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.

Graham Scott Hillis, C. V. Pearson, S. A. Harding, S. Sutherland, C. A. Ludlam, J. C. Marioni, R. J. Prescott, K. A. A. Fox, A. D. Flapan

    Research output: Contribution to journalArticle

    21 Citations (Scopus)

    Abstract

    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.

    Original languageEnglish
    Pages (from-to)72-79
    Number of pages7
    JournalAmerican Heart Journal
    Volume148
    DOIs
    Publication statusPublished - 2004

    Keywords

    • CHLAMYDIA-PNEUMONIAE INFECTION
    • FUTURE MYOCARDIAL-INFARCTION
    • SECONDARY PREVENTION TRIAL
    • UNSTABLE ANGINA-PECTORIS
    • HEART-DISEASE EVENTS
    • SMOOTH-MUSCLE-CELLS
    • ENDOTHELIAL-CELLS
    • ARTERY-DISEASE
    • HELICOBACTER-PYLORI
    • CARDIOVASCULAR EVENTS

    Cite this

    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. / Hillis, Graham Scott; Pearson, C. V.; Harding, S. A.; Sutherland, S.; Ludlam, C. A.; Marioni, J. C.; Prescott, R. J.; Fox, K. A. A.; Flapan, A. D.

    In: American Heart Journal, Vol. 148, 2004, p. 72-79.

    Research output: Contribution to journalArticle

    Hillis, Graham Scott ; Pearson, C. V. ; Harding, S. A. ; Sutherland, S. ; Ludlam, C. A. ; Marioni, J. C. ; Prescott, R. J. ; Fox, K. A. A. ; Flapan, A. D. / 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. In: American Heart Journal. 2004 ; Vol. 148. pp. 72-79.
    @article{60dabdb7646645cd8353af70b8029cc3,
    title = "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.",
    abstract = "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.",
    keywords = "CHLAMYDIA-PNEUMONIAE INFECTION, FUTURE MYOCARDIAL-INFARCTION, SECONDARY PREVENTION TRIAL, UNSTABLE ANGINA-PECTORIS, HEART-DISEASE EVENTS, SMOOTH-MUSCLE-CELLS, ENDOTHELIAL-CELLS, ARTERY-DISEASE, HELICOBACTER-PYLORI, CARDIOVASCULAR EVENTS",
    author = "Hillis, {Graham Scott} and Pearson, {C. V.} and Harding, {S. A.} and S. Sutherland and Ludlam, {C. A.} and Marioni, {J. C.} and Prescott, {R. J.} and Fox, {K. A. A.} and Flapan, {A. D.}",
    year = "2004",
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    T1 - 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.

    AU - Hillis, Graham Scott

    AU - Pearson, C. V.

    AU - Harding, S. A.

    AU - Sutherland, S.

    AU - Ludlam, C. A.

    AU - Marioni, J. C.

    AU - Prescott, R. J.

    AU - Fox, K. A. A.

    AU - Flapan, A. D.

    PY - 2004

    Y1 - 2004

    N2 - 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.

    AB - 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.

    KW - CHLAMYDIA-PNEUMONIAE INFECTION

    KW - FUTURE MYOCARDIAL-INFARCTION

    KW - SECONDARY PREVENTION TRIAL

    KW - UNSTABLE ANGINA-PECTORIS

    KW - HEART-DISEASE EVENTS

    KW - SMOOTH-MUSCLE-CELLS

    KW - ENDOTHELIAL-CELLS

    KW - ARTERY-DISEASE

    KW - HELICOBACTER-PYLORI

    KW - CARDIOVASCULAR EVENTS

    U2 - 10.1016/j.ahj.2004.01.016

    DO - 10.1016/j.ahj.2004.01.016

    M3 - Article

    VL - 148

    SP - 72

    EP - 79

    JO - American Heart Journal

    JF - American Heart Journal

    SN - 0002-8703

    ER -