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EDITORIAL
Obesity, COPD, NIV and reverse epidemiology Key words: COPD, non-invasive ventilation, obesity, obstructive sleep apnoea. Abbreviations: BMI, body mass index; COPD, chronic obstructive pulmonary disease; FRC, functional residual capacity; NIV, non-invasive ventilation; OHS, obesity hypoventilation syndrome; OSA, obstructive sleep apnoea; RCT, randomized, controlled trial; T2RF, type 2 respiratory failure.
Chronic obstructive pulmonary disease (COPD) is the third most common cause of death in the USA at a cost of approximately $50 billion annually.1 The development of type 2 respiratory failure (T2RF) in COPD is associated with a poor prognosis and has led to COPD becoming the most common indication for noninvasive ventilation (NIV), in an effort to improve respiratory failure and symptoms, and reduce hospital admissions and mortality.2 Despite this, the evidence for NIV in this patient group is not strong. Chronic T2RF implies a ‘load capacity imbalance’ in the respiratory system whereby the output of the respiratory neuromuscular pump is insufficient to overcome the imposed respiratory mechanical loads and/or increased ventilatory requirements due to increased physiological deadspace or metabolic rate.3 The advent of NIV, usually utilizing bilevel positive pressure delivered mainly at night (NIV), has changed the natural history of neuromuscular and chest wall disorders causing T2RF.4 Obesity hypoventilation syndrome (OHS) is one such disorder. Obesity causes reduced lung and chest wall compliance, increased airway resistance and increased ventilatory requirements.5,6 In the face of this increased work of breathing, augmented central respiratory drive is required to maintain eucapnia. This fails in OHS with obstructive sleep apnoea (OSA), genetic predisposition and neurohormonal factors such as leptin resistance appearing to play a role.6 Severe COPD also imposes increased elastic, resistive and threshold loads7 with markedly increased ventilatory requirements.8 These increased loads are placed on muscles at a mechanical disadvantage primarily due to hyperinflation, both static and dynamic.9 Genetic factors and respiratory controller phenotype also appear to play a role in development of hypercapnia in COPD.3,9 The coexistence of OSA and COPD—termed ‘overlap syndrome’—appears to result in daytime hypercapnia at less severe levels of lung dysfunction10 presumably because the added loads imposed by the upper airway lead to hypoventilation at night, which in turn leads to daytime hypercapnia due to progressive renal bicarbonate retention.11 Treatment of overlap syndrome using either continuous positive airway pressure or bilevel NIV has been found to be effective in control© 2014 Asian Pacific Society of Respirology
ling hypercapnia and improving long-term health outcomes in uncontrolled trials.10,12,13 In contrast, while use of NIV for acute hypercapnic exacerbations of COPD improves survival and reduces length of hospital stay,14 results for long-term trials of NIV in hypercapnic COPD have been at best variable. The largest randomized, controlled trial (RCT) suggested a small increase in survival with NIV, which disappeared by 3.5 years.15 However, there has been no clear impact on hospital admissions, and quality-of-life results vary with one trial suggesting that NIV reduced quality of life.15–17 The reasons for this failure are uncertain, although it has been suggested that inadequate control of nocturnal hypoventilation may have been a factor.18,19 The coexistence of COPD and obesity results in complex changes in lung function, most notably that the two disorders have opposite effects on operational lung volume5,20 during wakefulness. To our knowledge, no study has systematically assessed physiological changes in sleep in this group. Overlap syndrome is more common as body mass index (BMI) increases,21 and BMI is independently associated with severity of sleep hypoventilation in hypercapnic COPD patients who do not have OSA.22 Obesity may also cause reductions in functional residual capacity (FRC) in sleep in COPD, whereas normally, FRC does not fall in these subjects.23–25 Nevertheless, overweight and mild-to-moderate obesity have been repeatedly found to be positive independent prognostic factors in COPD for reasons that are unexplained.26 This prognostic advantage does not appear to extend to morbid obesity.27 Despite this inconclusive literature, reflected in guideline recommendations,28,29 NIV continues to be widely used for COPD with chronic ventilatory failure in many countries.2,30 The previously mentioned trials of domiciliary NIV in hypercapnic