Ebook Prevention of cardiovascular diseases from current evidence to clinical practice: Part 1

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Ebook Prevention of cardiovascular diseases from current evidence to clinical practice: Part 1

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(BQ) Part 1 book Prevention of cardiovascular diseases from current evidence to clinical practice presents the following contents: Cardiovascular disease in women - An update, risk factors in childhood and youth, genetics of cardiovascular disease, raised blood cholesterol - Preventable risk factor for cardiovascular disease, tobacco and alcohol control - Preventable risk factors,...

Prevention of Cardiovascular Diseases From Current Evidence to Clinical Practice Jadelson P Andrade Fausto J Pinto Donna K Arnett Editors 123 Prevention of Cardiovascular Diseases Jadelson P Andrade • Fausto J Pinto Donna K Arnett Editors Prevention of Cardiovascular Diseases From Current Evidence to Clinical Practice Editors Jadelson P Andrade, M.D Director, Hospital da Bahia Salvador, Bahia, Brazil Donna K Arnett, M.S.P.H., Ph.D Professor and Chair of the Department of Epidemiology School of Public Health University of Alabama School of Medicine Birmingham, AL, USA Fausto J Pinto, M.D., Ph.D Head of Cardiology Department University Hospital of Santa Maria Faculty of Medicine University of Lisbon Lisbon, Portugal Originally published in Portuguese With the title Tratado de Prevenỗóo Cardiovascular Um Desao Global” Published by “Atheneu, 2014” ISBN 978-3-319-22356-8 ISBN 978-3-319-22357-5 DOI 10.1007/978-3-319-22357-5 (eBook) Library of Congress Control Number: 2015945957 Springer Cham Heidelberg New York Dordrecht London © Springer International Publishing Switzerland 2015 This work is subject to copyright All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed The use of general descriptive names, registered names, trademarks, service marks, etc in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made Printed on acid-free paper Springer International Publishing AG Switzerland is part of Springer Science+Business Media (www.springer.com) Preface by Jadelson P Andrade According to data released by the World Health Organization (WHO), 56.9 million deaths were reported worldwide in 2008, and of these about 17 million were caused by cardiovascular diseases From this alarming reported epidemiological reality, the WHO began to encourage all countries of the world to embrace the banner of cardiovascular prevention, proposing an alliance between the nations, governments, civil society, and private sectors to team up in your face The WHO proposal has the primary objective to promote working together to modify these serious epidemiological data and the gloomy future outlook projected for the following 30 years In line with the WHO global project, the Brazilian Society of Cardiology proposed an international partnership with the European Society of Cardiology and the American Heart Association to prepare the book “Cardiovascular Prevention – A Global Challenge.” Three editors were invited, Jadelson P Andrade, Donna K Arnett, and Fausto J Pinto, then president and president-elect of the aforementioned institutions The work was developed in 28 chapters addressing different themes of cardiovascular prevention with the original version in Portuguese and this edition in English with the title: “Prevention of Cardiovascular Diseases: From Current Evidence to Clinical Practice.” The authors of the chapters were distributed among Brazilian, European, and American experts, all with relevant scientific contributions on the subject The ultimate purpose of the editors, in line with the recent proposal from WHO, is to make available to the international medical community a valuable reference tool for proper addressing the alarming epidemiological index Salvador, Brazil Jadelson P Andrade, MD, FACC, FESC v Preface by Fausto J Pinto Cardiovascular diseases represent the main cause of mortality worldwide, accounting for 36 % of all deaths in the European Union in 2010 according to the latest available statistics published in the last OECD report They cover a range of diseases related to the circulatory system, including ischemic heart disease (IHD) and cerebro-vascular disease, which together comprise 60 % of all cardiovascular deaths, and caused more than one-fifth of all deaths in EU member states The occurrence of several risk factors, such as hypertension, diabetes, dyslipidemia, obesity, smoking, and others, accounts