% CI, 80.5-81.1 years]). The proportion (SE) of life-years lived in older adulthood with Gagne score of at least 1 was 0.38% (0.00%) in those with a normal BMI, 0.41% (0.00%) in those with overweight, and 0.43% (0.01%) in those with classes I and II obesity. Cumulative median per-person health care costs in older adulthood were significantly higher among overweight participants (10âŻ427 to 23âŻ396 [95% CI, 28âŻ319]) participants compared with those with a normal BMI (Pâ\u3câ.001).
Conclusions and Relevance: In this cohort study, overweight in midlife, compared with normal BMI, was associated with higher cumulative burden of morbidity and greater proportion of life lived with morbidity in the context of similar longevity. These findings translated to higher total health care expenditures in older adulthood for those who were overweight in midlife
Association of the degree of adiposity and duration of obesity with measures of cardiac structure and function: The CARDIA study
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/109634/1/oby20865.pd
Life\u27s Simple 7 and Incident Heart Failure: The MultiâEthnic Study of Atherosclerosis
Background The American Heart Association introduced the Life\u27s Simple 7 (LS7) metrics to assess and promote cardiovascular health. We sought to examine the association between the LS7 metrics and incident heart failure (HF) in a multiethnic cohort. Methods and Results We analyzed data from 6506 participants of the MultiâEthnic Study of Atherosclerosis free of cardiovascular disease at baseline. The LS7 metrics (smoking, physical activity, body mass index, diet, blood pressure, total cholesterol, and blood glucose) were graded on a scale of 0 to 2, with 2 indicating âidealâ status, 1 âintermediateâ status, and 0 âpoorâ status. Points were summed, thus the LS7 score ranged from 0 to 14. Cox proportional hazard ratios and incidence rates of HF per 1000 personâyears were calculated. During a median followâup of 12.2 years, 262 (4%) participants developed HF. Incidence of HF decreased as the number of ideal LS7 metrics increased; 5.9 per 1000 personâyears for participants with 0 to 1 ideal metrics and 0.6 per 1000 personâyears for those with 6 to 7 ideal metrics. Compared with inadequate scores (0â8 points), hazard ratios for HF were 0.57 (0.43â0.76) and 0.31 (0.19â0.49) for average (9â10 points) and optimal (11â14 points) scores, respectively. A similar pattern was observed when the results were stratified by 4 racial/ethnic groups: white, Chinese American, black, and Hispanic. Conclusions A lower risk of HF with more favorable LS7 status regardless of race/ethnicity suggests that efforts to achieve ideal cardiovascular health may reduce the burden of HF, a major source of morbidity and mortality
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