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SHAPE, the Society for Heart Attack Prevention and Eradication (http://www.shapesociety.org), a nonprofit grassroots organization dedicated to the mission of eradicating heart attacks, today announced the agenda of its first focus group meeting on prediction of near-future heart attacks using artificial intelligence. The meeting is led by Dr. Morteza Naghavi the founder and executive director of SHAPE and features leading cardiovascular researchers from around the world.. This will be the 20th scientific meeting held by SHAPE since 2001. Detailed agenda of the meeting is shown below. The First Machine Learning Vulnerable Patient Symposium A Focus Group Meeting on Developing an Artificial Intelligence-based Forecast System A Satellite Event in Conjunction with 2016 Annual Scientific Sessions of American Heart Association This event is open to public. Participation via GoToMeeting can be requested. Dinner will be served 7:30 PM. This is the 20th Vulnerable Plaque & Vulnerable Patient Symposium held by SHAPE since 2001. Welcome: Morteza Naghavi, M.D. Founder of SHAPE and Executive Chairman of the SHAPE Task Force Opening Remarks: Valentin Fuster, M.D., Ph.D. Professor of Medicine and Physician-in-Chief, Mount Sinai Hospital and Icahn School of Medicine Jagat Narula M.D., Ph.D. Chief of Cardiology, Mount Sinai West & St. Luke’s Hospitals Associate, Dean, Arnhold Institute for Global Health at Mount Sinai Icahn School of Medicine Ioannis Kakadiaris, Ph.D. Professor of Computer Science and Biomedical Engineering, Director of Machine Learning Laboratory University of Houston Topic: What is Machine Learning and How Can It Shape the Future of Healthcare? Invited Online Presentations: Two Examples of Machine Learning Studies in CVD Risk Assessment (10 minutes each) CVD prediction using support vector machine in a large Australian cohort. Dinesh Kumar, Ph.D. and Sridhar Arjunan, Ph.D. Biosignals Lab, School of Electrical and Computer Engineering, RMIT University, Melbourne, Australia (2) Prediction of revascularization after myocardial perfusion SPECT by machine learning in a large clinical population Piotr Slomka, Ph.D. Chief Scientist, Artificial Intelligence in Medicine Program, Department of Imaging Cedars-Sinai Medical Center, Professor, UCLA School of Medicine, Los Angeles, CA Moderated Discussions on the Vulnerable Patient Project Machine Learning for Prediction of Near-Term CHD Events All investigators will be asked to give a very brief introduction of their study and how it can fit in Background: Imagine instead of the existing daily weather forecasts and hurricane alerts we were told the probability of a storm within the next 10 years! This is how heart attacks are predicted today. We teach our physicians to calculate the 10-year probability of a heart attack and sudden cardiac death based on their patients’ risk factors. Long term predictions do not trigger immediate preventive actions. Although some people develop warning symptoms, half of men and two-thirds of women who die suddenly of coronary heart disease (CHD) have no previous symptoms. Imagine if we could alert people months, weeks, or even days before a heart attack and trigger immediate preventive actions. The Idea: Use machine learning to create new algorithms to detect who will experience a CHD event within a year (The Vulnerable Patient). Algorithms will be based on banked biospecimen and information collected days up to 12 months prior to the event. We will utilize existing cohorts such as MESA, Heinz Nixdorf Recall Study, Framingham Heart Study, BioImage Study and the Dallas Heart Study. External validation to test for discrimination and calibration will be conducted using other longitudinal observational studies that provide adjudicated cardiovascular event information such as the MiHeart, JHS, DANRISK and ROBINSCA. Additionally, we will use machine learning to characterize individuals who, despite high conventional risk, have lived over 80 years with no CHD events (The Invulnerable ). We expect to discover new targets for drug and possibly vaccine development. We will make the algorithms available as an open source tool to collect additional data over time and increase its predictive value. Organizers: SHAPE as the originating and organizing center for the entire project, recruiting new studies and biobanks, conducting workshops with researchers from each study, fundraising, creating an open source platform community for future enhancement and collaborations. Stanford as the coordinating center for collecting data and samples, and basic science labs. Mount Sinai as the data review and publication center. Machine Learning Lab to be decided, either Google, Apple, IBM, Facebook, Amazon or wherever we find a strong industry partner or sponsor. Director, Cardiac Computed Tomography, Associate Professor of Medicine, Johns Hopkins University Division of Cardiology, The Johns Hopkins Hospital Imagine the new machine learning Vulnerable Patient detection algorithm (heart attack forecaster) is created and validated. If studies confirm the algorithm is able to detect the Vulnerable Patient with 50% or more certainty. In other words, 1 out of 2 patients classified as Vulnerable Patient goes to have an ASCVD event in the following 12 months. Now the questions are: A)    What preventive actions would you take if your asymptomatic patient tested positive as a Vulnerable Patient? B)    What preventive actions would you take if the patient was you?! (This question is meant to circumvent regulatory and financial limitations that may apply to your patients but may not hold you back). Moderators will invite comments from all participants in the meeting. Invited Key Opinion Leaders (Alphabetic Order) Arthur Agatston, M.D. Founder of South Beach Diet, Director of Wellness at Baptist Hospital and Professor of Medicine at University of Miami, FL Daniel Berman, M.D. Professor of Medicine at UCLA, Director of Cardiac