COPD have mostly excluded those with overlap syndrome and had few obese patients with the average BMI at the upper end of the normal weight range (see table 1 in Elliott 2009).19 Observational studies that include more patients who also have obesity and/or OSA suggest that these groups may benefit more from long-term NIV.31,32 In this month’s issue of Respirology, Borel and colleagues33 report long-term data on death and hospitalization in a cohort of 213 patients commencing NIV primarily for COPD. The study suffers from the predictable issues of database data; baseline CO2 figures suggest that not all were hypercapnic, and presence or absence of OSA is characterized only by history. Obese subjects commencing NIV had a considerably better prognosis as measured by the composite Respirology (2014) 19, 777–779 doi: 10.1111/resp.12340
778 outcome of death or hospital readmission. They also had less severe lung function impairment. Nevertheless, on multivariate analysis, BMI remained a significant positive prognostic factor in a dose-dependent fashion. Surprisingly, a history of OSA was a significant negative prognostic factor. The authors also showed that in obese subjects, NIV adherence had a dose-dependent impact on survival. What lessons can we take from this study? It remains unclear why obesity is a positive prognostic factor in COPD patients, but this advantage appears to extend to those undergoing NIV, as has been previously suggested.34 The current study does not provide definitive information on whether obese COPD patients have ‘more to gain’ from NIV than their leaner counterparts because there was no control group. However, the dose-dependent effect of NIV adherence and the relatively mild lung function impairment at which NIV was considered necessary suggest that such patients respond to NIV more similarly to OHS patients than the COPD patients included in the randomized trials of NIV in COPD. It should be noted that these patients also had relatively mild levels of obesity (median (interquartile range) BMI 34.5 (32.2, 38.6) kg/m2. It follows that careful consideration should be given before excluding even mildly obese patients from NIV on the grounds that they have evidence of COPD. Future RCTs may provide more conclusive evidence of benefit in such patients. Fergal J. O’Donoghue1,2 MB, BCh, PhD and Mark E. Howard1,2 MBBS, PhD 1 Institute for Breathing and Sleep, Austin Health, Heidelberg and 2University of Melbourne, Parkville, Victoria, Australia
REFERENCES 1 Guarascio AJ, Ray SM, Finch CK, Self TH. The clinical and economic burden of chronic obstructive pulmonary disease in the USA. Clinicoecon. Outcomes Res. 2013; 5: 235–45. 2 Lloyd-Owen SJ, Donaldson GC, Ambrosino N, Escarabill J, Farre R, Fauroux B, Robert D, Schoenhofer B, Simonds AK, Wedzicha JA. Patterns of home mechanical ventilation use in Europe: results from the Eurovent survey. Eur. Respir. J. 2005; 25: 1025–31. 3 Roussos C, Koutsoukou A. Respiratory failure. Eur. Respir. J. Suppl. 2003; 47: 3s–14s. 4 Piper AJ, Sullivan CE. Effects of long-term nocturnal nasal ventilation on spontaneous breathing during sleep in neuromuscular and chest wall disorders. Eur. Respir. J. 1996; 9: 1515–22. 5 O’Donnell DE, Ciavaglia CE, Neder JA. When obesity and chronic obstructive pulmonary disease collide. Physiological and clinical consequences. Ann. Am. Thorac. Soc. 2014; 11: 635– 44. 6 Piper AJ, Grunstein RR. Big breathing: the complex interaction of obesity, hypoventilation, weight loss, and respiratory function. J. Appl. Physiol. (1985) 2010; 108: 199–205. 7 Smith TC, Marini JJ. Impact of PEEP on lung mechanics and work of breathing in severe airflow obstruction. J. Appl. Physiol. (1985) 1988; 65: 1488–99. 8 Loring SH, Garcia-Jacques M, Malhotra A. Pulmonary characteristics in COPD and mechanisms of increased work of breathing. J. Appl. Physiol. (1985) 2009; 107: 309–14. Respirology (2014) 19, 777–779
Editorial 9 McKenzie DK, Butler JE, Gandevia SC. Respiratory muscle function and activation in chronic obstructive pulmonary disease. J. Appl. Physiol. (1985) 2009; 107: 621–9. 10 McNicholas WT, Verbraecken J, Marin JM. Sleep disorders in COPD: the forgotten dimension. Eur. Respir. Rev. 2013; 22: 365–75. 11 Hukins CA, Hillman DR. Daytime predictors of sleep hypoventilation in Duchenne muscular dystrophy. Am. J. Respir. Crit. Care Med. 2000; 161: 166–70. 12 Jaoude P, Kufel T, El-Solh AA. Survival benefit of CPAP favors hypercapnic patients with the overlap syndrome. Lung 2014; 192: 251–8. 13 Marin JM, Soriano JB, Carrizo SJ, Boldova A, Celli BR. Outcomes in patients with chronic obstructive pulmonary disease and obstructive sleep apnea: the overlap syndrome. Am. J. Respir. Crit. Care Med. 2010; 182: 325–31. 