for an increase in the prevalence and severity of cardiovascular disease The uprising of some of these risk factors in some regions more than other may explain partially the differences observed among the different regions in the globe and even within the same continent There are underlying risk factors, such as diet, which may explain differences in IHD mortality across countries For instance, on average across EU member states, IHD mortality rates in 2010 were nearly two times greater for men The disparity was greatest in Cyprus, France, and Luxembourg, with male rates two-to three times higher, and least in Malta, Romania, and the Slovak Republic, at 60 % higher The success of different strategies in the treatment of cardiovascular disease has resulted in a decrease in IHD mortality rates in nearly all countries in Europe and the USA The decline has been most remarkable in Denmark, Ireland, the Netherlands, and the United Kingdom Estonia and Norway also saw IHD mortality rates cut by one-half or more, although rates in Estonia are still high Declining tobacco consumption contributed significantly to reducing the incidence of IHD, and consequently to reducing mortality rates However, the impact of treatment improvement should not undermine the absolute need to improve healthy lifestyles and reduce the weight of the different risk factors, particularly the ones who can be easily prevented if appropriate steps are taken (e.g., smoking, overweight-obesity, diabetes, hypertension, dyslipidemia) The relationship of prevention strategies with cardiovascular events and death rates is clearly established through different scientific studies Therefore, the efficacy of primary prevention programs in patients with recognized, treatable risk factors such as hypercholesterolemia, hypertension, diabetes, and smoking should be a vii viii Preface by Fausto J Pinto priority across the different countries It is also important to recognize the need of a tailored approach considering the differences among different countries, which reinforces the importance of putting in place surveillance systems in place that may be able to monitor properly the need and implementation of preventable measures This is of crucial importance for a successful fight against inequalities to access to appropriate health care among the different countries The role of scientific societies in the dissemination of information as well as in the promotion of different activities towards the populations as well as the decision makers can fill in an important gap in this regard This Book on Prevention, being a joint enterprise between the Brazilian Society of Cardiology, European Society of Cardiology and American Heart Association, will certainly fit into this common goal of improving Prevention of Cardiovascular Disease worldwide Cardiology Department, CCUL, CAML University of Lisbon, Lisbon, Portugal Fausto J Pinto, MD, PhD, FESCC, FACC faustopinto@medicina.ulisboa.pt Preface by Donna K Arnett For those of us who have devoted our lives to studying and treating cardiovascular disease (CVD), the idea that CVD prevention is critical is so obvious that further exposition on the subject may seem gratuitous It is decidedly not The successes that clinicians and public health practitioners have had in the realm of CVD prevention are not only reasons to exult, but also cause for redoubling our efforts with some assurance that prevention is eminently possible and further progress can be made And although some of the more alarming trends observed in some parts of the world (rising prevalence of obesity, for example) are cause for deep concern, they are also cause for increased and improved preventive action It is precisely this changing landscape of CVD and its risk factors that makes continued assessment and discussion of CVD-prevention strategies so critically important Programs in the USA such as the Centers for Disease Control and Prevention’s Million Hearts Initiative and the American Heart Association’s 2020 Impact Goal (to improve cardiovascular health by 20 % by 2020 while reducing CVD and stroke mortality by 20 %) and analogous efforts in other countries are tangible representations of population evaluation, goal setting, policy making, and program development that drive progress in this realm Each of the chapters in this book represents a primer in CVD and its prevention With its calculated mix of CVD and risk factor fundamentals and trenchant foresight, this volume will be welcomed by all those around the