Sleep Strategies

 

The definition of mild obstructive sleep apnea (OSA) has varied over the years depending upon several factors, but based upon all definitions, it is highly prevalent. Depending upon presence of symptoms and gender, the prevalence may be as high 28% in men and 26% in women. (Young et al. N Engl J Med. 1993;328:1230).

Typically, a combination of symptoms and frequency of respiratory events is required to make the diagnosis. Based upon the International Classification of Sleep Disorders-3rd edition (ICSD-3), the threshold apnea hypopnea index (AHI) for diagnosis depends upon the presence or absence of symptoms. If an individual has no symptoms, an AHI of 15 events per hour or more is required to make a diagnosis of OSA. However, there are several concerns about whether or not an individual may be “symptomatic.” This is most relevant when driving privileges may be at risk, such as with a commercial drivers’ licensing.

If a person knows that their response to a list of questions could lead to further testing, additional costs, and/or treatment, then symptoms could be unreported or underestimated. Notwithstanding, specific symptoms that are typically noted include some sign of sleepiness or non-restorative sleep and apneic episodes. The presence of snoring, gasping, choking, or breathing interruptions, either witnessed or noted by the individuals themselves, are included in the criteria. The Epworth Sleepiness Scale is the most common measure of sleepiness, which includes the likelihood of falling asleep in eight different scenarios. However, there is only a weak correlation between the scale and severity of OSA with sensitivity as low as 0.36 reported in some studies, especially if only mild OSA is present.

The presence of other comorbid disease can be used as criteria, including hypertension, mood disorder, cognitive dysfunction, coronary artery disease, stroke, congestive heart failure, atrial fibrillation, and type 2 diabetes mellitus. If no signs, symptoms, or comorbid diseases are present, then an AHI greater than 15 events per hour or more is required to make the diagnosis of OSA (Chowdrui et al. Am J Respir Crit Care Med. 2016;193:e37).

There is still debate regarding the association of mild OSA and cardiovascular disease and whether treatment may prevent or reduce cardiovascular outcomes. The four main clinical outcomes typically reported are hypertension, cardiovascular events, cardiovascular and all-cause mortality, and arrhythmias.

Regarding mild OSA and hypertension, 5 prospective and 18 cross-sectional studies have been reported with the two main studies being the Wisconsin Sleep Cohort study and the Sleep Heart Health Study. The Wisconsin Sleep Cohort study found mild OSA was associated with an increased risk of hypertension (Peppard et al. N Engl J Med. 2000;342:1378). However, the Sleep Heart Health study followed individuals without hypertension, including 629 with mild OSA, for 5.2 years and assessed risk of incident hypertension. Stratified analyses found no evidence for an elevated risk of hypertension in subgroups defined by age, sex, BMI, or degree of sleepiness (O’Connor et al. Am J Respir Crit Care Med. 2009;179:1159). Therefore, it appears current data are contradictory when it comes to mild OSA and subsequent risk of hypertension when stratified by age, sex, and BMI. Only retrospective analyses have been used to assess the risk of cardiovascular events.

A large clinical cohort of patients referred for sleep studies showed no association of mild OSA with different composite outcomes. Kendzerska and colleagues evaluated a composite outcome (myocardial infarction, stroke, CHF, revascularization procedures, or death from any cause) during a median follow-up of 68 months. No association of mild OSA with the composite cardiovascular endpoint was identified compared with those without OSA (Kendzerska et al. PLoS Med. 2014;11[2]:e1001599). Only one population-based study (MrOS Sleep Study) looked at the association between mild OSA and nocturnal arrhythmias in elderly men. The study did not find an increased risk for atrial fibrillation or complex ventricular ectopy in patients with mild OSA vs no OSA (Mehra et al. Arch Intern Med. 2009; 169:1147).

