Sleep Medicine

African American smokers who logged more total sleep time and greater sleep efficacy performed better on a functional walk test than did those with poorer sleep, based on data from 209 adults.

beichh4046/Getty Images

African American smokers tend to develop COPD sooner and also report more sleep problems, compared with white smokers, wrote Andrew J. Gangemi, MD, of Temple University Hospital, Philadelphia, and colleagues.

In addition, African Americans tend to develop COPD at a younger age and with lower levels of smoking than do non-Hispanic whites, they said. “Sleep health may be a contributing factor to the lung and cardiovascular health disparity experienced by AA smokers,” in part because data suggest that insufficient sleep may be associated with increased risk of COPD exacerbation in smokers in general, they said.

In a study published in Chest, the researchers reviewed data from 209 African American adults aged 40-65 years who had smoked at least one cigarette in the past month. The average age of the participants was 55 years, 59% were women, and the average smoking habit was nine cigarettes per day.

The researchers measured functional exercise capacity of the participants using the 6-minute walk test (6MWT). Total sleep time (TST) and sleep efficacy (SE) were measured by way of a finger-based device.

Smokers of at least 10 cigarettes per day gained an additional 0.05-0.58 meters in distance covered on the 6MWT for every added minute of total sleep time in a multivariable regression analysis. Similarly, smokers of at least 10 cigarettes per day gained an additional 0.84-6.17–meter increase in distance covered on the 6MWT for every added percentage of sleep efficacy.

The reasons for the impact of SE and TST on functional exercise capacity in smokers remain unclear, the researchers said. “Heavier smokers have higher levels of autonomic imbalance, including higher resting heart rate and heart rate variability, impaired 24-hour cardiovascular sympathetic tone, and blunted cerebrovascular autonomic regulation and baroreflex response to hypercapnia,” they said.

Also unclear is the reason for the large magnitude of the association between SE and smoking vs. the lesser association between TST and smoking on 6MWT results, the researchers wrote. “Poor sleep efficiency, outside of traditional OSA scoring, is predictive of myocardial infarction, stroke, and cardiovascular-related mortality risk. Moreover, deficits in sleep efficiency have been consistently demonstrated in smokers versus nonsmokers,” they said.

The study findings were limited by several factors including inability to extrapolate data to other demographic groups and the cross-sectional design, the researchers noted. In addition, they did not address how TST and SE may relate to lung function.

However, the results “extend current knowledge about the potential role of improved sleep health to functional exercise capacity in AA smokers,” and set the stage for future studies of how changes in sleep health may affect lung and functional exercise capacity in smokers over time, as well as effects on inflammation and autonomic imbalance, the researchers concluded.

The study was supported by the National Institute on Minority Health and Health Disparities and by the National Institute of General Medical Sciences, both part of the National Institutes Health. The researchers had no financial conflicts to disclose.

SOURCE: Gangemi A et al. Chest 2020 Apr 23. doi: 10.1016/j.chest.2020.03.070.

African American smokers who logged more total sleep time and greater sleep efficacy performed better on a functional walk test than did those with poorer sleep, based on data from 209 adults.

beichh4046/Getty Images

African American smokers tend to develop COPD sooner and also report more sleep problems, compared with white smokers, wrote Andrew J. Gangemi, MD, of Temple University Hospital, Philadelphia, and colleagues.

In addition, African Americans tend to develop COPD at a younger age and with lower levels of smoking than do non-Hispanic whites, they said. “Sleep health may be a contributing factor to the lung and cardiovascular health disparity experienced by AA smokers,” in part because data suggest that insufficient sleep may be associated with increased risk of COPD exacerbation in smokers in general, they said.

In a study published in Chest, the researchers reviewed data from 209 African American adults aged 40-65 years who had smoked at least one cigarette in the past month. The average age of the participants was 55 years, 59% were women, and the average smoking habit was nine cigarettes per day.

The researchers measured functional exercise capacity of the participants using the 6-minute walk test (6MWT). Total sleep time (TST) and sleep efficacy (SE) were measured by way of a finger-based device.

Smokers of at least 10 cigarettes per day gained an additional 0.05-0.58 meters in distance covered on the 6MWT for every added minute of total sleep time in a multivariable regression analysis. Similarly, smokers of at least 10 cigarettes per day gained an additional 0.84-6.17–meter increase in distance covered on the 6MWT for every added percentage of sleep efficacy.

The reasons for the impact of SE and TST on functional exercise capacity in smokers remain unclear, the researchers said. “Heavier smokers have higher levels of autonomic imbalance, including higher resting heart rate and heart rate variability, impaired 24-hour cardiovascular sympathetic tone, and blunted cerebrovascular autonomic regulation and baroreflex response to hypercapnia,” they said.

Also unclear is the reason for the large magnitude of the association between SE and smoking vs. the lesser association between TST and smoking on 6MWT results, the researchers wrote. “Poor sleep efficiency, outside of traditional OSA scoring, is predictive of myocardial infarction, stroke, and cardiovascular-related mortality risk. Moreover, deficits in sleep efficiency have been consistently demonstrated in smokers versus nonsmokers,” they said.

The study findings were limited by several factors including inability to extrapolate data to other demographic groups and the cross-sectional design, the researchers noted. In addition, they did not address how TST and SE may relate to lung function.

However, the results “extend current knowledge about the potential role of improved sleep health to functional exercise capacity in AA smokers,” and set the stage for future studies of how changes in sleep health may affect lung and functional exercise capacity in smokers over time, as well as effects on inflammation and autonomic imbalance, the researchers concluded.

The study was supported by the National Institute on Minority Health and Health Disparities and by the National Institute of General Medical Sciences, both part of the National Institutes Health. The researchers had no financial conflicts to disclose.

SOURCE: Gangemi A et al. Chest 2020 Apr 23. doi: 10.1016/j.chest.2020.03.070.

African American smokers who logged more total sleep time and greater sleep efficacy performed better on a functional walk test than did those with poorer sleep, based on data from 209 adults.

beichh4046/Getty Images

African American smokers tend to develop COPD sooner and also report more sleep problems, compared with white smokers, wrote Andrew J. Gangemi, MD, of Temple University Hospital, Philadelphia, and colleagues.

In addition, African Americans tend to develop COPD at a younger age and with lower levels of smoking than do non-Hispanic whites, they said. “Sleep health may be a contributing factor to the lung and cardiovascular health disparity experienced by AA smokers,” in part because data suggest that insufficient sleep may be associated with increased risk of COPD exacerbation in smokers in general, they said.

In a study published in Chest, the researchers reviewed data from 209 African American adults aged 40-65 years who had smoked at least one cigarette in the past month. The average age of the participants was 55 years, 59% were women, and the average smoking habit was nine cigarettes per day.

The researchers measured functional exercise capacity of the participants using the 6-minute walk test (6MWT). Total sleep time (TST) and sleep efficacy (SE) were measured by way of a finger-based device.

Smokers of at least 10 cigarettes per day gained an additional 0.05-0.58 meters in distance covered on the 6MWT for every added minute of total sleep time in a multivariable regression analysis. Similarly, smokers of at least 10 cigarettes per day gained an additional 0.84-6.17–meter increase in distance covered on the 6MWT for every added percentage of sleep efficacy.

The reasons for the impact of SE and TST on functional exercise capacity in smokers remain unclear, the researchers said. “Heavier smokers have higher levels of autonomic imbalance, including higher resting heart rate and heart rate variability, impaired 24-hour cardiovascular sympathetic tone, and blunted cerebrovascular autonomic regulation and baroreflex response to hypercapnia,” they said.

Also unclear is the reason for the large magnitude of the association between SE and smoking vs. the lesser association between TST and smoking on 6MWT results, the researchers wrote. “Poor sleep efficiency, outside of traditional OSA scoring, is predictive of myocardial infarction, stroke, and cardiovascular-related mortality risk. Moreover, deficits in sleep efficiency have been consistently demonstrated in smokers versus nonsmokers,” they said.

The study findings were limited by several factors including inability to extrapolate data to other demographic groups and the cross-sectional design, the researchers noted. In addition, they did not address how TST and SE may relate to lung function.

However, the results “extend current knowledge about the potential role of improved sleep health to functional exercise capacity in AA smokers,” and set the stage for future studies of how changes in sleep health may affect lung and functional exercise capacity in smokers over time, as well as effects on inflammation and autonomic imbalance, the researchers concluded.

The study was supported by the National Institute on Minority Health and Health Disparities and by the National Institute of General Medical Sciences, both part of the National Institutes Health. The researchers had no financial conflicts to disclose.

SOURCE: Gangemi A et al. Chest 2020 Apr 23. doi: 10.1016/j.chest.2020.03.070.

The risk for suicide is higher at night than at any other time of day, new research shows.

In findings that may offer an opportunity for suicide prevention, investigators found that the risk of dying by suicide between midnight and 6:00 a.m. was roughly three times higher than at other times of day regardless of month, method of suicide, or a wide range of other factors.

“The take-home message is that helping at-risk patients sleep through the night may be an excellent way to reduce suicide risk,” lead author Andrew Tubbs, an MD/PhD candidate at the Sleep and Health Research Program, department of psychiatry, University of Arizona, Tucson, said in an interview.

The study was published in the March/April issue of the Journal of Clinical Psychiatry.

Time, method of suicide

Previous research suggests that waking at night is linked to a heightened risk for suicidal thoughts and behaviors, the investigators note.

“The motivation for this study was to expand our understanding of factors that increase suicide risk at night. Since night length changes across seasons, we wondered if suicide risk at night would be lower during summer months and higher during winter months,” he said.

“Similarly, we thought the availability of some suicide methods may vary by time of day — for example, perhaps nighttime would involve more ‘silent’ methods, such as poisoning or asphyxiation, over ‘louder methods,’ such as firearms or vehicle suicides,” Mr. Tubbs added.

The investigators also examined whether the risk for nocturnal suicide was influenced by demographic or geographic factors.

They analyzed data on 35,338 suicides from the U.S. National Violent Death Reporting System for the years 2003-2010.

Time of suicide was divided into four categories: night (12:00 a.m.–5:59 a.m.), morning (6:00 a.m.–11:59 a.m.), afternoon (12:00 p.m.–5:59 p.m.), and evening (6:00 p.m.–11:59 p.m.).

Suicide methods included guns, asphyxiation, poisons, falls, vehicles, sharp weapons, drowning, and fire. Demographics included sex, age, race, and ethnicity. Geographic analyses were based on latitude (at or above 40° N or below 35° N) and region (West, Midwest, South, and Northeast).

Raw data revealed that more males than females died by suicide (n = 28,700 vs. 6636), that most suicides occurred in May (n = 3196), and that the most common method of suicide was by firearms (n = 21,937). Most suicides occurred in those aged 45-54 years (n = 7252) and in whites (n = 31,239) and non-Hispanics (33,384).

Interestingly, most suicides occurred during the afternoon (n = 11,381). Mr. Tubbs explained that suicides are more common during the day, typically around midday, when most people are awake, “so the ‘eligible’ population for suicide is highest at noon,” he said. However, this does not translate into level of risk, so the researchers accounted for nocturnal wakefulness in the analyses.

“When reason sleeps”

The incidence rate ratio at night was 3.18, significantly higher than at any other time of day across all months. The highest IRR was in May (3.90), and the lowest was in November (2.74).

An analysis of variance (ANOVA) for month and time of day indicated that the IRR varied significantly only by time of day (P < .001), not across months (P = .33) or by interaction (P = 1.00).

Initially, a two-way ANOVA showed that the risk for suicide varied both by time of day and by suicide method (both Ps < .001), but the interaction between them was not significant (P = .3026). The mean (SD) nocturnal IRR was 3.09 (.472) across all methods.

Although more than half of suicides involved firearms, “no method had a significantly higher risk at a specific time than any other method at that same time,” the authors note. In addition, an analysis of nocturnal risk by method showed no differences on the basis of sex, age, ethnicity, latitude, and region.

“There are probably many overlapping reasons why the risk of suicide is highest at night. Certainly, social and family supports are minimized if you are awake and everyone you know and love is asleep – you’re isolated, no one’s reaching out to you, and there’s no one there to stop you,” said Mr. Tubbs.

On the other hand, “recent evidence indicates nighttime changes in brain function can impair impulse control, decision making, and long-term planning, which can definitely increase suicidal behaviors.

“Whether these changes are due to sleep deprivation or circadian rhythms is unknown, but it is clearly dangerous to be awake when reason sleeps,” he said.

Clinicians who treat suicidal patients, said Mr. Tubbs, should ask about sleep. If a patient has a problem with sleep, cognitive-behavioral therapy for insomnia should be initiated. This first-line treatment, he said, is more effective and much safer than prescribing a hypnotic.
 

Difficult hours

Commenting on the study, Christopher W. Drapeau, PhD, of the department of education, Valparaiso University, Indiana, said that sleep disturbances “may be a modifiable risk factor for suicide, especially when sleep disturbances are cited by patients as a primary reason for wanting to attempt suicide.”

Dr. Drapeau, who was not involved in the study, said that this “presents an area for health professionals to focus on when developing treatment approaches based on patient information collected during suicide-risk screenings and comprehensive risk assessments.”

Also commenting on the study, Michael Nadorff, PhD, of the department of psychology, Mississippi State University, Starkville, who was not involved with the study, said the study findings are clinically relevant.

These data, he said, inform clinicians about when patients are most likely to be struggling with suicide intent and offer an opportunity to develop safety plans to mitigate suicide risk during these “difficult hours” when coping mechanisms are at a low ebb and sources of support are unavailable.

Support for the study was provided by grants from the National Institutes of Health and the Veterans Administration. Mr. Tubbs and Dr. Drapeau, and Dr. Nadorff report no relevant financial relationships.

This article first appeared on Medscape.com.

The risk for suicide is higher at night than at any other time of day, new research shows.

In findings that may offer an opportunity for suicide prevention, investigators found that the risk of dying by suicide between midnight and 6:00 a.m. was roughly three times higher than at other times of day regardless of month, method of suicide, or a wide range of other factors.

“The take-home message is that helping at-risk patients sleep through the night may be an excellent way to reduce suicide risk,” lead author Andrew Tubbs, an MD/PhD candidate at the Sleep and Health Research Program, department of psychiatry, University of Arizona, Tucson, said in an interview.

The study was published in the March/April issue of the Journal of Clinical Psychiatry.

Time, method of suicide

Previous research suggests that waking at night is linked to a heightened risk for suicidal thoughts and behaviors, the investigators note.

“The motivation for this study was to expand our understanding of factors that increase suicide risk at night. Since night length changes across seasons, we wondered if suicide risk at night would be lower during summer months and higher during winter months,” he said.

“Similarly, we thought the availability of some suicide methods may vary by time of day — for example, perhaps nighttime would involve more ‘silent’ methods, such as poisoning or asphyxiation, over ‘louder methods,’ such as firearms or vehicle suicides,” Mr. Tubbs added.

The investigators also examined whether the risk for nocturnal suicide was influenced by demographic or geographic factors.

They analyzed data on 35,338 suicides from the U.S. National Violent Death Reporting System for the years 2003-2010.

Time of suicide was divided into four categories: night (12:00 a.m.–5:59 a.m.), morning (6:00 a.m.–11:59 a.m.), afternoon (12:00 p.m.–5:59 p.m.), and evening (6:00 p.m.–11:59 p.m.).

Suicide methods included guns, asphyxiation, poisons, falls, vehicles, sharp weapons, drowning, and fire. Demographics included sex, age, race, and ethnicity. Geographic analyses were based on latitude (at or above 40° N or below 35° N) and region (West, Midwest, South, and Northeast).

Raw data revealed that more males than females died by suicide (n = 28,700 vs. 6636), that most suicides occurred in May (n = 3196), and that the most common method of suicide was by firearms (n = 21,937). Most suicides occurred in those aged 45-54 years (n = 7252) and in whites (n = 31,239) and non-Hispanics (33,384).

Interestingly, most suicides occurred during the afternoon (n = 11,381). Mr. Tubbs explained that suicides are more common during the day, typically around midday, when most people are awake, “so the ‘eligible’ population for suicide is highest at noon,” he said. However, this does not translate into level of risk, so the researchers accounted for nocturnal wakefulness in the analyses.

“When reason sleeps”

The incidence rate ratio at night was 3.18, significantly higher than at any other time of day across all months. The highest IRR was in May (3.90), and the lowest was in November (2.74).

An analysis of variance (ANOVA) for month and time of day indicated that the IRR varied significantly only by time of day (P < .001), not across months (P = .33) or by interaction (P = 1.00).

Initially, a two-way ANOVA showed that the risk for suicide varied both by time of day and by suicide method (both Ps < .001), but the interaction between them was not significant (P = .3026). The mean (SD) nocturnal IRR was 3.09 (.472) across all methods.

Although more than half of suicides involved firearms, “no method had a significantly higher risk at a specific time than any other method at that same time,” the authors note. In addition, an analysis of nocturnal risk by method showed no differences on the basis of sex, age, ethnicity, latitude, and region.

“There are probably many overlapping reasons why the risk of suicide is highest at night. Certainly, social and family supports are minimized if you are awake and everyone you know and love is asleep – you’re isolated, no one’s reaching out to you, and there’s no one there to stop you,” said Mr. Tubbs.

On the other hand, “recent evidence indicates nighttime changes in brain function can impair impulse control, decision making, and long-term planning, which can definitely increase suicidal behaviors.

“Whether these changes are due to sleep deprivation or circadian rhythms is unknown, but it is clearly dangerous to be awake when reason sleeps,” he said.

Clinicians who treat suicidal patients, said Mr. Tubbs, should ask about sleep. If a patient has a problem with sleep, cognitive-behavioral therapy for insomnia should be initiated. This first-line treatment, he said, is more effective and much safer than prescribing a hypnotic.
 

Difficult hours

Commenting on the study, Christopher W. Drapeau, PhD, of the department of education, Valparaiso University, Indiana, said that sleep disturbances “may be a modifiable risk factor for suicide, especially when sleep disturbances are cited by patients as a primary reason for wanting to attempt suicide.”

Dr. Drapeau, who was not involved in the study, said that this “presents an area for health professionals to focus on when developing treatment approaches based on patient information collected during suicide-risk screenings and comprehensive risk assessments.”

Also commenting on the study, Michael Nadorff, PhD, of the department of psychology, Mississippi State University, Starkville, who was not involved with the study, said the study findings are clinically relevant.

These data, he said, inform clinicians about when patients are most likely to be struggling with suicide intent and offer an opportunity to develop safety plans to mitigate suicide risk during these “difficult hours” when coping mechanisms are at a low ebb and sources of support are unavailable.

Support for the study was provided by grants from the National Institutes of Health and the Veterans Administration. Mr. Tubbs and Dr. Drapeau, and Dr. Nadorff report no relevant financial relationships.

This article first appeared on Medscape.com.

The risk for suicide is higher at night than at any other time of day, new research shows.

In findings that may offer an opportunity for suicide prevention, investigators found that the risk of dying by suicide between midnight and 6:00 a.m. was roughly three times higher than at other times of day regardless of month, method of suicide, or a wide range of other factors.

“The take-home message is that helping at-risk patients sleep through the night may be an excellent way to reduce suicide risk,” lead author Andrew Tubbs, an MD/PhD candidate at the Sleep and Health Research Program, department of psychiatry, University of Arizona, Tucson, said in an interview.

The study was published in the March/April issue of the Journal of Clinical Psychiatry.

Time, method of suicide

Previous research suggests that waking at night is linked to a heightened risk for suicidal thoughts and behaviors, the investigators note.

“The motivation for this study was to expand our understanding of factors that increase suicide risk at night. Since night length changes across seasons, we wondered if suicide risk at night would be lower during summer months and higher during winter months,” he said.

“Similarly, we thought the availability of some suicide methods may vary by time of day — for example, perhaps nighttime would involve more ‘silent’ methods, such as poisoning or asphyxiation, over ‘louder methods,’ such as firearms or vehicle suicides,” Mr. Tubbs added.

The investigators also examined whether the risk for nocturnal suicide was influenced by demographic or geographic factors.

They analyzed data on 35,338 suicides from the U.S. National Violent Death Reporting System for the years 2003-2010.

Time of suicide was divided into four categories: night (12:00 a.m.–5:59 a.m.), morning (6:00 a.m.–11:59 a.m.), afternoon (12:00 p.m.–5:59 p.m.), and evening (6:00 p.m.–11:59 p.m.).

Suicide methods included guns, asphyxiation, poisons, falls, vehicles, sharp weapons, drowning, and fire. Demographics included sex, age, race, and ethnicity. Geographic analyses were based on latitude (at or above 40° N or below 35° N) and region (West, Midwest, South, and Northeast).

Raw data revealed that more males than females died by suicide (n = 28,700 vs. 6636), that most suicides occurred in May (n = 3196), and that the most common method of suicide was by firearms (n = 21,937). Most suicides occurred in those aged 45-54 years (n = 7252) and in whites (n = 31,239) and non-Hispanics (33,384).

Interestingly, most suicides occurred during the afternoon (n = 11,381). Mr. Tubbs explained that suicides are more common during the day, typically around midday, when most people are awake, “so the ‘eligible’ population for suicide is highest at noon,” he said. However, this does not translate into level of risk, so the researchers accounted for nocturnal wakefulness in the analyses.

“When reason sleeps”

The incidence rate ratio at night was 3.18, significantly higher than at any other time of day across all months. The highest IRR was in May (3.90), and the lowest was in November (2.74).

An analysis of variance (ANOVA) for month and time of day indicated that the IRR varied significantly only by time of day (P < .001), not across months (P = .33) or by interaction (P = 1.00).

Initially, a two-way ANOVA showed that the risk for suicide varied both by time of day and by suicide method (both Ps < .001), but the interaction between them was not significant (P = .3026). The mean (SD) nocturnal IRR was 3.09 (.472) across all methods.

Although more than half of suicides involved firearms, “no method had a significantly higher risk at a specific time than any other method at that same time,” the authors note. In addition, an analysis of nocturnal risk by method showed no differences on the basis of sex, age, ethnicity, latitude, and region.