globe who aim to rise to the challenge of CVD prevention Birmingham, AL, USA Donna K Arnett, MSPH, PhD ix 126 S.A Claas et al Jensen HK The molecular genetic basis and diagnosis of familial hypercholesterolemia in Denmark Dan Med Bull 2002;49:318–45 De Castro-Oros I, Pocovi M, Civeira F The genetic basis of familial hypercholesterolemia: inheritance, linkage, and mutations Appl Clin Genet 2010;3:53–64 Goldstein J, Hobbs H, Brown M Familial hypercholesterolemia In: Beaudet A, Sly W, Valle D, editors The metabolic and molecular bases of inherited disease New York: McGraw-Hill; 2001 p 2863–913 Robinson JG Management of familial hypercholesterolemia: a review of the recommendations from the National Lipid Association Expert Panel on familial hypercholesterolemia J Manag Care Pharm 2013;19:139–49 Horton JD, Cohen JC, Hobbs HH PCSK9: a convertase that coordinates LDL catabolism J Lipid Res 2009;50 Suppl:S172–7 Cohen J, Pertsemlidis A, Kotowski IK, et al Low LDL cholesterol in individuals of African descent resulting from frequent nonsense mutations in PCSK9 Nat Genet 2005;37:161–5 10 Wierzbicki AS, Hardman TC, Viljoen A Inhibition of pro-protein convertase subtilisin kexin [corrected] (PCSK-9) as a treatment for hyperlipidaemia Expert Opin Investig Drugs 2012;21:667–76 11 Ahmad Z, Adams-Huet B, Chen C, et al Low prevalence of mutations in known loci for autosomal dominant hypercholesterolemia in a multiethnic patient cohort Circ Cardiovasc Genet 2012;5:666–75 12 Maron BJ, Maron MS Hypertrophic cardiomyopathy Lancet 2013;381:242–55 13 Subasic K Hypertrophic cardiomyopathy Nurs Clin North Am 2013;48:571–84 14 Yingchoncharoen T, Tang WW Recent advances 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for coronary artery disease Nat Genet 2013;45:25–33 20 Schunkert H, Konig IR, Kathiresan S, et al Large-scale association analysis identifies 13 new susceptibility loci for coronary artery disease Nat Genet 2011;43:333–8 21 Saha N, Tay JS, Low PS, et al Guanidine to adenine (G/A) substitution in the promoter region of the apolipoprotein AI gene is associated with elevated serum apolipoprotein AI levels in Chinese non-smokers Genet Epidemiol 1994;11:255–64 22 Minnich A, DeLangavant G, Lavigne J, et al G→A substitution at position −75 of the apolipoprotein A-I gene promoter Evidence against a direct effect on HDL cholesterol levels Arterioscler Thromb Vasc Biol 1995;15:1740–5 23 Barre DE, Guerra R, Verstraete R, et al Genetic analysis of a polymorphism in the human apolipoprotein A-I gene promoter: effect on plasma HDL-cholesterol levels J Lipid Res 1994;35:1292–6 24 Miettinen HE, Korpela K, Hamalainen L, et al Polymorphisms of the apolipoprotein and angiotensin converting enzyme genes in young North Karelian patients with coronary heart disease Hum Genet 1994;94:189–92 25 Akita H, Chiba H, Tsuji M, et al Evaluation of G-to-A substitution in the apolipoprotein A-I gene promoter as a determinant of high-density lipoprotein cholesterol level in subjects with and without cholesteryl ester transfer protein deficiency Hum Genet 1995;96:521–6 Genetics of Cardiovascular Disease 127 26 Teslovich TM, Musunuru K, Smith AV, et al Biological, clinical and population relevance of 95 loci for blood lipids Nature 2010;466:707–13 27 Kathiresan S, Willer CJ, Peloso GM, et al Common variants at 30 loci contribute to polygenic dyslipidemia Nat Genet 2009;41:56–65 28 Williams RR, Hunt SC, Hasstedt SJ, et al Genetics of hypertension: what we know and don’t know Clin Exp Hypertens A 1990;12:865–76 29 Ji W, Foo JN, O’Roak BJ, et al Rare independent mutations in renal salt handling genes contribute to blood pressure variation Nat Genet 2008;40:592–9 30 Ehret GB, Munroe PB, Rice KM, et al Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk Nature 2011;478:103–9 31 Kato N, Takeuchi F, Tabara Y, et al Meta-analysis of genome-wide association studies identifies common variants associated with blood pressure variation in east Asians Nat Genet 2011;43:531–8 32 Ganesh SK, Arnett DK, Assimes TL, et al Genetics and genomics for the prevention and treatment of cardiovascular disease: update: a scientific statement from the American Heart Association Circulation 2013;128:2813–51 33 Mega JL, Close SL, Wiviott SD, et al Cytochrome P450 genetic polymorphisms and the response to prasugrel: relationship to pharmacokinetic, pharmacodynamic, and clinical outcomes Circulation 2009;119:2553–60 34 Holmes MV, Perel P, Shah T, et al CYP2C19 genotype, clopidogrel metabolism, platelet function, and cardiovascular events: a systematic