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Hypertension: HELP
Articles by Donna K. Arnett
Based on 58 articles published since 2010
(Why 58 articles?)
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Between 2010 and 2020, D. Arnett wrote the following 58 articles about Hypertension.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3
1 Editorial Analysis of Large Electronic Health Record Databases Supports Blood Pressure-Incident Diabetes Association. 2015

Arnett, Donna K. ·Department of Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama. Electronic address: arnett@uab.edu. ·J Am Coll Cardiol · Pubmed #26429080.

ABSTRACT: -- No abstract --

2 Editorial Wicked problems and worthy pursuits: resolving to meet American Heart Association 2020 Impact Goals. 2012

Arnett, Donna K. · ·Circulation · Pubmed #22547668.

ABSTRACT: -- No abstract --

3 Review A Clinician's Guide to Healthy Eating for Cardiovascular Disease Prevention. 2019

Pallazola, Vincent A / Davis, Dorothy M / Whelton, Seamus P / Cardoso, Rhanderson / Latina, Jacqueline M / Michos, Erin D / Sarkar, Sudipa / Blumenthal, Roger S / Arnett, Donna K / Stone, Neil J / Welty, Francine K. ·Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease, Baltimore, MD. · Division of Endocrinology, Diabetes, and Metabolism, Johns Hopkins University School of Medicine, Baltimore, MD. · Department of Epidemiology, School of Public Health, University of Alabama at Birmingham. · Cardiology Division, Feinberg School of Medicine, Northwestern University, Chicago, IL. · Cardiology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA. ·Mayo Clin Proc Innov Qual Outcomes · Pubmed #31485563.

ABSTRACT: Despite continued advances in health care, the cardiovascular disease (CVD) mortality rate has plateaued in recent years and appears to be trending upward. Poor diet is a leading cause of obesity and type 2 diabetes mellitus, which are leading contributors to CVD morbidity and mortality. Although dietary modification is a cornerstone of CVD prevention, implementation in clinical practice is limited by inadequate formal training in nutrition science. In this report, we review the individual components of a heart-healthy diet, evidence-based dietary recommendations, and the impact of diet on CVD risk factor prevention and management. Furthermore, we examine the unique difficulties of dietary counseling in low-socioeconomic-status environments and provide an evidence-based approach to better serve these populations. We utilized PubMed searches in adults with no date restriction with the following search terms: "carbohydrate," "fat," protein," "DASH," "Mediterranean," "plant-based," "vegetarian," "cardiovascular disease," "obesity," "weight loss," "diabetes," "socioeconomic status," and "race." In this review, we demonstrate that patients should focus on implementing a general diet plan that is high in fruits, whole grains, legumes, and nonstarchy vegetables while low in

4 Review Omics of Blood Pressure and Hypertension. 2018

Arnett, Donna K / Claas, Steven A. ·From the College of Public Health, University of Kentucky, Lexington. donna.arnett@uky.edu. · From the College of Public Health, University of Kentucky, Lexington. ·Circ Res · Pubmed #29748366.

ABSTRACT: Essential hypertension is a common, complex disorder affecting ≤1 billion adults globally. Blood pressure is a highly heritable trait, with ≤50% of the variation between individuals accounted for by familial relationships. Despite this strong heritability, determining the genetic architecture of hypertension in humans has proved challenging. Recent technological and methodological developments have given rise to what is now known as omics-a domain of study that includes genomics, as well as epigenomics, transcriptomics, proteomics, and metabolomics. For complex traits like hypertension, which involve multiple pathways and organs, omic approaches offer the advantage of allowing identification of novel hypertensive mechanisms to help further dissect and characterize the disorder's pathophysiology. This review provides a primer on the genomics, transcriptomics, proteomics, and metabolomics of blood pressure and hypertension. We provide an introduction to each approach with examples chosen to illustrate its potential. We conclude with a brief assessment of current methods aimed at integrating multiomic data. A review of the literature found genomic, epigenomic, transcriptomic, proteomic, and metabolomic methods have been applied to dissect the pathophysiology of blood pressure and hypertension. Omic methods and integration of multiomic data represent a potentially fruitful approach to illuminating the complex pathophysiology of hypertension and, ultimately, may point to novel diagnostics and treatments.

5 Review Research Needs to Improve Hypertension Treatment and Control in African Americans. 2016

Whelton, Paul K / Einhorn, Paula T / Muntner, Paul / Appel, Lawrence J / Cushman, William C / Diez Roux, Ana V / Ferdinand, Keith C / Rahman, Mahboob / Taylor, Herman A / Ard, Jamy / Arnett, Donna K / Carter, Barry L / Davis, Barry R / Freedman, Barry I / Cooper, Lisa A / Cooper, Richard / Desvigne-Nickens, Patrice / Gavini, Nara / Go, Alan S / Hyman, David J / Kimmel, Paul L / Margolis, Karen L / Miller, Edgar R / Mills, Katherine T / Mensah, George A / Navar, Ann M / Ogedegbe, Gbenga / Rakotz, Michael K / Thomas, George / Tobin, Jonathan N / Wright, Jackson T / Yoon, Sung Sug Sarah / Cutler, Jeffrey A / Anonymous7660880. ·From the Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine (P.K.W., K.C.F.), and Department of Medicine, Tulane University School of Medicine (P.K.W., K.C.F.), New Orleans, LA · Division of Cardiovascular Sciences (P.T.E., P.D.-N., G.A.M., J.A.C.), and Center for Translation Research and Implementation Science (N.G., G.A.M.), National Heart, Lung, and Blood Institute, Bethesda, MD · Department of Epidemiology, School of Public Health, University of Alabama at Birmingham (P.M.) · Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins University, Baltimore, MD (L.J.A., L.A.C., E.R.M.) · Preventive Medicine Section, Veterans Affairs Medical Center, Memphis, TN (W.C.C.) · Department of Epidemiology and Biostatistics, Dornsife School of Public Health, Drexel University, Philadelphia, PA (A.V.D.R.) · Department of Medicine, Case Western Reserve University, University Hospitals Case Medical Center, Louis Stokes Cleveland VA Medical Center, OH (M.R., J.T.W.) · Cardiovascular Research Institute, Morehouse School of Medicine, Atlanta, GA (H.A.T.) · Department of Epidemiology and Prevention (J.A.) and Department of Medicine (B.I.F., J.A.), Wake Forest School of Medicine, Wake Forest University, Winston Salem, NC · Dean's Office, University of Kentucky College of Public Health, Lexington (D.K.A.) · Department of Pharmacy Practice and Science, College of Pharmacy, University of Iowa, Iowa City (B.L.C.) · Department of Biostatistics, University of Texas School of Public Health, Houston (B.R.D.) · Department of Public Health Sciences, Stritch School of Medicine, Loyola University Chicago, Maywood, IL (R.C.) · Division of Research, Kaiser Permanente Northern California, Oakland (A.S.G.) · Department of Internal Medicine, Baylor College of Medicine, Houston, TX (D.J.H.) · National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD (P.L.K.) · HealthPartners Institute, Minneapolis, MN (K.L.M.) · Duke Clinical Research Institute, Duke University Medical Center, Durham, NC (A.M.N.) · Department of Population Health, NYU School of Medicine, New York (G.O.) · American Medical Association, Chicago, IL (M.K.R.) · Department of Nephrology and Hypertension, Cleveland Clinic, OH (G.T.) · Clinical Directors Network (CND) and The Rockefeller University Center for Clinical and Translational Science, New York (J.N.T.) · and National Center for Health Statistics, Centers for Disease Control and Prevention, Hyattsville, MD (S.S.(S.)Y.). ·Hypertension · Pubmed #27620388.

