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1. Association of macular pigment optical density with retinal layer thicknesses in eyes with and without manifest primary open-angle glaucoma

Author

Steven Bailey, Zhe Liu, Yao Liu, Robert B Wallace, Elizabeth Johnson, JoAnn E Manson, Ronald Gangnon, J A Mares, Barbara E K Klein, Charles Kooperberg, Julie Mares, Barbara V Howard, Shari Ludlam, Joan McGowan, Leslie Ford, Nancy Geller, Ross Prentice, Andrea LaCroix, Marcia L Stefanick, Cynthia A Thomson, Jennifer Robinson, Barbara Blodi, Lesley F Tinker, Ann Lundquist, Heather Stockman, Amitha Domalpally, Thomas Lawler, Catherine Thuruthumaly, Tyler Etheridge, Thasarat S Vajaranant, Billy R Hammond, Marine Nalbandyan, Corinne Engelman, Gloria Sarto, Erin LeBlanc, Karen Gehrs, Lesley Tinker, D Max Snodderly, Randy Hammond, Amy Millen, Bill Wooten, Jennifer Maykoski Portland, Chris Smith Madison, Kim Wood, Jennie Perry Raymond, Iowa City, Jean Walshire, Christine Sinkey, Courtney Blomme, Kristen Hall, Diane Pauk, Esther Mezhibovsky, Krista Christensen, Jacques Rossouw Bethesda, Garnet Anderson Seattle, Rebecca Jackson Columbus, Tucson Phoenix, Jean Wactawski Wende, Gainesville Jacksonville, Lewis Kuller Pittsburgh, Sally Shumaker Winston-Salem, Robert Brunner Reno, and Mark Espeland Winston-Salem

Subjects
Ophthalmology, RE1-994
Abstract

Objective To investigate associations between baseline macular pigment optical density (MPOD) and retinal layer thicknesses in eyes with and without manifest primary open-angle glaucoma (POAG) in the Carotenoids in Age-Related Eye Disease Study 2 (CAREDS2).Methods and analysis MPOD was measured at CAREDS baseline (2001–2004) via heterochromatic flicker photometry (0.5° from foveal centre). Peripapillary retinal nerve fibre layer (RNFL), macular ganglion cell complex (GCC), ganglion cell layer (GCL), inner plexiform layer (IPL), and RNFL thicknesses were measured at CAREDS2 (2016–2019) via spectral-domain optical coherence tomography. Associations between MPOD and retinal thickness were assessed using multivariable linear regression.Results Among 742 eyes (379 participants), manifest POAG was identified in 50 eyes (32 participants). In eyes without manifest POAG, MPOD was positively associated with macular GCC, GCL and IPL thicknesses in the central subfield (P-trend ≤0.01), but not the inner or outer subfields. Among eyes with manifest POAG, MPOD was positively associated with macular GCC, GCL, IPL and RNFL in the central subfield (P-trend ≤0.03), but not the inner or outer subfields, and was positively associated with peripapillary RNFL thickness in the superior and temporal quadrants (P-trend≤0.006).Conclusion We observed a positive association between MPOD and central subfield GCC thickness 15 years later. MPOD was positively associated with peripapillary RNFL superior and temporal quadrant thicknesses among eyes with manifest POAG. Our results linking low MPOD to retinal layers that are structural indicators of early glaucoma provide further evidence that carotenoids may be protective against manifest POAG.

Published
2023
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2. Both Light Intensity and Moderate‐to‐Vigorous Physical Activity Measured by Accelerometry Are Favorably Associated With Cardiometabolic Risk Factors in Older Women: The Objective Physical Activity and Cardiovascular Health (OPACH) Study

Author

Michael J. LaMonte, Cora E. Lewis, David M. Buchner, Kelly R. Evenson, Eileen Rillamas‐Sun, Chongzhi Di, I‐Min Lee, John Bellettiere, Marcia L. Stefanick, Charles B. Eaton, Barbara V. Howard, Chloe Bird, Andrea Z. LaCroix, Jacques Rossouw, Shari Ludlam, Dale Burwen, Joan McGowan, Leslie Ford, Nancy Geller, Garnet Anderson, Ross Prentice, Charles Kooperberg, JoAnn E. Manson, Rebecca Jackson, Cynthia A. Thomson, Jean Wactawski‐Wende, Marian Limacher, Robert Wallace, Lewis Kuller, and Sally Shumaker

Subjects
aging, coronary heart disease, exercise, risk factor, women and minorities, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

BackgroundThe relationship between light intensity physical activity (PA), which is common in older adults, and cardiovascular disease (CVD) risk factors is unclear. This study examined associations of accelerometer‐measured PA intensity with CVD risk factors in older women of different race‐ethnicities. Methods and ResultsCross‐sectional analyses were conducted in 4832 women (mean age 78.9 years; 52.5% white, 30.5% black, 17.1% Hispanic) who were without known CVD and wore triaxial accelerometers a minimum of 4 of 7 days with ≥10 hours/d awake wear‐time. Vector magnitude counts per 15‐s epoch were used to define time spent in low light (19–225 counts/15 s), high light (226–518), and moderate‐to‐vigorous; ≥519) intensity PA. Fasting CVD biomarkers, resting blood pressure, waist girth, body mass index, and 10‐year predicted CVD risk (Reynolds Risk Score) were measured. After adjusting for age, wear time, race‐ethnicity, and potential confounders, each PA measure was favorably associated with mean high‐density lipoprotein, triglyceride, glucose, C‐reactive protein, body mass index, waist girth, and Reynolds Risk Score (P

