Accumulation of Gene Polymorphisms Related to Plaque Disruption and Thrombosis Is Associated With Cerebral Infarction in Subjects With Type 2 Diabetes
OBJECTIVE: It is believed that disruption of vulnerable atherosclerotic plaque and subsequent thrombus formation play critical roles in the pathogenesis of cerebral infarction. We simultaneously determined four relatively common genetic variants related to plaque rupture or subsequent local thrombus...
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| Published in | Diabetes care Vol. 33; no. 2; pp. 390 - 395 |
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| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Alexandria, VA
American Diabetes Association
01.02.2010
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0149-5992 1935-5548 1935-5548 |
| DOI | 10.2337/dc09-1518 |
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| Abstract | OBJECTIVE: It is believed that disruption of vulnerable atherosclerotic plaque and subsequent thrombus formation play critical roles in the pathogenesis of cerebral infarction. We simultaneously determined four relatively common genetic variants related to plaque rupture or subsequent local thrombus formation and evaluated the combined effect on cerebral infarction. RESEARCH DESIGN AND METHODS: We enrolled 3,094 Japanese type 2 diabetic subjects (62.7% male; aged 61.5 ± 8.4 years) and determined their genotypes regarding matrix metalloproteinase 9 C-1562T, coagulation factor XII (F12) C46T, von Willebrand factor (VWF) G-1051A, and plasminogen activator inhibitor (PAI-1) 675 4G/5G polymorphisms. The diagnosis of cerebral infarction was performed based on history, physical examination, and neuroimaging. RESULTS: The single association analysis revealed that there were no statistically significant associations between each polymorphism and the prevalence of cerebral infarction. Interestingly, the prevalence of cerebral infarction was higher with the increase of the total number of four concomitant unfavorable proatherothrombotic alleles in each subject (P value for linear trend = 0.004). Furthermore, a multiple logistic regression analysis showed that the number of proatherothrombotic alleles was a risk factor for cerebral infarction independently of conventional risk factors (odds ratio for one-point increase in the number of proatherothrombotic allele 1.15 [95% CI 1.05-1.26], P = 0.004). CONCLUSIONS: Accumulation of gene polymorphisms related to plaque rupture and thrombus formation is likely associated with the prevalence of cerebral infarction in type 2 diabetic patients, suggesting that the combined information about these variants is useful to assess the risk of cerebral infarction. |
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| AbstractList | It is believed that disruption of vulnerable atherosclerotic plaque and subsequent thrombus formation play critical roles in the pathogenesis of cerebral infarction. We simultaneously determined four relatively common genetic variants related to plaque rupture or subsequent local thrombus formation and evaluated the combined effect on cerebral infarction. We enrolled 3,094 Japanese type 2 diabetic subjects (62.7% male; aged 61.5 ± 8.4 years) and determined their genotypes regarding matrix metalloproteinase 9 C-1562T, coagulation factor XII (F12) C46T, von Willebrand factor (VWF) G-1051A, and plasminogen activator inhibitor (PAT-1) 675 4G/5G polymorphisms. The diagnosis of cerebral infarction was performed based on history, physical examination, and neuroimaging. The single association analysis revealed that there were no statistically significant associations between each polymorphism and the prevalence of cerebral infarction. Interestingly, the prevalence of cerebral infarction was higher with the increase of the total number of four concomitant unfavorable proatherothrombotic alleles in each subject (P value for linear trend = 0.004). Furthermore, a multiple logistic regression analysis showed that the number of proatherothrombotic alleles was a risk factor for cerebral infarction independently of conventional risk factors (odds ratio for one-point increase in the number of proatherothrombotic allele 1.15 [95% CI 1.05-1.26], P = 0.004). Accumulation of gene polymorphisms related to plaque rupture and thrombus formation is likely associated with the prevalence of cerebral infarction in type 2 diabetic patients, suggesting that the combined information about these variants is useful to assess the risk of cerebral infarction. OBJECTIVE: It is believed that disruption