Relationship between the endothelium biomarkers endocan and thrombomodulin and slow coronary flow. Sadettin Selçuk Baysal 1* , Şahbender Koç 2 , Bedri Caner Kaya 1 , Ahmet Güneş 1 , Naime Meriç Konar 3 , İbrahim Halil Altiparmak 4 1 Cardiology Department, Şanlıurfa Mehmet Akif İnan Training and Research Hospital, Şanlıurfa, Turkey 2 Cardiology Department, Keçiören Training and Research Hospital, Ankara, Turkey 3 Department of Biostatistics, Hacettepe University, Ankara, Turkey 4 Department of Cardiology, Harran University, Şanlıurfa, Turkey Abstract Background: Growing evidence suggests that endothelial dysfunction plays a key role in the pathophysiology of Slow Coronary Flow (SCF). This study investigated the association between endothelial biomarkers endocan and soluble Thrombomodulin (sTM) and SCF. Methods: The study population consisted of 89 subjects (54 patients with SCF and 35 controls). Coronary flow rate was assessed using the Thrombolysis in Myocardial Infarction (TIMI) Frame Count (TFC) method. The serum endocan and sTM levels of all subjects were analysed. Results: Significantly higher endocan levels (1.14 ± 0.22 vs. 0.96 ± 0.32 ng/ml; p=0.009) and sTM levels (657.06 ± 198.18 vs. 592.76 ± 128.45 pg/ml; p=0.119) were observed in the SCF group relative to the control group. A positive correlation was detected between endocan and TFC (r=0.563; p=0.016). Multivariate logistic regression analysis revealed endocan as a predictor of SCF. Conclusions: The endocan level in SCF patients was significantly higher than in controls and the sTM level was also increased, although the difference was not significant. These results suggest that endocan may serve as a biomarker to predict SCF. Keywords: Slow coronary flow, Endocan, Thrombomodulin, Endothelial dysfunction. Accepted on January 19, 2018 Introduction The Slow Coronary Flow (SCF) phenomenon is an angiographic finding described as retarded flow of contrast agent to the end branch of a coronary artery without significant coronary stenosis [1]. Although it is well-known among interventional cardiologists that coronary angiography is performed in approximately 1% of patients, the mechanisms underlying this entity have not yet been elucidated [2]. Microvascular dysfunction, endothelial dysfunction, diffuse atherosclerosis, and platelet and vasomotor dysfunction have been proposed in the etiology of SCF [3,4]. Endothelial cell-specific molecule-1, or endocan, is a soluble proteoglycan secreted by human vascular endothelial cells and can be found in the circulation [5]. Previous studies have suggested that endocan plays a key role in the pathophysiology of endothelial dysfunction [5,6]. Thrombomodulin (TM) is an integral membrane type-1 glycoprotein that is widely distributed on the lumenal surface of vascular endothelial cells and has been implicated in the endothelial regulation of fibrinolysis and coagulation. Soluble Thrombomodulin (sTM) can be detected in serum after proteolysis of TM on the endothelium [7]. Previous studies have suggested that the sTM concentration reflects the degree of endothelial damage [7,8]. Because endothelial dysfunction plays an important role in the pathophysiology of SCF, we aimed to determine whether sTM and endocan, two endothelial dysfunction biomarkers, are associated with SCF. Therefore, we investigated the relationship between these two biomarkers and SCF. Few studies have investigated the relationship between endocan and SCF; to the best of our knowledge, this was the first study to measure the concentration of sTM in the circulation of SCF patients. Subjects and Methods This was a cross-sectional study, in which 6,517 patients underwent coronary angiography between February 2015 and January 2016. During this period, a total of 89 patients with an initial diagnosis of stable angina pectoris, and who had angiographically confirmed normal coronary arteries without ISSN 0970-938X www.biomedres.info Biomed Res 2018 Volume 29 Issue 7 1345 Biomedical Research 2018; 29 (7): 1345-1350