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Coronary Artery Disease: HELP
Articles from NIH Bethesda
Based on 201 articles published since 2008
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These are the 201 published articles about Coronary Artery Disease that originated from NIH Bethesda during 2008-2019.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7 · 8 · 9
51 Article Understanding bias in relationships between the food environment and diet quality: the Coronary Artery Risk Development in Young Adults (CARDIA) study. 2017

Rummo, Pasquale E / Guilkey, David K / Ng, Shu Wen / Meyer, Katie A / Popkin, Barry M / Reis, Jared P / Shikany, James M / Gordon-Larsen, Penny. ·Department of Nutrition, Gillings School of Public Health, University of North Carolina, Chapel Hill, North Carolina, USA. · Department of Population Health, NYU School of Medicine, New York, NY, USA. · Department of Economics, University of North Carolina, Chapel Hill, North Carolina, USA. · Carolina Population Center, Chapel Hill, North Carolina, USA. · Division of Cardiovascular Sciences, National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA. · Division of Preventive Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA. ·J Epidemiol Community Health · Pubmed #28983065.

ABSTRACT: BACKGROUND: The relationship between food environment exposures and diet behaviours is unclear, possibly because the majority of studies ignore potential residual confounding. METHODS: We used 20 years (1985-1986, 1992-1993 2005-2006) of data from the Coronary Artery Risk Development in Young Adults (CARDIA) study across four US cities (Birmingham, Alabama; Chicago, Illinois; Minneapolis, Minnesota; Oakland, California) and instrumental variables (IV) regression to obtain causal estimates of longitudinal associations between the percentage of neighbourhood food outlets (per total food outlets within 1 km network distance of respondent residence) and an RESULTS: The mean diet quality score across follow-up was 63.4 (SD=12.7). A 10% increase in fast food restaurants (relative to full-service restaurants) was associated with a lower diet quality score over time using IV regression (β=-1.01, 95% CI -1.99 to -0.04); estimates were attenuated using non-causal models. The percentage of neighbourhood convenience and grocery stores (relative to supermarkets) was not associated with diet quality in any model, but estimates from non-causal models were similarly attenuated compared with causal models. CONCLUSION: Ignoring residual confounding may generate biased estimated effects of neighbourhood food outlets on diet outcomes and may have contributed to weak findings in the food environment literature.

52 Article Quantifying sociodemographic and income disparities in medical therapy and lifestyle among symptomatic patients with suspected coronary artery disease: a cross-sectional study in North America. 2017

Ladapo, Joseph A / Coles, Adrian / Dolor, Rowena J / Mark, Daniel B / Cooper, Lawton / Lee, Kerry L / Goldberg, Jonathan / Shapiro, Michael D / Hoffmann, Udo / Douglas, Pamela S. ·Division of General Internal Medicine and Health Services Research, David Geffen School of Medicine at UCLA, Los Angeles, California, USA. · Department of Medicine, Duke Clinical Research Institute, Duke University School of Medicine, Durham, North Carolina, USA. · National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA. · Louis Stokes Cleveland VA Medical Center, Cleveland, Ohio, USA. · Oregon Health and Science University, Portland, Oregon, USA. · Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA. ·BMJ Open · Pubmed #28965093.

ABSTRACT: OBJECTIVES: To evaluate potential gaps in preventive medical therapy and healthy lifestyle practices among symptomatic patients with suspected coronary artery disease (CAD) seeing primary care physicians and cardiologists and how gaps vary by sociodemographic characteristics and baseline cardiovascular risk. DESIGN: Cross-sectional study assessing potential preventive gaps. PARTICIPANTS: 10 003 symptomatic outpatients evaluated by primary care physicians, cardiologists or other specialists for suspected CAD. SETTING: PROspective Multicenter Imaging Study for Evaluation of Chest Painfrom 2010 to 2014. MEASURES: Primary measures were absence of an antihypertensive, statin or angiotensin-converting enzyme inhibitor/angiotensin receptor blocker for renal protection in patients with hypertension, dyslipidaemia or diabetes, respectively, and being sedentary, smoking or being obese. RESULTS: Preventive treatment gaps affected 14% of patients with hypertension, 36% of patients with dyslipidaemia and 32% of patients with diabetes. Overall, 49% of patients were sedentary, 18% currently smoked and 48% were obese. Women were significantly more likely to not take a statin for dyslipidaemia and to be sedentary. Patients with lower socioeconomic status were also significantly more likely to not take a statin. Compared with Whites, Blacks were significantly more likely to be obese, while Asians were less likely to smoke or be obese. High-risk patients sometimes experienced larger preventive care gaps than low-risk patients. For patients with dyslipidaemia, the presence of a treatment gap was associated with a higher risk of an adverse event (HR 1.35, 95% CI 1.02 to 1.82). CONCLUSIONS: Among contemporary, symptomatic patients with suspected CAD, significant gaps exist in preventive care and lifestyle practices, and high-risk patients sometimes had larger gaps. Differences by sex, age, race/ethnicity, socioeconomic status and geography are modest but contribute to disparities and have implications for improving opulation health. For patients with dyslipidaemia, the presence of a treatment gap was associated with a higher risk of an adverse event. CLINICAL TRIAL REGISTRATION: Clinical Trials.gov identifier NCT01174550.

53 Article Sudden Cardiac Death in Women With Suspected Ischemic Heart Disease, Preserved Ejection Fraction, and No Obstructive Coronary Artery Disease: A Report From the Women's Ischemia Syndrome Evaluation Study. 2017

Mehta, Puja K / Johnson, B Delia / Kenkre, Tanya S / Eteiba, Wafia / Sharaf, Barry / Pepine, Carl J / Reis, Steven E / Rogers, William J / Kelsey, Sheryl F / Thompson, Diane V / Bittner, Vera / Sopko, George / Shaw, Leslee J / Bairey Merz, C Noel. ·Emory University School of Medicine, Atlanta, GA puja.kiran.mehta@emory.edu. · Graduate School of Public Health, University of Pittsburgh, PA. · Rhode Island Hospital, Providence, RI. · University of Florida, Gainesville, FL. · University of Pittsburgh Medical Center, Pittsburgh, PA. · University of Alabama at Birmingham, AL. · Allegheny General Hospital, Pittsburgh, PA. · National Institutes of Health, Bethesda, MD. · Emory University School of Medicine, Atlanta, GA. · Cedars Sinai Heart Institute, Los Angeles, CA. ·J Am Heart Assoc · Pubmed #28862961.

ABSTRACT: BACKGROUND: Sudden cardiac death (SCD) is often the first presentation of ischemic heart disease; however, there is limited information on SCD among women with and without obstructive coronary artery disease (CAD). We evaluated SCD incidence in the WISE (Women's Ischemia Syndrome Evaluation) study. METHODS AND RESULTS: Overall, 904 women with suspected ischemic heart disease with preserved ejection fraction and core laboratory coronary angiography were followed for outcomes. In case of death, a death certificate and/or a physician or family narrative of the circumstances of death was obtained. A clinical events committee rated all deaths as cardiovascular or noncardiovascular and as SCD or non-SCD. In total, 96 women (11%) died over a median of 6 years (maximum: 8 years). Among 65 cardiovascular deaths, 42% were SCD. Mortality per 1000 person-hours increased linearly with CAD severity (no CAD: 5.8; minimal: 15.9; obstructive: 38.6; CONCLUSIONS: SCD contributes substantially to mortality in women with and without obstructive CAD. Corrected QT interval is the single independent SCD risk factor in women without obstructive CAD. In addition to management of traditional risk factors, these data indicate that further investigation should address mechanistic understanding and interventions targeting depression and corrected QT interval in women.

54 Article Coronary Artery Calcium Volume and Density: Potential Interactions and Overall Predictive Value: The Multi-Ethnic Study of Atherosclerosis. 2017

Criqui, Michael H / Knox, Jessica B / Denenberg, Julie O / Forbang, Nketi I / McClelland, Robyn L / Novotny, Thomas E / Sandfort, Veit / Waalen, Jill / Blaha, Michael J / Allison, Matthew A. ·Department of Family Medicine and Public Health, University of California, San Diego, La Jolla, California. Electronic address: mcriqui@ucsd.edu. · Department of Family Medicine and Public Health, University of California, San Diego, La Jolla, California. · Department of Biostatistics, University of Washington, Seattle, Washington. · Division of Epidemiology and Biostatistics, San Diego State University, San Diego, California. · National Institutes of Health Clinical Center, Department of Radiology and Imaging Sciences, Bethesda, Maryland. · Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, Maryland. ·JACC Cardiovasc Imaging · Pubmed #28797404.

ABSTRACT: OBJECTIVES: This study sought to determine the possibility of interactions between coronary artery calcium (CAC) volume or CAC density with each other, and with age, sex, ethnicity, the new atherosclerotic cardiovascular disease (ASCVD) risk score, diabetes status, and renal function by estimated glomerular filtration rate, and, using differing CAC scores, to determine the improvement over the ASCVD risk score in risk prediction and reclassification. BACKGROUND: In MESA (Multi-Ethnic Study of Atherosclerosis), CAC volume was positively and CAC density inversely associated with cardiovascular disease (CVD) events. METHODS: A total of 3,398 MESA participants free of clinical CVD but with prevalent CAC at baseline were followed for incident CVD events. RESULTS: During a median 11.0 years of follow-up, there were 390 CVD events, 264 of which were coronary heart disease (CHD). With each SD increase of ln CAC volume (1.62), risk of CHD increased 73% (p < 0.001) and risk of CVD increased 61% (p < 0.001). Conversely, each SD increase of CAC density (0.69) was associated with 28% lower risk of CHD (p < 0.001) and 25% lower risk of CVD (p < 0.001). CAC density was inversely associated with risk at all levels of CAC volume (i.e., no interaction was present). In multivariable Cox models, significant interactions were present for CAC volume with age and ASCVD risk score for both CHD and CVD, and CAC density with ASCVD risk score for CVD. Hazard ratios were generally stronger in the lower risk groups. Receiver-operating characteristic area under the curve and Net Reclassification Index analyses showed better prediction by CAC volume than by Agatston, and the addition of CAC density to CAC volume further significantly improved prediction. CONCLUSIONS: The inverse association between CAC density and incident CHD and CVD events is robust across strata of other CVD risk factors. Added to the ASCVD risk score, CAC volume and density provided the strongest prediction for CHD and CVD events, and the highest correct reclassification.