“There are probably many overlapping reasons why the risk of suicide is highest at night. Certainly, social and family supports are minimized if you are awake and everyone you know and love is asleep – you’re isolated, no one’s reaching out to you, and there’s no one there to stop you,” said Mr. Tubbs.

On the other hand, “recent evidence indicates nighttime changes in brain function can impair impulse control, decision making, and long-term planning, which can definitely increase suicidal behaviors.

“Whether these changes are due to sleep deprivation or circadian rhythms is unknown, but it is clearly dangerous to be awake when reason sleeps,” he said.

Clinicians who treat suicidal patients, said Mr. Tubbs, should ask about sleep. If a patient has a problem with sleep, cognitive-behavioral therapy for insomnia should be initiated. This first-line treatment, he said, is more effective and much safer than prescribing a hypnotic.
 

Difficult hours

Commenting on the study, Christopher W. Drapeau, PhD, of the department of education, Valparaiso University, Indiana, said that sleep disturbances “may be a modifiable risk factor for suicide, especially when sleep disturbances are cited by patients as a primary reason for wanting to attempt suicide.”

Dr. Drapeau, who was not involved in the study, said that this “presents an area for health professionals to focus on when developing treatment approaches based on patient information collected during suicide-risk screenings and comprehensive risk assessments.”

Also commenting on the study, Michael Nadorff, PhD, of the department of psychology, Mississippi State University, Starkville, who was not involved with the study, said the study findings are clinically relevant.

These data, he said, inform clinicians about when patients are most likely to be struggling with suicide intent and offer an opportunity to develop safety plans to mitigate suicide risk during these “difficult hours” when coping mechanisms are at a low ebb and sources of support are unavailable.

Support for the study was provided by grants from the National Institutes of Health and the Veterans Administration. Mr. Tubbs and Dr. Drapeau, and Dr. Nadorff report no relevant financial relationships.

This article first appeared on Medscape.com.

Hypersomnolence, or excessive daytime sleepiness, in older adults is a risk factor for developing several serious medical conditions, including hypertension, heart disease, cancer, and diabetes, new research suggests. A study of almost 11,000 participants shows those who reported excessive sleepiness were twice as likely as their nonsleepy counterparts to develop these conditions. Hypersomnolence was also linked to development of musculoskeletal and connective tissue conditions.

“Paying attention to sleepiness in older adults could help doctors predict and prevent future medical conditions,” study investigator Maurice M. Ohayon, MD, PhD, Stanford University, California, said in a news release.

The findings were released March 1 ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology. The AAN canceled the meeting and released abstracts and access to presenters for press coverage.
 

Early warning sign

Prior research has suggested an association between hypersomnolence and several psychiatric disorders, as well as cognitive decline and Alzheimer’s disease. However, its role in the development of other medical conditions is not as well studied.

The current investigation included 10,930 adults who were interviewed by phone on two separate occasions 3 years apart. At the second interview, 3,701 participants were at least 65 years old and 59% were women.

About 23% of the elderly participants reported hypersomnolence in the first interview and 24% reported it in the second interview. Of these individuals, 41% said during the first and second interviews that excessive daytime sleepiness was a chronic problem.

After adjusting for gender and obstructive sleep apnea status, participants who reported hypersomnolence in the first interview had more than a twofold greater risk of developing diabetes (relative risk [RR], 2.3; 95% CI, 1.5 - 3.4) or hypertension (RR, 2.3; 95% CI, 1.5 - 3.4) 3 years later than those who did not report this problem. They were also twice as likely to develop cancer (RR, 2.0; 95% CI, 1.1 - 3.8).

Of the 840 participants who reported hypersomnolence at the first interview, 52 (6.2%) developed diabetes compared with 74 (2.9%) who did not have excessive daytime sleepiness. Twenty (2.4%) individuals who reported hypersomnolence developed cancer compared with 21 (0.8%) who did not have it. Chronic hypersomnolence was associated with a greater than twofold increased risk of developing heart disease (RR, 2.5; 95% CI, 1.8 - 3.4).

Those who reported hypersomnolence at the second interview also were 50% more likely to have diseases of the musculoskeletal system and connective tissue, such as arthritis, tendinitis, and lupus, than their peers who did not have excessive daytime sleepiness.

The findings suggest that hypersomnolence in the elderly “can be an early sign of a developing medical condition,” the investigators wrote.

A limitation of the study is that it relied on participants’ memories rather than monitoring their sleep length and quality and daytime sleepiness in a sleep clinic, they noted.

Sleep as a vital sign?

Commenting on the findings, Harly Greenberg, MD, medical director at the Northwell Health Sleep Disorders Center, New York City, called the study “informative.”

However, because the findings were associations, “the study does not necessarily indicate that hypersomnolence itself is causal for these conditions. Rather excessive sleepiness may be a marker of sleep disorders that can cause sleepiness as well as contribute to the risk of these medical conditions,” said Dr. Greenberg, who was not involved with the research.

“The takeaway point from this study is that excessive sleepiness should not be ignored. Not only does it impair quality of life, daytime function, and vigilance and increase risk of sleepiness-related accidents, it may also be a marker for serious sleep disorders that can increase risk for medical disorders,” he said.

Also commenting on the study, Nathaniel Watson, MD, professor of neurology at the University of Washington (UW) and director of the UW Medicine Sleep Clinic, said it is “not surprising” that excessive daytime sleepiness might contribute to diabetes, hypertension, and other diseases.

“Sleep is something we spend a third of our lives doing. It impacts nearly every aspect of human physiology and we have a lot of basic science and epidemiologic research that shows when sleep is either inadequate or of poor quality or not timed correctly it can be associated with some of these untoward health outcomes,” said Watson, who is a past president of the American Academy of Sleep Medicine.

“This research just provides further evidence in support of the importance of sleep for overall health and well-being,” he added.

Asking patients about sleepiness, sleep, or sleep quality should be a “vital sign just like temperature, blood pressure, weight, and these other measures,” Dr. Watson said.

The study was supported by the Arrillaga Foundation. Drs. Ohayon, Greenberg, and Watson have reported no relevant financial relationships.

This article first appeared on Medscape.com.

Hypersomnolence, or excessive daytime sleepiness, in older adults is a risk factor for developing several serious medical conditions, including hypertension, heart disease, cancer, and diabetes, new research suggests. A study of almost 11,000 participants shows those who reported excessive sleepiness were twice as likely as their nonsleepy counterparts to develop these conditions. Hypersomnolence was also linked to development of musculoskeletal and connective tissue conditions.

“Paying attention to sleepiness in older adults could help doctors predict and prevent future medical conditions,” study investigator Maurice M. Ohayon, MD, PhD, Stanford University, California, said in a news release.

The findings were released March 1 ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology. The AAN canceled the meeting and released abstracts and access to presenters for press coverage.
 

Early warning sign

Prior research has suggested an association between hypersomnolence and several psychiatric disorders, as well as cognitive decline and Alzheimer’s disease. However, its role in the development of other medical conditions is not as well studied.

The current investigation included 10,930 adults who were interviewed by phone on two separate occasions 3 years apart. At the second interview, 3,701 participants were at least 65 years old and 59% were women.

About 23% of the elderly participants reported hypersomnolence in the first interview and 24% reported it in the second interview. Of these individuals, 41% said during the first and second interviews that excessive daytime sleepiness was a chronic problem.

After adjusting for gender and obstructive sleep apnea status, participants who reported hypersomnolence in the first interview had more than a twofold greater risk of developing diabetes (relative risk [RR], 2.3; 95% CI, 1.5 - 3.4) or hypertension (RR, 2.3; 95% CI, 1.5 - 3.4) 3 years later than those who did not report this problem. They were also twice as likely to develop cancer (RR, 2.0; 95% CI, 1.1 - 3.8).

Of the 840 participants who reported hypersomnolence at the first interview, 52 (6.2%) developed diabetes compared with 74 (2.9%) who did not have excessive daytime sleepiness. Twenty (2.4%) individuals who reported hypersomnolence developed cancer compared with 21 (0.8%) who did not have it. Chronic hypersomnolence was associated with a greater than twofold increased risk of developing heart disease (RR, 2.5; 95% CI, 1.8 - 3.4).

Those who reported hypersomnolence at the second interview also were 50% more likely to have diseases of the musculoskeletal system and connective tissue, such as arthritis, tendinitis, and lupus, than their peers who did not have excessive daytime sleepiness.

The findings suggest that hypersomnolence in the elderly “can be an early sign of a developing medical condition,” the investigators wrote.

A limitation of the study is that it relied on participants’ memories rather than monitoring their sleep length and quality and daytime sleepiness in a sleep clinic, they noted.

Sleep as a vital sign?

Commenting on the findings, Harly Greenberg, MD, medical director at the Northwell Health Sleep Disorders Center, New York City, called the study “informative.”

However, because the findings were associations, “the study does not necessarily indicate that hypersomnolence itself is causal for these conditions. Rather excessive sleepiness may be a marker of sleep disorders that can cause sleepiness as well as contribute to the risk of these medical conditions,” said Dr. Greenberg, who was not involved with the research.

“The takeaway point from this study is that excessive sleepiness should not be ignored. Not only does it impair quality of life, daytime function, and vigilance and increase risk of sleepiness-related accidents, it may also be a marker for serious sleep disorders that can increase risk for medical disorders,” he said.

Also commenting on the study, Nathaniel Watson, MD, professor of neurology at the University of Washington (UW) and director of the UW Medicine Sleep Clinic, said it is “not surprising” that excessive daytime sleepiness might contribute to diabetes, hypertension, and other diseases.

“Sleep is something we spend a third of our lives doing. It impacts nearly every aspect of human physiology and we have a lot of basic science and epidemiologic research that shows when sleep is either inadequate or of poor quality or not timed correctly it can be associated with some of these untoward health outcomes,” said Watson, who is a past president of the American Academy of Sleep Medicine.

“This research just provides further evidence in support of the importance of sleep for overall health and well-being,” he added.

Asking patients about sleepiness, sleep, or sleep quality should be a “vital sign just like temperature, blood pressure, weight, and these other measures,” Dr. Watson said.

The study was supported by the Arrillaga Foundation. Drs. Ohayon, Greenberg, and Watson have reported no relevant financial relationships.

This article first appeared on Medscape.com.

Hypersomnolence, or excessive daytime sleepiness, in older adults is a risk factor for developing several serious medical conditions, including hypertension, heart disease, cancer, and diabetes, new research suggests. A study of almost 11,000 participants shows those who reported excessive sleepiness were twice as likely as their nonsleepy counterparts to develop these conditions. Hypersomnolence was also linked to development of musculoskeletal and connective tissue conditions.

“Paying attention to sleepiness in older adults could help doctors predict and prevent future medical conditions,” study investigator Maurice M. Ohayon, MD, PhD, Stanford University, California, said in a news release.

The findings were released March 1 ahead of the study’s scheduled presentation at the annual meeting of the American Academy of Neurology. The AAN canceled the meeting and released abstracts and access to presenters for press coverage.
 

Early warning sign

Prior research has suggested an association between hypersomnolence and several psychiatric disorders, as well as cognitive decline and Alzheimer’s disease. However, its role in the development of other medical conditions is not as well studied.

The current investigation included 10,930 adults who were interviewed by phone on two separate occasions 3 years apart. At the second interview, 3,701 participants were at least 65 years old and 59% were women.

About 23% of the elderly participants reported hypersomnolence in the first interview and 24% reported it in the second interview. Of these individuals, 41% said during the first and second interviews that excessive daytime sleepiness was a chronic problem.

After adjusting for gender and obstructive sleep apnea status, participants who reported hypersomnolence in the first interview had more than a twofold greater risk of developing diabetes (relative risk [RR], 2.3; 95% CI, 1.5 - 3.4) or hypertension (RR, 2.3; 95% CI, 1.5 - 3.4) 3 years later than those who did not report this problem. They were also twice as likely to develop cancer (RR, 2.0; 95% CI, 1.1 - 3.8).

Of the 840 participants who reported hypersomnolence at the first interview, 52 (6.2%) developed diabetes compared with 74 (2.9%) who did not have excessive daytime sleepiness. Twenty (2.4%) individuals who reported hypersomnolence developed cancer compared with 21 (0.8%) who did not have it. Chronic hypersomnolence was associated with a greater than twofold increased risk of developing heart disease (RR, 2.5; 95% CI, 1.8 - 3.4).

Those who reported hypersomnolence at the second interview also were 50% more likely to have diseases of the musculoskeletal system and connective tissue, such as arthritis, tendinitis, and lupus, than their peers who did not have excessive daytime sleepiness.

The findings suggest that hypersomnolence in the elderly “can be an early sign of a developing medical condition,” the investigators wrote.

A limitation of the study is that it relied on participants’ memories rather than monitoring their sleep length and quality and daytime sleepiness in a sleep clinic, they noted.

Sleep as a vital sign?

Commenting on the findings, Harly Greenberg, MD, medical director at the Northwell Health Sleep Disorders Center, New York City, called the study “informative.”

However, because the findings were associations, “the study does not necessarily indicate that hypersomnolence itself is causal for these conditions. Rather excessive sleepiness may be a marker of sleep disorders that can cause sleepiness as well as contribute to the risk of these medical conditions,” said Dr. Greenberg, who was not involved with the research.

“The takeaway point from this study is that excessive sleepiness should not be ignored. Not only does it impair quality of life, daytime function, and vigilance and increase risk of sleepiness-related accidents, it may also be a marker for serious sleep disorders that can increase risk for medical disorders,” he said.

Also commenting on the study, Nathaniel Watson, MD, professor of neurology at the University of Washington (UW) and director of the UW Medicine Sleep Clinic, said it is “not surprising” that excessive daytime sleepiness might contribute to diabetes, hypertension, and other diseases.

“Sleep is something we spend a third of our lives doing. It impacts nearly every aspect of human physiology and we have a lot of basic science and epidemiologic research that shows when sleep is either inadequate or of poor quality or not timed correctly it can be associated with some of these untoward health outcomes,” said Watson, who is a past president of the American Academy of Sleep Medicine.

“This research just provides further evidence in support of the importance of sleep for overall health and well-being,” he added.

Asking patients about sleepiness, sleep, or sleep quality should be a “vital sign just like temperature, blood pressure, weight, and these other measures,” Dr. Watson said.

The study was supported by the Arrillaga Foundation. Drs. Ohayon, Greenberg, and Watson have reported no relevant financial relationships.

This article first appeared on Medscape.com.

Mass social distancing and social isolation to prevent the spread of a deadly disease, along with technological tools that allow social communication and continued work and school, is an unprecedented situation.

Stockbyte/Thinkstock.com

The current reality of most people’s lives during the COVID-19 pandemic has the potential to induce or exacerbate sleep problems, though it may also present some with an opportunity to improve sleep, wrote Ellemarije Altena, PhD, of the University of Bordeaux (France), and her colleagues in a recent research review in the Journal of Sleep Research.

The review was conducted by a task force of the European Academy for Cognitive Behavioural Therapy for Insomnia. The European CBT-I Academy is an initiative of the European Insomnia Network to promote implementation and dissemination of treatment.

After discussing the known effects of stress, confinement, and altered schedules on sleep, the authors present recommendations on ways to manage sleep problems such as insomnia in the general public and potentially encourage people to take advantage of the opportunity to align their schedules with their natural circadian rhythms. Physicians may find the recommendations helpful in advising patients with sleep problems related to the COVID-19 emergency.

“Being forced to stay at home, work from home, do homeschooling with children, drastically minimize outings, reduce social interaction or work many more hours under stressful circumstances, and in parallel manage the attendant health risks, can have a major impact on daily functioning and nighttime sleep,” Dr. Altena and colleagues wrote.

There may also be a lag time in physicians hearing about changes in sleep or sleeping problems from patients, said Krishna M. Sundar, MD, FCCP, medical director of the Sleep-Wake Center at the University of Utah in Salt Lake City. “There may actually be some improvement in sleep durations given that most folks are working from home with more time with family and less work-related stress,” he said in an interview. “In terms of sleep or other effects on worsening of psychiatric problems, it is still not clear what the overall effects are going to be.”

Although daylight has the biggest impact on regulating circadian rhythms, artificial light, meal times, diet, and amount of physical activity can also have an influence. Negative effects on sleep can result from both excessively high activity levels, such as stress and work overload, or excessively low levels, such as from depression or confinement, the authors note.

The current situation also opens the door to interactions between stress, sleep, anxiety, and risk of PTSD. “Those sensitive to stress-related sleep disruption are more likely to develop chronic insomnia,” which, in combination with a major stressor, is a risk factor for PTSD, the authors write. They note that 7% of Wuhan residents, the city in China where the virus appears to have originated, particularly women, reported PTSD symptoms after the COVID-19 outbreak, and anxiety was highest in those under age 35 years and those who followed news about the disease for more than 3 hours a day.

Better sleep quality and fewer early morning awakenings, however, appeared to be protective against PTSD symptoms. The authors note the value of physical exercise, cognitive interventions, and relaxation techniques, including meditation, for reducing stress and milder symptoms of PTSD.

“Some patients are sleeping a bit better because of the pace of things has slowed down a bit,” said Anne C. Trainor, a nurse practitioner and instructor in the neurology department’s sleep disorders program at Oregon Health & Science University in Portland, who was not involved in the study. “Keeping a regular schedule for sleeping and eating, getting exercise daily – preferably in sunlight and not just before bedtime – and using relaxation or mindfulness practice and cognitive interventions to help manage anxiety” were the key takeaways from this review, Ms. Trainor said in an interview.


 

Home confinement, stressors and sleep

A wide range of stressors could affect sleep during COVID-19 social distancing interventions, including “major changes in routines, living with uncertainty,” and anxiety about health, the economic situation, and how long this situation will last, the authors write.

Parents must juggle work, homeschooling, and ordinary household errands and management. Meanwhile, entrepreneurs, small business owners ,and workers in entertainment, hospitality and food service must contend with anxiety about job uncertainty and financial security. For anyone working from home, disruptions to work and home routines can make it difficult to associate being home with relaxation – and sleep.

“The more regular our sleep schedule is the better quality our sleep tends to be, but it is a struggle when we don’t have separate spaces to work and parent in,” Ms. Trainor said.

At the same time, “confinement-related stress may be caused by an inability to engage in rewarding activities, such as visiting friends and family, shopping, attending cultural and sports events, and visiting bars or restaurants,” the authors write. “Spending more time with family in a limited space can also induce stress, particularly in situations where there are preexisting family difficulties.”

Being stuck at home may lead to less daylight exposure than usual, reduced physical activity, and increased eating, which can contribute to weight gain and other health risks. However, “the effect of stress from confinement, loss of work, and health concerns needs to be individualized and may be difficult to generalize,” Dr. Sundar said.

The authors of the review note the established associations between too little social interaction, increased stress, and poor sleep quality, though loneliness mediates this relationship. Loneliness is also a risk during this time, with or without online social interaction.

Children and teens may also have difficulty sleeping, which can affect their behavioral and emotional regulation, and primary caregivers experience more stress while juggling childcare, household duties, and work.

“While many parents share childcare and household responsibilities, in most families these tasks are still predominantly managed by mothers,” the authors added.

“Sharing responsibilities between parents and not overworking just one parent is key,” said Brandon M. Seay MD, a pediatric pulmonologist and sleep specialist at Children’s Healthcare of Atlanta. He also recommended trying to incorporate work into the day while kids are doing online learning.

Ms. Trainor agreed that trading off responsibilities between parents is ideal, though the challenge is greater for single parents. It may be possible for some to take family leave, but not all families have that option, she said.

The study authors also point out a Catch-22 for many people: The blurred boundary between home life and work life can undermine work productivity and efficiency, thereby increasing stress. “Healthy sleep may be a key protective factor to cope positively with these challenges, although adequate opportunity to sleep may be affected by increased time pressure of work, childcare, and household requirements.”

Dr. Seay advises adults to try to get at least 6-8 hours of sleep each night, even taking advantage of a later waking time – if the kids also sleep in – to help. “If anything, the ability to sleep later and wake up later is of benefit for a lot of my teenage patients,” he said in an interview.

In fact, the study authors also address possible positive effects on sleep for some people during the current situation. Since social support can improve sleep quality, social media interaction might provide some social support, though it’s not the same as meeting people in person and “screen exposure may hamper sleep quality when used close to bedtime.”

Some people may actually have an opportunity to get more daylight exposure or exercise, which can improve sleep, and some, especially night owls and teenagers, may be able to align their daily schedules more closely to their natural circadian rhythms.

“Given that we are not bound by usual work or social schedules, there may be a tendency to drift to our sleep chronotypes,” especially for teenagers, Dr. Sundar said.

For some, this may be their first opportunity to learn what their chronotype is, Dr. Seay said.

“It is always advantageous to ‘obey’ your natural sleep timing, [although] it simply isn’t always the most efficient outside of our current situation,” he said. “Use this as a time to figure out your natural sleep timing if you constantly have issues being able to wake up in the morning. Now that you don’t have to be up for work or school, you can figure out what time works for you.”

At the same time, if you have an extreme circadian rhythm disorder, especially an irregular one, it may still be best to try to keep a regular sleep schedule to avoid feeling isolated if others are socializing while you’re asleep, Ms. Trainor said.

The authors similarly note the limits of potential benefits during this time, noting that they “may not be enough to counteract the negative effects of the increased work and family requirements, as well as the overwhelming levels of stress and anxiety about the well-being of oneself and others, and the negative effects of confinement for family social reactions.”
 

Treating stress, anxiety, and insomnia

The first-line treatment for chronic insomnia is cognitive-behavioral therapy for insomnia, but “recent evidence shows that cognitive-behavioral therapy can also serve to treat sudden-onset (acute) insomnia due to rapid stress-causing situation changes,” the authors noted. They also reviewed the key elements of CBT-I: stimulus control, sleep hygiene, relaxation interventions, cognitive reappraisal, paradoxical intention, and sleep restriction.

