Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Tuesday, January 31, 2017

Sleep Apnea Device Improves Breathing, But Maybe Not Heart Risk - No benefit for endothelial function, blood pressure

So you can have your doctor decipher between these two.

Untreated Sleep Apnea Boosts Risk of Heart Disease, Stroke


Sleep Apnea Device Improves Breathing, But Maybe Not Heart Risk - No benefit for endothelial function, blood pressure

  • by
    Contributing Writer
  • This article is a collaboration between MedPage Today® and:
    Medpage Today

Action Points

  • Jaw repositioning with mandibular advancement therapy significantly improved sleep scores and symptoms, but the treatment did not improve key measures of heart disease risk among CPAP-intolerant patients with severe sleep apnea.
  • Note that these findings from a sham-controlled, randomized trial thus cast doubt on the belief that successful treatment of sleep apnea will reduce the cardiovascular risk associated with the condition.
Jaw repositioning with mandibular advancement therapy significantly improved sleep scores and symptoms, but the treatment did not improve key measures of heart disease risk among CPAP-intolerant patients with severe sleep apnea in a newly reported study.
Use of a mandibular advancement device (MAD) was associated with improvements in apnea-hypopnea index (AHI) scores, micro-arousal index scores and snoring, daytime fatigue and sleepiness in the study, but the treatment did not appear to improve endothelial function or lower blood pressure.
These findings from a sham-controlled, randomized trial thus cast doubt on the belief that successful treatment of sleep apnea will reduce the cardiovascular risk associated with the condition.
The multicenter study is among the first to examine the impact of MAD therapy on cardiovascular risk factors in patients with obstructive sleep apnea (OSA), wrote study leader Frederic Gagnadoux, MD, of the University Hospital of Angers in France, and colleagues.
Their research was published online Friday in the American Journal of Respiratory and Critical Care Medicine.
Endothelial dysfunction, which is a major predictor of atherosclerosis, as well as myocardial infarction (MI) and stroke risk, can be caused or exacerbated by OSA. Untreated sleep apnea is an independent risk factor for MI and stroke, and evidence has suggested that successful treatment of OSA could lower this risk.
Continuous positive airway pressure (CPAP) is considered the front-line treatment for OSA, but patient compliance remains a challenge. Studies suggest that 29% to 84% of patients on CPAP are nonadherent, meaning they use their CPAP device for 4 hours or less each night.
Mandibular advancement therapy has emerged as the main alternative to CPAP. The oral devices open the airways by moving the lower jaw forward.
In the newly reported study, Gagnadoux and colleagues assessed the impact of MAD therapy on key measures of sleep and cardiovascular risk in patients with severe sleep apnea and no known cardiovascular disease.
A total of 150 patients with severe sleep apnea (mean apnea-hypopnea index [AHI] score of 41), but only moderate daytime sleepiness, were randomized to either MAD therapy (n=75) or sham device therapy (n=75) for 2 months.
In the effective MAD group, mean mandibular advancement was 7.9 (1.5) mm, corresponding to an average of 106% of maximum voluntary advancement. Eleven effective MAD patients and 10 sham treatment patients dropped out of the study.
The primary study outcome was change in the reactive hyperemia index (RHI), which is a validated measurement of endothelial function.
Among the main findings:
  • In the intention-to-treat analysis, RHI decreased by 0.03 points in the effective MAD group (P=0.95) and by 0.13 points (P=0.13) in the sham device group.
  • After adjustment for baseline values, age, gender, BMI, AHI, and smoking habits, the difference in RHI outcome between effective MAD and sham device groups was not statistically significant (adjusted intergroup difference 0.15, 95% CI -0.08 to 0.38; P=0.20).
  • In the overall population, change in RHI from baseline to follow-up was not correlated with either change in AHI (r=-0.08; P=0.41) or change in 3% oxygen desaturation index.
  • In a post-hoc analysis in which the median value of baseline RHI was used to classify patients into low and high RHI groups, a significant improvement in RHI was observed in the low RHI group with both effective MAD and sham device, with no significant adjusted intergroup difference between the two treatments.
The mean objective compliance with effective MAD was 6.7 hours per night, which corresponded to approximately 90% of reported sleep duration.
"Interestingly, we found that reported and objective compliance were highly correlated in the effective MAD group but not in the sham device group, which emphasizes the importance of objective compliance measurement in sham-controlled trials of MAD therapy," the researchers wrote.
They further noted that several recent studies have shown little or no improvement in cardiovascular outcomes associated with treatment for OSA. Research published last year in the New England Journal of Medicine showed no evidence of a reduction in such outcomes among patients with moderate to severe OSA treated with CPAP.
The researchers added that the exclusion of patients with cardiovascular disease may have been a limitation of their study.
"Although our post hoc analysis showed no intergroup differences in RHI outcome in patients with low baseline RHI, further studies are required to determine whether MAD therapy for OSA can improve endothelial function in patients with overt cardiovascular disease and metabolic disorders who exhibit more severe endothelial dysfunction at baseline," they wrote.
Funding for this research was provided by the French Ministry of Health.
  • Reviewed by Robert Jasmer, MD Associate Clinical Professor of Medicine, University of California, San Francisco and Dorothy Caputo, MA, BSN, RN, Nurse Planner
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