ABSTRACT: -- No abstract --

6 Review The Role of Healthy Lifestyle in the Primordial Prevention of Cardiovascular Disease. 2016

Claas, Steven A / Arnett, Donna K. ·Department of Epidemiology, School of Public Health, University of Alabama at Birmingham, Birmingham, AL, USA. · Dean's Office, College of Public Health, University of Kentucky, Lexington, KY, USA. donna.arnett@uky.edu. ·Curr Cardiol Rep · Pubmed #27142061.

ABSTRACT: Whereas primary prevention seeks to forestall development of disease in individuals with elevated risk, primordial prevention seeks to preempt the development of risk factors. Health behaviors-characterized as "lifestyle" factors-are key interventional targets in primordial prevention of cardiovascular disease. Appropriate dietary intake, including limiting salt and saturated fat consumption, can reduce the risk of developing hypertension and dyslipidemias. Regular physical activity is associated with lower blood pressure and healthier lipid profiles. Diet and exercise are critical to maintaining weight conducive to cardiovascular health. Behavioral factors such as stress management, sleep duration, portion control, and meal timing may play a role in weight management and offer additional routes of intervention. Any smoking elevates cardiovascular risk. Although lifestyle modification programs can be instrumental in reaching public health goals, maintaining cardiovascular health should not be a matter solely of willpower. Ideally, structural and social forces should make healthy lifestyles the default option.

7 Review Genetics, ancestry, and hypertension: implications for targeted antihypertensive therapies. 2014

Franceschini, Nora / Chasman, Daniel I / Cooper-DeHoff, Rhonda M / Arnett, Donna K. ·Department of Epidemiology, University of North Carolina Gillings School of Global Public Health, 137 E. Franklin St., Suite 306, Chapel Hill, NC, USA, noraf@unc.edu. ·Curr Hypertens Rep · Pubmed #24903233.

ABSTRACT: Hypertension is the most common chronic condition seen by physicians in ambulatory care and a condition for which life-long medications are commonly prescribed. There is evidence for genetic factors influencing blood pressure variation in populations and response to medications. This review summarizes recent genetic discoveries that surround blood pressure, hypertension, and antihypertensive drug response from genome-wide association studies, while highlighting ancestry-specific findings and any potential implication for drug therapy targets. Genome-wide association studies have identified several novel loci for inter-individual variation of blood pressure and hypertension risk in the general population. Evidence from pharmacogenetic studies suggests that genes influence the blood pressure response to antihypertensive drugs, although results are somewhat inconsistent across studies. There is still much work that remains to be done to identify genes both for efficacy and adverse events of antihypertensive medications.

8 Review Genetics of hypertension and cardiovascular disease and their interconnected pathways: lessons from large studies. 2011

Kraja, Aldi T / Hunt, Steven C / Rao, D C / Dávila-Román, Victor G / Arnett, Donna K / Province, Michael A. ·Division of Statistical Genomics, Washington University School of Medicine, 4444 Forest Park Avenue, St. Louis, MO 63108, USA. aldi@wustl.edu ·Curr Hypertens Rep · Pubmed #21128019.

ABSTRACT: Blood pressure (BP), hypertension (HT) and cardiovascular disease (CVD) are common complex phenotypes, which are affected by multiple genetic and environmental factors. This article describes recent genome-wide association studies (GWAS) that have reported causative variants for BP/HT and CVD/heart traits and analyzes the overlapping associated gene polymorphisms. It also examines potential replication of findings from the HyperGEN data on African Americans and whites. Several genes involved in BP/HT regulation also appear to be involved in CVD. A better picture is emerging, with overlapping hot-spot regions and with interconnected pathways between BP/HT and CVD. A systemic approach to full understanding of BP/HT and CVD development and their progression to disease may lead to the identification of gene targets and pathways for the development of novel therapeutic interventions.

9 Clinical Trial Association between family risk of stroke and myocardial infarction with prevalent risk factors and coexisting diseases. 2012

Kennedy, Richard E / Howard, George / Go, Rodney C / Rothwell, Peter M / Tiwari, Hemant K / Feng, Rui / McClure, Leslie A / Prineas, Ronald J / Banerjee, Amitava / Arnett, Donna K. ·Department of Biostatistics, School of Public Health, 1665 University Boulevard, University of Alabama at Birmingham, Birmingham, AL 35294-0022, USA. ·Stroke · Pubmed #22328552.

ABSTRACT: BACKGROUND AND PURPOSE: Familial transmission of stroke and myocardial infarction (MI) is partially mediated by transmission of cerebrovascular and cardiovascular risk factors. We examined relationships between family risk of stroke and MI with risk factors for these phenotypes. METHODS: A cross-sectional association between the stratified log-rank family score for stroke and MI with prevalent risk factors was assessed in the REasons for Geographic And Racial Differences in Stroke (REGARDS) cohort. RESULTS: Individuals in the fourth quartile of stratified log-rank family scores for stroke were more likely to have prevalent risk factors including hypertension (OR, 1.43; 95% CI, 1.30-1.58), left ventricular hypertrophy (OR, 1.42; 95% CI, 1.16-1.42), diabetes (OR, 1.26; 95% CI, 1.12-1.43), and atrial fibrillation (OR, 1.23; 95% CI, 1.03-1.45) compared with individuals in the first quartile. Likewise, individuals in the fourth quartile of stratified log-rank family scores for MI were more likely to have prevalent risk factors including hypertension (OR, 1.57; 95% CI, 1.27-1.94) and diabetes (OR, 1.29; 95% CI, 1.12-1.43) than the first quartile. In contrast to stroke, the family risk score for MI was associated with dyslipidemia (OR, 1.38; 95% CI, 1.23-1.55) and overweight/obesity (OR, 1.22; 95% CI, 1.10-1.37). CONCLUSIONS: Family risk of stroke and MI is strongly associated with the majority of risk factors associated with each disease. Family history and genetic studies separating nonspecific contributions of intermediate phenotypes from specific contributions to the disease phenotype may lead to a more thorough understanding of transmission for these complex disorders.

10 Clinical Trial Pharmacogenetic effect of the stromelysin (MMP3) polymorphism on stroke risk in relation to antihypertensive treatment: the genetics of hypertension associated treatment study. 2011

Sherva, Richard / Ford, Charles E / Eckfeldt, John H / Davis, Barry R / Boerwinkle, Eric / Arnett, Donna K. ·Department of Epidemiology, University of Alabama at Birmingham, Birmingham, AL 32594, USA. ·Stroke · Pubmed #21183746.

ABSTRACT: BACKGROUND AND PURPOSE: Atherothrombotic diseases including stroke share a common etiology of atherosclerosis, and susceptibility to atherosclerosis has a genetic component. Stromelysin-1 (matrix metalloproteinase-3 [MMP3]) regulates arterial matrix composition and is a candidate gene for atherothrombosis. A common polymorphism of MMP3 alters expression levels and affects atherosclerotic progression and plaque stability. As part of the Genetics of Hypertension Associated Treatment study, ancillary to the Antihypertensive and Lipid Lowering to Prevent Heart Attack Trial, we evaluated the 5A/6A polymorphism in MMP3 to determine its association with stroke and determine whether it modifies clinical outcome response to blood pressure-lowering drugs. METHODS: The effect of the MMP3 5A/6A polymorphism on stroke rates was examined by using multivariate-adjusted Cox regression models, including a test for interactions between genotype and antihypertensive drug class. RESULTS: Compared with participants treated with chlorthalidone with the 6A/6A genotype, individuals with the 6A/6A genotype randomized to lisinopril had higher stroke rates (hazard ratio=1.32; 95% CI, 1.08 to 1.61; P=0.007) and 5A/6A individuals taking lisinopril had lower stroke rates (hazard ratio(interaction)=0.74; 95% CI, 0.53 to 1.04; P(interaction)=0.08), whereas 5A/5A individuals taking lisinopril had the lowest stroke rate (hazard ratio(interaction)=0.51; 95% CI, 0.31 to 0.85; P(interaction)=0.009). There were no pharmacogenetic differences in stroke rate by genotype in patients taking amlodipine or doxazosin vs chlorthalidone. CONCLUSIONS: The MMP3 6A/6A genotype is associated with an increased risk of stroke in hypertensive subjects taking lisinopril compared with patients treated with chlorthalidone, whereas a protective effect was found for 5A/5A individuals treated with lisinopril. Genetic screening for the MMP3 5A/6A genotype might be a useful tool to select optimal antihypertensive therapy if this finding is replicated. Clinical Trial Registration- URL: http://www.clinicaltrials.gov. Unique identifier: NCT00563901.

