[Characteristics of atherosclerotic plaque in diabetics]

Diabetes is associated with a high risk for early atherosclerosis. 3/4 of all Type-2 diabetic patients exhibit coronary artery disease.

Microcirculatory disturbances precede morphologic changes. Especially fluctuations in blood glucose which occur i.e. in the postprandial state in badly controlled diabetic subjects, lead to an activation of protein kinase C beta and to stimulation of extracellular matrix proteins and cytokines. NO-dependent vasodilation is reduced. Postprandial blood glucose peaks are correlated with the intima-media thickness of the carotid artery and appear to be more important than fasting glucose values in multivariate analyses. After coronary interventions there is an enhanced plasminogen activator inhibitor-1 synthesis in diabetic patients compared to controls. This enhanced synthesis contributes to an exaggerated intravascular thrombogenicity. Already within a few days statin therapy leads to an increase in vasodilatory capacity irrespective of plasma lipid concentrations.

Atherosclerosis and development of plaques are functionally and morphologically different between diabetic patients and controls. Blood glucose fluctuations, mainly occurring in the postprandial state enhance atherosclerotic lesions in diabetic patients and in patients with impaired glucose tolerance. In addition to an optimized antidiabetic treatment, statin treatment is inhibitory concerning the development of atherosclerotic lesions.