55 Article Hemoglobin Glycation Index Is Associated With Cardiovascular Diseases in People With Impaired Glucose Metabolism. 2017

Ahn, Chang Ho / Min, Se Hee / Lee, Dong-Hwa / Oh, Tae Jung / Kim, Kyoung Min / Moon, Jae Hoon / Choi, Sung Hee / Park, Kyong Soo / Jang, Hak Chul / Ha, Joon / Sherman, Arthur S / Lim, Soo. ·Department of Internal Medicine, Seoul National University College of Medicine, Seoul 03080, South Korea. · Department of Internal Medicine, Seoul National University Hospital, Seoul 03080, South Korea. · Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam 13620, South Korea. · Laboratory of Biological Modeling, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. ·J Clin Endocrinol Metab · Pubmed #28541544.

ABSTRACT: Context: There is a substantial interindividual variation in the association between glycated hemoglobin (HbA1c) and plasma glucose concentrations. Its impact on cardiovascular disease (CVD) has not been comprehensively evaluated. Objective: We examined associations between interindividual variations in HbA1c, which was estimated as the hemoglobin glycation index (HGI), and CVD. Design, Setting, and Participants: We performed a cross-sectional analysis with 1248 treatment-naïve subjects with prediabetes or diabetes. The HGI was defined as the measured HbA1c minus predicted HbA1c, which was calculated from the linear relationship between HbA1c and fasting plasma glucose levels. Main Outcome Measures: The prevalence of composite and individual CVDs including coronary artery disease (CAD), stroke, and peripheral artery disease (PAD). Results: The overall prevalence of composite CVD was 10.3% and individual prevalences of CAD, stroke, and PAD were 5.7%, 5.1%, and 1.3%, respectively. All prevalences significantly increased from the first to third tertile of HGI. In multivariate analysis, the highest HGI tertile was independently associated with composite CVD [odds ratio (95% confidence interval): 2.81 (1.59-4.98)], and individual CAD [2.30 (1.12-4.73)], stroke [3.40 (1.50-7.73)], and PAD [6.37 (1.18-34.33)] after adjustment for other CVD risk factors including HbA1c levels. Two consecutive measurements of HGI obtained on different days showed good correlation (r = 0.651, P < 0.001) and high concordance rate in the tertile classification (69.1%). Conclusions: High HGI was independently associated with overall and individual CVDs. This result suggests that discrepancy between HbA1c and fasting glucose levels can reflect vascular health in subjects with impaired glucose metabolism.

56 Article Fifteen new risk loci for coronary artery disease highlight arterial-wall-specific mechanisms. 2017

Howson, Joanna M M / Zhao, Wei / Barnes, Daniel R / Ho, Weang-Kee / Young, Robin / Paul, Dirk S / Waite, Lindsay L / Freitag, Daniel F / Fauman, Eric B / Salfati, Elias L / Sun, Benjamin B / Eicher, John D / Johnson, Andrew D / Sheu, Wayne H H / Nielsen, Sune F / Lin, Wei-Yu / Surendran, Praveen / Malarstig, Anders / Wilk, Jemma B / Tybjærg-Hansen, Anne / Rasmussen, Katrine L / Kamstrup, Pia R / Deloukas, Panos / Erdmann, Jeanette / Kathiresan, Sekar / Samani, Nilesh J / Schunkert, Heribert / Watkins, Hugh / Anonymous2140907 / Do, Ron / Rader, Daniel J / Johnson, Julie A / Hazen, Stanley L / Quyyumi, Arshed A / Spertus, John A / Pepine, Carl J / Franceschini, Nora / Justice, Anne / Reiner, Alex P / Buyske, Steven / Hindorff, Lucia A / Carty, Cara L / North, Kari E / Kooperberg, Charles / Boerwinkle, Eric / Young, Kristin / Graff, Mariaelisa / Peters, Ulrike / Absher, Devin / Hsiung, Chao A / Lee, Wen-Jane / Taylor, Kent D / Chen, Ying-Hsiang / Lee, I-Te / Guo, Xiuqing / Chung, Ren-Hua / Hung, Yi-Jen / Rotter, Jerome I / Juang, Jyh-Ming J / Quertermous, Thomas / Wang, Tzung-Dau / Rasheed, Asif / Frossard, Philippe / Alam, Dewan S / Majumder, Abdulla Al Shafi / Di Angelantonio, Emanuele / Chowdhury, Rajiv / Anonymous2150907 / Chen, Yii-Der Ida / Nordestgaard, Børge G / Assimes, Themistocles L / Danesh, John / Butterworth, Adam S / Saleheen, Danish. ·MRC/BHF Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. · Department of Biostatistics and Epidemiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA. · Department of Applied Mathematics, University of Nottingham Malaysia Campus, Semenyih, Malaysia. · Robertson Centre for Biostatistics, University of Glasgow, Glasgow, UK. · HudsonAlpha Institute for Biotechnology, Huntsville, Alabama, USA. · Pfizer Worldwide Research and Development, Cambridge, Massachusetts, USA. · Department of Medicine, Division of Cardiovascular Medicine, Stanford University, Stanford, California, USA. · Stanford Cardiovascular Institute, Stanford University, Stanford, California, USA. · National Heart, Lung, and Blood Institute, Population Sciences Branch, Bethesda, Maryland, USA. · NHLBI and Boston University's The Framingham Heart Study, Framingham, Massachusetts, USA. · Division of Endocrine and Metabolism, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan. · School of Medicine, National Yang-Ming University, Taipei, Taiwan. · College of Medicine, National Defense Medical Center, Taipei, Taiwan. · Department of Clinical Biochemistry, Herlev and Gentofte Hospital, Copenhagen University Hospital, Copenhagen, Denmark. · Northern Institute for Cancer Research, Newcastle University, Newcastle-upon-Tyne, UK. · Pfizer Worldwide Research and Development, Stockholm, Sweden. · Pfizer Worldwide Research and Development, Human Genetics, Cambridge, Massachusetts, USA. · Department of Clinical Biochemistry, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark. · Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. · William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. · Centre for Genomic Health, Queen Mary University of London, London, UK. · Institute for Cardiogenetics, University of Lübeck, Lübeck, Germany. · DZHK (German Research Centre for Cardiovascular Research), partner site Hamburg/Lübeck/Kiel, Lübeck, Germany. · University Heart Center Lübeck, Lübeck, Germany. · Center for Genomic Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA. · Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA. · Department of Cardiovascular Sciences, University of Leicester, Leicester, UK. · NIHR Leicester Biomedical Research Centre, Glenfield Hospital, Leicester, UK. · Deutsches Herzzentrum München, Technische Universität München, Munich, Germany. · DZHK (German Center for Cardiovascular Research), partner site Munich Heart Alliance, Munich, Germany. · Radcliffe Department of Medicine, University of Oxford, Oxford, UK. · Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK. · Charles Bronfman Institute for Personalized Medicine, Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA. · Departments of Genetics, Medicine, and Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA. · University of Florida College of Pharmacy, Gainesville, Florida, USA. · Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland, Ohio, USA. · Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia, USA. · Saint Luke's Mid America Heart Institute, Kansas City, Missouri, USA. · Department of Biomedical and Health Informatics, University of Missouri-Kansas City, Kansas City, Missouri, USA. · College of Medicine, University of Florida, Gainesville, Florida, USA. · Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, North Carolina, USA. · Department of Epidemiology, University of Washington, Seattle, Washington, USA. · Department of Statistics and Biostatistics, Rutgers University, Piscataway, New Jersey, USA. · Division of Genomic Medicine, National Human Genome Research Institute, US National Institutes of Health, Bethesda,Maryland, USA. · Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA. · Carolina Center for Genome Sciences, Chapel Hill, North Carolina, USA. · Human Genetics Center, School of Public Health, University of Texas Health Science Center at Houston, Houston, Texas, USA. · Human Genome Sequencing Center, Baylor College of Medicine, Houston, Texas, USA. · Division of Biostatistics and Bioinformatics, Institute of Population Health Sciences, National Health Research Institutes, Miaoli, Taiwan. · Department of Medical Research, Taichung Veterans General Hospital, Taichung, Taiwan. · Institute for Translational Genomics and Population Sciences, Department of Pediatrics, LABioMed at Harbor-UCLA Medical Center, Torrance, California, USA. · School of Medicine, Chung Shan Medical University, Taichung, Taiwan. · Division of Endocrinology and Metabolism, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan. · Institute for Translational Genomics and Population Sciences, Departments of Pediatrics and Medicine, LABioMed at Harbor-UCLA Medical Center, Torrance, California, USA. · Cardiovascular Center and Division of Cardiology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan. · National Taiwan University College of Medicine, Taipei, Taiwan. · Centre for Non-Communicable Disease, Karachi, Pakistan. · School of Kinesiology and Health Science, York University, Toronto, Ontario, Canada. · National Institute of Cardiovascular Diseases, Sher-e-Bangla Nagar, Bangladesh. · National Institute for Health Research Blood and Transplant Research Unit in Donor Health and Genomics, University of Cambridge, Cambridge, UK. · Wellcome Trust Sanger Institute, Hinxton, UK. · British Heart Foundation Cambridge Centre of Excellence, Department of Medicine, University of Cambridge, Cambridge, UK. ·Nat Genet · Pubmed #28530674.

