Sleep-Disordered Breathing: Implications in Cerebrovascular Disease

Vahid Mohsenin, MD

Disclosures

Prev Cardiol. 2003;6(3) 

In This Article

Increased Prevalence of Sleep Apnea in Stroke

The strong association between sleep apnea and stroke is further supported by a number of studies examining the prevalence of sleep apnea in patients with recent stroke or TIAs. Mohsenin and Valor[17] demonstrated a high prevalence of OSA (80%) in a group of patients recovering from hemispheric stroke without a previous history of sleep apnea compared with age-matched patients with a similar frequency of hypertension and smoking without stroke. A subsequent study by Dyken et al.[20] showed a similar result where 77% of men and 64% of women with stroke had OSA compared with age-matched controls with a prevalence of sleep apnea of 23% (p=0.01) in males and 14% (p=0.01) in females without stroke. In a larger study on 128 patients with TIA and stroke, Bassetti and Aldrich[21] found OSA in 62.5% of the patients compared to 12.5% in the normal control group. They observed a high frequency of OSA in patients with TIA suggesting the preexisting OSA prior to cerebrovascular events rather than as a consequence of it. This latter observation strongly supports the role of sleep apnea as an independent risk factor for cerebrovascular disease ( Table IV ).

Regardless of whether sleep apnea precedes or follows a stroke, it is associated with poor functional outcome in survivors and higher mortality after 1 year compared with those patients with stroke but without sleep apnea.[19] The high prevalence of sleep apnea and poor functional outcome in stroke should prompt the physicians to evaluate the patients for underlying SDB.

There are several pathophysiologic mechanisms that may underlie the diurnal development of stroke. The alteration of cerebral hemodynamics, hypoxemia, and dysfunction of cerebral autoregulation appear to be the main mechanisms of cerebral ischemia in patients with SDB.[41,42] Pronounced cerebral blood flow velocity changes during apneic episodes and the concomitant alterations of vessel wall tension might lead to chronic strain on the brain vessels and formation of atherosclerosis.[51] Another important factor that increases the risk of thromboembolic stroke is enhanced platelet aggregability during sleep and immediately after rising. Platelets from normal individuals show increased responsiveness to epinephrine and adenosine diphosphate with enhanced aggregability between 6 a.m. and 9 a.m.[52] Both spontaneous and post-activation platelet aggregation are significantly enhanced in patients with severe OSA during the night compared with normal individuals.[53] The abnormality reverses with treatment of sleep apnea with one night treatment with continuous positive airway pressure.[53] Likewise, increased platelet aggregability during the early morning hours has been shown to increase the risk of myocardial infarction and sudden death.[52,54] The elevated plasma fibrinogen level is believed to be associated with an increased risk of stroke and other vascular events.[55] Plasma fibrinogen has been shown to be elevated in patients with stroke and sleep apnea.[56] In the same study, the investigators found a correlation between the severity of coexisting sleep apnea and fibrinogen level in patients with stroke. Taken together, the combination of cerebral hypoperfusion and hypercoagulability in sleep apnea disorder is possibly the main pathophysiologic mechanism for increased risk of stroke in this population.

The relationship between the severity of sleep apnea and the development of hypertension as indicated by the respiratory disturbance index (RDI) and odds ratios. Data derived from N Engl J Med. 2000;342;1378-1384.[56]

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