Several cohort studies have reported mild OSA is not associated with increased cardiovascular mortality. In the 18-year follow-up of the Wisconsin Cohort Study, it was found that mild OSA was not associated with cardiovascular mortality (HR, 1.8; 95% CI, 0.7–4.9). All-cause mortality was also not significantly increased in the mild OSA group compared with the no-OSA group in the Wisconsin cohort after 8 years of follow-up (adjusted HR, 1.6; 95% CI, 0.8–2.8). In summary, compared with subjects without OSA, available evidence from population-based longitudinal studies indicates that mild OSA is not associated with increased cardiovascular or all-cause mortality.

Does treatment of mild OSA vs no treatment change cardiovascular or mortality outcomes? This is still debated with no definitive answer. There have been several studies that have examined different therapies for OSA to reduce cardiovascular events. Typical events include coronary artery disease, hypertension, heart failure, stroke, arrhythmias, and cardiovascular disease-related mortality. However, most studies have examined cohorts with moderate to severe OSA with limited evaluation in the mild OSA category.

The effect of treatment of mild OSA on hypertension has been evaluated. A single clinical trial randomized patients with mild OSA to either a very low calorie diet with supervised lifestyle modifications vs control arm and followed patients for 1 year (Tuomilehto et al. Am J Respir Crit Care Med. 2009;179:320). Participants in the intervention arm lost more weight than the control group. Hypertension was a secondary outcome measured from the study. There was no significant change in systolic and diastolic blood pressure after successful weight loss with diet and lifestyle modifications. Follow-up at 2 and 5 years did not show significant changes in systolic and diastolic blood pressure. Patients in the treatment group lost more weight than the control group (10.7kg vs 2.4kg, respectively) and had greater resolution of sleep apnea (63% vs 35%, respectively).

An observational study evaluated the effects of CPAP specifically in patients with mild OSA. There was no significant difference in the risk of developing hypertension among those patients ineligible for CPAP therapy, active on therapy, or those who declined therapy (Marin et al. JAMA. 2012; 307:2169). In contrast, a retrospective longitudinal cohort with normal blood pressure at baseline (mild OSA without preexisting cardiovascular disease, diabetes, or hyperlipidemia) did show decrease in mean arterial blood pressure of 2 mm Hg in the treatment group (Jaimchariyatam et al. Sleep Med. 2010;11:837). The MOSAIC trial was a multicenter randomized trial that evaluated the effects of CPAP on cardiac function in minimally symptomatic patients with OSA. The use of CPAP reduced the oxygen desaturation index (ODI) and Epworth Sleepiness Scale values. However, 6 months of therapy did not change functional or structural parameters measured by echocardiogram or cardiac magnetic resonance scanning in patients with mild to moderate OSA (Craig et al. J Clin Sleep Med. 2015;11[9]:967). A single retrospective study reported the effects of CPAP in patients with mild OSA and all-cause mortality. The study compared treatment with patients using CPAP more than 4 hours vs a combined group of nonadherent and those who refused therapy (Hudgel et al. J Clin Sleep Med. 2012;8:9). There was no significant difference in all-cause mortality in the two groups. However, this study did not analyze the impact of therapy on cardiovascular-specific mortality.

To date, there have been no studies that have evaluated the impact of treatment of mild OSA on cardiovascular events, arrhythmias, or stroke. In addition, there have been no randomized studies assessing treatment of mild OSA on fatal and nonfatal cardiovascular events. There is inadequate evidence regarding the effect of mild OSA on elevated blood pressure, neurologic cognition, quality of life, and cardiovascular consequences. Future research is needed to investigate the impact of mild OSA on these outcomes.

In summary, mild OSA is a very prevalent disease but the association with hypertension remains unclear and the literature to date suggests no association with other cardiovascular outcomes. In addition, no clear prevention of cardiovascular outcomes with treatment has been proven in the setting of mild OSA.

Dr. Duthuluru is Assistant Professor, Dr. Nazir is Assistant Professor, and Dr. Stevens is Associate Professor at the University of Kansas Medical Center.