11 Article Genome-Wide Association Study of Apparent Treatment-Resistant Hypertension in the CHARGE Consortium: The CHARGE Pharmacogenetics Working Group. 2019

Irvin, Marguerite R / Sitlani, Colleen M / Floyd, James S / Psaty, Bruce M / Bis, Joshua C / Wiggins, Kerri L / Whitsel, Eric A / Sturmer, Til / Stewart, James / Raffield, Laura / Sun, Fangui / Liu, Ching-Ti / Xu, Hanfei / Cupples, Adrienne L / Tanner, Rikki M / Rossing, Peter / Smith, Albert / Zilhão, Nuno R / Launer, Lenore J / Noordam, Raymond / Rotter, Jerome I / Yao, Jie / Li, Xiaohui / Guo, Xiuqing / Limdi, Nita / Sundaresan, Aishwarya / Lange, Leslie / Correa, Adolfo / Stott, David J / Ford, Ian / Jukema, J Wouter / Gudnason, Vilmundur / Mook-Kanamori, Dennis O / Trompet, Stella / Palmas, Walter / Warren, Helen R / Hellwege, Jacklyn N / Giri, Ayush / O'donnell, Christopher / Hung, Adriana M / Edwards, Todd L / Ahluwalia, Tarunveer S / Arnett, Donna K / Avery, Christy L. ·Department of Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama, USA. · Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle, Washington, USA. · Department of Epidemiology, University of Washington, Seattle, Washington, USA. · Department of Health Services, University of Washington, Seattle, Washington, USA. · Kaiser Permanente Washington Health Research Institute, Seattle, Washington, USA. · Department of Medicine, University of North Carolina, Chapel Hill, North Carolina, USA. · Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina, USA. · Department of Genetics, University of North Carolina, Chapel Hill, North Carolina, USA. · Department of Biostatistics, Boston University, Boston, Maryland, USA. · Steno Diabetes Center Copenhagen, Gentofte, Denmark. · Icelandic Heart Association, Kopavogur, Iceland. · University of Iceland, Reykjavik, Iceland. · Laboratory of Epidemiology and Population Science, Intramural Research Program, National Institute on Aging, Bethesda, Maryland, USA. · Department of Internal Medicine, Section of Gerontology and Geriatrics, Leiden University Medical Center, Leiden, The Netherlands. · Institute for Translational Genomics and Population Sciences, Departments of Pediatrics and Medicine, LABioMed at Harbor-UCLA Medical Center, Torrance, California, USA. · Department of Neurology, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA. · Department of Biostatistics, University of Alabama at Birmingham, Birmingham, Alabama, USA. · Department of Medicine, University of Colorado-Denver, Aurora, Colorado, USA. · Department of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA. · Institute of Cardiovascular and Medical Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK. · Robertson Center for Biostatistics, University of Glasgow, Glasgow, UK. · Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands. · Department of Clinical Epidemiology, Leiden University Medical Center, Leiden, The Netherlands. · Department of Public Health and Primary Care, Leiden University Medical Center, Leiden, The Netherlands. · Department of Medicine, Columbia University Medical Center, New York, New York, USA. · William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK. · National Institute for Health Research Barts Cardiovascular Biomedical Research Unit, Queen Mary University of London, London, UK. · Biomedical Laboratory Research and Development, Tennessee Valley Healthcare System (626)/Vanderbilt University, Nashville, Tennessee, USA. · Division of Genetic Medicine, Department of Medicine, Vanderbilt Genetics Institute, Vanderbilt University Medical Center, Nashville, Tennessee, USA. · Division of Quantitative Sciences, Department of Obstetrics and Gynecology, Vanderbilt Genetics Institute, Vanderbilt Epidemiology Center, Institute for Medicine and Public Health, Vanderbilt University Medical Center, Nashville, Tennessee, USA. · VA Boston Health Care System, Boston, Massachusetts, USA. · Section of Cardiology and Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. · Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA. · Division of Epidemiology, Department of Medicine, Vanderbilt Genetics Institute, Vanderbilt University Medical Center, Nashville, Tennessee, USA. · Deans Office, School of Public Health, University of Kentucky, Lexington, Kentucky, USA. ·Am J Hypertens · Pubmed #31545351.

ABSTRACT: BACKGROUND: Only a handful of genetic discovery efforts in apparent treatment-resistant hypertension (aTRH) have been described. METHODS: We conducted a case-control genome-wide association study of aTRH among persons treated for hypertension, using data from 10 cohorts of European ancestry (EA) and 5 cohorts of African ancestry (AA). Cases were treated with 3 different antihypertensive medication classes and had blood pressure (BP) above goal (systolic BP ≥ 140 mm Hg and/or diastolic BP ≥ 90 mm Hg) or 4 or more medication classes regardless of BP control (nEA = 931, nAA = 228). Both a normotensive control group and a treatment-responsive control group were considered in separate analyses. Normotensive controls were untreated (nEA = 14,210, nAA = 2,480) and had systolic BP/diastolic BP < 140/90 mm Hg. Treatment-responsive controls (nEA = 5,266, nAA = 1,817) had BP at goal (<140/90 mm Hg), while treated with one antihypertensive medication class. Individual cohorts used logistic regression with adjustment for age, sex, study site, and principal components for ancestry to examine the association of single-nucleotide polymorphisms with case-control status. Inverse variance-weighted fixed-effects meta-analyses were carried out using METAL. RESULTS: The known hypertension locus, CASZ1, was a top finding among EAs (P = 1.1 × 10-8) and in the race-combined analysis (P = 1.5 × 10-9) using the normotensive control group (rs12046278, odds ratio = 0.71 (95% confidence interval: 0.6-0.8)). Single-nucleotide polymorphisms in this locus were robustly replicated in the Million Veterans Program (MVP) study in consideration of a treatment-responsive control group. There were no statistically significant findings for the discovery analyses including treatment-responsive controls. CONCLUSION: This genomic discovery effort for aTRH identified CASZ1 as an aTRH risk locus.

12 Article Gene Variants at Loci Related to Blood Pressure Account for Variation in Response to Antihypertensive Drugs Between Black and White Individuals. 2019

Iniesta, Raquel / Campbell, Desmond / Venturini, Cristina / Faconti, Luca / Singh, Sonal / Irvin, Marguerite R / Cooper-DeHoff, Rhonda M / Johnson, Julie A / Turner, Stephen T / Arnett, Donna K / Weale, Michael E / Warren, Helen / Munroe, Patricia B / Cruickshank, Kennedy / Padmanabhan, Sandosh / Lewis, Cathryn / Chowienczyk, Phil. ·From the Department of Medical and Molecular Genetics (R.I., M.E.W., C.L.), King's College London, United Kingdom. · Department of Twin Research (C.V.), King's College London, United Kingdom. · Department of Clinical Pharmacology, King's College London British Heart Foundation Centre, School of Cardiovascular Medicine and Sciences (L.F., P.C.), King's College London, United Kingdom. · Department of Pharmacotherapy and Translational Research and Center for Pharmacogenetics, College of Pharmacy (R.M.C.-D., S.S., J.A.J.), University of Florida. · Department of Epidemiology, University of Alabama (M.R.I.). · Division of Cardiovascular Medicine, College of Medicine (R.M.C.-D., J.A.J.), University of Florida. · Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN (S.T.T.). · Department of Epidemiology, University of Kentucky College of Public Health (D.K.A). · Department of Clinical Pharmacology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry and Barts Cardiovascular Biomedical Research Center, Queen Mary University of London, United Kingdom (H.W., P.B.M). · Department of Nutrition and Dietetics (K.C.), King's College London, United Kingdom. · Division of Cardiovascular and Medical Sciences, University of Glasgow, United Kingdom (S.P.). · Department of Genetic Epidemiology and Statistics, Social, Genetic and Developmental Psychiatry Centre (C.L.), King's College London, United Kingdom. ·Hypertension · Pubmed #31327267.