Imaging and Nuclear Cardiology at Cedars-Sinai, Los Angeles, CA Michael Blaha, M.D., M.P.H., Director of Clinical Research, Ciccarone Center for the Prevention of Heart Disease, Johns Hopkins University, Baltimore, MD Mathew Budoff, M.D. Professor of Medicine and Director of Preventive Cardiology, UCLA Harbor, Los Angeles, CA Adolfo Correa, M.D., Ph.D. Chief Science Officer, Jackson Heart Study, Professor of Medicine and Pediatrics, University of Mississippi, Jackson, MS Rahul Deo, M.D., Ph.D. Assistant Professor of Medicine, Division of Cardiology, University of California, San Francisco, CA Raimund Erbel, M.D. Professor of Medicine, Chief of Cardiology and Director of West German Heart Centre, University Essen, Germany Sergio Fazio, M.D., Ph.D. Chair of Preventive Cardiology and Professor of Medicine, Oregon Health and Science University, Portland, OR Zahi Fayad, M.D. Professor of Radiology and Medicine (Cardiology), Director of the Translational and Molecular Imaging Institute, Mount Sinai Hospital, New York, NY Philip Greenland, M.D., Professor of Cardiology, Director, Institute for Public Health and Medicine, Center for Population Health Sciences, Chicago, IL Robert Harrington, M.D. Chair of the Department of Medicine, Professor of Medicine, Stanford University School of Medicine, Stanford, CA Harvey Hecht, M.D., Director of Cardiac CT Imaging Laboratory, Mount Sinai School of Medicine, New York, NY Karl-Heinz Jöckel, Ph.D. Institute for Medical Informatics, Biometry and Epidemiology, University of Duisburg-Essen, Germany Ioannis Kakadiaris, Ph.D. Professor of Computer Science and Biomedical Engineering, University of Houston, Houston, TX Stanley Kleis, Ph.D. Professor of Mechanical Engineering and Biomedical Engineering, University of Houston, Houston, TX Tatiana Kuznetsova, M.D. Professor and Director, Hypertension and Cardiovascular Epidemiology, University of Leuven, Leuven, Belgium Daniel Levy, M.D. Director of Framingham Heart Study, and Intramural Investigator, National Institute of Health, Bethesda, MD Roxana Mehran, M.D. Professor of Medicine and Director of Interventional Clinical Trials, Mount Sinai School of Medicine, New York, NY Ralph Metcalfe, Ph.D. Professor of Mechanical and Biomedical Engineering, University of Houston, Houston, TX Susanne Moebus, Ph.D., M.P.H. Biologist & Epidemiologist, Head of the Centre for Urban Epidemiology, University Essen, Germany Morteza Naghavi, M.D. Founder and Executive Chairman of the SHAPE Task Force, President of MEDITEX, Houston, TX Tasneem Z. Naqvi, M.D. Professor of Medicine and Director of Echocardiography, College of Medicine, May Clinic, Scottsdale, AZ Jagat Narula, M.D., Ph.D. Associate Dean for Global Affairs, Professor of Medicine (Cardiology), Mount Sinai Hospital and School of Medicine, New York, NY Ulla Roggenbuck, Ph.D. Institute for Medical Informatics, Biometry and Epidemiology, University Hospital of Essen, Germany Henrik Sillesen, M.D. Professor and Head of Dept. of Vascular Surgery, Rigs Hospitalet, University of Copenhagen, Copenhagen, Denmark Robert Superko, M.D. Professor of Medicine and President at Cholesterol, Genetics, and Heart Disease Institute, Carmel, CA Pierre-Jean Touboul, M.D. Professor of Neurology, Department of Neurology and Stroke Center, AP-HP Bichat University Hospital, Neurology and Stroke Center, Paris, France Nathan Wong, M.P.H., Ph.D. Professor of Epidemiology and Director, Heart Disease Prevention Program, University of California, Irvine, CA Symposium Registration http://shapesociety.org/the-first-machine-learning-heart-attack-forecast-symposium/ About SHAPE The Society for Heart Attack Prevention and Eradication (SHAPE) is a non-profit organization that promotes education and research related to prevention, detection, and treatment of heart attacks. SHAPE is committed to raising public awareness about revolutionary discoveries that are opening exciting avenues that can lead to the eradication of heart attacks. SHAPE's mission is to eradicate heart attacks in the 21st century. SHAPE has recently embarked on “Machine Learning Heart Attack Forecast System (Vulnerable Patient Project)” Project which is a collaborative effort between world’s leading cardiovascular researchers to develop a new Heart Attack Forecast System empowered by artificial intelligence. Additional information on this innovative project will be announced soon. To learn more about SHAPE visit http://www.shapesociety.org. Contact information: 1-877-SHAPE11 and info(at)shapesociety(dot)org. Learn more about the Vulnerable Patient http://shapesociety.org/the-first-machine-learning-heart-attack-forecast-symposium About SHAPE Task Force The SHAPE Task Force, an international group of leading cardiovascular physicians and researchers, has created the SHAPE Guidelines, which educates physicians on how to identify asymptomatic atherosclerosis (hidden plaques) and implement proper therapies to prevent a future heart attack. According to the SHAPE Guidelines, men 45-75 and women 55-75 need to be tested for hidden plaques in coronary or carotid arteries. Individuals with high risk atherosclerosis (high plaque score) should be treated even if their cholesterol level is within statistical “normal range.” If they have plaques, the so-called normal is not normal for them. The higher the amount of plaque burden in the arteries the higher the risk and the more vulnerable to heart attack. SHAPE Guideline aims to identify the asymptomatic “Vulnerable Patient” and offer them intensive preventive therapy to prevent a future heart attack. Knowing one's plaque score can be a matter of life and death. The SHAPE Task Force includes the following: Click below to learn about SHAPE Centers of Excellence http://shapesociety.org/centers-of-excellence/ Drs Naghavi, PK Shah, Daniel Berman, and Mathew Budoff members of the SHAPE Task Force explain how hospitals and community clinics can become a SHAPE Center of Excellence and establish themselves a leader in preventive health.


