@article {6240, title = {Racial and regional differences in venous thromboembolism in the United States in 3 cohorts.}, journal = {Circulation}, volume = {129}, year = {2014}, month = {2014 Apr 08}, pages = {1502-9}, abstract = {

BACKGROUND: Blacks are thought to have a higher risk of venous thromboembolism (VTE) than whites. However, prior studies are limited to administrative databases that lack specific information on VTE risk factors or have limited geographic scope.

METHODS AND RESULTS: We ascertained VTE from 3 prospective studies: the Atherosclerosis Risk in Communities Study (ARIC), the Cardiovascular Health Study (CHS), and the Reasons for Geographic and Racial Differences in Stroke study (REGARDS). We tested the association of race with VTE using Cox proportional hazard models adjusted for VTE risk factors. Over 438 090 person-years, 916 incident VTE events (302 in blacks) occurred in 51 149 individuals (17 318 blacks) who were followed up. In risk factor-adjusted models, blacks had a higher rate of VTE than whites in the CHS (hazard ratio, 1.81; 95\% confidence interval, 1.20-2.73) but not ARIC (hazard ratio, 1.21; 95\% confidence interval, 0.96-1.54). In REGARDS, there was a significant region-by-race interaction (P=0.01): Blacks in the Southeast had a significantly higher rate of VTE than blacks in the rest of the United States (hazard ratio, 1.63; 95\% confidence interval, 1.08-2.48) that was not seen in whites (hazard ratio, 0.83; 95\% confidence interval, 0.61-1.14).

CONCLUSIONS: The association of race with VTE differed in each cohort, which may reflect the different time periods of the studies or different regional rates of VTE. Further studies of environmental and genetic risk factors for VTE are needed to determine which underlie racial and perhaps regional differences in VTE.

}, keywords = {African Continental Ancestry Group, Aged, Cohort Studies, European Continental Ancestry Group, Female, Humans, Longitudinal Studies, Male, Middle Aged, Prevalence, Proportional Hazards Models, Prospective Studies, Residence Characteristics, Risk Factors, United States, Venous Thromboembolism}, issn = {1524-4539}, doi = {10.1161/CIRCULATIONAHA.113.006472}, author = {Zakai, Neil A and McClure, Leslie A and Judd, Suzanne E and Safford, Monika M and Folsom, Aaron R and Lutsey, Pamela L and Cushman, Mary} } @article {7448, title = {PCSK9 Loss-of-Function Variants, Low-Density Lipoprotein Cholesterol, and Risk of Coronary Heart Disease and Stroke: Data From 9 Studies of Blacks and Whites.}, journal = {Circ Cardiovasc Genet}, volume = {10}, year = {2017}, month = {2017 Aug}, pages = {e001632}, abstract = {

BACKGROUND: PCSK9 loss-of-function (LOF) variants allow for the examination of the effects of lifetime reduced low-density lipoprotein cholesterol (LDL-C) on cardiovascular events. We examined the association of PCSK9 LOF variants with LDL-C and incident coronary heart disease and stroke through a meta-analysis of data from 8 observational cohorts and 1 randomized trial of statin therapy.

METHODS AND RESULTS: These 9 studies together included 17 459 blacks with 403 (2.3\%) having at least 1 Y142X or C679X variant and 31 306 whites with 955 (3.1\%) having at least 1 R46L variant. Unadjusted odds ratios for associations between PCSK9 LOF variants and incident coronary heart disease (851 events in blacks and 2662 events in whites) and stroke (523 events in blacks and 1660 events in whites) were calculated using pooled Mantel-Haenszel estimates with continuity correction factors. Pooling results across studies using fixed-effects inverse-variance-weighted models, PCSK9 LOF variants were associated with 35 mg/dL (95\% confidence interval [CI], 32-39) lower LDL-C in blacks and 13 mg/dL (95\% CI, 11-16) lower LDL-C in whites. PCSK9 LOF variants were associated with a pooled odds ratio for coronary heart disease of 0.51 (95\% CI, 0.28-0.92) in blacks and 0.82 (95\% CI, 0.63-1.06) in whites. PCSK9 LOF variants were not associated with incident stroke (odds ratio, 0.84; 95\% CI, 0.48-1.47 in blacks and odds ratio, 1.06; 95\% CI, 0.80-1.41 in whites).

CONCLUSIONS: PCSK9 LOF variants were associated with lower LDL-C and coronary heart disease incidence. PCSK9 LOF variants were not associated with stroke risk.