of vulnerable atherosclerotic plaque and subsequent thrombus formation play critical roles in the pathogenesis of cerebral infarction. We simultaneously determined four relatively common genetic variants related to plaque rupture or subsequent local thrombus formation and evaluated the combined effect on cerebral infarction. RESEARCH DESIGN AND METHODS: We enrolled 3,094 Japanese type 2 diabetic subjects (62.7% male; aged 61.5 ± 8.4 years) and determined their genotypes regarding matrix metalloproteinase 9 C-1562T, coagulation factor XII (F12) C46T, von Willebrand factor (VWF) G-1051A, and plasminogen activator inhibitor (PAI-1) 675 4G/5G polymorphisms. The diagnosis of cerebral infarction was performed based on history, physical examination, and neuroimaging. RESULTS: The single association analysis revealed that there were no statistically significant associations between each polymorphism and the prevalence of cerebral infarction. Interestingly, the prevalence of cerebral infarction was higher with the increase of the total number of four concomitant unfavorable proatherothrombotic alleles in each subject (P value for linear trend = 0.004). Furthermore, a multiple logistic regression analysis showed that the number of proatherothrombotic alleles was a risk factor for cerebral infarction independently of conventional risk factors (odds ratio for one-point increase in the number of proatherothrombotic allele 1.15 [95% CI 1.05-1.26], P = 0.004). CONCLUSIONS: Accumulation of gene polymorphisms related to plaque rupture and thrombus formation is likely associated with the prevalence of cerebral infarction in type 2 diabetic patients, suggesting that the combined information about these variants is useful to assess the risk of cerebral infarction. It is believed that disruption of vulnerable atherosclerotic plaque and subsequent thrombus formation play critical roles in the pathogenesis of cerebral infarction. We simultaneously determined four relatively common genetic variants related to plaque rupture or subsequent local thrombus formation and evaluated the combined effect on cerebral infarction.OBJECTIVEIt is believed that disruption of vulnerable atherosclerotic plaque and subsequent thrombus formation play critical roles in the pathogenesis of cerebral infarction. We simultaneously determined four relatively common genetic variants related to plaque rupture or subsequent local thrombus formation and evaluated the combined effect on cerebral infarction.We enrolled 3,094 Japanese type 2 diabetic subjects (62.7% male; aged 61.5 +/- 8.4 years) and determined their genotypes regarding matrix metalloproteinase 9 C-1562T, coagulation factor XII (F12) C46T, von Willebrand factor (VWF) G-1051A, and plasminogen activator inhibitor (PAI-1) 675 4G/5G polymorphisms. The diagnosis of cerebral infarction was performed based on history, physical examination, and neuroimaging.RESEARCH DESIGN AND METHODSWe enrolled 3,094 Japanese type 2 diabetic subjects (62.7% male; aged 61.5 +/- 8.4 years) and determined their genotypes regarding matrix metalloproteinase 9 C-1562T, coagulation factor XII (F12) C46T, von Willebrand factor (VWF) G-1051A, and plasminogen activator inhibitor (PAI-1) 675 4G/5G polymorphisms. The diagnosis of cerebral infarction was performed based on history, physical examination, and neuroimaging.The single association analysis revealed that there were no statistically significant associations between each polymorphism and the prevalence of cerebral infarction. Interestingly, the prevalence of cerebral infarction was higher with the increase of the total number of four concomitant unfavorable proatherothrombotic alleles in each subject (P value for linear trend = 0.004). Furthermore, a multiple logistic regression analysis showed that the number of proatherothrombotic alleles was a risk factor for cerebral infarction independently of conventional risk factors (odds ratio for one-point increase in the number of proatherothrombotic allele 1.15 [95% CI 1.05-1.26], P = 0.004).RESULTSThe single association analysis revealed that there were no statistically significant associations between each polymorphism and the prevalence of cerebral infarction. Interestingly, the prevalence of cerebral infarction was higher with the increase of the total number of four concomitant unfavorable proatherothrombotic alleles in each subject (P value for linear trend = 0.004). Furthermore, a multiple logistic regression analysis showed that the number of proatherothrombotic alleles was a risk factor for cerebral infarction independently of