Can increased intestinal permeability and low-grade endotoxemia be the triggering pathogenesis in isolated coronary artery ectasia?


Toprak K., KAPLANGÖRAY M., Altiparmak İ. H., Taşcanov M. B., Güngören F., Fedai H., ...Daha Fazla

Coronary Artery Disease, cilt.34, sa.2, ss.102-110, 2023 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 34 Sayı: 2
  • Basım Tarihi: 2023
  • Doi Numarası: 10.1097/mca.0000000000001209
  • Dergi Adı: Coronary Artery Disease
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, CINAHL, EMBASE, MEDLINE
  • Sayfa Sayıları: ss.102-110
  • Anahtar Kelimeler: coronary artery disease, intestinal permeability, isolated coronary artery ectasia, lipopolysaccharide, low-grade endotoxemia, zonulin
  • Bilecik Şeyh Edebali Üniversitesi Adresli: Evet

Özet

Purpose Isolated coronary artery ectasia (ICAE) is a rare coronary artery disease (CAD) encountered during coronary angiography. Although many mechanisms have been suggested today that may be associated with ICAE, the underlying pathogenesis has not been fully understood. In this study, we aimed to reveal the possible relationship between intestinal permeability and ICAE. Methods Of the 12 850 patients who underwent coronary angiography, 138 consecutive patients with ICAE and 140 age- and sex-matched subjects with normal coronary arteries as the control group and 140 subjects with stenotic CAD were included in the study. Results Serum zonulin and lipopolysaccharide levels were significantly higher in patients with ICAE than in the control group and CAD group. Additionally, zonulin and lipopolysaccharide levels were significantly higher in the CAD group than in the ICAE group. In the correlation analysis, serum zonulin levels were correlated with the mean diameter and length of the ecstatic segment. In multivariate analysis, zonulin and lipopolysaccharide were identified as independent predictors for ICAE. Conclusion These results suggest that there may be a pathophysiological relationship between increased intestinal permeability and ICAE.