Abstract 005: Cumulative Stress Exposure is Associated With Incident Hypertension in African Americans: Findings From the Jackson Heart Study

Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Tanya M Spruill ◽  
Mark J Butler ◽  
S J Thomas ◽  
Gabriel S Tajeu ◽  
Sheila F Castaneda ◽  
...  
Keyword(s):  
Risk Factors ◽  
African Americans ◽  
Chronic Stress ◽  
Cumulative Exposure ◽  
Stress Exposure ◽  
Jackson Heart Study ◽  
Incident Hypertension ◽  
Heart Study ◽  
Increased Risk

Introduction and Hypothesis: Chronic stress has been associated with incident hypertension but evidence is mixed, particularly in African Americans. We tested the hypothesis that higher cumulative exposure to stress would be associated with increased risk of developing hypertension in the Jackson Heart Study (JHS), a prospective study of cardiovascular disease in African Americans. Methods: Analyses included 1,442 JHS participants free of hypertension at baseline (2000-2004) who completed at least 3 annual follow-up telephone interviews. Incident hypertension was defined as systolic blood pressure (SBP) ≥140 mm Hg or diastolic BP (DBP) ≥90 mm Hg or use of antihypertensive medications at Exam 2 (2005-2008) or Exam 3 (2009-2013). A single-item measure of stress (“How much stress have you experienced over the past year?”) was completed during annual interviews, and the percentage of assessments in each measurement interval (i.e., between Exams 1 and 2, between Exams 2 and 3) in which high stress was reported was categorized as No Chronic Stress (0%), Low Chronic Stress (1-33.3%) or High Chronic Stress (>33.3%). Chronic stress exposure in each interval was used to predict incident hypertension at the following exam among participants free of hypertension at the start of the interval using repeated measures Poisson regression models with progressive adjustment for age, sex, years between exams and other relevant risk factors (education, marital status, parental history of hypertension, baseline SBP and DBP, body mass index, diabetes, chronic kidney disease). Results: The 1,442 participants in this analysis contributed data to 1,987 measurement intervals. The mean age was 49±0.26 years and 41% were male. During follow-up (median, 8 years), 44.0% of participants developed hypertension. The percentage of intervals with No, Low and High chronic stress was 62.3%, 9.2% and 28.6%, respectively. Multivariable-adjusted risk ratios (95% confidence interval) for incident hypertension associated with Low (vs. No) and High (vs. No) chronic stress were 1.11 (0.90-1.37) and 1.21 (1.06-1.38), respectively ( P trend=0.005). This association remained statistically significant after further adjustment for baseline stress ( P trend=0.014) and potential behavioral mediators (smoking, alcohol use, physical activity, diet; P trend=0.03). In stratified analyses, the association was present in women ( P trend=0.002), younger participants (<50 years old; P trend=0.007) and those with normal BP at baseline ( P trend=0.001). Conclusion: We found that African Americans reporting higher chronic stress over time are at increased risk of developing hypertension, independent of baseline stress levels and cardiovascular and behavioral risk factors. Future studies should evaluate the use of stress management interventions to support primary prevention of hypertension in this high risk population.

Abstract P488: Discrimination and Hypertension Risk Among African Americans in The Jackson Heart Study

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Allana T Forde ◽  
Mario Sims ◽  
Paul Muntner ◽  
Tené Lewis ◽  
Amanda Onwuka ◽  
...  
Keyword(s):  
Risk Factors ◽  
Blood Pressure ◽  
African Americans ◽  
The United States ◽  
Jackson Heart Study ◽  
Incident Hypertension ◽  
Hypertension Risk ◽  
Heart Study ◽  
Low Levels