News Article | December 7, 2016
Site: www.eurekalert.org

DALLAS, Dec. 7, 2016 -- Even modest increases in high blood pressure were linked to a greater risk of death and heart failure among African American adults of all ages, according to new research in Journal of the American Heart Association, the Open Access Journal of the American Heart Association/American Stroke Association. In 2014, the eighth Joint National Committee (JNC) panel increased the recommended blood pressure for people 60 years and older without other medical conditions from less than 140/90 mm Hg to less than 150/90 mm Hg. These recommendations were published after the National Heart, Lung and Blood Institute elected to stop issuing clinical practice guidelines. The effects of the new recommendations on African Americans were unclear due to limited study data available for this population. "Given that blood pressure targets are not attained in up to 50 percent of clinical practice, providers may want to proceed cautiously when liberalizing these targets in a group at higher risk of all the downstream effects of hypertension, such as heart attack, stroke, and chronic kidney disease," said Tiffany C. Randolph, M.D., study lead author and cardiologist at Cone Health Medical Group HeartCare in Greensboro, North Carolina. At the time of the study, Randolph was a research fellow at Duke University Medical Center in Durham, North Carolina. In this study, researchers analyzed high blood pressure and the risk of death and hospitalization for heart failure in 5,280 patients enrolled in the Jackson Heart Study between 2000 and 2011 in Jackson, Mississippi. All participants were African American, nearly two-thirds were women, average age 56 years. The median follow-up was nine years for death, and seven years for hospitalization due to heart failure. "This observational study should make us question whether the current JNC guidelines have identified the optimal target for blood pressure control in the African American population," Randolph said. "To fully answer this question, we will need additional large, randomized, controlled trials that enroll a diverse population. Until then, providers will have to continue assessing risk and working with patients to set blood pressure goals based on all the available data and individual patient concerns." High blood pressure is a common disease that affects about 80 million -- one out of every three -- adults over age 20 in the United States. Often called the "silent killer" because of its lack of symptoms, high blood pressure is one of the main causes of serious diseases such as heart attack, stroke, kidney disease, and heart failure. Anyone can develop high blood pressure, but African Americans and women age 65 or older are at greater risk. High blood pressure is manageable with heart-healthy lifestyle changes, including maintaining a healthy weight, following a healthy diet, being physically active, avoiding smoking and in some cases taking blood pressure-lowering medication. Co-authors are Melissa A. Greiner, M.S.; Chidiebube Egwim, M.D.; Adrian F. Hernandez, M.D., M.H.S.; Kevin L. Thomas, M.D.; Lesley H. Curtis, Ph.D.; Paul Muntner, Ph.D.; Wei Wang, Ph.D.; Robert J. Mentz, M.D.; and Emily C. O'Brien, Ph.D. Author disclosures are on the manuscript. The National Heart, Lung, and Blood Institute and the National Institute on Minority Health and Health Disparities supported the study. Blood pressure images are located in the right column of the release link http://newsroom. After Dec. 7 view the manuscript online. Rise above heart failure Follow AHA/ASA news on Twitter @HeartNews For updates and new science from JAHA, follow @JAHA_AHA Statements and conclusions of study authors published in American Heart Association scientific journals are solely those of the study authors and do not necessarily reflect the association's policy or position. The association makes no representation or guarantee as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations are available at http://www. .


