Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Coronary Artery Disease: HELP
Articles by Traci M. Bartz
Based on 4 articles published since 2010
(Why 4 articles?)
||||

Between 2010 and 2020, Traci M. Bartz wrote the following 4 articles about Coronary Artery Disease.
 
+ Citations + Abstracts
1 Article A genome-wide association study identifies new loci for factor VII and implicates factor VII in ischemic stroke etiology. 2019

de Vries, Paul S / Sabater-Lleal, Maria / Huffman, Jennifer E / Marten, Jonathan / Song, Ci / Pankratz, Nathan / Bartz, Traci M / de Haan, Hugoline G / Delgado, Graciela E / Eicher, John D / Martinez-Perez, Angel / Ward-Caviness, Cavin K / Brody, Jennifer A / Chen, Ming-Huei / de Maat, Moniek P M / Frånberg, Mattias / Gill, Dipender / Kleber, Marcus E / Rivadeneira, Fernando / Soria, José Manuel / Tang, Weihong / Tofler, Geoffrey H / Uitterlinden, André G / van Hylckama Vlieg, Astrid / Seshadri, Sudha / Boerwinkle, Eric / Davies, Neil M / Giese, Anne-Katrin / Ikram, M Kamran / Kittner, Steven J / McKnight, Barbara / Psaty, Bruce M / Reiner, Alex P / Sargurupremraj, Muralidharan / Taylor, Kent D / Anonymous15491124 / Anonymous15501124 / Fornage, Myriam / Hamsten, Anders / März, Winfried / Rosendaal, Frits R / Souto, Juan Carlos / Dehghan, Abbas / Johnson, Andrew D / Morrison, Alanna C / O'Donnell, Christopher J / Smith, Nicholas L. ·Human Genetics Center, Department of Epidemiology, Human Genetics, and Environmental Sciences, School of Public Health, The University of Texas Health Science Center at Houston, Houston, TX. · Department of Epidemiology, Erasmus University Medical Center, Rotterdam, The Netherlands. · Unit of Genomics of Complex Diseases, Institut d'Investigació Biomèdica Sant Pau (IIB-Sant Pau), Barcelona, Spain. · Cardiovascular Medicine Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden. · Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden. · Population Sciences Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Framingham, MA. · The Framingham Heart Study, Framingham, MA. · Center for Population Genomics, Veterans Affairs (VA) Boston Healthcare System, Jamaica Plain, MA. · Medical Research Council (MRC) Human Genetics Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom. · Department of Medical Sciences and. · Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden. · Department of Laboratory Medicine and Pathology, School of Medicine, University of Minnesota, Minneapolis, MN. · Department of Biostatistics, University of Washington, Seattle, WA. · Department of Clinical Epidemiology, Leiden University Medical Center, Leiden, The Netherlands. · Vth Department of Medicine, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany. · National Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, Chapel Hill, NC. · Department of Medicine, University of Washington, Seattle, WA. · Department of Hematology, Erasmus University Medical Center, Rotterdam, The Netherlands. · Department of Epidemiology and Biostatistics and. · Department of Stroke Medicine, Imperial College London, London, United Kingdom. · Institute of Nutrition, Friedrich Schiller University Jena, Mannheim, Germany. · Department of Internal Medicine, Erasmus University Medical Center, Rotterdam, The Netherlands. · Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN. · Royal North Shore Hospital, University of Sydney, Sydney, Australia. · Department of Neurology, Boston University, Boston, MA. · Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases, University of Texas Health Sciences Center, San Antonio, TX. · Human Genome Sequencing Center, College of Medicine, Baylor University, Houston, TX. · MRC Integrative Epidemiology Unit, Bristol Medical School, University of Bristol, Bristol, United Kingdom. · Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA. · Department of Neurology, Erasmus University Medical Center, Rotterdam, The Netherlands. · Department of Neurology, School of Medicine, University of Maryland, Baltimore, MD. · Baltimore VA Medical Center, Baltimore, MD. · Department of Medicine. · Department of Epidemiology, and. · Department of Health Services, University of Washington, Seattle, WA. · Kaiser Permanente Washington Research Institute, Kaiser Permanente Washington, Seattle, WA. · Fred Hutchinson Cancer Research Center, Seattle, WA. · Department of Epidemiology, University of Washington, Seattle, WA. · INSERM U1219, Bordeaux Population Health Research Center, University of Bordeaux, Bordeaux, France. · The Institute for Translational Genomics and Population Sciences, Department of Pediatrics, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA. · Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center at Houston, Houston, TX. · Synlab Academy, Synlab Holding Deutschland GmbH, Mannheim, Germany. · Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University Graz, Graz, Austria. · Einthoven Laboratory of Experimental Vascular Medicine, Leiden University Medical Center, Leiden, The Netherlands. · Department of Thrombosis and Hemostasis, Leiden University Medical Center, Leiden, The Netherlands. · Unitat d'Hemostasia i Trombosi, Hospital de la Sant Creu i Sant Pau, Barcelona, Spain. · MRC-Public Health England Centre for Environment and Health, School of Public Health and. · UK Dementia Research Institute, Imperial College London, London, United Kingdom. · Cardiology Section, VA Boston Healthcare System, West Roxbury, MA; and. · Seattle Epidemiologic Research and Information Center, Office of Research and Development, Department of Veteran Affairs, Seattle, WA. ·Blood · Pubmed #30642921.