Background: African Americans have a higher risk for hypertension compared to other racial or ethnic groups in the United States. One possible explanation for this health disparity is perceived discrimination. Few studies have prospectively examined the association between discrimination and the incidence of hypertension. Methods: We examined the associations of everyday, lifetime, and stress from lifetime discrimination with incident hypertension and whether these associations differed by sex, discrimination attribution (i.e. the main reason for the discrimination event), and coping responses to discrimination among African Americans enrolled in the Jackson Heart Study. Discrimination was self-reported by 1845 African Americans aged 21 to 85 years without hypertension at baseline (2000-2004). Participants completed two follow-up study visits from 2005-2008 and 2009-2013. We used interval-censored Cox regression to estimate associations of discrimination with incident hypertension (antihypertensive medication use; and/or systolic blood pressure ≥ 140 mm Hg and diastolic blood pressure ≥ 90 mm Hg at follow-up visits 2 or 3) after adjustment for confounding variables. Results: Overall, 52% (954 of 1845) of participants developed hypertension over the follow-up period. After adjustment for age, sex, education and hypertension risk factors (body mass index, alcohol use, smoking, diet and physical activity), medium versus low levels of lifetime discrimination (hazard ratio-HR: 1.45, 95% confidence interval-CI: 1.15-1.82) and high versus low levels of lifetime discrimination (HR: 1.35, CI: 1.08-1.68) were associated with a higher incidence of hypertension. High versus low stress from lifetime discrimination was associated with hypertension risk after adjustment for demographics (HR: 1.20, CI: 1.02-1.41), but the association was attenuated after adjustment for hypertension risk factors (HR: 1.14, CI: 0.97-1.35). Lifetime discrimination and stress from discrimination were associated with an increased hypertension risk among females, but not males. No interactions with age, attribution or coping were present for any type of discrimination. Conclusions: Findings from this study support an association between lifetime discrimination and incident hypertension in African Americans.

scholarly journals Discrimination and Hypertension Risk Among African Americans in the Jackson Heart Study

Hypertension ◽  
2020 ◽  
Vol 76 (3) ◽  
pp. 715-723 ◽  
Author(s):  
Allana T. Forde ◽  
Mario Sims ◽  
Paul Muntner ◽  
Tené Lewis ◽  
Amanda Onwuka ◽  
...  
Keyword(s):  
Risk Factors ◽  
African Americans ◽  
The United States ◽  
Hazard Ratio ◽  
Jackson Heart Study ◽  
Incident Hypertension ◽  
Hypertension Risk ◽  
Heart Study ◽  
Low Levels

African Americans have a higher risk of hypertension compared with other racial or ethnic groups in the United States. One possible explanation for this disparity is discrimination. Few studies have examined the association between discrimination and incidence of hypertension. We examined whether everyday discrimination, lifetime discrimination, and stress from discrimination were associated with incident hypertension and whether these associations differed by gender, age, discrimination attribution, and coping responses to discrimination among African Americans in the Jackson Heart Study. Discrimination was self-reported by 1845 African Americans aged 21 to 85 years without hypertension at baseline (2000–2004). Participants completed 2 follow-up study visits from 2005 to 2008 and 2009 to 2013. We used Cox proportional hazards regression to estimate associations of discrimination with incident hypertension. Overall, 52% (n=954) of the participants developed hypertension over the follow-up period. After adjustment for age, gender, socioeconomic status and hypertension risk factors, medium versus low levels of lifetime discrimination (hazard ratio, 1.49 [95% CI, 1.18–1.89]), and high versus low levels of lifetime discrimination (hazard ratio, 1.34 [95% CI, 1.07–1.68]) were associated with a higher incidence of hypertension. No statistically significant interactions with gender, age, attribution, or coping were present. Higher stress from lifetime discrimination was associated with higher hypertension risk after adjustment for demographics (hazard ratio for high versus low, 1.19 [95% CI, 1.01–1.40]), but the association was attenuated after adjustment for hypertension risk factors (hazard ratio, 1.14 [95% CI, 0.97–1.35]). Lifetime discrimination may increase the risk of hypertension in African Americans.

scholarly journals Neighborhood social environment as risk factors to health behavior among African Americans: The Jackson Heart Study