14 Ram FSF, Picot J, Lightowler J, Wedzicha JA. Non-invasive positive pressure ventilation for treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst. Rev. 2004; (3): CD004104. 15 McEvoy RD, Pierce RJ, Hillman D, Esterman A, Ellis EE, Catcheside PG, O’Donoghue FJ, Barnes DJ, Grunstein RR; Australian trial of non-invasive Ventilation in Chronic Airflow Limitation (AVCAL) Study Group. Nocturnal non-invasive nasal ventilation in stable hypercapnic COPD: a randomised controlled trial. Thorax 2009; 64: 561–6. 16 Casanova C, Celli BR, Tost L, Soriano E, Abreu J, Velasco V, Santolaria F. Long-term controlled trial of nocturnal nasal positive pressure ventilation in patients with severe COPD. Chest 2000; 118: 1582–90. 17 Clini E, Sturani C, Rossi A, Viaggi S, Corrado A, Donner CF, Ambrosino N; Rehabilitation and Chronic Care Study Group, Italian Association of Hospital Pulmonologists (AIPO). The Italian multicentre study on noninvasive ventilation in chronic obstructive pulmonary disease patients. Eur. Respir. J. 2002; 20: 529–38. 18 Dreher M, Storre JH, Schmoor C, Windisch W. High-intensity versus low-intensity non-invasive ventilation in patients with stable hypercapnic COPD: a randomised crossover trial. Thorax 2010; 65: 303–8. 19 Elliott MW. Domiciliary non-invasive ventilation in stable COPD? Thorax 2009; 64: 553–6. 20 Ora J, Laveneziana P, Ofir D, Deesomchok A, Webb KA, O’Donnell DE. Combined effects of obesity and chronic obstructive pulmonary disease on dyspnea and exercise tolerance. Am. J. Respir. Crit. Care Med. 2009; 180: 964–71. 21 Sanders MH, Newman AB, Haggerty CL, Redline S, Lebowitz M, Samet J, O’Connor GT, Punjabi NM, Shahar E; Sleep Heart Health Study. Sleep and sleep-disordered breathing in adults with predominantly mild obstructive airway disease. Am. J. Respir. Crit. Care Med. 2003; 167: 7–14. 22 O’Donoghue FJ, Catcheside PG, Ellis EE, Grunstein RR, Pierce RJ, Rowland LS, Collins ER, Rochford SE, McEvoy RD; Australian trial of Noninvasive Ventilation in Chronic Airflow Limitation investigators. Sleep hypoventilation in hypercapnic chronic obstructive pulmonary disease: prevalence and associated factors. Eur. Respir. J. 2003; 21: 977–84. 23 Ballard RD, Clover CW, Suh BY. Influence of sleep on respiratory function in emphysema. Am. J. Respir. Crit. Care Med. 1995; 151: 945–51. 24 Hudgel DW, Martin RJ, Capehart M, Johnson B, Hill P. Contribution of hypoventilation to sleep oxygen desaturation in chronic obstructive pulmonary disease. J. Appl. Physiol. Respir. Environ. Exerc. Physiol. 1983; 55: 669–77. 25 O’Donoghue FJ, Catcheside PG, Eckert DJ, McEvoy RD. Changes in respiration in NREM sleep in hypercapnic chronic obstructive pulmonary disease. J. Physiol. 2004; 559(Pt 2): 663–73. 26 Cao C, Wang R, Wang J, Bunjhoo H, Xu Y, Xiong W. Body mass index and mortality in chronic obstructive pulmonary disease: a meta-analysis. PLoS ONE 2012; 7: e43892. © 2014 Asian Pacific Society of Respirology
Editorial 27 Jordan JG Jr, Mann JR. Obesity and mortality in persons with obstructive lung disease using data from the NHANES III. South. Med. J. 2010; 103: 323–30. 28 Global Initiative for Chronic Obstructive Lung Disease (GOLD). 2014. Available from URL: http://www.goldcopd.org/uploads/ users/files/GOLD_Report2014_Feb07.pdf 29 McKim DA, Road J, Avendano M, Abdool S, Cote F, Duguid N, Fraser J, Maltais F, Morrison DL, O’Connell C et al. Home mechanical ventilation: a Canadian Thoracic Society clinical practice guideline. Can. Respir. J. 2011; 18: 197–215. 30 Garner DJ, Berlowitz DJ, Douglas J, Harkness N, Howard M, McArdle N, Naughton MT, Neill A, Piper A, Yeo A et al. Home mechanical ventilation in Australia and New Zealand. Eur. Respir. J. 2013; 41: 39–45. 31 Jones SE, Packham S, Hebden M, Smith AP. Domiciliary nocturnal intermittent positive pressure ventilation in patients with
© 2014 Asian Pacific Society of Respirology
779 respiratory failure due to severe COPD: long-term follow up and effect on survival. Thorax 1998; 53: 495–8. 32 Meecham Jones DJ, Paul EA, Jones PW, Wedzicha JA. Nasal pressure support ventilation plus oxygen compared with oxygen therapy alone in hypercapnic COPD. Am. J. Respir. Crit. Care Med. 1995; 152: 538–44. 33 Borel J-C, Pepin J-L, Pison C, Vesin A, Gonzalez-Bermejo J, Court-Fortune I, Timsit J-F. Long-term adherence with noninvasive ventilation improves prognosis in obese COPD patients. Respirology 2014; 19: 857–65 34 Budweiser S, Jorres RA, Riedl T, Heinemann F, Hitzl AP, Windisch W, Pfeifer M. Predictors of survival in COPD patients with chronic hypercapnic respiratory failure receiving noninvasive home ventilation. Chest 2007; 131: 1650–8.
