Low‐grade inflammation, endothelial activation and carotid intima‐media thickness in type 2 diabetes

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Abstract
Objectives. The objective of this study was to assess the relationship between inflammation, endothelial activation and incipient atherosclerosis in type 2 diabetes. Design. Cross‐sectional study. Setting and subjects. We studied 239 type 2 diabetic patients [71 with clinical cardiovascular disease (CVD)] and 78 healthy control subjects, aged 50–75 in a single research centre. Methods. Carotid intima‐media thickness (IMT) was determined by ultrasound. Circulating intracellular adhesion molecule‐1, vascular cell adhesion molecule‐1, E‐selectin, ultra‐sensitive C‐reactive protein, human serum amyloid A, interleukin‐6, monocyte colony‐stimulating factor, secretory nonpancreatic phospholipase A2 type IIA, glucose, HbA1c, and lipid/lipoprotein variables were measured. Results. Carotid IMT was significantly thicker in diabetic patients than healthy controls across the whole age range. IMT was also thicker in diabetic patients with, than without, CVD, but this difference disappeared after controlling for confounding factors. Concentrations of the inflammatory and endothelial markers except IL‐6 were significantly higher in the diabetic patients than in healthy controls, but comparable in diabetic patients with and without CVD. The main determinants of IMT in the diabetic patients were blood pressure, age and diabetes duration. Conclusions. Low‐grade inflammation and endothelial activation are increased in diabetic patients but do not associate with IMT or clinical CVD. The inflammatory reaction seems to be rather a feature of the metabolic syndrome than a direct determinant of atherosclerosis.