ABSTRACT: Factor VII (FVII) is an important component of the coagulation cascade. Few genetic loci regulating FVII activity and/or levels have been discovered to date. We conducted a meta-analysis of 9 genome-wide association studies of plasma FVII levels (7 FVII activity and 2 FVII antigen) among 27 495 participants of European and African ancestry. Each study performed ancestry-specific association analyses. Inverse variance weighted meta-analysis was performed within each ancestry group and then combined for a

2 Article Relation of the Myocardial Contraction Fraction, as Calculated from M-Mode Echocardiography, With Incident Heart Failure, Atherosclerotic Cardiovascular Disease and Mortality (Results from the Cardiovascular Health Study). 2017

Maurer, Mathew S / Koh, William J H / Bartz, Traci M / Vullaganti, Sirish / Barasch, Eddy / Gardin, Julius M / Gottdiener, John S / Psaty, Bruce M / Kizer, Jorge R. ·Columbia University Medical Center, Division of Cardiology, New York, New York. Electronic address: msm10@cumc.columbia.edu. · University of Washington, Department of Biostatistics, Seattle, Washington. · Columbia University Medical Center, Division of Cardiology, New York, New York. · Department of Research and Education, St. Francis Hospital/SUNY at Stony Brook, The Heart Center, Roslyn, New York. · Department of Medicine, Hackensack University Medical Center, Hackensack, New Jersey. · University of Maryland Medical Center, Baltimore, Maryland. · University of Washington, Seattle, Washington; Group Health Research Institute, Group Health Cooperative, Seattle, Washington. · Department of Medicine, Albert Einstein College of Medicine, Bronx, New York; Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York. ·Am J Cardiol · Pubmed #28073429.

ABSTRACT: We evaluated the association between 2-dimensional (2D) echocardiography (echo)-determined myocardial contraction fraction (MCF) and adverse cardiovascular outcomes including incident heart failure (HF), atherosclerotic cardiovascular disease (ASCVD), and mortality. The MCF, the ratio of left ventricular (LV) stroke volume (SV) to myocardial volume (MV), is a volumetric measure of myocardial shortening that can distinguish pathologic from physiological hypertrophy. Using 2D echo-guided M-mode data from the Cardiovascular Health Study, we calculated MCF in subjects with LV ejection fraction (EF) ≥55% and used Cox models to evaluate its association with incident HF, ASCVD, and all-cause mortality after adjusting for clinical and echo parameters. We assessed whether log

