Abstract

Cardiovascular autonomic neuropathy (CAN) is the most frequent complication of diabetes and one of the major components of diabetic dysautonomia. CAN occurs early in the course of diabetes, and several pathophysiological factors are involved. It is associated with an impairment in cardiovascular prognosis. Cardiac autonomic function should be assessed in most diabetic patients as it contributes to the evaluation of cardiovascular risk. The presence of CAN should lead to further awareness of possible complications and optimal control of risk factors. Pathophysiology As for peripheral neuropathy, both metabolic and vascular mechanisms are probably involved in the pathogenesis of diabetic CAN. Metabolic changes consecutive to chronic hyperglycaemia include polyol pathway activation, oxidative stress, accumulation of advanced glycated endproducts, proteine kinase C activation and impairment of essential fatty acid metabolism. As for the role of microvascular factors, reduced endoneurial blood flow and oxygen tension, endothelial dysfunction, increased capillary permeability that may induce endoneurial oedema and rheological changes have been shown in experimental diabetes. In addition, oxidative stress may be the link between the metabolic and vascular hypotheses.1 Malnutrition may also be implicated, as suggested in Asian populations.2 Carbohydrate intake may also impair vagosympathetic balance.3 Finally, in patients with type 1 diabetes, several studies stand in favour of immunological factors.4

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