Copyright © 1998 by the European Society of Cardiology.
Increased fibrinogen levels are associated with persistentChlamydia pneumoniaeinfection in unstable coronary artery disease
a Department of Cardiology, University of Uppsala
b Department of Clinical Microbiology, Gävle Central Hospital and Institute of Infectious Diseases and Clinical Microbiology, University of Uppsala
c Laboratory for Coagulation Research, Department of Clinical Laboratory Sciences, University of Uppsala, Uppsala, Sweden
accepted September 9, 1997
Aim
Increased levels of acute phase proteins, e.g. fibrinogen, are related to a poor outcome in unstable coronary artery disease, but the cause of inflammation is unknown. We therefore investigated the prevalence of persistent Chlamydia pneumoniae infection, and its relationship to inflammation in this condition.
Methods and Results
In 256 patients participating in the FRISC trial, evaluating the effects of dalteparin (a low molecular weight heparin) in unstable angina or non-Q wave myocardial infarction, Chlamydia pneumoniae IgA antibody titres and levels of fibrinogen, C-reactive protein and troponin T were determined at inclusion. Increased C. pneumoniae IgA antibody titres were significantly more common in the patients (36%) than in a reference popu-lation of similar age (19%); P<0·001. Raised titres were associated with male gender, increasing age, smoking, and elevated concentrations of fibrinogen, C-reactive protein and troponin T. The association between persistent C. pneumoniae infection and increased fibrinogen levels was independent of other risk factors evaluated in multivariate analysis (P=0·009).
Conclusion
Persistent C. pneumoniae infection is common in unstable coronary artery disease. The independent association between increased C. pneumoniae IgA antibody titres and fibrinogen levels indicates that chronic infection could be of importance for disease activity.
Key Words: Chlamydia pneumoniae • unstable angina • acute myocardial infarction • fibrinogen • C-reactive protein
f1 Correspondence: Henrik Toss, Department of Cardiology, University Hospital, Uppsala, S-751 85 Sweden.
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