CMS to Review NCD for CPAP Therapy; Study Links Obstructive Sleep Apnea to Higher Risk of Stroke
Last week, the Centers for Medicare & Medicaid Services (CMS) announced that it plans to review the national coverage determination (NCD) for CPAP therapy.
CMS received a formal request from the American Academy of Otolaryngology-Head and Neck Surgery to modify the decision to include the use of portable multi-channel home sleep testing devices as an alternative to facility-based polysomnography in the evaluation of OSA.
The current national coverage policy specifies that only polysomnography done in a facility-based sleep study laboratory can be used to identify patients with OSA requiring CPAP.
In addition, CMS has received an incomplete request from a Medicare beneficiary, numerous informal requests from stakeholders, and interest from Medicare contractors concerning the criteria for determining the Apnea-Hypopnea Index (AHI). It has been suggested by some that the requirement be changed to "the AHI is equal to the average number of episodes of apnea and hypopnea per hour and must be based on a minimum of two hours of sleep or less, if the actual number of AHI episodes recorded is 30 or more in less than two hours, recorded by polysomnography using actual recorded hours of sleep (i.e., the AHI may not be extrapolated or projected)."
CMS also stated that it is aware of recently published research suggesting a benefit for the use of CPAP without prior sleep testing in selected populations (trial of CPAP).
The scope of the reconsideration will include all aspects of the NCD.
The public cmment priod is open until April 13, 2007. MS considers all public comments, and is particularly interested in clinical studies and other scientific information relevant to the technology under review. Instructions on submitting comments can be found at http://www.cms.hhs.gov/InfoExchange/02_publiccomments.asp#TopOfPage.
Study Links Obstructive Sleep Apnea to Higher Risk of Stroke
Patients with moderate to severe sleep apnea who have significantly higher serum levels of inflammatory markers that serve as precursors to coronary artery disease, as well as lesions associated with silent brain infarction, have an elevated risk of stroke, according to a group of 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.
In an editorial on this research in the same issue of the journal, Brian J. Murray, M.D., of Sunnybrook Health Sciences Center and the University of Toronto, Canada, wrote:
"The article by Drs. Minoguchi and colleagues provides further important observations on the association between stroke and obstructive sleep apnea, with significant public health implications. The authors, using brain magnetic resonance imaging, demonstrate that patients with obstructive sleep apnea have a higher incidence of so-called silent brain infarction (i.e., those devoid of obvious clinical symptoms leading to self-detection or identification by physician examination). 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."
"Clinically identified stroke represents the tip of the iceberg in terms of cerebral vascular disease by a least an order of magnitude," he continued. "Small, but strategically placed lesions in the brain can produce clinically obvious stroke. For example, a lesion of only a few millimeters in diameter that is located in the posterior limb of the inner capsule may leave a patient with devastating hemiplegia (paralysis affecting one side of the body), that would be obvious clinically. The need to prevent these types of strokes from developing is obvious."
"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."
This article originally appeared in the March 2007 issue of HME Business.