| Tumor necrosis factor-alpha gene -308G>A polymorphism is associated with ST-elevation myocardial infarction and with high plasma levels of biochemical ischemia markers. | |
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MedLine Citation:
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PMID: 16319659 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVES: As is well known, acute myocardial infarction presents two electrocardiogram (EKG) patterns, ST-elevation (STEMI) and no ST-elevation (NSTEMI), characterized by different coronary artery thrombotic occlusion. Growing evidence shows that inflammation plays a central role in the pathogenesis of acute myocardial infarction. Among the factors that promote inflammation and arterial thrombosis, one of the most important is the proinflammatory cytokine tumor necrosis factor-alpha. The expression of this cytokine is modulated by a polymorphism located at nucleotide -308 of tumor necrosis factor-alpha promoter gene. The objective of our study is to verify whether tumor necrosis factor-alpha -308 polymorphism is associated with risk of acute myocardial infarction (STEMI and NSTEMI) or with biochemical myocardial ischemia markers, such as troponin I, creatine kinase-MB, lactate dehydrogenase and myoglobin. METHODS: We analyzed tumor necrosis factor-alpha -308 polymorphism in a total of 603 study participants: 293 elderly patients affected by acute myocardial infarction (STEMI and NSTEMI) and 310 healthy controls. RESULTS: We found that individuals carrying the tumor necrosis factor-alpha -308 AG+AA genotypes are significantly more represented among acute myocardial infarction patients affected by STEMI than among NSTEMI patients (OR = 1.86, 95% CI 1.08-3.21, p = 0.027) and healthy controls (OR = 1.64, 95% CI 1.03-2.64, p = 0.046). Furthermore, the patients carrying tumor necrosis factor-alpha -308 AG+AA genotypes displayed significant increased levels of biochemical myocardial ischemia markers. CONCLUSIONS: Our study shows a significant association between the tumor necrosis factor-alpha -308 polymorphism and the occurrence of STEMI, and suggests that the tumor necrosis factor-alpha -308 polymorphism could play a role in the pathogenesis of cardiac ischemic damage, AA+AG genotype carrier individuals being likely to be affected by more severe ischemic damage than the rest of the population. |
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Authors:
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Roberto Antonicelli; Fabiola Olivieri; Luca Cavallone; Liana Spazzafumo; Massimiliano Bonaf?; Francesca Marchegiani; Maurizio Cardelli; Roberta Galeazzi; Simona Giovagnetti; Gian Piero Perna; Claudio Franceschi |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Coronary artery disease Volume: 16 ISSN: 0954-6928 ISO Abbreviation: Coron. Artery Dis. Publication Date: 2005 Dec |
Date Detail:
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Created Date: 2005-12-01 Completed Date: 2006-12-11 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9011445 Medline TA: Coron Artery Dis Country: England |
Other Details:
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Languages: eng Pagination: 489-93 Citation Subset: IM |
Affiliation:
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Center of Molecular Biology, Department of Cardiology-CCU and Center of Statistics, Italian National Research Centers on Aging (I.N.R.C.A.), Ancona, Italy. r.antonicelli@inrca.it |
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| MeSH Terms | |
Descriptor/Qualifier:
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Aged Aged, 80 and over Biological Markers / blood Creatine Kinase, MB Form / blood Electrocardiography* Female Humans L-Lactate Dehydrogenase / blood Male Myocardial Infarction / genetics*, physiopathology Myocardial Ischemia / genetics*, physiopathology Myoglobin / blood Polymorphism, Genetic* Risk Factors Troponin I / blood Tumor Necrosis Factor-alpha / genetics* |
| Chemical | |
Reg. No./Substance:
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0/Biological Markers; 0/Myoglobin; 0/TNF protein, human; 0/Troponin I; 0/Tumor Necrosis Factor-alpha; EC 1.1.1.27/L-Lactate Dehydrogenase; EC 2.7.3.2/Creatine Kinase, MB Form |
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