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The genetics of heart disease: An update

Philadelphia: Lippincott-Raven Publishers, Reichl D, Miller NE. Pathophysiology of reverse cholesterol transport: insights from inherited disorders of lipoprotein metabolism. Arteriosclerosis ; 9: Inhibition of lipoprotein lipase by an apoprotein of human very low density lipoprotein. Biochem Biophys Res Commun ; Arteriosclerosis ; 4: Karathanasis SK. DNA polymorphism adjacent to the human apolipoprotein AI gene: relation to hypertriglyceridemia.

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Lancet ; 1: J Clin Invest ; Atherosclerosis ; Restriction fragment length polymorphisms of the apolipoprotein A-I, C-III, A-IV gene locus: relationships with lipids, apolipoproteins, and premature coronary artery disease. Estimation of the concentration of low-density lipoprotein cholesterol in plasma without use of the preparative ultracentrifuge. Clin Chem ; Clauss A.


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Quick method to estimate fibrinogen by a functional clotting assay. Acta Haematol ; Hyperlipidemia in coronary artery disease: II. Genetic analysis of lipid levels in families and delineation of a new inherited disorder, combined hyperlipidemia. Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults. The Bogalusa Heart Study. Natural history and risk factors of atherosclerosis in children and youth: the PDAY study. Pediatr Pathol Mol Med ; Faergeman O. Methods for detecting coronary disease: epidemiology and clinical management.

Assessment of clinically silent atherosclerotic disease and established and novel risk factors for predicting myocardial infarction and cardiac death in healthy middle-aged subjects: rationale and design of the Heinz Nixdorf RECALL Study. Results of follow-up at eight years. Relationship of baseline major risk factors to coronary and all-cause mortality and to longevity: findings from long-term follow-up of Chicago cohorts. Cardiology ; Multicenter study of the prevalence of diabetes mellitus and impaired glucose tolerance in the urban Brazilian population aged yr.

Diabetes Care ; Effects of serum lipoproteins and smoking on atherosclerosis in young men and women. Arterioscler Thromb Vasc Biol ; The influence of smoking on soluble adhesion molecules and endothelial cell markers. Thromb Res ; Relationship of baseline serum cholesterol levels in 3 large cohorts of younger men to long-term coronary, cardiovascular, and all-cause mortality and to longevity. Factors associated with low and elevated plasma high density lipoprotein cholesterol and apolipoprotein A-I levels in the Framingham Offspring Study. J Lipid Res b; Relation of plasma levels and composition of apolipoprotein B containing lipoproteins to angiographically defined coronary artery disease in young patients with myocardial infarction.

Apo a isoforma predicts risk for coronary heart disease: a study in six populations.

The genetics of heart disease: An update - Harvard Health

Arterioscler Thromb ; Association of fibrinogen, C-reactive protein, albumin or leukocyte count with coronary heart disease: meta-analysis of prospective studies. Plasma fibrinogen and coronary heart disease in urban Japanese. Am J Epidemiol ; Prospective Epidemiological Study of Myocardial Infarction. Thromb Haemost ; Association of fibrinolytic parameters with early atherosclerosis.


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D-Dimers in relation to the severity of arteriosclerosis in patients with stable angina pectoris after myocardial infarction. Eur Heart J ; Thrombogenic factors and recurrent coronary events. Davies MJ. Stability and instability: the two faces of coronary atherosclerosis. The Paul Dudley White Lecture, Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris.

European Concerted Action on Thrombosis and Disabilities. Our second example concerns the prodrug clopidogrel, which is converted into an active metabolite that selectively and irreversibly binds to the P2Y12 receptor on the platelet membrane. Conversion is achieved by the hepatic cytochrome P system in a two-step oxidative process, and cytochrome P 2C19 is involved in both of these steps.

The response to treatment with clopidogrel varies markedly between individuals, and the causes of a poor response are not clearly understood, but have been suggested to be related to clinical, cellular, or genetic factors. Moreover, three recent meta-analyses question the validity of this warning based on the fact that the reported associations are mainly driven by studies with small sample sizes; 78 , 81 , 82 thus, they concluded that current evidence does not support the use of individualized clopidogrel regimens guided by the CYP2C19 genotype.

In the past 7 years, GWAS have contributed substantially to our understanding of the genetic architecture of complex diseases, including CAD. To date, approximately 40 unique loci have been found to be robustly associated with disease risk in large samples from several populations, a much higher number than those identified by linkage and candidate gene association studies.

However, these variants explain only a small proportion of the heritability of CAD. Although it is not yet clear if or how all of this information on the genetic architecture of CAD can be translated into clinical practice, 86 we already have some exciting examples of its potential utility. To identify new therapeutic targets, we must first make the difficult transition from the statistical associations reported in GWAS to the functional mechanisms behind these associations.

Research on the use of genetic information to improve cardiovascular risk estimation in individuals at intermediate risk can be carried out as a second step or in parallel, and further studies to develop new ways to include this information in risk functions, to evaluate its cost-effectiveness, and to explore the ethical issues are also warranted. Disability-adjusted life years DALYs for diseases and injuries in 21 regions, — a systematic analysis for the Global Burden of Disease Study Lluis-Ganella C.