CBT-I lends very naturally to telemedicine, Dr. Seay, Dr. Sundar, and Ms. Trainor all agreed.

“I actually see this current situation as an opportunity for health care practices and providers to expand the reach of telemedicine – due to necessity – which will hopefully continue after confinement has been lifted worldwide,” Dr. Seay said.  

Dr. Sundar pointed to research supporting CBT-I online and several apps that can be used for it, such as SHUTi and Sleepio. Ms. Trainor noted that the Cleveland Clinic offers a basic CBT-I online class for $40.

The authors note that prescribing medication is generally discouraged because it lacks evidence for long-term effectiveness of chronic insomnia, but it might be worth considering as a second-line therapy for acute insomnia from outside stressors, such as home confinement, if CBT-I doesn’t work or isn’t possible. Pharmacologic treatment can include benzodiazepines, hypnotic benzodiazepine receptor agonists, or sedating antidepressants, particularly if used for a comorbid mood disorder.

The authors then offer general recommendations for improving sleep that doctors can pass on to their patients:

• Get up and go to bed at approximately the same times daily.
• Schedule 15-minute breaks during the day to manage stress and reflect on worries and the situation.
• Reserve the bed for sleep and sex only; not for working, watching TV, using the computer, or doing other activities.
• Try to follow your natural sleep rhythm as much as possible.
• Use social media as stress relief, an opportunity to communicate with friends and family, and distraction, especially with uplifting stories or humor.
• Leave devices out of the bedroom.
• Limit your exposure to news about the COVID-19 pandemic.
• Exercise regularly, ideally in daylight.
• Look for ways to stay busy and distracted, including making your home or bedroom more comfortable if possible.
• Get as much daylight during the day as possible, and keep lights dim or dark at night.
• Engage in familiar, comfortable, relaxing activities before bedtime.
• If your daily activity level is lower, eat less as well, ideally at least 2 hours before going to bed.

The authors also offered recommendations specifically for families:

• Divide child care, home maintenance, and chores between adults, being sure not to let the lion’s share fall on women.
• Maintain regular sleep times for children and spend the 30 minutes before their bedtime doing a calming, familiar activity that both the children and parents enjoy.
• “While using computer, smartphones, and watching TV more than usual may be inevitable in confinement, avoid technological devices after dinner or too close to bedtime.”
• Ensure your child has daily physical activity, keep a relatively consistent schedule or routine, expose them to as much daylight or bright light as possible during the day, and try to limit their bed use only to sleeping if possible. “Parents need to be involved in setting schedules for sleep and meal times so that kids do not get into sleep patterns that are difficult to change when school starts back,” Dr. Sundar said. “Limiting screen time is also important especially during nighttime.”
• Reassure children if they wake up anxious at night.

SOURCE: Altena E et al. J Sleep Res. 2020 Apr 4. doi: 10.1111/jsr.13052.

Mass social distancing and social isolation to prevent the spread of a deadly disease, along with technological tools that allow social communication and continued work and school, is an unprecedented situation.

Stockbyte/Thinkstock.com

The current reality of most people’s lives during the COVID-19 pandemic has the potential to induce or exacerbate sleep problems, though it may also present some with an opportunity to improve sleep, wrote Ellemarije Altena, PhD, of the University of Bordeaux (France), and her colleagues in a recent research review in the Journal of Sleep Research.

The review was conducted by a task force of the European Academy for Cognitive Behavioural Therapy for Insomnia. The European CBT-I Academy is an initiative of the European Insomnia Network to promote implementation and dissemination of treatment.

After discussing the known effects of stress, confinement, and altered schedules on sleep, the authors present recommendations on ways to manage sleep problems such as insomnia in the general public and potentially encourage people to take advantage of the opportunity to align their schedules with their natural circadian rhythms. Physicians may find the recommendations helpful in advising patients with sleep problems related to the COVID-19 emergency.

“Being forced to stay at home, work from home, do homeschooling with children, drastically minimize outings, reduce social interaction or work many more hours under stressful circumstances, and in parallel manage the attendant health risks, can have a major impact on daily functioning and nighttime sleep,” Dr. Altena and colleagues wrote.

There may also be a lag time in physicians hearing about changes in sleep or sleeping problems from patients, said Krishna M. Sundar, MD, FCCP, medical director of the Sleep-Wake Center at the University of Utah in Salt Lake City. “There may actually be some improvement in sleep durations given that most folks are working from home with more time with family and less work-related stress,” he said in an interview. “In terms of sleep or other effects on worsening of psychiatric problems, it is still not clear what the overall effects are going to be.”

Although daylight has the biggest impact on regulating circadian rhythms, artificial light, meal times, diet, and amount of physical activity can also have an influence. Negative effects on sleep can result from both excessively high activity levels, such as stress and work overload, or excessively low levels, such as from depression or confinement, the authors note.

The current situation also opens the door to interactions between stress, sleep, anxiety, and risk of PTSD. “Those sensitive to stress-related sleep disruption are more likely to develop chronic insomnia,” which, in combination with a major stressor, is a risk factor for PTSD, the authors write. They note that 7% of Wuhan residents, the city in China where the virus appears to have originated, particularly women, reported PTSD symptoms after the COVID-19 outbreak, and anxiety was highest in those under age 35 years and those who followed news about the disease for more than 3 hours a day.

Better sleep quality and fewer early morning awakenings, however, appeared to be protective against PTSD symptoms. The authors note the value of physical exercise, cognitive interventions, and relaxation techniques, including meditation, for reducing stress and milder symptoms of PTSD.

“Some patients are sleeping a bit better because of the pace of things has slowed down a bit,” said Anne C. Trainor, a nurse practitioner and instructor in the neurology department’s sleep disorders program at Oregon Health & Science University in Portland, who was not involved in the study. “Keeping a regular schedule for sleeping and eating, getting exercise daily – preferably in sunlight and not just before bedtime – and using relaxation or mindfulness practice and cognitive interventions to help manage anxiety” were the key takeaways from this review, Ms. Trainor said in an interview.


 

Home confinement, stressors and sleep

A wide range of stressors could affect sleep during COVID-19 social distancing interventions, including “major changes in routines, living with uncertainty,” and anxiety about health, the economic situation, and how long this situation will last, the authors write.

Parents must juggle work, homeschooling, and ordinary household errands and management. Meanwhile, entrepreneurs, small business owners ,and workers in entertainment, hospitality and food service must contend with anxiety about job uncertainty and financial security. For anyone working from home, disruptions to work and home routines can make it difficult to associate being home with relaxation – and sleep.

“The more regular our sleep schedule is the better quality our sleep tends to be, but it is a struggle when we don’t have separate spaces to work and parent in,” Ms. Trainor said.

At the same time, “confinement-related stress may be caused by an inability to engage in rewarding activities, such as visiting friends and family, shopping, attending cultural and sports events, and visiting bars or restaurants,” the authors write. “Spending more time with family in a limited space can also induce stress, particularly in situations where there are preexisting family difficulties.”

Being stuck at home may lead to less daylight exposure than usual, reduced physical activity, and increased eating, which can contribute to weight gain and other health risks. However, “the effect of stress from confinement, loss of work, and health concerns needs to be individualized and may be difficult to generalize,” Dr. Sundar said.

The authors of the review note the established associations between too little social interaction, increased stress, and poor sleep quality, though loneliness mediates this relationship. Loneliness is also a risk during this time, with or without online social interaction.

Children and teens may also have difficulty sleeping, which can affect their behavioral and emotional regulation, and primary caregivers experience more stress while juggling childcare, household duties, and work.

“While many parents share childcare and household responsibilities, in most families these tasks are still predominantly managed by mothers,” the authors added.

“Sharing responsibilities between parents and not overworking just one parent is key,” said Brandon M. Seay MD, a pediatric pulmonologist and sleep specialist at Children’s Healthcare of Atlanta. He also recommended trying to incorporate work into the day while kids are doing online learning.

Ms. Trainor agreed that trading off responsibilities between parents is ideal, though the challenge is greater for single parents. It may be possible for some to take family leave, but not all families have that option, she said.

The study authors also point out a Catch-22 for many people: The blurred boundary between home life and work life can undermine work productivity and efficiency, thereby increasing stress. “Healthy sleep may be a key protective factor to cope positively with these challenges, although adequate opportunity to sleep may be affected by increased time pressure of work, childcare, and household requirements.”

Dr. Seay advises adults to try to get at least 6-8 hours of sleep each night, even taking advantage of a later waking time – if the kids also sleep in – to help. “If anything, the ability to sleep later and wake up later is of benefit for a lot of my teenage patients,” he said in an interview.

In fact, the study authors also address possible positive effects on sleep for some people during the current situation. Since social support can improve sleep quality, social media interaction might provide some social support, though it’s not the same as meeting people in person and “screen exposure may hamper sleep quality when used close to bedtime.”

Some people may actually have an opportunity to get more daylight exposure or exercise, which can improve sleep, and some, especially night owls and teenagers, may be able to align their daily schedules more closely to their natural circadian rhythms.

“Given that we are not bound by usual work or social schedules, there may be a tendency to drift to our sleep chronotypes,” especially for teenagers, Dr. Sundar said.

For some, this may be their first opportunity to learn what their chronotype is, Dr. Seay said.

“It is always advantageous to ‘obey’ your natural sleep timing, [although] it simply isn’t always the most efficient outside of our current situation,” he said. “Use this as a time to figure out your natural sleep timing if you constantly have issues being able to wake up in the morning. Now that you don’t have to be up for work or school, you can figure out what time works for you.”

At the same time, if you have an extreme circadian rhythm disorder, especially an irregular one, it may still be best to try to keep a regular sleep schedule to avoid feeling isolated if others are socializing while you’re asleep, Ms. Trainor said.

The authors similarly note the limits of potential benefits during this time, noting that they “may not be enough to counteract the negative effects of the increased work and family requirements, as well as the overwhelming levels of stress and anxiety about the well-being of oneself and others, and the negative effects of confinement for family social reactions.”
 

Treating stress, anxiety, and insomnia

The first-line treatment for chronic insomnia is cognitive-behavioral therapy for insomnia, but “recent evidence shows that cognitive-behavioral therapy can also serve to treat sudden-onset (acute) insomnia due to rapid stress-causing situation changes,” the authors noted. They also reviewed the key elements of CBT-I: stimulus control, sleep hygiene, relaxation interventions, cognitive reappraisal, paradoxical intention, and sleep restriction.

CBT-I lends very naturally to telemedicine, Dr. Seay, Dr. Sundar, and Ms. Trainor all agreed.

“I actually see this current situation as an opportunity for health care practices and providers to expand the reach of telemedicine – due to necessity – which will hopefully continue after confinement has been lifted worldwide,” Dr. Seay said.  

Dr. Sundar pointed to research supporting CBT-I online and several apps that can be used for it, such as SHUTi and Sleepio. Ms. Trainor noted that the Cleveland Clinic offers a basic CBT-I online class for $40.

The authors note that prescribing medication is generally discouraged because it lacks evidence for long-term effectiveness of chronic insomnia, but it might be worth considering as a second-line therapy for acute insomnia from outside stressors, such as home confinement, if CBT-I doesn’t work or isn’t possible. Pharmacologic treatment can include benzodiazepines, hypnotic benzodiazepine receptor agonists, or sedating antidepressants, particularly if used for a comorbid mood disorder.

The authors then offer general recommendations for improving sleep that doctors can pass on to their patients:

• Get up and go to bed at approximately the same times daily.
• Schedule 15-minute breaks during the day to manage stress and reflect on worries and the situation.
• Reserve the bed for sleep and sex only; not for working, watching TV, using the computer, or doing other activities.
• Try to follow your natural sleep rhythm as much as possible.
• Use social media as stress relief, an opportunity to communicate with friends and family, and distraction, especially with uplifting stories or humor.
• Leave devices out of the bedroom.
• Limit your exposure to news about the COVID-19 pandemic.
• Exercise regularly, ideally in daylight.
• Look for ways to stay busy and distracted, including making your home or bedroom more comfortable if possible.
• Get as much daylight during the day as possible, and keep lights dim or dark at night.
• Engage in familiar, comfortable, relaxing activities before bedtime.
• If your daily activity level is lower, eat less as well, ideally at least 2 hours before going to bed.

The authors also offered recommendations specifically for families:

• Divide child care, home maintenance, and chores between adults, being sure not to let the lion’s share fall on women.
• Maintain regular sleep times for children and spend the 30 minutes before their bedtime doing a calming, familiar activity that both the children and parents enjoy.
• “While using computer, smartphones, and watching TV more than usual may be inevitable in confinement, avoid technological devices after dinner or too close to bedtime.”
• Ensure your child has daily physical activity, keep a relatively consistent schedule or routine, expose them to as much daylight or bright light as possible during the day, and try to limit their bed use only to sleeping if possible. “Parents need to be involved in setting schedules for sleep and meal times so that kids do not get into sleep patterns that are difficult to change when school starts back,” Dr. Sundar said. “Limiting screen time is also important especially during nighttime.”
• Reassure children if they wake up anxious at night.

SOURCE: Altena E et al. J Sleep Res. 2020 Apr 4. doi: 10.1111/jsr.13052.

Mass social distancing and social isolation to prevent the spread of a deadly disease, along with technological tools that allow social communication and continued work and school, is an unprecedented situation.

Stockbyte/Thinkstock.com

The current reality of most people’s lives during the COVID-19 pandemic has the potential to induce or exacerbate sleep problems, though it may also present some with an opportunity to improve sleep, wrote Ellemarije Altena, PhD, of the University of Bordeaux (France), and her colleagues in a recent research review in the Journal of Sleep Research.

The review was conducted by a task force of the European Academy for Cognitive Behavioural Therapy for Insomnia. The European CBT-I Academy is an initiative of the European Insomnia Network to promote implementation and dissemination of treatment.

After discussing the known effects of stress, confinement, and altered schedules on sleep, the authors present recommendations on ways to manage sleep problems such as insomnia in the general public and potentially encourage people to take advantage of the opportunity to align their schedules with their natural circadian rhythms. Physicians may find the recommendations helpful in advising patients with sleep problems related to the COVID-19 emergency.

“Being forced to stay at home, work from home, do homeschooling with children, drastically minimize outings, reduce social interaction or work many more hours under stressful circumstances, and in parallel manage the attendant health risks, can have a major impact on daily functioning and nighttime sleep,” Dr. Altena and colleagues wrote.

There may also be a lag time in physicians hearing about changes in sleep or sleeping problems from patients, said Krishna M. Sundar, MD, FCCP, medical director of the Sleep-Wake Center at the University of Utah in Salt Lake City. “There may actually be some improvement in sleep durations given that most folks are working from home with more time with family and less work-related stress,” he said in an interview. “In terms of sleep or other effects on worsening of psychiatric problems, it is still not clear what the overall effects are going to be.”

Although daylight has the biggest impact on regulating circadian rhythms, artificial light, meal times, diet, and amount of physical activity can also have an influence. Negative effects on sleep can result from both excessively high activity levels, such as stress and work overload, or excessively low levels, such as from depression or confinement, the authors note.

The current situation also opens the door to interactions between stress, sleep, anxiety, and risk of PTSD. “Those sensitive to stress-related sleep disruption are more likely to develop chronic insomnia,” which, in combination with a major stressor, is a risk factor for PTSD, the authors write. They note that 7% of Wuhan residents, the city in China where the virus appears to have originated, particularly women, reported PTSD symptoms after the COVID-19 outbreak, and anxiety was highest in those under age 35 years and those who followed news about the disease for more than 3 hours a day.

Better sleep quality and fewer early morning awakenings, however, appeared to be protective against PTSD symptoms. The authors note the value of physical exercise, cognitive interventions, and relaxation techniques, including meditation, for reducing stress and milder symptoms of PTSD.

“Some patients are sleeping a bit better because of the pace of things has slowed down a bit,” said Anne C. Trainor, a nurse practitioner and instructor in the neurology department’s sleep disorders program at Oregon Health & Science University in Portland, who was not involved in the study. “Keeping a regular schedule for sleeping and eating, getting exercise daily – preferably in sunlight and not just before bedtime – and using relaxation or mindfulness practice and cognitive interventions to help manage anxiety” were the key takeaways from this review, Ms. Trainor said in an interview.


 

Home confinement, stressors and sleep

A wide range of stressors could affect sleep during COVID-19 social distancing interventions, including “major changes in routines, living with uncertainty,” and anxiety about health, the economic situation, and how long this situation will last, the authors write.

Parents must juggle work, homeschooling, and ordinary household errands and management. Meanwhile, entrepreneurs, small business owners ,and workers in entertainment, hospitality and food service must contend with anxiety about job uncertainty and financial security. For anyone working from home, disruptions to work and home routines can make it difficult to associate being home with relaxation – and sleep.

“The more regular our sleep schedule is the better quality our sleep tends to be, but it is a struggle when we don’t have separate spaces to work and parent in,” Ms. Trainor said.

At the same time, “confinement-related stress may be caused by an inability to engage in rewarding activities, such as visiting friends and family, shopping, attending cultural and sports events, and visiting bars or restaurants,” the authors write. “Spending more time with family in a limited space can also induce stress, particularly in situations where there are preexisting family difficulties.”

Being stuck at home may lead to less daylight exposure than usual, reduced physical activity, and increased eating, which can contribute to weight gain and other health risks. However, “the effect of stress from confinement, loss of work, and health concerns needs to be individualized and may be difficult to generalize,” Dr. Sundar said.

The authors of the review note the established associations between too little social interaction, increased stress, and poor sleep quality, though loneliness mediates this relationship. Loneliness is also a risk during this time, with or without online social interaction.

Children and teens may also have difficulty sleeping, which can affect their behavioral and emotional regulation, and primary caregivers experience more stress while juggling childcare, household duties, and work.

“While many parents share childcare and household responsibilities, in most families these tasks are still predominantly managed by mothers,” the authors added.

“Sharing responsibilities between parents and not overworking just one parent is key,” said Brandon M. Seay MD, a pediatric pulmonologist and sleep specialist at Children’s Healthcare of Atlanta. He also recommended trying to incorporate work into the day while kids are doing online learning.

Ms. Trainor agreed that trading off responsibilities between parents is ideal, though the challenge is greater for single parents. It may be possible for some to take family leave, but not all families have that option, she said.

The study authors also point out a Catch-22 for many people: The blurred boundary between home life and work life can undermine work productivity and efficiency, thereby increasing stress. “Healthy sleep may be a key protective factor to cope positively with these challenges, although adequate opportunity to sleep may be affected by increased time pressure of work, childcare, and household requirements.”

Dr. Seay advises adults to try to get at least 6-8 hours of sleep each night, even taking advantage of a later waking time – if the kids also sleep in – to help. “If anything, the ability to sleep later and wake up later is of benefit for a lot of my teenage patients,” he said in an interview.

In fact, the study authors also address possible positive effects on sleep for some people during the current situation. Since social support can improve sleep quality, social media interaction might provide some social support, though it’s not the same as meeting people in person and “screen exposure may hamper sleep quality when used close to bedtime.”

Some people may actually have an opportunity to get more daylight exposure or exercise, which can improve sleep, and some, especially night owls and teenagers, may be able to align their daily schedules more closely to their natural circadian rhythms.

“Given that we are not bound by usual work or social schedules, there may be a tendency to drift to our sleep chronotypes,” especially for teenagers, Dr. Sundar said.

For some, this may be their first opportunity to learn what their chronotype is, Dr. Seay said.

“It is always advantageous to ‘obey’ your natural sleep timing, [although] it simply isn’t always the most efficient outside of our current situation,” he said. “Use this as a time to figure out your natural sleep timing if you constantly have issues being able to wake up in the morning. Now that you don’t have to be up for work or school, you can figure out what time works for you.”

At the same time, if you have an extreme circadian rhythm disorder, especially an irregular one, it may still be best to try to keep a regular sleep schedule to avoid feeling isolated if others are socializing while you’re asleep, Ms. Trainor said.

The authors similarly note the limits of potential benefits during this time, noting that they “may not be enough to counteract the negative effects of the increased work and family requirements, as well as the overwhelming levels of stress and anxiety about the well-being of oneself and others, and the negative effects of confinement for family social reactions.”
 

Treating stress, anxiety, and insomnia

The first-line treatment for chronic insomnia is cognitive-behavioral therapy for insomnia, but “recent evidence shows that cognitive-behavioral therapy can also serve to treat sudden-onset (acute) insomnia due to rapid stress-causing situation changes,” the authors noted. They also reviewed the key elements of CBT-I: stimulus control, sleep hygiene, relaxation interventions, cognitive reappraisal, paradoxical intention, and sleep restriction.

CBT-I lends very naturally to telemedicine, Dr. Seay, Dr. Sundar, and Ms. Trainor all agreed.

“I actually see this current situation as an opportunity for health care practices and providers to expand the reach of telemedicine – due to necessity – which will hopefully continue after confinement has been lifted worldwide,” Dr. Seay said.  

Dr. Sundar pointed to research supporting CBT-I online and several apps that can be used for it, such as SHUTi and Sleepio. Ms. Trainor noted that the Cleveland Clinic offers a basic CBT-I online class for $40.

The authors note that prescribing medication is generally discouraged because it lacks evidence for long-term effectiveness of chronic insomnia, but it might be worth considering as a second-line therapy for acute insomnia from outside stressors, such as home confinement, if CBT-I doesn’t work or isn’t possible. Pharmacologic treatment can include benzodiazepines, hypnotic benzodiazepine receptor agonists, or sedating antidepressants, particularly if used for a comorbid mood disorder.

