Evaluation of the endothelial glycocalyx damage in patients with acute coronary syndrome
Abstract Background Endothelial glycocalyx (EG) is sugar-based cell-bound surface molecules linked to transmembrane proteins observed on the endothelial surface of the vessels. Damage to this structure causes an increase in platelet and leucocyte adhesion and shear stress in the vessel. We hypothesi...
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Veröffentlicht in: | Atherosclerosis 2016-04, Vol.247, p.184-188 |
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Zusammenfassung: | Abstract Background Endothelial glycocalyx (EG) is sugar-based cell-bound surface molecules linked to transmembrane proteins observed on the endothelial surface of the vessels. Damage to this structure causes an increase in platelet and leucocyte adhesion and shear stress in the vessel. We hypothesized a possible link between EG damage and acute coronary syndrome (ACS). Methods We measured the syndecan-1 levels (a biomarker of EG damage) in 141 patients (99 men) with ACS and compared to those of 45 patients (24 men) with non-coronary chest pain (NCCP) and of 24 (14 men) healthy individuals (CONTROL). Results The baseline characteristics of the ACS and NCCP groups were similar. Syndecan-1 levels were significantly higher in the ACS group than in the NCCP (p = 0.01) and CONTROL (p = 0.001) groups but did not differ between the NCCP and CONTROL groups (p = 0.83). In analysis according to gender category, the difference among the groups remained significant only for men (p = 0.0009). A syndecan-1 level higher than 148 ng/ml was associated with ACS diagnosis with an odds ratio of 14 (95% confidence interval (CI): 1.8 to 102), p = 0.011. After adjusting for gender, age and current or past tobacco use, this syndecan-1 level remained positively associated with ACS diagnosis with an odds ratio of 12 (95% CI: 1.6 to 93), p = 0.016. Conclusion Higher syndecan-1 levels were observed during ACS, mostly in men, suggesting that EG damage could participate in the atherosclerotic plaque vulnerability process in these patients. |
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ISSN: | 0021-9150 1879-1484 |
DOI: | 10.1016/j.atherosclerosis.2016.02.023 |