BACKGROUND: Smoke‐free legislation has been associated with reductions in secondhand smoke exposure and cardiovascular disease. However, it remains unknown whether smoke‐free policies are associated with reductions in blood pressure (BP). METHODS AND RESULTS: Longitudinal data from 2606 nonsmoking adult participants of the CARDIA (Coronary Artery Risk Development in Young Adults) Study (1995–2011) were linked to state, county, and local‐level 100% smoke‐free policies in bars, restaurants, and/or nonhospitality workplaces based on participants' census tract of residence. Mixed‐effects models estimated associations of policies with BP and hypertension trajectories over 15 years of follow‐up. Fixed‐effects regression estimated associations of smoke‐free policies with within‐person changes in systolic and diastolic BP and hypertension. Models were adjusted for sociodemographic, health‐related, and policy/geographic covariates. Smoke‐free policies were associated with between‐person differences and within‐person changes in systolic BP. Participants living in areas with smoke‐free policies had lower systolic BP on average at the end of follow‐up compared with those in areas without policies (adjusted predicted mean differences [in mm Hg]: restaurant: −1.14 [95% confidence interval: −2.15, −0.12]; bar: −1.52 [−2.48, −0.57]; workplace: −1.41 [−2.32, −0.50]). Smoke‐free policies in restaurants and bars were associated with mean within‐person reductions in systolic BP of −0.85 (−1.61, −0.09) and −1.08 (−1.82, −0.34), respectively. Only restaurant policies were associated with a significant within‐person reduction in diastolic BP, of −0.58 (−1.15, −0.01). CONCLUSIONS: While the magnitude of associations was small at the individual level, results suggest a potential mechanism through which reductions in secondhand smoke because of smoke‐free policies may improve population‐level cardiovascular health.
BACKGROUND: Smoke-free legislation has been associated with lower rates of cardiovascular disease hospital admissions in ecologic studies. However, prior studies lacked detailed information on individual-level factors (e.g. socio-demographic and clinical characteristics) that could potentially confound associations. Our objective was to estimate associations of smoke-free policies with incident cardiovascular disease in a longitudinal cohort after controlling for socio-demographics, cardiovascular disease risk factors, and policy covariates. METHODS: Longitudinal data from 3,783 black and white adults in the Coronary Artery Risk Development in Young Adults (CARDIA) study (1995-2015) were linked to state, county and local 100% smoke-free policies in bars, restaurants, and non-hospitality workplaces by census tract. Extended Cox regression estimated hazard ratios (HRs) of incident cardiovascular disease associated with time-dependent smoke-free policy exposures. Models were adjusted for socio-demographic characteristics, cardiovascular disease risk factors, state cigarette tax, participant-reported presence of a smoking ban at their workplace, field center, and metropolitan statistical area poverty. RESULTS: During a median follow-up of 20 years (68,332 total person-years), 172 participants had an incident cardiovascular disease event (2.5 per 1,000 person-years). Over the follow-up period, 80% of participants lived in areas with smoke-free policies in restaurants, 67% in bars, and 65% in non-hospitality workplaces. In fully adjusted models, participants living in an area with a restaurant, bar, or workplace smoke-free policy had lower risk of incident cardiovascular disease compared to those in areas without smoke-free policies (HR: 0.75, 95% CI: 0.49, 1.15; HR: 0.76, 95% CI: 0.47, 1.24; HR: 0.54, 95% CI: 0.34, 0.86, respectively; HR 0.58, 95% CI: 0.33, 1.00 for living in an area with all 3 types of policies compared to none). The estimated preventive fraction was 25% for restaurant policies, 24% for bar ...
