You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT JAMA
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 290 No. 11, September 17, 2003 TABLE OF CONTENTS
  JAMA
  •  Online Features
  Editorial
 This Article
 •Full text
 •PDF
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Citing articles on HighWire
 •Citing articles on Web of Science (5)
 •Contact me when this article is cited
 Related Content
 •Related article
 •Similar articles in JAMA
 Topic Collections
 •Bacterial Infections
 •Cardiovascular System
 •Cardiovascular Disease/ Myocardial Infarction
 •Infectious Diseases
 •Alert me on articles by topic
 Social Bookmarking
  Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit Add to Technorati Add to Twitter What's this?

Antibiotic Therapy for Coronary Artery Disease

Can a WIZARD Change It All?

Sorin V. Pislaru, MD, PhD; Frans Van de Werf, MD, PhD

JAMA. 2003;290:1515-1516.

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

The possible association between Chlamydia pneumoniae and atherosclerosis was first reported in 1988 by Saikku et al1 who noted that antichlamydial antibodies were present more often among patients with acute myocardial infarction (MI) than among matched controls. Since then, several other serological studies have yielded conflicting results about this association, possibly due to lack of uniformity in methods used (ie, different classes of antibodies tested, different methods, different cutoff points) and by the high prevalence of C pneumoniae exposure in the population. On the other hand, data from basic laboratory studies have strongly suggested a possible role of C pneumoniae in the etiology of atherosclerosis. Cells involved in atherogenesis (vascular endothelial cells, smooth muscle cells, macrophages, and platelets) have been found to be infected by C pneumoniae.2 In mouse and rabbit models, C pneumoniae has been detected in . . . [Full Text of this Article]

Author Affiliations: Department of Cardiology, Mayo Clinic and Foundation, Rochester, Minn (Dr Pislaru) and Department of Cardiology, Gasthuisberg University Hospital and University of Leuven, Leuven, Belgium (Dr Van de Werf).



Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter     What's this?

RELATED ARTICLE

Azithromycin for the Secondary Prevention of Coronary Heart Disease Events: The WIZARD Study: A Randomized Controlled Trial
Christopher M. O'Connor, Michael W. Dunne, Marc A. Pfeffer, Joseph B. Muhlestein, Louis Yao, Sandeep Gupta, Rebecca J. Benner, Marian R. Fisher, and Thomas D. Cook
JAMA. 2003;290(11):1459-1466.
ABSTRACT | FULL TEXT  


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Chlamydia pneumoniae infections in mouse models: relevance for atherosclerosis research
de Kruif et al.
Cardiovasc Res 2005;65:317-327.
ABSTRACT | FULL TEXT  

Antibiotics and Coronary Heart Disease
Nieto
JAMA 2004;291 :302-303.
FULL TEXT  

Short-Term Antibiotic Therapy Not Effective for Secondary Prevention of CAD
Journal Watch Cardiology 2003;2003:2-2.
FULL TEXT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 2003 American Medical Association. All Rights Reserved.