ABSTRACT: Selection of antihypertensive treatment according to self-defined ethnicity is recommended by some guidelines but might be better guided by individual genotype rather than ethnicity or race. We compared the extent to which variation in blood pressure response across different ethnicities may be explained by genetic factors: genetically defined ancestry and gene variants at loci known to be associated with blood pressure. We analyzed data from 5 trials in which genotyping had been performed (n=4696) and in which treatment responses to β-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blocker, thiazide or thiazide-like diuretic and calcium channel blocker were available. Genetically defined ancestry for proportion of African ancestry was computed using the 1000 genomes population database as a reference. Differences in response to the thiazide diuretic hydrochlorothiazide, the β-blockers atenolol and metoprolol, the angiotensin-converting enzyme inhibitor lisinopril, and the angiotensin receptor blocker candesartan were more closely associated to genetically defined ancestry than self-defined ethnicity in admixed subjects. A relatively small number of gene variants related to loci associated with drug-signaling pathways (KCNK3, SULT1C3, AMH, PDE3A, PLCE1, PRKAG2) with large effect size (-3.5 to +3.5 mm Hg difference in response per allele) and differing allele frequencies in black versus white individuals explained a large proportion of the difference in response to candesartan and hydrochlorothiazide between these groups. These findings suggest that a genomic precision medicine approach can be used to individualize antihypertensive treatment within and across populations without recourse to surrogates of genetic structure such as self-defined ethnicity.

13 Article 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. 2019

Arnett, Donna K / Blumenthal, Roger S / Albert, Michelle A / Buroker, Andrew B / Goldberger, Zachary D / Hahn, Ellen J / Himmelfarb, Cheryl Dennison / Khera, Amit / Lloyd-Jones, Donald / McEvoy, J William / Michos, Erin D / Miedema, Michael D / Muñoz, Daniel / Smith, Sidney C / Virani, Salim S / Williams, Kim A / Yeboah, Joseph / Ziaeian, Boback. · ·J Am Coll Cardiol · Pubmed #30894319.

ABSTRACT: -- No abstract --

14 Article 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. 2019

Arnett, Donna K / Blumenthal, Roger S / Albert, Michelle A / Buroker, Andrew B / Goldberger, Zachary D / Hahn, Ellen J / Himmelfarb, Cheryl Dennison / Khera, Amit / Lloyd-Jones, Donald / McEvoy, J William / Michos, Erin D / Miedema, Michael D / Muñoz, Daniel / Smith, Sidney C / Virani, Salim S / Williams, Kim A / Yeboah, Joseph / Ziaeian, Boback. · ·J Am Coll Cardiol · Pubmed #30894318.

ABSTRACT: -- No abstract --

15 Article Differential Impact of Risk Factors on Stroke Occurrence Among Men Versus Women in West Africa. 2019

Akpalu, Albert / Gebregziabher, Mulugeta / Ovbiagele, Bruce / Sarfo, Fred / Iheonye, Henry / Akinyemi, Rufus / Akpa, Onoja / Tiwari, Hemant K / Arnett, Donna / Wahab, Kolawole / Lackland, Daniel / Abiodun, Adeoye / Ogbole, Godwin / Jenkins, Carolyn / Arulogun, Oyedunni / Akpalu, Josephine / Obiako, Reginald / Olowoyo, Paul / Fawale, Michael / Komolafe, Morenikeji / Osaigbovo, Godwin / Obiabo, Yahaya / Chukwuonye, Innocent / Owolabi, Lukman / Adebayo, Philip / Sunmonu, Taofiki / Owolabi, Mayowa. ·From the Department of Medicine, School of Medicine and Dentistry, University of Ghana, Accra (A.A., J.A.). · Department of Public Health Sciences, Medical University of South Carolina, Charleston (M.G.). · Department of Neurology, Medical University of South Carolina, Charleston (B.O). · Department of Medicine, Komfo Anokye Teaching Hospital, Kumasi, Ghana (F.S.). · Department of Radiology, Ahmadu Bello University, Zaria, Nigeria (H.I.). · Centre for Genomic and Precision Medicine, University of Ibadan, Nigeria (R.A., A.A., M.O.). · Department of Epidemiology and Medical Statistics, University of Ibadan, Nigeria (O. Akpa). · Department of Biostatistics, University of Alabama at Birmingham (H.K.T.). · Faculty of Public Health, University of Kentucky, Lexington (D.A.). · Department of Medicine, University of Ilorin Teaching Hospital, Nigeria (K.W.). · Department of Neurology, Medical University of South Carolina, Charleston (D.L.). · Department of Radiology, University of Ibadan, Nigeria (G. Ogbole). · College of Nursing, Medical University of South Carolina, Charleston (C.J.). · Department of Health Promotion and Education, University of Ibadan, Nigeria (O. Arulogun). · Department of Medicine, Ahmadu Bello University, Zaria, Nigeria (R.O). · Department of Medicine, Federal University Teaching Hospital, Ido Ekiti, Nigeria (P.O.). · Department of Medicine, Obafemi Awolowo University Teaching Hospital, Ile-Ife, Nigeria (M.F., M.K.). · Department of Medicine, Jos University Teaching Hospital, Nigeria (G. Osaigbovo). · Department of Medicine, Delta State University Teaching Hospital, Ogara, Nigeria (Y.O.). · Department of Medicine, Federal Medical Center, Umuahia, Abia State (I.C.). · Department of Medicine, Aminu Kano Teaching Hospital, Nigeria (L.O.). · Department of Medicine, Ladoke Akintola University of Technology, Ogbomoso, Nigeria (P.A.). · Department of Medicine, Federal Medical Center, Owo, Ondo, Nigeria (T.S.). ·Stroke · Pubmed #30879432.

ABSTRACT: Background and Purpose- The interplay between sex and the dominant risk factors for stroke occurrence in sub-Saharan Africa has not been clearly delineated. We compared the effect sizes of risk factors of stroke by sex among West Africans. Methods- SIREN study (Stroke Investigative Research and Educational Networks) is a case-control study conducted at 15 sites in Ghana and Nigeria. Cases were adults aged >18 years with computerized tomography/magnetic resonance imaging confirmed stroke, and controls were age- and sex-matched stroke-free adults. Comprehensive evaluation for vascular, lifestyle, and psychosocial factors was performed using validated tools. We used conditional logistic regression to estimate odds ratios and reported risk factor specific and composite population attributable risks with 95% CIs. Results- Of the 2118 stroke cases, 1193 (56.3%) were males. The mean±SD age of males was 58.1±13.2 versus 60.15±14.53 years among females. Shared modifiable risk factors for stroke with adjusted odds ratios (95% CI) among females versus males, respectively, were hypertension [29.95 (12.49-71.77) versus 16.1 0(9.19-28.19)], dyslipidemia [2.08 (1.42-3.06) versus 1.83 (1.29-2.59)], diabetes mellitus [3.18 (2.11-4.78) versus 2.19 (1.53-3.15)], stress [2.34 (1.48-3.67) versus 1.61 (1.07-2.43)], and low consumption of green leafy vegetables [2.92 (1.89-4.50) versus 2.00 (1.33-3.00)]. However, salt intake and income were significantly different between males and females. Six modifiable factors had a combined population attributable risk of 99.1% (98.3%-99.6%) among females with 9 factors accounting for 97.2% (94.9%-98.7%) among males. Hemorrhagic stroke was more common among males (36.0%) than among females (27.6%), but stroke was less severe among males than females. Conclusions- Overall, risk factors for stroke occurrence are commonly shared by both sexes in West Africa favoring concerted interventions for stroke prevention in the region.