The authors then offer general recommendations for improving sleep that doctors can pass on to their patients:

• Get up and go to bed at approximately the same times daily.
• Schedule 15-minute breaks during the day to manage stress and reflect on worries and the situation.
• Reserve the bed for sleep and sex only; not for working, watching TV, using the computer, or doing other activities.
• Try to follow your natural sleep rhythm as much as possible.
• Use social media as stress relief, an opportunity to communicate with friends and family, and distraction, especially with uplifting stories or humor.
• Leave devices out of the bedroom.
• Limit your exposure to news about the COVID-19 pandemic.
• Exercise regularly, ideally in daylight.
• Look for ways to stay busy and distracted, including making your home or bedroom more comfortable if possible.
• Get as much daylight during the day as possible, and keep lights dim or dark at night.
• Engage in familiar, comfortable, relaxing activities before bedtime.
• If your daily activity level is lower, eat less as well, ideally at least 2 hours before going to bed.

The authors also offered recommendations specifically for families:

• Divide child care, home maintenance, and chores between adults, being sure not to let the lion’s share fall on women.
• Maintain regular sleep times for children and spend the 30 minutes before their bedtime doing a calming, familiar activity that both the children and parents enjoy.
• “While using computer, smartphones, and watching TV more than usual may be inevitable in confinement, avoid technological devices after dinner or too close to bedtime.”
• Ensure your child has daily physical activity, keep a relatively consistent schedule or routine, expose them to as much daylight or bright light as possible during the day, and try to limit their bed use only to sleeping if possible. “Parents need to be involved in setting schedules for sleep and meal times so that kids do not get into sleep patterns that are difficult to change when school starts back,” Dr. Sundar said. “Limiting screen time is also important especially during nighttime.”
• Reassure children if they wake up anxious at night.

SOURCE: Altena E et al. J Sleep Res. 2020 Apr 4. doi: 10.1111/jsr.13052.

Among patients admitted to a hospital with chronic obstructive pulmonary disease (COPD) exacerbation, obstructive sleep apnea (OSA) is prevalent and increases the likelihood of hospital readmission more than threefold, according to results from a single-center study published in CHEST.

Mario Naranjo, MD, and colleagues retrospectively examined data from Albert Einstein Medical Center in Philadelphia to assess the impact of OSA on hospital readmission within 30 days of discharge after treatment for a COPD exacerbation. Dr. Naranjo is affiliated with Johns Hopkins Medicine, Baltimore.

The researchers analyzed data from 238 patients admitted for COPD exacerbation between May 2017 and July 2018 who were screened for previously unrecognized and untreated OSA and underwent a high-resolution pulse-oximetry or portable sleep monitoring study. In all, 111 (46.6%) had OSA; 28.6% had mild OSA, 9.7% had moderate OSA, and 8.4% had severe OSA.

Most baseline characteristics were similar among patients with and without OSA, but patients with OSA had a greater mean body mass index (33.9 vs. 30.3 kg/m²) and were more likely to have comorbid heart failure (19.8% vs. 7.1%), compared with patients without OSA. In addition, the proportion of male patients was greater in the cohort with OSA (60.4% vs. 49.6%).

For patients with mild OSA (oxygen desaturation index [ODI] ≥ 5 and < 15/hour), the odds of 30-day readmission were 2.05 times higher, compared with patients without OSA (32.4% vs. 18.9%). With moderate OSA (ODI ≥ 15 and < 30/hour), the odds of 30-day readmission were 6.68 times higher (60.9% vs. 18.9%). For severe OSA (ODI ≥ 30/hour), the odds were 10.01 times higher (70.0% vs. 18.9%). “For combined OSA severity categories, the odds of 30-day readmission were 3.5 times higher,” said Dr. Naranjo and colleagues. In addition, 90- and 180-day readmission rates and 6-month mortality rates were higher among patients with OSA.

“These findings have important implications for the evaluation and care of patients admitted to the hospital for COPD exacerbations,” Dr. Naranjo and colleagues said. “Although the combination of COPD and OSA (also known as the “overlap syndrome”) in ambulatory settings has been shown to have worse outcomes in terms of COPD exacerbations and mortality, these findings have not been reported previously for hospitalized COPD patients.”

Greater degrees of nocturnal hypoxemia and hypercapnia, worse functional status, and daytime sleepiness and fatigue may contribute to the relationship between OSA and the likelihood of hospital readmission, according to the authors. A multicenter study is warranted to confirm the results, they said.

Dr. Naranjo had no conflicts of interest. Coauthors have received grants from ResMed, Dayzz, and the National Institutes of Health and consulted for Jazz Pharmaceuticals, Best Doctors, and ResMed. One author is a committee chair for the American Academy of Sleep Medicine.

[email protected]

SOURCE: Naranjo M et al. Chest. 2020 Apr 2. doi: 10.1016/j.chest.2020.03.036.

Among patients admitted to a hospital with chronic obstructive pulmonary disease (COPD) exacerbation, obstructive sleep apnea (OSA) is prevalent and increases the likelihood of hospital readmission more than threefold, according to results from a single-center study published in CHEST.

Mario Naranjo, MD, and colleagues retrospectively examined data from Albert Einstein Medical Center in Philadelphia to assess the impact of OSA on hospital readmission within 30 days of discharge after treatment for a COPD exacerbation. Dr. Naranjo is affiliated with Johns Hopkins Medicine, Baltimore.

The researchers analyzed data from 238 patients admitted for COPD exacerbation between May 2017 and July 2018 who were screened for previously unrecognized and untreated OSA and underwent a high-resolution pulse-oximetry or portable sleep monitoring study. In all, 111 (46.6%) had OSA; 28.6% had mild OSA, 9.7% had moderate OSA, and 8.4% had severe OSA.

Most baseline characteristics were similar among patients with and without OSA, but patients with OSA had a greater mean body mass index (33.9 vs. 30.3 kg/m²) and were more likely to have comorbid heart failure (19.8% vs. 7.1%), compared with patients without OSA. In addition, the proportion of male patients was greater in the cohort with OSA (60.4% vs. 49.6%).

For patients with mild OSA (oxygen desaturation index [ODI] ≥ 5 and < 15/hour), the odds of 30-day readmission were 2.05 times higher, compared with patients without OSA (32.4% vs. 18.9%). With moderate OSA (ODI ≥ 15 and < 30/hour), the odds of 30-day readmission were 6.68 times higher (60.9% vs. 18.9%). For severe OSA (ODI ≥ 30/hour), the odds were 10.01 times higher (70.0% vs. 18.9%). “For combined OSA severity categories, the odds of 30-day readmission were 3.5 times higher,” said Dr. Naranjo and colleagues. In addition, 90- and 180-day readmission rates and 6-month mortality rates were higher among patients with OSA.

“These findings have important implications for the evaluation and care of patients admitted to the hospital for COPD exacerbations,” Dr. Naranjo and colleagues said. “Although the combination of COPD and OSA (also known as the “overlap syndrome”) in ambulatory settings has been shown to have worse outcomes in terms of COPD exacerbations and mortality, these findings have not been reported previously for hospitalized COPD patients.”

Greater degrees of nocturnal hypoxemia and hypercapnia, worse functional status, and daytime sleepiness and fatigue may contribute to the relationship between OSA and the likelihood of hospital readmission, according to the authors. A multicenter study is warranted to confirm the results, they said.

Dr. Naranjo had no conflicts of interest. Coauthors have received grants from ResMed, Dayzz, and the National Institutes of Health and consulted for Jazz Pharmaceuticals, Best Doctors, and ResMed. One author is a committee chair for the American Academy of Sleep Medicine.

[email protected]

SOURCE: Naranjo M et al. Chest. 2020 Apr 2. doi: 10.1016/j.chest.2020.03.036.

Among patients admitted to a hospital with chronic obstructive pulmonary disease (COPD) exacerbation, obstructive sleep apnea (OSA) is prevalent and increases the likelihood of hospital readmission more than threefold, according to results from a single-center study published in CHEST.

Mario Naranjo, MD, and colleagues retrospectively examined data from Albert Einstein Medical Center in Philadelphia to assess the impact of OSA on hospital readmission within 30 days of discharge after treatment for a COPD exacerbation. Dr. Naranjo is affiliated with Johns Hopkins Medicine, Baltimore.

The researchers analyzed data from 238 patients admitted for COPD exacerbation between May 2017 and July 2018 who were screened for previously unrecognized and untreated OSA and underwent a high-resolution pulse-oximetry or portable sleep monitoring study. In all, 111 (46.6%) had OSA; 28.6% had mild OSA, 9.7% had moderate OSA, and 8.4% had severe OSA.

Most baseline characteristics were similar among patients with and without OSA, but patients with OSA had a greater mean body mass index (33.9 vs. 30.3 kg/m²) and were more likely to have comorbid heart failure (19.8% vs. 7.1%), compared with patients without OSA. In addition, the proportion of male patients was greater in the cohort with OSA (60.4% vs. 49.6%).

For patients with mild OSA (oxygen desaturation index [ODI] ≥ 5 and < 15/hour), the odds of 30-day readmission were 2.05 times higher, compared with patients without OSA (32.4% vs. 18.9%). With moderate OSA (ODI ≥ 15 and < 30/hour), the odds of 30-day readmission were 6.68 times higher (60.9% vs. 18.9%). For severe OSA (ODI ≥ 30/hour), the odds were 10.01 times higher (70.0% vs. 18.9%). “For combined OSA severity categories, the odds of 30-day readmission were 3.5 times higher,” said Dr. Naranjo and colleagues. In addition, 90- and 180-day readmission rates and 6-month mortality rates were higher among patients with OSA.

“These findings have important implications for the evaluation and care of patients admitted to the hospital for COPD exacerbations,” Dr. Naranjo and colleagues said. “Although the combination of COPD and OSA (also known as the “overlap syndrome”) in ambulatory settings has been shown to have worse outcomes in terms of COPD exacerbations and mortality, these findings have not been reported previously for hospitalized COPD patients.”

Greater degrees of nocturnal hypoxemia and hypercapnia, worse functional status, and daytime sleepiness and fatigue may contribute to the relationship between OSA and the likelihood of hospital readmission, according to the authors. A multicenter study is warranted to confirm the results, they said.

Dr. Naranjo had no conflicts of interest. Coauthors have received grants from ResMed, Dayzz, and the National Institutes of Health and consulted for Jazz Pharmaceuticals, Best Doctors, and ResMed. One author is a committee chair for the American Academy of Sleep Medicine.

[email protected]

SOURCE: Naranjo M et al. Chest. 2020 Apr 2. doi: 10.1016/j.chest.2020.03.036.

Obstructive sleep apnea (OSA) is a common disorder in the US and other industrialized countries. The Wisconsin Sleep Cohort Study reported prevalence rates as high as 20% to 30% in men and 10% to 15% in women.^1,2 Several studies have shown high prevalence of OSA among veterans. Ancoli-Israel and colleagues reported a OSA rate of 36% in a cohort of elderly patients at a US Department of Veterans Affairs (VA) medical center.³ A study by Kreis and colleagues showed that OSA was present in 27% of patients hospitalized on the medical ward at a VA hospital.⁴ Incidence of sleep apnea among veterans in the US will likely increase over time as obesity is becoming more prevalent. Rates of obesity have increased from 14% in 2000 to 18% in 2010 among both male and female veterans.⁵

Untreated OSA is associated with increased risk of coronary artery disease, cerebrovascular accidents, uncontrolled diabetes mellitus, and other complications. Patients with OSA are less productive, have increased health care utilization, and have a higher risk of motor vehicle accidents.⁶ Continuous positive airway pressure (CPAP) is the main form of treatment of OSA. However, despite the adverse outcomes of untreated sleep apnea, suboptimal CPAP adherence remains a major problem in clinical practice. When adherence is defined as > 4 hours of nightly use, 29% to 83% of patients with OSA have been reported to be nonadherent to treatment.⁷ Stepnowsky and colleagues estimated that 50% of patients with OSA for whom CPAP was recommended were no longer using it 1 year later.⁸ CPAP adherence among veterans also has been poor. Wallace and colleagues reported that about one-third of patients with OSA at a VA Miami Healthcare System had mean daily use ≥ 4 hours.⁹ Typical reasons for poor CPAP adherence include pressure intolerance, mask discomfort, nasal and oropharyngeal dryness and irritation.¹⁰ Development and implementation of alternate treatment strategies for OSA is important to reduce disease burden of this widespread and debilitating condition.

Upper airway stimulation (UAS) is a novel therapy for management of OSA that has been gaining popularity and acceptance within the sleep medicine community in the past few years. This treatment option involves implantation of a neurostimulator with a sensing lead and a stimulation lead. The device is similar to a pacemaker and is surgically implanted in chest wall. The sensing lead is placed close to the diaphragm for monitoring of pleural pressure to help assess ventilation. The stimulation lead is placed under the tongue in proximity to the hypoglossal nerve (cranial nerve XII). The neurostimulator delivers electrical pulses to the hypoglossal nerve through the stimulation lead. These stimulating pulses are synchronized with the ventilation detected by the sensing lead. This electrical stimulation results in anterior displacement of the tongue via action of the genioglossus and geniohyoid muscles. Mechanical coupling with the palate also is common and leads to additional airway opening within the oropharynx to prevent apneic episodes. The patient turns on the stimulation through the use of a portable remote control and is turned off in the morning. The patient is able to operate the UAS device by placing the remote control on the skin in proximity of the device. The patient also is able to adjust device voltage within a range set by their physician. The effective voltage range is determined via an overnight sleep study titration performed 1 month after device activation. UAS therapy is not considered first-line treatment for OSA as it requires surgical implantation under general anesthesia; however, it provides an alternative to patients with OSA who are unable to tolerate traditional therapy with CPAP.

The landmark Stimulation Therapy for Apnea Reduction (STAR) trial showed effectiveness of UAS therapy at 12 months postimplantation.¹¹ Follow-up of these participants has proven the sustainability of this effect at 18, 24, 36, and 48 months of therapy.^12-15 Inclusion criteria of the study was moderate-to-severe sleep apnea with predominantly obstructive events. Subjects were excluded if there were anatomical abnormalities of the upper airway or if the pattern of airway collapse was not conducive to UAS on sedated endoscopy evaluation. Participants in the trial were predominantly white males, the average age was 54.5 years, and the average body mass index (BMI) was 28.4. The outcomes measured included Functional Outcomes of Sleep Questionnaire, Epworth Sleepiness Scale (ESS), percentage of sleep time with oxygen saturation < 90%, and subjective snoring. All of these objective and subjective markers of sleep improved significantly with UAS therapy at 12 months and were maintained at improved levels at 48 months of therapy.

The adverse effects (AEs) associated with device implantation and subsequent UAS therapy have been infrequent and mostly transient. Out of 126 device implantations, there were 2 participants who had serious AEs due to implantation and required repositioning and fixation of the neurostimulator to resolve discomfort. Other AEs related to the procedure, including sore throat and muscle soreness, were considered nonserious and resolved with supportive care. AEs related to subsequent UAS therapy included temporary tongue weakness and tongue soreness/abrasion. These complications also have either resolved spontaneously or with use of supportive strategies such as a mouth guard. Due to the sustained clinical benefit and acceptable AE profile as demonstrated by the STAR trial, UAS has emerged as a realistic alternative for management of OSA.

Development of a successful program that provides and supports all aspects of UAS, including device implantation and follow-up, necessitates a multispecialty team approach. Ideally surgical and nonsurgical sleep physicians as well as clinical and administrative support staff should be part of this group.

This study is based on the experience of the development of the UAS program at the Clement J. Zablocki VA Medical Center (CJZ VAMC) in Milwaukee. Currently, there are 25 patients who are part of this UAS program. The inclusion and exclusion criteria were adopted from the STAR trial. The patient population is similar to the population in that trial. They are all white males with average age of 57.2 years and BMI of 31.3. The CJZVAMC UAS Program consists of multidisciplinary group of health care professionals. This article describes the role of a nonsurgical sleep medicine physician that was crucial in the development of this UAS program.

Process

Introduction of this novel alternative therapy has sparked much interest among health care providers (HCPs) at CJZVAMC. However, there has been much misunderstanding among patients and HCPs about what this treatment involves and how it is implemented. For example, many patients that called the sleep clinic to set up an evaluation for UAS did not realize that this is a surgical procedure that requires general anesthesia. One of the most important tasks for a nonsurgical sleep physician is to educate patients and HCPs about this therapy. Most of patient education at CJZVAMC has been done during individual clinic appointments; however, setting up group educational classes for patients is a more efficient strategy to deliver this information. Similarly, giving a lecture on UAS at medicine (or another specialty) grand rounds has been effective in the education of HCPs who refer patients to the sleep clinic. If possible, a combined lecture with a surgical colleague could provide a more balanced and complete depiction of UAS and help to answer a broader range of questions for the audience.

Screening

Screening and identification of appropriate candidates is an important first step in the patient pathway in the UAS therapy. Failure of CPAP therapy is a key starting point in this screening process. When patients present to the sleep clinic with difficulty tolerating CPAP therapy, an extensive and thorough troubleshooting process needs to take place to make sure that all CPAP options have been exhausted. This process would typically include trial of various masks, including different mask interfaces. A dedicated appointment with a registered polysomnographic technologist (RPSGT) or another clinic staff member with vast experience in PAP mask fitting is typically part of this effort.

Adjustment of CPAP pressure settings also may be helpful as high PAP pressure may be another obstacle. Patients frequently have trouble tolerating higher pressure settings especially when they are new to this therapy. Pressure restriction to 4-cm to 7-cm water pressure on auto CPAP has been a helpful technique to allow patients to become more comfortable with this therapy. Once patients are able to use PAP at lower pressures, these settings can be titrated up gradually for optimal effectiveness. Other desensitization techniques, such as use during daytime while distracted by other activities (such as watching TV) can be helpful in adjustment to PAP therapy. Addressing problems with nasal congestion can help improve PAP adherence. Finally, patients should be offered opportunities for education about their PAP machine on an ongoing basis. Lack of proficiency with humidifier use is a very common obstacle and frequently leads to PAP nonadherence. Teaching PAP operation should correspond to the patient’s level of education to be effective. PAP therapy remains the first-line treatment strategy for OSA as it is not invasive and highly effective. Nonsurgical sleep medicine physicians are uniquely positioned to implement and troubleshoot this therapy for sleep apnea patients before considering UAS.

As part of the screening process, it can be helpful to conduct routine multidisciplinary meetings to discuss patients who are being evaluated for UAS implantation. These meetings should include the otolaryngologist, nonsurgical sleep medicine physician, as well as additional staff (nurses, respiratory therapists, etc) who are involved in the UAS process. Having a mental health care provider as part of the multidisciplinary team during the screening process also could be a valuable addition as this specialist could evaluate and provide insight into a patient’s emotional status prior to implantation. This is common practice during evaluation for organ transplantation and would help to predict patient’s psychological well-being after this life-changing procedure.¹⁶ Having multidisciplinary agreement on patient’s candidacy for UAS therapy could improve long-term success of this treatment. Additionally, these multidisciplinary meetings as part of the UAS program can improve team camaraderie and prevent miscommunications during this therapy.

Drug-Induced Sedated Endoscopy

Patient pathway to neurostimulator implantation involves evaluation of the upper airway using drug-induced sedated endoscopy (DISE). This procedure helps determine whether the patient’s anatomy is appropriate for UAS. DISE also can evaluate the pattern of airway closure during an apneic episode. Anterior-posterior pattern of closure is associated with greater UAS effectiveness compared with concentric pattern of airway closure. DISE is typically performed by the otolaryngologist scheduled to implant the UAS. However, nonsurgical physicians who are part of the patient’s care team can be trained to perform this procedure especially if they have experience in performing endoscopy of the upper airway (such as a pulmonary specialist). This can make the evaluation process more efficient and dramatically improve access to care.

Coordination of Care

In order for the UAS program to be successful, the patient’s care team has to work closely with the device manufacturer throughout the implantation pathway and for ongoing patient care. The device manufacturer can assist with education of HCPs, surgical physicians, clinical support staff, and the patient. However, an even more essential role for industry support is during UAS device activation and subsequent titration of UAS via an overnight in-laboratory sleep study.

After surgical implantation, the UAS device activation can be performed in the nonsurgical sleep clinic and is done about 1 month later. This period allows for tissue healing after the surgery and for the patient to get accustomed to having this new device in their body. This activation can be done with assistance from an industry technician until the HCP is comfortable with this process. The multidisciplinary UAS team could choose to delegate device activation to a technician with specialized relevant training, such as RPSGT or respiratory therapist (RT).

This procedure involves determination of sensory and functional threshold for UAS. Sensory threshold is minimum voltage required for the patient to feel the stimulation. The functional threshold is the minimum voltage required to move the tongue past the lower front teeth during stimulation. After these thresholds are established, a voltage range is set on the device. The voltage at functional threshold is typically set at the lower level of this range, and the maximum level is set at 1 volt higher. Patients are able to adjust voltage within this range and are instructed to increase the voltage gradually (0.1-volt increments) while maintaining levels that are comfortable during sleep.

About a month after device activation, patients undergo another overnight polysomnogram for titration of UAS device. In order to educate and train the institutional RPSGT on how to perform this type of titration, an industry technician is required for the first few overnight titrations. The goal of this study is to establish appropriate voltage to resolve sleep-disordered breathing and insure patient comfort at this setting. Patients typically leave the study with a new voltage range. They are asked to keep effective voltage in mind and make appropriate adjustments to maintain comfortable therapy.

Successful UAS therapy includes multiple steps, such as implantation, activation, and titration. This protocol requires effective coordination of care that includes communication with surgical staff, patients, support staff, and industry liaison. Nonsurgical sleep medicine physicians can play a vital role by helping to coordinate care at the early stages of UAS therapy and facilitate effective communication among various providers involved in this process.

Follow-Up

After completion of the initial therapeutic pathway, patients continue to follow up regularly, monitoring for AEs from UAS therapy and sleep apnea symptoms. Patients can be followed in the nonsurgical sleep clinic after the initial postoperative appointment with the surgeon. Frequency of follow-up depends on the presence and severity of any AEs and residual symptoms of sleep apnea. Even though most AEs related to UAS therapy reported in the STAR trial were nonserious and transient, 2% of participants required surgical revision.³ Therefore, maintaining open channels of communication among the entire UAS patient care team even months and years after surgical implantation is important. The nonsurgical sleep medicine physician who will continue to monitor the patient’s progress may need to consult with the surgical colleague or industry liaison at any point during treatment.
 