Genetic Polymorphisms and Ischemic Heart Disease

Barcelona, Spain: Universitat Pompeu Fabra; Feto-placental atherosclerotic lesions in intrauterine fetal demise: role of parental cigarette smoking. Open Cardiovasc Med J. Genetics of atherosclerosis. Annu Rev Genomics Hum Genet. The year in atherothrombosis. J Am Coll Cardiol. Tabas I, Glass CK. Anti-inflammatory therapy in chronic disease: challenges and opportunities.

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Pathophysiology of atherosclerosis plaque progression. Heart Lung Circ. Monocytes in coronary artery disease and atherosclerosis: where are we now? Progress and challenges in translating the biology of atherosclerosis. The influence of innate and adaptive immune responses on atherosclerosis.

Annu Rev Pathol. August 7, Libby P. Inflammation in atherosclerosis. Arterioscler Thromb Vasc Biol. Tabas I. Macrophage death and defective inflammation resolution in atherosclerosis. Nat Rev Immunol.

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Doyle B, Caplice N. Plaque neovascularization and antiangiogenic therapy for atherosclerosis. Heritability in the genomics era — concepts and misconceptions. Nat Rev Genet. Research into the genetic component of heart disease: from linkage studies to genome-wide genotyping. Rev Esp Cardiol Suppl. Peden JF, Farrall M. Thirty-five common variants for coronary artery disease: the fruits of much collaborative labour. Hum Mol Genet.

Chial H. Mendelian genetics: patterns of inheritance and single-gene disorders. Nature Education. Accessed November 4, Lobo I. Multifactorial inheritance and genetic disease. Nature Education ;1 1. Large-scale association analysis identifies new risk loci for coronary artery disease. Nat Genet. Genetic linkage studies. Kathiresan S, Srivastava D. Genetics of human cardiovascular disease.

Systolic and diastolic blood pressure lowering as determinants of cardiovascular outcome. The gene encoding 5-lipoxygenase activating protein confers risk of myocardial infarction and stroke. Mutation of MEF2A in an inherited disorder with features of coronary artery disease. A third major locus for autosomal dominant hypercholesterolemia maps to 1p Am J Hum Genet.

Risch N, Merikangas K. The future of genetic studies of complex human diseases. Zhu M, Zhao S. Candidate gene identification approach: progress and challenges. Int J Biol Sci. Candidate-gene approaches for studying complex genetic traits: practical considerations. How to use an article about genetic association. C: What are the results and will they help me in caring for my patients?

Meta-analysis of genetic association studies supports a contribution of common variants to susceptibility to common disease. Five years of GWAS discovery. The International HapMap Consortium. A haplotype map of the human genome. Arking DE, Chakravarti A. Understanding cardiovascular disease through the lens of genome-wide association studies. Trends Genet. PLINK: a tool set for whole-genome association and population-based linkage analyses. Roberts R, Stewart AF. Genes and coronary artery disease: where are we? Finding the missing heritability of complex diseases.

A catalog of published genome-wide association studies. Marian AJ. Trends Cardiovasc Med. Almasy L. The role of phenotype in gene discovery in the whole genome sequencing era. Hum Genet. A common variant on chromosome 9p21 affects the risk of myocardial infarction. A common allele on chromosome 9 associated with coronary heart disease. Wellcome Trust Case Control Consortium. Genome-wide association study of 14, cases of seven common diseases and 3, shared controls. New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.

Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk. Meta-analysis identifies 13 new loci associated with waist-hip ratio and reveals sexual dimorphism in the genetic basis of fat distribution. Association analyses of , individuals reveal 18 new loci associated with body mass index. Biological, clinical and population relevance of 95 loci for blood lipids.

Here's the lowdown on where those numbers need to be:. Stroke recovery is difficult at best and you could be disabled for life. Shake that salt habit, take your medications as recommended by your doctor and get moving. Those numbers need to get down and stay down. Be physically active every day. Research has shown that at least minutes per week of moderate-intensity physical activity can help lower blood pressure, lower cholesterol and keep your weight at a healthy level.

And something IS better than nothing. If you're inactive now, start out slow. Even a few minutes at a time may offer some health benefits. Studies show that people who have achieved even a moderate level of fitness are much less likely to die early than those with a low fitness level. Obesity is highly prevalent in America, not only for adults but also for children.

Fad diets and supplements are not the answer. Good nutrition, controlling calorie intake and physical activity are the only way to maintain a healthy weight. Obesity places you at risk for high cholesterol, high blood pressure and insulin resistance, a precursor of type 2 diabetes — the very factors that heighten your risk of cardiovascular disease. Learn 5 goals to losing weight. Visit Weight Management. For example, people under stress may overeat, start smoking or smoke more than they otherwise would.

Research has even shown that stress reaction in young adults predicts middle-age blood pressure risk. Get stress management tips and tools. Learn more about s tress and heart health. However, there is a cardioprotective effect of moderate alcohol consumption.