Decreased cerebral vasomotor reactivity in patients with obstructive sleep apnea syndrome

Abstract

ObjectiveIn obstructive sleep apnea syndrome (OSAS), any of the activated neural, vascular, hemodynamic, metabolic, inflammatory, and thrombotic mechanisms may be related to increased cerebrovascular disease and risk of death; however, the possible pathophysiological process between obstructive sleep apnea syndrome and stroke has not been clearly explained. We hypothesize that alterations in vasomotor reactivity in patients may be responsible for their altered cerebral blood flow, and may contribute to the increased risk of ischemic stroke. MethodsA total of 30 untreated patients with severe obstructive sleep apnea and 26 control subjects were included in the study. The mean blood flow velocity and breath holding index were measured in middle cerebral artery bilaterally in both patient and control groups by using transcranial Doppler ultrasound. We compared the values between two groups. ResultsThe mean blood flow velocity and breath holding indexes were significantly decreased in the patient group when compared with the control group. There were no correlations between cerebral hemodynamic parameters and polysomnographic findings in patients. ConclusionOur findings suggest that there was a deteriorated vasodilator response to hypercapnia in patients with OSAS. This deterioration may stem from chemoreceptors or endothelial damages that lead to vascular relaxation and vasodilatation in cerebrovascular circulation. This impaired cerebral vascular regulation may contribute to the increased risk of stroke in patients with OSAS.