News Article | November 10, 2016
Site: www.eurekalert.org

A study published Nov. 9 in the journal Science Translational Medicine is the first to show that mutations in certain cancer and cardiovascular genes put individuals at an increased risk for dominantly inherited, actionable conditions, regardless of family medical history. The study, carried out in two separate populations of African-Americans and European-Americans, finds that individuals carrying these mutations are at higher risk for developing one of these cancer or cardiac syndromes, respectively. The new work, led by Robert C. Green, MD, MPH, of Brigham and Women's Hospital, Broad Institute and Harvard Medical School, has important implications for the use of genomic sequencing as a future clinical screening tool. "The field of clinical genetics has been uncertain about recommending genome screening in healthy individuals for two reasons. First, we do not know if those individuals will be at increased risk regardless of their family history. Second, we do not know if identifying individuals carrying these mutations will make a positive difference in their eventual clinical outcomes," said Green, senior author on the research. "This analysis addresses only the first of these questions, but demonstrates that in the aggregate, mutations in a subset of genes are associated with a substantial risk of developing the related condition." The study combined the work of investigators in genomics, informatics, molecular biology, epidemiology and statistics at multiple institutions to seek insights into a question that has been extremely difficult to answer. If people carry a genetic mutation, what are the chances that they will develop the related condition over a number of years? Addressing this question has been difficult because very few population-based cohorts have had both genetic sequencing and systematic medical testing recorded over time, and highly heritable conditions are relatively rare. To explore this question, the investigators used data previously collected in two longitudinal cohort studies that investigated heart disease but also collected data on cancer. Data were analyzed from 462 European-Americans from the Massachusetts-based Framingham Heart Study who had been followed for two decades, and 3,223 African-American participants in the Mississippi-based Jackson Heart Study who had been followed for a shorter period. The researchers screened participants for disease-causing mutations using a panel of 56 genes representing 24 hereditary cancer and cardiac syndromes while blinded to the clinical outcomes in these participants. The researchers also collected clinical and diagnostic test information on the participants while blinded to the genome sequencing results. The research team then analyzed whether those who carried the mutations went on to develop associated conditions (cancer, heart disease and high cholesterol) more frequently than those who did not carry the mutations. The results were highly significant, indicating that carrying a mutation in one of the 56 genes conferred greater risk of eventually developing an associated disease in both African-Americans and European-Americans. The risk differences were not thought to be due to racial differences, but rather to the fact that the European Americans in the Framingham study were followed longer than the African Americans in the Jackson study, and had more time to develop the clinical features associated with their genetic changes. Importantly, the study combined risks from very different mutations and very different genes into an "aggregate" estimation of the genetic penetrance (the likelihood that someone with a mutation will develop the condition). While these results establish that as group, those who carry one of these mutations have a higher risk to develop the related disease than those who do not, the results are less relevant to individuals within that population. Nevertheless, it is the first such study to attempt to estimate the effects of such aggregate penetrance within a group. "These populations are uniquely suited for a study like this because everyone in the Framingham and Jackson cohorts received regular EKGs, echocardiograms and lipid measurements, not just those who had medical problems," said Pradeep Natarajan, MD, MMSc, one of the lead authors based at Massachusetts General Hospital. "Data of this nature is not available from a typical health care system where only those who have come to medical attention get blood testing or certain types of diagnostic testing." Eventually, using an individual's genomic variants to predict and prevent future illness may become a routine part of health care. However, it remains to be seen whether identifying individuals with genetic mutations will result in sufficient clinical benefit to merit the risks and costs of downstream imaging studies or procedures. The authors caution that this study does not provide evidence that recognizing genetic mutations directly confers medical benefit. In seeking to explore the related question of clinical outcomes, Green and his team have also implemented a separate randomized clinical trial of medical sequencing called the MedSeq Project, and have organized a Consortium to track medical outcomes among any ostensibly healthy individuals who have been sequenced for predictive purposes. In addition to Natarajan, lead authors on the study included Alexander Bick, MD, PhD, of Massachusetts General Hospital, and Nina Gold, MD, of Boston Children's Hospital. The study involved screening thousands of variants from each person's genome, followed by rigorous manual classification of the variants, supervised by Heidi Rehm, PhD, FACMG, director of the Partners Laboratory for Molecular Medicine and a clinical molecular geneticist at Brigham and Women's Hospital and Harvard Medical School. The study also used sophisticated statistical modeling by simulation, designed by Peter Kraft, PhD, at the Harvard School of Public Health. Researchers from the University of Mississippi Medical Center contributed Jackson Heart Study data. This work was supported by the National Human Genome Research Institute, the Howard Hughes Medical Institute, the National Heart, Lung and Blood Institute and the National Institute on Minority Health and Health Disparities. Brigham and Women's Hospital (BWH) is a 793-bed nonprofit teaching affiliate of Harvard Medical School and a founding member of Partners HealthCare. BWH has more than 4.2 million annual patient visits and nearly 46,000 inpatient stays, is the largest birthing center in Massachusetts and employs nearly 16,000 people. The Brigham's medical preeminence dates back to 1832, and today that rich history in clinical care is coupled with its national leadership in patient care, quality improvement and patient safety initiatives, and its dedication to research, innovation, community engagement and educating and training the next generation of health care professionals. Through investigation and discovery conducted at its Brigham Research Institute (BRI), BWH is an international leader in basic, clinical and translational research on human diseases, more than 3,000 researchers, including physician-investigators and renowned biomedical scientists and faculty supported by nearly $666 million in funding. For the last 25 years, BWH ranked second in research funding from the National Institutes of Health (NIH) among independent hospitals. BWH is also home to major landmark epidemiologic population studies, including the Nurses' and Physicians' Health Studies and the Women's Health Initiative as well as the TIMI Study Group, one of the premier cardiovascular clinical trials groups. For more information, resources and to follow us on social media, please visit BWH's online newsroom.