Limitations

This review outlines the UAS therapy pathway and emphasizes the role of the nonsurgical sleep medicine provider. However, the experience describes a UAS program development at a single VA medical center. Since this UAS device and therapy have already been approved by the VA on a national level, we did not face any challenges with authorization and insurance compensation. Therefore, this review does not provide any guidance with these matters. These are certainly common concerns for sleep medicine providers who offer UAS therapy in medical practices outside the VA, and these would hopefully be addressed in the future.

Furthermore, this review is based on the pulmonary sleep medicine provider’s experience and perspective. Therefore, certain aspects of UAS therapy could be better addressed by nonsurgical sleep medicine providers in different fields of expertise. For example, a study by a psychiatrist or psychologist could provide insight into the emotional concerns of patients who are undergoing this novel and life-altering treatment that includes surgical implantation of hardware into the body. A neurologist could explore the long-term effects of recurrent electrical stimulation on the autonomic and somatic nervous system as well as the musculature of the upper airway.

Conclusion

Multidisciplinary perspectives are needed to provide guidance for practitioners and institutions looking to set up and improve established UAS programs. As the long-term outcomes of the STAR trial continue to be published and provide more validation for UAS, this novel therapy will likely continue to gain acceptance as a safe and effective treatment for OSA.¹¹

Obstructive sleep apnea (OSA) is a common disorder in the US and other industrialized countries. The Wisconsin Sleep Cohort Study reported prevalence rates as high as 20% to 30% in men and 10% to 15% in women.^1,2 Several studies have shown high prevalence of OSA among veterans. Ancoli-Israel and colleagues reported a OSA rate of 36% in a cohort of elderly patients at a US Department of Veterans Affairs (VA) medical center.³ A study by Kreis and colleagues showed that OSA was present in 27% of patients hospitalized on the medical ward at a VA hospital.⁴ Incidence of sleep apnea among veterans in the US will likely increase over time as obesity is becoming more prevalent. Rates of obesity have increased from 14% in 2000 to 18% in 2010 among both male and female veterans.⁵

Untreated OSA is associated with increased risk of coronary artery disease, cerebrovascular accidents, uncontrolled diabetes mellitus, and other complications. Patients with OSA are less productive, have increased health care utilization, and have a higher risk of motor vehicle accidents.⁶ Continuous positive airway pressure (CPAP) is the main form of treatment of OSA. However, despite the adverse outcomes of untreated sleep apnea, suboptimal CPAP adherence remains a major problem in clinical practice. When adherence is defined as > 4 hours of nightly use, 29% to 83% of patients with OSA have been reported to be nonadherent to treatment.⁷ Stepnowsky and colleagues estimated that 50% of patients with OSA for whom CPAP was recommended were no longer using it 1 year later.⁸ CPAP adherence among veterans also has been poor. Wallace and colleagues reported that about one-third of patients with OSA at a VA Miami Healthcare System had mean daily use ≥ 4 hours.⁹ Typical reasons for poor CPAP adherence include pressure intolerance, mask discomfort, nasal and oropharyngeal dryness and irritation.¹⁰ Development and implementation of alternate treatment strategies for OSA is important to reduce disease burden of this widespread and debilitating condition.

Upper airway stimulation (UAS) is a novel therapy for management of OSA that has been gaining popularity and acceptance within the sleep medicine community in the past few years. This treatment option involves implantation of a neurostimulator with a sensing lead and a stimulation lead. The device is similar to a pacemaker and is surgically implanted in chest wall. The sensing lead is placed close to the diaphragm for monitoring of pleural pressure to help assess ventilation. The stimulation lead is placed under the tongue in proximity to the hypoglossal nerve (cranial nerve XII). The neurostimulator delivers electrical pulses to the hypoglossal nerve through the stimulation lead. These stimulating pulses are synchronized with the ventilation detected by the sensing lead. This electrical stimulation results in anterior displacement of the tongue via action of the genioglossus and geniohyoid muscles. Mechanical coupling with the palate also is common and leads to additional airway opening within the oropharynx to prevent apneic episodes. The patient turns on the stimulation through the use of a portable remote control and is turned off in the morning. The patient is able to operate the UAS device by placing the remote control on the skin in proximity of the device. The patient also is able to adjust device voltage within a range set by their physician. The effective voltage range is determined via an overnight sleep study titration performed 1 month after device activation. UAS therapy is not considered first-line treatment for OSA as it requires surgical implantation under general anesthesia; however, it provides an alternative to patients with OSA who are unable to tolerate traditional therapy with CPAP.

The landmark Stimulation Therapy for Apnea Reduction (STAR) trial showed effectiveness of UAS therapy at 12 months postimplantation.¹¹ Follow-up of these participants has proven the sustainability of this effect at 18, 24, 36, and 48 months of therapy.^12-15 Inclusion criteria of the study was moderate-to-severe sleep apnea with predominantly obstructive events. Subjects were excluded if there were anatomical abnormalities of the upper airway or if the pattern of airway collapse was not conducive to UAS on sedated endoscopy evaluation. Participants in the trial were predominantly white males, the average age was 54.5 years, and the average body mass index (BMI) was 28.4. The outcomes measured included Functional Outcomes of Sleep Questionnaire, Epworth Sleepiness Scale (ESS), percentage of sleep time with oxygen saturation < 90%, and subjective snoring. All of these objective and subjective markers of sleep improved significantly with UAS therapy at 12 months and were maintained at improved levels at 48 months of therapy.

The adverse effects (AEs) associated with device implantation and subsequent UAS therapy have been infrequent and mostly transient. Out of 126 device implantations, there were 2 participants who had serious AEs due to implantation and required repositioning and fixation of the neurostimulator to resolve discomfort. Other AEs related to the procedure, including sore throat and muscle soreness, were considered nonserious and resolved with supportive care. AEs related to subsequent UAS therapy included temporary tongue weakness and tongue soreness/abrasion. These complications also have either resolved spontaneously or with use of supportive strategies such as a mouth guard. Due to the sustained clinical benefit and acceptable AE profile as demonstrated by the STAR trial, UAS has emerged as a realistic alternative for management of OSA.

Development of a successful program that provides and supports all aspects of UAS, including device implantation and follow-up, necessitates a multispecialty team approach. Ideally surgical and nonsurgical sleep physicians as well as clinical and administrative support staff should be part of this group.

This study is based on the experience of the development of the UAS program at the Clement J. Zablocki VA Medical Center (CJZ VAMC) in Milwaukee. Currently, there are 25 patients who are part of this UAS program. The inclusion and exclusion criteria were adopted from the STAR trial. The patient population is similar to the population in that trial. They are all white males with average age of 57.2 years and BMI of 31.3. The CJZVAMC UAS Program consists of multidisciplinary group of health care professionals. This article describes the role of a nonsurgical sleep medicine physician that was crucial in the development of this UAS program.

Process

Introduction of this novel alternative therapy has sparked much interest among health care providers (HCPs) at CJZVAMC. However, there has been much misunderstanding among patients and HCPs about what this treatment involves and how it is implemented. For example, many patients that called the sleep clinic to set up an evaluation for UAS did not realize that this is a surgical procedure that requires general anesthesia. One of the most important tasks for a nonsurgical sleep physician is to educate patients and HCPs about this therapy. Most of patient education at CJZVAMC has been done during individual clinic appointments; however, setting up group educational classes for patients is a more efficient strategy to deliver this information. Similarly, giving a lecture on UAS at medicine (or another specialty) grand rounds has been effective in the education of HCPs who refer patients to the sleep clinic. If possible, a combined lecture with a surgical colleague could provide a more balanced and complete depiction of UAS and help to answer a broader range of questions for the audience.

Screening

Screening and identification of appropriate candidates is an important first step in the patient pathway in the UAS therapy. Failure of CPAP therapy is a key starting point in this screening process. When patients present to the sleep clinic with difficulty tolerating CPAP therapy, an extensive and thorough troubleshooting process needs to take place to make sure that all CPAP options have been exhausted. This process would typically include trial of various masks, including different mask interfaces. A dedicated appointment with a registered polysomnographic technologist (RPSGT) or another clinic staff member with vast experience in PAP mask fitting is typically part of this effort.

Adjustment of CPAP pressure settings also may be helpful as high PAP pressure may be another obstacle. Patients frequently have trouble tolerating higher pressure settings especially when they are new to this therapy. Pressure restriction to 4-cm to 7-cm water pressure on auto CPAP has been a helpful technique to allow patients to become more comfortable with this therapy. Once patients are able to use PAP at lower pressures, these settings can be titrated up gradually for optimal effectiveness. Other desensitization techniques, such as use during daytime while distracted by other activities (such as watching TV) can be helpful in adjustment to PAP therapy. Addressing problems with nasal congestion can help improve PAP adherence. Finally, patients should be offered opportunities for education about their PAP machine on an ongoing basis. Lack of proficiency with humidifier use is a very common obstacle and frequently leads to PAP nonadherence. Teaching PAP operation should correspond to the patient’s level of education to be effective. PAP therapy remains the first-line treatment strategy for OSA as it is not invasive and highly effective. Nonsurgical sleep medicine physicians are uniquely positioned to implement and troubleshoot this therapy for sleep apnea patients before considering UAS.

As part of the screening process, it can be helpful to conduct routine multidisciplinary meetings to discuss patients who are being evaluated for UAS implantation. These meetings should include the otolaryngologist, nonsurgical sleep medicine physician, as well as additional staff (nurses, respiratory therapists, etc) who are involved in the UAS process. Having a mental health care provider as part of the multidisciplinary team during the screening process also could be a valuable addition as this specialist could evaluate and provide insight into a patient’s emotional status prior to implantation. This is common practice during evaluation for organ transplantation and would help to predict patient’s psychological well-being after this life-changing procedure.¹⁶ Having multidisciplinary agreement on patient’s candidacy for UAS therapy could improve long-term success of this treatment. Additionally, these multidisciplinary meetings as part of the UAS program can improve team camaraderie and prevent miscommunications during this therapy.

Drug-Induced Sedated Endoscopy

Patient pathway to neurostimulator implantation involves evaluation of the upper airway using drug-induced sedated endoscopy (DISE). This procedure helps determine whether the patient’s anatomy is appropriate for UAS. DISE also can evaluate the pattern of airway closure during an apneic episode. Anterior-posterior pattern of closure is associated with greater UAS effectiveness compared with concentric pattern of airway closure. DISE is typically performed by the otolaryngologist scheduled to implant the UAS. However, nonsurgical physicians who are part of the patient’s care team can be trained to perform this procedure especially if they have experience in performing endoscopy of the upper airway (such as a pulmonary specialist). This can make the evaluation process more efficient and dramatically improve access to care.

Coordination of Care

In order for the UAS program to be successful, the patient’s care team has to work closely with the device manufacturer throughout the implantation pathway and for ongoing patient care. The device manufacturer can assist with education of HCPs, surgical physicians, clinical support staff, and the patient. However, an even more essential role for industry support is during UAS device activation and subsequent titration of UAS via an overnight in-laboratory sleep study.

After surgical implantation, the UAS device activation can be performed in the nonsurgical sleep clinic and is done about 1 month later. This period allows for tissue healing after the surgery and for the patient to get accustomed to having this new device in their body. This activation can be done with assistance from an industry technician until the HCP is comfortable with this process. The multidisciplinary UAS team could choose to delegate device activation to a technician with specialized relevant training, such as RPSGT or respiratory therapist (RT).

This procedure involves determination of sensory and functional threshold for UAS. Sensory threshold is minimum voltage required for the patient to feel the stimulation. The functional threshold is the minimum voltage required to move the tongue past the lower front teeth during stimulation. After these thresholds are established, a voltage range is set on the device. The voltage at functional threshold is typically set at the lower level of this range, and the maximum level is set at 1 volt higher. Patients are able to adjust voltage within this range and are instructed to increase the voltage gradually (0.1-volt increments) while maintaining levels that are comfortable during sleep.

About a month after device activation, patients undergo another overnight polysomnogram for titration of UAS device. In order to educate and train the institutional RPSGT on how to perform this type of titration, an industry technician is required for the first few overnight titrations. The goal of this study is to establish appropriate voltage to resolve sleep-disordered breathing and insure patient comfort at this setting. Patients typically leave the study with a new voltage range. They are asked to keep effective voltage in mind and make appropriate adjustments to maintain comfortable therapy.

Successful UAS therapy includes multiple steps, such as implantation, activation, and titration. This protocol requires effective coordination of care that includes communication with surgical staff, patients, support staff, and industry liaison. Nonsurgical sleep medicine physicians can play a vital role by helping to coordinate care at the early stages of UAS therapy and facilitate effective communication among various providers involved in this process.

Follow-Up

After completion of the initial therapeutic pathway, patients continue to follow up regularly, monitoring for AEs from UAS therapy and sleep apnea symptoms. Patients can be followed in the nonsurgical sleep clinic after the initial postoperative appointment with the surgeon. Frequency of follow-up depends on the presence and severity of any AEs and residual symptoms of sleep apnea. Even though most AEs related to UAS therapy reported in the STAR trial were nonserious and transient, 2% of participants required surgical revision.³ Therefore, maintaining open channels of communication among the entire UAS patient care team even months and years after surgical implantation is important. The nonsurgical sleep medicine physician who will continue to monitor the patient’s progress may need to consult with the surgical colleague or industry liaison at any point during treatment.
 

Limitations

This review outlines the UAS therapy pathway and emphasizes the role of the nonsurgical sleep medicine provider. However, the experience describes a UAS program development at a single VA medical center. Since this UAS device and therapy have already been approved by the VA on a national level, we did not face any challenges with authorization and insurance compensation. Therefore, this review does not provide any guidance with these matters. These are certainly common concerns for sleep medicine providers who offer UAS therapy in medical practices outside the VA, and these would hopefully be addressed in the future.

Furthermore, this review is based on the pulmonary sleep medicine provider’s experience and perspective. Therefore, certain aspects of UAS therapy could be better addressed by nonsurgical sleep medicine providers in different fields of expertise. For example, a study by a psychiatrist or psychologist could provide insight into the emotional concerns of patients who are undergoing this novel and life-altering treatment that includes surgical implantation of hardware into the body. A neurologist could explore the long-term effects of recurrent electrical stimulation on the autonomic and somatic nervous system as well as the musculature of the upper airway.

Conclusion

Multidisciplinary perspectives are needed to provide guidance for practitioners and institutions looking to set up and improve established UAS programs. As the long-term outcomes of the STAR trial continue to be published and provide more validation for UAS, this novel therapy will likely continue to gain acceptance as a safe and effective treatment for OSA.¹¹

Obstructive sleep apnea (OSA) is a common disorder in the US and other industrialized countries. The Wisconsin Sleep Cohort Study reported prevalence rates as high as 20% to 30% in men and 10% to 15% in women.^1,2 Several studies have shown high prevalence of OSA among veterans. Ancoli-Israel and colleagues reported a OSA rate of 36% in a cohort of elderly patients at a US Department of Veterans Affairs (VA) medical center.³ A study by Kreis and colleagues showed that OSA was present in 27% of patients hospitalized on the medical ward at a VA hospital.⁴ Incidence of sleep apnea among veterans in the US will likely increase over time as obesity is becoming more prevalent. Rates of obesity have increased from 14% in 2000 to 18% in 2010 among both male and female veterans.⁵

Untreated OSA is associated with increased risk of coronary artery disease, cerebrovascular accidents, uncontrolled diabetes mellitus, and other complications. Patients with OSA are less productive, have increased health care utilization, and have a higher risk of motor vehicle accidents.⁶ Continuous positive airway pressure (CPAP) is the main form of treatment of OSA. However, despite the adverse outcomes of untreated sleep apnea, suboptimal CPAP adherence remains a major problem in clinical practice. When adherence is defined as > 4 hours of nightly use, 29% to 83% of patients with OSA have been reported to be nonadherent to treatment.⁷ Stepnowsky and colleagues estimated that 50% of patients with OSA for whom CPAP was recommended were no longer using it 1 year later.⁸ CPAP adherence among veterans also has been poor. Wallace and colleagues reported that about one-third of patients with OSA at a VA Miami Healthcare System had mean daily use ≥ 4 hours.⁹ Typical reasons for poor CPAP adherence include pressure intolerance, mask discomfort, nasal and oropharyngeal dryness and irritation.¹⁰ Development and implementation of alternate treatment strategies for OSA is important to reduce disease burden of this widespread and debilitating condition.

Upper airway stimulation (UAS) is a novel therapy for management of OSA that has been gaining popularity and acceptance within the sleep medicine community in the past few years. This treatment option involves implantation of a neurostimulator with a sensing lead and a stimulation lead. The device is similar to a pacemaker and is surgically implanted in chest wall. The sensing lead is placed close to the diaphragm for monitoring of pleural pressure to help assess ventilation. The stimulation lead is placed under the tongue in proximity to the hypoglossal nerve (cranial nerve XII). The neurostimulator delivers electrical pulses to the hypoglossal nerve through the stimulation lead. These stimulating pulses are synchronized with the ventilation detected by the sensing lead. This electrical stimulation results in anterior displacement of the tongue via action of the genioglossus and geniohyoid muscles. Mechanical coupling with the palate also is common and leads to additional airway opening within the oropharynx to prevent apneic episodes. The patient turns on the stimulation through the use of a portable remote control and is turned off in the morning. The patient is able to operate the UAS device by placing the remote control on the skin in proximity of the device. The patient also is able to adjust device voltage within a range set by their physician. The effective voltage range is determined via an overnight sleep study titration performed 1 month after device activation. UAS therapy is not considered first-line treatment for OSA as it requires surgical implantation under general anesthesia; however, it provides an alternative to patients with OSA who are unable to tolerate traditional therapy with CPAP.

The landmark Stimulation Therapy for Apnea Reduction (STAR) trial showed effectiveness of UAS therapy at 12 months postimplantation.¹¹ Follow-up of these participants has proven the sustainability of this effect at 18, 24, 36, and 48 months of therapy.^12-15 Inclusion criteria of the study was moderate-to-severe sleep apnea with predominantly obstructive events. Subjects were excluded if there were anatomical abnormalities of the upper airway or if the pattern of airway collapse was not conducive to UAS on sedated endoscopy evaluation. Participants in the trial were predominantly white males, the average age was 54.5 years, and the average body mass index (BMI) was 28.4. The outcomes measured included Functional Outcomes of Sleep Questionnaire, Epworth Sleepiness Scale (ESS), percentage of sleep time with oxygen saturation < 90%, and subjective snoring. All of these objective and subjective markers of sleep improved significantly with UAS therapy at 12 months and were maintained at improved levels at 48 months of therapy.

The adverse effects (AEs) associated with device implantation and subsequent UAS therapy have been infrequent and mostly transient. Out of 126 device implantations, there were 2 participants who had serious AEs due to implantation and required repositioning and fixation of the neurostimulator to resolve discomfort. Other AEs related to the procedure, including sore throat and muscle soreness, were considered nonserious and resolved with supportive care. AEs related to subsequent UAS therapy included temporary tongue weakness and tongue soreness/abrasion. These complications also have either resolved spontaneously or with use of supportive strategies such as a mouth guard. Due to the sustained clinical benefit and acceptable AE profile as demonstrated by the STAR trial, UAS has emerged as a realistic alternative for management of OSA.

Development of a successful program that provides and supports all aspects of UAS, including device implantation and follow-up, necessitates a multispecialty team approach. Ideally surgical and nonsurgical sleep physicians as well as clinical and administrative support staff should be part of this group.

This study is based on the experience of the development of the UAS program at the Clement J. Zablocki VA Medical Center (CJZ VAMC) in Milwaukee. Currently, there are 25 patients who are part of this UAS program. The inclusion and exclusion criteria were adopted from the STAR trial. The patient population is similar to the population in that trial. They are all white males with average age of 57.2 years and BMI of 31.3. The CJZVAMC UAS Program consists of multidisciplinary group of health care professionals. This article describes the role of a nonsurgical sleep medicine physician that was crucial in the development of this UAS program.

Process

Introduction of this novel alternative therapy has sparked much interest among health care providers (HCPs) at CJZVAMC. However, there has been much misunderstanding among patients and HCPs about what this treatment involves and how it is implemented. For example, many patients that called the sleep clinic to set up an evaluation for UAS did not realize that this is a surgical procedure that requires general anesthesia. One of the most important tasks for a nonsurgical sleep physician is to educate patients and HCPs about this therapy. Most of patient education at CJZVAMC has been done during individual clinic appointments; however, setting up group educational classes for patients is a more efficient strategy to deliver this information. Similarly, giving a lecture on UAS at medicine (or another specialty) grand rounds has been effective in the education of HCPs who refer patients to the sleep clinic. If possible, a combined lecture with a surgical colleague could provide a more balanced and complete depiction of UAS and help to answer a broader range of questions for the audience.

Screening

Screening and identification of appropriate candidates is an important first step in the patient pathway in the UAS therapy. Failure of CPAP therapy is a key starting point in this screening process. When patients present to the sleep clinic with difficulty tolerating CPAP therapy, an extensive and thorough troubleshooting process needs to take place to make sure that all CPAP options have been exhausted. This process would typically include trial of various masks, including different mask interfaces. A dedicated appointment with a registered polysomnographic technologist (RPSGT) or another clinic staff member with vast experience in PAP mask fitting is typically part of this effort.

Adjustment of CPAP pressure settings also may be helpful as high PAP pressure may be another obstacle. Patients frequently have trouble tolerating higher pressure settings especially when they are new to this therapy. Pressure restriction to 4-cm to 7-cm water pressure on auto CPAP has been a helpful technique to allow patients to become more comfortable with this therapy. Once patients are able to use PAP at lower pressures, these settings can be titrated up gradually for optimal effectiveness. Other desensitization techniques, such as use during daytime while distracted by other activities (such as watching TV) can be helpful in adjustment to PAP therapy. Addressing problems with nasal congestion can help improve PAP adherence. Finally, patients should be offered opportunities for education about their PAP machine on an ongoing basis. Lack of proficiency with humidifier use is a very common obstacle and frequently leads to PAP nonadherence. Teaching PAP operation should correspond to the patient’s level of education to be effective. PAP therapy remains the first-line treatment strategy for OSA as it is not invasive and highly effective. Nonsurgical sleep medicine physicians are uniquely positioned to implement and troubleshoot this therapy for sleep apnea patients before considering UAS.