Published
2017
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3. Change in Physical Activity and Sitting Time After Myocardial Infarction and Mortality Among Postmenopausal Women in the Women's Health Initiative‐Observational Study

Author

Anna M. Gorczyca, Charles B. Eaton, Michael J. LaMonte, JoAnn E. Manson, Jeanne D. Johnston, Aurelian Bidulescu, Molly E. Waring, Todd Manini, Lisa W. Martin, Marcia L. Stefanick, Ka He, Andrea K. Chomistek, Jacques Rossouw, Shari Ludlam, Dale Burwen, Joan McGowan, Leslie Ford, Nancy Geller, Garnet Anderson, Ross Prentice, Andrea LaCroix, Charles Kooperberg, Barbara V. Howard, Rebecca Jackson, Cynthia A. Thomson, Jean Wactawski‐Wende, Marian Limacher, Robert Wallace, Lewis Kuller, and Sally Shumaker

Subjects
exercise, mortality, myocardial infarction, physical exercise, sitting time, women, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

BackgroundHow physical activity (PA) and sitting time may change after first myocardial infarction (MI) and the association with mortality in postmenopausal women is unknown. Methods and ResultsParticipants included postmenopausal women in the Women's Health Initiative‐Observational Study, aged 50 to 79 years who experienced a clinical MI during the study. This analysis included 856 women who had adequate data on PA exposure and 533 women for sitting time exposures. Sitting time was self‐reported at baseline, year 3, and year 6. Self‐reported PA was reported at baseline through year 8. Change in PA and sitting time were calculated as the difference between the cumulative average immediately following MI and the cumulative average immediately preceding MI. The 4 categories of change were: maintained low, decreased, increased, and maintained high. The cut points were ≥7.5 metabolic equivalent of task hours/week versus

Published
2017
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4. Factors Associated With New‐Onset Depression Following Ischemic Stroke: The Women's Health Initiative

Author

Joel Salinas, Roberta M. Ray, Rami Nassir, Kamakshi Lakshminarayan, Christina Dording, Jordan Smoller, Sylvia Wassertheil‐Smoller, Jonathan Rosand, Erin C. Dunn, Jacques Rossouw, Shari Ludlam, Dale Burwen, Joan McGowan, Leslie Ford, Nancy Geller, Garnet Anderson, Ross Prentice, Andrea LaCroix, Charles Kooperberg, JoAnn E. Manson, Barbara V. Howard, Marcia L. Stefanick, Rebecca Jackson, Cynthia A. Thomson, Jean Wactawski‐Wende, Marian Limacher, Robert Wallace, Lewis Kuller, and Sally Shumaker

Subjects
epidemiology, risk factor, stroke, women, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

BackgroundPsychosocial characteristics have a strong effect on risk of depression, and their direct treatment with behavioral interventions reduces rates of depression. Because new‐onset poststroke depression (NPSD) is frequent, devastating, and often treatment‐resistant, novel preventive efforts are needed. As a first step toward developing behavioral interventions for NPSD, we investigated whether prestroke psychosocial factors influenced rates of NPSD in a manner similar to the general population. Methods and ResultsUsing the Women's Health Initiative, we analyzed 1424 respondents who were stroke‐free at enrollment and had no self‐reported history of depression from enrollment to their nonfatal ischemic stroke based on initiation of treatment for depression or the Burnam screening instrument for detecting depressive disorders. NPSD was assessed using the same method during the 5‐year poststroke period. Logistic regression provided odds ratios of NPSD controlling for multiple covariates. NPSD occurred in 21.4% (305/1424) of the analytic cohort and varied by stroke severity as measured by the Glasgow scale, ranging from 16.7% of those with good recovery to 31.6% of those severely disabled. Women with total anterior circulation infarction had the highest level (31.4%) of NPSD while those with lacunar infarction had the lowest (16.1%). Prestroke psychosocial measures had different associations with NPSD depending on functional recovery of the individual. ConclusionsThere is a difference in the relationship of prestroke psychosocial status and risk of NPSD depending on stroke severity; thus it may be that the same preventive interventions might not work for all stroke patients. One size does not fit all.