Respirology (2014) 19, 777–779
EDITORIAL
Obesity, COPD, NIV and reverse epidemiology Key words: COPD, non-invasive ventilation, obesity, obstructive sleep apnoea. Abbreviations: BMI, body mass index; COPD, chronic obstructive pulmonary disease; FRC, functional residual capacity; NIV, non-invasive ventilation; OHS, obesity hypoventilation syndrome; OSA, obstructive sleep apnoea; RCT, randomized, controlled trial; T2RF, type 2 respiratory failure.
Chronic obstructive pulmonary disease (COPD) is the third most common cause of death in the USA at a cost of approximately $50 billion annually.1 The development of type 2 respiratory failure (T2RF) in COPD is associated with a poor prognosis and has led to COPD becoming the most common indication for noninvasive ventilation (NIV), in an effort to improve respiratory failure and symptoms, and reduce hospital admissions and mortality.2 Despite this, the evidence for NIV in this patient group is not strong. Chronic T2RF implies a ‘load capacity imbalance’ in the respiratory system whereby the output of the respiratory neuromuscular pump is insufficient to overcome the imposed respiratory mechanical loads and/or increased ventilatory requirements due to increased physiological deadspace or metabolic rate.3 The advent of NIV, usually utilizing bilevel positive pressure delivered mainly at night (NIV), has changed the natural history of neuromuscular and chest wall disorders causing T2RF.4 Obesity hypoventilation syndrome (OHS) is one such disorder. Obesity causes reduced lung and chest wall compliance, increased airway resistance and increased ventilatory requirements.5,6 In the face of this increased work of breathing, augmented central respiratory drive is required to maintain eucapnia. This fails in OHS with obstructive sleep apnoea (OSA), genetic predisposition and neurohormonal factors such as leptin resistance appearing to play a role.6 Severe COPD also imposes increased elastic, resistive and threshold loads7 with markedly increased ventilatory requirements.8 These increased loads are placed on muscles at a mechanical disadvantage primarily due to hyperinflation, both static and dynamic.9 Genetic factors and respiratory controller phenotype also appear to play a role in development of hypercapnia in COPD.3,9 The coexistence of OSA and COPD—termed ‘overlap syndrome’—appears to result in daytime hypercapnia at less severe levels of lung dysfunction10 presumably because the added loads imposed by the upper airway lead to hypoventilation at night, which in turn leads to daytime hypercapnia due to progressive renal bicarbonate retention.11 Treatment of overlap syndrome using either continuous positive airway pressure or bilevel NIV has been found to be effective in control© 2014 Asian Pacific Society of Respirology
ling hypercapnia and improving long-term health outcomes in uncontrolled trials.10,12,13 In contrast, while use of NIV for acute hypercapnic exacerbations of COPD improves survival and reduces length of hospital stay,14 results for long-term trials of NIV in hypercapnic COPD have been at best variable. The largest randomized, controlled trial (RCT) suggested a small increase in survival with NIV, which disappeared by 3.5 years.15 However, there has been no clear impact on hospital admissions, and quality-of-life results vary with one trial suggesting that NIV reduced quality of life.15–17 The reasons for this failure are uncertain, although it has been suggested that inadequate control of nocturnal hypoventilation may have been a factor.18,19 The coexistence of COPD and obesity results in complex changes in lung function, most notably that the two disorders have opposite effects on operational lung volume5,20 during wakefulness. To our knowledge, no study has systematically assessed physiological changes in sleep in this group. Overlap syndrome is more common as body mass index (BMI) increases,21 and BMI is independently associated with severity of sleep hypoventilation in hypercapnic COPD patients who do not have OSA.22 Obesity may also cause reductions in functional residual capacity (FRC) in sleep in COPD, whereas normally, FRC does not fall in these subjects.23–25 Nevertheless, overweight and mild-to-moderate obesity have been repeatedly found to be positive independent prognostic