News Article | November 16, 2016
Site: www.eurekalert.org

(Boston)--Philip A. Wolf, MD, professor of neurology and research professor of medicine (epidemiology and preventive medicine) at Boston University School of Medicine (BUSM), recently delivered the American Heart Association (AHA) 2016 Distinguished Scientist Lecture. Presented during Scientific Session 2016 in New Orleans, LA, the Distinguished Scientist Lectureship was established in 2006 and is viewed as a major honor and recognition of excellence by the AHA. Wolf was co-principal investigator on the Framingham Heart Study Physical Examination, Testing and Surveillance awarded by the National Heart Lung Blood Institute (NHLBI) to BUSM from 1983 to 1989 and was the principal investigator (PI) from 1989 until 2014. Up until 2014 he was PI of continuously funded research grants, Precursors of Stroke incidence and Prognosis from the National Institute of Neurological Diseases and Stroke from 1981 and Epidemiology of Dementia from the National Institute on Aging from 1989. In 2002, he stepped down from the post of chief of the Cerebrovascular Disease Section of the department of neurology at Boston Medical Center, a post he held for more than 30 years. In that role he participated in a number of international cooperative clinical studies of stroke. He was a PI or executive committee member for several key projects: the National Institute of Neurological Disorders and Stroke (NINDS) Data Bank; the Ticlopidine-Aspirin Stroke Study (TASS); Boston Area Anticoagulation Trial in Atrial Fibrillation (BAATAF); North American Symptomatic Carotid Endarterectomy Trial (NASCET); and the Clopidogrel-Aspirin Prevention of Ischemic Events Study (CAPRIE). Wolf served on Executive Committees and Data Safety Monitoring Boards for a number of National Institute of Health (NIH) and industry supported studies of Stroke: BRAVO, VISP, TRENDS, WHI Stroke Study, and PRoFESS. He serves on the Monitoring Boards of two NHLBI observational studies, the Cardiovascular Health Study and The Jackson Heart Study. He is a member of the Stroke Council and Epidemiology and Disease Prevention Councils of the AHA and served on the Executive Committees of both councils. He was a member of the Science Affairs Council of the AHA and of the Scientific Issues Committee of the American Academy of Neurology. In 1992, Wolf was selected by the National Advisory Neurological Disorders and Stroke Council to receive a Jacob A. Javits Neuroscience Investigator Award and was the first to receive the Humana Award for Excellence in Clinical Stroke of the Stroke Council of the AHA. He was selected as the Connor Memorial Lecturer in 1992 by the AHA. He also received the Mihara Cerebrovascular Disorder Research Fund Mihara Award of the International Stroke Society in 1996. He was the recipient of the American Stroke Association New England Chapter's C. Miller Fisher Award in 2000. Wolf's publications focused on the topics of the epidemiology of stroke, dementia and cognitive decline and he has authored or co-authored more than 350 original articles, as well as book chapters, and abstracts. His research has appeared in such journals as The New England Journal of Medicine, Journal of the American Medical Association, Neurology, Stroke and The American Journal of Epidemiology. He has served on the editorial boards of Stroke-A Journal of Cerebral Circulation, and Neuroepidemiology. He has been elected to a number of professional associations including the American Neurologic Association, the American Epidemiologic Society, and the American Academy of Neurology. Wolf received his medical degree from the State University of New York College of Medicine at Syracuse cum laude and was elected to Alpha Omega Alpha. He completed his residency at the Massachusetts General Hospital in Boston. In 2010, he received the honorary Doctor of Science degree from his alma mater.


