title: [Mechanisms of macrovascular involvement in diabetic subjects].
abstract: Diabetic macroangiopathy is often viewed as an accelerated and aggravated form of atherosclerosis. Several biological disturbances that are associated with diabetes partially account for a possible aggravation of atherosclerosis. Such are disorders of blood lipids (increased triglyceride concentration, modifications of low density lipoproteins) of haemostatis (increased platelet activity, decreased fibrinolytic activity) or of arterial vasomotility. Yet, many uncertainties and inconsistencies still obfuscate the links between diabetes and atherosclerosis, which remain hypothetical, and debatable. Clinical experience and all clinical epidemiological studies show that the incidence and severity of ischaemic arterial diseases (coronary heart disease, lower limb ischaemia, cerebral ischaemic events) are increased in diabetic individuals. However, intermediates other than worsened atherosclerosis may account for these associations. For instance, several anatomical epidemiological studies, based on routine autopsies, have note consistently found that atherosclerotic lesions (plaques) are larger and more extensive in diabetic than in non-diabetic individuals. The basic mechanisms of diabetic macroangiopathy could therefore be not as closely related to atherosclerosis as is usually thought. Among the non-atherosclerotic lesions that could explain the increased arterial risk in diabetic patients, the best documented and most plausible is arteriosclerosis--a pure sclerosis of the arterial wall (without lipid deposition) which, in its advanced forms, can compromise tissue vascularization. Arteriosclerosis is considered as a normal consequence of arterial ageing which would be accelerated in diabetes. Chronic hyperglycaemia is and independent and influent marker of arterial risk in diabetic patients. It could stimulate arterial sclerosis by enhancing non-enzymatic glycation of various components of the arterial matrix, through formation of advanced glycation end-products (AGEs).(ABSTRACT TRUNCATED AT 250 WORDS)
authors: Service de médecine vasculaire, Hôpital Broussais, Paris, France.
authors: L
authors: L
authors: Capron
mesh_terms: D001161:Arteriosclerosis / Q000209:etiology; D003925:Diabetic Angiopathies / Q000503:physiopathology*; D006801:Humans; D007511:Ischemia / Q000209:etiology
vernacular_title: Mécanismes de l'atteinte macrovasculaire du sujet diabétique.