16 Article 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. 2019

Arnett, Donna K / Blumenthal, Roger S / Albert, Michelle A / Buroker, Andrew B / Goldberger, Zachary D / Hahn, Ellen J / Himmelfarb, Cheryl Dennison / Khera, Amit / Lloyd-Jones, Donald / McEvoy, J William / Michos, Erin D / Miedema, Michael D / Muñoz, Daniel / Smith, Sidney C / Virani, Salim S / Williams, Kim A / Yeboah, Joseph / Ziaeian, Boback. ·ACC/AHA Representative. · Lay Representative. · ACC/AHA Task Force on Clinical Practice Guidelines Liaison. · Task Force Performance Measures Representative. ·Circulation · Pubmed #30879355.

ABSTRACT: -- No abstract --

17 Article 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. 2019

Arnett, Donna K / Blumenthal, Roger S / Albert, Michelle A / Buroker, Andrew B / Goldberger, Zachary D / Hahn, Ellen J / Himmelfarb, Cheryl Dennison / Khera, Amit / Lloyd-Jones, Donald / McEvoy, J William / Michos, Erin D / Miedema, Michael D / Muñoz, Daniel / Smith, Sidney C / Virani, Salim S / Williams, Kim A / Yeboah, Joseph / Ziaeian, Boback. ·ACC/AHA Representative. · Lay Representative. · ACC/AHA Task Force on Clinical Practice Guidelines Liaison. · Task Force Performance Measures Representative. ·Circulation · Pubmed #30879339.

ABSTRACT: -- No abstract --

18 Article The Interaction of a Diabetes Gene Risk Score With 3 Different Antihypertensive Medications for Incident Glucose-level Elevation. 2019

Barzilay, Joshua I / Lai, Dejian / Davis, Barry R / Pressel, Sara / Previn, Hannah E / Arnett, Donna K. ·Division of Endocrinology, Kaiser Permanente of Georgia and Division of Endocrinology, Emory University School of Medicine, Atlanta, Georgia, USA. · Department of Biostatistics, University of Texas School of Public Health, Houston, Texas, USA. · Clinical Trial Center, University of Texas School of Public Health, Houston, Texas, USA. · Department of Epidemiology, University of Kentucky College of Public Health, Lexington, Kentucky, USA. ·Am J Hypertens · Pubmed #30590387.

ABSTRACT: BACKGROUND: Elevations of fasting glucose (FG) levels are frequently encountered in people treated with thiazide diuretics. The risk is lower in people treated with ACE inhibitors (ACEi). To determine if genetic factors play a role in FG elevation, we examined the interaction of a diabetes gene risk score (GRS) with the use of 3 different antihypertensive medications. METHODS: We examined 376 nondiabetic hypertensive individuals with baseline FG <100 mg/dl who were genotyped for 24 genes associated with risk of elevated glucose levels. All participants had ≥1 follow-up FG level over 6 years of follow-up. Participants were randomized to treatment with a thiazide-like diuretic (chlorthalidone), a calcium channel blocker (CCB; amlodipine), or an ACEi (lisinopril). Outcomes were an FG increase of ≥13 or ≥27 mg/dl, the upper 75% and 90% FG increase in the parent cohort from which the present cohort was obtained. Odds ratios were adjusted for factors that increase FG levels. RESULTS: For every 1 allele increase in GRS, the adjusted odds ratios (ORs) were 1.06 (95% confidence interval (CI): 0.99, 1.14; P = 0.06) and 1.09 (95% CI: 0.99, 1.20; P = 0.08). When results were examined by randomized medications, participants randomized to amlodipine had statistically significant odds for either outcome (OR: 1.23; 95% CI: 1.03, 1.48; P = 0.01 and OR: 1.31; 95% CI: 1.06, 1.62; P = 0.01). No such risk increase was found in participants randomized to the other 2 medications. CONCLUSIONS: A diabetes GRS predicts FG elevation in people treated with a CCB, but not with an ACEi or diuretic. These findings require confirmation. CLINICAL TRIALS REGISTRATION: Trial number NCT00000542.

19 Article Combined linkage and association analysis identifies rare and low frequency variants for blood pressure at 1q31. 2019

Wang, Heming / Nandakumar, Priyanka / Tekola-Ayele, Fasil / Tayo, Bamidele O / Ware, Erin B / Gu, C Charles / Lu, Yingchang / Yao, Jie / Zhao, Wei / Smith, Jennifer A / Hellwege, Jacklyn N / Guo, Xiuqing / Edwards, Todd L / Loos, Ruth J F / Arnett, Donna K / Fornage, Myriam / Rotimi, Charles / Kardia, Sharon L R / Cooper, Richard S / Rao, D C / Ehret, Georg / Chakravarti, Aravinda / Zhu, Xiaofeng. ·Department of Population and Quantitative Health Sciences, Case Western Reserve University, Cleveland, OH, 44106, USA. · Division of Sleep and Circadian Disorders, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA. · Center for Complex Disease Research, Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. · Center for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, 20892, USA. · Department of Public Health Sciences, Stritch School of Medicine, Loyola University Chicago, Maywood, IL, 60153, USA. · Survey Research Center, Institute for Social Research, University of Michigan, Ann Arbor, MI, 48104, USA. · Division of Biostatistics, Washington University School of Medicine, St. Louis, MO, 63110, USA. · The Charles Bronfman Institute for Personalized Medicine, The Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA. · The Mindich Child Health and Development Institute, The Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA. · Institute for Translational Genomics and Population Sciences, Department of Pediatrics, LABioMed at Harbor-UCLA Medical Center, Torrance, CA, USA. · Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI, 48109, USA. · Division of Epidemiology, Department of Medicine, Vanderbilt Genetics Institute, Vanderbilt University Medical Center, Nashville, TN, 37203, USA. · College of Public Health, University of Kentucky, Lexington, 40536, KY, USA. · Human Genetics Center, Department of Epidemiology, Human Genetics, and Environmental Sciences, School of Public Health, University of Texas Health Science Center at Houston, Houston, TX, 77030, USA. · Center for Complex Disease Research, Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. aravinda.chakravarti@nyulangone.org. · Human Genetics Center, Department of Epidemiology, Human Genetics, and Environmental Sciences, School of Public Health, University of Texas Health Science Center at Houston, Houston, TX, 77030, USA. aravinda.chakravarti@nyulangone.org. · Department of Population and Quantitative Health Sciences, Case Western Reserve University, Cleveland, OH, 44106, USA. xiaofeng.zhu@case.edu. ·Eur J Hum Genet · Pubmed #30262922.