review and meta-analysis JAMA 2011; 306:2704–14 35 Scott SA, Sangkuhl K, Stein CM, et al Clinical Pharmacogenetics Implementation Consortium guidelines for CYP2C19 genotype and clopidogrel therapy: 2013 update Clin Pharmacol Ther 2013;94:317–23 36 Rettie AE, Wienkers LC, Gonzalez FJ, et al Impaired (S)-warfarin metabolism catalysed by the R144C allelic variant of CYP2C9 Pharmacogenetics 1994;4:39–42 37 Limdi NA, McGwin G, Goldstein JA, et al Influence of CYP2C9 and VKORC1 1173C/T genotype on the risk of hemorrhagic complications in African-American and EuropeanAmerican patients on warfarin Clin Pharmacol Ther 2008;83:312–21 38 Finkelman BS, Gage BF, Johnson JA, et al Genetic warfarin dosing: tables versus algorithms J Am Coll Cardiol 2011;57:612–8 39 Kimmel SE, French B, Kasner SE, et al A pharmacogenetic versus a clinical algorithm for warfarin dosing N Engl J Med 2013;369:2283–93 40 Pirmohamed M, Burnside G, Eriksson N, et al A randomized trial of genotype-guided dosing of warfarin N Engl J Med 2013;369:2294–303 41 Lynch AI, Boerwinkle E, Davis BR, et al Pharmacogenetic association of the NPPA T2238C genetic variant with cardiovascular disease outcomes in patients with hypertension JAMA 2008;299:296–307 42 Barber MJ, Mangravite LM, Hyde CL, et al Genome-wide association of lipid-lowering response to statins in combined study populations PLoS One 2010;5, e9763 43 Frazier-Wood AC, Aslibekyan S, Borecki IB, et al Genome-wide association study indicates variants associated with insulin signaling and inflammation mediate lipoprotein responses to fenofibrate Pharmacogenet Genomics 2012;22:750–7 44 Evaluation of Genomic Applications in Practice and Prevention (EGAPP) Working Group EGAPP Working Group Recommendations 2009 http://www.egappreviews.org/recommendations/index htm Accessed 18 Mar 2014 45 Recommendations from the EGAPP Working Group: genomic profiling to assess cardiovascular risk to improve cardiovascular health Genet Med 2010;12:839–43 46 Recommendations from the EGAPP Working Group: routine testing for Factor V Leiden (R506Q) and prothrombin (20210G>A) mutations in adults with a history of idiopathic venous thromboembolism and their adult family members Genet Med 2011;13:67–76 Cardiovascular Disease in Women: An Update Helen C Huang, Puja K Mehta, and C Noel Bairey Merz Introduction CVD ranks number one in all-cause mortality in women around the world annually [1] According to the World Health Organization (WHO) 2008 data, one-third of women died from heart attacks due to ischemic heart disease (IHD) and strokes globally Although men and women share similar health challenges, the presentation of CVD in women deserves additional attention Emerging studies have shown that women not present or respond the same way as men Unfortunately, though public awareness of CVD in men has increased over the years, women remain understudied and under-promoted The presentation of CVD in women warrants further study due to its growing incidence and prevalence in the aging female population around the world H.C Huang, M.D Barbra Streisand Women’s Heart Center, Cedars-Sinai Heart Institute, Los Angeles, CA, USA P.K Mehta, M.D Cedars-Sinai Medical Center, Los Angeles, CA, USA Women’s Heart Center in the Division of Cardiology in the Cedars-Sinai Heart Institute, Los Angeles, CA, USA e-mail: puja.mehta@cshs.org C.N.B Merz, M.D., F.A.C.C., F.A.H.A (*) Barbra Streisand Women’s Heart Center, Preventive and Rehabilitative Cardiac Center, Women’s Guild Chair in Women’s Health, Los Angeles, CA, USA e-mail: noel.baireymerz@cshs.org © Springer International Publishing Switzerland 2015 J.P Andrade et al (eds.), Prevention of Cardiovascular Diseases, DOI 10.1007/978-3-319-22357-5_14 129 130 H.C Huang et al Risk Factors There are numerous non-modifiable risk factors of CVD, such as age, race, and genetic factors However, 90 % of CVD in women is attributable to modifiable risk factors, which stratifies women into three risk categories: “at high risk,” denoting a 10-year predicted risk for CVD >20 % based on documented CVD, diabetes mellitus, or end-stage or chronic kidney disease; “at risk” based one or more CVD risk factors, metabolic syndrome, or poor exercise tolerance on treadmill testing or evidence of subclinical atherosclerotic disease; and “at optimal risk,” denoting the absence of CVD risk factors or a healthy lifestyle in the setting of a Framingham risk score 185 were times more likely to develop CVD compared to women with SBP

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