ABSTRACT: Coronary artery disease (CAD) is a leading cause of morbidity and mortality worldwide. Although 58 genomic regions have been associated with CAD thus far, most of the heritability is unexplained, indicating that additional susceptibility loci await identification. An efficient discovery strategy may be larger-scale evaluation of promising associations suggested by genome-wide association studies (GWAS). Hence, we genotyped 56,309 participants using a targeted gene array derived from earlier GWAS results and performed meta-analysis of results with 194,427 participants previously genotyped, totaling 88,192 CAD cases and 162,544 controls. We identified 25 new SNP-CAD associations (P < 5 × 10

57 Article Coronary Plaque Characterization in Psoriasis Reveals High-Risk Features That Improve After Treatment in a Prospective Observational Study. 2017

Lerman, Joseph B / Joshi, Aditya A / Chaturvedi, Abhishek / Aberra, Tsion M / Dey, Amit K / Rodante, Justin A / Salahuddin, Taufiq / Chung, Jonathan H / Rana, Anshuma / Teague, Heather L / Wu, Jashin J / Playford, Martin P / Lockshin, Benjamin A / Chen, Marcus Y / Sandfort, Veit / Bluemke, David A / Mehta, Nehal N. ·From National Institutes of Health, National Heart, Lung, and Blood Institute, Bethesda, MD (J.B.L., A.A.J., A.C., T.M.A., A.K.D., J.A.R., T.S., J.H.C., A.R., H.L.T., M.P.P., M.Y.C., V.S., D.A.B., N.N.M.) · Department of Dermatology, Kaiser Permanente Los Angeles Medical Center, CA (J.J.W.) · and DermAssociates, Silver Spring, MD (B.A.L.). ·Circulation · Pubmed #28483812.

ABSTRACT: BACKGROUND: Psoriasis, a chronic inflammatory disease associated with an accelerated risk of myocardial infarction, provides an ideal human model to study inflammatory atherogenesis in vivo. We hypothesized that the increased cardiovascular risk observed in psoriasis would be partially attributable to an elevated subclinical coronary artery disease burden composed of noncalcified plaques with high-risk features. However, inadequate efforts have been made to directly measure coronary artery disease in this vulnerable population. As such, we sought to compare total coronary plaque burden and noncalcified coronary plaque burden (NCB) and high-risk plaque (HRP) prevalence between patients with psoriasis (n=105), patients with hyperlipidemia eligible for statin therapy under National Cholesterol Education Program-Adult Treatment Panel III guidelines (n=100) who were ≈10 years older, and healthy volunteers without psoriasis (n=25). METHODS: Patients underwent coronary computed-tomography angiography for total coronary plaque burden and NCB quantification and HRP identification, defined as low attenuation (<30 hounsfield units), positive remodeling (>1.10), and spotty calcification. A consecutive sample of the first 50 patients with psoriasis was scanned again 1 year after therapy. RESULTS: Despite being younger and at lower traditional risk than patients with hyperlipidemia, patients with psoriasis had increased NCB (mean±SD: 1.18±0.33 versus 1.11±0.32, CONCLUSIONS: Patients with psoriasis had greater NCB and increased HRP prevalence than healthy volunteers. In addition, patients with psoriasis had elevated NCB and equivalent HRP prevalence as older patients with hyperlipidemia. Last, modulation of target organ inflammation (eg, skin) was associated with an improvement in NCB at 1 year, suggesting that control of remote sites of inflammation may translate into reduced coronary artery disease risk.

58 Article Progression of Coronary Artery Calcium and Incident Heart Failure: The Multi-Ethnic Study of Atherosclerosis. 2017

Bakhshi, Hooman / Ambale-Venkatesh, Bharath / Yang, Xiaoying / Ostovaneh, Mohammad R / Wu, Colin O / Budoff, Matthew / Bahrami, Hossein / Wong, Nathan D / Bluemke, David A / Lima, João A C. ·Cardiology Division, Department of Medicine, Johns Hopkins Hospital, Baltimore, MD. · George Washington University, Washington, DC. · Office of Biostatistics Research, National Heart Lung and Blood Institute, Bethesda, MD. · Division of Cardiology, Harbor-UCLA Medical Center, Torrance, CA. · Division of Cardiovascular Medicine, Keck School of Medicine of University of Southern California, Los Angeles, CA. · Division of Cardiology, University of California, Irvine, Irvine, CA. · Radiology and Imaging Sciences, National Institutes of Health (NIH), Bethesda, MD. · Cardiology Division, Department of Medicine, Johns Hopkins Hospital, Baltimore, MD jlima@jhmi.edu. ·J Am Heart Assoc · Pubmed #28428195.

ABSTRACT: BACKGROUND: Although the association between coronary artery calcium (CAC) and future heart failure (HF) has been shown previously, the value of CAC progression in the prediction of HF has not been investigated. In this study, we investigated the association of CAC progression with subclinical left ventricular (LV) dysfunction and incident HF in the Multi-Ethnic Study of Atherosclerosis. METHODS AND RESULTS: The Multi-Ethnic Study of Atherosclerosis is a population-based study consisting of 6814 men and women aged 45 to 84, free of overt cardiovascular disease at enrollment, who were recruited from 4 ethnicities. We included 5644 Multi-Ethnic Study of Atherosclerosis participants who had baseline and follow-up cardiac computed tomography and were free of HF and coronary heart disease before the second cardiac computed tomography. Mean (±SD) age was 61.7±10.2 years and 47.2% were male. The Cox proportional hazard models and multivariable linear regression models were deployed to determine the association of CAC progression with incident HF and subclinical LV dysfunction, respectively. Over a median follow-up of 9.6 (interquartile range: 8.8-10.6) years, 182 participants developed incident HF. CAC progression of 10 units per year was associated with 3% of increased risk of HF independent of overt coronary heart disease ( CONCLUSIONS: CAC progression was associated with incident HF and modestly increased LV end diastolic volume and LV end systolic volume at follow-up exam independent of overt coronary heart disease.

59 Article A longitudinal study of smokeless tobacco use and mortality in the United States. 2017

Timberlake, David S / Nikitin, Dmitriy / Johnson, Norman J / Altekruse, Sean F. ·Program in Public Health, University of California, Irvine, Irvine, CA. · School of Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC. · The United States Census Bureau, Suitland, MD. · Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, MD. ·Int J Cancer · Pubmed #28411395.

ABSTRACT: Few studies in the United States have examined longitudinally the mortality risks associated with use of smokeless tobacco (SLT). The sample of our study was composed of participants from the National Longitudinal Mortality Study who completed a single Tobacco Use Supplement to the Current Population Survey between the years 1985 and 2011. Using survival methods, SLT use at the baseline survey was examined as a predictor of all-cause mortality and cause-specific mortalities in models that excluded individuals who had ever smoked cigarettes, cigars or used pipes (final n = 349,282). The participants had median and maximum follow-up times of 8.8 and 26.3 years, respectively. Regression analyses indicated that compared to the never tobacco users, the current SLT users did not have elevated mortality risks from all cancers combined, the digestive system cancers and cerebrovascular disease. However, current SLT users had a higher mortality risk for coronary heart disease (CHD) [hazard ratio (HR) (95% CI) = 1.24 (1.05, 1.46)] relative to never tobacco users. In a separate model, the elevated risk for CHD mortality corresponded to the use of moist snuff [HR (95% CI) = 1.30 (1.03, 1.63)]. The associations with CHD mortality could be attributed to long-term nicotine exposure, other SLT constituents (e.g., metals) or the confounding effects of CHD risk factors not accounted for in our study. The study's findings contribute to the ongoing dialogue on tobacco harm reduction and the US FDA's evaluation of Modified Risk Tobacco Product applications submitted by American SLT manufacturers.

60 Article Prognostic Value of Combined CT Angiography and Myocardial Perfusion Imaging versus Invasive Coronary Angiography and Nuclear Stress Perfusion Imaging in the Prediction of Major Adverse Cardiovascular Events: The CORE320 Multicenter Study. 2017

Chen, Marcus Y / Rochitte, Carlos E / Arbab-Zadeh, Armin / Dewey, Marc / George, Richard T / Miller, Julie M / Niinuma, Hiroyuki / Yoshioka, Kunihiro / Kitagawa, Kakuya / Sakuma, Hajime / Laham, Roger / Vavere, Andrea L / Cerci, Rodrigo J / Mehra, Vishal C / Nomura, Cesar / Kofoed, Klaus F / Jinzaki, Masahiro / Kuribayashi, Sachio / Scholte, Arthur J / Laule, Michael / Tan, Swee Yaw / Hoe, John / Paul, Narinder / Rybicki, Frank J / Brinker, Jeffrey A / Arai, Andrew E / Matheson, Matthew B / Cox, Christopher / Clouse, Melvin E / Di Carli, Marcelo F / Lima, João A C. ·From the Laboratory of Cardiac Energetics, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Md (M.Y.C., A.E.A.) · InCor Heart Institute, University of São Paulo Medical School, Brazil, São Paulo, Brazil (C.E.R.) · Johns Hopkins Hospital and School of Medicine, 600 N Wolfe St, Blalock 524, Baltimore, MD 21287 (A.A., R.T.G., J.M.M., A.L.V., R.J.C., V.C.M., J.A.B., J.A.C.L.) · Department of Radiology, Charité Medical School-Humboldt, Berlin, Germany (M.D., M.L.) · Memorial Heart Center, Iwate Medical University, Morioka, Japan (H.N., K.Y.) · Department of Radiology, St. Luke's International Hospital, Tokyo, Japan (H.N.) · Department of Radiology, Mie University Hospital, Tsu, Japan (K.K., H.S.) · Department of Radiology, Beth Israel Deaconess Medical Center, Harvard University, Boston, Mass (R.L., M.E.C.) · and Radiology Sector, Hospital Israelita Albert Einstein, São Paulo, Brazil (C.N.) · From the Department of Cardiology, Rigshospitalet, University of Copenhagen, Denmark (K.F.K.) · Keio University School of Medicine, Tokyo, Japan (M.J., S.K.) · Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands (A.J.S.) · Department of Cardiology, National Heart Centre, Singapore (S.Y.T.) · Medi-Rad Associates, CT Centre, Mount Elizabeth Hospital, Singapore (J.H.) · Department of Medical Imaging, Toronto General Hospital, Toronto, Ontario, Canada (N.P.) · Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada (F.J.R.) · Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Md (M.B.M., C.C.) · and Department of Nuclear Medicine and Cardiovascular Imaging, Brigham and Women's Hospital, Boston, Mass (M.F.D.C.). ·Radiology · Pubmed #28290782.

