Macroangiopathy in diabetes mellitus

Abstract

In patients with diabetic angiopathy until today, no histological nor histochemical evidence has been found to define a specific type of diabetic arteriopathy. Consequently, diabetic arteriosclerosis is considered as a more serious form of atherosclerosis characterized by its premature onset. Hyperglycemia is assumed to be the crucial pathophysiological cause of the development of macro- and microangiopathy in diabetes mellitus. Apparently, hyperglycemia has a direct toxic influence on the arterial wall by increased accumulation of irreversible glycosylation end products, and secondly, it provokes endothelial dysfunction. The frequently occurring ulcerations of the diabetic foot are primarily caused by neuropathy; however, peripheral vascular disease (PVD) is often associated. The risk of suffering from PVD in diabetic patients is approximately four-fold. Usually, the distal segments of the lower leg arteries are concerned, where reconstructive intervention is complicated or even impossible. Diabetes is considered as an independent risk factor for cardio- and cerebrovascular diseases with almost twice as high rates for recurrent myocardial infarction, and a 3.7 fold higher relative risk for stroke in diabetic, compared to non-diabetic patients. This review looks at the correlations between hyperglycemia and arteriosclerosis, but also the treatment options in diabetic patients. Until now, there is no evidence for an association between an optimal control of blood glucose levels and a decrease in the risk of coronary heart disease, stroke, or PVD. In contrast, an attenuation of microvascular lesions is achieved by stringent control of blood glucose levels. Thus, although the development of macroangiopathy may not be significantly influenced, the conduction of a stringent control regimen of plasmatic glucose levels is advisable.