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J Appl Physiol 105: 1852-1857, 2008. First published October 16, 2008; doi:10.1152/japplphysiol.90900.2008
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Impaired cerebral autoregulation in obstructive sleep apnea

¹Yale Center for Sleep Medicine, Department of Medicine, ²Department of Neurology, and ³John B. Pierce Foundation Laboratory, Yale University School of Medicine New Haven, Connecticut

Submitted 14 July 2008 ; accepted in final form 8 October 2008

Obstructive sleep apnea (OSA) increases the risk of stroke independent of known vascular and metabolic risk factors. Although patients with OSA have higher prevalence of hypertension and evidence of hypercoagulability, the mechanism of this increased risk is unknown. Obstructive apnea events are associated with surges in blood pressure, hypercapnia, and fluctuations in cerebral blood flow. These perturbations can adversely affect the cerebral circulation. We hypothesized that patients with OSA have impaired cerebral autoregulation, which may contribute to the increased risk of cerebral ischemia and stroke. We examined cerebral autoregulation in patients with and without OSA by measuring cerebral artery blood flow velocity (CBFV) by using transcranial Doppler ultrasound and arterial blood pressure using finger pulse photoplethysmography during orthostatic hypotension and recovery as well as during 5% CO₂ inhalation. Cerebral vascular conductance and reactivity were determined. Forty-eight subjects, 26 controls (age 41.0±2.3 yr) and 22 OSA (age 46.8±2.3 yr) free of cerebrovascular and active coronary artery disease participated in this study. OSA patients had a mean apnea-hypopnea index of 78.4±7.1 vs. 1.8±0.3 events/h in controls. The oxygen saturation during sleep was significantly lower in the OSA group (78±2%) vs. 91±1% in controls. The dynamic vascular analysis showed mean CBFV was significantly lower in OSA patients compared with controls (48±3 vs. 55±2 cm/s; P <0.05, respectively). The OSA group had a lower rate of recovery of cerebrovascular conductance for a given drop in blood pressure compared with controls (0.06±0.02 vs. 0.20±0.06 cm·s^–2·mmHg^–1; P <0.05). There was no difference in cerebrovascular vasodilatation in response to CO₂. The findings showed that patients with OSA have decreased CBFV at baseline and delayed cerebrovascular compensatory response to changes in blood pressure but not to CO₂. These perturbations may increase the risk of cerebral ischemia during obstructive apnea.

stroke; cerebral blood flow; orthostatic hypotension; hypercapnia

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