ABSTRACT: Purpose To compare the prognostic importance (time to major adverse cardiovascular event [MACE]) of combined computed tomography (CT) angiography and CT myocardial stress perfusion imaging with that of combined invasive coronary angiography (ICA) and stress single photon emission CT myocardial perfusion imaging. Materials and Methods This study was approved by all institutional review boards, and written informed consent was obtained. Between November 2009 and July 2011, 381 participants clinically referred for ICA and aged 45-85 years were enrolled in the Combined Noninvasive Coronary Angiography and Myocardial Perfusion Imaging Using 320-Detector Row Computed Tomography (CORE320) prospective multicenter diagnostic study. All images were analyzed in blinded independent core laboratories, and a panel of physicians adjudicated all adverse events. MACE was defined as revascularization (>30 days after index ICA), myocardial infarction, or cardiac death; hospitalization for chest pain or congestive heart failure; or arrhythmia. Late MACE was defined similarly, except for patients who underwent revascularization within the first 182 days after ICA, who were excluded. Comparisons of 2-year survival (time to MACE) used standard Kaplan-Meier curves and restricted mean survival times bootstrapped with 2000 replicates. Results An MACE (49 revascularizations, five myocardial infarctions, one cardiac death, nine hospitalizations for chest pain or congestive heart failure, and one arrhythmia) occurred in 51 of 379 patients (13.5%). The 2-year MACE-free rates for combined CT angiography and CT perfusion findings were 94% negative for coronary artery disease (CAD) versus 82% positive for CAD and were similar to combined ICA and single photon emission CT findings (93% negative for CAD vs 77% positive for CAD, P < .001 for both). Event-free rates for CT angiography and CT perfusion versus ICA and single photon emission CT for either positive or negative results were not significantly different for MACE or late MACE (P > .05 for all). The area under the receiver operating characteristic curve (AUC) for combined CT angiography and CT perfusion (AUC = 68; 95% confidence interval [CI]: 62, 75) was similar (P = .36) to that for combined ICA and single photon emission CT (AUC = 71; 95% CI: 65, 79) in the identification of MACE at 2-year follow-up. Conclusion Combined CT angiography and CT perfusion enables similar prediction of 2-year MACE, late MACE, and event-free survival similar to that enabled by ICA and single photon emission CT.

61 Article High levels of serum β2-microglobulin predict severity of coronary artery disease. 2017

You, Ling / Xie, Ruiqin / Hu, Haijuan / Gu, Guoqiang / Zheng, Hongmei / Zhang, Jidong / Yang, Xiaohong / He, Ximiao / Cui, Wei. ·Division of Cardiology, The Second Hospital of Hebei Medical University, 215 Heping West Rd, Xinhua, Shijiazhuang, Hebei, 050000, People's Republic of China. · Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Bethesda, MD, 20892, USA. Ximiao.He@gmail.com. · Division of Cardiology, The Second Hospital of Hebei Medical University, 215 Heping West Rd, Xinhua, Shijiazhuang, Hebei, 050000, People's Republic of China. cuiwei@medmail.com.cn. ·BMC Cardiovasc Disord · Pubmed #28249620.

ABSTRACT: BACKGROUND: The identification of new risk factors for coronary artery disease (CAD) is increasingly sought in an effort to tackle this threatening disease. β2-microglobulin (B2M) is reported to associate with peripheral arterial disease and adverse cardiovascular outcomes. However, the association between B2M and cardiovascular disease remains under-researched. This study evaluated the effects of B2M on CAD without renal dysfunction. METHODS: One thousand seven hundred sixty-two subjects (403 non-CAD subjects and 1,359 CAD subjects) were investigated. Fasting samples were collected to determine B2M level. The Gensini and SYNTAX scores were used to assess the severity of CAD. RESULTS: CAD subjects were significantly higher in serum B2M level comparing with non-CAD subjects (1.25 ± 0.46 vs 1.14 ± 0.28 mg/L, p < 0.001). Serum B2M level was a risk factor of CAD after adjusting potential confounders (Odds Ratio (OR) = 2.363, 95% confidence interval (CI): 1.467-3.906, p = 0.001). Receiver operating characteristics (ROC) showed B2M level moderately predicted diagnosis of CAD (the area under the ROC curve (AUC) = 0.608, 95% CI: 0.577-0.639, p < 0.001). Furthermore, serum B2M level was positively associated with Gensini score system, SYNTAX score system and the number of disease vessels (NDV ≥ 2). CONCLUSIONS: The significant association between serum B2M and CAD suggests that B2M could be a biomarker for CAD.

62 Article Association of Coronary Artery Calcium in Adults Aged 32 to 46 Years With Incident Coronary Heart Disease and Death. 2017

Carr, John Jeffrey / Jacobs, David R / Terry, James G / Shay, Christina M / Sidney, Stephen / Liu, Kiang / Schreiner, Pamela J / Lewis, Cora E / Shikany, James M / Reis, Jared P / Goff, David C. ·Department of Radiology and Radiological Sciences, Vanderbilt University Medical Center, Nashville, Tennessee. · Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis. · Center for Health Metrics and Evaluation, American Heart Association, Dallas, Texas. · Division of Research, Kaiser Permanente, Oakland, California. · Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois. · Division of Preventive Medicine, Department of Medicine, University of Alabama at Birmingham. · Division of Cardiovascular Sciences, National Heart, Lung, and Blood Institute, Bethesda, Maryland. · Department of Epidemiology, Colorado School of Public Health, Aurora. ·JAMA Cardiol · Pubmed #28196265.

ABSTRACT: Importance: Coronary artery calcium (CAC) is associated with coronary heart disease (CHD) and cardiovascular disease (CVD); however, prognostic data on CAC are limited in younger adults. Objective: To determine if CAC in adults aged 32 to 46 years is associated with incident clinical CHD, CVD, and all-cause mortality during 12.5 years of follow-up. Design, Setting, and Participants: The Coronary Artery Risk Development in Young Adults (CARDIA) Study is a prospective community-based study that recruited 5115 black and white participants aged 18 to 30 years from March 25, 1985, to June 7, 1986. The cohort has been under surveillance for 30 years, with CAC measured 15 (n = 3043), 20 (n = 3141), and 25 (n = 3189) years after recruitment. The mean follow-up period for incident events was 12.5 years, from the year 15 computed tomographic scan through August 31, 2014. Main Outcomes and Measures: Incident CHD included fatal or nonfatal myocardial infarction, acute coronary syndrome without myocardial infarction, coronary revascularization, or CHD death. Incident CVD included CHD, stroke, heart failure, and peripheral arterial disease. Death included all causes. The probability of developing CAC by age 32 to 56 years was estimated using clinical risk factors measured 7 years apart between ages 18 and 38 years. Results: At year 15 of the study among 3043 participants (mean [SD] age, 40.3 [3.6] years; 1383 men and 1660 women), 309 individuals (10.2%) had CAC, with a geometric mean Agatston score of 21.6 (interquartile range, 17.3-26.8). Participants were followed up for 12.5 years, with 57 incident CHD events and 108 incident CVD events observed. After adjusting for demographics, risk factors, and treatments, those with any CAC experienced a 5-fold increase in CHD events (hazard ratio [HR], 5.0; 95% CI, 2.8-8.7) and 3-fold increase in CVD events (HR, 3.0; 95% CI, 1.9-4.7). Within CAC score strata of 1-19, 20-99, and 100 or more, the HRs for CHD were 2.6 (95% CI, 1.0-5.7), 5.8 (95% CI, 2.6-12.1), and 9.8 (95% CI, 4.5-20.5), respectively. A CAC score of 100 or more had an incidence of 22.4 deaths per 100 participants (HR, 3.7; 95% CI, 1.5-10.0); of the 13 deaths in participants with a CAC score of 100 or more, 10 were adjudicated as CHD events. Risk factors for CVD in early adult life identified those above the median risk for developing CAC and, if applied, in a selective CAC screening strategy could reduce the number of people screened for CAC by 50% and the number imaged needed to find 1 person with CAC from 3.5 to 2.2. Conclusions and Relevance: The presence of CAC among individuals aged between 32 and 46 years was associated with increased risk of fatal and nonfatal CHD during 12.5 years of follow-up. A CAC score of 100 or more was associated with early death. Adults younger than 50 years with any CAC, even with very low scores, identified on a computed tomographic scan are at elevated risk of clinical CHD, CVD, and death. Selective use of screening for CAC might be considered in individuals with risk factors in early adulthood to inform discussions about primary prevention.

