Compliance with nasal CPAP therapy for obstructive sleep apnoea: how much is enough?

McNicholas, WT

doi:10.1183/09031936.97.10050969

Cited by 48 publications

(16 citation statements)

References 25 publications

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“…day -1 ) to define compliance, previous studies found it to range 50±90% [2,15,16]. However, there is no general consensus on the cut-off point for acceptable compliance [17]. In a recent French study [12] following-up 3,225 patients, mean hours of CPAP use was approximately 6.5 h in patients accepting treatment.…”

Section: Discussionmentioning

confidence: 99%

Therapy with nCPAP: incomplete elimination of Sleep Related Breathing Disorder

Grote¹,

Hedner²,

Grunstein³

et al. 2000

Eur Respir J

141

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Correct assessment of the overall treatment effectiveness requires knowledge about therapy compliance and efficacy. This study aimed to determine overall long-term apnoea alleviation after continuous positive airway pressure (CPAP) in a complete sleep laboratory cohort.Out of 209 consecutive CPAP candidates (mean age 5712 yrs, body mass index (BMI) 30.05.1 kg . m 2 , respiratory disturbance index (RDI) 32.929 h), follow-up treatment was performed in 149 of them at 9, 18 and 30 months after CPAP prescription. Compliance with CPAP (machine run time/days CPAP available) was adjusted for the individual subjective sleep-time. Apnoea alleviation was defined as adjusted compliance multiplied by the CPAP effect (RDI with CPAP applied), remaining RDI was calculated.The baseline RDI, age or BMI in 75 patients, who did not tolerate nasal continuous positive airway pressure (nCPAP), did not differ from those accepting CPAP (acceptors, n=74). In acceptors at 9 months follow-up RDI with CPAP applied was 1.42.6 (CPAP effect, n=66), mean CPAP use was 3.62.5 . 24 h -1 (n=68), mean apnoea alleviation was 52.432.0% (range 1±100%, n=47), the average remaining wholenight RDI was 17.826. At 9, 18 and 30 months (n=47), the mean daily CPAP use increased from 3.62.5 h to 4.12.5 h and 4.42.4 h (p<0.01).Effectiveness of continuous positive airway pressure is potentially high but acceptance was low. When accounting for sleep-time, its actual effect and use, only 50% adjusted continuous positive airway pressure effectiveness was observed. Eur Respir J 2000; 16: 921±927.

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Section: Discussionmentioning

confidence: 99%

Therapy with nCPAP: incomplete elimination of Sleep Related Breathing Disorder

Grote¹,

Hedner²,

Grunstein³

et al. 2000

Eur Respir J

141

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“…It effectively ameliorates the symptoms of the disease and reduces the associated long-term cardiovascular morbidity and mortality [10]. However, many patients stop using it because of discomfort and compliance rates vary [122,123]. Current therapeutic alternatives to CPAP therapy are often suboptimal, particularly for patients with severe disease.…”

Section: Therapeutic Potentialmentioning

confidence: 99%

Cardiovascular disease in obstructive sleep apnoea syndrome: the role of intermittent hypoxia and inflammation

Taylor²,

2009

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There is increasing evidence that intermittent hypoxia plays a role in the development of cardiovascular risk in obstructive sleep apnoea syndrome (OSAS) through the activation of inflammatory pathways. The development of translational models of intermittent hypoxia has allowed investigation of its role in the activation of inflammatory mechanisms and promotion of cardiovascular disease in OSAS. There are noticeable differences in the response to intermittent hypoxia between body tissues but the hypoxia-sensitive transcription factors hypoxia-inducible factor-1 and nuclear factor-kB appear to play a key role in mediating the inflammatory and cardiovascular consequences of OSAS. Expanding our understanding of these pathways, the cross-talk between them and the activation of inflammatory mechanisms by intermittent hypoxia in OSAS will provide new avenues of therapeutic opportunity for the disease.

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“…Previous reports that have evaluated compliance with CPAP in OSAS have found average nightly compliance to range from 4 to 6 hours per night. [32][33][34] Another HIF-1-dependent gene, VEGF, has been reported to be increased in serum 35,36 and plasma 37 of OSAS patients. We chose not to measure VEGF in the present study as a marker of HIF-1 activation because VEGF activation is complex and can be regulated by a wide range of transcription factors other than HIF-1, including Sp1, Sp3, or activating protein 2.…”

Section: Baseline Characteristics In Osas Patients and Control Subjectsmentioning

confidence: 99%

Selective Activation of Inflammatory Pathways by Intermittent Hypoxia in Obstructive Sleep Apnea Syndrome

2005

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Background-Obstructive sleep apnea syndrome (OSAS), characterized by intermittent hypoxia/reoxygenation (IHR), is an independent risk factor for cardiovascular disease. We investigated the underlying molecular mechanisms of this association in a translational study. Methods and Results-In a novel in vitro model of IHR, we used HeLa cells transfected with reporter constructs and DNA binding assays for the master transcriptional regulators of the inflammatory and adaptive pathways (NFB and HIF-1, respectively) to investigate underlying transcriptional events initiated by repeated cell exposure to IHR. Furthermore, we prospectively studied 19 male OSAS patients (median apnea-hypopnea frequency, 48.5 episodes per hour; interquartile range [IQR], 28.5 to 72.9) and 17 matched normal control subjects. Circulating levels of the proinflammatory cytokine tumor necrosis factor-␣ and the adaptive factor erythropoietin were assayed in all subjects at baseline and again after 6 weeks of continuous positive airway pressure therapy in patients. Full blood count was measured as part of a detailed baseline evaluation. HeLa cells exposed to IHR demonstrated selective activation of the proinflammatory transcription factor NFB (PϽ0.001 by ANOVA), whereas the adaptive regulator HIF-1 was not activated, as demonstrated by luciferase reporter assays and DNA binding studies. Circulating tumor necrosis factor-␣ levels were higher in OSAS patients (2.56 pg/mL; IQR, 2.01 to 3.42 pg/mL) than in control subjects (1.25 pg/mL; IQR, 0.94 to 1.87; PϽ0.001) but normalized with continuous positive airway pressure therapy (1.24 pg/mL; IQR, 0.78 to 2.35 pg/mL; Pϭ0.002). In contrast, erythropoietin levels were similar throughout. Furthermore, circulating neutrophil levels were higher in OSAS patients than in control subjects, whereas the hematocrit was unaltered. Conclusions-These data demonstrate selective activation of inflammatory over adaptive pathways in IHR and OSAS, which may be an important molecular mechanism of cardiovascular disease.

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Compliance with nasal CPAP therapy for obstructive sleep apnoea: how much is enough?

Cited by 48 publications

References 25 publications

Therapy with nCPAP: incomplete elimination of Sleep Related Breathing Disorder

Therapy with nCPAP: incomplete elimination of Sleep Related Breathing Disorder

Cardiovascular disease in obstructive sleep apnoea syndrome: the role of intermittent hypoxia and inflammation

Selective Activation of Inflammatory Pathways by Intermittent Hypoxia in Obstructive Sleep Apnea Syndrome

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