2017 ◽  
Vol 45 ◽  
pp. 199-207 ◽  
Author(s):  
Xu Wang ◽  
Amy H. Auchincloss ◽  
Sharrelle Barber ◽  
Stephanie L. Mayne ◽  
Michael E. Griswold ◽  
...  
Keyword(s):  
Risk Factors ◽  
African Americans ◽  
Health Behavior ◽  
Social Environment ◽  
Jackson Heart Study ◽  
Heart Study

Abstract P053: Diabetes Risk Prediction and Sickle Cell Trait in African Americans From CARDIA and the Jackson Heart Study

Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Mary E Lacy ◽  
Gregory A Wellenius ◽  
Adolfo Correa ◽  
Mercedes R Carnethon ◽  
Robert I Leim ◽  
...  
Keyword(s):  
African Americans ◽  
Risk Prediction ◽  
Sickle Cell ◽  
Prediction Models ◽  
Sickle Cell Trait ◽  
Model Performance ◽  
Jackson Heart Study ◽  
Discriminative Ability ◽  
Heart Study

Introduction: Existing models to predict incident diabetes mellitus (DM) perform better in Whites than African Americans. In models that incorporate hemoglobin A1c (A1C) as a predictor of DM, the difference in model performance by race is more pronounced. In a recent study, we found that A1C was systematically underestimating glycemia in African Americans with sickle cell trait (SCT). Hypothesis: Given the poorer performance of DM prediction models in African Americans than Whites and the impact of SCT on the A1C-glycemia association, we hypothesized that incorporating sickle cell trait into DM prediction models would improve the ability of the model to predict future risk of DM. Methods: We pooled data collected from 2000-2012 on 3,122 African Americans (8.6% with SCT) from the Jackson Heart Study (JHS; n=2,065; mean age=54.71 years) and CARDIA (n=1,057; mean age=44.53). Over 5 years of follow-up in CARDIA and 10 years of follow-up in JHS, 85 CARDIA participants (8.1%) and 342 JHS participants (16.6%) developed DM. Using generalized estimating equations to account for correlation of repeated measures, we compared the discriminative ability and net reclassification improvement (NRI) resulting from the addition of SCT for a series of prediction models. Results: Overall, the addition of SCT to prediction models did not result in significant improvement in the discriminative ability. However, by the NRI index, the addition of SCT to measures of glycemia and to a fuller risk prediction model did improve prediction of DM. In the full model, adding SCT*A1C as a predictor resulted in 2% of events being reclassified as higher risk and 45% of non-events being reclassified as lower risk. Conclusion: Our results suggest that incorporating SCT into DM prediction for African Americans may result in modest improvement in model performance.

Abstract P345: Prediction of Cardiovascular Disease Events and Death using Multiple Biomarkers in African Americans: the Jackson Heart Study

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Solomon K Musani ◽  
Ramachandran Vasan ◽  
Aurelian Bidulescu ◽  
Jung Lee ◽  
Gregory Wilson ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
African Americans ◽  
High Sensitivity ◽  
Serum Cortisol ◽  
Jackson Heart Study ◽  
Cvd Risk ◽  
Risk Reclassification ◽  
Heart Study ◽  
Traditional Risk Factors