 

The definition of mild obstructive sleep apnea (OSA) has varied over the years depending upon several factors, but based upon all definitions, it is highly prevalent. Depending upon presence of symptoms and gender, the prevalence may be as high 28% in men and 26% in women. (Young et al. N Engl J Med. 1993;328:1230).

Typically, a combination of symptoms and frequency of respiratory events is required to make the diagnosis. Based upon the International Classification of Sleep Disorders-3rd edition (ICSD-3), the threshold apnea hypopnea index (AHI) for diagnosis depends upon the presence or absence of symptoms. If an individual has no symptoms, an AHI of 15 events per hour or more is required to make a diagnosis of OSA. However, there are several concerns about whether or not an individual may be “symptomatic.” This is most relevant when driving privileges may be at risk, such as with a commercial drivers’ licensing.

If a person knows that their response to a list of questions could lead to further testing, additional costs, and/or treatment, then symptoms could be unreported or underestimated. Notwithstanding, specific symptoms that are typically noted include some sign of sleepiness or non-restorative sleep and apneic episodes. The presence of snoring, gasping, choking, or breathing interruptions, either witnessed or noted by the individuals themselves, are included in the criteria. The Epworth Sleepiness Scale is the most common measure of sleepiness, which includes the likelihood of falling asleep in eight different scenarios. However, there is only a weak correlation between the scale and severity of OSA with sensitivity as low as 0.36 reported in some studies, especially if only mild OSA is present.

The presence of other comorbid disease can be used as criteria, including hypertension, mood disorder, cognitive dysfunction, coronary artery disease, stroke, congestive heart failure, atrial fibrillation, and type 2 diabetes mellitus. If no signs, symptoms, or comorbid diseases are present, then an AHI greater than 15 events per hour or more is required to make the diagnosis of OSA (Chowdrui et al. Am J Respir Crit Care Med. 2016;193:e37).

There is still debate regarding the association of mild OSA and cardiovascular disease and whether treatment may prevent or reduce cardiovascular outcomes. The four main clinical outcomes typically reported are hypertension, cardiovascular events, cardiovascular and all-cause mortality, and arrhythmias.

Regarding mild OSA and hypertension, 5 prospective and 18 cross-sectional studies have been reported with the two main studies being the Wisconsin Sleep Cohort study and the Sleep Heart Health Study. The Wisconsin Sleep Cohort study found mild OSA was associated with an increased risk of hypertension (Peppard et al. N Engl J Med. 2000;342:1378). However, the Sleep Heart Health study followed individuals without hypertension, including 629 with mild OSA, for 5.2 years and assessed risk of incident hypertension. Stratified analyses found no evidence for an elevated risk of hypertension in subgroups defined by age, sex, BMI, or degree of sleepiness (O’Connor et al. Am J Respir Crit Care Med. 2009;179:1159). Therefore, it appears current data are contradictory when it comes to mild OSA and subsequent risk of hypertension when stratified by age, sex, and BMI. Only retrospective analyses have been used to assess the risk of cardiovascular events.

A large clinical cohort of patients referred for sleep studies showed no association of mild OSA with different composite outcomes. Kendzerska and colleagues evaluated a composite outcome (myocardial infarction, stroke, CHF, revascularization procedures, or death from any cause) during a median follow-up of 68 months. No association of mild OSA with the composite cardiovascular endpoint was identified compared with those without OSA (Kendzerska et al. PLoS Med. 2014;11[2]:e1001599). Only one population-based study (MrOS Sleep Study) looked at the association between mild OSA and nocturnal arrhythmias in elderly men. The study did not find an increased risk for atrial fibrillation or complex ventricular ectopy in patients with mild OSA vs no OSA (Mehra et al. Arch Intern Med. 2009; 169:1147).

