Cerebral hemodynamics and systemic endothelial function are impaired in metabolic diseases

Metabolic diseases are associated with an increased risk of cerebrovascular and cardiovascular diseases. Several mechanisms could contribute to this increased risk of vascular events; among them the role of an impairment in vascular reactivity has been considered. Cerebral vasomotor reactivity (VMR) represents the capability of cerebral vessels to modify their caliber in response to a stimulus. Impaired VMR is associated with an increased risk of ischemic events in subjects with carotid disease. Endothelial dysfunction is considered an important pathogenic factor for atherosclerosis and can be non-invasively assessed by flow-mediated vasodilation (FMD) evaluation. We found that VMR and FMD did not correlate in subjects without a history of vascular diseases probably due to physiological differences between cerebral and peripheral vascular districts and vasodilatatory stimulus used. We also found a slight still significant impairment in cerebral hemodynamics and systemic endothelial function in patients with type-2 diabetes with optimal metabolic control and preserved autonomic balance, but with clinical features of metabolic syndrome. This change in vasomotor function could be responsible for the increased risk of stroke and silent cerebral ischemia observed in patients with diabetes mellitus. Finally, acute hyperglycemia was found to reduce VMR both in patients with metabolic syndrome and in controls. Glycemic variability, increased in a condition of insulin resistance (i.e. metabolic syndrome), appeared to be the major predictor of this VMR reduction induced by hyperglycemia, possibly representing the earliest cause of cerebrovascular damage in diabetes.