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Published on: January 23, 2019
Antiendothelial cell antibodies in patients with coronary artery ectasia
Demosthenes G Katritsis1, Theodoros Zografos, Socrates Korovesis
1Department of Cardiology, Athens Euroclinic, Athens, Greece. dkatritsis@euroclinic.gr
Insights
Increased IgA antiendothelial cell antibodies (AECA) were found in coronary artery ectasia (CAE) patients, suggesting autoimmunity may play a role in CAE pathogenesis.
Area of Science:
- Cardiology
- Immunology
- Vascular Biology
Background:
- Mechanisms of coronary artery ectasia (CAE) pathogenesis remain unclear.
- Circulating antiendothelial cell antibodies (AECA) are linked to endothelial injury in vasculitis.
- AECA prevalence in CAE is currently unknown.
Purpose of the Study:
- To investigate the prevalence of AECA in patients with CAE.
- To explore the potential role of autoimmunity in CAE pathogenesis.
Main Methods:
- Coronary angiography identified 27 CAE patients and 30 controls.
- Serum AECA (IgG, IgM, IgA), antinuclear antibodies (ANA), and antineutrophil cytoplasmic antibodies (ANCA) were measured.
- Anticardiolipin antibodies (aCL) were also assessed.
Main Results:
- ANA and ANCA prevalence did not differ between CAE patients and controls.
- No significant differences in IgG or IgM aCL reactivity were observed.
- IgA AECA prevalence was significantly higher in CAE patients (37.0%) compared to controls (10%).
Conclusions:
- A higher prevalence of IgA AECA in CAE patients suggests a potential autoimmune contribution.
- These findings provide evidence for autoimmunity in the pathogenesis of some CAE cases.
Background:
The mechanisms involved in the pathogenesis of coronary artery ectasia (CAE) have not been elucidated. Circulating antiendothelial cell antibodies (AECA) are often detectable in systemic vasculitis and have been implicated in the pathogenesis of endothelial injury. Their prevalence in CAE is not known.
Methods And Results:
Out of 475 consecutive patients subjected to coronary angiography, 27 patients were diagnosed with CAE. Thirty patients matched for age, body mass index, sex, and coronary artery disease prevalence, served as controls. Serum AECA of IgG, IgM, and IgA isotypes were detected using a cell-based enzyme-linked immunosorbent assay (ELISA). Antinuclear antibodies (ANA) and antineutrophil cytoplasmic antibodies (ANCA) were detected using indirect immunofluorescence. IgG and IgM anticardiolipin antibodies (aCL) were detected using commercial ELISA. The prevalence of ANA and ANCA was similar in CAE patients and controls (33.3 vs. 43.3%, and 3.3 vs. 7.4%, respectively). There was no significant difference in IgG or IgM aCL reactivity between patients and controls. Both CAE patients and controls were negative for IgG AECA. The frequency of IgM AECA positivity was similar in CAE patients and controls. The prevalence of AECA of the IgA isotype was significantly higher in CAE patients (37.0 vs. 10%, P<0.05).
Conclusion:
There is increased prevalence of circulating AECA of the IgA isotype in patients with CAE. This provides evidence for a role of autoimmunity in the pathogenesis of certain cases of CAE.
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