The prospective association of Chlamydia pneumoniae and four other pathogens with development of coronary artery calcium: The Multi-Ethnic Study of Atherosclerosis (MESA)

- First prospective study of the association between pathogens and CAC development.
- No independent associations of Chlamydia pneumoniae with CAC development.
- Similar null results in all of the subgroups according to age, sex, and race.
- No independent associations for H. pylori, CMV, HSV and hepatitis A virus.
- Unlikely that these pathogens play important roles in the development and progression of CAC.

ObjectivePrevious basic and cross-sectional studies obtained conflicting results regarding the association of pathogens with coronary artery calcium (CAC). The aim of this study is to prospectively evaluate this association in a population-based cohort.MethodsWe examined 5744 individuals aged 45-84 years at baseline (2000-02) who underwent repeated CAC assessment on average 2.4 years later (a half at visit 2 [2002-04] and the other half at visit 3 [2004-05]). CAC incidence was defined as newly detectable CAC at follow-up (475 cases of 2942 participants). CAC progression was defined as annualized change in CAC Agatston score ≥10 units/year if baseline CAC score >0 to <100 or ≥10%/year if baseline score ≥ 100 (1537 cases of 2802 participants). Seropositivity was assessed in the entire cohort for Chlamydia pneumoniae and in a random sample (n = 873) for Helicobacter pylori, cytomegalovirus, herpes simplex virus, and hepatitis A virus.ResultsSeropositivity to C. pneumoniae was not significantly associated with CAC incidence (odds ratio [OR] 1.11 [95% CI, 0.88-1.39], P = 0.371) or progression (1.14 [0.96-1.36], P = 0.135) even in unadjusted models. When CAC incidence and progression were combined, we observed significant association with C. pneumoniae seropositivity before adjustment (OR 1.17 [1.03-1.33], P = 0.016) but not in a model adjusting for traditional risk factors (1.04 [0.90-1.19], P = 0.611). The results were consistent across subgroups according to age, sex, and race/ethnicity. None of five pathogens or their accrual was associated with CAC incidence and progression in the subsample.ConclusionOur prospective study does not support the pathophysiological involvement of these pathogens in CAC development.