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The effect of chronic azithromycin therapy on soluble endothelium-derived adhesion molecules in patients with

H B Semaan1, P A Gurbel, J L Anderson

  • 1Department of Medicine, Union Memorial Hospital, Baltimore, Maryland, USA.

Journal of Cardiovascular Pharmacology
|October 12, 2000
PubMed

Insights

Azithromycin therapy did not significantly alter levels of vascular cell-adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin in coronary artery disease (CAD) patients. These markers of endothelial activation were elevated in CAD patients but unaffected by prolonged azithromycin treatment.

Area of Science:

  • Cardiovascular Medicine
  • Infectious Diseases
  • Immunology

Background:

  • Coronary artery disease (CAD) involves inflammation and atherosclerosis, potentially linked to Chlamydia pneumoniae (C.Pn) infection.
  • Cell-adhesion molecules like VCAM-1, ICAM-1, and E-selectin play a role in inflammatory cell recruitment during plaque development.
  • Azithromycin has shown anti-inflammatory effects in CAD patients, reducing cytokine levels.

Purpose of the Study:

  • To investigate the impact of azithromycin treatment on circulating levels of soluble vascular cell-adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin in patients with CAD.
  • To assess if azithromycin influences endothelial activation markers in CAD patients with evidence of C.Pn infection.

Main Methods:

  • Plasma concentrations of VCAM-1, ICAM-1, and E-selectin were measured in 40 CAD patients, 20 subjects with normal coronary arteries, and 14 healthy volunteers.
  • CAD patients with a positive IgG titer against C.Pn were randomly assigned to receive either azithromycin (500 mg/wk) or placebo for 3 months.
  • Serum samples were collected at baseline, 3 months, and a 6-month follow-up visit.

Main Results:

  • Patients with CAD exhibited significantly elevated plasma levels of VCAM-1 and E-selectin compared to controls.
  • No significant difference was observed in ICAM-1 levels between CAD patients and controls.
  • Prolonged azithromycin treatment (3 months) did not significantly alter the plasma concentrations of VCAM-1, ICAM-1, or E-selectin over a 6-month period.

Conclusions:

  • Soluble markers of endothelial activation (VCAM-1, E-selectin) are significantly increased in patients with documented CAD.
  • Long-term azithromycin treatment did not demonstrate a significant effect on plasma levels of these endothelial activation markers in CAD patients.
  • The findings suggest that azithromycin, at the tested dosage and duration, does not modulate key markers of endothelial activation in CAD patients, despite its known anti-inflammatory properties.

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