Published
2017
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5. Social Isolation and Incident Heart Failure Hospitalization in Older Women: Women's Health Initiative Study Findings

Author

Crystal W. Cené, Xiaoyan Iris Leng, Khushnood Faraz, Matthew Allison, Khadijah Breathett, Chloe Bird, Mace Coday, Giselle Corbie‐Smith, Randi Foraker, Nkechinyere N. Ijioma, Milagros C. Rosal, Shawnita Sealy‐Jefferson, Tetyana P. Shippee, Candyce H. Kroenke, Jacques Rossouw, Shari Ludlam, Joan McGowan, Leslie Ford, Nancy Geller, Garnet Anderson, Ross Prentice, Andrea LaCroix, Charles Kooperberg, JoAnn E. Manson, Barbara V. Howard, Marcia L. Stefanick, Rebecca Jackson, Cynthia A. Thomson, Jean Wactawski‐Wende, Marian Limacher, Jennifer Robinson, Lewis Kuller, Sally Shumaker, and Robert Brunner

Subjects
Heart Failure, Hospitalization, Postmenopause, Social Isolation, Risk Factors, Incidence, Humans, Women's Health, Female, Cardiology and Cardiovascular Medicine, Aged
Abstract

Background The association of social isolation or lack of social network ties in older adults is unknown. This knowledge gap is important since the risk of heart failure (HF) and social isolation increase with age. The study examines whether social isolation is associated with incident HF in older women, and examines depressive symptoms as a potential mediator and age and race and ethnicity as effect modifiers. Methods and Results This study included 44 174 postmenopausal women of diverse race and ethnicity from the WHI (Women's Health Initiative) study who underwent annual assessment for HF adjudication from baseline enrollment (1993–1998) through 2018. We conducted a mediation analysis to examine depressive symptoms as a potential mediator and further examined effect modification by age and race and ethnicity. Incident HF requiring hospitalization was the main outcome. Social isolation was a composite variable based on marital/partner status, religious ties, and community ties. Depressive symptoms were assessed using CES‐D (Center for Epidemiology Studies‐Depression). Over a median follow‐up of 15.0 years, we analyzed data from 36 457 women, and 2364 (6.5%) incident HF cases occurred; 2510 (6.9%) participants were socially isolated. In multivariable analyses adjusted for sociodemographic, behavioral, clinical, and general health/functioning; socially isolated women had a higher risk of incident HF than nonisolated women (HR, 1.23; 95% CI, 1.08–1.41). Adding depressive symptoms in the model did not change this association (HR, 1.22; 95% CI, 1.07–1.40). Neither race and ethnicity nor age moderated the association between social isolation and incident HF. Conclusions Socially isolated older women are at increased risk for developing HF, independent of traditional HF risk factors. Registration URL: http://www.clinicaltrials.gov ; Unique identifier: NCT00000611.

Published
2022

6. Sedentary Behavior and Cardiovascular Disease in Older Women

Author

John Bellettiere, Michael J. LaMonte, Kelly R. Evenson, Eileen Rillamas-Sun, Jacqueline Kerr, I-Min Lee, Chongzhi Di, Dori E. Rosenberg, Marcia L. Stefanick, David M. Buchner, Melbourne F. Hovell, Andrea Z. LaCroix, Jacques Rossouw, Shari Ludlam, Dale Burwen, Joan McGowan, Leslie Ford, Nancy Geller, Garnet Anderson, Ross Prentice, Charles Kooperberg, JoAnn E. Manson, Barbara V. Howard, Rebecca Jackson, Cynthia A. Thomson, Jean Wactawski-Wende, Marian Limacher, Robert Wallace, Lewis Kuller, and Sally Shumaker

Subjects
Sedentary time, Gerontology, medicine.medical_specialty, business.industry, Cardiovascular health, Physical activity, Sedentary behavior, Disease, 030204 cardiovascular system & hematology, 03 medical and health sciences, 0302 clinical medicine, Physiology (medical), Epidemiology, Medicine, 030212 general & internal medicine, Cardiology and Cardiovascular Medicine, business
Abstract

Background: Evidence that higher sedentary time is associated with higher risk for cardiovascular disease (CVD) is based mainly on self-reported measures. Few studies have examined whether patterns of sedentary time are associated with higher risk for CVD. Methods: Women from the OPACH Study (Objective Physical Activity and Cardiovascular Health; n=5638, aged 63–97 years, mean age 79±7 years) with no history of myocardial infarction or stroke wore accelerometers for 4 to 7 days and were followed up for up to 4.9 years for CVD events. Average daily sedentary time and mean sedentary bout duration were the exposures of interest. Cox regression models were used to estimate hazard ratios (HRs) and 95% CIs for CVD using models adjusted for covariates and subsequently adjusted for potential mediators (body mass index, diabetes mellitus, hypertension, and CVD risk biomarkers [fasting glucose, high-density lipoprotein, triglycerides, and systolic blood pressure]). Restricted cubic spline regression characterized dose-response relationships. Results: There were 545 CVD events during 19 350 person-years. With adjustment for covariates, women in the highest (≈11 h/d or more) versus the lowest (≈9 h/d or less) quartile of sedentary time had higher risk for CVD (HR, 1.62; 95% CI, 1.21–2.17; P trend P trend P trend=0.003) after adjustment for covariates. Additional adjustment for CVD risk biomarkers attenuated associations, resulting in a quartile 4 versus quartile 1 HR of 1.36 (95% CI, 1.01–1.83; P trend=0.10). Dose-response associations of sedentary time and bout duration with CVD were linear ( P nonlinear >0.05, each). Women jointly classified as having both high sedentary time and long bout durations had significantly higher risk for CVD (HR, 1.34; 95% CI, 1.08–1.65) than women with low sedentary time and short bout duration. All analyses were repeated for incident coronary heart disease (myocardial infarction or CVD death), and associations were similar, with notably stronger HRs. Conclusions: Both high sedentary time and long mean bout durations were associated in a dose-response manner with increased CVD risk in older women, which suggests that efforts to reduce CVD burden might benefit from addressing either or both components of sedentary behavior.