Campbell Jenkins B.W.,Jackson Heart Study | Sarpong D.F.,Xavier University of Louisiana | Addison C.,Jackson Heart Study | White M.S.,Hinds Community College | And 3 more authors.
International Journal of Environmental Research and Public Health | Year: 2014

This study examined: (a) differences in lung function between current and non current smokers who had sedentary lifestyles and non sedentary lifestyles and (b) the mediating effect of sedentary lifestyle on the association between smoking and lung function in African Americans. Sedentary lifestyle was defined as the lowest quartile of the total physical activity score. The results of linear and logistic regression analyses revealed that non smokers with non sedentary lifestyles had the highest level of lung function, and smokers with sedentary lifestyles had the lowest level. The female non-smokers with sedentary lifestyles had a significantly higher FEV1% predicted and FVC% predicted than smokers with non sedentary lifestyles (93.3% vs. 88.6%; p = 0.0102 and 92.1% vs. 86.9%; p = 0.0055 respectively). FEV1/FVC ratio for men was higher in non smokers with sedentary lifestyles than in smokers with non sedentary lifestyles (80.9 vs. 78.1; p = 0.0048). Though smoking is inversely associated with lung function, it seems to have a more deleterious effect than sedentary lifestyle on lung function. Physically active smokers had higher lung function than their non physically active counterparts. © 2014 by the authors; licensee MDPI, Basel, Switzerland.


Hickson D.A.,Jackson Heart Study | Roux A.V.D.,University of Michigan | Gebreab S.Y.,University of Michigan | Wyatt S.B.,University of Mississippi Medical Center | And 4 more authors.
American Journal of Public Health | Year: 2012

Objectives. We examined the social patterning of cumulative dysregulation of multiple systems, or allostatic load, among African Americans adults. Methods. We examined the cross-sectional associations of socioeconomic status (SES) with summary indices of allostatic load and neuroendocrine, metabolic, autonomic, and immune function components in 4048 Jackson Heart Study participants. Results. Lower education and income were associated with higher allostatic load scores in African American adults. Patterns were most consistent for the metabolic and immune dimensions, less consistent for the autonomic dimension, and absent for the neuroendocrine dimension among African American women. Associations of SES with the global allostatic load score and the metabolic and immune domains persisted after adjustment for behavioral factors and were stronger for income than for education. There was some evidence that the neuroendocrine dimension was inversely associated with SES after behavioral adjustment in men, but the immune and autonomic components did not show clear dose-response trends, and we observed no associations for the metabolic component. Conclusions. Findings support our hypothesis that allostatic load is socially patterned in African American women, but this pattern is less consistent in African American men.


Patel S.R.,Brigham and Women's Hospital | Goodloe R.,Vanderbilt University | De G.,Harvard University | Kowgier M.,Samuel Lunenfeld Research Institute | And 20 more authors.
PLoS ONE | Year: 2012