Several cohort studies have reported mild OSA is not associated with increased cardiovascular mortality. In the 18-year follow-up of the Wisconsin Cohort Study, it was found that mild OSA was not associated with cardiovascular mortality (HR, 1.8; 95% CI, 0.7–4.9). All-cause mortality was also not significantly increased in the mild OSA group compared with the no-OSA group in the Wisconsin cohort after 8 years of follow-up (adjusted HR, 1.6; 95% CI, 0.8–2.8). In summary, compared with subjects without OSA, available evidence from population-based longitudinal studies indicates that mild OSA is not associated with increased cardiovascular or all-cause mortality.

Does treatment of mild OSA vs no treatment change cardiovascular or mortality outcomes? This is still debated with no definitive answer. There have been several studies that have examined different therapies for OSA to reduce cardiovascular events. Typical events include coronary artery disease, hypertension, heart failure, stroke, arrhythmias, and cardiovascular disease-related mortality. However, most studies have examined cohorts with moderate to severe OSA with limited evaluation in the mild OSA category.

The effect of treatment of mild OSA on hypertension has been evaluated. A single clinical trial randomized patients with mild OSA to either a very low calorie diet with supervised lifestyle modifications vs control arm and followed patients for 1 year (Tuomilehto et al. Am J Respir Crit Care Med. 2009;179:320). Participants in the intervention arm lost more weight than the control group. Hypertension was a secondary outcome measured from the study. There was no significant change in systolic and diastolic blood pressure after successful weight loss with diet and lifestyle modifications. Follow-up at 2 and 5 years did not show significant changes in systolic and diastolic blood pressure. Patients in the treatment group lost more weight than the control group (10.7kg vs 2.4kg, respectively) and had greater resolution of sleep apnea (63% vs 35%, respectively).

An observational study evaluated the effects of CPAP specifically in patients with mild OSA. There was no significant difference in the risk of developing hypertension among those patients ineligible for CPAP therapy, active on therapy, or those who declined therapy (Marin et al. JAMA. 2012; 307:2169). In contrast, a retrospective longitudinal cohort with normal blood pressure at baseline (mild OSA without preexisting cardiovascular disease, diabetes, or hyperlipidemia) did show decrease in mean arterial blood pressure of 2 mm Hg in the treatment group (Jaimchariyatam et al. Sleep Med. 2010;11:837). The MOSAIC trial was a multicenter randomized trial that evaluated the effects of CPAP on cardiac function in minimally symptomatic patients with OSA. The use of CPAP reduced the oxygen desaturation index (ODI) and Epworth Sleepiness Scale values. However, 6 months of therapy did not change functional or structural parameters measured by echocardiogram or cardiac magnetic resonance scanning in patients with mild to moderate OSA (Craig et al. J Clin Sleep Med. 2015;11[9]:967). A single retrospective study reported the effects of CPAP in patients with mild OSA and all-cause mortality. The study compared treatment with patients using CPAP more than 4 hours vs a combined group of nonadherent and those who refused therapy (Hudgel et al. J Clin Sleep Med. 2012;8:9). There was no significant difference in all-cause mortality in the two groups. However, this study did not analyze the impact of therapy on cardiovascular-specific mortality.

To date, there have been no studies that have evaluated the impact of treatment of mild OSA on cardiovascular events, arrhythmias, or stroke. In addition, there have been no randomized studies assessing treatment of mild OSA on fatal and nonfatal cardiovascular events. There is inadequate evidence regarding the effect of mild OSA on elevated blood pressure, neurologic cognition, quality of life, and cardiovascular consequences. Future research is needed to investigate the impact of mild OSA on these outcomes.

In summary, mild OSA is a very prevalent disease but the association with hypertension remains unclear and the literature to date suggests no association with other cardiovascular outcomes. In addition, no clear prevention of cardiovascular outcomes with treatment has been proven in the setting of mild OSA.

Dr. Duthuluru is Assistant Professor, Dr. Nazir is Assistant Professor, and Dr. Stevens is Associate Professor at the University of Kansas Medical Center.