As part of the screening process, it can be helpful to conduct routine multidisciplinary meetings to discuss patients who are being evaluated for UAS implantation. These meetings should include the otolaryngologist, nonsurgical sleep medicine physician, as well as additional staff (nurses, respiratory therapists, etc) who are involved in the UAS process. Having a mental health care provider as part of the multidisciplinary team during the screening process also could be a valuable addition as this specialist could evaluate and provide insight into a patient’s emotional status prior to implantation. This is common practice during evaluation for organ transplantation and would help to predict patient’s psychological well-being after this life-changing procedure.¹⁶ Having multidisciplinary agreement on patient’s candidacy for UAS therapy could improve long-term success of this treatment. Additionally, these multidisciplinary meetings as part of the UAS program can improve team camaraderie and prevent miscommunications during this therapy.

Drug-Induced Sedated Endoscopy

Patient pathway to neurostimulator implantation involves evaluation of the upper airway using drug-induced sedated endoscopy (DISE). This procedure helps determine whether the patient’s anatomy is appropriate for UAS. DISE also can evaluate the pattern of airway closure during an apneic episode. Anterior-posterior pattern of closure is associated with greater UAS effectiveness compared with concentric pattern of airway closure. DISE is typically performed by the otolaryngologist scheduled to implant the UAS. However, nonsurgical physicians who are part of the patient’s care team can be trained to perform this procedure especially if they have experience in performing endoscopy of the upper airway (such as a pulmonary specialist). This can make the evaluation process more efficient and dramatically improve access to care.

Coordination of Care

In order for the UAS program to be successful, the patient’s care team has to work closely with the device manufacturer throughout the implantation pathway and for ongoing patient care. The device manufacturer can assist with education of HCPs, surgical physicians, clinical support staff, and the patient. However, an even more essential role for industry support is during UAS device activation and subsequent titration of UAS via an overnight in-laboratory sleep study.

After surgical implantation, the UAS device activation can be performed in the nonsurgical sleep clinic and is done about 1 month later. This period allows for tissue healing after the surgery and for the patient to get accustomed to having this new device in their body. This activation can be done with assistance from an industry technician until the HCP is comfortable with this process. The multidisciplinary UAS team could choose to delegate device activation to a technician with specialized relevant training, such as RPSGT or respiratory therapist (RT).

This procedure involves determination of sensory and functional threshold for UAS. Sensory threshold is minimum voltage required for the patient to feel the stimulation. The functional threshold is the minimum voltage required to move the tongue past the lower front teeth during stimulation. After these thresholds are established, a voltage range is set on the device. The voltage at functional threshold is typically set at the lower level of this range, and the maximum level is set at 1 volt higher. Patients are able to adjust voltage within this range and are instructed to increase the voltage gradually (0.1-volt increments) while maintaining levels that are comfortable during sleep.

About a month after device activation, patients undergo another overnight polysomnogram for titration of UAS device. In order to educate and train the institutional RPSGT on how to perform this type of titration, an industry technician is required for the first few overnight titrations. The goal of this study is to establish appropriate voltage to resolve sleep-disordered breathing and insure patient comfort at this setting. Patients typically leave the study with a new voltage range. They are asked to keep effective voltage in mind and make appropriate adjustments to maintain comfortable therapy.

Successful UAS therapy includes multiple steps, such as implantation, activation, and titration. This protocol requires effective coordination of care that includes communication with surgical staff, patients, support staff, and industry liaison. Nonsurgical sleep medicine physicians can play a vital role by helping to coordinate care at the early stages of UAS therapy and facilitate effective communication among various providers involved in this process.

Follow-Up

After completion of the initial therapeutic pathway, patients continue to follow up regularly, monitoring for AEs from UAS therapy and sleep apnea symptoms. Patients can be followed in the nonsurgical sleep clinic after the initial postoperative appointment with the surgeon. Frequency of follow-up depends on the presence and severity of any AEs and residual symptoms of sleep apnea. Even though most AEs related to UAS therapy reported in the STAR trial were nonserious and transient, 2% of participants required surgical revision.³ Therefore, maintaining open channels of communication among the entire UAS patient care team even months and years after surgical implantation is important. The nonsurgical sleep medicine physician who will continue to monitor the patient’s progress may need to consult with the surgical colleague or industry liaison at any point during treatment.
 

Limitations

This review outlines the UAS therapy pathway and emphasizes the role of the nonsurgical sleep medicine provider. However, the experience describes a UAS program development at a single VA medical center. Since this UAS device and therapy have already been approved by the VA on a national level, we did not face any challenges with authorization and insurance compensation. Therefore, this review does not provide any guidance with these matters. These are certainly common concerns for sleep medicine providers who offer UAS therapy in medical practices outside the VA, and these would hopefully be addressed in the future.

Furthermore, this review is based on the pulmonary sleep medicine provider’s experience and perspective. Therefore, certain aspects of UAS therapy could be better addressed by nonsurgical sleep medicine providers in different fields of expertise. For example, a study by a psychiatrist or psychologist could provide insight into the emotional concerns of patients who are undergoing this novel and life-altering treatment that includes surgical implantation of hardware into the body. A neurologist could explore the long-term effects of recurrent electrical stimulation on the autonomic and somatic nervous system as well as the musculature of the upper airway.

Conclusion

Multidisciplinary perspectives are needed to provide guidance for practitioners and institutions looking to set up and improve established UAS programs. As the long-term outcomes of the STAR trial continue to be published and provide more validation for UAS, this novel therapy will likely continue to gain acceptance as a safe and effective treatment for OSA.¹¹

Among community-dwelling adults aged 65 years and older with sleep-disordered breathing, Alzheimer’s-associated brain changes may occur in the absence of cognitive impairment, investigators have found.

Among 127 adults enrolled in a randomized clinical trial of interventions to promote mental well-being in older adults, those with sleep-disordered breathing had significantly greater amyloid burden and gray-matter volume, as well as increased perfusion and metabolism in parietal-occipital regions, reported Claire André, PhD, from the French Institute of Health and Medical Research (INSERM) unit in Caen, and colleagues.

“Our findings highlight the need to treat sleep disorders in the older population, even in the absence of cognitive or behavioral manifestations,” they wrote in a study published in JAMA Neurology.

Previous studies of the possible association between sleep-disordered breathing and dementia risk have shown conflicting or inconsistent results, the authors noted.

“These discrepancies may be explained by the characteristics of patients with sleep-disordered breathing (e.g., recruited from sleep clinics versus from the community, differences in age and disease duration), the scoring criteria of respiratory events, sample sizes, or the lack of controls for possibly biasing covariates,” they wrote.

To see whether they could clear up the confusion, the investigators conducted a retrospective analysis of 127 patients who were enrolled in the Age-Well randomized, controlled trial of the Medit-Ageing European project. The participants were community-dwelling adults (mean age, 69.1 years; 63% women), who were enrolled in the trial and underwent evaluation from 2016 to 2018 at the Cyceron Cancer Center in Caen.

The participants, all of whom were cognitively unimpaired at baseline, underwent neuropsychological assessment, polysomnography, MRI, plus florbetapir- and fluorodeoxyglucose-labeled PET.

The investigators defined sleep-disordered breathing as 15 apnea-hypopnea index events per hour or higher, and compared results between those with sleep-disordered breathing and those without for each imaging modality.

Participants with sleep-disordered breathing has significantly greater amyloid burden (P = .04), gray-matter volume (P = .04), perfusion (P = .04), and metabolism (P = .001), primarily overlapping the posterior cingulate cortex and precuneus, areas known to be significantly involved in Alzheimer’s disease.

When the investigators looked for behavioral and cognitive correlates of sleep-disordered breathing severity with associated brain changes, however, they found no associations with either cognitive performance, self-reported cognitive or sleep difficulties, or symptoms of daytime sleepiness.

“Importantly, to the best of our knowledge, our results show in vivo for the first time that greater amyloid burden colocalizes with greater gray-matter volume, perfusion, and metabolism in older participants with sleep-disordered breathing who are cognitively unimpaired. We believe that these overlapping patterns reinforce the likelihood of common underlying mechanisms,” they wrote.

The Age-Well randomized clinical trial is part of the Medit-Ageing project and is funded through the European Union’s Horizon 2020 Research and Innovation Program, INSERM, and Fondation d’ Entreprise MMA des Entrepreneurs du Futur. Dr. André reported no conflicts of interest to disclose.

SOURCE: André C et al. JAMA Neurol. 2020 Mar 23. doi: 10.1001/jamaneurol.2020.0311.

Among community-dwelling adults aged 65 years and older with sleep-disordered breathing, Alzheimer’s-associated brain changes may occur in the absence of cognitive impairment, investigators have found.

Among 127 adults enrolled in a randomized clinical trial of interventions to promote mental well-being in older adults, those with sleep-disordered breathing had significantly greater amyloid burden and gray-matter volume, as well as increased perfusion and metabolism in parietal-occipital regions, reported Claire André, PhD, from the French Institute of Health and Medical Research (INSERM) unit in Caen, and colleagues.

“Our findings highlight the need to treat sleep disorders in the older population, even in the absence of cognitive or behavioral manifestations,” they wrote in a study published in JAMA Neurology.

Previous studies of the possible association between sleep-disordered breathing and dementia risk have shown conflicting or inconsistent results, the authors noted.

“These discrepancies may be explained by the characteristics of patients with sleep-disordered breathing (e.g., recruited from sleep clinics versus from the community, differences in age and disease duration), the scoring criteria of respiratory events, sample sizes, or the lack of controls for possibly biasing covariates,” they wrote.

To see whether they could clear up the confusion, the investigators conducted a retrospective analysis of 127 patients who were enrolled in the Age-Well randomized, controlled trial of the Medit-Ageing European project. The participants were community-dwelling adults (mean age, 69.1 years; 63% women), who were enrolled in the trial and underwent evaluation from 2016 to 2018 at the Cyceron Cancer Center in Caen.

The participants, all of whom were cognitively unimpaired at baseline, underwent neuropsychological assessment, polysomnography, MRI, plus florbetapir- and fluorodeoxyglucose-labeled PET.

The investigators defined sleep-disordered breathing as 15 apnea-hypopnea index events per hour or higher, and compared results between those with sleep-disordered breathing and those without for each imaging modality.

Participants with sleep-disordered breathing has significantly greater amyloid burden (P = .04), gray-matter volume (P = .04), perfusion (P = .04), and metabolism (P = .001), primarily overlapping the posterior cingulate cortex and precuneus, areas known to be significantly involved in Alzheimer’s disease.

When the investigators looked for behavioral and cognitive correlates of sleep-disordered breathing severity with associated brain changes, however, they found no associations with either cognitive performance, self-reported cognitive or sleep difficulties, or symptoms of daytime sleepiness.

“Importantly, to the best of our knowledge, our results show in vivo for the first time that greater amyloid burden colocalizes with greater gray-matter volume, perfusion, and metabolism in older participants with sleep-disordered breathing who are cognitively unimpaired. We believe that these overlapping patterns reinforce the likelihood of common underlying mechanisms,” they wrote.

The Age-Well randomized clinical trial is part of the Medit-Ageing project and is funded through the European Union’s Horizon 2020 Research and Innovation Program, INSERM, and Fondation d’ Entreprise MMA des Entrepreneurs du Futur. Dr. André reported no conflicts of interest to disclose.

SOURCE: André C et al. JAMA Neurol. 2020 Mar 23. doi: 10.1001/jamaneurol.2020.0311.

Among community-dwelling adults aged 65 years and older with sleep-disordered breathing, Alzheimer’s-associated brain changes may occur in the absence of cognitive impairment, investigators have found.

Among 127 adults enrolled in a randomized clinical trial of interventions to promote mental well-being in older adults, those with sleep-disordered breathing had significantly greater amyloid burden and gray-matter volume, as well as increased perfusion and metabolism in parietal-occipital regions, reported Claire André, PhD, from the French Institute of Health and Medical Research (INSERM) unit in Caen, and colleagues.

“Our findings highlight the need to treat sleep disorders in the older population, even in the absence of cognitive or behavioral manifestations,” they wrote in a study published in JAMA Neurology.

Previous studies of the possible association between sleep-disordered breathing and dementia risk have shown conflicting or inconsistent results, the authors noted.

“These discrepancies may be explained by the characteristics of patients with sleep-disordered breathing (e.g., recruited from sleep clinics versus from the community, differences in age and disease duration), the scoring criteria of respiratory events, sample sizes, or the lack of controls for possibly biasing covariates,” they wrote.

To see whether they could clear up the confusion, the investigators conducted a retrospective analysis of 127 patients who were enrolled in the Age-Well randomized, controlled trial of the Medit-Ageing European project. The participants were community-dwelling adults (mean age, 69.1 years; 63% women), who were enrolled in the trial and underwent evaluation from 2016 to 2018 at the Cyceron Cancer Center in Caen.

The participants, all of whom were cognitively unimpaired at baseline, underwent neuropsychological assessment, polysomnography, MRI, plus florbetapir- and fluorodeoxyglucose-labeled PET.

The investigators defined sleep-disordered breathing as 15 apnea-hypopnea index events per hour or higher, and compared results between those with sleep-disordered breathing and those without for each imaging modality.

Participants with sleep-disordered breathing has significantly greater amyloid burden (P = .04), gray-matter volume (P = .04), perfusion (P = .04), and metabolism (P = .001), primarily overlapping the posterior cingulate cortex and precuneus, areas known to be significantly involved in Alzheimer’s disease.

When the investigators looked for behavioral and cognitive correlates of sleep-disordered breathing severity with associated brain changes, however, they found no associations with either cognitive performance, self-reported cognitive or sleep difficulties, or symptoms of daytime sleepiness.

“Importantly, to the best of our knowledge, our results show in vivo for the first time that greater amyloid burden colocalizes with greater gray-matter volume, perfusion, and metabolism in older participants with sleep-disordered breathing who are cognitively unimpaired. We believe that these overlapping patterns reinforce the likelihood of common underlying mechanisms,” they wrote.

The Age-Well randomized clinical trial is part of the Medit-Ageing project and is funded through the European Union’s Horizon 2020 Research and Innovation Program, INSERM, and Fondation d’ Entreprise MMA des Entrepreneurs du Futur. Dr. André reported no conflicts of interest to disclose.

SOURCE: André C et al. JAMA Neurol. 2020 Mar 23. doi: 10.1001/jamaneurol.2020.0311.

Insomnia symptoms and use of sleep medications is linked to motor vehicle accidents (MVA), and young women with insomnia and reported daytime sleepiness represent a subpopulation at specific risk, according to an analysis of a 5-year population sample. The new research was published online in Sleep and led by Charles Morin, PhD, of Laval University, Quebec City.

The risks of daytime sleepiness and MVA are generally thought of in the context of obstructive sleep apnea (OSA) or men, but the results of the new work suggest that insomnia should not be overlooked, according to Krishna Sundar, MD, clinical professor of pulmonary, critical care, and sleep medicine, and medical director of the Sleep-Wake Center, at the University of Utah, Salt Lake City.

“The notion has been that it may keep them more hypervigilant and less prone to motor vehicle accidents because they are less able to fall asleep even if they want to during the daytime, as compared to other conditions like sleep apnea where there is a higher tendency to doze off,” Dr. Sundar said in an interview.

It should also be remembered that patients aren’t always completely reliable when it comes to self-assessment, according to Brandon M. Seay, MD, a pediatric pulmonologist and sleep specialist at Children’s Healthcare of Atlanta. “Most people with insomnia won’t say they are sleepy in the daytime, but when you objectively look, you do see an element of daytime sleepiness even if it’s not perceived that well by insomnia patients,” said Dr. Seay.

SOURCE: Morin C et al. Sleep. 2020 Feb 29. DOI: 10.1093/sleep/zsaa032.

Insomnia symptoms and use of sleep medications is linked to motor vehicle accidents (MVA), and young women with insomnia and reported daytime sleepiness represent a subpopulation at specific risk, according to an analysis of a 5-year population sample. The new research was published online in Sleep and led by Charles Morin, PhD, of Laval University, Quebec City.

The risks of daytime sleepiness and MVA are generally thought of in the context of obstructive sleep apnea (OSA) or men, but the results of the new work suggest that insomnia should not be overlooked, according to Krishna Sundar, MD, clinical professor of pulmonary, critical care, and sleep medicine, and medical director of the Sleep-Wake Center, at the University of Utah, Salt Lake City.

“The notion has been that it may keep them more hypervigilant and less prone to motor vehicle accidents because they are less able to fall asleep even if they want to during the daytime, as compared to other conditions like sleep apnea where there is a higher tendency to doze off,” Dr. Sundar said in an interview.

It should also be remembered that patients aren’t always completely reliable when it comes to self-assessment, according to Brandon M. Seay, MD, a pediatric pulmonologist and sleep specialist at Children’s Healthcare of Atlanta. “Most people with insomnia won’t say they are sleepy in the daytime, but when you objectively look, you do see an element of daytime sleepiness even if it’s not perceived that well by insomnia patients,” said Dr. Seay.

SOURCE: Morin C et al. Sleep. 2020 Feb 29. DOI: 10.1093/sleep/zsaa032.

Insomnia symptoms and use of sleep medications is linked to motor vehicle accidents (MVA), and young women with insomnia and reported daytime sleepiness represent a subpopulation at specific risk, according to an analysis of a 5-year population sample. The new research was published online in Sleep and led by Charles Morin, PhD, of Laval University, Quebec City.

The risks of daytime sleepiness and MVA are generally thought of in the context of obstructive sleep apnea (OSA) or men, but the results of the new work suggest that insomnia should not be overlooked, according to Krishna Sundar, MD, clinical professor of pulmonary, critical care, and sleep medicine, and medical director of the Sleep-Wake Center, at the University of Utah, Salt Lake City.

“The notion has been that it may keep them more hypervigilant and less prone to motor vehicle accidents because they are less able to fall asleep even if they want to during the daytime, as compared to other conditions like sleep apnea where there is a higher tendency to doze off,” Dr. Sundar said in an interview.

It should also be remembered that patients aren’t always completely reliable when it comes to self-assessment, according to Brandon M. Seay, MD, a pediatric pulmonologist and sleep specialist at Children’s Healthcare of Atlanta. “Most people with insomnia won’t say they are sleepy in the daytime, but when you objectively look, you do see an element of daytime sleepiness even if it’s not perceived that well by insomnia patients,” said Dr. Seay.

SOURCE: Morin C et al. Sleep. 2020 Feb 29. DOI: 10.1093/sleep/zsaa032.

People who frequently alter the amount of sleep and time they go to bed each night are twofold more likely to develop cardiovascular disease, independent of traditional CVD risk factors, new research suggests.

Prior studies have focused on shift workers because night shift work will influence circadian rhythm and increase CVD risk. But it is increasingly recognized that circadian disruption may occur outside of shift work and accumulate over time, particularly given modern lifestyle factors such as increased use of mobile devices and television at night, said study coauthor Tianyi Huang, ScD, MSc, of Brigham and Women’s Hospital and Harvard Medical School in Boston, Massachusetts.

“Even if they tend to go to sleep at certain times, by following that lifestyle or behavior, it can interfere with their planned sleep timing,” he said.

“One thing that surprised me in this sample is that about one third of participants have irregular sleep patterns that can put them at increased risk of cardiovascular disease. So I think the prevalence is higher than expected,” Huang added.

As reported today in the Journal of the American College of Cardiology, the investigators used data from 7-day wrist actigraphy, 1 night of at-home polysomnography, and sleep questionnaires to assess sleep duration and sleep-onset timing among 1,992 Multi-Ethnic Study of Atherosclerosis () participants, aged 45 to 84 years, who were free of CVD and prospectively followed for a me MESA dian of 4.9 years.

A total of 786 patients (39.5%) had sleep duration standard deviation (SD) > 90 minutes and 510 (25.6%) had sleep-onset timing SD > 90 minutes.

During follow-up, there were 111 incident CVD events, including myocardial infarction, coronary heart disease death, stroke, and other coronary events.

Compared with people who had less than 1 hour of variation in sleep duration, the risk for incident CVD was 9% higher for people whose sleep duration varied 61 to 90 minutes (hazard ratio [HR], 1.09; 95% confidence interval [CI], 0.62 - 1.92), even after controlling for a variety of cardiovascular and sleep-related risk factors such as body mass index, systolic blood pressure, smoking status, total cholesterol, average sleep duration, insomnia symptoms, and sleep apnea.

Moreover, the adjusted CVD risk was substantially increased with 91 to 120 minutes of variation (HR, 1.59; 95% CI, 0.91 - 2.76) and more than 120 minutes of variation in sleep duration (HR, 2.14; 95% CI, 1.24 - 3.68).

Every 1-hour increase in sleep duration SD was associated with 36% higher CVD risk (95% CI; 1.07 - 1.73).

Compared with people with no more than a half hour of variation in nightly bedtimes, the adjusted hazard ratios for CVD were 1.16 (95% CI, 0.64 - 2.13), 1.52 (95% CI, 0.81 - 2.88), and 2.11 (95% CI, 1.13 - 3.91) when bedtimes varied by 31 to 60 minutes, 61 to 90 minutes, and more than 90 minutes.

For every 1-hour increase in sleep-onset timing SD, the risk of CVD was 18% higher (95% CI; 1.06 - 1.31).

“The results are similar for the regularity of sleep timing and the regularity of sleep duration, which means that both can contribute to circadian disruption and then lead to development of cardiovascular disease,” Huang said.

This is an important article and signals how sleep is an important marker and possibly a mediator of cardiovascular risk, said Harlan Krumholz, MD, of Yale School of Medicine in New Haven, Connecticut, who was not involved with the study.

