Association of Multiple Genetic Variants with the Extension and Severity of Coronary Artery Disease
Autor(a) principal: | |
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Data de Publicação: | 2018 |
Outros Autores: | , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Arquivos Brasileiros de Cardiologia (Online) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0066-782X2018000100016 |
Resumo: | Abstract Background: Metabolic syndrome (MS) is a condition that, when associated with ischemic heart disease and cardiovascular events, can be influenced by genetic variants and determine more severe coronary atherosclerosis. Objectives: To examine the contribution of genetic polymorphisms to the extension and severity of coronary disease in subjects with MS and recent acute coronary syndrome (ACS). Methods: Patients (n = 116, 68% males) aged 56 (9) years, with criteria for MS, were prospectively enrolled to the study during the hospitalization period after an ACS. Clinical and laboratory parameters, high-sensitivity C-reactive protein, thiobarbituric acid reactive substances, adiponectin, endothelial function, and the Gensini score were assessed. Polymorphisms of paraoxonase-1 (PON-1), methylenotetrahydrofolate reductase (MTHFR), endothelial nitric oxide synthase (ENOS), angiotensin-converting enzyme (ACE), angiotensin II type 1 receptor (AT1R), apolipoprotein C3 (APOC3), lipoprotein lipase (LPL) were analysed by polymerase chain reaction (PCR) technique, followed by the identification of restriction fragment length polymorphisms (RFLP, and a genetic score was calculated. Parametric and non-parametric tests were used, as appropriate. Significance was set at p < 0.05. Results: Polymorphisms of PON-1, MTHFR and ENOS were not in the Hardy-Weinberg equilibrium. The DD genotype of LPL was associated with higher severity and greater extension of coronary lesions. Genetic score tended to be higher in patients with Gensini score < P50 (13.7 ± 1.5 vs. 13.0 ± 1.6, p = 0.066), with an inverse correlation between genetic and Gensini scores (R = -0.194, p = 0.078). Conclusions: The LPL polymorphism contributed to the severity of coronary disease in patients with MS and recent ACS. Combined polymorphisms were associated with the extension of coronary disease, and the lower the genetic score the more severe the disease. |
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Arquivos Brasileiros de Cardiologia (Online) |
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Association of Multiple Genetic Variants with the Extension and Severity of Coronary Artery DiseaseCoronary Artery Disease / geneticPolymorphism, GeneticMetabolic SyndromeSedentary LifestyleAbstract Background: Metabolic syndrome (MS) is a condition that, when associated with ischemic heart disease and cardiovascular events, can be influenced by genetic variants and determine more severe coronary atherosclerosis. Objectives: To examine the contribution of genetic polymorphisms to the extension and severity of coronary disease in subjects with MS and recent acute coronary syndrome (ACS). Methods: Patients (n = 116, 68% males) aged 56 (9) years, with criteria for MS, were prospectively enrolled to the study during the hospitalization period after an ACS. Clinical and laboratory parameters, high-sensitivity C-reactive protein, thiobarbituric acid reactive substances, adiponectin, endothelial function, and the Gensini score were assessed. Polymorphisms of paraoxonase-1 (PON-1), methylenotetrahydrofolate reductase (MTHFR), endothelial nitric oxide synthase (ENOS), angiotensin-converting enzyme (ACE), angiotensin II type 1 receptor (AT1R), apolipoprotein C3 (APOC3), lipoprotein lipase (LPL) were analysed by polymerase chain reaction (PCR) technique, followed by the identification of restriction fragment length polymorphisms (RFLP, and a genetic score was calculated. Parametric and non-parametric tests were used, as appropriate. Significance was set at p < 0.05. Results: Polymorphisms of PON-1, MTHFR and ENOS were not in the Hardy-Weinberg equilibrium. The DD genotype of LPL was associated with higher severity and greater extension of coronary lesions. Genetic score tended to be higher in patients with Gensini score < P50 (13.7 ± 1.5 vs. 13.0 ± 1.6, p = 0.066), with an inverse correlation between genetic and Gensini scores (R = -0.194, p = 0.078). Conclusions: The LPL polymorphism contributed to the severity of coronary disease in patients with MS and recent ACS. Combined polymorphisms were associated with the extension of coronary disease, and the lower the genetic score the more severe the disease.Sociedade Brasileira de Cardiologia - SBC2018-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0066-782X2018000100016Arquivos Brasileiros de Cardiologia v.110 n.1 2018reponame:Arquivos Brasileiros de Cardiologia (Online)instname:Sociedade Brasileira de Cardiologia (SBC)instacron:SBC10.5935/abc.20170177info:eu-repo/semantics/openAccessFischer,Simone Cristina Pinto MatheusPinto,Simone PiresLins,Lívia Campos do Amaral SilvaBianco,Henrique TriaMonteiro,Carlos Manoel de CastroPinheiro,Luiz Fernando MunizFonseca,Francisco Antonio HelfensteinIzar,Maria Cristina de Oliveiraeng2018-03-05T00:00:00Zoai:scielo:S0066-782X2018000100016Revistahttp://www.arquivosonline.com.br/https://old.scielo.br/oai/scielo-oai.php||arquivos@cardiol.br1678-41700066-782Xopendoar:2018-03-05T00:00Arquivos Brasileiros de Cardiologia (Online) - Sociedade Brasileira de Cardiologia (SBC)false |