conventional risk factors (odds ratio for one-point increase in the number of proatherothrombotic allele 1.15 [95% CI 1.05-1.26], P = 0.004).Accumulation of gene polymorphisms related to plaque rupture and thrombus formation is likely associated with the prevalence of cerebral infarction in type 2 diabetic patients, suggesting that the combined information about these variants is useful to assess the risk of cerebral infarction.CONCLUSIONSAccumulation of gene polymorphisms related to plaque rupture and thrombus formation is likely associated with the prevalence of cerebral infarction in type 2 diabetic patients, suggesting that the combined information about these variants is useful to assess the risk of cerebral infarction. Accumulation of Gene Polymorphisms Related to Plaque Disruption and Thrombosis Is Associated With Cerebral Infarction in Subjects With Type 2 Diabetes Naoto Katakami , MD, PHD 1 , Mitsuyoshi Takahara , MD, PHD 1 , Hideaki Kaneto , MD, PHD 1 , Ikki Shimizu , MD, PHD 2 , Keizo Ohno , MD, PHD 3 , Fukashi Ishibashi , MD, PHD 4 , Takeshi Osonoi , MD, PHD 5 , Atsunori Kashiwagi , MD, PHD 6 , Ryuzo Kawamori , MD, PHD 7 , Iichiro Shimomura , MD, PHD 1 , Munehide Matsuhisa , MD, PHD 1 and Yoshimitsu Yamasaki , MD, PHD 8 1 Department of Metabolic Medicine, Osaka University Graduate School of Medicine, Osaka, Japan; 2 Ehime Prefectural Central Hospital, Osaka, Japan; 3 Ehime Prefectural Imabari Hospital, Osaka, Japan; 4 Ishibashi Clinic, Osaka, Japan; 5 Naka Kinen Clinic, Osaka, Japan; 6 Department of Medicine, Shiga, University of Medical Science, Shiga, Japan; 7 Department of Medicine, Metabolism and Endocrinology, Juntendo University School of Medicine, Juntendo, Japan; 8 Center for Advanced Science and Innovation, Osaka University, Osaka, Japan. Corresponding author: Naoto Katakami, katakami{at}medone.med.osaka-u.ac.jp . Abstract OBJECTIVE It is believed that disruption of vulnerable atherosclerotic plaque and subsequent thrombus formation play critical roles in the pathogenesis of cerebral infarction. We simultaneously determined four relatively common genetic variants related to plaque rupture or subsequent local thrombus formation and evaluated the combined effect on cerebral infarction. RESEARCH DESIGN AND METHODS We enrolled 3,094 Japanese type 2 diabetic subjects (62.7% male; aged 61.5 ± 8.4 years) and determined their genotypes regarding matrix metalloproteinase 9 C-1562T, coagulation factor XII ( F12 ) C46T, von Willebrand factor ( VWF ) G-1051A, and plasminogen activator inhibitor ( PAI-1 ) 675 4G/5G polymorphisms. The diagnosis of cerebral infarction was performed based on history, physical examination, and neuroimaging. RESULTS The single association analysis revealed that there were no statistically significant associations between each polymorphism and the prevalence of cerebral infarction. Interestingly, the prevalence of cerebral infarction was higher with the increase of the total number of four concomitant unfavorable proatherothrombotic alleles in each subject ( P value for linear trend = 0.004). Furthermore, a multiple logistic regression analysis showed that the number of proatherothrombotic alleles was a risk factor for cerebral infarction independently of conventional risk factors (odds ratio for one-point increase in the number of proatherothrombotic allele 1.15 [95% CI 1.05–1.26], P = 0.004). CONCLUSIONS Accumulation of gene polymorphisms related to plaque rupture and thrombus formation is likely associated with the prevalence of cerebral infarction in type 2 diabetic patients, suggesting that the combined information about these variants is useful to assess the risk of cerebral infarction. Footnotes The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Received August 14, 2009. Accepted November 13, 2009. © 2010 by the American Diabetes Association. It is believed that disruption of vulnerable atherosclerotic plaque and subsequent thrombus formation play critical roles in the pathogenesis of cerebral infarction. We simultaneously determined four relatively common genetic variants related to plaque rupture or subsequent local thrombus formation and evaluated the combined effect on cerebral infarction. We enrolled 3,094 Japanese type 2 diabetic subjects (62.7% male; aged 61.5 +/- 8.4 years) and determined their genotypes regarding matrix metalloproteinase 9 C-1562T, coagulation factor XII (F12) C46T, von Willebrand factor (VWF) G-1051A, and plasminogen activator inhibitor (PAI-1) 675 4G/5G polymorphisms. The diagnosis of cerebral infarction was performed based on history, physical