“What I like about this is it’s a nice longitudinal, epidemiologic study with not just self-report, but sensor-detected sleep, that has been correlated with well-curated and adjudicated outcomes to give us a strong sense of this association,” he told theheart.org/Medscape Cardiology. “And also, that it goes beyond just the duration — they combine the duration and timing in order to give a fuller picture of sleep.”

Nevertheless, Krumholz said researchers are only at the beginning of being able to quantify the various dimensions of sleep and the degree to which sleep is a reflection of underlying physiologic issues, or whether patients are having erratic sleep patterns that are having a toxic effect on their overall health.

Questions also remain about the mechanism behind the association, whether the increased risk is universal or more harmful for some people, and the best way to measure factors during sleep that can most comprehensively and precisely predict risk.

“As we get more information flowing in from sensors, I think we will begin to develop more sophisticated approaches toward understanding risk, and it will be accompanied by other studies that will help us understand whether, again, this is a reflection of other processes that we should be paying attention to or whether it is a cause of disease and risk,” Krumholz said.

Subgroup analyses suggested positive associations between irregular sleep and CVD in African Americans, Hispanics, and Chinese Americans but not in whites. This could be because sleep irregularity, both timing and duration, was substantially higher in minorities, especially African Americans, but may also be as a result of chance because the study sample is relatively small, Huang explained.

The authors note that the overall findings are biologically plausible because of their previous work linking sleep irregularity with metabolic risk factors that predispose to atherosclerosis, such as obesity, diabetes, and hypertension. Participants with irregular sleep tended to have worse baseline cardiometabolic profiles, but this only explained a small portion of the associations between sleep irregularity and CVD, they note.

Other possible explanations include circadian clock genes, such as clock, per2 and bmal1, which have been shown experimentally to control a broad range of cardiovascular functions, from blood pressure and endothelial functions to vascular thrombosis and cardiac remodeling.

Irregular sleep may also influence the rhythms of the autonomic nervous system, and behavioral rhythms with regard to timing and/or amount of eating or exercise.

Further research is needed to understand the mechanisms driving the associations, the impact of sleep irregularity on individual CVD outcomes, and to determine whether a 7-day SD of more than 90 minutes for either sleep duration or sleep-onset timing can be used clinically as a threshold target for promoting cardiometabolically healthy sleep, Huang said.

“When providers communicate with their patients regarding strategies for CVD prevention, usually they focus on healthy diet and physical activity; and even when they talk about sleep, they talk about whether they have good sleep quality or sufficient sleep,” he said. “But one thing they should provide is advice regarding sleep regularity and [they should] recommend their patients follow a regular sleep pattern for the purpose of cardiovascular prevention.”

In a related editorial, Olaf Oldenburg, MD, Luderus-Kliniken Münster, Clemenshospital, Münster, Germany, and Jens Spiesshoefer, MD, Institute of Life Sciences, Scuola Superiore Sant’Anna, Pisa, Italy, write that the observed independent association between sleep irregularity and CVD “is a particularly striking finding given that impaired circadian rhythm is likely to be much more prevalent than the extreme example of shift work.”

They call on researchers to utilize big data to facilitate understanding of the association and say it is essential to test whether experimental data support the hypothesis that altered circadian rhythms would translate into unfavorable changes in 24-hour sympathovagal and neurohormonal balance, and ultimately CVD.

The present study “will, and should, stimulate much needed additional research on the association between sleep and CVD that may offer novel approaches to help improve the prognosis and daily symptom burden of patients with CVD, and might make sleep itself a therapeutic target in CVD,” the editorialists conclude.

This research was supported by contracts from the National Heart, Lung, and Blood Institute (NHLBI), and by grants from the National Center for Advancing Translational Sciences. The MESA Sleep Study was supported by an NHLBI grant. Huang was supported by a career development grant from the National Institutes of Health.

Krumholz and Oldenburg have disclosed no relevant financial relationships. Spiesshoefer is supported by grants from the Else-Kröner-Fresenius Stiftung, the Innovative Medical Research program at the University of Münster, and Deutsche Herzstiftung; and by young investigator research support from Scuola Superiore Sant’Anna Pisa. He also has received travel grants and lecture honoraria from Boehringer Ingelheim and Chiesi.
 

Source: J Am Coll Cardiol. 2020 Mar 2. doi: 10.1016/j.jacc.2019.12.054.

This article first appeared on Medscape.com.

People who frequently alter the amount of sleep and time they go to bed each night are twofold more likely to develop cardiovascular disease, independent of traditional CVD risk factors, new research suggests.

Prior studies have focused on shift workers because night shift work will influence circadian rhythm and increase CVD risk. But it is increasingly recognized that circadian disruption may occur outside of shift work and accumulate over time, particularly given modern lifestyle factors such as increased use of mobile devices and television at night, said study coauthor Tianyi Huang, ScD, MSc, of Brigham and Women’s Hospital and Harvard Medical School in Boston, Massachusetts.

“Even if they tend to go to sleep at certain times, by following that lifestyle or behavior, it can interfere with their planned sleep timing,” he said.

“One thing that surprised me in this sample is that about one third of participants have irregular sleep patterns that can put them at increased risk of cardiovascular disease. So I think the prevalence is higher than expected,” Huang added.

As reported today in the Journal of the American College of Cardiology, the investigators used data from 7-day wrist actigraphy, 1 night of at-home polysomnography, and sleep questionnaires to assess sleep duration and sleep-onset timing among 1,992 Multi-Ethnic Study of Atherosclerosis () participants, aged 45 to 84 years, who were free of CVD and prospectively followed for a me MESA dian of 4.9 years.

A total of 786 patients (39.5%) had sleep duration standard deviation (SD) > 90 minutes and 510 (25.6%) had sleep-onset timing SD > 90 minutes.

During follow-up, there were 111 incident CVD events, including myocardial infarction, coronary heart disease death, stroke, and other coronary events.

Compared with people who had less than 1 hour of variation in sleep duration, the risk for incident CVD was 9% higher for people whose sleep duration varied 61 to 90 minutes (hazard ratio [HR], 1.09; 95% confidence interval [CI], 0.62 - 1.92), even after controlling for a variety of cardiovascular and sleep-related risk factors such as body mass index, systolic blood pressure, smoking status, total cholesterol, average sleep duration, insomnia symptoms, and sleep apnea.

Moreover, the adjusted CVD risk was substantially increased with 91 to 120 minutes of variation (HR, 1.59; 95% CI, 0.91 - 2.76) and more than 120 minutes of variation in sleep duration (HR, 2.14; 95% CI, 1.24 - 3.68).

Every 1-hour increase in sleep duration SD was associated with 36% higher CVD risk (95% CI; 1.07 - 1.73).

Compared with people with no more than a half hour of variation in nightly bedtimes, the adjusted hazard ratios for CVD were 1.16 (95% CI, 0.64 - 2.13), 1.52 (95% CI, 0.81 - 2.88), and 2.11 (95% CI, 1.13 - 3.91) when bedtimes varied by 31 to 60 minutes, 61 to 90 minutes, and more than 90 minutes.

For every 1-hour increase in sleep-onset timing SD, the risk of CVD was 18% higher (95% CI; 1.06 - 1.31).

“The results are similar for the regularity of sleep timing and the regularity of sleep duration, which means that both can contribute to circadian disruption and then lead to development of cardiovascular disease,” Huang said.

This is an important article and signals how sleep is an important marker and possibly a mediator of cardiovascular risk, said Harlan Krumholz, MD, of Yale School of Medicine in New Haven, Connecticut, who was not involved with the study.

“What I like about this is it’s a nice longitudinal, epidemiologic study with not just self-report, but sensor-detected sleep, that has been correlated with well-curated and adjudicated outcomes to give us a strong sense of this association,” he told theheart.org/Medscape Cardiology. “And also, that it goes beyond just the duration — they combine the duration and timing in order to give a fuller picture of sleep.”

Nevertheless, Krumholz said researchers are only at the beginning of being able to quantify the various dimensions of sleep and the degree to which sleep is a reflection of underlying physiologic issues, or whether patients are having erratic sleep patterns that are having a toxic effect on their overall health.

Questions also remain about the mechanism behind the association, whether the increased risk is universal or more harmful for some people, and the best way to measure factors during sleep that can most comprehensively and precisely predict risk.

“As we get more information flowing in from sensors, I think we will begin to develop more sophisticated approaches toward understanding risk, and it will be accompanied by other studies that will help us understand whether, again, this is a reflection of other processes that we should be paying attention to or whether it is a cause of disease and risk,” Krumholz said.

Subgroup analyses suggested positive associations between irregular sleep and CVD in African Americans, Hispanics, and Chinese Americans but not in whites. This could be because sleep irregularity, both timing and duration, was substantially higher in minorities, especially African Americans, but may also be as a result of chance because the study sample is relatively small, Huang explained.

The authors note that the overall findings are biologically plausible because of their previous work linking sleep irregularity with metabolic risk factors that predispose to atherosclerosis, such as obesity, diabetes, and hypertension. Participants with irregular sleep tended to have worse baseline cardiometabolic profiles, but this only explained a small portion of the associations between sleep irregularity and CVD, they note.

Other possible explanations include circadian clock genes, such as clock, per2 and bmal1, which have been shown experimentally to control a broad range of cardiovascular functions, from blood pressure and endothelial functions to vascular thrombosis and cardiac remodeling.

Irregular sleep may also influence the rhythms of the autonomic nervous system, and behavioral rhythms with regard to timing and/or amount of eating or exercise.

Further research is needed to understand the mechanisms driving the associations, the impact of sleep irregularity on individual CVD outcomes, and to determine whether a 7-day SD of more than 90 minutes for either sleep duration or sleep-onset timing can be used clinically as a threshold target for promoting cardiometabolically healthy sleep, Huang said.

“When providers communicate with their patients regarding strategies for CVD prevention, usually they focus on healthy diet and physical activity; and even when they talk about sleep, they talk about whether they have good sleep quality or sufficient sleep,” he said. “But one thing they should provide is advice regarding sleep regularity and [they should] recommend their patients follow a regular sleep pattern for the purpose of cardiovascular prevention.”

In a related editorial, Olaf Oldenburg, MD, Luderus-Kliniken Münster, Clemenshospital, Münster, Germany, and Jens Spiesshoefer, MD, Institute of Life Sciences, Scuola Superiore Sant’Anna, Pisa, Italy, write that the observed independent association between sleep irregularity and CVD “is a particularly striking finding given that impaired circadian rhythm is likely to be much more prevalent than the extreme example of shift work.”

They call on researchers to utilize big data to facilitate understanding of the association and say it is essential to test whether experimental data support the hypothesis that altered circadian rhythms would translate into unfavorable changes in 24-hour sympathovagal and neurohormonal balance, and ultimately CVD.

The present study “will, and should, stimulate much needed additional research on the association between sleep and CVD that may offer novel approaches to help improve the prognosis and daily symptom burden of patients with CVD, and might make sleep itself a therapeutic target in CVD,” the editorialists conclude.

This research was supported by contracts from the National Heart, Lung, and Blood Institute (NHLBI), and by grants from the National Center for Advancing Translational Sciences. The MESA Sleep Study was supported by an NHLBI grant. Huang was supported by a career development grant from the National Institutes of Health.

Krumholz and Oldenburg have disclosed no relevant financial relationships. Spiesshoefer is supported by grants from the Else-Kröner-Fresenius Stiftung, the Innovative Medical Research program at the University of Münster, and Deutsche Herzstiftung; and by young investigator research support from Scuola Superiore Sant’Anna Pisa. He also has received travel grants and lecture honoraria from Boehringer Ingelheim and Chiesi.
 

Source: J Am Coll Cardiol. 2020 Mar 2. doi: 10.1016/j.jacc.2019.12.054.

This article first appeared on Medscape.com.

People who frequently alter the amount of sleep and time they go to bed each night are twofold more likely to develop cardiovascular disease, independent of traditional CVD risk factors, new research suggests.

Prior studies have focused on shift workers because night shift work will influence circadian rhythm and increase CVD risk. But it is increasingly recognized that circadian disruption may occur outside of shift work and accumulate over time, particularly given modern lifestyle factors such as increased use of mobile devices and television at night, said study coauthor Tianyi Huang, ScD, MSc, of Brigham and Women’s Hospital and Harvard Medical School in Boston, Massachusetts.

“Even if they tend to go to sleep at certain times, by following that lifestyle or behavior, it can interfere with their planned sleep timing,” he said.

“One thing that surprised me in this sample is that about one third of participants have irregular sleep patterns that can put them at increased risk of cardiovascular disease. So I think the prevalence is higher than expected,” Huang added.

As reported today in the Journal of the American College of Cardiology, the investigators used data from 7-day wrist actigraphy, 1 night of at-home polysomnography, and sleep questionnaires to assess sleep duration and sleep-onset timing among 1,992 Multi-Ethnic Study of Atherosclerosis () participants, aged 45 to 84 years, who were free of CVD and prospectively followed for a me MESA dian of 4.9 years.

A total of 786 patients (39.5%) had sleep duration standard deviation (SD) > 90 minutes and 510 (25.6%) had sleep-onset timing SD > 90 minutes.

During follow-up, there were 111 incident CVD events, including myocardial infarction, coronary heart disease death, stroke, and other coronary events.

Compared with people who had less than 1 hour of variation in sleep duration, the risk for incident CVD was 9% higher for people whose sleep duration varied 61 to 90 minutes (hazard ratio [HR], 1.09; 95% confidence interval [CI], 0.62 - 1.92), even after controlling for a variety of cardiovascular and sleep-related risk factors such as body mass index, systolic blood pressure, smoking status, total cholesterol, average sleep duration, insomnia symptoms, and sleep apnea.

Moreover, the adjusted CVD risk was substantially increased with 91 to 120 minutes of variation (HR, 1.59; 95% CI, 0.91 - 2.76) and more than 120 minutes of variation in sleep duration (HR, 2.14; 95% CI, 1.24 - 3.68).

Every 1-hour increase in sleep duration SD was associated with 36% higher CVD risk (95% CI; 1.07 - 1.73).

Compared with people with no more than a half hour of variation in nightly bedtimes, the adjusted hazard ratios for CVD were 1.16 (95% CI, 0.64 - 2.13), 1.52 (95% CI, 0.81 - 2.88), and 2.11 (95% CI, 1.13 - 3.91) when bedtimes varied by 31 to 60 minutes, 61 to 90 minutes, and more than 90 minutes.

For every 1-hour increase in sleep-onset timing SD, the risk of CVD was 18% higher (95% CI; 1.06 - 1.31).

“The results are similar for the regularity of sleep timing and the regularity of sleep duration, which means that both can contribute to circadian disruption and then lead to development of cardiovascular disease,” Huang said.

This is an important article and signals how sleep is an important marker and possibly a mediator of cardiovascular risk, said Harlan Krumholz, MD, of Yale School of Medicine in New Haven, Connecticut, who was not involved with the study.

“What I like about this is it’s a nice longitudinal, epidemiologic study with not just self-report, but sensor-detected sleep, that has been correlated with well-curated and adjudicated outcomes to give us a strong sense of this association,” he told theheart.org/Medscape Cardiology. “And also, that it goes beyond just the duration — they combine the duration and timing in order to give a fuller picture of sleep.”

Nevertheless, Krumholz said researchers are only at the beginning of being able to quantify the various dimensions of sleep and the degree to which sleep is a reflection of underlying physiologic issues, or whether patients are having erratic sleep patterns that are having a toxic effect on their overall health.

Questions also remain about the mechanism behind the association, whether the increased risk is universal or more harmful for some people, and the best way to measure factors during sleep that can most comprehensively and precisely predict risk.

“As we get more information flowing in from sensors, I think we will begin to develop more sophisticated approaches toward understanding risk, and it will be accompanied by other studies that will help us understand whether, again, this is a reflection of other processes that we should be paying attention to or whether it is a cause of disease and risk,” Krumholz said.

Subgroup analyses suggested positive associations between irregular sleep and CVD in African Americans, Hispanics, and Chinese Americans but not in whites. This could be because sleep irregularity, both timing and duration, was substantially higher in minorities, especially African Americans, but may also be as a result of chance because the study sample is relatively small, Huang explained.

The authors note that the overall findings are biologically plausible because of their previous work linking sleep irregularity with metabolic risk factors that predispose to atherosclerosis, such as obesity, diabetes, and hypertension. Participants with irregular sleep tended to have worse baseline cardiometabolic profiles, but this only explained a small portion of the associations between sleep irregularity and CVD, they note.

Other possible explanations include circadian clock genes, such as clock, per2 and bmal1, which have been shown experimentally to control a broad range of cardiovascular functions, from blood pressure and endothelial functions to vascular thrombosis and cardiac remodeling.

Irregular sleep may also influence the rhythms of the autonomic nervous system, and behavioral rhythms with regard to timing and/or amount of eating or exercise.

Further research is needed to understand the mechanisms driving the associations, the impact of sleep irregularity on individual CVD outcomes, and to determine whether a 7-day SD of more than 90 minutes for either sleep duration or sleep-onset timing can be used clinically as a threshold target for promoting cardiometabolically healthy sleep, Huang said.

“When providers communicate with their patients regarding strategies for CVD prevention, usually they focus on healthy diet and physical activity; and even when they talk about sleep, they talk about whether they have good sleep quality or sufficient sleep,” he said. “But one thing they should provide is advice regarding sleep regularity and [they should] recommend their patients follow a regular sleep pattern for the purpose of cardiovascular prevention.”

In a related editorial, Olaf Oldenburg, MD, Luderus-Kliniken Münster, Clemenshospital, Münster, Germany, and Jens Spiesshoefer, MD, Institute of Life Sciences, Scuola Superiore Sant’Anna, Pisa, Italy, write that the observed independent association between sleep irregularity and CVD “is a particularly striking finding given that impaired circadian rhythm is likely to be much more prevalent than the extreme example of shift work.”

They call on researchers to utilize big data to facilitate understanding of the association and say it is essential to test whether experimental data support the hypothesis that altered circadian rhythms would translate into unfavorable changes in 24-hour sympathovagal and neurohormonal balance, and ultimately CVD.

The present study “will, and should, stimulate much needed additional research on the association between sleep and CVD that may offer novel approaches to help improve the prognosis and daily symptom burden of patients with CVD, and might make sleep itself a therapeutic target in CVD,” the editorialists conclude.

This research was supported by contracts from the National Heart, Lung, and Blood Institute (NHLBI), and by grants from the National Center for Advancing Translational Sciences. The MESA Sleep Study was supported by an NHLBI grant. Huang was supported by a career development grant from the National Institutes of Health.

Krumholz and Oldenburg have disclosed no relevant financial relationships. Spiesshoefer is supported by grants from the Else-Kröner-Fresenius Stiftung, the Innovative Medical Research program at the University of Münster, and Deutsche Herzstiftung; and by young investigator research support from Scuola Superiore Sant’Anna Pisa. He also has received travel grants and lecture honoraria from Boehringer Ingelheim and Chiesi.
 

Source: J Am Coll Cardiol. 2020 Mar 2. doi: 10.1016/j.jacc.2019.12.054.

This article first appeared on Medscape.com.

LAS VEGAS – Clinicians should spend 1 hour with patients who present with a chief complaint of insomnia, rather than rushing to a treatment after a 10- to 15-minute office visit, according to John W. Winkelman, MD, PhD.

Doug Brunk/MDedge News

“Why? Because sleep problems are usually multifactorial, involving psychiatric illness, sleep disorders, medical illness, medication, and poor sleep hygiene/stress,” he said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “There are usually many contributing problems, and sleep quality is only as strong as the weakest link. Maybe you don’t have an hour [to meet with new patients], but you need to give adequate time, otherwise you’re not going to do justice to the problem.”

During that first visit, Dr. Winkelman recommends establishing and prioritizing goals with the patient. “Ask, ‘what is it that bothers you most about your insomnia? Is it the time awake at night, your total sleep time, or how you feel during the day?’ Because we’re going to use different approaches based on that chief complaint of the insomnia,” said Dr. Winkelman, chief of the Massachusetts General Sleep Disorders Clinical Research Program in the department of psychiatry at Harvard Medical School, Boston. “Cognitive-behavioral therapy for insomnia [CBT-I], for instance, is very good at reducing time awake at night. It won’t increase total sleep time, but it reduces time awake at night dramatically.”

According to the DSM-5, insomnia disorder is marked by dissatisfaction with sleep quality or quantity associated with at least one of the following: difficulty initiating sleep, difficulty maintaining sleep, and early morning awakening. “Just getting up to pee five times a night is not insomnia,” he said. “Just taking an hour and a half to fall asleep at the beginning of the night is not insomnia. There has to be distress or dysfunction related to the sleep disturbance, for a minimum of three times per week for 3 months.”

Most sleep problems are transient, but 25%-30% last more than 1 year. The differential diagnosis for chronic insomnia includes primary psychiatric disorders, medications, substances, restless legs syndrome, sleep schedule disorders, and obstructive sleep apnea.

“In general, we do not order sleep studies in people with insomnia unless we suspect sleep apnea; it’s just a waste of time,” said Dr. Winkelman, who is also a professor of psychiatry at Harvard Medical School. Indications for polysomnography include loud snoring plus one of the following: daytime sleepiness, witnessed apneas, or refractory hypertension. Other indications include abnormal behaviors or movements during sleep, unexplained excessive daytime sleepiness, and refractory sleep complaints, especially repetitive brief awakenings.

Many common cognitive and behavioral issues can produce or worsen insomnia, including inconsistent bedtimes and wake times. “That irregular schedule wreaks havoc with sleep,” he said. “It messes up the circadian rhythm. Also, homeostatic drive needs to build up: We need to be awake 16 or more hours in order to be sleepy. If people are sleeping until noon on Sundays and then trying to go to bed at their usual time, 10 or 11 at night, they’ve only been awake 10 or 11 hours. That’s why they’re going to have problems falling asleep. Also, a lot of people doze off after dinner in front of the TV. That doesn’t help.”

