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      Genetic Testing for Early Detection of Individuals at Risk of Coronary Heart Disease and Monitoring Response to Therapy: Challenges and Promises

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          Abstract

          Coronary heart disease (CHD) often presents suddenly with little warning. Traditional risk factors are inadequate to identify the asymptomatic high-risk individuals. Early identification of patients with subclinical coronary artery disease using noninvasive imaging modalities would allow the early adoption of aggressive preventative interventions. Currently, it is impractical to screen the entire population with noninvasive coronary imaging tools. The use of relatively simple and inexpensive genetic markers of increased CHD risk can identify a population subgroup in which benefit of atherosclerotic imaging modalities would be increased despite nominal cost and radiation exposure. Additionally, genetic markers are fixed and need only be measured once in a patient’s lifetime, can help guide therapy selection, and may be of utility in family counseling.

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          Genomewide association analysis of coronary artery disease.

          Nilesh J. Samani, Jeanette Erdmann, Alistair S. Hall … (2007)
          Modern genotyping platforms permit a systematic search for inherited components of complex diseases. We performed a joint analysis of two genomewide association studies of coronary artery disease. We first identified chromosomal loci that were strongly associated with coronary artery disease in the Wellcome Trust Case Control Consortium (WTCCC) study (which involved 1926 case subjects with coronary artery disease and 2938 controls) and looked for replication in the German MI [Myocardial Infarction] Family Study (which involved 875 case subjects with myocardial infarction and 1644 controls). Data on other single-nucleotide polymorphisms (SNPs) that were significantly associated with coronary artery disease in either study (P 80%) of a true association: chromosomes 1p13.3 (rs599839), 1q41 (rs17465637), 10q11.21 (rs501120), and 15q22.33 (rs17228212). We identified several genetic loci that, individually and in aggregate, substantially affect the risk of development of coronary artery disease. Copyright 2007 Massachusetts Medical Society.
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            Charting a course for genomic medicine from base pairs to bedside.

            Eric Green, Mark Guyer (2011)
            There has been much progress in genomics in the ten years since a draft sequence of the human genome was published. Opportunities for understanding health and disease are now unprecedented, as advances in genomics are harnessed to obtain robust foundational knowledge about the structure and function of the human genome and about the genetic contributions to human health and disease. Here we articulate a 2011 vision for the future of genomics research and describe the path towards an era of genomic medicine.
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              Susceptibility to coronary artery disease and diabetes is encoded by distinct, tightly linked SNPs in the ANRIL locus on chromosome 9p.

              Helen M Broadbent, John F. Peden, Stefan Lorkowski … (2008)
              Genome-wide association studies have identified a region on chromosome 9p that is associated with coronary artery disease (CAD). The region is also associated with type 2 diabetes (T2D), a risk factor for CAD, although different SNPs were reported to be associated to each disease in separate studies. We have undertaken a case-control study in 4251 CAD cases and 4443 controls in four European populations using previously reported ('literature') and tagging SNPs. We replicated the literature SNPs (P = 8x10(-13); OR = 1.29; 95% CI: 1.20-1.38) and showed that the strong consistent association detected by these SNPs is a consequence of a 'yin-yang' haplotype pattern spanning 53 kb. There was no evidence of additional CAD susceptibility alleles over the major risk haplotype. CAD patients without myocardial infarction (MI) showed a trend towards stronger association than MI patients. The CAD susceptibility conferred by this locus did not differ by sex, age, smoking, obesity, hypertension or diabetes. A simultaneous test of CAD and diabetes susceptibility with CAD and T2D-associated SNPs indicated that these associations were independent of each other. Moreover, this region was not associated with differences in plasma levels of low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, fibrinogen, albumin, uric acid, bilirubin or homocysteine, although the CAD-high-risk allele was paradoxically associated with lower triglyceride levels. A large antisense non-coding RNA gene (ANRIL) collocates with the high-risk haplotype, is expressed in tissues and cell types that are affected by atherosclerosis and is a prime candidate gene for the chromosome 9p CAD locus.
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                Author and article information

                Contributors
                : +1-510-7491658 , +1-510-7491854 , HighHDL@mac.com
                : +1-613-7614779 , +1-613-7614650 , rroberts@ottawaheart.ca
                : +1-305-5383828 , +1-305-5381979 , Arthur.agatston@southbeachdietlp.com
                : +1-404-2721413 , SFrohwein@sjha.org
                : +1-404-2721413 , jreingold@gmail.com
                : +1-510-7494254 , +1-510-7496248 , Thomas.White@celera.com
                : +1-510-749420 , +1-510-7496247 , John.Sninsky@celera.com
                : +1-678-5577748 , basilMargolis@gmail.com
                : +1-678-5476000 , MOMARY_KM@mercer.edu
                : +1-678-7634533 , Superbrenda@mac.com
                : +1-404-3556562 , sking@sjha.org
                Journal
                Journal ID (nlm-ta): Curr Atheroscler Rep
                Title: Current Atherosclerosis Reports
                Publisher: Current Science Inc. (New York )
                ISSN (Print): 1523-3804
                ISSN (Electronic): 1534-6242
                Publication date (Electronic): 10 August 2011
                Publication date PMC-release: 10 August 2011
                Publication date (Print): October 2011
                Volume: 13
                Issue: 5
                Pages: 396-404
                Affiliations
                [1 ]Celera Corporation, 1401 Harbor Bay Parkway, Alameda, CA 94502 USA
                [2 ]Ruddy Canadian Cardiovascular Genetics Centre, University of Ottawa Heart Institute, 40 Ruskin Street, Ottawa, ON K1Y 4W7 Canada
                [3 ]South Beach Preventive Cardiology, 1691 Michigan Ave, #500, Miami Beach, FL 33139 USA
                [4 ]Saint Joseph’s Hospital of Atlanta, 665 Peachtree Dunwoody Road, N.E., Atlanta, GA 30342 USA
                [5 ]College of Pharmacy and Health Sciences, Mercer University, 3001 Mercer University Drive, Atlanta, GA 30341-4415 USA
                [6 ]Cholesterol, Genetics, and Heart Disease Institute, 40 Bear Paw, Portola Valley, CA 94028 USA
                [7 ]Emory University, Atlanta, GA USA
                Article
                Publisher ID: 198
                DOI: 10.1007/s11883-011-0198-8
                PMC ID: 3165136
                PubMed ID: 21830102
                SO-VID: 85140044-01df-45e8-a22a-14a0f8468134
                Copyright © © The Author(s) 2011
                History
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © Springer Science+Business Media, LLC 2011

                ScienceOpen disciplines: Immunology
                Keywords: imaging,coronary heart disease,risk factor,genetic,screening
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: imaging, coronary heart disease, risk factor, genetic, screening

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