Although obstructive sleep apnea (OSA) is known to have a strong familial basis, no genetic polymorphisms influencing apnea risk have been identified in cross-cohort analyses. We utilized the National Heart, Lung, and Blood Institute (NHLBI) Candidate Gene Association Resource (CARe) to identify sleep apnea susceptibility loci. Using a panel of 46,449 polymorphisms from roughly 2,100 candidate genes on a customized Illumina iSelect chip, we tested for association with the apnea hypopnea index (AHI) as well as moderate to severe OSA (AHI≥15) in 3,551 participants of the Cleveland Family Study and two cohorts participating in the Sleep Heart Health Study. Among 647 African-Americans, rs11126184 in the pleckstrin (PLEK) gene was associated with OSA while rs7030789 in the lysophosphatidic acid receptor 1 (LPAR1) gene was associated with AHI using a chip-wide significance threshold of p-value<2×10-6. Among 2,904 individuals of European ancestry, rs1409986 in the prostaglandin E2 receptor (PTGER3) gene was significantly associated with OSA. Consistency of effects between rs7030789 and rs1409986 in LPAR1 and PTGER3 and apnea phenotypes were observed in independent clinic-based cohorts. Novel genetic loci for apnea phenotypes were identified through the use of customized gene chips and meta-analyses of cohort data with replication in clinic-based samples. The identified SNPs all lie in genes associated with inflammation suggesting inflammation may play a role in OSA pathogenesis.


Riestra P.,Human Genome Research Institutes | Gebreab S.Y.,Human Genome Research Institutes | Xu R.,Human Genome Research Institutes | Khan R.J.,Human Genome Research Institutes | And 4 more authors.
BMC Medical Genetics | Year: 2015

Background: Despite the important role of adiponectin in regulating general metabolic homeostasis, analysis of genetic determinants of adiponectin and the related cardio-metabolic traits in African American population has been limited and inconsistent. Considering the high genetic admixture of African Americans and thus the important population stratification that may confound the genetic-trait associations, the objective of this work was to perform a comprehensive analysis of the associations between ADIPOQ variants and adiponectin levels and obesity phenotypes in a large African American population from the Jackson Heart Study (JHS) cohort. Methods: Genotype data was available for 2968 JHS participants (1131men; 1837women). Single Nucleotide Polymorphisms (SNPs) were selected by a Tag-SNP Approach and literature review. The genotype imputation was performed using IMPUTE2 software and reference phased data from the 1000G project. PLINK software was used for the genetic analysis. Plasma specimens were analyzed by ELISA for adiponectin levels. All analyses were controlled for population stratification assessed by Individual Proportions of European Ancestry (PEA) estimates calculated in HAPMIX using ancestry informative markers (AIMs). Results: We found a gender-dependent association of some ADIPOQ variants and adiponectin levels. In women four of the studied polymorphisms (rs6444174, rs16861205, rs1403697, rs7641507) were associated with adiponectin levels after Bonferroni correction and controlling for the percentage of PEA, age, annual household income and smoking. These results were consistent with the haplotype analysis. The association between the rs12495941 variant and obesity is modulated by the PEA, so that the relationship between the G allele and a higher incidence of obesity was present in those individuals within the lower PEA group. In addition we found an effect modification of obesity on the association between the ADIPOQ rs6444174 SNP and BMI so that the presence of the T allele was negatively and significantly associated with BMI only in participants with a normal weight. Conclusions: In this large African American cohort, ADIPOQ variants were associated with adiponectin levels in a gender-dependent manner and the relationship of some of these variants with obesity and BMI was modulated by the PEA and obesity status respectively. This suggests that the effects of these polymorphisms on adiponectin and obesity phenotypes are subject to a strong interaction with genetic and environmental factors in African American population. © 2015 Riestra et al.


PubMed | Human Genome Research Institutes, Indiana University Bloomington and Jackson Heart Study
Type: | Journal: BMC medical genetics | Year: 2015

Despite the important role of adiponectin in regulating general metabolic homeostasis, analysis of genetic determinants of adiponectin and the related cardio-metabolic traits in African American population has been limited and inconsistent. Considering the high genetic admixture of African Americans and thus the important population stratification that may confound the genetic-trait associations, the objective of this work was to perform a comprehensive analysis of the associations between ADIPOQ variants and adiponectin levels and obesity phenotypes in a large African American population from the Jackson Heart Study (JHS) cohort.Genotype data was available for 2968 JHS participants (1131men; 1837women). Single Nucleotide Polymorphisms (SNPs) were selected by a Tag-SNP Approach and literature review. The genotype imputation was performed using IMPUTE2 software and reference phased data from the 1000G project. PLINK software was used for the genetic analysis. Plasma specimens were analyzed by ELISA for adiponectin levels. All analyses were controlled for population stratification assessed by Individual Proportions of European Ancestry (PEA) estimates calculated in HAPMIX using ancestry informative markers (AIMs).We found a gender-dependent association of some ADIPOQ variants and adiponectin levels. In women four of the studied polymorphisms (rs6444174, rs16861205, rs1403697, rs7641507) were associated with adiponectin levels after Bonferroni correction and controlling for the percentage of PEA, age, annual household income and smoking. These results were consistent with the haplotype analysis. The association between the rs12495941 variant and obesity is modulated by the PEA, so that the relationship between the G allele and a higher incidence of obesity was present in those individuals within the lower PEA group. In addition we found an effect modification of obesity on the association between the ADIPOQ rs6444174 SNP and BMI so that the presence of the T allele was negatively and significantly associated with BMI only in participants with a normal weight.In this large African American cohort, ADIPOQ variants were associated with adiponectin levels in a gender-dependent manner and the relationship of some of these variants with obesity and BMI was modulated by the PEA and obesity status respectively. This suggests that the effects of these polymorphisms on adiponectin and obesity phenotypes are subject to a strong interaction with genetic and environmental factors in African American population.