Spending excessive time in bed can also trigger or worsen insomnia. Dr. Winkelman recommends that people restrict their access to bed to the number of hours it is reasonable to sleep. “I see a lot of people in their 70s and 80s spending 10 hours in bed,” he said. “It doesn’t sound that crazy, but there is no way they’re going to get 10 hours of sleep. It’s physically impossible, so they spend 2 or 3 hours awake at night.” Clock-watching is another no-no. “In the middle of the night you wake up, look at the clock, and say to yourself: ‘Oh my god, I’ve been awake for 3 hours. I have 4 hours left. I need 7 hours. That means I need to go to sleep now!’ ”

An estimated 30%-40% of people with chronic insomnia have a psychiatric disorder. That means “you have to be thorough in your evaluation and act as if you’re doing a structured interview,” Dr. Winkelman said. “Ask about obsessive-compulsive disorder, generalized anxiety disorder, PTSD, et cetera, so that you understand the complete myriad of psychiatric illnesses, because psychiatric illnesses run in gangs. Comorbidity is generally the rule.”

The first-line treatment for chronic insomnia disorder is CBT-I, a multicomponent approach that includes time-in-bed restriction, stimulus control, cognitive therapy, relaxation therapy, and sleep hygiene. According to Dr. Winkelman, the cornerstone of CBT-I is time-in-bed restriction. “Many people with insomnia are spending 8.5 hours in bed to get 6.5 hours of sleep,” he said. “What you do is restrict access to bed to 6.5 hours; you initially sleep deprive them. Over the first few weeks, they hate you. After a few weeks when they start sleeping well, you start gradually increasing time in bed, but they rarely get back to the 8.5 hours in bed they were spending beforehand.”

Online CBT-I programs such as Sleepio can also be effective for improving sleep latency and wake after sleep onset, but not for total sleep time (JAMA Psychiatry. 2017;74[1]:68-75). “Not everybody responds to CBT; 50% don’t respond at a couple of months,” he said. “These are the people you need to think about medication for.”

Medications commonly used for chronic insomnia include benzodiazepine receptor agonists (BzRAs) – temazepam, eszopiclone, triazolam, zolpidem, and zaleplon are Food and Drug Administration approved – melatonin agonists, orexin antagonists, sedating antidepressants, anticonvulsants, and dopaminergic antagonists. “Each of the agents in these categories has somewhat similar mechanisms of action, and similar efficacy and contraindications,” Dr. Winkelman said. “The best way to divide the benzodiazepine receptor agonists is based on half-life. How long do you want drug on receptor in somebody with insomnia? Probably not much longer than 8 hours. Nevertheless, some psychiatrists love clonazepam, which has a 40-hour half-life. The circumstances under which clonazepam should be used for insomnia are small, such as in people with a daytime anxiety disorder.”

Consider trying triazolam, zolpidem, and zaleplon for patients who have problems falling asleep, he said, while oxazepam and eszopiclone are sensible options for people who have difficulty falling and staying asleep. Clinical response to BzRAs is common, yet only about half of people who have insomnia remit with one of these agents.

Dr. Winkelman said that patients and physicians often ask him whether BzRAs and other agents used as sleep aids are addictive. Abuse is identified when recurrent use causes clinically and functionally significant impairment, such as health problems; disability; and failure to meet major responsibilities at work, home, or school. “These are concerns with BzRAs. Misuse and abuse generally occur in younger people. Once you get to 35 years old, misuse rates get very low. In older people, rates of side effects go up.

“Tolerance, physiological and psychological dependence, and nonmedical diversion are also of concern,” he said. However, for the majority of people, BzRA hypnotics are effective and safe.

As for other agents, meta-analyses have demonstrated that melatonin 1-3 mg can help people fall asleep when it’s not being endogenously released. “That’s during the day,” he said. “That might be most relevant for jet lag and for people doing shift work.” Two orexin antagonists on the market for insomnia include suvorexant and lemborexant 10-20 mg. Advantages of these include little abuse liability and few side effects. “In one head-to-head polysomnography study in the elderly, lemborexant was superior to zolpidem 6.25 mg CR on both objective and subjective ability to fall asleep and stay asleep,” Dr. Winkelman said. (JAMA Netw Open. 2019;2[12]:e1918254).

Antidepressants are another treatment option, including mirtazapine 15-30 mg, trazodone 25-100 mg, and amitriptyline and doxepin (10-50 mg). Advantages include little abuse liability, while potential drawbacks include daytime sedation, weight gain, and anticholinergic side effects. Meanwhile, atypical antipsychotics such as quetiapine 25-100 mg have long been known to be helpful for sleep. “Advantages are that they’re anxiolytic, they’re mood stabilizing, and there is little abuse liability,” Dr. Winkelman said. “Drawbacks are that they’re probably less effective than BzRAs, they cause daytime sedation, weight gain, risks of extrapyramidal symptoms and glucose and lipid abnormalities.”

Dr. Winkelman said that he uses “a fair amount” of the anticonvulsant gabapentin as a second- or third-line hypnotic agent. “I usually start with 300 mg [at bedtime],” he added. “Drawbacks are that it’s probably less effective than BzRAs; it affects cognition; and can cause daytime sedation, dizziness, and weight gain. There are also concerns about abuse.”

Dr. Winkelman reported that he has received grant/research support from Merck, the RLS Foundation, and Luitpold Pharmaceuticals. He is also a consultant for Advance Medical, Avadel Pharmaceuticals, and UpToDate and is a member of the speakers’ bureau for Luitpold.

[email protected]

LAS VEGAS – Clinicians should spend 1 hour with patients who present with a chief complaint of insomnia, rather than rushing to a treatment after a 10- to 15-minute office visit, according to John W. Winkelman, MD, PhD.

Doug Brunk/MDedge News

“Why? Because sleep problems are usually multifactorial, involving psychiatric illness, sleep disorders, medical illness, medication, and poor sleep hygiene/stress,” he said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “There are usually many contributing problems, and sleep quality is only as strong as the weakest link. Maybe you don’t have an hour [to meet with new patients], but you need to give adequate time, otherwise you’re not going to do justice to the problem.”

During that first visit, Dr. Winkelman recommends establishing and prioritizing goals with the patient. “Ask, ‘what is it that bothers you most about your insomnia? Is it the time awake at night, your total sleep time, or how you feel during the day?’ Because we’re going to use different approaches based on that chief complaint of the insomnia,” said Dr. Winkelman, chief of the Massachusetts General Sleep Disorders Clinical Research Program in the department of psychiatry at Harvard Medical School, Boston. “Cognitive-behavioral therapy for insomnia [CBT-I], for instance, is very good at reducing time awake at night. It won’t increase total sleep time, but it reduces time awake at night dramatically.”

According to the DSM-5, insomnia disorder is marked by dissatisfaction with sleep quality or quantity associated with at least one of the following: difficulty initiating sleep, difficulty maintaining sleep, and early morning awakening. “Just getting up to pee five times a night is not insomnia,” he said. “Just taking an hour and a half to fall asleep at the beginning of the night is not insomnia. There has to be distress or dysfunction related to the sleep disturbance, for a minimum of three times per week for 3 months.”

Most sleep problems are transient, but 25%-30% last more than 1 year. The differential diagnosis for chronic insomnia includes primary psychiatric disorders, medications, substances, restless legs syndrome, sleep schedule disorders, and obstructive sleep apnea.

“In general, we do not order sleep studies in people with insomnia unless we suspect sleep apnea; it’s just a waste of time,” said Dr. Winkelman, who is also a professor of psychiatry at Harvard Medical School. Indications for polysomnography include loud snoring plus one of the following: daytime sleepiness, witnessed apneas, or refractory hypertension. Other indications include abnormal behaviors or movements during sleep, unexplained excessive daytime sleepiness, and refractory sleep complaints, especially repetitive brief awakenings.

Many common cognitive and behavioral issues can produce or worsen insomnia, including inconsistent bedtimes and wake times. “That irregular schedule wreaks havoc with sleep,” he said. “It messes up the circadian rhythm. Also, homeostatic drive needs to build up: We need to be awake 16 or more hours in order to be sleepy. If people are sleeping until noon on Sundays and then trying to go to bed at their usual time, 10 or 11 at night, they’ve only been awake 10 or 11 hours. That’s why they’re going to have problems falling asleep. Also, a lot of people doze off after dinner in front of the TV. That doesn’t help.”

Spending excessive time in bed can also trigger or worsen insomnia. Dr. Winkelman recommends that people restrict their access to bed to the number of hours it is reasonable to sleep. “I see a lot of people in their 70s and 80s spending 10 hours in bed,” he said. “It doesn’t sound that crazy, but there is no way they’re going to get 10 hours of sleep. It’s physically impossible, so they spend 2 or 3 hours awake at night.” Clock-watching is another no-no. “In the middle of the night you wake up, look at the clock, and say to yourself: ‘Oh my god, I’ve been awake for 3 hours. I have 4 hours left. I need 7 hours. That means I need to go to sleep now!’ ”

An estimated 30%-40% of people with chronic insomnia have a psychiatric disorder. That means “you have to be thorough in your evaluation and act as if you’re doing a structured interview,” Dr. Winkelman said. “Ask about obsessive-compulsive disorder, generalized anxiety disorder, PTSD, et cetera, so that you understand the complete myriad of psychiatric illnesses, because psychiatric illnesses run in gangs. Comorbidity is generally the rule.”

The first-line treatment for chronic insomnia disorder is CBT-I, a multicomponent approach that includes time-in-bed restriction, stimulus control, cognitive therapy, relaxation therapy, and sleep hygiene. According to Dr. Winkelman, the cornerstone of CBT-I is time-in-bed restriction. “Many people with insomnia are spending 8.5 hours in bed to get 6.5 hours of sleep,” he said. “What you do is restrict access to bed to 6.5 hours; you initially sleep deprive them. Over the first few weeks, they hate you. After a few weeks when they start sleeping well, you start gradually increasing time in bed, but they rarely get back to the 8.5 hours in bed they were spending beforehand.”

Online CBT-I programs such as Sleepio can also be effective for improving sleep latency and wake after sleep onset, but not for total sleep time (JAMA Psychiatry. 2017;74[1]:68-75). “Not everybody responds to CBT; 50% don’t respond at a couple of months,” he said. “These are the people you need to think about medication for.”

Medications commonly used for chronic insomnia include benzodiazepine receptor agonists (BzRAs) – temazepam, eszopiclone, triazolam, zolpidem, and zaleplon are Food and Drug Administration approved – melatonin agonists, orexin antagonists, sedating antidepressants, anticonvulsants, and dopaminergic antagonists. “Each of the agents in these categories has somewhat similar mechanisms of action, and similar efficacy and contraindications,” Dr. Winkelman said. “The best way to divide the benzodiazepine receptor agonists is based on half-life. How long do you want drug on receptor in somebody with insomnia? Probably not much longer than 8 hours. Nevertheless, some psychiatrists love clonazepam, which has a 40-hour half-life. The circumstances under which clonazepam should be used for insomnia are small, such as in people with a daytime anxiety disorder.”

Consider trying triazolam, zolpidem, and zaleplon for patients who have problems falling asleep, he said, while oxazepam and eszopiclone are sensible options for people who have difficulty falling and staying asleep. Clinical response to BzRAs is common, yet only about half of people who have insomnia remit with one of these agents.

Dr. Winkelman said that patients and physicians often ask him whether BzRAs and other agents used as sleep aids are addictive. Abuse is identified when recurrent use causes clinically and functionally significant impairment, such as health problems; disability; and failure to meet major responsibilities at work, home, or school. “These are concerns with BzRAs. Misuse and abuse generally occur in younger people. Once you get to 35 years old, misuse rates get very low. In older people, rates of side effects go up.

“Tolerance, physiological and psychological dependence, and nonmedical diversion are also of concern,” he said. However, for the majority of people, BzRA hypnotics are effective and safe.

As for other agents, meta-analyses have demonstrated that melatonin 1-3 mg can help people fall asleep when it’s not being endogenously released. “That’s during the day,” he said. “That might be most relevant for jet lag and for people doing shift work.” Two orexin antagonists on the market for insomnia include suvorexant and lemborexant 10-20 mg. Advantages of these include little abuse liability and few side effects. “In one head-to-head polysomnography study in the elderly, lemborexant was superior to zolpidem 6.25 mg CR on both objective and subjective ability to fall asleep and stay asleep,” Dr. Winkelman said. (JAMA Netw Open. 2019;2[12]:e1918254).

Antidepressants are another treatment option, including mirtazapine 15-30 mg, trazodone 25-100 mg, and amitriptyline and doxepin (10-50 mg). Advantages include little abuse liability, while potential drawbacks include daytime sedation, weight gain, and anticholinergic side effects. Meanwhile, atypical antipsychotics such as quetiapine 25-100 mg have long been known to be helpful for sleep. “Advantages are that they’re anxiolytic, they’re mood stabilizing, and there is little abuse liability,” Dr. Winkelman said. “Drawbacks are that they’re probably less effective than BzRAs, they cause daytime sedation, weight gain, risks of extrapyramidal symptoms and glucose and lipid abnormalities.”

Dr. Winkelman said that he uses “a fair amount” of the anticonvulsant gabapentin as a second- or third-line hypnotic agent. “I usually start with 300 mg [at bedtime],” he added. “Drawbacks are that it’s probably less effective than BzRAs; it affects cognition; and can cause daytime sedation, dizziness, and weight gain. There are also concerns about abuse.”

Dr. Winkelman reported that he has received grant/research support from Merck, the RLS Foundation, and Luitpold Pharmaceuticals. He is also a consultant for Advance Medical, Avadel Pharmaceuticals, and UpToDate and is a member of the speakers’ bureau for Luitpold.

[email protected]

LAS VEGAS – Clinicians should spend 1 hour with patients who present with a chief complaint of insomnia, rather than rushing to a treatment after a 10- to 15-minute office visit, according to John W. Winkelman, MD, PhD.

Doug Brunk/MDedge News

“Why? Because sleep problems are usually multifactorial, involving psychiatric illness, sleep disorders, medical illness, medication, and poor sleep hygiene/stress,” he said at an annual psychopharmacology update held by the Nevada Psychiatric Association. “There are usually many contributing problems, and sleep quality is only as strong as the weakest link. Maybe you don’t have an hour [to meet with new patients], but you need to give adequate time, otherwise you’re not going to do justice to the problem.”

During that first visit, Dr. Winkelman recommends establishing and prioritizing goals with the patient. “Ask, ‘what is it that bothers you most about your insomnia? Is it the time awake at night, your total sleep time, or how you feel during the day?’ Because we’re going to use different approaches based on that chief complaint of the insomnia,” said Dr. Winkelman, chief of the Massachusetts General Sleep Disorders Clinical Research Program in the department of psychiatry at Harvard Medical School, Boston. “Cognitive-behavioral therapy for insomnia [CBT-I], for instance, is very good at reducing time awake at night. It won’t increase total sleep time, but it reduces time awake at night dramatically.”

According to the DSM-5, insomnia disorder is marked by dissatisfaction with sleep quality or quantity associated with at least one of the following: difficulty initiating sleep, difficulty maintaining sleep, and early morning awakening. “Just getting up to pee five times a night is not insomnia,” he said. “Just taking an hour and a half to fall asleep at the beginning of the night is not insomnia. There has to be distress or dysfunction related to the sleep disturbance, for a minimum of three times per week for 3 months.”

Most sleep problems are transient, but 25%-30% last more than 1 year. The differential diagnosis for chronic insomnia includes primary psychiatric disorders, medications, substances, restless legs syndrome, sleep schedule disorders, and obstructive sleep apnea.

“In general, we do not order sleep studies in people with insomnia unless we suspect sleep apnea; it’s just a waste of time,” said Dr. Winkelman, who is also a professor of psychiatry at Harvard Medical School. Indications for polysomnography include loud snoring plus one of the following: daytime sleepiness, witnessed apneas, or refractory hypertension. Other indications include abnormal behaviors or movements during sleep, unexplained excessive daytime sleepiness, and refractory sleep complaints, especially repetitive brief awakenings.

Many common cognitive and behavioral issues can produce or worsen insomnia, including inconsistent bedtimes and wake times. “That irregular schedule wreaks havoc with sleep,” he said. “It messes up the circadian rhythm. Also, homeostatic drive needs to build up: We need to be awake 16 or more hours in order to be sleepy. If people are sleeping until noon on Sundays and then trying to go to bed at their usual time, 10 or 11 at night, they’ve only been awake 10 or 11 hours. That’s why they’re going to have problems falling asleep. Also, a lot of people doze off after dinner in front of the TV. That doesn’t help.”

Spending excessive time in bed can also trigger or worsen insomnia. Dr. Winkelman recommends that people restrict their access to bed to the number of hours it is reasonable to sleep. “I see a lot of people in their 70s and 80s spending 10 hours in bed,” he said. “It doesn’t sound that crazy, but there is no way they’re going to get 10 hours of sleep. It’s physically impossible, so they spend 2 or 3 hours awake at night.” Clock-watching is another no-no. “In the middle of the night you wake up, look at the clock, and say to yourself: ‘Oh my god, I’ve been awake for 3 hours. I have 4 hours left. I need 7 hours. That means I need to go to sleep now!’ ”

An estimated 30%-40% of people with chronic insomnia have a psychiatric disorder. That means “you have to be thorough in your evaluation and act as if you’re doing a structured interview,” Dr. Winkelman said. “Ask about obsessive-compulsive disorder, generalized anxiety disorder, PTSD, et cetera, so that you understand the complete myriad of psychiatric illnesses, because psychiatric illnesses run in gangs. Comorbidity is generally the rule.”

The first-line treatment for chronic insomnia disorder is CBT-I, a multicomponent approach that includes time-in-bed restriction, stimulus control, cognitive therapy, relaxation therapy, and sleep hygiene. According to Dr. Winkelman, the cornerstone of CBT-I is time-in-bed restriction. “Many people with insomnia are spending 8.5 hours in bed to get 6.5 hours of sleep,” he said. “What you do is restrict access to bed to 6.5 hours; you initially sleep deprive them. Over the first few weeks, they hate you. After a few weeks when they start sleeping well, you start gradually increasing time in bed, but they rarely get back to the 8.5 hours in bed they were spending beforehand.”

Online CBT-I programs such as Sleepio can also be effective for improving sleep latency and wake after sleep onset, but not for total sleep time (JAMA Psychiatry. 2017;74[1]:68-75). “Not everybody responds to CBT; 50% don’t respond at a couple of months,” he said. “These are the people you need to think about medication for.”

Medications commonly used for chronic insomnia include benzodiazepine receptor agonists (BzRAs) – temazepam, eszopiclone, triazolam, zolpidem, and zaleplon are Food and Drug Administration approved – melatonin agonists, orexin antagonists, sedating antidepressants, anticonvulsants, and dopaminergic antagonists. “Each of the agents in these categories has somewhat similar mechanisms of action, and similar efficacy and contraindications,” Dr. Winkelman said. “The best way to divide the benzodiazepine receptor agonists is based on half-life. How long do you want drug on receptor in somebody with insomnia? Probably not much longer than 8 hours. Nevertheless, some psychiatrists love clonazepam, which has a 40-hour half-life. The circumstances under which clonazepam should be used for insomnia are small, such as in people with a daytime anxiety disorder.”

Consider trying triazolam, zolpidem, and zaleplon for patients who have problems falling asleep, he said, while oxazepam and eszopiclone are sensible options for people who have difficulty falling and staying asleep. Clinical response to BzRAs is common, yet only about half of people who have insomnia remit with one of these agents.

Dr. Winkelman said that patients and physicians often ask him whether BzRAs and other agents used as sleep aids are addictive. Abuse is identified when recurrent use causes clinically and functionally significant impairment, such as health problems; disability; and failure to meet major responsibilities at work, home, or school. “These are concerns with BzRAs. Misuse and abuse generally occur in younger people. Once you get to 35 years old, misuse rates get very low. In older people, rates of side effects go up.

“Tolerance, physiological and psychological dependence, and nonmedical diversion are also of concern,” he said. However, for the majority of people, BzRA hypnotics are effective and safe.

As for other agents, meta-analyses have demonstrated that melatonin 1-3 mg can help people fall asleep when it’s not being endogenously released. “That’s during the day,” he said. “That might be most relevant for jet lag and for people doing shift work.” Two orexin antagonists on the market for insomnia include suvorexant and lemborexant 10-20 mg. Advantages of these include little abuse liability and few side effects. “In one head-to-head polysomnography study in the elderly, lemborexant was superior to zolpidem 6.25 mg CR on both objective and subjective ability to fall asleep and stay asleep,” Dr. Winkelman said. (JAMA Netw Open. 2019;2[12]:e1918254).

Antidepressants are another treatment option, including mirtazapine 15-30 mg, trazodone 25-100 mg, and amitriptyline and doxepin (10-50 mg). Advantages include little abuse liability, while potential drawbacks include daytime sedation, weight gain, and anticholinergic side effects. Meanwhile, atypical antipsychotics such as quetiapine 25-100 mg have long been known to be helpful for sleep. “Advantages are that they’re anxiolytic, they’re mood stabilizing, and there is little abuse liability,” Dr. Winkelman said. “Drawbacks are that they’re probably less effective than BzRAs, they cause daytime sedation, weight gain, risks of extrapyramidal symptoms and glucose and lipid abnormalities.”

Dr. Winkelman said that he uses “a fair amount” of the anticonvulsant gabapentin as a second- or third-line hypnotic agent. “I usually start with 300 mg [at bedtime],” he added. “Drawbacks are that it’s probably less effective than BzRAs; it affects cognition; and can cause daytime sedation, dizziness, and weight gain. There are also concerns about abuse.”

Dr. Winkelman reported that he has received grant/research support from Merck, the RLS Foundation, and Luitpold Pharmaceuticals. He is also a consultant for Advance Medical, Avadel Pharmaceuticals, and UpToDate and is a member of the speakers’ bureau for Luitpold.

[email protected]