 

The definition of mild obstructive sleep apnea (OSA) has varied over the years depending upon several factors, but based upon all definitions, it is highly prevalent. Depending upon presence of symptoms and gender, the prevalence may be as high 28% in men and 26% in women. (Young et al. N Engl J Med. 1993;328:1230).

Typically, a combination of symptoms and frequency of respiratory events is required to make the diagnosis. Based upon the International Classification of Sleep Disorders-3rd edition (ICSD-3), the threshold apnea hypopnea index (AHI) for diagnosis depends upon the presence or absence of symptoms. If an individual has no symptoms, an AHI of 15 events per hour or more is required to make a diagnosis of OSA. However, there are several concerns about whether or not an individual may be “symptomatic.” This is most relevant when driving privileges may be at risk, such as with a commercial drivers’ licensing.

If a person knows that their response to a list of questions could lead to further testing, additional costs, and/or treatment, then symptoms could be unreported or underestimated. Notwithstanding, specific symptoms that are typically noted include some sign of sleepiness or non-restorative sleep and apneic episodes. The presence of snoring, gasping, choking, or breathing interruptions, either witnessed or noted by the individuals themselves, are included in the criteria. The Epworth Sleepiness Scale is the most common measure of sleepiness, which includes the likelihood of falling asleep in eight different scenarios. However, there is only a weak correlation between the scale and severity of OSA with sensitivity as low as 0.36 reported in some studies, especially if only mild OSA is present.

The presence of other comorbid disease can be used as criteria, including hypertension, mood disorder, cognitive dysfunction, coronary artery disease, stroke, congestive heart failure, atrial fibrillation, and type 2 diabetes mellitus. If no signs, symptoms, or comorbid diseases are present, then an AHI greater than 15 events per hour or more is required to make the diagnosis of OSA (Chowdrui et al. Am J Respir Crit Care Med. 2016;193:e37).

There is still debate regarding the association of mild OSA and cardiovascular disease and whether treatment may prevent or reduce cardiovascular outcomes. The four main clinical outcomes typically reported are hypertension, cardiovascular events, cardiovascular and all-cause mortality, and arrhythmias.

Regarding mild OSA and hypertension, 5 prospective and 18 cross-sectional studies have been reported with the two main studies being the Wisconsin Sleep Cohort study and the Sleep Heart Health Study. The Wisconsin Sleep Cohort study found mild OSA was associated with an increased risk of hypertension (Peppard et al. N Engl J Med. 2000;342:1378). However, the Sleep Heart Health study followed individuals without hypertension, including 629 with mild OSA, for 5.2 years and assessed risk of incident hypertension. Stratified analyses found no evidence for an elevated risk of hypertension in subgroups defined by age, sex, BMI, or degree of sleepiness (O’Connor et al. Am J Respir Crit Care Med. 2009;179:1159). Therefore, it appears current data are contradictory when it comes to mild OSA and subsequent risk of hypertension when stratified by age, sex, and BMI. Only retrospective analyses have been used to assess the risk of cardiovascular events.

A large clinical cohort of patients referred for sleep studies showed no association of mild OSA with different composite outcomes. Kendzerska and colleagues evaluated a composite outcome (myocardial infarction, stroke, CHF, revascularization procedures, or death from any cause) during a median follow-up of 68 months. No association of mild OSA with the composite cardiovascular endpoint was identified compared with those without OSA (Kendzerska et al. PLoS Med. 2014;11[2]:e1001599). Only one population-based study (MrOS Sleep Study) looked at the association between mild OSA and nocturnal arrhythmias in elderly men. The study did not find an increased risk for atrial fibrillation or complex ventricular ectopy in patients with mild OSA vs no OSA (Mehra et al. Arch Intern Med. 2009; 169:1147).