Background: The usefulness of biomarkers from different biologic pathways for predicting cardiovascular disease (CVD) events among African Americans is not well understood. Methods: We evaluated prospectively 3,102 Jackson Heart Study participants (mean age 54 years; 64% women) with data on a panel of 9 biomarkers representing inflammation (high sensitivity C - reactive protein), adiposity (adiponectin, leptin), neurohormonal activation (B-type natriuretic peptide [BNP], aldosterone, and cortisol); insulin resistance (HOMA-IR); and endothelial function (endothelin and homocysteine). We used Cox proportional hazard regression to relate the biomarker panel to the incidence of CVD (stroke, coronary heart disease, angina, heart failure and intermittent claudication) adjusting for standard CVD risk factors. Results: On follow-up (median 8.2 years), 224 participants (141 women) experienced a first CVD event, and 238 (140 women) died. Circulating concentrations of aldosterone, BNP and HOMA-IR were associated with CVD (multivariable-adjusted hazard ratios [HR] and 95% confidence interval [CI] per standard deviation (SD) increase in log-biomarker) were, respectively 1.15, (95% CI 1.01-1.30, p=0.016), 1.97, (95% CI 1.22-2.41, p<0.0001), and 1.30, (95% CI 1.10-1.52, p=0.0064). Blood cortisol and homocysteine were associated with death (HR per SD increment log-biomarker, respectively, 1.17, (95% CI 1.01-1.35, p=0.042), and 1.24, (95% CI 1.10-1.40, pvalue=0.0005). Biomarkers improved risk reclassification by 0.135; 0.120 of which was gained in classification of participants that experienced CVD events and 0.015 from participants that did not. Also, biomarkers marginally increased the model c-statistic beyond traditional risk factors. Conclusions: In our community-based sample of African Americans, circulating aldosterone, BNP and HOMA-IR predicted CVD risk, whereas serum cortisol and homocysteine predicted death. However, the incremental yield of biomarkers over traditional risk factors for risk prediction was minimal.

Abstract P146: Telomere Length, DNA Methylation, and Risk of Cardiovascular Diseases: Meta-EWAS of Four Multi-ethnic Prospective Cohorts

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Pooja Subedi ◽  
Huaizhen Qin ◽  
Shelley A Cole ◽  
Maria T Plaza ◽  
Arce Domingo-Relloso ◽  
...  
Keyword(s):  
Risk Factors ◽  
Dna Methylation ◽  
African Americans ◽  
Telomere Length ◽  
Cox Regression ◽  
Heart Study ◽  
Methylation Score ◽  
Prospective Cohorts ◽  
Reduced Risk

Background: Biological aging assessed by both leukocyte telomere length (LTL) and DNA methylation (DNAm) has been associated with CVD and its risk factors. Moreover, LTL is epigenetically regulated. We hypothesized that LTL-associated epigenetic changes are associated with risk of CVD in the community. Objective: To test whether LTL-associated loci are associated with incident CVD, independent of standard risk factors in multi-ethnic cohorts. Method: We evaluated 3,628 participants with complete LTL and DNAm data in four prospective cohorts, including 1,531 American Indians from the Strong Heart Study (SHS, mean age 56, 60% women), 821 non-Hispanic Whites (NHW) from the Framingham Heart Study (FHS, mean age 60, 51% women), 471 NHW, 150 Hispanics, and 162 African Americans from the Multi-ethnic Study of Atherosclerosis (MESA, mean age 70 , 55% women), and 471 NHW and 342 African Americans from the Women’s Health Initiative (WHI, mean age 65 , all women). LTL was quantified by qPCR (SHS, MESA) or Southern blot (FHS, WHI). DNAm was assayed by Illumina EPIC (SHS) or 450K (FHS, MESA and WHI) arrays. We imputed 450K to 850K using random forest algorithms. CVD events included fatal and nonfatal MI, CHD, heart failure, stroke, peripheral artery diseases, and cardiovascular deaths. Cohort-specific EWAS was conducted to identify CpGs associated with LTL, adjusting for age, sex, race/ethnicity, smoking, alcohol, BMI, site, cell proportion, and batch. Multiple testing was Bonferroni-corrected (genome-wide P < 2.4 x10 -7 ). Results across studies were combined by random-effects meta-analysis. To examine whether LTL-associated epigenetic loci are associated with CVD risk, we used a weighted methylation score to predict incident CVD by Cox regression, adjusting for age, sex, site, smoking, alcohol, BMI, glucose, SBP, LDL-C, and total cholesterol. Results: We ascertained 2,001 CVD events, including 986 in the SHS (average follow-up 15.2 years), 208 in FHS (average follow-up 7.7 years), 74 in MESA (average follow-up 4.9 years), and 733 in WHI (average follow-up 12.2 years). Meta-EWAS identified 22 CpGs (mapped to 17 unique genes) associated with LTL. Of these, 19 loci (15 negatively and 4 positively associated with LTL) had consistent directionality of association across four cohorts. The most significant genes harboring altered CpG sites included TLL2 (cg10549018, P= 2.42 x 10 -12 ) and TPST1 ( cg10691866, P =8.6 x 10 -10 ). A higher composite methylation score, which reflects longer LTL ( P <0.0001), was significantly associated with a reduced risk of CVD in the SHS (HR=0.16, 95% CI: 0.07–0.37), FHS (HR=0.08, 95% CI: 0.01–0.40), and WHI (HR=0.32, 95%CI: 0.13–0.82), but not MESA (HR=0.47, 95% CI: 0.04–5.09). Conclusion: Altered DNA methylation at 19 CpG loci was significantly associated with LTL. Their combined effects may predict a reduced risk of CVD. The observed associations warrant further investigation.