63 Article Association of Body Mass Index with DNA Methylation and Gene Expression in Blood Cells and Relations to Cardiometabolic Disease: A Mendelian Randomization Approach. 2017

Mendelson, Michael M / Marioni, Riccardo E / Joehanes, Roby / Liu, Chunyu / Hedman, Åsa K / Aslibekyan, Stella / Demerath, Ellen W / Guan, Weihua / Zhi, Degui / Yao, Chen / Huan, Tianxiao / Willinger, Christine / Chen, Brian / Courchesne, Paul / Multhaup, Michael / Irvin, Marguerite R / Cohain, Ariella / Schadt, Eric E / Grove, Megan L / Bressler, Jan / North, Kari / Sundström, Johan / Gustafsson, Stefan / Shah, Sonia / McRae, Allan F / Harris, Sarah E / Gibson, Jude / Redmond, Paul / Corley, Janie / Murphy, Lee / Starr, John M / Kleinbrink, Erica / Lipovich, Leonard / Visscher, Peter M / Wray, Naomi R / Krauss, Ronald M / Fallin, Daniele / Feinberg, Andrew / Absher, Devin M / Fornage, Myriam / Pankow, James S / Lind, Lars / Fox, Caroline / Ingelsson, Erik / Arnett, Donna K / Boerwinkle, Eric / Liang, Liming / Levy, Daniel / Deary, Ian J. ·Framingham Heart Study, Framingham, Massachusetts, United States of America. · Boston University School of Medicine, Boston, Massachusetts, United States of America. · Department of Cardiology, Boston Children's Hospital, Boston, Massachusetts, United States of America. · Population Sciences Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, United States of America. · Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, United Kingdom. · Medical Genetics Section, Centre for Genomic and Experimental Medicine, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom. · Queensland Brain Institute, University of Queensland, Brisbane, Queensland, Australia. · Hebrew SeniorLife, Harvard Medical School, Boston, Massachusetts, United States of America. · Department of Biostatistics, Boston University, Boston, Massachusetts, United States of America. · Molecular Epidemiology and Science for Life Laboratory, Department of Medical Sciences, Uppsala University, Uppsala, Sweden. · Department of Epidemiology, School of Public Health, University of Alabama at Birmingham, Birmingham, Alabama, United States of America. · Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota, United States of America. · Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, Minnesota, United States of America. · Department of Biostatistics, School of Public Health, University of Alabama at Birmingham, Birmingham, Alabama, United States of America. · Center for Epigenetics, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America. · Icahn Institute for Genomics and Multiscale Biology and Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America. · Human Genetics Center, School of Public Health, University of Texas Health Science Center at Houston, Houston, Texas, United States of America. · Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America. · Cardiovascular Epidemiology, Department of Medical Sciences, Uppsala University, Uppsala, Sweden. · Institute for Molecular Bioscience, University of Queensland, Brisbane, Queensland, Australia. · Wellcome Trust Clinical Research Facility, Western General Hospital, University of Edinburgh, Edinburgh, United Kingdom. · Department of Psychology, University of Edinburgh, Edinburgh, United Kingdom. · Alzheimer Scotland Dementia Research Centre, University of Edinburgh, Edinburgh, United Kingdom. · Center for Molecular Medicine and Genetics and Department of Neurology, Wayne State University, Detroit, Michigan, United States of America. · Children's Hospital Oakland Research Institute, Oakland, California, United States of America. · HudsonAlpha Institute for Biotechnology, Huntsville, Alabama, United States of America. · Brown Foundation Institute of Molecular Medicine, University of Texas, Houston, Texas, United States of America. · Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California, United States of America. · College of Public Health, University of Kentucky, Lexington, Kentucky, United States of America. · Human Genome Sequencing Center, Baylor College of Medicine, Houston, Texas, United States of America. · Departments of Epidemiology and Biostatistics, School of Public Health, Harvard University, Boston, Massachusetts, United States of America. ·PLoS Med · Pubmed #28095459.

ABSTRACT: BACKGROUND: The link between DNA methylation, obesity, and adiposity-related diseases in the general population remains uncertain. METHODS AND FINDINGS: We conducted an association study of body mass index (BMI) and differential methylation for over 400,000 CpGs assayed by microarray in whole-blood-derived DNA from 3,743 participants in the Framingham Heart Study and the Lothian Birth Cohorts, with independent replication in three external cohorts of 4,055 participants. We examined variations in whole blood gene expression and conducted Mendelian randomization analyses to investigate the functional and clinical relevance of the findings. We identified novel and previously reported BMI-related differential methylation at 83 CpGs that replicated across cohorts; BMI-related differential methylation was associated with concurrent changes in the expression of genes in lipid metabolism pathways. Genetic instrumental variable analysis of alterations in methylation at one of the 83 replicated CpGs, cg11024682 (intronic to sterol regulatory element binding transcription factor 1 [SREBF1]), demonstrated links to BMI, adiposity-related traits, and coronary artery disease. Independent genetic instruments for expression of SREBF1 supported the findings linking methylation to adiposity and cardiometabolic disease. Methylation at a substantial proportion (16 of 83) of the identified loci was found to be secondary to differences in BMI. However, the cross-sectional nature of the data limits definitive causal determination. CONCLUSIONS: We present robust associations of BMI with differential DNA methylation at numerous loci in blood cells. BMI-related DNA methylation and gene expression provide mechanistic insights into the relationship between DNA methylation, obesity, and adiposity-related diseases.

64 Article Coronary Plaque Progression and Regression in Asymptomatic African American Chronic Cocaine Users With Obstructive Coronary Stenoses: A Preliminary Study. 2017

Sandfort, Veit / Bluemke, David A / Vargas, Jose / Brinker, Jeffrey A / Gerstenblith, Gary / Kickler, Thomas / Zheng, Gang / Li, Ji / Chen, Shaoguang / Lai, Hong / Fishman, Elliot K / Lai, Shenghan. ·Department of Radiology and Imaging Sciences (VS, DAB, JV), National Institutes of Health Clinical, Center, Bethesda · Department of Radiology (DAB, HL, EKF, SL), Johns Hopkins School of Medicine, Baltimore, MD · MedStar Health Research Institute (JV), Georgetown University Hospital, Washington, DC · Department of Medicine (JAB, GG, SL) · and Department of Pathology (TK, GZ, JL, SC, SL), Johns Hopkins School of Medicine, Baltimore, MD. ·J Addict Med · Pubmed #28060223.

ABSTRACT: OBJECTIVE: Although rapid progression of coronary atherosclerosis was observed in chronic cocaine users, it is unknown whether reduced cocaine use retards the progression of atherosclerosis. We investigated whether reduced cocaine use over a 12-month period was associated with coronary plaque regression in cocaine users. METHODS: Fifteen African American chronic cocaine users with previously coronary computed tomography angiography (CCTA)-confirmed >50% coronary stenosis in Baltimore, Maryland, were enrolled in a study to investigate whether reduced cocaine use is associated with changes in coronary plaque burden over a 12-month period of cash-based incentive intervention, which was implemented to systematically reinforce cocaine abstinence. In addition to previous CCTA (preintervention), CCTA was performed at the intervention baseline and at postintervention. Plaque analyses were performed to determine the trajectory of plaque changes in the absence of intervention by comparing the preintervention with the intervention baseline studies; the trajectory of plaque changes associated with the intervention by comparing the intervention baseline with the postintervention studies; and (3) whether reduced cocaine use was independently associated with changes in coronary plaque burden. RESULTS: During the 12-month cash-based incentive intervention period, cocaine use in participants was lower. The medians of noncalcified plaque indices were 37.8 (interquartile range [IQR] 29.3-44.0), 43.1 (IQR 38.3-49.0), and 38.7 (IQR 31.2-46.8) mm at preintervention, intervention baseline, and postintervention, respectively. Multivariable generalized estimating equation analysis showed that both total plaque and noncalcified plaque indices at preintervention were significantly lowered as compared with intervention baseline levels; both total plaque and noncalcified plaque indices after intervention were significantly lowered as compared with intervention baseline levels; and reduced cocaine use was independently associated with lower total plaque volume index (P < 0.0001) and noncalcified plaque volume index (P = 0.010). CONCLUSIONS: Our findings suggest that continued cocaine use may be associated with noncalcified plaque progression, whereas reduced cocaine use may be associated with noncalcified plaque regression. Larger studies are needed to confirm these findings.

65 Article Transition in the mechanism of flow-mediated dilation with aging and development of coronary artery disease. 2017

Beyer, Andreas M / Zinkevich, Natalya / Miller, Bradley / Liu, Yanping / Wittenburg, April L / Mitchell, Michael / Galdieri, Ralph / Sorokin, Andrey / Gutterman, David D. ·Department of Medicine, Medical College of Wisconsin, Milwaukee, USA. abeyer@mcw.edu. · Department of Physiology, Cardiovascular Center, Medical College of Wisconsin, HRC H4875, 8701 Watertown Plank Rd., Milwaukee, WI, 53226, USA. abeyer@mcw.edu. · Department of Medicine, Medical College of Wisconsin, Milwaukee, USA. · Department of Health and Medicine, Carroll University, Waukesha, USA. · NIH NIGMS, Bethesda, USA. · Department of Physiology, Cardiovascular Center, Medical College of Wisconsin, HRC H4875, 8701 Watertown Plank Rd., Milwaukee, WI, 53226, USA. · Children's Hospital of Wisconsin, Wauwatosa, USA. · Wheaton Franciscan Healthcare, Wheaton, USA. · Clement J. Zablocki VA Medical Center Milwaukee, Milwaukee, USA. ·Basic Res Cardiol · Pubmed #27995364.

