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      Enfoque genómico en la enfermedad cardiovascular Translated title: Genomic approach to cardiovascular disease

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          Abstract

          Introducción: las enfermedades cardiovasculares (EC) constituyen la principal causa de muerte a nivel mundial. La etiología es multifactorial, pueden influir diversos factores como la dieta, los hábitos de vida, el nivel de ejercicio físico o la carga genética. El gran número de genes implicados, así como sus diversas variantes, pueden influir sobre el riesgo de padecer enfermedades cardiovasculares por medio de distintas vías. Objetivo: determinar la relación existente entre diferentes polimorfismos genéticos y el riesgo individual de EC en población infantil y adulta. Métodos: se llevó a cabo una búsqueda bibliográfica utilizando la base de datos PubMed. La búsqueda se limitó a un periodo de diez años y a metaanálisis realizados en humanos. Resultados: se establece relación entre el riesgo de enfermedad cardiovascular y los siguientes polimorfismos genéticos: cromosoma 9p21, apolipoproteína A5, apolipoproteínas E2, E3 y E4, gen PPARG o PPARΥ, genes implicados en el metabolismo lipídico, gen MTHFR, citocromo P450, factor V de coagulación o factor de Leiden (FVL) y gen VKORC. Conclusiones: Se han identificado un gran número de genes relacionados con la enfermedad cardiovascular. La carga genética puede influir de manera directa o indirecta sobre el riesgo cardiovascular, modificando factores de riesgo para enfermedad cardiovascular o actuando sobre la medicación empleada para tratarla.

          Translated abstract

          Introduction: Cardiovascular diseases are the most important cause of death worldwide. The etiology is multifactorial, they may be influenced by various factors such as diet, lifestyle, level of exercise or genetics. The large number of genes involved, as well as its various forms, can influence the risk of cardiovascular diseases through different forms. Aim: To determine the relationship between different genetic polymorphisms and individual risk of CHD in child and adult population. Methods: A literature search was performed using PubMed database. The search was limited to a period of ten years and meta-analysis performed in humans. Results: The relationship between the risk of cardiovascular disease and the following genetic polymorphisms: chromosome 9p21, apolipoprotein A5, apolipoprotein E2, E3 and E4, gen PPARG or PPARϒ, genes involved in lipid metabolism, MTHFR gene, cytochrome P450, factor V, coagulation factor Leiden (FVL) and gen VKORC was reviewed. Conclusions: We have identified a number of genes related to cardiovascular disease. The genetic can influence directly or indirectly on cardiovascular risk by modifying risk factors for cardiovascular or acting on the medication used to treat it.

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          Most cited references133

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          Genetic associations with valvular calcification and aortic stenosis.

          Limited information is available regarding genetic contributions to valvular calcification, which is an important precursor of clinical valve disease. We determined genomewide associations with the presence of aortic-valve calcification (among 6942 participants) and mitral annular calcification (among 3795 participants), as detected by computed tomographic (CT) scanning; the study population for this analysis included persons of white European ancestry from three cohorts participating in the Cohorts for Heart and Aging Research in Genomic Epidemiology consortium (discovery population). Findings were replicated in independent cohorts of persons with either CT-detected valvular calcification or clinical aortic stenosis. One SNP in the lipoprotein(a) (LPA) locus (rs10455872) reached genomewide significance for the presence of aortic-valve calcification (odds ratio per allele, 2.05; P=9.0×10(-10)), a finding that was replicated in additional white European, African-American, and Hispanic-American cohorts (P<0.05 for all comparisons). Genetically determined Lp(a) levels, as predicted by LPA genotype, were also associated with aortic-valve calcification, supporting a causal role for Lp(a). In prospective analyses, LPA genotype was associated with incident aortic stenosis (hazard ratio per allele, 1.68; 95% confidence interval [CI], 1.32 to 2.15) and aortic-valve replacement (hazard ratio, 1.54; 95% CI, 1.05 to 2.27) in a large Swedish cohort; the association with incident aortic stenosis was also replicated in an independent Danish cohort. Two SNPs (rs17659543 and rs13415097) near the proinflammatory gene IL1F9 achieved genomewide significance for mitral annular calcification (P=1.5×10(-8) and P=1.8×10(-8), respectively), but the findings were not replicated consistently. Genetic variation in the LPA locus, mediated by Lp(a) levels, is associated with aortic-valve calcification across multiple ethnic groups and with incident clinical aortic stenosis. (Funded by the National Heart, Lung, and Blood Institute and others.).
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            Physical Activity and Risk of Cardiovascular Disease—A Meta-Analysis of Prospective Cohort Studies

