Association between vimentin, a new biomarker of atherosclerosis, and the degree of coronary atherosclerosis

Background. Atherosclerosis is a major risk factor for the development of coronary syndromes and myocardial ischaemia [1]. Initial studies show that vimentin, an endothelium damage marker, levels correlate with the presence of coronary artery disease (CAD) [2]. New biomarkers could be an important prognostic tool to identify patients at an increased risk of atherosclerosis at early stages. Aim. We aimed to assess the association of vimentin relationship with inflammation level in stabile angina pectoris (SAP) patients. Methods. This is a retrospective study of 131 eligible patients who met the inclusion criteria (no comorbidities except hypertension, dyslipidaemia) and were diagnosed with stabile angina pectoris (SAP). Patients underwent ankle-brachial index (ABI) assessments, carotid artery ultrasound (CAU), and necessary blood tests. Patients were divided into: 1) four groups according to high-sensitivity C-reactive protein (hs-CRP): normal hs-CRP levels, slightly elevated, moderately elevated, and highly elevated; and 2) two groups according to ABI (normal ABI — value between 1 and 1.4 and abnormal ABI ? 0.9 or 1.4), 3) two groups according to SAP presence. The presence and severity of CAD was assessed by coronary angiography (CA) or computed tomographic coronary angiography (CCTA). In the CA group, the severity of CAD was assessed by the Gensini score and in the CCTA group, the severity of CAD was assessed by the CAD-RADS score. The Systemic Inflammatory Response Index (SIRI) — monocyte to lymphocyte ratio (MLR) multiplied by neutrophils, the Systemic Immune Inflammation Index (SII) — platelets multiplied by neutrophil to lymphocyte ratio (NLR) and lymphocyte to monocyte ratio (LMR) — were calculated to assess the inflammatory status. Statistical analysis was performed using Mann–Whitney-U, Kruskal–Wallis, ÷2 tests, and Spearman correlation coefficient. Data are presented as percentage (number) or median (minimum-maximum) or mean (standard deviation) according to the sample distribution. Results. The mean age was 55.24 (10.19) years and 52.7% (69) were male. Vimentin concentration in CAD patients was higher in comparison with those without CAD (186.93 (7.81–2081.0), and 70.82 (7.81–399.0), p = 0.022, respectively). There was a significant weak correlation between vimentin levels and CAD severity as assessed by the CAD-RADS score (r = 0.298, p = 0.023) and a strong correlation between CAD severity as assessed by the Gensini score (r = 0.640, p = 0.002). Vimentin levels correlated statistically significantly with hs-CRP levels (r = 0.277, p = 0.017). Vimentin level (146.54 ng/ml (7.81–2081)) in the normal ABI group was significant lower than in the abnormal ABI group (320.78 ng/ml (76.81–823.68), (p = 0.014)). Vimentin concentrations correlated reversibly with ABI values in right and left limbs. (r = –0.286, p = 0.020; r = –0.273, p = 0.026, respectively). Accordingly, vimentin levels correlated with age (r = 0.273, p = 0.019), leukocyte (r = 0.266, p = 0.023), neutrophil (r = 0.250, p = 0.033 ) counts, SIRI (r = 0.231, p = 0.049), and NLR (r = 0.259, p = 0.027), and right carotid artery intima-media thickness (r = 0.268, p = 0.034). No significant correlations were found between vimentin levels and uric acid, lipid markers. Conclusions. Vimentin levels were higher in the higher hs-CRP groups. Vimentin concentration correlated with CAD severity as assessed by the Gensini score, ABI values, thickening of the carotid intima media and SIRI. Vimentin concentration in the serum may reflect the degree of atherosclerosis development.