ABSTRACT: High blood pressure (BP) is a major risk factor for cardiovascular disease (CVD) and is more prevalent in African Americans as compared to other US groups. Although large, population-based genome-wide association studies (GWAS) have identified over 300 common polymorphisms modulating inter-individual BP variation, largely in European ancestry subjects, most of them do not localize to regions previously identified through family-based linkage studies. This discrepancy has remained unexplained despite the statistical power differences between current GWAS and prior linkage studies. To address this issue, we performed genome-wide linkage analysis of BP traits in African-American families from the Family Blood Pressure Program (FBPP) and genotyped on the Illumina Human Exome BeadChip v1.1. We identified a genomic region on chromosome 1q31 with LOD score 3.8 for pulse pressure (PP), a region we previously implicated in DBP studies of European ancestry families. Although no reported GWAS variants map to this region, combined linkage and association analysis of PP identified 81 rare and low frequency exonic variants accounting for the linkage evidence. Replication analysis in eight independent African ancestry cohorts (N = 16,968) supports this specific association with PP (P = 0.0509). Additional association and network analyses identified multiple potential candidate genes in this region expressed in multiple tissues and with a strong biological support for a role in BP. In conclusion, multiple genes and rare variants on 1q31 contribute to PP variation. Beyond producing new insights into PP, we demonstrate how family-based linkage and association studies can implicate specific rare and low frequency variants for complex traits.

20 Article Clinical correlates and heritability of cardiac mechanics: The HyperGEN study. 2019

Khan, Sadiya S / Kim, Kwang-Youn A / Peng, Jie / Aguilar, Frank G / Selvaraj, Senthil / Martinez, Eva E / Baldridge, Abigail S / Sha, Jin / Irvin, Marguerite R / Broeckel, Ulrich / Arnett, Donna K / Rasmussen-Torvik, Laura J / Shah, Sanjiv J. ·Division of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, United States; Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, United States. · Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, United States. · Division of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, United States. · Departments of Epidemiology and Biostatistics, School of Public Health, University of Alabama Birmingham, Birmingham, AL 35294, United States. · Human and Molecular Genetics Center, Medical College of Wisconsin, Milwaukee, WI 53226, United States. · Division of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, United States. Electronic address: sanjiv.shah@northwestern.edu. ·Int J Cardiol · Pubmed #30045819.

ABSTRACT: BACKGROUND: Indices of cardiac mechanics are sensitive markers of subclinical myocardial dysfunction. Improved understanding of the clinical correlates and heritability of cardiac mechanics could result in novel insight into the acquired and genetic risk factors for myocardial dysfunction. Therefore, we sought to determine the clinical correlates and heritability of indices of cardiac mechanics in whites and African Americans (AAs). METHODS: We examined 2058 participants stratified by race (1104 whites, 954 AA) in the Hypertension Genetic Epidemiology Network (HyperGEN), a population- and family-based study, and performed digitization of analog echocardiograms with subsequent speckle-tracking analysis. We used linear mixed effects models to determine the clinical correlates of indices of cardiac mechanics (longitudinal, circumferential, radial strain; early diastolic strain rate; and early diastolic tissue velocities). Heritability estimates for cardiac mechanics were calculated using maximum-likelihood variance component analyses in Sequential Oligogenic Linkage Analysis Routine (SOLAR), with adjustment for clinical and echocardiographic covariates. RESULTS: Several clinical characteristics and conventional echocardiographic parameters were found to be associated with speckle-tracking traits of cardiac mechanics. Male sex, blood pressure, and fasting glucose were associated with worse longitudinal strain (LS) (P < 0.05 for all) after multivariable adjustment. After adjustment for covariates, LS, e' velocity, and early diastolic strain rate were found to be heritable; LS and e' velocity had higher heritability estimates in AAs compared to whites. CONCLUSIONS: Indices of cardiac mechanics are heritable traits even after adjustment for clinical and conventional echocardiographic correlates. These findings provide the basis for future studies of genetic determinants of these traits that may elucidate race-based differences in heart failure development.

21 Article Association of Estimated Sodium Intake With Adverse Cardiac Structure and Function: From the HyperGEN Study. 2017

Selvaraj, Senthil / Djoussé, Luc / Aguilar, Frank G / Martinez, Eva E / Polsinelli, Vincenzo B / Irvin, Marguerite R / Arnett, Donna K / Shah, Sanjiv J. ·Division of Aging, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts. Electronic address: senthil.selvaraj@uphs.upenn.edu. · Division of Aging, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts. · Division of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois. · Department of Epidemiology, School of Public Health, University of Alabama-Birmingham, Birmingham, Alabama. ·J Am Coll Cardiol · Pubmed #28774377.

ABSTRACT: BACKGROUND: The optimal level of sodium intake remains controversial. OBJECTIVES: This study sought to determine whether examination of left ventricular longitudinal strain (LS), circumferential strain, and e' velocity can provide insight into thresholds for the detrimental effects of estimated sodium intake (ESI) on subclinical cardiovascular disease. METHODS: We performed speckle-tracking analysis on HyperGEN (Hypertension Genetic Epidemiology Network) study echocardiograms with available urinary sodium data (N = 2,996). We evaluated the associations among ESI and LS, circumferential strain, and e' velocity using multivariable-adjusted linear mixed-effects models (to account for relatedness among subjects) with linear splines (spline 1: ESI ≤3.7 g/day, spline 2: ESI >3.7 g/day based on visual inspection of fractional polynomial plots of the association between ESI and indices of strain and e' velocity). We performed mediation analysis to understand the indirect effects of systolic blood pressure and serum aldosterone on the relationship between ESI and strain and e' velocity. RESULTS: Mean age of participants was 49 ± 14 years, 57% were female, 50% were African American, and 54% had hypertension. The median ESI was 3.73 (interquartile range: 3.24, 4.25) g/day. ESI >3.7 g/day was associated with larger left atrial and left ventricular dimensions (p < 0.05). After adjusting for speckle-tracking analyst, image quality, study site, age, sex, smoking status, alcohol use, daily blocks walked, diuretic use, estimated glomerular filtration rate, left ventricular mass, ejection fraction, and wall motion score index, ESI >3.7 g/day was associated with both strain parameters and e' velocity (p < 0.05 for all comparisons), but ESI ≤3.7 g/day was not (p > 0.05 for all comparisons). There were significant interactions by potassium excretion for circumferential strain. Mediation analysis suggested that systolic blood pressure explained 14% and 20% of the indirect effects between ESI and LS and e' velocity, respectively, whereas serum aldosterone explained 19% of the indirect effects between ESI and LS. CONCLUSIONS: ESI >3.7 g/day is associated with adverse cardiac remodeling and worse systolic strain and diastolic e' velocity.

22 Article Single-trait and multi-trait genome-wide association analyses identify novel loci for blood pressure in African-ancestry populations. 2017