Published
2019

7. Metabolically Healthy/Unhealthy Overweight/Obesity Associations With Incident Heart Failure in Postmenopausal Women: The Women's Health Initiative

Author

Amber R. Cordola Hsu, Bin Xie, Darleen V. Peterson, Michael J. LaMonte, Lorena Garcia, Charles B. Eaton, Scott B. Going, Lawrence S. Phillips, JoAnn E. Manson, Hoda Anton-Culver, Nathan D. Wong, Jacques Rossouw, Shari Ludlam, Joan McGowan, Leslie Ford, Nancy Geller, Garnet Anderson, Ross Prentice, Andrea LaCroix, Charles Kooperberg, Barbara V. Howard, Marcia L. Stefanick, Rebecca Jackson, Cynthia A. Thomson, Jean Wactawski-Wende, Marian Limacher, Jennifer Robinson, Lewis Kuller, Sally Shumaker, Robert Brunner, and Mark Espeland

Subjects
Gerontology, Risk Assessment, Body Mass Index, Risk Factors, Diabetes mellitus, medicine, Diabetes Mellitus, Humans, Obesity, Aged, Heart Failure, Postmenopausal women, business.industry, Women's Health Initiative, Incidence, Overweight obesity, Middle Aged, Overweight, medicine.disease, Lipids, Hospitalization, Postmenopause, Increased risk, Heart failure, Hypertension, Female, Waist Circumference, Cardiology and Cardiovascular Medicine, business
Abstract

Background: Obesity is associated with an increased risk of heart failure (HF); however, how metabolic weight groups relate to HF risk, especially in postmenopausal women, has not been demonstrated. Methods: We included 19 412 postmenopausal women ages 50 to 79 without cardiovascular disease from the Women’s Health Initiative. Normal weight was defined as a body mass index ≥18.5 and 2 and waist circumference 2 or waist circumference ≥88 cm. Metabolically healthy was based on Results: Among our sample, 455 (2.34%) participants experienced HF hospitalizations over a mean follow-up time of 11.3±1.1 years. Compared with metabolically healthy normal weight individuals, HF risk was greater in metabolically unhealthy normal weight (HR, 1.66 [95% CI, 1.01–2.72], P =0.045) and metabolically unhealthy overweight/obese individuals (HR, 1.95 [95% CI, 1.35–2.80], P =0.0004), but not metabolically healthy overweight/obese individuals (HR, 1.15 [95% CI, 0.78–1.71], P =0.48). Subdividing the overweight/obese into separate groups showed HRs for metabolically unhealthy obese of 2.62 (95% CI, 1.80–3.83; P P =0.06). Conclusions: Metabolically unhealthy overweight/obese and metabolically unhealthy normal weight are associated with an increased risk of HF in postmenopausal women.

Published
2021

8. Risk factor burden, heart failure, and survival in women of different ethnic groups insights from the women's health initiative

Author

Khadijah Breathett, Iris Leng, Randi E. Foraker, William T. Abraham, Laura Coker, Keith E. Whitfield, Sally Shumaker, JoAnn E. Manson, Charles B. Eaton, Barbara V. Howard, Nkechinyere Ijioma, Crystal W. Cené, Lisa W. Martin, Karen C. Johnson, Liviu Klein, Jacques Rossouw, Shari Ludlam, Dale Burwen, Joan McGowan, Leslie Ford, Nancy Geller, Garnet Anderson, Ross Prentice, Andrea LaCroix, Charles Kooperberg, Marcia L. Stefanick, Rebecca Jackson, Cynthia A. Thomson, Jean Wactawski-Wende, Marian Limacher, Robert Wallace, and Lewis Kuller

Subjects
genetic structures, Medical Physiology, Ethnic group, 030204 cardiovascular system & hematology, Cardiorespiratory Medicine and Haematology, Cardiovascular, ethnic groups, survival, Article, 03 medical and health sciences, 0302 clinical medicine, Clinical Research, Risk Factors, medicine, Ethnicity, Humans, 030212 general & internal medicine, Risk factor, skin and connective tissue diseases, Socioeconomic status, Survival analysis, Aged, Proportional Hazards Models, African Americans, Heart Failure, Continental Population Groups, Proportional hazards model, business.industry, Women's Health Initiative, Prevention, Racial Groups, Middle Aged, medicine.disease, Survival Analysis, Confidence interval, Black or African American, Heart Disease, Cardiovascular System & Hematology, Heart failure, Women's Health, Female, women, Biochemistry and Cell Biology, Cardiology and Cardiovascular Medicine, business, Demography
Abstract

