Obstructive Sleep Apnea, Stroke Risk Due to Impaired Cerebral Autoregulation
Obstructive Sleep Apnea, Stroke Risk Due to Impaired Cerebral Autoregulation
Abstract & Commentary
By Alan Z. Segal, MD, Associate Professor of Clinical Neurology, Weill Cornell Medical College. Dr. Segal reports no financial relationships relevant to this field of study.
Synopsis: Obstructive sleep apnea causes a variety of alterations in the control of cerebral blood flow, contributing to the risk for stroke.
Source: Nasr N, et al. Cerebral autoregulation in patients with obstructive sleep apnea syndrome during wakefulness. European J Neurol 2009;16:386-391.
Obstructive sleep apnea (OSA) is a known independent risk factor for stroke. OSA may promote hypertension, cause increased platelet aggregation, impair endothelial cell function, and induce cardiac arrhythmias. During an episode of OSA, cerebral blood flow (CBF) is known to rise initially, but then falls below baseline levels as respirations are resumed. While the CBF rise is clearly related to vasodilation resulting from increased in C02, the late fall is less well understood. Intracranial pressure (ICP) is also known to rise during episodes of OSA due to alterations in venous return. In the setting of elevated ICP, cerebral perfusion pressure can be compromised, especially if blood pressure fluctuates widely. The process of cerebral autoregulation under normal circumstances keeps blood flow constant, protecting the brain from these blood pressure variations.
Daytime studies of patients with known OSA have additionally shown them to have impaired cerebral vasomotor reactivity to C02 challenge. CBF, as demonstrated by transcranial Doppler (TCD) and Xenon CT, has been shown to show impaired vasodilation in OSA patients compared to controls in response to C02 inhalation. It has also been shown that OSA patients have more impaired cerebral vasoreactivity in the morning, after a full night of chemoreceptor exposure to elevated C02 levels, than when tested in the evening.
In the current study, Nasr and colleagues compared 11 OSA patients to nine controls matched for age, body mass index, and blood pressure. Of note, seven of the control patients had snoring, but were not diagnosed with OSA. The study was done in the morning following an all-night polysomnogram. CBF was measured for 15 minutes during wakefulness using flow velocities by TCD mounted on a head frame. An autoregulatory index (Mx) was calculated, based on continuous CBF and systemic arterial blood pressure (ABP) readings. An Mx close to 1 implies sustained changes in CBF as a function of ABP (poor autoregulation), while an Mx of 0 implies no significant effect of ABP on CBF (intact autoregulation). Higher Mx values are therefore abnormal, with Mx < 0.3 consistent with a normal range of autoregulation. Subject patients had moderate to severe OSA, with an Apnea/Hypopnea Index (AHI) of 22.7 events per hour.
OSA patients were found to have an Mx of 0.4 compared with 0.2 among controls (p = 0.009). There was a direct correlation between the severity of Mx and the AHI (p = 0.003).
Commentary
As the authors note, prior data has suggested that OSA patients have impaired "chemoregulation" (poor reactivity to hypoxia and hypercapnia). This study now indicates that, in addition, they have impaired "mechanoregulation," with impairments in the relationship between ABP and CBF. Although the precise relationship between stroke and OSA is not well understood, these factors, taken together, imply a dramatic cerebrovascular deficiency in OSA patients. While only a small subset of strokes occur on a "low flow" basis, most being embolic or atherothrombotic, it is clear that OSA patients have little reserve to sustain any cerebrovascular insult. It has been previously shown that impaired cerebrovascular reactivity in OSA patients could be improved with CPAP ventilation. It will be a subject for future studies to determine if CPAP can also correct the autoregulatory failure that was demonstrated by these data in patients with OSA.
Obstructive sleep apnea causes a variety of alterations in the control of cerebral blood flow, contributing to the risk for stroke.Subscribe Now for Access
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