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      Association of the genetic markers for myocardial infarction with sudden cardiac death

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          Abstract

          Objective

          Investigate the association of rs17465637 gene MIAF3 (1q41), rs1376251 gene TAS2R50 (12p13), rs4804611 gene ZNF627 (19p13), rs619203 gene ROS1 (6q22), rs1333049 (9p21), rs10757278 (9p21), rs2549513 (16q23), rs499818 (6p24) associated with myocardial infarction available from the international genome-wide studies with sudden cardiac death (SCD) in a case–control study.

          Methods

          A sample of SCD cases ( n = 285) was formed using the WHO criteria; the control sample ( n = 421) was selected according to sex and age. DNA was isolated by phenol–chloroform extraction from the myocardial tissue of SCD cases and blood of control cases. The groups were genotyped for the selected SNPs by real-time PCR using TaqMan probes (Applied Biosystems, United States).

          Results

          No statistically significant differences in the genotype and allelic frequencies of studied single nucleotide polymorphisms between sudden cardiac death cases and control were detectable in general group. By separating the groups of sex and age differences in the genotype frequencies of rs1333049, rs10757278 and rs499818 are statistical significance. Genotypes CC of rs1333049 and GG of rs10757278 are associated with an increased sudden cardiac death risk in men ( p = 0.019, OR = 1.7, 95% CI 1.1–2.8; p = 0.011, OR = 1.8, 95% CI 1.2–2.8, respectively). Genotype AG of rs499818 is associated with an increased sudden cardiac death risk in the women over 50 years old ( p = 0.009, OR = 2.4, 95% CI 1.3–4.6).

          Conclusion

          Polymorphisms rs1333049 and rs10757278 are associated with SCD in men and rs499818 in the women aged over 50 years.

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          Most cited references25

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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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            Framingham Heart Study 100K project: genome-wide associations for cardiovascular disease outcomes

            Martin Larson, Larry D Atwood, Emelia Benjamin … (2007)
            Background Cardiovascular disease (CVD) and its most common manifestations – including coronary heart disease (CHD), stroke, heart failure (HF), and atrial fibrillation (AF) – are major causes of morbidity and mortality. In many industrialized countries, cardiovascular disease (CVD) claims more lives each year than any other disease. Heart disease and stroke are the first and third leading causes of death in the United States. Prior investigations have reported several single gene variants associated with CHD, stroke, HF, and AF. We report a community-based genome-wide association study of major CVD outcomes. Methods In 1345 Framingham Heart Study participants from the largest 310 pedigrees (54% women, mean age 33 years at entry), we analyzed associations of 70,987 qualifying SNPs (Affymetrix 100K GeneChip) to four major CVD outcomes: major atherosclerotic CVD (n = 142; myocardial infarction, stroke, CHD death), major CHD (n = 118; myocardial infarction, CHD death), AF (n = 151), and HF (n = 73). Participants free of the condition at entry were included in proportional hazards models. We analyzed model-based deviance residuals using generalized estimating equations to test associations between SNP genotypes and traits in additive genetic models restricted to autosomal SNPs with minor allele frequency ≥0.10, genotype call rate ≥0.80, and Hardy-Weinberg equilibrium p-value ≥ 0.001. Results Six associations yielded p < 10-5. The lowest p-values for each CVD trait were as follows: major CVD, rs499818, p = 6.6 × 10-6; major CHD, rs2549513, p = 9.7 × 10-6; AF, rs958546, p = 4.8 × 10-6; HF: rs740363, p = 8.8 × 10-6. Of note, we found associations of a 13 Kb region on chromosome 9p21 with major CVD (p 1.7 – 1.9 × 10-5) and major CHD (p 2.5 – 3.5 × 10-4) that confirm associations with CHD in two recently reported genome-wide association studies. Also, rs10501920 in CNTN5 was associated with AF (p = 9.4 × 10-6) and HF (p = 1.2 × 10-4). Complete results for these phenotypes can be found at the dbgap website . Conclusion No association attained genome-wide significance, but several intriguing findings emerged. Notably, we replicated associations of chromosome 9p21 with major CVD. Additional studies are needed to validate these results. Finding genetic variants associated with CVD may point to novel disease pathways and identify potential targeted preventive therapies.
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              Identification of four gene variants associated with myocardial infarction.

