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Differential Effects of Lipid-lowering Drugs in Modulating Morphology of Cholesterol Particles
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Published on: November 10, 2017

Association of Chlamydia pneumoniae antibody with the cholesterol-lowering effect of statins

Yasunori Sawayama1, Masafumi Tatsukawa, Kyoko Okada

  • 1Department of General Medicine, Kyushu University Hospital, Higashi-ku, Fukuoka 812-8582, Japan.

Atherosclerosis
|December 4, 2003
PubMed

Insights

Chlamydia pneumoniae infection may reduce the effectiveness of lipid-lowering drugs in treating atherosclerosis. Patients without C. pneumoniae antibodies showed improved carotid intima-media thickness, unlike infected patients.

Area of Science:

  • Cardiology
  • Infectious Diseases
  • Vascular Biology

Background:

  • Atherosclerosis is a significant cardiovascular disease.
  • The role of Chlamydia pneumoniae (C. pneumoniae) infection in atherosclerosis progression is debated.
  • Lipid-lowering therapies are standard treatments for hypercholesterolemia.

Purpose of the Study:

  • To investigate the association between C. pneumoniae infection and atherosclerosis.
  • To compare the efficacy of lipid-lowering drugs on carotid intima-media thickness (IMT) in patients with and without C. pneumoniae antibodies.

Main Methods:

  • 165 asymptomatic hypercholesterolemic patients were randomized to probucol or pravastatin for 2 years.
  • Carotid intima-media thickness (IMT) change was measured as the primary endpoint.
  • C. pneumoniae antibodies (IgA and IgG) were detected using enzyme-linked immunosorbent assay.

Main Results:

  • Patients without C. pneumoniae antibodies showed a significant reduction in IMT progression (-19%).
  • Patients with C. pneumoniae antibodies showed no significant change in IMT (-6%).
  • No significant differences in lipid reduction or drug efficacy were observed between groups.

Conclusions:

  • C. pneumoniae infection appears to reduce the effectiveness of lipid-lowering therapy on carotid atherosclerosis.
  • This suggests C. pneumoniae may play a role in the progression of atherosclerosis.
  • Further research is warranted to elucidate the mechanisms involved.

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