Patients with sleep apnea having significantly higher serum levels of inflammatory markers, as well as lesions associated with silent brain infarction, have an elevated risk of stroke, according to Japanese medical researchers. The results appear in the second issue for March 2007 of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society.
Kenji Minoguchi, M.D., Ph.D., of Showa University School of Medicine in Tokyo, and nine associates studied silent brain infarction, brain tissue death from lack of blood supply, in 50 male patients with obstructive sleep apnea (OSA). The researchers also examined the effects of three months of treatment with nasal continuous positive airway pressure (nCPAP) on serum inflammatory marker levels in 24 male patients who had moderate to severe OSA.According to the authors, the occurrence of stroke in patients with OSA is likely preceded by subclinical cerebrovascular disease, or silent brain infarction, which is detectable with brain magnetic resonance imaging (MRI). The lesions identified as silent brain infarction were either wedge-shaped or round and showed up in brain white matter on MRI scans.
'The percentage of silent brain infarction in patients with moderate to severe OSA at 25 percent was higher than that for obese control subjects at 6.7 percent, or even patients with mild OSA who had 7.7 percent,' said Dr. Minoguchi.
The investigators noted that cardiovascular disease is commonly characterized by ongoing inflammatory responses that can enhance platelet activation and increase the prevalence of silent brain infarction. Platelets are small, colorless, irregular blood cells that promote blood clotting. Two important proteins called soluble C40 ligand and soluble P-selectin are markers of platelet activation and appear to forecast future cerebrovascular events.
The researchers found that use of nCPAP, a treatment designed to reduce the number of episodes of breathing stoppage associated with sleep apnea, significantly lowered serum levels of C-reactive protein and the levels of the two platelet-activating proteins, all associated with cerebrovascular disease.
'As a result, nCPAP may be an important treatment intervention for decreasing the cerebrovascular risk in this susceptible population of obstructive sleep apnea patients,' said Dr. Minoguchi.
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The well-designed and executed study excluded patients with known risk-factor co-morbidities, thereby establishing the relationship between brain infarcts and obstructive sleep apnea itself. The significance of this finding pertains not only to stroke pathophysiology, but to dementia as well.'
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'Silent infarction identified on routine neuroimaging studies, on the other hand, may occur in areas of the brain that can only be detected clinically by detailed neurophysical assessment, or perhaps not at all with currently available tests. It is hard to believe, however, that loss of brain tissue should go without consequences. The brain may reorganize functional networks to adapt to lesions and recover function. But with each subsequent stroke, the capacity to do so is diminished. This at least partially accounts for the finding that patients with stroke and obstructive sleep apnea tend to have a longer rehabilitation stay and worse functional recovery than those patients without obstructive sleep apnea.'
Dr. Murray concluded: 'Treating obstructive sleep apnea with continuous positive airway pressure appears to reduce the incidence of clinically obvious stroke. This study provides a novel potential mechanism for this finding. In particular, those patients with silent infarcts and sleep apnea had elevated markers of platelet activation, such as soluble CD40 ligand and soluble P-selectin. Furthermore, continuous positive airway pressure therapy for 3 months can lower such markers in this population, thereby providing a link between the white matter lesions and their pathogenesis. Treatment with continuous positive airway pressure may therefore lead to a reduced incidence of subsequent ischemic brain lesions.'
Source-Eurekalert
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