            In order to update and improve available evidence on associations of physical activity (PA) with cardiovascular disease (CVD) by applying meta-analytic random effects modeling to data from prospective cohort studies, using high quality criteria of study selection, we searched the PubMed database from January 1980 to December 2010 for prospective cohort studies of PA and incident CVD, distinguishing occupational PA and leisure time PA, coronary heart disease (CHD) and stroke, respectively. Inclusion criteria were peer-reviewed English papers with original data, studies with large sample size (n ≥ 1,000) and substantial follow-up (≥5 years), available data on major confounders and on estimates of relative risk (RR) or hazard ratio (HR), with 95% confidence intervals (CI). We included 21 prospective studies in the overall analysis, with a sample size of more than 650,000 adults who were initially free from CVD, and with some 20,000 incident cases documented during follow-up. Among men, RR of overall CVD in the group with the high level of leisure time PA was 0.76 (95% CI 0.70–0.82, p < 0.001), compared to the reference group with low leisure time PA, with obvious dose-response relationship. A similar effect was observed among women (RR = 0.73, 95% CI 0.68–0.78, p < 0.001). A strong protective effect of occupational PA was observed for moderate level in both men (RR = 0.89, 95% CI 0.82–0.97, p = 0.008) and women (RR = 0.83, 95% CI 0.67–1.03, p = 0.089). No publication bias was observed. Our findings suggest that high level of leisure time PA and moderate level of occupational PA have a beneficial effect on cardiovascular health by reducing the overall risk of incident coronary heart disease and stroke among men and women by 20 to 30 percent and 10 to 20 percent, respectively. This evidence from high quality studies supports efforts of primary and secondary prevention of CVD in economically advanced as well as in rapidly developing countries.
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              Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose-response meta-analysis of prospective cohort studies

              We have been informed about a slight error in this Research paper by Wang and colleagues (BMJ 2014;349:g4490, doi:10.1136/bmj.g4490). From one of the studies (Leenders et al, Am J Epidemiol 2013;178:590-602) included in the meta-analysis, the authors inadvertently used data for women only rather than for the whole population. They have re-run their analyses using the correct hazard ratio for overall mortality of 1.00 (95% confidence interval 0.99 to 1.01) for 100 g/day fruit consumption. The revised pooled hazard ratio for all cause mortality should be 0.94 (0.89 to 0.98; P=0.006) for an increment of one serving of fruit a day, which is almost identical to that reported in the paper (0.94, 0.90 to 0.98; P=0.002) and hence does not affect the conclusions.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                nh
                Nutrición Hospitalaria
                Nutr. Hosp.
                Grupo Arán (Madrid, Madrid, Spain )
                0212-1611
                1699-5198
                February 2016
                : 33
                : 1
                : 148-155
                Affiliations
                [02] Madrid orgnameCentros de Investigación en Nutrición y Salud
                [01] Madrid orgnameUniversidad Complutense de Madrid orgdiv1Departmento de Medicina
                Article
                S0212-16112016000100025
                10.20960/nh.23
                44055ade-b911-454d-b57c-49ad85f7feef

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 International License.

                History
                : 27 October 2015
                : 17 September 2015
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 83, Pages: 8
                Product

                SciELO Spain


                Enfermedad cardiovascular,Polimorfismo,Infancia,Genética,Cardiovascular disease,Polymorphism,Childhood,Genomic

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