Liang, Jingjing / Le, Thu H / Edwards, Digna R Velez / Tayo, Bamidele O / Gaulton, Kyle J / Smith, Jennifer A / Lu, Yingchang / Jensen, Richard A / Chen, Guanjie / Yanek, Lisa R / Schwander, Karen / Tajuddin, Salman M / Sofer, Tamar / Kim, Wonji / Kayima, James / McKenzie, Colin A / Fox, Ervin / Nalls, Michael A / Young, J Hunter / Sun, Yan V / Lane, Jacqueline M / Cechova, Sylvia / Zhou, Jie / Tang, Hua / Fornage, Myriam / Musani, Solomon K / Wang, Heming / Lee, Juyoung / Adeyemo, Adebowale / Dreisbach, Albert W / Forrester, Terrence / Chu, Pei-Lun / Cappola, Anne / Evans, Michele K / Morrison, Alanna C / Martin, Lisa W / Wiggins, Kerri L / Hui, Qin / Zhao, Wei / Jackson, Rebecca D / Ware, Erin B / Faul, Jessica D / Reiner, Alex P / Bray, Michael / Denny, Joshua C / Mosley, Thomas H / Palmas, Walter / Guo, Xiuqing / Papanicolaou, George J / Penman, Alan D / Polak, Joseph F / Rice, Kenneth / Taylor, Ken D / Boerwinkle, Eric / Bottinger, Erwin P / Liu, Kiang / Risch, Neil / Hunt, Steven C / Kooperberg, Charles / Zonderman, Alan B / Laurie, Cathy C / Becker, Diane M / Cai, Jianwen / Loos, Ruth J F / Psaty, Bruce M / Weir, David R / Kardia, Sharon L R / Arnett, Donna K / Won, Sungho / Edwards, Todd L / Redline, Susan / Cooper, Richard S / Rao, D C / Rotter, Jerome I / Rotimi, Charles / Levy, Daniel / Chakravarti, Aravinda / Zhu, Xiaofeng / Franceschini, Nora. ·Department of Epidemiology & Biostatistics, School of Medicine, Case Western Reserve University, Cleveland, OH, United States of America. · Department of Medicine, Division of Nephrology, University of Virginia, Charlottesville, Virginia, United States of America. · Department of Obstetrics and Gynecology, Institute for Medicine and Public Health, Vanderbilt Genetics Institute, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America. · Department of Public Health Sciences, Loyola University Chicago Stritch School of Medicine, Maywood, Illinois, United States of America. · Department of Pediatrics, University of California San Diego, La Jolla, California, United States of America. · Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, Michigan, United States of America. · The Charles Bronfman Institute for Personalized Medicine, Icahn School of Medicine at Mount Sinai, New York City, New York, United States of America. · The Genetics of Obesity and Related Metabolic Traits Program, Ichan School of Medicine at Mount Sinai, New York City, New York, United States of America. · Division of Epidemiology, Department of Medicine, Vanderbilt-Ingram Cancer Center, Vanderbilt Epidemiology Center, Vanderbilt University School of Medicine, Nashville, Tennessee, United States of America. · Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle, Washington, United States of America. · Center for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, United States of America. · Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America. · Division of Biostatistics, School of Medicine, Washington University in St. Louis, St. Louis, Missouri, United States of America. · Laboratory of Epidemiology and Population Sciences, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America. · Department of Biostatistics, University of Washington, Seattle, Washington, United States of America. · Interdisciplinary Program of Bioinformatics, Seoul National University, Seoul, Republic of Korea. · Division of Adult Cardiology, Uganda Heart Institute, Makerere University College of Health Sciences, Kampala, Uganda. · Department of Medicine, Makerere University College of Health Sciences, Kampala, Uganda. · Tropical Metabolism Research Unit, Caribbean Institute for Health Research, University of the West Indies, Mona, Jamaica. · Department of Preventive Medicine, University of Mississippi Medical Center, Jackson, Mississippi, United States of America. · Data Tecnica International, Glen Echo, MD, United States of America and Laboratory of Neurogenetics, National Institute on Aging, National Institute of Health, Bethesda, Maryland, United States of America. · Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia, United States of America. · Center for Genomic Medicine, Massachusetts General Hospital, Boston, Massachusetts, United States of America. · Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, United States of America. · Program in Medical and Population Genetics, Broad Institute, Cambridge, Massachusetts, United States of America. · Department of Genetics, Stanford University School of Medicine, Stanford, California, United States of America. · Institute of Molecular Medicine and Human Genetics Center, University of Texas Health Science Center at Houston, Houston, TX, United States of America. · Division of Structural and Functional Genomics, Center for Genome Science, Korea National Institute of Health, Cheongju, Republic of Korea. · Department of Internal Medicine, Graduate Institute of Biomedical and Pharmaceutical Science, College of Medicine, Fu Jen Catholic University, New Taipei City, Taiwan. · Division of Endocrinology, Diabetes, and Metabolism, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, United States of America. · Human Genetics Center, School of Public Health, University of Texas Health Science Center, Houston, Texas, United States of America. · The George Washington University School of Medicine and Health Sciences, Washington DC. United States of America. · Department of Internal Medicine, Ohio State University, Columbus, Ohio, United States of America. · Survey Research Center, Institute for Social Research, University of Michigan Ann Arbor, Michigan, United States of America. · Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America. · Department of Biomedical Informatics, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America. · Department of Medicine, Columbia University, New York City, New York, United States of America. · Medical Genetics Institute, Cedars-Sinai Medical Center, Los Angeles, CA, United States of America. · Division of Cardiovascular Sciences, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, United States of America. · Tufts Medical Center, Tufts University School of Medicine, Boston, Massachusetts, United States of America. · Institute for Translational Genomics and Population Sciences, Los Angeles Biomedical Research Institute and Department of Pediatrics, Harbor-UCLA Medical Center, Torrance, CA. · Department of Preventive Medicine, Northwestern University Medical School, Chicago, Illinois, United States of America. · Institute for Human Genetics, University of California, San Francisco, California, United States of America. · Cardiovascular Genetics, University of Utah, Salt Lake City, Utah, United States of America. · Department of Biostatistics, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, United States of America. · The Mindich Child Health and Development Institute, Ichan School of Medicine at Mount Sinai, New York City, New York, United States of America. · Kaiser Permanente Washington Health Research Institute, Seattle, Washington, United States of America. · University of Kentucky, College of Public Health, Lexington, KY. · Department of Public Health Science, Seoul National University, Seoul, Republic of Korea. · Division of Epidemiology, Department of Medicine, Institute of Medicine and Public Health, Vanderbilt Genetics Institute, Vanderbilit University Medical Center, Nashville, Tennessee, United States of America. · Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America. · Population Sciences Branch, National Heart, Lung, and Blood Institute of the National Institutes of Health, Bethesda, MD, and the Framingham Heart Study, Framingham, Massachusetts, United States of America. · McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America. · Epidemiology, Gilling School of Global Public Health, University of North Carolina, Chapel Hill, North Carolina, United States of America. ·PLoS Genet · Pubmed #28498854.

ABSTRACT: Hypertension is a leading cause of global disease, mortality, and disability. While individuals of African descent suffer a disproportionate burden of hypertension and its complications, they have been underrepresented in genetic studies. To identify novel susceptibility loci for blood pressure and hypertension in people of African ancestry, we performed both single and multiple-trait genome-wide association analyses. We analyzed 21 genome-wide association studies comprised of 31,968 individuals of African ancestry, and validated our results with additional 54,395 individuals from multi-ethnic studies. These analyses identified nine loci with eleven independent variants which reached genome-wide significance (P < 1.25×10-8) for either systolic and diastolic blood pressure, hypertension, or for combined traits. Single-trait analyses identified two loci (TARID/TCF21 and LLPH/TMBIM4) and multiple-trait analyses identified one novel locus (FRMD3) for blood pressure. At these three loci, as well as at GRP20/CDH17, associated variants had alleles common only in African-ancestry populations. Functional annotation showed enrichment for genes expressed in immune and kidney cells, as well as in heart and vascular cells/tissues. Experiments driven by these findings and using angiotensin-II induced hypertension in mice showed altered kidney mRNA expression of six genes, suggesting their potential role in hypertension. Our study provides new evidence for genes related to hypertension susceptibility, and the need to study African-ancestry populations in order to identify biologic factors contributing to hypertension.

