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Circulation. 1999;99:1538-1539

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(Circulation. 1999;99:1538-1539.)
© 1999 American Heart Association, Inc.


Editorials

Antibiotic Treatment Trials for Secondary Prevention of Coronary Artery Disease Events

J. Thomas Grayston, MD

From the Department of Epidemiology, University of Washington, Seattle, Wash.

Correspondence to J. Thomas Grayston, MD, Professor of Epidemiology, University of Washington, F-262 Health Sciences Center, Seattle, WA 98195-7236. E-mail grayston@u.washington.edu


Key Words: Editorials • Chlamydia pneumoniae • antibiotics • coronary disease


*    Introduction
 
The TWAR organism was described as a cause of respiratory infection in 1986.1 In 1989, it was declared a new species of Chlamydia and named Chlamydia pneumoniae.2 In 1988, Saikku et al3 reported a small seroepidemiological study suggesting a possible association between TWAR infection and atherosclerosis. Information on the association of C pneumoniae and atherosclerosis has accumulated rapidly since that time. More than 20 seroepidemiological studies have confirmed an association, and several have failed to find it.4 The seroepidemiological studies have been most useful in calling attention to the possibility of an association rather than suggesting possible mechanisms.

That an association between C pneumoniae and atherosclerosis exists has been shown definitively in a series of studies demonstrating C pneumoniae organisms in atherosclerotic tissues. The organism has been demonstrated in atherosclerotic plaques by electron microscopy, by immunocytochemistry using monoclonal antibodies, by polymerase chain reaction (PCR), and by isolation of the organism.5 6 7 More than 20 reports have appeared that demonstrate the presence of the organism in atherosclerotic plaques by 1 or more of these techniques. Except for a few studies using PCR only, the organism has been found in from 50% to 100% of the lesions studied. In most of the studies, the organism could not be found in normal-artery tissue.

Although the association of C pneumoniae and atherosclerosis has been established beyond a reasonable doubt, the significance of the association for the etiology of atherosclerosis and its progression and complications is unknown. Studies of this association should now be directed . . . [Full Text of this Article]




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