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

ABSTRACT

OBJECTIVE: 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. METHODS: 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 Chlamydia pneumoniae, and to measure the level of certain biochemistry markers interleukin-2, 6, 10 and 18 (IL-2, 6, 10 and 18), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), endothelin-1 (ET-1), soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1). RESULTS: 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-α, IFN-γ, ET-1, sICAM-1 and sVCAM-1 in patients with AMI were significantly higher than those of the controls (P < 0.01). CONCLUSIONS: 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.