The prospective association of Chlamydia pneumoniae and four other pathogens with development of coronary artery calcium: the multi-ethnic study of atherosclerosis (MESA).

Atherosclerosis 2013 Oct 7;230(2):268-74. Epub 2013 Aug 7.

Department of Epidemiology, Johns Hopkins University, 615 North Wolfe Street, Baltimore, MD 21205, USA; Netherlands Institute for Health Sciences, Erasmus University, Dr. Molewaterplein 60, 3015 GJ Rotterdam, The Netherlands. Electronic address:

Objective: Previous 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.

Methods: We 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.

Results: Seropositivity 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.

Conclusion: Our prospective study does not support the pathophysiological involvement of these pathogens in CAC development.

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http://dx.doi.org/10.1016/j.atherosclerosis.2013.07.053DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3815605PMC
October 2013
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