Background: The higher risk of heart failure (HF) in African-American and Hispanic women compared with white women is related to the higher burden of risk factors (RFs) in minorities. However, it is unclear if there are differences in the association between the number of RFs for HF and the risk of development of HF and death within racial/ethnic groups. Methods and Results: In the WHI (Women’s Health Initiative; 1993–2010), African-American (n=11 996), white (n=18 479), and Hispanic (n=5096) women with 1, 2, or 3+ baseline RFs were compared with women with 0 RF within their respective racial/ethnic groups to assess risk of developing HF or all-cause mortality before and after HF, using survival analyses. After adjusting for age, socioeconomic status, and hormone therapy, the subdistribution hazard ratio (95% confidence interval) of developing HF increased as number of RFs increased ( P P =0.18)—African-Americans 1 RF: 1.80 (1.01–3.20), 2 RFs: 3.19 (1.84–5.54), 3+ RFs: 7.31 (4.26–12.56); Whites 1 RF: 1.27 (1.04–1.54), 2 RFs: 1.95 (1.60–2.36), 3+ RFs: 4.07 (3.36–4.93); Hispanics 1 RF: 1.72 (0.68–4.34), 2 RFs: 3.87 (1.60–9.37), 3+ RFs: 8.80 (3.62–21.42). Risk of death before developing HF increased with subsequent RFs ( P P =0.001). The number of RFs was not associated with the risk of death after developing HF in any group ( P =0.25; interaction P =0.48). Conclusions: Among diverse racial/ethnic groups, an increase in the number of baseline RFs was associated with higher risk of HF and death before HF but was not associated with death after HF. Early RF prevention may reduce the burden of HF across multiple racial/ethnic groups.

Published
2018
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9. Coronary Artery Calcification (CAC) and Post‐Trial Cardiovascular Events and Mortality Within the Women's Health Initiative (WHI) Estrogen‐Alone Trial

Author

Indu G. Poornima, Rachel H. Mackey, Matthew A. Allison, JoAnn E. Manson, J. Jeffrey Carr, Michael J. LaMonte, Yuefang Chang, Lewis H. Kuller, J.E. Rossouw, S. Ludlam, B.B. Cochrane, J.R. Hunt, B. Lund, R. Prentice, C. O'Rourke, L. Du, S. Pillsbury, C. Hightower, R. Ellison, J. Tan, S. Wassertheil‐Smoller, M. Magnani, D.H. Noble, T. Dellicarpini, M. Bueche, A.D. McGinnis, F.J. Rybicki, A.R. Assaf, G. Sloane, L.S. Phillips, V. Butler, M. Huber, J. Vitali, J. Hsia, C. LeBrun, R. Palm, D. Embersit, E. Whitlock, K. Arnold, S. Sidney, V. Cantrell, J.M. Kotchen, C. Feltz, B.V. Howard, A. Thomas‐Geevarghese, G. Boggs, J.S. Jelinick, P. Greenland, A. Neuman, G. Carlson‐Lund, S.M. Giovanazzi, M.L. Stefanick, S. Swope, R. Jackson, K. Toussant, C.E. Lewis, P. Pierce, C. Stallings, J. Wactawski‐Wende, S. Goel, R. Laughlin, J. Robbins, S. Zaragoza, D. Macias, D. Belisle, L. Nathan, B. Voigt, J. Goldin, M. Woo, R.D. Langer, X. Lien, C.M. Wright, M. Gass, S. Sheridan, J.G. Robinson, D. Feddersen, K. Kelly‐Brake, J. Carroll, J. Ockene, L. Churchill, N.L. Lasser, B. Miller, P.D. Maldjian, J. Pierre‐Louis, J. Fishman, M.J. O'Sullivan, D. Fernandez, K.L. Margolis, C.L. Bjerk, C. Truwit, J.A. Hearity, W.B. Hyslop, K. Darroch, C. Murphy, G. Heiss, D. Edmundowicz, D. Ives, K.C. Johnson, S. Satterfield, S.A. Connelly, E.L. Jones, R. Brzyski, M.A. Nashawati, S. Torchia, A. Rodriguez, R. Garza, P. Nentwich, G.E. Sarto, L. Broderick, N.K. Sweitzer, Jacques Rossouw, Shari Ludlam, Joan McGowan, Leslie Ford, Nancy Geller, Garnet Anderson, Ross Prentice, Andrea LaCroix, Barbara V. Howard, Rebecca Jackson, Cynthia A. Thomson, Jean Wactawski‐Wende, Marian Limacher, Jennifer Robinson, Lewis Kuller, Sally Shumaker, and Robert Brunner