ABSTRACT: In microvessels of patients with coronary artery disease (CAD), flow-mediated dilation (FMD) is largely dependent upon the endothelium-derived hyperpolarizing factor H

66 Article Coronary Artery Calcium to Guide a Personalized Risk-Based Approach to Initiation and Intensification of Antihypertensive Therapy. 2017

McEvoy, John W / Martin, Seth S / Dardari, Zeina A / Miedema, Michael D / Sandfort, Veit / Yeboah, Joseph / Budoff, Matthew J / Goff, David C / Psaty, Bruce M / Post, Wendy S / Nasir, Khurram / Blumenthal, Roger S / Blaha, Michael J. ·From Ciccarone Center for the Prevention of Heart Disease, Johns Hopkins University School of Medicine, Baltimore, MD (J.W.M., S.S.M., Z.A.D., W.S.P., K.N., R.S.B., M.J.Blaha) · Minneapolis Heart Institute and Minneapolis Heart Institute Foundation, MN (M.D.M.) · Radiology and Imaging Sciences, National Institutes of Health, Bethesda, MD (V.S.) · Heart and Vascular Center of Excellence, Wake Forest Baptist Health, Winston-Salem, NC (J.Y.) · Los Angeles Biomedical Research Institute at Harbor-UCLA, Torrance, CA (M.J.Budoff) · Department of Epidemiology, Colorado School of Public Health, Aurora (D.C.G.) · Cardiovascular Health Research Unit, Departments of Medicine, Epidemiology, and Health Services, University of Washington, Seattle (B.M.P.) · and Center for Healthcare Advancement and Outcomes and Miami Cardiac and Vascular Institute, Baptist Health South Florida (K.N.). ·Circulation · Pubmed #27881560.

ABSTRACT: BACKGROUND: The use of atherosclerotic cardiovascular disease (ASCVD) risk to personalize systolic blood pressure (SBP) treatment goals is a topic of increasing interest. Therefore, we studied whether coronary artery calcium (CAC) can further guide the allocation of anti-hypertensive treatment intensity. METHODS: We included 3733 participants from the Multi-Ethnic Study of Atherosclerosis (MESA) with SBP between 120 and 179 mm Hg. Within subgroups categorized by both SBP (120-139 mm Hg, 140-159 mm Hg, and 160-179 mm Hg) and estimated 10-year ASCVD risk (using the American College of Cardiology/American Heart Assocation pooled-cohort equations), we compared multivariable-adjusted hazard ratios for the composite outcome of incident ASCVD or heart failure after further stratifying by CAC (0, 1-100, or >100). We estimated 10-year number-needed-to-treat for an intensive SBP goal of 120 mm Hg by applying the treatment benefit recorded in meta-analyses to event rates within CAC strata. RESULTS: The mean age was 65 years, and 642 composite events took place over a median of 10.2 years. In persons with SBP <160 mm Hg, CAC stratified risk for events. For example, among those with an ASCVD risk of <15% and who had an SBP of either 120 to 139 mm Hg or 140 to 159 mm Hg, respectively, we found increasing hazard ratios for events with CAC 1 to 100 (1.7 [95% confidence interval, 1.0-2.6] or 2.0 [1.1-3.8]) and CAC >100 (3.0 [1.8-5.0] or 5.7 [2.9-11.0]), all relative to CAC=0. There appeared to be no statistical association between CAC and events when SBP was 160 to 179 mm Hg, irrespective of ASCVD risk level. Estimated 10-year number-needed-to-treat for a SBP goal of 120mmHg varied substantially according to CAC levels when predicted ASCVD risk <15% and SBP <160mmHg (eg, 10-year number-needed-to-treat of 99 for CAC=0 and 24 for CAC>100, when SBP 120-139mm Hg). However, few participants with ASCVD risk <5% had elevated CAC. Furthermore, 10-year number-needed-to-treat estimates were consistently low and varied less among CAC strata when SBP was 160 to 179 mm Hg or when ASCVD risk was ≥15% at any SBP level. CONCLUSIONS: Combined CAC imaging and assessment of global ASCVD risk has the potential to guide personalized SBP goals (eg, choosing a traditional goal of 140 or a more intensive goal of 120 mm Hg), particularly among adults with an estimated ASCVD risk of 5% to 15% and prehypertension or mild hypertension.

67 Article Guideline-based statin/lipid-lowering therapy eligibility for primary prevention and accuracy of coronary artery calcium and clinical cardiovascular events: The Multi-Ethnic Study of Atherosclerosis (MESA). 2017

Flueckiger, Peter / Qureshi, Waqas / Michos, Erin D / Blaha, Michael / Burke, Gregory / Sandfort, Veit / Herrington, David / Yeboah, Joseph. ·Heart and Vascular Center of Excellence, Wake Forest School of Medicine, Winston-Salem, North Carolina. · Ciccarone Center for the Prevention of Heart Disease, Johns Hopkins University School of Medicine, Baltimore, Maryland. · Division of Public Health Sciences, Wake Forest School of Medicine, Winston-Salem, North Carolina. · Radiology and Imaging Services, National Institutes of Health, Bethesda, Maryland. ·Clin Cardiol · Pubmed #27859433.

ABSTRACT: BACKGROUND: With multiple cholesterol guidelines, we evaluated the accuracy of recommended statin therapy on identifying coronary artery calcium (CAC) and cardiovascular disease (CVD) events by 2004 NCEP/ ATP III, 2016 ESC/EAS, and 2013 ACC/AHA guidelines. HYPOTHESIS: ACC/AHA guidelines are more accurate in identifying persons at risk for CVD. METHODS: 5002/6814 participants age <75 years and free of CVD were included. CAC categories (>0, ≥100, and ≥300) and 10 years of CVD outcomes were considered. Sensitivity (SN), specificity (SP), positive and negative predictive value (PPV and NPV), and likelihood ratios (LR) were calculated. Mean age was 59 years; 47% of subjects were males. RESULTS: 1297 (26%), 1381 (28%), and 2538 (51%) had class I indications for statin/LLT by the NCEP ATP III, ESC/EAS, and AHA/ACC guidelines, respectively. SN, SP, NPV, and PPV for CAC ≥300 were: NCEP ATP III (41.1%, 75.5%, 93.3% and 13.4%), ESC/EAS (54.1%, 74.8%, 94.6% and16.6%), and ACC/AHA (87.2%, 52.6%, 97.8% and 14.5%). SN, SP, PPV, and NPV for corresponding CVD outcomes were: NCEP ATP III (45.8%, 75.1%, 96.3%, and 8.9%), ESC/EAS (50.5%, 72.9%, 98.7%, and 3.6%), and AHA/ACC (79.6%, 50.7%, 98%, and 7.7%). ESC/EAS had significantly higher positive LR 2.15 (95% CI, 1.95 - 2.38) and ACC/AHA had significantly lower negative LR [0.24, (95% CI 0.19 - 0.31)] for corresponding CVD. CONCLUSIONS: Despite the increased in SN of statin eligibility by the ACC/AHA, it has similar NPV and PPV for CAC/future CVD events. The ACC/AHA class I indications for statin may be a superior screening tool for subclinical and clinical CVD.

68 Article Longevity-Associated FOXO3 Genotype and its Impact on Coronary Artery Disease Mortality in Japanese, Whites, and Blacks: A Prospective Study of Three American Populations. 2017

Willcox, Bradley J / Morris, Brian J / Tranah, Gregory J / Chen, Randi / Masaki, Kamal H / He, Qimei / Willcox, D Craig / Allsopp, Richard C / Moisyadi, Stefan / Gerschenson, Mariana / Davy, Philip M C / Poon, Leonard W / Rodriguez, Beatriz / Newman, Anne B / Harris, Tamara B / Cummings, Steven R / Liu, Yongmei / Parimi, Neeta / Evans, Daniel S / Donlon, Timothy A. ·Department of Research, Kuakini Medical Center, Honolulu, Hawaii. · Department of Geriatric Medicine, John A. Burns School of Medicine, University of Hawaii, Honolulu. · School of Medical Sciences and Bosch Institute, University of Sydney, New South Wales, Australia. · California Pacific Medical Center Research Institute, San Francisco. · Department of Human Welfare, Okinawa International University, Ginowan, Japan. · Institute for Biogenesis Research, University of Hawaii, Honolulu. · Department of Cell and Molecular Biology, John A. Burns School of Medicine, University of Hawaii, Honolulu. · Institute of Gerontology, University of Georgia, Athens. · Department of Epidemiology, University of Pittsburgh, Pennsylvania. · Laboratory of Neurogenetics, Intramural Research Program, National Institute on Aging, Bethesda, Maryland. · Division of Public Health Sciences, Wake Forest School of Medicine, Winston-Salem, North Carolina. · Department of Pathology, John A. Burns School of Medicine, University of Hawaii, Honolulu, Hawaii. ·J Gerontol A Biol Sci Med Sci · Pubmed #27694344.

ABSTRACT: Background: We recently reported that protection against coronary artery disease (CAD) mortality is the major contributor to longer life associated with FOXO3 genotype. The present study examined this relation in more detail. Methods: We performed a 15-year observational study of 3,584 older American men of Japanese ancestry from the Kuakini Honolulu Heart Program cohort and 1,595 White and 1,067 Black elderly individuals from the Health Aging and Body Composition study. Results: Multivariate Cox regression models demonstrated that carriage of the longevity-associated G allele of FOXO3 single nucleotide polymorphisms rs2802292 was a protective factor against CAD mortality in all three populations. In Japanese and Whites, but not in Blacks, the protective effect of the G allele was little changed in models adjusted for other major risk factors. Population-attributable risk (PAR) models found that the nonprotective TT genotype contributed 15%, 9%, and 3% to CAD mortality risk in Japanese, White, and Black Americans, respectively, and was one of the top three contributing factors to CAD mortality. In Japanese, this effect size was comparable with hypertension (15%), but in Whites and Blacks PAR for hypertension was higher (29% and 26%, respectively). G-allele carriers had lower plasma TNF-α than noncarriers, suggesting inflammation as a potential mediating factor for CAD mortality risk. Conclusion: FOXO3 genotype is an important risk factor for CAD mortality in older populations. More research is needed to identify potential mechanisms and targets for intervention.

