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      Identifying genetic markers associated with susceptibility to cardiovascular diseases.

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          Abstract

          The development of cardiovascular diseases (CVDs) is due to a complex interaction between the genome and the environment. Understanding how genetic differences in individuals contribute to their susceptibility to CVDs can help guide practitioners to give the best advice to achieve a favorable outcome for the patient. As genome technologies evolve, genotyping of individuals could be available to all patients using a simple saliva test. Large-scale genome-wide association studies and meta analyses have provided powerful insights into polymorphisms that may be predictive of disease and an individual's response to certain nutrients, but moving forward it is imperative that these insights can be applied in the medical setting to reduce the incidence and mortality of CVDs.

          Most cited references75

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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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            Newly identified loci that influence lipid concentrations and risk of coronary artery disease.

            Cristen J Willer, Serena Sanna, Anne U. Jackson … (2008)
            To identify genetic variants influencing plasma lipid concentrations, we first used genotype imputation and meta-analysis to combine three genome-wide scans totaling 8,816 individuals and comprising 6,068 individuals specific to our study (1,874 individuals from the FUSION study of type 2 diabetes and 4,184 individuals from the SardiNIA study of aging-associated variables) and 2,758 individuals from the Diabetes Genetics Initiative, reported in a companion study in this issue. We subsequently examined promising signals in 11,569 additional individuals. Overall, we identify strongly associated variants in eleven loci previously implicated in lipid metabolism (ABCA1, the APOA5-APOA4-APOC3-APOA1 and APOE-APOC clusters, APOB, CETP, GCKR, LDLR, LPL, LIPC, LIPG and PCSK9) and also in several newly identified loci (near MVK-MMAB and GALNT2, with variants primarily associated with high-density lipoprotein (HDL) cholesterol; near SORT1, with variants primarily associated with low-density lipoprotein (LDL) cholesterol; near TRIB1, MLXIPL and ANGPTL3, with variants primarily associated with triglycerides; and a locus encompassing several genes near NCAN, with variants strongly associated with both triglycerides and LDL cholesterol). Notably, the 11 independent variants associated with increased LDL cholesterol concentrations in our study also showed increased frequency in a sample of coronary artery disease cases versus controls.
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              Plasma triglyceride level is a risk factor for cardiovascular disease independent of high-density lipoprotein cholesterol level: a meta-analysis of population-based prospective studies.

              J Hokanson, M. Austin (1996)
              Despite nearly 40 years of research, the role of plasma triglyceride as a risk factor for cardiovascular disease remains elusive. The objectives of the present study were to quantify the magnitude of the association between triglyceride and cardiovascular disease in the general population, and to determine whether this relationship is independent of high-density lipoprotein (HDL) cholesterol, using the semi-quantitative techniques of metaanalysis. Seventeen studies were selected for the analysis based on published reports of population-based, prospective studies, including 46413 men and 10864 women. To insure comparability, only studies reporting the association between fasting triglyceride levels and incident cardiovascular endpoints were included. Using standard meta-analysis calculations, relative risks (RR) and 95% confidence intervals (CI) were calculated and standardized with respect to a 1 mmol/l increase in triglyceride. Multivariable-adjusted RRs were determined for the six studies in men and two studies in women that reported adjustments for HDL cholesterol. For men and women, the univariate RRs for triglyceride were 1.32 (95% Cl 1.26-1.39) and 1.76 (95% Cl 1.50-2.07), respectively, indicating an approximately 30% increased risk in men and a 75% increase in women. Adjustment of HDL cholesterol and other risk factors attenuated these RRs to 1.14 (95% Cl 1.05-1.28) and 1.37 (95% Cl 1.13-1.66), respectively, which were still statistically significant values. Based on combined data from prospective studies, triglyceride is a risk factor for cardiovascular disease for both men and women in the general population, independent of HDL cholesterol. These finding demonstrate the necessity for clinical trials to evaluate whether lowering plasma triglyceride decreases the risk of cardiovascular disease.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Future Sci OA
                Title: Future science OA
                Publisher: Future Science Ltd
                ISSN: 2056-5623
                ISSN (Print): 2056-5623
                Publication date (Electronic): Jan 2019
                Volume: 5
                Issue: 1
                Affiliations
                [1 ] Rightangled Ltd, The Relay Building, 114 Whitechapel High St, London E1 7PT, UK.
                Article
                DOI: 10.4155/fsoa-2018-0031
                PMC ID: 6331704
                PubMed ID: 30652019
                SO-VID: 3398e538-efea-45ec-95bd-043a04a4b68e
                History

                Keywords: DNA,SNP,cardiovascular disease,genetic,genotyping,heart,medicine,personalised,pharmacogenetics,polymorphism
                Data availability:
                Keywords: DNA, SNP, cardiovascular disease, genetic, genotyping, heart, medicine, personalised, pharmacogenetics, polymorphism

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