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Sleep‐Disordered Breathing: Implications in Cerebrovascular Disease

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Stroke and sleep‐disordered breathing (SDB) are both common and are associated with significant morbidity and mortality. Several recent large epidemiologic studies have shown a strong association between these two disorders independent of known risk factors for stroke. This review will outline the scientific basis for this relationship and suggest SDB as a modifiable risk factor for stroke. Several studies have shown a characteristic circadian rhythmicity in stroke. The authors discussed the influence of normal sleep states as well as the effect of SDB on cerebral hemodynamics. The hemodynamic, metabolic, and hematologic changes during SDB in the form of decreased cerebral perfusion and increased coagulability are the possible pathogenetic mechanisms for stroke. There are accumulating lines of evidence that SDB may indeed cause diurnal hypertension. However, the increased risk of stroke in patients with SDB appears to be independent of coexisting hypertension, but the presence of hypertension would greatly increase the risk even further. Furthermore, several studies have documented high prevalence of sleep apnea in patients with transient ischemic attacks and stroke. SDB appears to contribute as a risk factor for stroke through hemodynamic and hematologic changes. Because of high prevalence of SDB in this population, patients with transient ischemic attacks and stroke should be screened for these disorders.
Title: Sleep‐Disordered Breathing: Implications in Cerebrovascular Disease
Description:
Stroke and sleep‐disordered breathing (SDB) are both common and are associated with significant morbidity and mortality.
Several recent large epidemiologic studies have shown a strong association between these two disorders independent of known risk factors for stroke.
This review will outline the scientific basis for this relationship and suggest SDB as a modifiable risk factor for stroke.
Several studies have shown a characteristic circadian rhythmicity in stroke.
The authors discussed the influence of normal sleep states as well as the effect of SDB on cerebral hemodynamics.
The hemodynamic, metabolic, and hematologic changes during SDB in the form of decreased cerebral perfusion and increased coagulability are the possible pathogenetic mechanisms for stroke.
There are accumulating lines of evidence that SDB may indeed cause diurnal hypertension.
However, the increased risk of stroke in patients with SDB appears to be independent of coexisting hypertension, but the presence of hypertension would greatly increase the risk even further.
Furthermore, several studies have documented high prevalence of sleep apnea in patients with transient ischemic attacks and stroke.
SDB appears to contribute as a risk factor for stroke through hemodynamic and hematologic changes.
Because of high prevalence of SDB in this population, patients with transient ischemic attacks and stroke should be screened for these disorders.

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