Relationship of vimentin and endocan with severity of coronary artery disease

Background. New biomarkers are now emerging to predict the early stages of atherosclerosis, a major cause of coronary artery disease (CAD). One such biomarker is vimentin, with studies showing that vimentin levels correlate with the presence of CAD. Another promising biomarker is endocan. Elevated plasma levels of this biomarker may reflect endothelial dysfunction and may therefore be associated with cardiovascular disease. Aim. The aim was to assess the association of vimentin and endocan with CAD severity. Methods. This was a retrospective pilot study involving 131 coronary artery disease (CAD) patients. All the CAD underwent coronary angiography (CA) or multi-slice computed tomographic coronary angiography (CTCA). CAD severity in patients undergoing CA was assessed by Gensini score: between 0 and 11; between 12 and 35; greater than 35. The severity of CAD in patients undergoing CTCA was assessed according to the CAD-RADS score: CAD-RADS 0; CAD-RADS 1 and 2; CAD-RADS 3; CAD-RADS 4 and 5. Statistical analysis was performed using Mann–Whitney-U, Kruskal–Wallis, ÷2 tests, Spearman correlation coefficient. Data are presented as percentage (number) or median (minimum-maximum) or mean (standard deviation) according to the sample distribution. Results. CTCA was performed in the vast majority of patients — 84.73% (n = 111), CA was performed in approximately one third of patients — 30.53% (n = 40), and some patients (14.5% (n = 19)) had both tests. 73.3% (n = 96) of patients had CAD, and 26.7% — did not (n = 35). Those with CAD were older in comparison with non-CAD (p < 0.001). Vimentin levels were much higher in patients with CAD compared to non-CAD (186.93 (7.81–2081.0) vs. 70.82 (7.81–399.0), p = 0.022). In contrast, there was no significant difference in endocan levels between the groups ( p = 0.498). There was a trend for vimentin levels to increase with the severity of CAD, as assessed by the Gensini score. There was no statistically significant difference in the severity of CAD according to CAD RADS, either in terms of vimentine (p = 0.112) or endocan (p = 0.492) levels. Interestingly, vimentin levels were lower in patients without atherosclerotic lesions than in those with the most significant atherosclerotic lesions (CAD-RADS 4 and 5), (p = 0.019). There was a significant correlation between vimentin levels and the severity of CAD as assessed by the CAD-RADS score (r = 0.298; p = 0.023). Vimentin and endocan levels did not differ by sex, arterial hypertension, dyslipidaemia, obesity or family history, but vimentin concentrations were much higher in smokers in comparison with no-smokers (298.18 (48.24–2081) vs 149.17 (7.81–1485)); p = 0.006). In contrast, endocan levels were lower in smokers compared to non-smokers (159.5 (48.37–1276.09) vs 187.2 (47.12–2173.52); p = 0.090). Vimentin levels were statistically significantly higher in patients requiring revascularisation (percutaneous coronary intervention in 13% (n = 17) or coronary artery bypass grafting in 1.5% (n = 2)), (p = 0.011), while endocan levels were not statistically significantly different in these groups (p = 0.552). Conclusions. Vimentin levels may reflect the severity of CAD. Relationship between the levels of Endocan and CAD severity have to be clarified.