BACKGROUND: The relationship of coronary artery calcium (CAC) with adverse cardiac remodeling is not well established. To study the association of CAC in middle age and change in CAC from early adulthood to middle age with left ventricular (LV) function. METHODS: CAC score was measured by computed tomography at CARDIA study year-15 (Y15) and at Y25 examinations in 3,043 and 3,189 participants, respectively. CAC score was assessed as a continuous variable and log-transformed to account for nonlinearity. Change in CAC from Y15 to Y25 was evaluated as the absolute difference of log-transformed CAC from Y15 to Y25. LV structure and function were evaluated by echocardiography at Y25. RESULTS: At Y25, mean age was 50.1±3.6 yr, 56.6% women, 52.4% black. In the multivariable analysis at Y25, higher CAC was related to higher LV mass (β=1.218, adjusted-p=0.007), higher LV end-diastolic volume (β=0.811, adjusted-p=0.007), higher LV end-systolic volume (β=0.350, adjusted-p=0.048), higher LA volume (β=0.214, adjusted-p=0.009), and higher E/e' ratio (β=0.059, adjusted-p= 0.014). CAC was measured at both Y15 and Y25 in 2,449 individuals. Higher change in CAC score during follow-up was independently related to higher LV mass index in blacks (β=4.789, adjusted-p<0.001), but not in whites (β=1.051, adjusted-p=0.283). CONCLUSIONS: Higher CAC in middle age is associated to higher LV mass and volumes, and worse LV diastolic function. Being free of CAC from young adulthood to middle age correlates to better LV function at middle age. Higher change in CAC score during follow-up is independently related to higher LV mass index in blacks.
Objective: There are currently five widely used definition of prediabetes. We compared the ability of these to predict 5-year conversion to diabetes and investigated whether there were other cut-points identifying risk of progression to diabetes that may be more useful. Research design and methods: We conducted an individual participant meta-analysis using longitudinal data included in the Obesity, Diabetes and Cardiovascular Disease Collaboration. Cox regression models were used to obtain study-specific HRs for incident diabetes associated with each prediabetes definition. Harrell's C-statistics were used to estimate how well each prediabetes definition discriminated 5-year risk of diabetes. Spline and receiver operating characteristic curve (ROC) analyses were used to identify alternative cut-points. Results: Sixteen studies, with 76 513 participants and 8208 incident diabetes cases, were available. Compared with normoglycemia, current prediabetes definitions were associated with four to eight times higher diabetes risk (HRs (95% CIs): 3.78 (3.11 to 4.60) to 8.36 (4.88 to 14.33)) and all definitions discriminated 5-year diabetes risk with good accuracy (C-statistics 0.79-0.81). Cut-points identified through spline analysis were fasting plasma glucose (FPG) 5.1 mmol/L and glycated hemoglobin (HbA1c) 5.0% (31 mmol/mol) and cut-points identified through ROC analysis were FPG 5.6 mmol/L, 2-hour postload glucose 7.0 mmol/L and HbA1c 5.6% (38 mmol/mol). Conclusions: In terms of identifying individuals at greatest risk of developing diabetes within 5 years, using prediabetes definitions that have lower values produced non-significant gain. Therefore, deciding which definition to use will ultimately depend on the goal for identifying individuals at risk of diabetes. ; This work was supported by the National Health and Medical Research Council of Australia (grant number 1103242). The Atherosclerosis Risk in Communities study has been funded in whole or in part with Federal funds from the National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, under contract nos. HHSN268201700001I, HHSN268201700002I, HHSN268201700003I, HHSN268201700005I, HHSN268201700004I. ES was supported by NIH/NIDDK grant K24DK106414. The Coronary Artery Risk Development in Young Adults Study (CARDIA) is supported by contracts HHSN2682018000031, HHSN2682018000041, HHSN2682018000051, HHSN2682018000061 and HHSN2682018000071 from the National Heart, Lung, and Blood Institute (NHLBI). The Jackson Heart Study (JHS) is supported and conducted in collaboration with Jackson State University (HHSN268201800013I), Tougaloo College (HHSN268201800014I), the Mississippi State Department of Health (HHSN268201800015I) and the University of Mississippi Medical Center (HHSN268201800010I, HHSN268201800011I and HHSN268201800012I) contracts from the National Heart, Lung, and Blood Institute (NHLBI) and the National Institute for Minority Health and Health Disparities (NIMHD). The Melbourne Collaborative Cohort Study (MCCS) recruitment was funded by VicHealth and Cancer Council Victoria. The MCCS was further augmented by Australian National Health and Medical