69 Article Sustained Economic Hardship and Cognitive Function: The Coronary Artery Risk Development in Young Adults Study. 2017

Zeki Al Hazzouri, Adina / Elfassy, Tali / Sidney, Stephen / Jacobs, David / Pérez Stable, Eliseo J / Yaffe, Kristine. ·Division of Epidemiology and Population Health Sciences, Department of Public Health Sciences, University of Miami, Miami, Florida. Electronic address: axz122@miami.edu. · Division of Epidemiology and Population Health Sciences, Department of Public Health Sciences, University of Miami, Miami, Florida. · Kaiser Permanente Division of Research, Oakland, California. · Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota. · National Institute on Minority Health and Health Disparities, Bethesda, Maryland. · Departments of Psychiatry, Neurology, and Epidemiology, University of California San Francisco, San Francisco, California;; San Francisco Veterans Affairs Medical Center, San Francisco, California. ·Am J Prev Med · Pubmed #27692543.

ABSTRACT: INTRODUCTION: The relationship between low income and worse health outcomes is evident, yet its association with cognitive outcomes is less explored. Most studies have measured income at one time and none have examined how sustained exposure to low income influences cognition in a relatively young cohort. This study examined the effect of sustained poverty and perceived financial difficulty on cognitive function in midlife. METHODS: Income data were collected six times between 1985 and 2010 for 3,383 adults from the Coronary Artery Risk Development in Young Adults prospective cohort study. Sustained poverty was defined by the percentage of time participants' household income was <200% of the federal poverty level-"never" in poverty, "0< to <1/3," "≥1/3 to <100%" or "all-time." In 2010, at a mean age of 50 years, participants underwent a cognitive battery. Data were analyzed in 2015. RESULTS: In demographic-adjusted linear regression models, individuals with all-time poverty performed significantly worse than individuals never in poverty: 0.92 points worse on verbal memory (z-score, -0.28; 95% CI=-0.43, -0.13), 11.60 points worse on processing speed (z-score, -0.72; 95% CI=-0.85, -0.58), and 3.50 points worse on executive function (z-score, -0.32; 95% CI=-0.47, -0.17). Similar results were observed with perceived financial difficulty. Findings were robust when restricted to highly educated participants, suggesting little evidence for reverse causation. CONCLUSIONS: Cumulative exposure to low income over 2 decades was strongly associated with worse cognitive function of a relatively young cohort. Poverty and perceived hardship may be important contributors to premature aging among disadvantaged populations.

70 Article Synergistic and Non-synergistic Associations for Cigarette Smoking and Non-tobacco Risk Factors for Cardiovascular Disease Incidence in the Atherosclerosis Risk In Communities (ARIC) Study. 2017

Lubin, Jay H / Couper, David / Lutsey, Pamela L / Yatsuya, Hiroshi. ·Biostatistics Branch, Division of Cancer Epidemiology and Genetics, US National Cancer Institute, National Institutes of Health, Bethesda, MD. · Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC. · Division of Epidemiology and Community Health, University of Minnesota School of Public Health, Minneapolis, MN. · Department of Public Health, Fujita Health University School of Medicine, Kutsukake-cho, Japan. ·Nicotine Tob Res · Pubmed #27651477.

ABSTRACT: Introduction: Cigarette smoking, various metabolic and lipid-related factors and hypertension are well-recognized cardiovascular disease (CVD) risk factors. Since smoking affects many of these factors, use of a single imprecise smoking metric, for example, ever or never smoked, may allow residual confounding and explain inconsistencies in current assessments of interactions. Methods: Using a comprehensive model in pack-years and cigarettes/day for the complex smoking-related relative risk (RR) of CVD to reduce residual confounding, we evaluated interactions with non-tobacco risk factors, including additive (non-synergistic) and multiplicative (synergistic) forms. Data were from the prospective Atherosclerosis Risk in Communities (ARIC) Study from four areas of the United States recruited in 1987-1989 with follow-up through 2008. Analyses included 14 127 participants, 207 693 person-years and 2857 CVD events. Results: Analyses revealed distinct interactions with smoking: including statistical consistency with additive (body mass index [BMI], waist to hip ratio [WHR], diabetes mellitus [DM], glucose, insulin, high density lipoproteins [HDL] and HDL(2)); and multiplicative (hypertension, total cholesterol [TC], low density lipoproteins [LDLs], apolipoprotein B [apoB], TC to HDL ratio and HDL(3)) associations, as well as indeterminate (apolipoprotein A-I [apoA-I] and triglycerides) associations. Conclusions: The forms of the interactions were revealing but require confirmation. Improved understanding of joint associations may help clarify the public health burden of smoking for CVD, links between etiologic factors and biological mechanisms, and the consequences of joint exposures, whereby synergistic associations highlight joint effects and non-synergistic associations suggest distinct contributions. Implications: Joint associations for cigarette smoking and non-tobacco risk factors were distinct, revealing synergistic/multiplicative (hypertension, TC, LDL, apoB, TC/HDL, HDL(3)), non-synergistic/additive (BMI, WHR, DM, glucose, insulin, HDL, HDL(2)) and indeterminate (apoA-I and TRIG) associations. If confirmed, these results may help better define the public health burden of smoking on CVD risk and identify links between etiologic factors and biologic mechanisms, where synergistic associations highlight joint impacts and non-synergistic associations suggest distinct contributions from each factor.

71 Article Associations of Coffee, Tea, and Caffeine Intake with Coronary Artery Calcification and Cardiovascular Events. 2017

Miller, P Elliott / Zhao, Di / Frazier-Wood, Alexis C / Michos, Erin D / Averill, Michelle / Sandfort, Veit / Burke, Gregory L / Polak, Joseph F / Lima, Joao A C / Post, Wendy S / Blumenthal, Roger S / Guallar, Eliseo / Martin, Seth S. ·Department of Critical Care Medicine, National Institutes of Health, Bethesda, Md; Division of Cardiology, Department of Medicine, Ciccarone Center for the Prevention of Heart Disease, Johns Hopkins University School of Medicine, Baltimore, Md. Electronic address: Elliott.miller@nih.gov. · Department of Epidemiology, Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, Md. · Children's Nutrition Research Center, Baylor College of Medicine, Houston, Tex. · Division of Cardiology, Department of Medicine, Ciccarone Center for the Prevention of Heart Disease, Johns Hopkins University School of Medicine, Baltimore, Md. · Department of Environmental and Occupational Health, University of Washington, Seattle. · Department of Radiology and Imaging Sciences, National Institutes of Health, Bethesda, Md. · Division of Public Health Sciences, Department of Epidemiology and Prevention, Wake Forest School of Medicine, Winston-Salem, NC. · Department of Radiology, Tufts Medical Center, Tufts University School of Medicine, Boston, Mass. · Division of Cardiology, Department of Medicine, Johns Hopkins Hospital, Baltimore, Md. · Division of Cardiology, Department of Medicine, Ciccarone Center for the Prevention of Heart Disease, Johns Hopkins University School of Medicine, Baltimore, Md; Department of Epidemiology, Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, Md. ·Am J Med · Pubmed #27640739.

ABSTRACT: BACKGROUND: Coffee and tea are 2 of the most commonly consumed beverages in the world. The association of coffee and tea intake with coronary artery calcium and major adverse cardiovascular events remains uncertain. METHODS: We examined 6508 ethnically diverse participants with available coffee and tea data from the Multi-Ethnic Study of Atherosclerosis. Intake for each was classified as never, occasional (<1 cup per day), and regular (≥1 cup per day). A coronary artery calcium progression ratio was derived from mixed effect regression models using loge(calcium score+1) as the outcome, with coefficients exponentiated to reflect coronary artery calcium progression ratio versus the reference. Cox proportional hazards analyses were used to evaluate the association between beverage intake and incident cardiovascular events. RESULTS: Over a median follow-up of 5.3 years for coronary artery calcium and 11.1 years for cardiovascular events, participants who regularly drank tea (≥1 cup per day) had a slower progression of coronary artery calcium compared with never drinkers after multivariable adjustment. This correlated with a statistically significant lower incidence of cardiovascular events for ≥1 cup per day tea drinkers (adjusted hazard ratio 0.71; 95% confidence interval 0.53-0.95). Compared with never coffee drinkers, regular coffee intake (≥1 cup per day) was not statistically associated with coronary artery calcium progression or cardiovascular events (adjusted hazard ratio 0.97; 95% confidence interval 0.78-1.20). Caffeine intake was marginally inversely associated with coronary artery calcium progression. CONCLUSIONS: Moderate tea drinkers had slower progression of coronary artery calcium and reduced risk for cardiovascular events. Future research is needed to understand the potentially protective nature of moderate tea intake.

72 Article Allometric scaling of brain regions to intra-cranial volume: An epidemiological MRI study. 2017

de Jong, Laura W / Vidal, Jean-Sébastien / Forsberg, Lars E / Zijdenbos, Alex P / Haight, Thaddeus / Anonymous2500879 / Sigurdsson, Sigurdur / Gudnason, Vilmundur / van Buchem, Mark A / Launer, Lenore J. ·Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands. · Geriatrics Department, AP-HP, Broca Hospital, Paris, 75013, France. · Université Paris Descartes, Sorbonne Paris V, Paris, EA, 4468, 75006, France. · Department of Clinical Neuroscience Karolinska Institute, Stockholm, Sweden. · Biospective Inc, Montreal, Quebec, Canada. · Intramural Research Program of the National Institute on Aging, Bethesda, Maryland. · Icelandic Heart Association, Kopavogur, Iceland. ·Hum Brain Mapp · Pubmed #27557999.