Subjects
medicine.medical_specialty, Time Factors, Randomization, Epidemiology, Computed Tomography Angiography, medicine.drug_class, Coronary Artery Disease, 030204 cardiovascular system & hematology, Coronary Angiography, Placebo, 03 medical and health sciences, 0302 clinical medicine, cardiovascular disease, Risk Factors, Internal medicine, medicine, Humans, cardiovascular diseases, 030212 general & internal medicine, Vascular Calcification, Original Research, Proportional Hazards Models, hormonal therapy, Chi-Square Distribution, Estrogens, Conjugated (USP), Computerized Tomography (CT), business.industry, Incidence, Women's Health Initiative, Estrogen Replacement Therapy, Middle Aged, mortality, coronary artery calcification, United States, Surgery, Postmenopause, Treatment Outcome, Estrogen, Coronary artery calcification, Multivariate Analysis, Women's Health, Hormonal therapy, Female, women, Mortality/Survival, Cardiology and Cardiovascular Medicine, business, Mortality survival
Abstract

Background Among women aged 50 to 59 years at baseline in the Women's Health Initiative (WHI) Estrogen‐Alone (E‐Alone) trial, randomization to conjugated equine estrogen‐alone versus placebo was associated with lower risk of myocardial infarction and mortality, and, in an ancillary study, the WHI‐CACS (WHI Coronary Artery Calcification Study) with lower CAC, measured by cardiac computed tomography ≈8.7 years after baseline randomization. We hypothesized that higher CAC would be related to post‐trial coronary heart disease (CHD), cardiovascular disease (CVD), and total mortality, independent of baseline randomization or risk factors. Methods and Results WHI‐CACS participants (n=1020) were followed ≈8 years from computed tomography scan in 2005 (mean age=64.4) through 2013 for incident CHD (myocardial infarction and fatal CHD, n=17), CVD (n=69), and total mortality (n=55). Incident CHD and CVD analyses excluded women with CVD before scan (n=89). Women with CAC=0 (n=54%) had very low age‐adjusted rates/1000 person‐years of CHD (0.91), CVD (5.56), and mortality (3.45). In comparison, rates were ≈2‐fold higher for women with any CAC (>0). Associations were not modified by baseline randomization to conjugated equine estrogen–alone versus placebo. Adjusted for baseline randomization and risk factors, the hazard ratio (95% confidence interval) for CAC >100 (19%) was 4.06 (2.11, 7.80) for CVD and 2.70 (1.26, 5.79) for mortality. Conclusions Among a subset of postmenopausal women aged 50 to 59 years at baseline in the WHI E‐Alone Trial, CAC at mean age of 64 years was strongly related to incident CHD, CVD, and to total mortality over ≈8 years, independent of baseline randomization to conjugated equine estrogen–alone versus placebo or CVD risk factors. Clinical Trial Registration URL: https://www.clinicaltrials.gov . Unique identifier: NCT00000611.