Research Council grants 209057, 396414 and 1074383 and by infrastructure provided by Cancer Council Victoria. Cases and their vital status were ascertained through the Victorian Cancer Registry and the Australian Institute of Health and Welfare, including the National Death Index and the Australian Cancer Database. The Multi-Ethnic Study of Atherosclerosis was supported by contracts HHSN268201500003I, N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168 and N01-HC-95169 from the National Heart, Lung, and Blood Institute and by grants UL1-TR-000040 and UL1-TR-001079 from NCRR. The Population Study of Women in Gothenburg (PSWG) was financed in part by grants from the Swedish state under the agreement between the Swedish government and the county councils, the ALF-agreement ALFGBG-720201. VIVA Study received grants 95/0029 and 06/90270 from the Instituto de Salud Carlos III, Spain. ; Sí
Publisher's version (útgefin grein). ; Heavy alcohol consumption is an established risk factor for hypertension; the mechanism by which alcohol consumption impact blood pressure (BP) regulation remains unknown. We hypothesized that a genome-wide association study accounting for gene-alcohol consumption interaction for BP might identify additional BP loci and contribute to the understanding of alcohol-related BP regulation. We conducted a large two-stage investigation incorporating joint testing of main genetic effects and single nucleotide variant (SNV)-alcohol consumption interactions. In Stage 1, genome-wide discovery meta-analyses in ≈131K individuals across several ancestry groups yielded 3, 514 SNVs (245 loci) with suggestive evidence of association (P < 1.0 × 10-5). In Stage 2, these SNVs were tested for independent external replication in ≈440K individuals across multiple ancestries. We identified and replicated (at Bonferroni correction threshold) five novel BP loci (380 SNVs in 21 genes) and 49 previously reported BP loci (2, 159 SNVs in 109 genes) in European ancestry, and in multi-ancestry meta-analyses (P < 5.0 × 10-8). For African ancestry samples, we detected 18 potentially novel BP loci (P < 5.0 × 10-8) in Stage 1 that warrant further replication. Additionally, correlated meta-analysis identified eight novel BP loci (11 genes). Several genes in these loci (e.g., PINX1, GATA4, BLK, FTO and GABBR2) have been previously reported to be associated with alcohol consumption. These findings provide insights into the role of alcohol consumption in the genetic architecture of hypertension. ; The following authors declare commercial private and/or governmental affiliations: Bruce M. Psaty (BMP) serves on the DSMB of a clinical trial funded by Zoll Lifecor and on the Steering Committee of the Yale Open Data Access Project funded by Johnson & Johnson. Barbara V. Howard (BVH) has a contract from National Heart, Lung, and Blood Institute (NHLBI). Brenda W.J.H. Penninx (BWJHP) has received research funding (non-related to the work reported here) from Jansen Research and Boehringer Ingelheim. Mike A. Nalls (MAN) is supported by a consulting contract between Data Tecnica International LLC and the National Institute on Aging (NIA), National Institutes of Health (NIH), Bethesda, MD, USA. MAN also consults for Illumina Inc., the Michael J. Fox Foundation, and the University of California Healthcare. MAN also has commercial affiliation with Data Tecnica International, Glen Echo, MD, USA. Mark J. Caulfield (MJC) has commercial affiliation and is Chief Scientist for Genomics England, a UK government company. Oscar H Franco (OHF) is supported by grants from Metagenics (on women's health and epigenetics) and from Nestlé (on child health). Peter S. Sever (PSS) is financial supported from several pharmaceutical companies which manufacture either blood pressure lowering or lipid lowering agents, or both, and consultancy fees. Paul W. Franks (PWF) has been a paid consultant in the design of a personalized nutrition trial (PREDICT) as part of a private-public partnership at Kings College London, UK, and has received research support from several pharmaceutical companies as part of European Union Innovative Medicines Initiative (IMI) projects. Fimlab LTD provided support in the form of salaries for author Terho Lehtimäki (TL) but did not have any additional role in the study design to publish, or preparation of the manuscript. Gen‐info Ltd provided support in the form of salaries for author Ozren Polašek (OP) but did not have any additional role in the study design to publish, or preparation of the manuscript. The specific roles of these authors are articulated in the 'author contributions' section. There are no patents, products in development, or marked products to declare. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. ; Peer Reviewed