More fibrosis and thrombotic complications but similar expression patterns of markers for coagulation and inflammation in symptomatic plaques from DM2 patients

Abstract

Objective: One of the possible pathological mechanisms behind the increased vascular injury in diabetes mellitus type 2 (DM2) is the formation of advanced glycation end products (AGEs). The aim of this study was to investigate whether the presence of AGEs and specific markers for coagulation and inflammation in symptomatic atherosclerotic plaques from DM2 patients differs from plaques from nondiabetics. Methods and results: Carotid atherectomies were obtained from DM2 patients (n=11) and controls without DM2 matched for age and other cardiovascular risk factors (n=12) who were treated for symptomatic carotid artery stenosis. Plaques were graded according to the American Heart Association classification of lesions. More fibrosis and more thrombotic complications (p=0.007) were observed in carotid atherectomies from DM2 patients. Percentages of immunostained smooth muscle cells and macrophages in the lesions, quantified planimetrically, did not differ between the two groups. No differences were found in the immunostaining for T cells, tissue factor (TF), endothelial protein C receptor (EPCR), nuclear factor KB, and the AGE carboxymethyllysine. Conclusions: These findings demonstrate that DM2 is associated with increased plaque complications; however, a local changed presence of AGEs, TF, and EPCR seems not to be involved in this end stage of atherosclerosis.