ABSTRACT: There is growing evidence that sub-structures of the brain scale allometrically to total brain size, that is, in a non-proportional and non-linear way. Here, scaling of different volumes of interest (VOI) to intra-cranial volume (ICV) was examined. It was assessed whether scaling was allometric or isometric and whether scaling coefficients significantly differed from each other. We also tested to what extent allometric scaling of VOI was introduced by the automated segmentation technique. Furthermore, reproducibility of allometric scaling was studied different age groups and study populations. Study samples included samples of cognitively healthy adults from the community-based Age Gene/Environment Susceptibility-Reykjavik Study (AGES-Reykjavik Study) (N = 3,883), the Coronary Artery Risk Development in Young Adults Study (CARDIA) (N =709), and the Alzheimer's Disease Neuroimaging Initiative (ADNI) (N = 180). Data encompassed participants with different age, ethnicity, risk factor profile, and ICV and VOI obtained with different automated MRI segmentation techniques. Our analysis showed that (1) allometric scaling is a trait of all parts of the brain, (2) scaling of neo-cortical white matter, neo-cortical gray matter, and deep gray matter structures including the cerebellum are significantly different from each other, and (3) allometric scaling of brain structures cannot solely be explained by age-associated atrophy, sex, ethnicity, or a systematic bias from study-specific segmentation algorithm, but appears to be a true feature of brain geometry. Hum Brain Mapp 38:151-164, 2017. © 2016 Wiley Periodicals, Inc.

73 Article Risk score overestimation: the impact of individual cardiovascular risk factors and preventive therapies on the performance of the American Heart Association-American College of Cardiology-Atherosclerotic Cardiovascular Disease risk score in a modern multi-ethnic cohort. 2017

DeFilippis, Andrew Paul / Young, Rebekah / McEvoy, John W / Michos, Erin D / Sandfort, Veit / Kronmal, Richard A / McClelland, Robyn L / Blaha, Michael J. ·Jewish Hospital, Louisville, KY, USA. · Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA. · Division of Cardiovascular Medicine, University of Louisville, 550 South Jackson Street, Louisville, KY 40202, USA. · University of Washington, Seattle, WA, USA. · National Institutes of Health, Bethesda, MD, USA. ·Eur Heart J · Pubmed #27436865.

ABSTRACT: Aims: To evaluate the 2013 American Heart Association (AHA)-American College of Cardiology (ACC)-Atherosclerotic Cardiovascular Disease (ASCVD) risk score among four different race/ethnic groups and to ascertain which factors are most associated with risk overestimation by the AHA-ACC-ASCVD score. Methods and results: The Multi-Ethnic Study of Atherosclerosis (MESA), a prospective community-based cohort, was used to examine calibration and discrimination of the AHA-ACC-ASCVD risk score in 6441 White, Black, Chinese, and Hispanic Americans (aged 45-79 years and free of known ASCVD at baseline). Using univariable and multivariable absolute risk regression, we modelled the impact of individual risk factors on the discordance between observed and predicted 10-year ASCVD risk. Overestimation was observed in all race/ethnic groups in MESA and was highest among Chinese (252% for women and 314% for men) and lowest in White women (72%) and Hispanic men (67%). Higher age, Chinese race/ethnicity (when compared with White), systolic blood pressure (treated and untreated), diabetes, alcohol use, exercise, lipid-lowering medication, and aspirin use were all associated with more risk overestimation, whereas family history was associated with less risk overestimation in a multivariable model (all P < 0.05). Conclusion: The AHA-ACC-ASCVD risk score overestimates ASCVD risk among men, women, and all four race/ethnic groups evaluated in a modern American primary prevention cohort. Clinicians treating patients similar to those in MESA, particularly older individuals and those with factors associated with more risk overestimation, may consider interpreting absolute ASCVD risk estimates with caution.

74 Article Greater Volume but not Higher Density of Abdominal Aortic Calcium Is Associated With Increased Cardiovascular Disease Risk: MESA (Multi-Ethnic Study of Atherosclerosis). 2016

Forbang, Nketi I / Michos, Erin D / McClelland, Robyn L / Remigio-Baker, Rosemay A / Allison, Matthew A / Sandfort, Veit / Ix, Joachim H / Thomas, Isac / Rifkin, Dena E / Criqui, Michael H. ·From the Department of Family Medicine and Public Health, University of California, San Diego, La Jolla (N.I.F., R.A.R.-B., M.A.A., J.H.I., I.T., D.E.R., M.H.C.) · Department of Medicine, Johns Hopkins University, Baltimore, MD (E.D.M.) · Department of Biostatistics, University of Washington, Seattle (R.L.M.) · Veterans Administration San Diego Healthcare System, La Jolla, CA (M.A.A., J.H.I., D.E.R.) · and Clinical Center, National Institutes of Health, Bethesda, MD (V.S.). ·Circ Cardiovasc Imaging · Pubmed #27903540.

ABSTRACT: BACKGROUND: Abdominal aortic calcium (AAC) and coronary artery calcium (CAC) independently and similarly predict cardiovascular disease (CVD) events. The standard AAC and CAC score, the Agatston method, upweights for greater calcium density, thereby modeling higher calcium density as a CVD hazard. METHODS AND RESULTS: Computed tomography scans were used to measure AAC and CAC volume and density in a multiethnic cohort of community-dwelling individuals, and Cox proportional hazard was used to determine their independent association with incident coronary heart disease (CHD, defined as myocardial infarction, resuscitated cardiac arrest, or CHD death), cardiovascular disease (CVD, defined as CHD plus stroke and stroke death), and all-cause mortality. In 997 participants with Agatston AAC and CAC scores >0, the mean age was 66±9 years, and 58% were men. During an average follow-up of 9 years, there were 77 CHD, 118 CVD, and 169 all-cause mortality events. In mutually adjusted models, additionally adjusted for CVD risk factors, an increase in ln(AAC volume) per standard deviation was significantly associated with increased all-cause mortality (hazard ratio=1.20; 95% confidence interval, 1.08-1.33; P<0.01) and an increased ln(CAC volume) per standard deviation was significantly associated with CHD (hazard ratio=1.17; 95% confidence interval, 1.04-1.59; P=0.02) and CVD (hazard ratio=1.20; 95% confidence interval, 1.05-1.36; P<0.01). In contrast, both AAC and CAC density were not significantly associated with CVD events. CONCLUSIONS: The Agatston method of upweighting calcium scores for greater density may be inappropriate for CVD risk prediction in both the abdominal aorta and coronary arteries.

75 Article Computed Tomographic Perfusion Improves Diagnostic Power of Coronary Computed Tomographic Angiography in Women: Analysis of the CORE320 Trial (Coronary Artery Evaluation Using 320-Row Multidetector Computed Tomography Angiography and Myocardial Perfusion) According to Gender. 2016

Penagaluri, Ashritha / Higgins, Angela Y / Vavere, Andrea L / Miller, Julie M / Arbab-Zadeh, Armin / Betoko, Aisha / Steveson, Chloe / Zimmermann, Elke / Cox, Christopher / Rochitte, Carlos E / Dewey, Marc / Kofoed, Klaus F / Niinuma, Hiroyuki / Di Carli, Marcelo F / Lima, João A C / Chen, Marcus Y. ·From the Johns Hopkins Hospital and School of Medicine (A.P., A.L.V., J.M.M., A.A.-Z, J.A.C.L.) and Johns Hopkins Bloomberg School of Public Health (A.B., C.C.), Baltimore, MD · National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD (A.Y.H., M.Y.C.) · Toshiba Medical Systems Corporation, Japan (C.S) · Charité Medical School, Humboldt, Berlin, Germany (E.Z., M.D.) · Heart Institute, InCor, University of São Paulo Medical School, Brazil (C.E.R.) · Rigshospitalet, University of Copenhagen, Denmark (K.F.K) · St Luke's International Hospital, Tokyo, Japan (H.N.) · and Brigham and Women's Hospital, Boston, MA (M.F.D.C.). ·Circ Cardiovasc Imaging · Pubmed #27811151.

ABSTRACT: BACKGROUND: Coronary computed tomographic angiography (CTA) and myocardial perfusion imaging (CTP) is a validated approach for detection and exclusion of flow-limiting coronary artery disease (CAD), but little data are available on gender-specific performance of these modalities. In this study, we aimed to evaluate the diagnostic accuracy of combined coronary CTA and CTP in detecting flow-limiting CAD in women compared with men. METHODS AND RESULTS: Three hundred and eighty-one patients who underwent both CTA-CTP and single-photon emission computed tomography myocardial perfusion imaging preceding invasive coronary angiography as part of the CORE320 multicenter study (Coronary Artery Evaluation Using 320-row Multidetector Computed Tomography Angiography and Myocardial Perfusion) were included in this ancillary study. All 4 image modalities were analyzed in blinded, independent core laboratories. Prevalence of flow-limiting CAD defined by invasive coronary angiography equal to 50% or greater with an associated single-photon emission computed tomography myocardial perfusion imaging defect was 45% (114/252) and 23% (30/129) in males and females, respectively. Patient-based diagnostic accuracy defined by the area under the receiver operating curve for detecting flow-limiting CAD by CTA alone in females was 0.83 (0.75-0.89) and for CTA-CTP was 0.92 (0.86-0.97; P=0.003) compared with men where the area under the receiver operating curve for detecting flow-limiting CAD by CTA alone was 0.82 (0.77-0.87) and for CTA-CTP was 0.84 (0.80-0.89; P=0.29). CONCLUSIONS: The combination of CTA-CTP was performed similarly in men and women for identifying flow-limiting coronary stenosis; however, in women, CTP had incremental value over CTA alone, which was not the case in men. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00934037.

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