News Article | November 11, 2016
Site: www.sciencedaily.com

A study published Nov. 9 in the journal Science Translational Medicine is the first to show that mutations in certain cancer and cardiovascular genes put individuals at an increased risk for dominantly inherited, actionable conditions, regardless of family medical history. The study, carried out in two separate populations of African-Americans and European-Americans, finds that individuals carrying these mutations are at higher risk for developing one of these cancer or cardiac syndromes, respectively. The new work, led by Robert C. Green, MD, MPH, of Brigham and Women's Hospital, Broad Institute and Harvard Medical School, has important implications for the use of genomic sequencing as a future clinical screening tool. "The field of clinical genetics has been uncertain about recommending genome screening in healthy individuals for two reasons. First, we do not know if those individuals will be at increased risk regardless of their family history. Second, we do not know if identifying individuals carrying these mutations will make a positive difference in their eventual clinical outcomes," said Green, senior author on the research. "This analysis addresses only the first of these questions, but demonstrates that in the aggregate, mutations in a subset of genes are associated with a substantial risk of developing the related condition." The study combined the work of investigators in genomics, informatics, molecular biology, epidemiology and statistics at multiple institutions to seek insights into a question that has been extremely difficult to answer. If people carry a genetic mutation, what are the chances that they will develop the related condition over a number of years? Addressing this question has been difficult because very few population-based cohorts have had both genetic sequencing and systematic medical testing recorded over time, and highly heritable conditions are relatively rare. To explore this question, the investigators used data previously collected in two longitudinal cohort studies that investigated heart disease but also collected data on cancer. Data were analyzed from 462 European-Americans from the Massachusetts-based Framingham Heart Study who had been followed for two decades, and 3,223 African-American participants in the Mississippi-based Jackson Heart Study who had been followed for a shorter period. The researchers screened participants for disease-causing mutations using a panel of 56 genes representing 24 hereditary cancer and cardiac syndromes while blinded to the clinical outcomes in these participants. The researchers also collected clinical and diagnostic test information on the participants while blinded to the genome sequencing results. The research team then analyzed whether those who carried the mutations went on to develop associated conditions (cancer, heart disease and high cholesterol) more frequently than those who did not carry the mutations. The results were highly significant, indicating that carrying a mutation in one of the 56 genes conferred greater risk of eventually developing an associated disease in both African-Americans and European-Americans. The risk differences were not thought to be due to racial differences, but rather to the fact that the European Americans in the Framingham study were followed longer than the African Americans in the Jackson study, and had more time to develop the clinical features associated with their genetic changes. Importantly, the study combined risks from very different mutations and very different genes into an "aggregate" estimation of the genetic penetrance (the likelihood that someone with a mutation will develop the condition). While these results establish that as group, those who carry one of these mutations have a higher risk to develop the related disease than those who do not, the results are less relevant to individuals within that population. Nevertheless, it is the first such study to attempt to estimate the effects of such aggregate penetrance within a group. "These populations are uniquely suited for a study like this because everyone in the Framingham and Jackson cohorts received regular EKGs, echocardiograms and lipid measurements, not just those who had medical problems," said Pradeep Natarajan, MD, MMSc, one of the lead authors based at Massachusetts General Hospital. "Data of this nature is not available from a typical health care system where only those who have come to medical attention get blood testing or certain types of diagnostic testing." Eventually, using an individual's genomic variants to predict and prevent future illness may become a routine part of health care. However, it remains to be seen whether identifying individuals with genetic mutations will result in sufficient clinical benefit to merit the risks and costs of downstream imaging studies or procedures. The authors caution that this study does not provide evidence that recognizing genetic mutations directly confers medical benefit. In seeking to explore the related question of clinical outcomes, Green and his team have also implemented a separate randomized clinical trial of medical sequencing called the MedSeq Project, and have organized a Consortium to track medical outcomes among any ostensibly healthy individuals who have been sequenced for predictive purposes.

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