}, issn = {1942-3268}, doi = {10.1161/CIRCGENETICS.116.001632}, author = {Kent, Shia T and Rosenson, Robert S and Avery, Christy L and Chen, Yii-der I and Correa, Adolfo and Cummings, Steven R and Cupples, L Adrienne and Cushman, Mary and Evans, Daniel S and Gudnason, Vilmundur and Harris, Tamara B and Howard, George and Irvin, Marguerite R and Judd, Suzanne E and Jukema, J Wouter and Lange, Leslie and Levitan, Emily B and Li, Xiaohui and Liu, Yongmei and Post, Wendy S and Postmus, Iris and Psaty, Bruce M and Rotter, Jerome I and Safford, Monika M and Sitlani, Colleen M and Smith, Albert V and Stewart, James D and Trompet, Stella and Sun, Fangui and Vasan, Ramachandran S and Woolley, J Michael and Whitsel, Eric A and Wiggins, Kerri L and Wilson, James G and Muntner, Paul} } @article {8921, title = {Egg consumption, overall diet quality, and risk of type 2 diabetes and coronary heart disease: A pooling project of US prospective cohorts.}, journal = {Clin Nutr}, volume = {40}, year = {2021}, month = {2021 05}, pages = {2475-2482}, abstract = {

BACKGROUND AND AIMS: Data on the relation of egg consumption with risk of type 2 diabetes (T2D) and coronary heart disease (CHD) are limited and inconsistent. Few studies have controlled for overall dietary patterns in egg-T2D or egg-CHD analyses, and it is unclear whether any observed elevated risks of T2D and CHD with frequent egg consumption is real or due to confounding by dietary habits. We tested the hypothesis that frequent egg consumption is associated with a higher risk of T2D and CHD risk after adjustment for overall dietary patterns among adults.

DESIGN: We used prospective cohort design to complete time-to-event analyses.

METHODS: We pooled de novo, harmonized, individual-level analyses from nine US cohorts (n~=~103,811). Cox regression was used to estimate hazard ratios separately in each cohort adjusting for age, ethnicity, body mass index (BMI), exercise, smoking, alcohol intake, and dietary patterns. We pooled cohort-specific results using an inverse-variance weighted method to estimate summary relative risks.

RESULTS: Median age ranged from 25 to 72 years. Median egg consumption was 1 egg per week in most of the cohorts. While egg consumption up to one per week was not associated with T2D risk, consumption of >=2 eggs per week was associated with elevated risk [27\% elevated risk of T2D comparing 7+ eggs/week with none (95\% CI: 16\%-37\%)]. There was little evidence for heterogeneity across cohorts and we observed similar conclusions when stratified by BMI. Overall, egg consumption was not associated with the risk of CHD. However, in a sensitivity analysis, there was a 30\% higher risk of CHD (95\% CI: 3\%-56\%) restricted to older adults consuming 5-6 eggs/week.

CONCLUSIONS: Our data showed an elevated risk of T2D with egg consumption of >=2 eggs per week but not with <2 eggs/week. While there was no overall association of egg consumption with CHD risk, the elevated CHD observed with consumption of 5-6 eggs/week in older cohorts merits further investigation.

}, keywords = {Adult, Aged, Cohort Studies, Coronary Disease, Diabetes Mellitus, Type 2, Diet, Eggs, Humans, Middle Aged, Prospective Studies, Risk Factors, United States}, issn = {1532-1983}, doi = {10.1016/j.clnu.2021.03.003}, author = {Djouss{\'e}, Luc and Zhou, Guohai and McClelland, Robyn L and Ma, Nanxun and Zhou, Xia and Kabagambe, Edmond K and Talegawkar, Sameera A and Judd, Suzanne E and Biggs, Mary L and Fitzpatrick, Annette L and Clark, Cheryl R and Gagnon, David R and Steffen, Lyn M and Gaziano, J Michael and Lee, I-Min and Buring, Julie E and Manson, JoAnn E} } @article {9917, title = {Association Between Cigarette Smoking~and Subclinical Markers of Cardiovascular Harm.}, journal = {J Am Coll Cardiol}, volume = {85}, year = {2025}, month = {2025 Mar 18}, pages = {1018-1034}, abstract = {

BACKGROUND: Cigarette smoking is a strong risk factor for cardiovascular harm.

OBJECTIVES: The study sought to explore the detailed relationships between smoking intensity, pack-years, and~time since cessation with inflammation, thrombosis, and subclinical atherosclerosis markers of cardiovascular harm.

METHODS: We included 182,364 participants (mean age 58.2 years, 69.0\% female) from 22 cohorts of the Cross Cohort Collaboration with self-reported smoking status, including smoking intensity and/or pack-years, and concurrent subclinical marker measurements. Markers were categorized into 3 domains: inflammation (high-sensitivity C-reactive protein, interleukin-6, glycoprotein acetylation), thrombosis (fibrinogen, D-dimer), and subclinical atherosclerosis (coronary artery calcium, carotid intima-media thickness, carotid plaque, and ankle-brachial index). Utilizing multivariate regression models and restricted cubic splines, we assessed associations of smoking status, intensity, pack-years, time since cessation, and subclinical markers.

