Infectious agents, protein electrophoresis and immunoglobulin levels in patients with coronary artery ectasia

Gulay Yetkin1, Didem Tascioglu2, Selcuk Ozturk3

  • 1Istinye University Faculty of Medicine, Department of Microbiology, Liv Hospital Istanbul, Turkey; International Medical Center IMC Hospital Mersin, Turkey.

Indian Heart Journal
|September 28, 2025
PubMed

Insights

Coronary artery ectasia (CAE) may differ from atherosclerosis, with higher IgE and alpha-2 globulin levels in patients with CAE. Infectious agents like C. pneumoniae and H. pylori do not appear to play a significant role in CAE pathogenesis.

Area of Science:

  • Cardiology
  • Immunology
  • Biochemistry

Background:

  • Coronary artery ectasia (CAE) shares similarities with atherosclerosis but exhibits distinct pathophysiological features.
  • Investigating inflammatory markers and infectious agents may elucidate differences between CAE and atherosclerosis.

Purpose of the Study:

  • To investigate potential differences in the pathophysiology of CAE compared to coronary artery disease (CAD) alone.
  • To assess the role of inflammatory parameters, specifically IgE and protein electrophoresis, in CAE.

Main Methods:

  • Compared laboratory parameters, including IgG antibodies against C. pneumoniae and H. pylori, total IgE, and protein electrophoresis, between patients with CAD and those with both CAD and CAE.
  • Utilized logistic regression to identify independent predictors of CAE presence.

Main Results:

  • Patients with CAE + CAD showed significantly higher levels of IgE, Alpha 2 macroglobulin, and Beta-1 globulin compared to CAD alone.
  • Elevated IgE and Alpha 2 macroglobulin were independently associated with the presence of CAE.
  • No significant differences in IgG antibodies against C. pneumoniae and H. pylori were observed between groups.

Conclusions:

  • The independent association of serum IgE and alpha-2 globulins with CAE suggests distinct pathophysiological mechanisms compared to atherosclerosis.
  • Common infectious agents like C. pneumoniae and H. pylori do not seem to contribute additionally to CAE pathogenesis.
Abstract

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