Abstract
Increasing evidences have shown that pathogens might promote atherosclerosis and trigger acute myocardial infarction (AMI). But the conclusions from various studies on the correlation between previous influenza virus (IV) infection and AMI were inconsistent. We conducted a case-control study to assess the association of previous IV infection and AMI. Questionnaire survey was conducted to collect information about demographic characteristics and heart disease risk factors. Fasting blood sample was obtained to measure IgG antibodies to influenza virus A(IV-A), influenza virus B(IV-B), cytomegalovirus (CMV), herpes simplex virus type-1 (HSV-1) and type-2 (HSV-2), adenovirus (ADV), rubella virus (RV) and Chlamydia pneumoniae (CP) and measure the level of some biochemistry markers. Compared to controls, cases were more likely to have positive IgG antibodies to IV-A and IV-B (IV-A: OR, 3.3; 95%CI, 1.5 to 7.4; IV-B: OR, 17.2; 95%CI, 7.7 to 38.0). After adjustment for potential confounding variables, the risk of AMI was still associated with the presence of IgG antibodies to IV-A (adjusted OR, 7.5; 95%CI, 1.3 to 43.0) and IV-B (adjusted OR, 27.3; 95%CI, 6.6 to 113.8). The study supported the hypothesis that previous IV infection took part in the development of atherosclerosis and trigger the occurrence of AMI.
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Acknowledgements
Thanks were extended to the staff of the Medical Examination Center and the Cardiac Care Unit of the First Hospital of Harbin Medical University for their assistance. We acknowledge Dr. Wei-Min Li for his clinical advice to this study and Dr. E.J. Love for his critical review of the manuscript. Acknowledgement was extended to Jian-Ling Pan, Chun-Yan Lin, Lian-Ming Wang, Zhao-Zhen Xu and Li-Yan Wang for their laboratory tests and survey. This study was supported by Natural Science Foundation (grant D200613) and Health Department Foundation (grant 2006–058) of Heilongjiang Province in China.
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Guan, XR., Li, X., Xin, XM. et al. Influenza Virus Infection and Risk of Acute Myocardial Infarction. Inflammation 31, 266–272 (2008). https://doi.org/10.1007/s10753-008-9074-2
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DOI: https://doi.org/10.1007/s10753-008-9074-2