RESULTS: A total of 15.3\% of participants currently smoke (mean 16.7 cigarettes/day, mean 30.0 pack-years), and 34.6\% of participants formerly smoked (median 19.0 years since quitting, mean 22.4 pack-years). Participants with a history of smoking showed higher levels of all subclinical markers compared with those who have never smoked, with stronger associations observed in those currently smoke. Among participants who currently smoke, smoking intensity showed a clear dose-response relationship with all markers, except for D-dimer, specifically with incremental 1\% to 9\% higher levels of subclinical markers per 10 cigarettes. After 20 cigarettes, the patterns appeared to plateau for blood markers, while they continued to increase for atherosclerosis markers. Among those who have ever smoked, robust dose-response relationships were observed for pack-years with all subclinical markers, with incremental 1\% to 9\% higher levels per 10 pack-years. The dose-response effects persisted after 20 pack-years for all markers, though with a milder slope. Among participants who smoked formerly, there were substantially lower levels of biomarkers with longer time since quitting, and most markers were not different compared with those who have never smoked by 30 years, except for the coronary artery calcium score, which remained 19\% higher even beyond quitting after 30 years.

CONCLUSIONS: Smoking-relevant parameters show strong and dose-response relationships across 3 domains of subclinical markers of cardiovascular harm. The sensitivity of the tested subclinical markers to small increments in cigarette exposure suggests potential value in the regulation of new and existing tobacco products.

}, keywords = {Aged, Atherosclerosis, Biomarkers, Cardiovascular Diseases, Carotid Intima-Media Thickness, Cigarette Smoking, Cohort Studies, Female, Humans, Male, Middle Aged, Risk Factors}, issn = {1558-3597}, doi = {10.1016/j.jacc.2024.12.032}, author = {Yao, Zhiqi and Tasdighi, Erfan and Dardari, Zeina A and Jha, Kunal K and Osuji, Ngozi and Rajan, Tanuja and Boakye, Ellen and Rodriguez, Carlos J and Matsushita, Kunihiro and Simonsick, Eleanor M and Lima, Jo{\~a}o A C and Widome, Rachel and Cohen, Debbie L and Appel, Lawrence J and Khera, Amit and Hall, Michael E and Judd, Suzanne E and Cole, Shelley A and Vasan, Ramachandran S and Benjamin, Emelia J and Lotufo, Paulo A and Bensenor, Isabela M and El Khoudary, Samar R and Barinas-Mitchell, Emma and Janssen, Imke and Psaty, Bruce M and Eaton, Charles B and Lamonte, Michael J and Cawthon, Peggy M and Orwoll, Eric S and Irvin, Marguerite R and Bhatnagar, Aruni and DeFilippis, Andrew P and El-Shahaway, Omar and Blaha, Michael J} } @article {9904, title = {Association between spatial social polarisation and high blood pressure in older adults.}, journal = {J Epidemiol Community Health}, year = {2025}, month = {2025 Mar 24}, abstract = {

BACKGROUND: Using data from the Cardiovascular Health Study (CHS) and the REasons for Geographic And Racial Differences in Stroke (REGARDS) study, we investigate the association between socioeconomic polarisation and blood pressure outcomes in black and white adults. We also validate previous findings that joint racial/ethnic and income measures of spatial social polarisation (SSP) outperform single domain measures.

METHODS: We conducted a cross-sectional analysis using a retrospective cohort combining CHS (recruited 1989-1990 and 1992-1993) and REGARDS (recruited 2003-2007). The study included 5888 CHS participants aged >=65 years and 30 183 REGARDS participants aged >=45 years. SSP was measured using the Index of Concentration at the Extremes for education, race/ethnicity, income, home ownership, and joint race/ethnicity and income at ZIP code, census tract and county levels. The SSP measures were modelled against the presence of high blood pressure and systolic blood pressure.

RESULTS: The sample had a mean age of 66 (SD: 9), was majority female (56\%), white/other (63\%), and at least high school graduates (85\%). A total of 26\% had high blood pressure, with a mean systolic blood pressure of 129 mm Hg (SD: 18). Census tract-level models showed low-income black areas had 25\% (95\% CI 11\%-40\%) higher odds of high blood pressure and 1.8 mm Hg (95\% CI 1.0-2.5) higher mean systolic blood pressure than high-income White areas.

CONCLUSION: Greater SSP is associated with a higher risk of high blood pressure and higher systolic blood pressure. Further investigating and reducing polarisation could help mitigate cardiovascular health disparities, improving outcomes for socioeconomically deprived communities.

}, issn = {1470-2738}, doi = {10.1136/jech-2024-223191}, author = {Abdel Magid, Hoda S and Jaros, Samuel and Lovasi, Gina S and Rosso, Andrea L and Tan, Annabel X and Rehkopf, David H and Nelson, Lorene M and Carlson, Michelle and Judd, Suzanne E and Odden, Michelle C} }