3 Article Diagnostic Yield and Clinical Utility of Sequencing Familial Hypercholesterolemia Genes in Patients With Severe Hypercholesterolemia. 2016

Khera, Amit V / Won, Hong-Hee / Peloso, Gina M / Lawson, Kim S / Bartz, Traci M / Deng, Xuan / van Leeuwen, Elisabeth M / Natarajan, Pradeep / Emdin, Connor A / Bick, Alexander G / Morrison, Alanna C / Brody, Jennifer A / Gupta, Namrata / Nomura, Akihiro / Kessler, Thorsten / Duga, Stefano / Bis, Joshua C / van Duijn, Cornelia M / Cupples, L Adrienne / Psaty, Bruce / Rader, Daniel J / Danesh, John / Schunkert, Heribert / McPherson, Ruth / Farrall, Martin / Watkins, Hugh / Lander, Eric / Wilson, James G / Correa, Adolfo / Boerwinkle, Eric / Merlini, Piera Angelica / Ardissino, Diego / Saleheen, Danish / Gabriel, Stacey / Kathiresan, Sekar. ·Center for Human Genetic Research, Cardiovascular Research Center and Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; Program in Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts. · Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Samsung Medical Center, Seoul, Republic of Korea. · Program in Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts; Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts. · Human Genetics Center and Institute of Molecular Medicine, University of Texas-Houston Health Science Center, Houston, Texas. · Department of Biostatistics, University of Washington, Seattle, Washington. · Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts. · Department of Epidemiology, Erasmus Medical Center, Rotterdam, the Netherlands. · Program in Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts. · Cardiovascular Health Research Unit, University of Washington, Seattle, Washington. · Program in Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts; Division of Cardiovascular Medicine, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan. · Deutsches Herzzentrum München, Technische Universität München, Deutsches Zentrum für Herz-Kreislauf-Forschung, München, Germany, and Munich Heart Alliance, München, Germany. · Department of Biomedical Sciences, Humanitas University, Rozzano, Milan, Italy, and Humanitas Clinical and Research Center, Rozzano, Milan, Italy. · Cardiovascular Health Research Unit, University of Washington, Seattle, Washington; Departments of Medicine, Epidemiology, and Health Services, University of Washington, Seattle, Washington. · Departments of Genetics, University of Pennsylvania, Philadelphia, Pennsylvania. · Public Health and Primary Care, University of Cambridge, Cambridge, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge and National Institute for Health Research Blood and Transplant Research Unit in Donor Health and Genomics, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom. · University of Ottawa Heart Institute, Ottawa, Canada. · Division of Cardiovascular Medicine, Radcliffe Department of Medicine and the Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom. · Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi. · Jackson Heart Study, Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi. · Ospedale Niguarda, Milano, Italy. · Division of Cardiology, Azienda Ospedaliero-Universitaria di Parma, University of Parma, Parma, Italy, and ASTC: Associazione per lo Studio Della Trombosi in Cardiologia, Pavia, Italy. · Biostatistics and Epidemiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. · Center for Human Genetic Research, Cardiovascular Research Center and Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; Program in Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts. Electronic address: skathiresan1@mgh.harvard.edu. ·J Am Coll Cardiol · Pubmed #27050191.