23 Article Stroke in Indigenous Africans, African Americans, and European Americans: Interplay of Racial and Geographic Factors. 2017

Owolabi, Mayowa / Sarfo, Fred / Howard, Virginia J / Irvin, Marguerite R / Gebregziabher, Mulugeta / Akinyemi, Rufus / Bennett, Aleena / Armstrong, Kevin / Tiwari, Hemant K / Akpalu, Albert / Wahab, Kolawole W / Owolabi, Lukman / Fawale, Bimbo / Komolafe, Morenikeji / Obiako, Reginald / Adebayo, Philip / Manly, Jennifer M / Ogbole, Godwin / Melikam, Ezinne / Laryea, Ruth / Saulson, Raelle / Jenkins, Carolyn / Arnett, Donna K / Lackland, Daniel T / Ovbiagele, Bruce / Howard, George / Anonymous5240902. ·From the Department of Medicine (M.O., E.M.) and Department of Radiology (G.O.), University of Ibadan, Nigeria · Department of Medicine, Komfo Anokye Teaching Hospital, Kumasi, Ghana (F.S.) · Department of Epidemiology (V.J.H., M.R.I.) and Department of Biostatistics (A.B., H.K.T., G.H.), University of Alabama at Birmingham · Department of Public Health Sciences (M.G.), Department of Psychiatry and Behavioural Sciences (K.A.), Department of Neurology (R.S., D.T.L., B.O.), and Department of Nursing (C.J.), Medical University of South Carolina, Charleston · Department of Internal Medicine, Federal Medical Centre, Abeokuta, Nigeria (R.A.) · Department of Medicine and Therapeutics, University of Ghana, Accra (A.A., R.L.) · Department of Medicine, University of Ilorin, Nigeria (K.W.W.) · Department of Medicine, Aminu Kano Teaching Hospital, Nigeria (L.O.) · Department of Medicine, Obafemi Awolowo University Teaching Hospital, Ile-Ife, Nigeria (B.F., M.K.) · Department of Medicine, Ahmadu Bello University, Zaria, Nigeria (R.O.) · Department of Internal Medicine, Ladoke Akintola University of Technology, Ogbomoso, Nigeria (P.A.) · Department of Neurology, Columbia University, New York (J.M.M.) · and College of Public Health, University of Kentucky at Lexington (D.K.A.). ·Stroke · Pubmed #28389611.

ABSTRACT: BACKGROUND AND PURPOSE: The relative contributions of racial and geographic factors to higher risk of stroke in people of African ancestry have not been unraveled. We compared stroke type and contributions of vascular risk factors among indigenous Africans (IA), African Americans (AA), and European Americans (EA). METHODS: SIREN (Stroke Investigative Research and Educational Network) is a large multinational case-control study in West Africa-the ancestral home of 71% AA-whereas REGARDS (Reasons for Geographic and Racial Differences in Stroke) is a cohort study including AA and EA in the United States. Using harmonized assessments and standard definitions, we compared data on stroke type and established risk factors for stroke in acute stroke cases aged ≥55 years in both studies. RESULTS: There were 811 IA, 452 AA, and 665 EA stroke subjects, with mean age of 68.0±9.3, 73.0±8.3, and 76.0±8.3 years, respectively ( CONCLUSIONS: Environmental risk factors such as sedentary lifestyle may contribute to the higher proportion of ischemic stroke in AA compared with IA, whereas racial factors may contribute to the higher proportion of hypertension and diabetes mellitus among stroke subjects of African ancestry.

24 Article Phenomapping for the Identification of Hypertensive Patients with the Myocardial Substrate for Heart Failure with Preserved Ejection Fraction. 2017

Katz, Daniel H / Deo, Rahul C / Aguilar, Frank G / Selvaraj, Senthil / Martinez, Eva E / Beussink-Nelson, Lauren / Kim, Kwang-Youn A / Peng, Jie / Irvin, Marguerite R / Tiwari, Hemant / Rao, D C / Arnett, Donna K / Shah, Sanjiv J. ·Department of Medicine, Massachusetts General Hospital, Boston, MA, USA. · Division of Cardiology, Department of Medicine, Institute for Human Genetics, California Institute for Quantitative Biosciences, and Cardiovascular Research Institute, University of California, San Francisco, CA, USA. · Division of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, 676 N. St. Clair St., Suite 600, Chicago, IL, 60611, USA. · Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. · Departments of Epidemiology and Biostatistics, School of Public Health, University of Alabama at Birmingham, Birmingham, AL, USA. · Division of Biostatistics, Washington University in St. Louis School of Medicine, St. Louis, MO, USA. · School of Public Health, University of Kentucky, Lexington, KY, USA. · Division of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, 676 N. St. Clair St., Suite 600, Chicago, IL, 60611, USA. sanjiv.shah@northwestern.edu. ·J Cardiovasc Transl Res · Pubmed #28258421.

ABSTRACT: We sought to evaluate whether unbiased machine learning of dense phenotypic data ("phenomapping") could identify distinct hypertension subgroups that are associated with the myocardial substrate (i.e., abnormal cardiac mechanics) for heart failure with preserved ejection fraction (HFpEF). In the HyperGEN study, a population- and family-based study of hypertension, we studied 1273 hypertensive patients utilizing clinical, laboratory, and conventional echocardiographic phenotyping of the study participants. We used machine learning analysis of 47 continuous phenotypic variables to identify mutually exclusive groups constituting a novel classification of hypertension. The phenomapping analysis classified study participants into 2 distinct groups that differed markedly in clinical characteristics, cardiac structure/function, and indices of cardiac mechanics (e.g., phenogroup #2 had a decreased absolute longitudinal strain [12.8 ± 4.1 vs. 14.6 ± 3.5%] even after adjustment for traditional comorbidities [p < 0.001]). The 2 hypertension phenogroups may represent distinct subtypes that may benefit from targeted therapies for the prevention of HFpEF.

25 Article Association of Central Adiposity With Adverse Cardiac Mechanics: Findings From the Hypertension Genetic Epidemiology Network Study. 2016

Selvaraj, Senthil / Martinez, Eva E / Aguilar, Frank G / Kim, Kwang-Youn A / Peng, Jie / Sha, Jin / Irvin, Marguerite R / Lewis, Cora E / Hunt, Steven C / Arnett, Donna K / Shah, Sanjiv J. ·From the Division of Cardiology, Department of Medicine (S.S., E.E.M., F.G.A., S.J.S.) and the Department of Preventive Medicine (K.-Y.A.K., J.P.), Northwestern University Feinberg School of Medicine, Chicago, IL · Department of Epidemiology, School of Public Health, University of Alabama Birmingham (J.S., M.R.I., C.E.L., D.K.A.) · the Department of Genetic Medicine, Weill Cornell Medical College in Qatar, Doha, (S.C.H.) · and the Department of Medicine, University of Utah, Salt Lake City (S.C.H.). ·Circ Cardiovasc Imaging · Pubmed #27307550.

ABSTRACT: BACKGROUND: Central obesity, defined by increased waist circumference or waist:hip ratio (WHR), is associated with increased cardiovascular events, including heart failure. However, the pathophysiological link between central obesity and adverse cardiovascular outcomes remains poorly understood. We hypothesized that central obesity and larger WHR are independently associated with worse cardiac mechanics (reduced left ventricular strain and systolic [s'] and early diastolic [e'] tissue velocities). METHODS AND RESULTS: We performed speckle-tracking analysis of echocardiograms from participants in the Hypertension Genetic Epidemiology Network (HyperGEN) study, a population- and family-based epidemiological study (n=2181). Multiple indices of systolic and diastolic cardiac mechanics were measured. We evaluated the association between central obesity and cardiac mechanics using multivariable-adjusted linear mixed-effects models to account for relatedness among participants. The mean age of the cohort was 51±14 years, 58% were women, and 47% were black. Mean body mass index was 30.8±7.1 kg/m(2), waist circumference was 102±17 cm, WHR was 0.91±0.08, and 80% had central obesity based on waist circumference and WHR criteria. After adjusting for multiple potential confounders (including age, sex, race, physical activity, body mass index, heart rate, smoking status, systolic blood pressure, fasting glucose, total cholesterol, antihypertensive medication use, glomerular filtration rate, left ventricular mass index, wall motion abnormalities, and ejection fraction), central obesity and WHR remained associated with worse global longitudinal strain, early diastolic strain rate, s' velocity, and e' velocity (P<0.05 for all comparisons). There were no significant statistical interactions between WHR and obesity status. CONCLUSIONS: In this cross-sectional study of participants with multiple comorbidities, central obesity was found to be associated with adverse cardiac mechanics.

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