Published
2017

10. Whole-exome sequencing identifies rare and low-frequency coding variants associated with LDL cholesterol

Author

Leslie A. Lange, Youna Hu, He Zhang, Chenyi Xue, Ellen M. Schmidt, Zheng-Zheng Tang, Chris Bizon, Ethan M. Lange, Joshua D. Smith, Emily H. Turner, Goo Jun, Hyun Min Kang, Gina Peloso, Paul Auer, Kuo-ping Li, Jason Flannick, Ji Zhang, Christian Fuchsberger, Kyle Gaulton, Cecilia Lindgren, Adam Locke, Alisa Manning, Xueling Sim, Manuel A. Rivas, Oddgeir L. Holmen, Omri Gottesman, Yingchang Lu, Douglas Ruderfer, Eli A. Stahl, Qing Duan, Yun Li, Peter Durda, Shuo Jiao, Aaron Isaacs, Albert Hofman, Joshua C. Bis, Adolfo Correa, Michael E. Griswold, Johanna Jakobsdottir, Albert V. Smith, Pamela J. Schreiner, Mary F. Feitosa, Qunyuan Zhang, Jennifer E. Huffman, Jacy Crosby, Christina L. Wassel, Ron Do, Nora Franceschini, Lisa W. Martin, Jennifer G. Robinson, Themistocles L. Assimes, David R. Crosslin, Elisabeth A. Rosenthal, Michael Tsai, Mark J. Rieder, Deborah N. Farlow, Aaron R. Folsom, Thomas Lumley, Ervin R. Fox, Christopher S. Carlson, Ulrike Peters, Rebecca D. Jackson, Cornelia M. van Duijn, André G. Uitterlinden, Daniel Levy, Jerome I. Rotter, Herman A. Taylor, Vilmundur Gudnason, David S. Siscovick, Myriam Fornage, Ingrid B. Borecki, Caroline Hayward, Igor Rudan, Y. Eugene Chen, Erwin P. Bottinger, Ruth J.F. Loos, Pål Sætrom, Kristian Hveem, Michael Boehnke, Leif Groop, Mark McCarthy, Thomas Meitinger, Christie M. Ballantyne, Stacey B. Gabriel, Christopher J. O’Donnell, Wendy S. Post, Kari E. North, Alexander P. Reiner, Eric Boerwinkle, Bruce M. Psaty, David Altshuler, Sekar Kathiresan, Dan-Yu Lin, Gail P. Jarvik, L. Adrienne Cupples, Charles Kooperberg, James G. Wilson, Deborah A. Nickerson, Goncalo R. Abecasis, Stephen S. Rich, Russell P. Tracy, Cristen J. Willer, David M. Altshuler, Gonçalo R. Abecasis, Hooman Allayee, Sharon Cresci, Mark J. Daly, Paul I.W. de Bakker, Mark A. DePristo, Peter Donnelly, Tim Fennell, Kiran Garimella, Stanley L. Hazen, Daniel M. Jordan, Adam Kiezun, Guillaume Lettre, Bingshan Li, Mingyao Li, Christopher H. Newton-Cheh, Sandosh Padmanabhan, Sara Pulit, Daniel J. Rader, David Reich, Muredach P. Reilly, Steve Schwartz, Laura Scott, John A. Spertus, Nathaniel O. Stitziel, Nina Stoletzki, Shamil R. Sunyaev, Benjamin F. Voight, Ermeg Akylbekova, Larry D. Atwood, Maja Barbalic, R. Graham Barr, Emelia J. Benjamin, Joshua Bis, Donald W. Bowden, Jennifer Brody, Matthew Budoff, Greg Burke, Sarah Buxbaum, Jeff Carr, Donna T. Chen, Ida Y. Chen, Wei-Min Chen, Pat Concannon, Ralph D’Agostino, Anita L. DeStefano, Albert Dreisbach, Josée Dupuis, J. Peter Durda, Jaclyn Ellis, Caroline S. Fox, Ervin Fox, Vincent Funari, Santhi K. Ganesh, Julius Gardin, David Goff, Ora Gordon, Wayne Grody, Myron Gross, Xiuqing Guo, Ira M. Hall, Nancy L. Heard-Costa, Susan R. Heckbert, Nicholas Heintz, David M. Herrington, DeMarc Hickson, Jie Huang, Shih-Jen Hwang, David R. Jacobs, Nancy S. Jenny, Andrew D. Johnson, Craig W. Johnson, Steven Kawut, Richard Kronmal, Raluca Kurz, Martin G. Larson, Mark Lawson, Cora E. Lewis, Dalin Li, Honghuang Lin, Chunyu Liu, Jiankang Liu, Kiang Liu, Xiaoming Liu, Yongmei Liu, William T. Longstreth, Cay Loria, Kathryn Lunetta, Aaron J. Mackey, Rachel Mackey, Ani Manichaikul, Taylor Maxwell, Barbara McKnight, James B. Meigs, Alanna C. Morrison, Solomon K. Musani, Josyf C. Mychaleckyj, Jennifer A. Nettleton, Kari North, Daniel O’Leary, Frank Ong, Walter Palmas, James S. Pankow, Nathan D. Pankratz, Shom Paul, Marco Perez, Sharina D. Person, Joseph Polak, Aaron R. Quinlan, Leslie J. Raffel, Vasan S. Ramachandran, Kenneth Rice, Jill P. Sanders, Pamela Schreiner, Sudha Seshadri, Steve Shea, Stephen Sidney, Kevin Silverstein, Nicholas L. Smith, Nona Sotoodehnia, Asoke Srinivasan, Kent Taylor, Fridtjof Thomas, Michael Y. Tsai, Kelly A. Volcik, Chrstina L. Wassel, Karol Watson, Gina Wei, Wendy White, Kerri L. Wiggins, Jemma B. Wilk, O. Dale Williams, Gregory Wilson, Phillip Wolf, Neil A. Zakai, John Hardy, James F. Meschia, Michael Nalls, Andrew Singleton, Brad Worrall, Michael J. Bamshad, Kathleen C. Barnes, Ibrahim Abdulhamid, Frank Accurso, Ran Anbar, Terri Beaty, Abigail Bigham, Phillip Black, Eugene Bleecker, Kati Buckingham, Anne Marie Cairns, Daniel Caplan, Barbara Chatfield, Aaron Chidekel, Michael Cho, David C. Christiani, James D. Crapo, Julia Crouch, Denise Daley, Anthony Dang, Hong Dang, Alicia De Paula, Joan DeCelie-Germana, Allen DozorMitch Drumm, Maynard Dyson, Julia Emerson, Mary J. Emond, Thomas Ferkol, Robert Fink, Cassandra Foster, Deborah Froh, Li Gao, William Gershan, Ronald L. Gibson, Elizabeth Godwin, Magdalen Gondor, Hector Gutierrez, Nadia N. Hansel, Paul M. Hassoun, Peter Hiatt, John E. Hokanson, Michelle Howenstine, Laura K. Hummer, Jamshed Kanga, Yoonhee Kim, Michael R. Knowles, Michael Konstan, Thomas Lahiri, Nan Laird, Christoph Lange, Lin Lin, Xihong Lin, Tin L. Louie, David Lynch, Barry Make, Thomas R. Martin, Steve C. Mathai, Rasika A. Mathias, John McNamara, Sharon McNamara, Deborah Meyers, Susan Millard, Peter Mogayzel, Richard Moss, Tanda Murray, Dennis Nielson, Blakeslee Noyes, Wanda O’Neal, David Orenstein, Brian O’Sullivan, Rhonda Pace, Peter Pare, H. Worth Parker, Mary Ann Passero, Elizabeth Perkett, Adrienne Prestridge, Nicholas M. Rafaels, Bonnie Ramsey, Elizabeth Regan, Clement Ren, George Retsch-Bogart, Michael Rock, Antony Rosen, Margaret Rosenfeld, Ingo Ruczinski, Andrew Sanford, David Schaeffer, Cindy Sell, Daniel Sheehan, Edwin K. Silverman, Don Sin, Terry Spencer, Jackie Stonebraker, Holly K. Tabor, Laurie Varlotta, Candelaria I. Vergara, Robert Weiss, Fred Wigley, Robert A. Wise, Fred A. Wright, Mark M. Wurfel, Robert Zanni, Fei Zou, Phil Green, Jay Shendure, Joshua M. Akey, Carlos D. Bustamante, Evan E. Eichler, P. Keolu Fox, Wenqing Fu, Adam Gordon, Simon Gravel, Jill M. Johnsen, Mengyuan Kan, Eimear E. Kenny, Jeffrey M. Kidd, Fremiet Lara-Garduno, Suzanne M. Leal, Dajiang J. Liu, Sean McGee, Timothy D. O’Connor, Bryan Paeper, Peggy D. Robertson, Jeffrey C. Staples, Jacob A. Tennessen, Gao Wang, Qian Yi, Rebecca Jackson, Garnet Anderson, Hoda Anton-Culver, Paul L. Auer, Shirley Beresford, Henry Black, Robert Brunner, Robert Brzyski, Dale Burwen, Bette Caan, Cara L. Carty, Rowan Chlebowski, Steven Cummings, J. David Curb, Charles B. Eaton, Leslie Ford, Stephanie M. Fullerton, Margery Gass, Nancy Geller, Gerardo Heiss, Barbara V. Howard, Li Hsu, Carolyn M. Hutter, John Ioannidis, Karen C. Johnson, Lewis Kuller, Andrea LaCroix, Kamakshi Lakshminarayan, Dorothy Lane, Norman Lasser, Erin LeBlanc, Kuo-Ping Li, Marian Limacher, Benjamin A. Logsdon, Shari Ludlam, JoAnn E. Manson, Karen Margolis, Lisa Martin, Joan McGowan, Keri L. Monda, Jane Morley Kotchen, Lauren Nathan, Judith Ockene, Mary Jo O’Sullivan, Lawrence S. Phillips, Ross L. Prentice, John Robbins, Jacques E. Rossouw, Haleh Sangi-Haghpeykar, Gloria E. Sarto, Sally Shumaker, Michael S. Simon, Marcia L. Stefanick, Evan Stein, Hua Tang, Kira C. Taylor, Cynthia A. Thomson, Timothy A. Thornton, Linda Van Horn, Mara Vitolins, Jean Wactawski-Wende, Robert Wallace, Sylvia Wassertheil-Smoller, Donglin Zeng, Deborah Applebaum-Bowden, Michael Feolo, Weiniu Gan, Dina N. Paltoo, Phyliss Sholinsky, Anne Sturcke, Epidemiology, and Internal Medicine

