Hyperglycemia may lead to atherosclerosis by different pathogenic mechanisms. Nonenzymatic glycation and oxidation of LDL may increase its atherogenicity. Glycation may modify some arterial wall structural proteins. Increased blood glucose leads to hypertriglyceridemia which results in decrease of HDL-cholesterol level and in increase of atherogenic dense LDL particles. Hyperglycemia also adversely affects processes of platelet aggregation, hemocoagulation and fibrinolysis. It accelerates the development of diabetic nephropathy--a condition with a high prevalence of macrovascular diseases. Prospective epidemiologic studies have shown that diabetic patients in worse metabolic control had an increased cardiovascular morbidity and mortality. Therapeutic randomized studies in type 1 (DCCT) and type 2 (UKPDS) diabetic patients have shown that better diabetes control had a preventive effect against development of microvascular complications. The incidence of macrovascular complications both in type 1 diabetic patients on intensive insulin or sulfonylurea treatment has been decreased on the level of borderline statistical significance. Metformin lead to a significant decrease in myocardial infarction incidence in the subgroup of obese type 2 diabetic patients. In conclusion, maximal possible metabolic control of diabetes prevents the development of microvascular complication, but more impressive decrease in macrovascular disease incidence probably requires to affect another important risk factors for atherosclerosis, such as dyslipidemia and hypertension.

Keywords: Arteriosclerosis /complications/; Blood Glucose /physiology/; Causality; Diabetic Angiopathies /physiopathology/; Humans; Hyperglycemia /complications/