Several cohort studies have reported mild OSA is not associated with increased cardiovascular mortality. In the 18-year follow-up of the Wisconsin Cohort Study, it was found that mild OSA was not associated with cardiovascular mortality (HR, 1.8; 95% CI, 0.7–4.9). All-cause mortality was also not significantly increased in the mild OSA group compared with the no-OSA group in the Wisconsin cohort after 8 years of follow-up (adjusted HR, 1.6; 95% CI, 0.8–2.8). In summary, compared with subjects without OSA, available evidence from population-based longitudinal studies indicates that mild OSA is not associated with increased cardiovascular or all-cause mortality.

Does treatment of mild OSA vs no treatment change cardiovascular or mortality outcomes? This is still debated with no definitive answer. There have been several studies that have examined different therapies for OSA to reduce cardiovascular events. Typical events include coronary artery disease, hypertension, heart failure, stroke, arrhythmias, and cardiovascular disease-related mortality. However, most studies have examined cohorts with moderate to severe OSA with limited evaluation in the mild OSA category.

The effect of treatment of mild OSA on hypertension has been evaluated. A single clinical trial randomized patients with mild OSA to either a very low calorie diet with supervised lifestyle modifications vs control arm and followed patients for 1 year (Tuomilehto et al. Am J Respir Crit Care Med. 2009;179:320). Participants in the intervention arm lost more weight than the control group. Hypertension was a secondary outcome measured from the study. There was no significant change in systolic and diastolic blood pressure after successful weight loss with diet and lifestyle modifications. Follow-up at 2 and 5 years did not show significant changes in systolic and diastolic blood pressure. Patients in the treatment group lost more weight than the control group (10.7kg vs 2.4kg, respectively) and had greater resolution of sleep apnea (63% vs 35%, respectively).

An observational study evaluated the effects of CPAP specifically in patients with mild OSA. There was no significant difference in the risk of developing hypertension among those patients ineligible for CPAP therapy, active on therapy, or those who declined therapy (Marin et al. JAMA. 2012; 307:2169). In contrast, a retrospective longitudinal cohort with normal blood pressure at baseline (mild OSA without preexisting cardiovascular disease, diabetes, or hyperlipidemia) did show decrease in mean arterial blood pressure of 2 mm Hg in the treatment group (Jaimchariyatam et al. Sleep Med. 2010;11:837). The MOSAIC trial was a multicenter randomized trial that evaluated the effects of CPAP on cardiac function in minimally symptomatic patients with OSA. The use of CPAP reduced the oxygen desaturation index (ODI) and Epworth Sleepiness Scale values. However, 6 months of therapy did not change functional or structural parameters measured by echocardiogram or cardiac magnetic resonance scanning in patients with mild to moderate OSA (Craig et al. J Clin Sleep Med. 2015;11[9]:967). A single retrospective study reported the effects of CPAP in patients with mild OSA and all-cause mortality. The study compared treatment with patients using CPAP more than 4 hours vs a combined group of nonadherent and those who refused therapy (Hudgel et al. J Clin Sleep Med. 2012;8:9). There was no significant difference in all-cause mortality in the two groups. However, this study did not analyze the impact of therapy on cardiovascular-specific mortality.

To date, there have been no studies that have evaluated the impact of treatment of mild OSA on cardiovascular events, arrhythmias, or stroke. In addition, there have been no randomized studies assessing treatment of mild OSA on fatal and nonfatal cardiovascular events. There is inadequate evidence regarding the effect of mild OSA on elevated blood pressure, neurologic cognition, quality of life, and cardiovascular consequences. Future research is needed to investigate the impact of mild OSA on these outcomes.

In summary, mild OSA is a very prevalent disease but the association with hypertension remains unclear and the literature to date suggests no association with other cardiovascular outcomes. In addition, no clear prevention of cardiovascular outcomes with treatment has been proven in the setting of mild OSA.

Dr. Duthuluru is Assistant Professor, Dr. Nazir is Assistant Professor, and Dr. Stevens is Associate Professor at the University of Kansas Medical Center.