              Jennifer Luke, D Leong, Bosco C Rowland … (2005)
              Family history is a major risk factor for myocardial infarction (MI). However, known gene variants associated with MI cannot fully explain the genetic component of MI risk. We hypothesized that a gene-centric association study that was not limited to candidate genes could identify novel genetic associations with MI. We studied 11,053 single-nucleotide polymorphisms (SNPs) in 6,891 genes, focusing on SNPs that could influence gene function to increase the likelihood of identifying disease-causing gene variants. To minimize false-positive associations generated by multiple testing, two studies were used to identify a limited number of nominally associated SNPs; a third study tested the hypotheses that these SNPs are associated with MI. In the initial study (of 340 cases and 346 controls), 637 SNPs were associated with MI (P<.05); these were evaluated in a second study (of 445 cases and 606 controls), and 31 of the 637 SNPs were associated with MI (P<.05) and had the same risk allele as in the first study. For each of these 31 SNPs, we tested the hypothesis that it is associated with MI, using a third study (of 560 cases and 891 controls). We found that four of these gene variants were associated with MI (P<.05; false-discovery rate <10%) and had the same risk allele as in the first two studies. These gene variants encode the cytoskeletal protein palladin (KIAA0992 [odds ratio (OR) 1.40]), a tyrosine kinase (ROS1 [OR 1.75]), and two G protein-coupled receptors (TAS2R50 [OR 1.58] and OR13G1 [OR 1.40]); all ORs are for carriers of two versus zero risk alleles. These findings could lead to a better understanding of MI pathophysiology and improved patient risk assessment.
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                Author and article information

                Contributors
                Anastasiya A. Ivanova
                Vladimir N. Maksimov
                Pavel S. Orlov
                Dinara E. Ivanoshchuk
                Mikhail I. Voevoda
                Journal
                Journal ID (nlm-ta): Indian Heart J
                Journal ID (iso-abbrev): Indian Heart J
                Title: Indian Heart Journal
                Publisher: Elsevier
                ISSN (Print): 0019-4832
                Publication date (Print): April 2017
                Publication date (Electronic): 30 July 2016
                Volume: 69
                Issue: Suppl 1
                Pages: S8-S11
                Affiliations
                [a ]Federal State Budgetary of Scientific Institution “Institution of Internal and Preventive Medicine”, Novosibirsk, Russia
                [b ]Novosibirsk Regional Office of Forensic Medical Examination, Novosibirsk, Russia
                Author notes
                [* ]Corresponding author at: Laboratory of Molecular Genetic Studies of Internal Diseases, Federal State Budgetary of Scientific Institution “Institution of Internal and Preventive Medicine”, ul. B. Bogatkova 175/1, Novosibirsk 630089, Russia.Laboratory of Molecular Genetic Studies of Internal Diseases, Federal State Budgetary of Scientific Institution “Institution of Internal and Preventive Medicine”ul. B. Bogatkova 175/1Novosibirsk630089Russia ivanova_a_a@ 123456mail.ru
                Article
                Publisher ID: S0019-4832(16)30330-3
                DOI: 10.1016/j.ihj.2016.07.016
                PMC ID: 5388015
                PubMed ID: 28400043
                SO-VID: 81abd977-5a73-43df-9501-5370ed083e91
                Copyright © © 2016 Published by Elsevier B.V. on behalf of Cardiological Society of India.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 30 March 2016
                Date accepted : 27 July 2016
                Categories
                Subject: Original Article

                Keywords: sudden cardiac death,9p21,rs17465637,rs1376251,rs4804611,rs619203,rs2549513,rs499818
                Data availability:
                Keywords: sudden cardiac death, 9p21, rs17465637, rs1376251, rs4804611, rs619203, rs2549513, rs499818

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