Effects of a brief course of azithromycin on soluble cell adhesion molecules and markers of inflammation in survivors of an acute coronary syndrome: A double-blind, randomized, placebo-controlled study

被引:20
作者
Hillis, GS
Pearson, CV
Harding, SA
Sutherland, S
Ludlam, CA
Marioni, JC
Prescott, RJ
Fox, KAA
Flapan, AD
机构
[1] Royal Infirm Edinburgh NHS Trust, Dept Cardiol, Edinburgh, Midlothian, Scotland
[2] Royal Infirm Edinburgh NHS Trust, Dept Haematol, Edinburgh, Midlothian, Scotland
[3] Univ Edinburgh, Dept Microbiol, Edinburgh, Midlothian, Scotland
[4] Univ Edinburgh, Dept Publ Hlth Sci, Edinburgh, Midlothian, Scotland
关键词
D O I
10.1016/j.ahj.2004.01.016
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background The anti-chlamydial antibiotic, azithromycin, may improve outcome in patients who survive an acute coronary syndrome. The mechanisms are, however, poorly understood. The aims of this study were to define any relationship between Chlamydia pneumoniae seropositivity and levels of specific markers of endothelial activation (soluble cell adhesion molecules) and more general markers of inflammation (C-reactive protein [CRP] and interleukin-6 [IL-6]) and to assess whether azithromycin had any effect on such markers. Methods Patients who survived an acute coronary syndrome were randomized to receive treatment with azithromycin (n = 72) or placebo (n = 69) for 5 days. Before therapy, C pneumoniae IgA and IgG titers were checked, with serum levels of soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1, soluble E-selectin (sE-selectin), soluble P-selectin, high-sensitivity CRP, and IL-6. They were rechecked 3 months later. Results There were no significant correlations between C pneumoniae titers and levels of CRP, IL-6, or soluble cell adhesion molecules. However, azithromycin treatment significantly reduced mean sICAM-1 levels (P = .006). This effect was more marked in patients with elevated titers of C pneumoniae IgA and IgG. Soluble E-selectin levels were also reduced in patients who were seropositive, but no effects were seen on other endothelial or inflammatory markers. Conclusions After an acute coronary syndrome, a 5-day course of azithromycin reduces levels of sICAM-1, a marker of endothelial cell activation. Although these data suggest a potentially beneficial role for azithromycin, they should be interpreted with caution.
引用
收藏
页码:72 / 79
页数:8
相关论文
共 48 条
[1]   Randomized secondary prevention trial of azithromycin in patients with coronary artery disease and serological evidence for Chlamydia pneumoniae infection -: The azithromycin in coronary artery disease:: Elimination of myocardial infection with Chlamydia (ACADEMIC) study [J].
Anderson, JL ;
Muhlestein, JB ;
Carlquist, J ;
Allen, A ;
Trehan, S ;
Nielson, C ;
Hall, S ;
Brady, J ;
Egger, M ;
Horne, B ;
Lim, T .
CIRCULATION, 1999, 99 (12) :1540-1547
[2]   The role of inflammation and infection in coronary artery disease [J].
Becker, AE ;
de Boer, OJ ;
van der Wal, AC .
ANNUAL REVIEW OF MEDICINE, 2001, 52 :289-297
[3]   Effect of short-term treatment with azithromycin on recurrent ischaemic events in patients with acute coronary syndrome in the Azithromycin in Acute Coronary Syndrome (AZACS) trial: a randomised controlled trial [J].
Cercek, B ;
Shah, PK ;
Noc, M ;
Zahger, D ;
Zeymer, U ;
Matetzky, S ;
Maurer, G ;
Mahrer, P .
LANCET, 2003, 361 (9360) :809-813
[4]   Effect of prior exposure to Chlamydia pneumoniae, Helicobacter pylori, or cytomegalovirus on the degree of inflammation and one-year prognosis of patients with unstable angina pectoris or non-Q-wave acute myocardial infarction [J].
Choussat, R ;
Montalescot, G ;
Collet, JP ;
Jardel, C ;
Ankri, A ;
Fillet, AM ;
Thomas, D ;
Raymond, J ;
Bastard, JP ;
Drobinski, G ;
Orfila, J ;
Agut, H ;
Thomas, D .
AMERICAN JOURNAL OF CARDIOLOGY, 2000, 86 (04) :379-384
[5]   Chronic infections and coronary heart disease: is there a link? [J].
Danesh, J ;
Collins, R ;
Peto, R .
LANCET, 1997, 350 (9075) :430-436
[6]   Chlamydia pneumoniae IgG titres and coronary heart disease:: prospective study and meta-analysis [J].
Danesh, J ;
Whincup, P ;
Walker, M ;
Lennon, L ;
Thomson, A ;
Appleby, P ;
Wong, YK ;
Bernardes-Silva, M ;
Ward, M .
BRITISH MEDICAL JOURNAL, 2000, 321 (7255) :208-212
[7]   Parameters of inflammation and infection in a community based case-control study of coronary heart disease [J].
De Backer, J ;
Mak, R ;
De Bacquer, D ;
Van Renterghem, L ;
Verbraekel, E ;
Kornitzer, M ;
De Backer, G .
ATHEROSCLEROSIS, 2002, 160 (02) :457-463
[8]   Antibodies to Chlamydia pneumoniae and clinical course in patients with unstable angina pectoris [J].
de Maat, MPM ;
Ossewaarde, JM ;
Verheggen, PWHM ;
Kluft, C ;
Cats, VM ;
Haverkate, F .
ATHEROSCLEROSIS, 2000, 153 (02) :499-504
[9]   Chlamydia pneumoniae infection of vascular smooth muscle and endothelial cells activates NF-κB and induces tissue factor and PAI-1 expression -: A potential link to accelerated arteriosclerosis [J].
Dechend, R ;
Maass, M ;
Gieffers, J ;
Dietz, R ;
Scheidereit, C ;
Leutz, A ;
Gulba, DC .
CIRCULATION, 1999, 100 (13) :1369-1373
[10]  
Fryer RH, 1997, J INVEST MED, V45, P168