About The Practice

Serving Texas Children's Concerns about Neurology, Epilepsy Developmental & Sleep Disorders. Advanced spasticity management.

The Houston Area ( Bellaire Katy Sugar Land Richmond Missouri City Cypress The Woodlands Lake Jackson)

The Greater San Antonio Area ( New Braunfels Seguin Central Texas)

Dr Joshua Rotenberg. Board Certified in Neurology with Special Qualifications in Child Neurology.

Dr. Rotenberg has added subspecialty board certification in epilepsy AND sleep disorders (American Board of Psychiatry & Neurology-Child Neurology).

Member - American Epilepsy Society

Member - American Academy of Cerebral Palsy & Developmental Medicine

Texas Medical & Sleep Specialists - Children & Adults Welcome. WWW.TXMSS.COM 713-464-4107




Thursday, August 09, 2012

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,161718 but may provoke coagulation activation and elevation of inflammatory cytokines in subjects with chronic inflammatory lung diseases,1920 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.21222324 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.2627 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.2529 All the aforementioned factors favor thrombosis formation in patients with SA.


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