Volume 19 Supplement 2
Endothelial glycocalyx damage in patients with acute coronary syndrome
© Miranda et al. 2015
Published: 28 September 2015
The endothelial glycocalyx is a thin layer of proteinaceous material at the endothelial surface of the vessels. Damage to this structure can cause protein extravasation and tissue edema, increase platelet and leukocyte adhesion and increase of the shear stress in the vessel due to decreasing the nitric oxide production. On the other hand, a vulnerable atherosclerotic plaque with rupture or erosion characterizes the acute coronary syndrome (ACS). The glycocalyx damage could contribute to this process.
To evaluate the glycocalyx damage through syndecan-1 dosage in patients with ACS.
We included patients with ACS diagnosis (n = 140). These patients had ST-segment elevation myocardial infarction (n = 71), were without ST-segment elevation myocardial infarction (n = 58) and had unstable angina (n = 12). The syndecan-1 level was dosage through commercial ELISA kits (Abcam®, Cambridge, UK) at admission. These levels were compared with 45 patients with noncoronary chest pain (NCCP) in which the ACS diagnosis was ruled out through negative electrocardiogram, troponin and imaging test (tomographic or conventional coronary angiography, stress echocardiography) and 24 completely healthy individuals (CONTROL). The values were expressed in median plus percentiles 25 (P25) and 75 (P75).
The syndecan-1 levels were higher in the patients with ACS (77 ng/ml; 46-134) compared with the NCCP group (60 ng/ml; 32-79); p = 0.01 and CONTROL group (42 ng/ml; 27-80); p = 0.001. No difference was observed between the NCCP versus CONTROL group (p = 0.83). A syndecan-1 level higher than 148 ng/ml was associated with the ACS diagnosis (relative risk: 1.53; 95 % confidence interval: 1.33-1.80; p <0.0001).
The endothelial glycocalyx damage could contribute to the atherosclerotic plaque vulnerability and the establishment of an ACS.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.