Central Sleep Apnea on Commencement of Continuous Positive Airway        Pressure in Patients With a Primary Diagnosis of Obstructive Sleep        Apnea-Hypopnea

Lehman, Sanaz; Antic, Nick A.; Thompson, C; Catcheside, Peter; Mercer, Jeremy; McEvoy, R. Doug

doi:10.5664/jcsm.8424

Cited by 118 publications

(46 citation statements)

References 37 publications

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“…The BMI of our compSAS patients (27.7 ± 2.0) was much smaller than that reported from the USA or Australia, 1,3,4,9 which is usually over 30. This means that the stronger effect of craniofacial structure may have also contributed to the different prevalence of compSAS in Caucasian patients.…”

Section: Discussioncontrasting

confidence: 69%

“…CAI and AHI after CPAP in our compSAS patients (10.1 ± 2.6/h, 15.7 ± 4.0/h, respectively) are about one‐third–two‐thirds of those of previous reports 1,4 though the AHI before CPAP is comparable in both groups. This might suggest that CPAP treatment may be more effective for Japanese compSAS patients, even if the same proportion of the patients have the potential to become compSAS after using CPAP.…”

Section: Discussioncontrasting

confidence: 46%

“…However, as Lehman et al. reported that the compSAS patients had a larger AHI value on diagnostic polysomnography, 4 more of our patients would have had compSAS if other conditions were the same.…”

Section: Discussionmentioning

confidence: 54%

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Prevalence of complex sleep apnea syndrome in Japan

Ando

Ishitobi

Yagi

et al. 2008

Sleep and Biological Rhythms

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Though complex sleep apnea syndrome (compSAS) has recently been recognized as a new category of sleep apnea syndrome, its prevalence has not been determined, especially in Japan. Hence, we surveyed the prevalence of compSAS in Japan from the data of 4582 patients at eight sleep institutes who were diagnosed with obstructive SAS (apnea-hypopnea index [AHI] > 20). Using Morgenthaler's criteria we diagnosed as compSAS in 194 patients with a larger proportion of cardiac patients than in all titrated patients. Thus, the prevalence of compSAS in Japan was estimated to be 4.2%. We concluded that compSAS is an interesting condition but is not frequently found in Japan.

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Section: Discussioncontrasting

confidence: 69%

Section: Discussioncontrasting

confidence: 46%

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Prevalence of complex sleep apnea syndrome in Japan

Ando

Ishitobi

Yagi

et al. 2008

Sleep and Biological Rhythms

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“…Oral appliance therapy can also yield CSA in patients treated for OSA. [4][5][6][7] Although unproven, a likely mechanism of complex sleep apnoea involves the relief of inspiratory flow limitation. In some patients with pharyngeal compromise, increasing ventilatory drive with increasing CO 2 may not yield increased airflow due to the prevailing upper airway mechanics (i.e.…”

Section: Treatment Emergent Csa: 'Complex Sleep Apnoea'mentioning

confidence: 99%

Pathogenesis of central and complex sleep apnoea

2016

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Central sleep apnoea (CSA)—the temporary absence or diminution of ventilator effort during sleep—is seen in a variety of forms including periodic breathing in infancy and healthy adults at altitude and Cheyne-Stokes respiration in heart failure. In most circumstances, the cyclic absence of effort is paradoxically a consequence of hypersensitive ventilatory chemoreflex responses to oppose changes in airflow, i.e. elevated loop gain, leading to overshoot/undershoot ventilatory oscillations. Considerable evidence illustrates overlap between CSA and obstructive sleep apnoea (OSA), including elevated loop gain in patients with OSA and the presence of pharyngeal narrowing during central apnoeas. Indeed, treatment of OSA, whether via CPAP, tracheostomy, or oral appliances, can reveal CSA, an occurrence referred to as complex sleep apnoea. Factors influencing loop gain include increased chemosensitivity (increased controller gain), reduced damping of blood gas levels (increased plant gain) and increased lung to chemoreceptor circulatory delay. Sleep-wake transitions and pharyngeal dilator muscle responses effectively raise the controller gain and therefore also contribute to total loop gain and overall instability. In some circumstances, for example apnoea of infancy and central congenital hypoventilation syndrome, central apnoeas are the consequence of ventilatory depression and defective ventilatory responses, i.e. low loop gain. The efficacy of available treatments for CSA can be explained in terms of their effects on loop gain, e.g. CPAP improves lung volume (plant gain), stimulants reduce the alveolar-inspired PCO2 difference, supplemental oxygen lowers chemosensitivity. Understanding the magnitude of loop gain and the mechanisms contributing to instability may facilitate personalised interventions for CSA.

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“…In another retrospective study, patients with CompSA had a significantly higher likelihood of congestive heart failure and ischemic heart disease. 10 Due to financial constraints and the huge burden of potential sleep apnea patients, there has been considerable interest in developing treatment pathways that do not involve diagnostic and therapeutic sleep lab studies. 11,12 Auto CPAP in the home setting has been used to determine the pressure needed to treat sleep apnea.…”

Section: Introductionmentioning

confidence: 99%

Complex sleep apnea in patients with obstructive sleep apnea on opioids for chronic pain

Mogri

Nadler

Khan

et al. 2014

Sleep and Biological Rhythms

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Complex sleep apnea (CompSA) is defined as the development of central events during a continuous positive airway pressure (CPAP) titration in a patient with obstructive sleep apnea (OSA). We hypothesized that patients with OSA on chronic opioids would fail a CPAP titration more frequently than patients with OSA not on opioid therapy and that the increased failure rate would be due to a greater prevalence of CompSA. In a retrospective chart review, we identified 58 patients with OSA on opioids and compared them to 150 patients with OSA not on opioids. CPAP titration failure was defined as an apnea‐hypopnea index greater than 5/h at all CPAP pressures tested. CompSA was defined as the development of a central apnea index greater than 5/h during the CPAP titration study. Nineteen of the 58 patients (32.8%) with chronic opioid use and 18 of the 150 (12.0%) in the control group had CPAP titration failure (P‐value 0.001). Six of the 49 patients (12.2%) with pure OSA in the opioid group and 5 of the 146 (3.4%) with pure OSA in the control group developed CompSA (odds ratio: 3.93; 95% confidence interval: 1.14–13.52; P‐value: 0.03). Logistic regression showed that opiate use still predicted the presence of CompSA after coronary artery disease, hyperlipidemia, antidepressant usage and benzodiazepine use were accounted for. Patients on chronic opioid therapy had a higher percentage of treatment failure, and this was secondary to a higher prevalence of CompSA and persistence of central events seen on the diagnostic sleep study.

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Central Sleep Apnea on Commencement of Continuous Positive Airway Pressure in Patients With a Primary Diagnosis of Obstructive Sleep Apnea-Hypopnea

Abstract: Disclosure StatementThis is not an industry supported study. Drs. Catcheside, Mercer, McEvoy, Lehman, Antic, and Thompson have indicated no financial conflicts of interest.

Cited by 118 publications

References 37 publications

Prevalence of complex sleep apnea syndrome in Japan

Prevalence of complex sleep apnea syndrome in Japan

Pathogenesis of central and complex sleep apnoea

Complex sleep apnea in patients with obstructive sleep apnea on opioids for chronic pain

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