Despite the widespread belief that obstructive sleep apnea (OSA) causes cardiovascular events like strokes and heart attacks, there is actually no good evidence that treating OSA lowers the risk of such cardiovascular outcomes.
Observational data showing that OSA is associated with cardiovascular outcomes like atrial fibrillation (Afib), stroke, cardiovascular death, and myocardial infarction (MI) have been utilized by the sleep apnea academic-industrial complex (in ways very similar to the ) to market the need for sleep apnea diagnosis and treatment.
However, as we saw in the omega-fatty acid world, causality can only be proven with a randomized trial of effective therapy of the disease (given that there is no way to randomize patients to having OSA or not having it.) The most widely prescribed and effective therapy for OSA is continuous positive airway pressure (CPAP).
Healthy user bias is a major confounder of most CPAP and all observational studies as noted at :
Observational studies have demonstrated that among patients with OSA, CPAP is associated with a lower incidence of fatal and nonfatal cardiovascular events. A recent meta-analysis of observational studies corroborated these findings, noting a hazard ratio (HR) of 0.37 (95% CI, 0.16 to 0.54) for cardiovascular mortality in CPAP treated patients compared to untreated patients. However, these studies are marred by their lack of randomization. Therefore, the patients compliant with CPAP may have enjoyed their cardiovascular benefit from any number of downstream effects of their general aptitude towards making healthy lifestyle choices (the healthy user bias) rather than from CPAP alone.
A for OSA, from the Agency for Healthcare Research and Quality (AHRQ) of the U.S. Department of Health and Human Services, outlines some of the major unresolved questions:
Obstructive sleep apnea (OSA) is a disorder characterized by periods of airflow cessation (apnea) or reduced airflow (hypopnea) during sleep. The diagnosis and severity of OSA, and response to therapy, are typically assessed using the apnea-hypopnea index (AHI). However, no standard definition of this measure exists, and whether AHI (and associated measures) are valid surrogate measure of clinical outcomes is unknown. OSA is commonly treated with the use of continuous positive airway pressure (CPAP) devices during sleep. The efficacy of CPAP, including for Food and Drug Administration (FDA) clearance/approval, has been based on changes in AHI, but the long-term effect of CPAP on clinical outcomes and the role of disease severity (as measured by AHI) or sleepiness symptoms on the putative effect of CPAP are unclear.
After looking at 47 studies on this question, the concluded that there was no evidence to support the idea that CPAP treatment lowers "clinically important outcomes."
And there isn't evidence that CPAP treatment of OSA influences individual aspects of cardiovascular disease, including Afib, which totally counters the mantra that sleep centers and Afib experts have been spouting for years.
In fact, the two randomized controlled trials (RCTs) that report Afib came to opposite conclusions, with one showing it lowered risk and the other one showing that CPAP raised the risk of developing Afib!
Pretty much everything you thought would be helped by CPAP treatment has not been proven, says the AHRQ:
Regarding other assessed outcomes, CPAP does not affect the risk of driving accidents or the risk of incident diabetes (both low SoE [standard of evidence]). CPAP does not result in clinically significant changes in depression or anxiety scores, executive cognitive function measures, or nonspecific quality of life measures (all low SoE). There is insufficient evidence regarding the effect of CPAP on incident hypertension, functional status measures, male or female sexual function, or days of work missed.
There is a clear and obvious way to prove that diagnosing OSA matters (beyond improving daytime sleep and snoring) and that OSA is a life-threatening disease. That is to randomize patients diagnosed with OSA to treatment with effective therapy (i.e., CPAP), and several of these have been performed. Unfortunately for the OSA business, the results of these RCTs do not show a benefit of therapy, consequently sleep experts/centers and businesses that sell OSA diagnostic and therapeutic equipment tend to gloss over, dismiss, or ignore these data.
Clinical Correlations does a good job of summarizing the methods and outcomes of the major randomized trials for those interested and they concluded:
Recurrent patterns emerge from these data reviewed here. Typical use of CPAP does not ameliorate the risks of fatal and nonfatal cardiovascular events in patients with OSA, though it may reduce symptoms of daytime sleepiness and snoring. Subgroup analyses of patients wearing CPAP over 4 hours per night suggest that CPAP may lower cardiovascular events; however, these findings are subject to significant bias.
Post-hoc subgroup analyses like the association of CPAP usage >4 hours with lower events cannot be used to prove causality; they should serve as hypothesis-generating. However, if your business is diagnosing and treating sleep apnea you are highly biased to cherry-pick the available studies.
Thus, although the non-biased writers of the main analysis section at Clinical Correlations came to the proper conclusion -- no benefit -- a pulmonary/sleep medicine MD "commentary" addition concluded the exact opposite:
As multiple studies have shown, treatment of OSA with CPAP has numerous cardiovascular benefits, including arrhythmia control and prevention of recurrence, improved glycemic control, and reduction of the risk for stroke and MI.
This pro-sleep apnea treatment commentary focused on the CPAP>4 hour subgroup analysis without admitting the severe bias this introduces and without discussing how common this is.
Such cherry-picking of the data is common in marketing and surprisingly throughout peer-reviewed articles in major journals. Social and news media summaries of such articles invariably eliminate discussion of the weakness of the observational database supporting the Afib/OSA connection and ignore the lack of support from RCTs.
Screening and Marketing of OSA
Screening for OSA is often done by questionnaires such as STOP-BANG or the Epworth Sleepiness Scale.
asks questions about snoring, sleepiness, observed apnea or choking and hypertension plus 4 clinical attributes (hypertension, obesity, age, neck size, and gender) and classifies patients as low, intermediate or high risk. It has a high sensitivity of 90% but a of 36%. This means that two-thirds of individuals who take this screening who don't have OSA when tested formally will be told they may have OSA.
I just took the STOP-BANG questionnaire and scored 4 (age 50 years, hypertension, fatigued during the day, and male). This was classified as "high risk" for OSA.
A male over age 55 already has 2 points on the score and since 3 points is considered "high risk of OSA" and all wives tell me their husbands snore, every man over age 55 is going to be identified at high risk.
To summarize and answer the question in my title:
Despite numerous flawed observational studies suggesting an association between sleep apnea and cardiovascular outcomes including Afib, the gold standard, high-quality RCT data do not clearly show that treatment of sleep apnea with CPAP improves cardiovascular outcomes.
Until good scientific evidence proves that treatment of OSA really does save lives, reduces heart failure, Afib, or other important cardiovascular outcomes, widespread screening and marketing for the diagnosis and treatment of OSA other than reducing snoring and daytime sleepiness should cease.
Anthony C. Pearson, MD, is a noninvasive cardiologist and professor of medicine at St. Louis University School of Medicine. He blogs on nutrition, cardiac testing, quackery, and other things worthy of skepticism at , where a first appeared.