examination, and neuroimaging. The single association analysis revealed that there were no statistically significant associations between each polymorphism and the prevalence of cerebral infarction. Interestingly, the prevalence of cerebral infarction was higher with the increase of the total number of four concomitant unfavorable proatherothrombotic alleles in each subject (P value for linear trend = 0.004). Furthermore, a multiple logistic regression analysis showed that the number of proatherothrombotic alleles was a risk factor for cerebral infarction independently of conventional risk factors (odds ratio for one-point increase in the number of proatherothrombotic allele 1.15 [95% CI 1.05-1.26], P = 0.004). Accumulation of gene polymorphisms related to plaque rupture and thrombus formation is likely associated with the prevalence of cerebral infarction in type 2 diabetic patients, suggesting that the combined information about these variants is useful to assess the risk of cerebral infarction. |
| Audience | Professional |
| Author | Yamasaki, Yoshimitsu Katakami, Naoto Ishibashi, Fukashi Shimizu, Ikki Kaneto, Hideaki Ohno, Keizo Kawamori, Ryuzo Matsuhisa, Munehide Takahara, Mitsuyoshi Osonoi, Takeshi Kashiwagi, Atsunori Shimomura, Iichiro |
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| CitedBy_id | crossref_primary_10_1007_s12017_015_8367_5 crossref_primary_10_1016_j_jstrokecerebrovasdis_2016_12_036 crossref_primary_10_3389_fneur_2022_1077178 crossref_primary_10_1007_s12035_015_9549_8 crossref_primary_10_1002_dmrr_1025 crossref_primary_10_3892_etm_2018_5965 crossref_primary_10_18632_oncotarget_14468 crossref_primary_10_1007_s13340_013_0130_2 crossref_primary_10_1016_j_jdiacomp_2015_05_004 crossref_primary_10_1038_srep43834 crossref_primary_10_1038_nrendo_2013_102 crossref_primary_10_1089_gtmb_2018_0130 crossref_primary_10_1080_00207454_2019_1634072 |
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| Keywords | Endocrinopathy Type 2 diabetes Human Cerebral infarction Nervous system diseases Genetic variability Nutrition Cardiovascular disease Genotype Metabolic diseases Thrombosis Accumulation Cerebral disorder Vascular disease Association Central nervous system disease Cerebrovascular disease Endocrinology Polymorphism |
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| Snippet | OBJECTIVE: It is believed that disruption of vulnerable atherosclerotic plaque and subsequent thrombus formation play critical roles in the pathogenesis of... Accumulation of Gene Polymorphisms Related to Plaque Disruption and Thrombosis Is Associated With Cerebral Infarction in Subjects With Type 2 Diabetes Naoto... It is believed that disruption of vulnerable atherosclerotic plaque and subsequent thrombus formation play critical roles in the pathogenesis of cerebral... |
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| SubjectTerms | Adult Aged alleles Biological and medical sciences blood Blood clot blood coagulation factors Cardiovascular disease Cerebral Infarction Cerebral Infarction - epidemiology Cerebral Infarction - genetics Cholesterol, HDL Cholesterol, HDL - blood clinical examination coagulation Diabetes Mellitus, Type 2 Diabetes Mellitus, Type 2 - genetics Diabetes. Impaired glucose tolerance Diabetic Angiopathies Diabetic Angiopathies - genetics Endocrine pancreas. Apud cells (diseases) Endocrinopathies epidemiology Etiopathogenesis. Screening. Investigations. Target tissue resistance Factor XII Factor XII - genetics Female gelatinase B Genes Genetic aspects genetic polymorphism Genetic research genetics Genotype Glycated Hemoglobin Glycated Hemoglobin A - metabolism Hospitals Humans infarction Japan Male Matrix Metalloproteinase 9 Matrix Metalloproteinase 9 - genetics Medical sciences Metabolic diseases metabolism Middle Aged Miscellaneous noninsulin-dependent diabetes mellitus odds ratio Original Research pathogenesis patients plasminogen activator Plasminogen Activator Inhibitor 1 Plasminogen Activator Inhibitor 1 - genetics Polymorphism, Genetic Polymorphism, Single Nucleotide Proteins Public health. Hygiene Public health. Hygiene-occupational medicine regression analysis risk factors Thrombosis Thrombosis - genetics Triglycerides Triglycerides - blood Type 2 diabetes Von Willebrand factor von Willebrand Factor - genetics |
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| Title | Accumulation of Gene Polymorphisms Related to Plaque Disruption and Thrombosis Is Associated With Cerebral Infarction in Subjects With Type 2 Diabetes |
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