scholarly journals The contribution of stress to the social patterning of clinical and subclinical CVD risk factors in African Americans: The Jackson Heart Study

2012 ◽  
Vol 75 (9) ◽  
pp. 1697-1707 ◽  
Author(s):  
Samson Y. Gebreab ◽  
Ana V. Diez-Roux ◽  
DeMarc A. Hickson ◽  
Shawn Boykin ◽  
Mario Sims ◽  
...  
Keyword(s):  
Risk Factors ◽  
African Americans ◽  
Jackson Heart Study ◽  
Cvd Risk Factors ◽  
Cvd Risk ◽  
Heart Study ◽  
The Social ◽  
Subclinical Cvd

Abstract 273: HDL Particle Concentration Inversely Associates with Incident Metabolic Syndrome in the Multiethnic Dallas Heart Study

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Preethi Mani ◽  
Ian J Neeland ◽  
Darren K McGuire ◽  
Colby Ayers ◽  
Amit Khera ◽  
...  
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Visceral Fat ◽  
Particle Concentration ◽  
Atherosclerotic Cardiovascular Disease ◽  
Heart Study ◽  
Increased Risk ◽  
Ascvd Risk ◽  
Dallas Heart Study

Objective: Metabolic syndrome (MetS) increases atherosclerotic cardiovascular disease (ASCVD) risk. Low HDL cholesterol (HDL-C) is a diagnostic criterion of MetS and a major ASCVD risk factor. HDL particle concentration (HDL-P) associates with incident ASCVD independent of HDL-C, but its association with incident MetS has not been studied. We hypothesized that HDL-P would be inversely associated with incident metabolic syndrome independent of HDL-C and other recognized risk factors. Methods: HDL-P was measured by NMR and visceral fat by MRI in participants of the Dallas Heart Study, a probability-based population sample of adults age 30-65. Participants with prevalent MetS, DM, CVD, cirrhosis, cancer, HIV, or renal failure were excluded. Incident MetS as defined by NCEP ATPIII criteria was determined in all participants after median follow-up period of 9.4 years. Results: Among a cohort of 1120 participants without DM or MetS at baseline (57% women, 45% Black, mean age 43), 22.8% had incident MetS at follow-up. HDL-P and HDL-C were modestly correlated (r=0.54, p<0.0001). The lowest quartile of HDL-P was associated with younger age, men, Hispanic ethnicity, lower total, HDL, and LDL cholesterol levels and particle sizes, and less reported alcohol intake. Participants in the lowest sex and race stratified quartile of HDL-P had the highest incidence of MetS (Figure). In models adjusted for traditional risk factors, HDL-C, visceral fat, HOMA-IR, and hs-CRP, the lowest quartile of HDL-P was associated with 65% increased risk of incident MetS (Figure). Conclusion: HDL-P is independently associated with incident MetS after adjustment for HDL-C, adiposity, inflammation, and markers of insulin sensitivity. Further studies are warranted to validate these findings and elucidate the mechanisms underpinning this association.

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