Association of influenza virus infection and inflammatory cytokines with acute myocardial infarction

To explore the potential relationship between previous influenza virus (IV) infection and acute myocardial infarction (AMI), and the mechanism of atherosclerosis, we conducted a case-control study and examined inflammatory cytokines to assess the association of previous IV infection and AMI. A questionnaire-based survey was conducted to collect information about demographic characteristics and heart disease risk factors. Fasting blood samples were obtained to measure immunoglobulin (Ig) G antibodies to influenza virus A (IV-A), influenza virus B (IV-B), cytomegalovirus, herpes simplex virus type-1 and type-2, adenovirus, rubella virus and , and to measure the level of certain biochemistry markers: interleukin-2, 6, 10 and 18 (IL-2, 6, 10 and 18), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), endothelin-1 (ET-1), soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1). Compared with the controls, the cases were more likely to have positive IgG antibodies to IV-A and IV-B [IV-A: odds ratio (OR): 3.1, 95% confidence interval (CI): 1.5-6.4; IV-B: OR: 10.2, 95% CI: 5.7-20.0]. After adjustment for potential confounding variables, the risk of AMI was still associated with the presence of IgG antibodies to IV-A (adjusted OR: 5.5, 95% CI: 1.3-23.0) and IV-B (adjusted OR: 20.3, 95% CI: 5.6-40.8). The levels of IL-2, 6, 10 and18, TNF-alpha, IFN-gamma, ET-1, sICAM-1 and sVCAM-1 in patients with AMI were significantly higher than those of the controls ( < 0.01). Our study supports the hypothesis that previous IV infection is associated with AMI. Inflammatory cytokines may take part in the development of atherosclerosis and trigger the occurrence of AMI.