Subjects
Male, Genome-wide association study, 030204 cardiovascular system & hematology, Cohort Studies, 0302 clinical medicine, Gene Frequency, Receptors, Genotype, Dyslipidemias/blood, Receptors, LDL/genetics, Genetics(clinical), Exome, Genetics (clinical), Exome sequencing, Genetics, 0303 health sciences, Serine Endopeptidases, Single Nucleotide, Middle Aged, 3. Good health, Cholesterol, Phenotype, Genetic Code, Cholesterol, LDL/genetics, Female, lipids (amino acids, peptides, and proteins), Proprotein Convertases, Proprotein Convertase 9, Sequence Analysis, Adult, Apolipoproteins E/blood, LDL/genetics, Serine Endopeptidases/genetics, Single-nucleotide polymorphism, Biology, Polymorphism, Single Nucleotide, Article, 03 medical and health sciences, Apolipoproteins E, SDG 3 - Good Health and Well-being, Humans, Polymorphism, Allele frequency, 030304 developmental biology, Genetic association, Aged, Dyslipidemias, PCSK9, DNA, Cholesterol, LDL, Lipase, Sequence Analysis, DNA, Receptors, LDL, Lipase/genetics, Proprotein Convertases/genetics, Follow-Up Studies, Genome-Wide Association Study
Abstract

Elevated low-density lipoprotein cholesterol (LDL-C) is a treatable, heritable risk factor for cardiovascular disease. Genome-wide association studies (GWASs) have identified 157 variants associated with lipid levels but are not well suited to assess the impact of rare and low-frequency variants. To determine whether rare or low-frequency coding variants are associated with LDL-C, we exome sequenced 2,005 individuals, including 554 individuals selected for extreme LDL-C (>98(th) or

Published
2014

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