Sleep Apnea Diagnosis Plays Role in Stroke Prevention

New information shows the importance of being diagnosed with sleep apnea and how this can help stroke prevention.

Improvements to the diagnosis and screening of sleep apnea are critical to stroke prevention, according to new stroke care guidelines released October 2 at the Canadian Stroke Congress.

Obstructive sleep apnea, a disorder where the flow of air to the brain pauses or decreases during sleep, is both a risk factor for stroke and a complication following stroke, according to the Canadian Best Practice Recommendations for Stroke Care.

Among the general population sleep apnea increases the likelihood of having a stroke, even after controlling for other stroke risk factors, such as high blood pressure and diabetes, researchers say.

At absolute minimum, four per cent of men and two per cent of women have serious sleep apnea, says Dr. Brian Murray, an associate professor of neurology and sleep medicine at the University of Toronto. Dr. Murray adds that clinically significant forms of the disorder affect more than 10 per cent of the population.

"There are ways to prevent sleep apnea from occurring," says Dr. Murray. "Keep your body weight low as obesity is a major contributor to sleep apnea; avoid medications and substances that relax the airways and cause snoring, such as sedatives and alcohol; and sleeping on your side can minimize sleep disordered breathing."

Signs of sleep apnea include significant snoring, pauses in breathing during sleep and daytime fatigue despite adequate sleep time. If any of these symptoms are present, says Dr. Murray, you should be evaluated by your doctor to determine next steps.

Obstructive sleep apnea is common after stroke. According to the updated best practice recommendations, at least 60 per cent of stroke patients experience sleep apnea. The new recommendations call for more screening of stroke patients who say they experience snoring, fragmented sleep or fatigue. Although, in many cases with stroke patients, daytime fatigue does not appear as a symptom, says Dr. Murray.

It is crucial for stroke patients to be screened for sleep apnea because untreated sleep apnea increases the chances of a second stroke and small studies have found that stroke patients with sleep apnea tended to have worse rehabilitation outcomes, says Dr. Murray.

The best practices also describe "higher rates of mortality and other complications in patients with stroke and untreated obstructive sleep apnea."

"This innovative Canadian research continues to show that there is more to learn about rehabilitation and recovery following stroke," says Ian Joiner, director of stroke for the Heart and Stroke Foundation. "Reflecting these advances in tools such as the Best Practices Recommendations for Stroke Care will help improve outcomes for Canadians."

The new recommendations are the fourth update to the Canadian Best Practice Recommendations for Stroke Care and this is the first time the recommendations have included a section on sleep apnea. The best practices were first released in 2006 to improve stroke care for Canadians living with stroke and future stroke patients. They are updated every two years.

"The new recommendations take stroke care a step further," says Dr. Michael Hill, Canadian Stroke Congress Co-Chair. "Stroke care is not only about giving the best possible treatment to patients. It is also about preventing new and recurrent strokes."

The Canadian Stroke Congress is a joint initiative of the Canadian Stroke Network, Heart and Stroke Foundation of Canada and the Canadian Stroke Consortium.

Read more here

Sleep Apnea and Risk of Deep Vein Thrombosis: A Non-randomized, Pair-matched Cohort Study

Sleep apnea is a risk factor for blood clots. Consider this for prevention and to avoid recurrence! JR

Sleep Apnea and Risk of Deep Vein Thrombosis: A Non-randomized, Pair-matched Cohort Study

Background

Patients with sleep apnea have been reported to be associated with increased prevalence of deep vein thrombosis (DVT) in some papers, which were criticized for either a small sample size or lack of a prospective control. Our study strived to explore the relationship of sleep apnea and the subsequent development of DVT using a nationwide, population-based database.

Methods

From 2000 to 2007, we identified a study cohort consisting of newly diagnosed sleep apnea cases in the National Health Insurance Research Database. A control cohort without sleep apnea, matched for age, sex, comorbidities, major operation, and fractures, was selected for comparison. The 2 cohorts were followed-up, and we observed the occurrence of DVT by registry of DVT diagnosis.

Results

Of the 10,185 sampled patients (5680 sleep apnea patients vs. 4505 control), 40 (0.39%) cases developed DVT during a mean follow-up period of 3.56 years, including 30 (0.53%) from the sleep apnea cohort and 10 (0.22 %) from the control group. Subjects with sleep apnea experienced a 3.113-fold (95% confidence interval, 1.516-6.390; P=.002) increase in incident DVT, which was independent of age, sex, and comorbidities. Kaplan-Meier analysis also revealed the tendency of sleep apnea patients toward DVT development (log-rank test, P=.001). The risk of DVT was even higher in sleep apnea cases who needed continuous positive airway pressure treatment (hazard ratio 9.575; 95% confidence interval, 3.181-28.818; P <.001).

Conclusion

Sleep apnea may be an independent risk factor for DVT.

Discussion 

In our current study, we identified SA as an independent risk factor for future development of DVT using a large-scale nationwide database, which supports the concept that SA may contribute to the formation or progression of thrombosis in venous circulation. Additionally, the adjusted risks of DVT in SA patients who needed and did not need CPAP treatment were 9.575 (95% CI, 3.181-28.818; P <.001) and 2.751 (95% CI, 1.317-5.747; P=.007), respectively, suggesting increased risk with increasing severity of sleep apnea.

The mechanism underlying the link of SA and DVT may lie in intermittent nocturnal hypoxia and chronic systemic inflammation, which are characteristic of SA, especially OSA.¹⁵ Short-term hypoxia alone may not induce significant hemostatic derangement in healthy subjects,¹⁶, ¹⁷, ¹⁸ but may provoke coagulation activation and elevation of inflammatory cytokines in subjects with chronic inflammatory lung diseases,¹⁹, ²⁰ suggesting the interplay between inflammation and coagulation. For patients with SA, chronic intermittent hypoxia as a result of repetitive apnea/hypopnea events produces reactive oxygen species and activates proinflammatory transcription factor nuclear factor κB and hypoxia-inducible transcription factor-1, thereby increasing the production of inflammatory cytokines, such as interleukin-6 and tumor necrosis factor-α.²¹, ²², ²³, ²⁴ On the action of these inflammatory cytokines, vascular endothelial cells increase expression and release of tissue factor, triggering the extrinsic coagulation pathway.²⁵ Platelet aggregation also is enhanced owing to the release of von Willebrand factor by endothelium.²⁶, ²⁷ Endothelial function is further impaired by reactive oxygen species and inflammatory mediators, which reduce nitric oxide availability and repair capacity.²⁸ On the other hand, these inflammatory mediators also downregulate activated protein C and upregulate plasminogen activator inhibitor, thus suppressing fibrinolysis.²⁵, ²⁹ All the aforementioned factors favor thrombosis formation in patients with SA.

http://www.amjmed.com/article/S0002-9343(11)00569-9/fulltext