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J Am Coll Cardiol, 2000; 35:112-118 © 2000 by the American College of Cardiology Foundation |




* Department of Internal Medicine IICardiology, University of Ulm, Ulm, Germany
Department of Epidemiology, University of Ulm, Ulm, Germany
Department of Clinical Microbiology, Malmö General Hospital, University of Lund, Malmö, Sweden
Department of Internal Medicine IGastroenterology, University of Ulm, Ulm, Germany
Manuscript received March 9, 1999; revised manuscript received July 22, 1999, accepted September 21, 1999.
Reprint requests and correspondence: Dr. A. Hoffmeister, Abteilung Innere Medizin II, Medizinische Universitätsklinik, Robert-Koch Str. 8, D-89081 Ulm, Germany.
albrecht.hoffmeister{at}medizin.uni-ulm.de
OBJECTIVES
We investigated the association between seropositivity to chlamydial lipopolysaccharide (cLPS) or Chlamydia pneumoniae (CP) and angiographically documented coronary artery disease (CAD), and we examined the relationship between serostatus and markers of systemic inflammation.
BACKGROUND
The potential contribution of CP to atherogenesis is still a matter of debate, and inflammation has been suggested to represent the link between infection and atherosclerotic disease.
METHODS
Subjects age 40 to 68 years were recruited for this case-control study between October 1996 and November 1997: 312 patients with at least one coronary stenosis >50% and 479 age- and sex-matched blood donors without manifest CAD or history of angina. Antibodies against cLPS and CP, C-reactive protein (CRP), fibrinogen, plasma viscosity, leukocytes and neutrophils were determined. The study had a power of >80% to detect an odds ratio (OR) of 1.55 or above for the prevalence of immunoglobulin (IgG) antibodies against cLPS at a significance level of alpha = 0.05.
RESULTS
Prevalence of IgG antibodies against cLPS was not different between cases and controls (61% vs. 62%; p = 0.7). The adjusted OR for the presence of CAD given positive IgG serostatus against cLPS was 0.9 (95% CI; 0.6 to 1.3). Similarly, no difference in the prevalence of IgG antibodies against CP was seen (88% vs. 87%; p = 0.6); the adjusted OR was 1.0 (95% CI; 0.6 to 1.6). Markers of inflammation did not show any statistically significant difference between cLPS seropositives and seronegatives.
CONCLUSIONS
Our results indicate no strong association between CP and CAD, and increased systemic inflammation in patients with CAD does not seem to be due to seropositivity to cLPS or CP.
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