Unhealthy Sleep – Timothy Mooring, M.D.

Timothy S. Mooring, M.D.

Timothy S. Mooring, M.D.

Insufficient sleep is a very common problem and is a public health issue. Eight hours of restful sleep is an increasingly rare “luxury” in the United States. Beyond lifestyle related insufficient sleep, many diseases lead to insufficient sleep due to reductions in either quality or quantity. Insomnia falls into a quantity sleep reducer but has many causes and contributors. Other diseases don’t allow the person to perceive that they are sleep deprived through disrupting normal sleep patterns without noticeable awakenings. Sleep apnea, periodic limb movements of sleep, pain disorders, and sleep-related bruxism are common examples of disrupting sleep quality. Overlap between all of these types of disruptors of normalcy is very common.

Disrupted sleep and excessive sleepiness are long-standing, well-recognized consequences of obstructive sleep apnea. They are a common presenting complaint to physicians and healthcare providers. Treatment of sleep apnea frequently improves or alleviates these sypmtoms. The explosion of this area of medicine has led to rapidly growing body of publication into insufficient sleep and its other health and psychosocial consequences.

Although the risk factors for hypertension and obstructive sleep apnea (OSA) are very similar. It has become clear that there is a direct causal relationship between OSA and high blood pressure. 25-40% of patients with high blood pressure will suffer from OSA. The early data suggested a causal relationship but over the last ten years, we have seen growing evidence into the imrpvements in blood pressure control when moderate to server sleep apnea is treated with CPAP. Complete control is CPAP alone is rare but medication and medication dose reductions are not uncommon with effective treatment.

Hypertension certainly is a recognized contributor to the development of coronary and peripheral artery disease. Thus you would expect the now well-documented increased prevalance of these conditions in patients with OSA. The converse is true as well. Approximately 50% of patiences with coronaryartery desiease sffer form sone level of sleep apnea. However, the mechnism behind contributing to the development of plaque formation appeasr to extend beyond the effects of hypertension. Alterations in levels of many hormones and substrates that affect arterial narrowing have been discovered. The support for OSA as a cause lies in the improvements in these levels with CPAP treatment in both hypertensive and non-hypertensive patients.

Until recently the studies supporting the cardiovascular event reduction with sleep apnea treatment had been small and weekly supported. We now understand that treatment of moderate to sever OSA with CPAP does prevent stroke and myocardial infarction. Survival benefit appears to be real as well. Although several newer studies have shown, that other non-CPAP treatments can be highly effective in alleviating or improving sleep related airway obstructive, they have been been well-studied regarding health effects. Thus for patients with significant sleep apnea and cardiovascular comorbidities, CPAP remains the mainstay for first-line treatment. Other treatment modalities are appropriate when CPAP is not tolerated or is ineffective.

Stroke is disease that has a two-sided relationship with sleep apnea. Obstructive sleep apnea as we discussed earlier is associated with increased risk of ischemic stroke. Stroke is also suspected to contribute to the development of sleep apnea in a small group of patient. Central sleep apnea is not uncommon after acute stroke but usually resolves during recovery and treatment is rarely needed. Patients with significant deficits, especially involving face and neck, will have issues with increased airway restriction during sleep and facilitate the appearance of sleep related apneas and hypopneas. Obstructive apnea should be treated as potential benefit from CPAP in recover and future vent prevention is possible.

Another potential stroke association lies in the development of atrial fibrillation in some patients with OSA. Atrial fibrillation predisposes patients to embolic stroke through left atrial clot development. OSA has a similar causal relationship with atrial arrhythmias as coronary disease. Likewise, treatment with CPAP has been shown to improve maintenance of sinus rhythm in patients with atrial fibrillation. Prevalence rates likewise are near or above 50%. The mechanism is hypothesized to be multi-factorial: Hypertension, cardiac remodeling, and lack of nocturnal cathecholamine down-regulation. Untreated sleep disordered breathing has been proposed as an independent risk for development atrial fibrillation. It is clear that screening for sleep apnea in this group of patients is recommended.

Many other arrhythmias seem to have a relationship wo sleep apnea. There direct link is not as well-defined. Atrial and ventricular arrhythmias are commonly seen during sleep studies. Sinus pauses intermittent block are clearly the most commonly recorded. Sudden cardiac death has been documented. It is impossible to determine if unexplained sleep related death is OSA related, but the improved survival associated with CPAP use may provide some support for it as a contributing factor to this somewhat uncommon cause of death.

Many other diseases have some demonstrated relationship with OSA. The benefit on these diseases with CPAP treatment is clearly less impressive with some exceptions. Recent studies have shown a slight slowing of Alzheimer’s progression with successful CPAP treatment. However, this group remains very difficult to treat due to memory issues and CPAP compliance as well as disease associated sleep disruptions. Diastolic heart disease has been shown to improve modestly with long term CPAP treatment. My clinical experience and some limited data suggest gastroesophageal reflux disease benefits from treatment as well.

Beyond sleep disordered breathing we must also recognize other sleep diseases and their impact on health. Many of the diseases previously discussed are associated with sleep times totallying 6-7 hours per night. Obesity rates and diabetes mellitus are clearly more common in patients with inadequate amounts of sleep. The literature also strongly supports decreased immune function with sort sleep times, including a three-fold increased risk of common cold contraction. Appetite and metabolism are influenced negatively by poor sleep hygiene. Our understanding of the need for appropriate amounts of sleep is rapidly growing. We are starting to see emerging evidence regarding inappropriate sleep time and its impact on survival. Both too little and too much sleep seems to have a negative impact on long-term well-being.

Growing attention is being put on sleepiness and driving. The United States Department of Transportation has published guidelines regarding who warrants testing for sleep apnea and requires documented compliance for some persons pursuing commercial driver’s licenses. The screening process uses body mass index as the basis for testing, but clinical judgment about using other predictors should be employed. The support for this movement lies in the substantial increased risk of motor vehicle accedents associated with sleep disordered breathing. Even if not fully falling asleep while driving, imnpaired judgment and reactionary times are associated with excessive sleepiness. Defining sleepiness objectively is very difficult thus the government is taking an aggressive approach to help minimize public safety risk.

Healthcare providers are becoming increasingly more aware of the issues associated with insufficient sleep and sleep disorders. Continued close attention to screening, recognition, and treatment is needed to help impove quality of life and health-risk reduction. Growing public interest coupled with a rapidly expanding body of literature will continue to keep sleep disorders and there treatment in the limelight.

 For more, visit adcpa.com or call us at (806) 358-0200

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