Project/Area Number |
17590730
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Circulatory organs internal medicine
|
Research Institution | Osaka University |
Principal Investigator |
SATO Hiroshi Osaka University, Graduate School of Medicine, Assistant professor, 医学系研究科, 講師 (10294092)
|
Co-Investigator(Kenkyū-buntansha) |
OTSU Kinya Osaka University, Graduate School of Medicine, Associate professor, 医学系研究科, 助教授 (20294051)
MATSUMURA Yasushi Osaka University, Hospital, Associate professor, 医学部附属病院, 助教授 (90252642)
|
Project Period (FY) |
2005 – 2006
|
Project Status |
Completed (Fiscal Year 2006)
|
Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2006: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2005: ¥1,800,000 (Direct Cost: ¥1,800,000)
|
Keywords | myocardial infarction / gene polymorphism / prognosis / epidemiology / risk factors |
Research Abstract |
Although previous epidemiologic studies have suggested an association between the onset of myocardial infarction (MI) and some genetic variations, the impact of these variants on recurrent cardiovascular events after MI has not been fully elucidated. We genotyped about 150 polymorphisms of atherosclerosis-related genes in consecutive acute MI patients registered in the Osaka Acute Coronary Insufficiency Study and compared the incidence of death and major adverse cardiac events (MACE) among the polymorphisms of each gene. After initial screening in about 600 patients, we selected 9 polymorphisms for screening in all patients. Multivariate Cox regression analysis revealed that G allele carriers at the position 252 of the lymphotoxin-alpha (LTA) gene were independently associated with an increased risk of death. In subgroup analysis, patients were divided into two groups respectively one statin-present group (n=384) and one statin-absent group (n=1202). In each group, the death rate was compared between patients of G allele carriers and those with AA genotype. In the statin-absent group, G carriers had significantly higher mortality than non-G Carriers. On the other hand, in the statin-present group, the mortality of each genotype was rather low. The Hazard ratio diminished and it lost statistical significance. In conclusion, the use of statin reduce the increased risk of death caused by LTA 252G allele. It is recommended from the results of this study that G allele carriers undergo statin treatment.
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