Vascular cell adhesion molecule-1 levels in patients with coronary artery disease with type 2 diabetes mellitus

Chronic systemic inflammation is a key component of the pathogenesis of both type 2 diabetes mellitus (T2DM) and coronary artery disease (CAD). Soluble vascular cell adhesion molecule-1 (sVCAM-1) is considered as the indicator of vascular inflammation and endothelial activation. The aim of our study was to investigate sVCAM-1 levels in patients with CAD with T2DM and to determine their dependence on a previous history of myocardial infarction (MI). The study included 52 patients with stable CAD with T2DM, 20 CAD patients without diabetes and 14 control group persons. sVCAM-1 levels were measured in serum by the enzyme-linked immunosorbent assay. sVCAM-1 levels in patients with CAD with T2DM and patients with CAD without diabetes were higher than in the control group (p<0,001 and p<0,001, respectively). The difference in sVCAM-1 levels between CAD patients with T2DM and without diabetes was not significant (p=0,355). There were no significant correlations of sVCAM-1 levels with glucometabolic indices in any group. Only in patients with CAD with T2DM sVCAM-1 level negatively correlated with high-density lipoprotein cholesterol. CAD patients with and without T2DM with a history of myocardial infarction (MI) had higher sVCAM-1 levels than patients without previous MI (p=0,038, p=0,043, respectively). Only in diabetic CAD patients sVCAM-1 levels were increased in those without a history of MI (p=0,036, in comparison with the controls). There were no correlations between sVCAM-1 levels and left ventricular remodeling indices in patients either with or without MI. Conclusions. In patients with CAD with T2DM and patients with CAD without T2DM, sVCAM-1 levels increased in comparison with the controls. However, in patients without diabetes sVCAM-1 level was increased only in those with previous MI. In patients with T2DM, sVCAM-1 level increased in the absence of previous MI and there was the further significant increase of its level in postinfarction cardiosclerosis.