ABSTRACT: BACKGROUND: Approximately 7% of American adults have severe hypercholesterolemia (untreated low-density lipoprotein [LDL] cholesterol ≥190 mg/dl), which may be due to familial hypercholesterolemia (FH). Lifelong LDL cholesterol elevations in FH mutation carriers may confer coronary artery disease (CAD) risk beyond that captured by a single LDL cholesterol measurement. OBJECTIVES: This study assessed the prevalence of an FH mutation among those with severe hypercholesterolemia and determined whether CAD risk varies according to mutation status beyond the observed LDL cholesterol level. METHODS: Three genes causative for FH (LDLR, APOB, and PCSK9) were sequenced in 26,025 participants from 7 case-control studies (5,540 CAD case subjects, 8,577 CAD-free control subjects) and 5 prospective cohort studies (11,908 participants). FH mutations included loss-of-function variants in LDLR, missense mutations in LDLR predicted to be damaging, and variants linked to FH in ClinVar, a clinical genetics database. RESULTS: Among 20,485 CAD-free control and prospective cohort participants, 1,386 (6.7%) had LDL cholesterol ≥190 mg/dl; of these, only 24 (1.7%) carried an FH mutation. Within any stratum of observed LDL cholesterol, risk of CAD was higher among FH mutation carriers than noncarriers. Compared with a reference group with LDL cholesterol <130 mg/dl and no mutation, participants with LDL cholesterol ≥190 mg/dl and no FH mutation had a 6-fold higher risk for CAD (odds ratio: 6.0; 95% confidence interval: 5.2 to 6.9), whereas those with both LDL cholesterol ≥190 mg/dl and an FH mutation demonstrated a 22-fold increased risk (odds ratio: 22.3; 95% confidence interval: 10.7 to 53.2). In an analysis of participants with serial lipid measurements over many years, FH mutation carriers had higher cumulative exposure to LDL cholesterol than noncarriers. CONCLUSIONS: Among participants with LDL cholesterol ≥190 mg/dl, gene sequencing identified an FH mutation in <2%. However, for any observed LDL cholesterol, FH mutation carriers had substantially increased risk for CAD.

4 Article Inflammation and sudden cardiac death in a community-based population of older adults: the Cardiovascular Health Study. 2013

Hussein, Ayman A / Gottdiener, John S / Bartz, Traci M / Sotoodehnia, Nona / DeFilippi, Christopher / See, Vincent / Deo, Rajat / Siscovick, David / Stein, Phyllis K / Lloyd-Jones, Donald. ·University of Maryland, Baltimore, Maryland. Electronic address: jgottdie@medicine.umaryland.edu. ·Heart Rhythm · Pubmed #23906927.

ABSTRACT: BACKGROUND: Inflammation is linked to adverse cardiovascular events, but its association with sudden cardiac death (SCD) has been controversial. Older subjects, who are at particular risk for SCD, were underrepresented in previous studies addressing this issue. OBJECTIVE: The purpose of this study was to study the association between inflammation and SCD in a community-based population of older adults. METHODS: In the Cardiovascular Health Study, 5806 and 5382 participants had measurements of C-reactive protein (CRP) and interleukin-6 (IL6), respectively, and were followed for up to 17 years. SCD risk as a function of baseline IL-6 and CRP was assessed in the overall population and in a group of participants without known prevalent cardiac disease. RESULTS: In univariate analyses, both IL-6 (hazard ratio [HR] 1.79 for 1+ log IL-6, 95% confidence interval [CI] 1.50-2.13; 5th vs 1st quintile HR 3.36, 95% CI 2.24-5.05) and CRP (HR 1.31 for 1+ log CRP, 95% CI 1.18-1.45; 5th vs 1st quintile HR 2.00, 95% CI 1.40-2.87) were associated with SCD risk. In covariate-adjusted analyses, accounting for baseline risk factors, incident myocardial infarction, and heart failure, the association with SCD risk persisted for IL-6 (HR 1.26 for 1+ log IL-6, 95% CI 1.02-1.56; 5th vs 1st quintile HR 1.63, 95% CI 1.03-2.56) but was significantly attenuated for CRP (HR 1.13 for 1+ log CRP, 95% CI 1.00-1.28; 5th vs 1st quintile HR 1.34, 95% CI 0.88-2.05). Similar findings were observed in participants without prevalent cardiac disease. CONCLUSION: Greater burden of inflammation, assessed by IL-6 levels, is associated with SCD risk beyond traditional risk factors, incident myocardial infarction, and heart failure.