dc.title.none.fl_str_mv |
Association of Multiple Genetic Variants with the Extension and Severity of Coronary Artery Disease |
title |
Association of Multiple Genetic Variants with the Extension and Severity of Coronary Artery Disease |
spellingShingle |
Association of Multiple Genetic Variants with the Extension and Severity of Coronary Artery Disease Fischer,Simone Cristina Pinto Matheus Coronary Artery Disease / genetic Polymorphism, Genetic Metabolic Syndrome Sedentary Lifestyle |
title_short |
Association of Multiple Genetic Variants with the Extension and Severity of Coronary Artery Disease |
title_full |
Association of Multiple Genetic Variants with the Extension and Severity of Coronary Artery Disease |
title_fullStr |
Association of Multiple Genetic Variants with the Extension and Severity of Coronary Artery Disease |
title_full_unstemmed |
Association of Multiple Genetic Variants with the Extension and Severity of Coronary Artery Disease |
title_sort |
Association of Multiple Genetic Variants with the Extension and Severity of Coronary Artery Disease |
author |
Fischer,Simone Cristina Pinto Matheus |
author_facet |
Fischer,Simone Cristina Pinto Matheus Pinto,Simone Pires Lins,Lívia Campos do Amaral Silva Bianco,Henrique Tria Monteiro,Carlos Manoel de Castro Pinheiro,Luiz Fernando Muniz Fonseca,Francisco Antonio Helfenstein Izar,Maria Cristina de Oliveira |
author_role |
author |
author2 |
Pinto,Simone Pires Lins,Lívia Campos do Amaral Silva Bianco,Henrique Tria Monteiro,Carlos Manoel de Castro Pinheiro,Luiz Fernando Muniz Fonseca,Francisco Antonio Helfenstein Izar,Maria Cristina de Oliveira |
author2_role |
author author author author author author author |
dc.contributor.author.fl_str_mv |
Fischer,Simone Cristina Pinto Matheus Pinto,Simone Pires Lins,Lívia Campos do Amaral Silva Bianco,Henrique Tria Monteiro,Carlos Manoel de Castro Pinheiro,Luiz Fernando Muniz Fonseca,Francisco Antonio Helfenstein Izar,Maria Cristina de Oliveira |
dc.subject.por.fl_str_mv |
Coronary Artery Disease / genetic Polymorphism, Genetic Metabolic Syndrome Sedentary Lifestyle |
topic |
Coronary Artery Disease / genetic Polymorphism, Genetic Metabolic Syndrome Sedentary Lifestyle |
description |
Abstract Background: Metabolic syndrome (MS) is a condition that, when associated with ischemic heart disease and cardiovascular events, can be influenced by genetic variants and determine more severe coronary atherosclerosis. Objectives: To examine the contribution of genetic polymorphisms to the extension and severity of coronary disease in subjects with MS and recent acute coronary syndrome (ACS). Methods: Patients (n = 116, 68% males) aged 56 (9) years, with criteria for MS, were prospectively enrolled to the study during the hospitalization period after an ACS. Clinical and laboratory parameters, high-sensitivity C-reactive protein, thiobarbituric acid reactive substances, adiponectin, endothelial function, and the Gensini score were assessed. Polymorphisms of paraoxonase-1 (PON-1), methylenotetrahydrofolate reductase (MTHFR), endothelial nitric oxide synthase (ENOS), angiotensin-converting enzyme (ACE), angiotensin II type 1 receptor (AT1R), apolipoprotein C3 (APOC3), lipoprotein lipase (LPL) were analysed by polymerase chain reaction (PCR) technique, followed by the identification of restriction fragment length polymorphisms (RFLP, and a genetic score was calculated. Parametric and non-parametric tests were used, as appropriate. Significance was set at p < 0.05. Results: Polymorphisms of PON-1, MTHFR and ENOS were not in the Hardy-Weinberg equilibrium. The DD genotype of LPL was associated with higher severity and greater extension of coronary lesions. Genetic score tended to be higher in patients with Gensini score < P50 (13.7 ± 1.5 vs. 13.0 ± 1.6, p = 0.066), with an inverse correlation between genetic and Gensini scores (R = -0.194, p = 0.078). Conclusions: The LPL polymorphism contributed to the severity of coronary disease in patients with MS and recent ACS. Combined polymorphisms were associated with the extension of coronary disease, and the lower the genetic score the more severe the disease. |
publishDate |
2018 |
dc.date.none.fl_str_mv |
2018-01-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0066-782X2018000100016 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0066-782X2018000100016 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.5935/abc.20170177 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Sociedade Brasileira de Cardiologia - SBC |
publisher.none.fl_str_mv |
Sociedade Brasileira de Cardiologia - SBC |
dc.source.none.fl_str_mv |
Arquivos Brasileiros de Cardiologia v.110 n.1 2018 reponame:Arquivos Brasileiros de Cardiologia (Online) instname:Sociedade Brasileira de Cardiologia (SBC) instacron:SBC |
instname_str |
Sociedade Brasileira de Cardiologia (SBC) |
instacron_str |
SBC |
institution |
SBC |
reponame_str |
Arquivos Brasileiros de Cardiologia (Online) |
collection |
Arquivos Brasileiros de Cardiologia (Online) |
repository.name.fl_str_mv |
Arquivos Brasileiros de Cardiologia (Online) - Sociedade Brasileira de Cardiologia (SBC) |
repository.mail.fl_str_mv |
||arquivos@cardiol.br |
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1752126568114683904 |