The mechanism linking inflammation to atherosclerosis is unknown. We have previously demonstrated a high occurrence of inflammation in the aortic adventitia of patients with coronary artery disease (CAD), which was more pronounced in patients with inflammatory rheumatic diseases (IRDs), and which might be involved in the pathogenesis of cardiovascular disease. In theory, infections might play a role in the pathogenesis of vascular inflammation or atherosclerosis, or both. This study compared seropositivity and the burden of several common infections in patients with CAD, both with and without IRD, and in healthy controls (HCs). Moreover, we looked for relationships between the examined antibodies and inflammatory infiltrates in the aortic adventitia.
We examined sera for Chlamydophila pneumoniae, Mycoplasma pneumoniae, Helicobacter pylori, CMV, Streptococcus pyogenes, parvovirus B19, HBV and HCV with commercially available serological tests in 67 patients with IRD, 52 patients without IRD and 30 HCs.
We observed neither any statistically significant differences in the examined antibodies between the groups nor a difference in the burden of infection. Except for a protective effect of mycoplasma immunoglobulin A (IgA), we did not find any other associations between the examined antibodies and the occurrence of aortic adventitial mononuclear cell infiltrates.
Our study does not support the notion that chronic infections or infectious burden contribute to accelerated occurrence of CAD in IRD. Mycoplasma IgA was related to a lower occurrence of aortic adventitial inflammation.