Chlamydia pneumoniae Seropositivity and Acute Coronary Syndromes: A Case–Control Study of the Infectious–Inflammatory Axis

Background and Objectives: Classical cardiovascular risk factors account for only a fraction of acute coronary syndromes (ACSs), and chronic Chlamydia pneumoniae infection has been proposed as a contributor to atherogenesis through persistent inflammation and endothelial dysfunction. We tested whether C. pneumoniae infection is independently associated with ACS by quantifying seroprevalence, inflammatory markers, and their relationship with conventional cardiovascular risk factors. Materials and Methods: In a prospective case–control design, we enrolled 47 patients with ACSs (29 with acute myocardial infarction and 18 with unstable angina) and 53 age- and locality-matched controls at Alexandria University Hospital. The clinical evaluation comprised electrocardiography, echocardiography, lipid profile, and high-sensitivity C-reactive protein (CRP). C. pneumoniae-specific IgG and IgM were measured by ELISA, with positive samples confirmed by microimmunofluorescence. Logistic regression models were adjusted for age, sex, hypertension, diabetes, dyslipidemia, and smoking. Results: IgM was undetectable in all 100 participants, excluding acute infection. IgG seropositivity was higher in cases than in controls (83.0% vs. 60.4%; OR: 3.20; 95% CI: 1.23–8.30; p = 0.017) and remained suggestive after multivariable adjustment (adjusted OR: 4.59; 95% CI: 1.33–18.28; p = 0.021), although the estimate is imprecise and does not meet our prespecified multivariate threshold of p < 0.01. Within the ACS cohort, IgG seropositivity was not significantly associated with CRP elevation (Fisher’s exact p = 1.000). CRP elevation was near-universal in cases (93.6%) and absent in controls (0%; p < 0.001). Conclusions: Chronic C. pneumoniae infection was associated with ACS in unadjusted analysis, with a suggestive but underpowered signal after multivariable adjustment, although the observational design precludes causal inference, and reverse causality cannot be excluded. Prospective studies using direct pathogen detection are required to determine whether the association reflects a contributory mechanism or shared susceptibility.