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Sleep-disordered breathing (SDB) is characterized by repetitive episodes of partial or complete upper airway occlusion occurring during sleep, with resultant intermittent hypoxemia and sleep disruption. Its pathogenesis relates to alteration in upper airway respiratory neuromuscular control and responsiveness during sleep that, in the setting of an anatomically compromised airway with increased critical pressure, is inadequate to maintain nasopharyngeal patency.1 The disorder has a high prevalence, estimated to afflict between 9% and 24% of adults in the general community when using standard polysomnography-based definitions and 2% to 4% when considering polysomnogram findings in addition to daytime somnolence symptoms.2 An explosion of research indicates that SDB is associated with considerable morbidity and mortality,3-5 suggesting that the health burden of SDB is quite substantive.2 Additionally, with the increase in obesity, a major risk factor for SDB, the prevalence of SDB is anticipated to increase, further contributing to cardiovascular disease burden. Although SDB is a treatable condition, at least 75% of severe SDB cases are undiagnosed.6,7 Even in clinical settings such as cardiology or diabetes centers, SDB is often not recognized or addressed as a therapeutic target to improve cardiovascular and metabolic risk factors. In this chapter, risk factors, pathogenesis, and associations of SDB with cardiovascular disease will be reviewed as they relate to adult patients with cardiovascular disease and cardiovascular risk reduction.


A diagnosis of SDB requires the documentation by polysomnography of an elevated number of apneas and hypopneas per hour of sleep (the apnea-hypopnea index [AHI]), with severity related to the frequency of these events and levels of associated oxyhemoglobin desaturation. In adults, an AHI of <5 is usually considered within the normal range, whereas 15 to 30 events per hour is considered to be of moderate severity and >30 events per hour is considered severe. It is important to note the limitations of this approach. For example, this categorization of disease severity does not take into account length of respiratory events, overall hypoxia burden, or level of accompanying sympathetic nervous system activation.


SDB, with its attendant sleep disruption and fragmentation, is associated with a myriad of signs and symptoms adversely affecting quality of life, including snoring, daytime somnolence, neurocognitive deficits, and irritability. In addition, recurrent upper airway collapse causes a range of physiologic stressors including repetitive intermittent hypoxia, ventilatory overshoot hyperoxia, sympathetic nervous system surges, sleep fragmentation, reduced sleep duration, alterations in intrathoracic pressure, and local airway edema and inflammation. These stressors contribute to a state of enhanced systemic inflammation, oxidative stress, metabolic dysregulation, and increased thrombosis in toto, creating the milieu for adverse cardiovascular sequelae. Substantial morbidity and economic costs are associated with untreated SDB including those related to daytime sleepiness affecting work life/productivity and often resulting in drowsy driving, as well as hypertension and cardiovascular comorbidity.




The prevalence of SDB varies considerably across the age span. There is some evidence that there is a multimodal distribution of prevalence, with one peak occurring in children ages 4 to 8 years, after which there is a declining prevalence until early adulthood, ...

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