Published Online
on August 19, 2002

A more recent version of this article appeared on August 27, 2002

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Submitted on April 10, 2002
Revised on June 7, 2002
Accepted on June 7, 2002

Association of Chlamydia pneumoniae With Coronary Artery Disease and Its Progression Is Dependent on the Modifying Effect of Mannose-Binding Lectin

Szabolcs Rugonfalvi-Kiss MD, Valéria Endrész PhD, Hans O. Madsen PhD, Katalin Burián MD, Jenô Duba MD, Zoltán Prohászka MD, István Karádi MD, László Romics MD, Éva Gönczöl MD, George Füst MD, and Peter Garred MD^*

From the 3rd Department of Medicine (S.R.-K., Z.P., I.K., L.R., G.F.), Faculty of Medicine, Semmelweis University, Budapest; the Department of Medical Microbiology (V.E., K.B.), Szeged University, Szeged, Hungary; Tissue-Typing Laboratory-7631, Department of Clinical Immunology (H.O.M., P.G.), Rigshospitalet, Copenhagen, Denmark; National Institute of Cardiology (J.D.), Budapest; and the Research Group of Metabolism, Genetics and Immunology (Z.P., L.R., G.F.), Hungarian Academy of Sciences, Budapest, Hungary; and the Virus Department (É.G.), Bela Johan National Center for Epidemiology, Budapest, Hungary.

^* To whom correspondence should be addressed. E-mail: garred{at}post5.tele.dk.

Background—The possible association between coronary artery disease (CAD) and Chlamydia pneumoniae (C pneumoniae) infection is controversial. On the basis of the recent suggestion that mannose-binding lectin (MBL) variant alleles are related to an increased risk of severe atherosclerosis, and on the in vitro interaction of MBL with C pneumoniae, we asked whether MBL might contribute to CAD in conjunction with C pneumoniae.

Methods and Results—Antibodies to C pneumoniae were measured by immunofluorescence and MBL alleles were determined by polymerase chain reaction technique in samples from 210 patients with CAD and 257 healthy subjects from Hungary collected between 1995 and 1996. A higher percentage of patients with CAD were anti-C pneumoniae positive as compared with the control group (P=0.058). However, at logistic regression analysis adjusted to age, sex, and serum lipid levels, this difference was confined only to subjects carrying MBL variant alleles (P=0.035, odds ratio 2.63, [95% CI: 1.07 to 6.45]). In contrast, no significant difference was seen in those homozygous for the normal MBL allele (P=0.412). During a 65±5.8-month follow-up period, major outcomes (new myocardial infarction, and/or bypass operation or cardiovascular death) occurred in 11 C pneumoniae positive and 3 C pneumoniae negative patients. In the C pneumoniae positive group, the odds ratio of development of outcomes was 3.27 (95% CI: 1.10 to 9.71, P=0.033) in the carriers of the MBL variant alleles compared with the homozygous carriers of the normal MBL allele.

Conclusions—These results indicate that infection with C pneumoniae leads mainly to the development and progression of severe CAD in patients with variation in the MBL gene.

Key words: coronary disease • genetics • immunology • infection

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