Increased incidence of Chlamydia species within the coronary arteries of patients with symptomatic atherosclerotic versus other forms of cardiovascular disease
JB Muhlestein,
EH Hammond,
JF Carlquist,
E Radicke,
MJ Thomson,
LA Karagounis,
ML Woods,
and
JL Anderson
Department of Medicine, University of Utah School of Medicine, LDS Hospital, Salt Lake City 84143, USA.
OBJECTIVES: The objectives of this study were to test prospectively for an association between Chlamydia and atherosclerosis by comparing the incidence of the pathogen found within atherosclerotic plaques in patients undergoing directional coronary atherectomy with a variety of control specimens and comparing the clinical features between the groups. BACKGROUND: Previous work has suggested an association between Chlamydia pneumoniae infection and coronary atherosclerosis, based on the demonstration of increased serologic titers and the detection of bacteria within atherosclerotic tissue, but this association has not yet been regarded as established. METHODS: Coronary specimens from 90 symptomatic patients undergoing coronary atherectomy were tested for the presence of Chlamydia species using direct immunofluorescence. Control specimens from 24 subjects without atherosclerosis (12 normal coronary specimens and 12 coronary specimens from cardiac transplant recipients with subsequent transplant-induced coronary disease) were also examined. RESULTS: Coronary atherectomy specimens were definitely positive in 66 (73%) and equivocally positive in 5 (6%), resulting in 79% of specimens showing evidence for the presence of Chlamydia species within the atherosclerotic tissue. In contrast, only 1 (4%) of 24 nonatherosclerotic coronary specimens showed any evidence of Chlamydia. The statistical significance of this difference is a p value < 0.001. Transmission electron microscopy was used to confirm the presence of appropriate organisms in three of five positive specimens. No clinical factors except the presence of a primary nonrestenotic lesion (odds ratio 3.0, p = 0.057) predicted the presence of Chlamydia. CONCLUSIONS: This high incidence of Chlamydia only in coronary arteries diseased by atherosclerosis suggests an etiologic role for Chlamydia infection in the development of coronary atherosclerosis that should be further studied.
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R. P. Darveau, C. M. Belton, R. A. Reife, and R. J. Lamont
Local Chemokine Paralysis, a Novel Pathogenic Mechanism for Porphyromonas gingivalis
Infect. Immun.,
April 1, 1998;
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[Abstract]
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K. Yamashita, K. Ouchi, M. Shirai, T. Gondo, T. Nakazawa, and H. Ito
Distribution of Chlamydia pneumoniae Infection in the Atherosclerotic Carotid Artery
Stroke,
April 1, 1998;
29(4):
773 - 778.
[Abstract]
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[PDF]
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P. Theroux and V. Fuster
Acute Coronary Syndromes : Unstable Angina and Non–Q-Wave Myocardial Infarction
Circulation,
March 31, 1998;
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J. B. Muhlestein, J. L. Anderson, E. H. Hammond, L. Zhao, S. Trehan, E. P. Schwobe, and J. F. Carlquist
Infection With Chlamydia pneumoniae Accelerates the Development of Atherosclerosis and Treatment With Azithromycin Prevents It in a Rabbit Model
Circulation,
February 24, 1998;
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[Abstract]
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P. Libby, D. Egan, and S. Skarlatos
Roles of Infectious Agents in Atherosclerosis and Restenosis: An Assessment of the Evidence and Need for Future Research
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December 2, 1997;
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M. Maass, E. Krause, P.M. Engel, S. Kruger, and M. Maass
Endovascular Presence of Chlamydia pneumoniae in Patients with Hemodynamically Effective Carotid Artery Stenosis
Angiology,
August 1, 1997;
48(8):
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[Abstract]
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S. Gupta, E. W. Leatham, D. Carrington, M. A. Mendall, J. C. Kaski, and A. J. Camm
Elevated Chlamydia pneumoniae Antibodies, Cardiovascular Events, and Azithromycin in Male Survivors of Myocardial Infarction
Circulation,
July 15, 1997;
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[Abstract]
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More Evidence for Infectious Cause of Coronary Disease
Journal Watch Cardiology,
August 1, 1996;
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16 - 16.
[Full Text]
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MORE EVIDENCE FOR INFECTIOUS CAUSE OF CORONARY DISEASE
Journal Watch (General),
June 18, 1996;
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1 - 1.
[Full Text]
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F. Mach, G. K. Sukhova, M. Michetti, P. Libby, and P. Michetti
Influence of Helicobacter pylori Infection During Atherogenesis In Vivo in Mice
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[Abstract]
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