factors in COPD for reasons that are unexplained.26 This prognostic advantage does not appear to extend to morbid obesity.27 Despite this inconclusive literature, reflected in guideline recommendations,28,29 NIV continues to be widely used for COPD with chronic ventilatory failure in many countries.2,30 The previously mentioned trials of domiciliary NIV in hypercapnic COPD have mostly excluded those with overlap syndrome and had few obese patients with the average BMI at the upper end of the normal weight range (see table 1 in Elliott 2009).19 Observational studies that include more patients who also have obesity and/or OSA suggest that these groups may benefit more from long-term NIV.31,32 In this month’s issue of Respirology, Borel and colleagues33 report long-term data on death and hospitalization in a cohort of 213 patients commencing NIV primarily for COPD. The study suffers from the predictable issues of database data; baseline CO2 figures suggest that not all were hypercapnic, and presence or absence of OSA is characterized only by history. Obese subjects commencing NIV had a considerably better prognosis as measured by the composite Respirology (2014) 19, 777–779 doi: 10.1111/resp.12340
778 outcome of death or hospital readmission. They also had less severe lung function impairment. Nevertheless, on multivariate analysis, BMI remained a significant positive prognostic factor in a dose-dependent fashion. Surprisingly, a history of OSA was a significant negative prognostic factor. The authors also showed that in obese subjects, NIV adherence had a dose-dependent impact on survival. What lessons can we take from this study? It remains unclear why obesity is a positive prognostic factor in COPD patients, but this advantage appears to extend to those undergoing NIV, as has been previously suggested.34 The current study does not provide definitive information on whether obese COPD patients have ‘more to gain’ from NIV than their leaner counterparts because there was no control group. However, the dose-dependent effect of NIV adherence and the relatively mild lung function impairment at which NIV was considered necessary suggest that such patients respond to NIV more similarly to OHS patients than the COPD patients included in the randomized trials of NIV in COPD. It should be noted that these patients also had relatively mild levels of obesity (median (interquartile range) BMI 34.5 (32.2, 38.6) kg/m2. It follows that careful consideration should be given before excluding even mildly obese patients from NIV on the grounds that they have evidence of COPD. Future RCTs may provide more conclusive evidence of benefit in such patients. Fergal J. O’Donoghue1,2 MB, BCh, PhD and Mark E. Howard1,2 MBBS, PhD 1 Institute for Breathing and Sleep, Austin Health, Heidelberg and 2University of Melbourne, Parkville, Victoria, Australia
REFERENCES 1 Guarascio AJ, Ray SM, Finch CK, Self TH. The clinical and economic burden of chronic obstructive pulmonary disease in the USA. Clinicoecon. Outcomes Res. 2013; 5: 235–45. 2 Lloyd-Owen SJ, Donaldson GC, Ambrosino N, Escarabill J, Farre R, Fauroux B, Robert D, Schoenhofer B, Simonds AK, Wedzicha JA. Patterns of home mechanical ventilation use in Europe: results from the Eurovent survey. Eur. Respir. J. 2005; 25: 1025–31. 3 Roussos C, Koutsoukou A. Respiratory failure. Eur. Respir. J. Suppl. 2003; 47: 3s–14s. 4 Piper AJ, Sullivan CE. Effects of long-term nocturnal nasal ventilation on spontaneous breathing during sleep in neuromuscular and chest wall disorders. Eur. Respir. J. 1996; 9: 1515–22. 5 O’Donnell DE, Ciavaglia CE, Neder JA. When obesity and chronic obstructive pulmonary disease collide. Physiological and clinical consequences. Ann. Am. Thorac. Soc. 2014; 11: 635– 44. 6 Piper AJ, Grunstein RR. Big breathing: the complex interaction of obesity, hypoventilation, weight loss, and respiratory function. J. Appl. Physiol. (1985) 2010; 108: 199–205. 7 Smith TC, Marini JJ. Impact of PEEP on lung mechanics and work of breathing in severe airflow obstruction. J. Appl. Physiol. (1985) 1988; 65: 1488–99. 8 Loring SH, Garcia-Jacques M, Malhotra A. Pulmonary characteristics in COPD and mechanisms of increased work of breathing. J. Appl. Physiol. (1985) 2009; 107: 309–14. Respirology (2014) 19, 777–779
Editorial 9 McKenzie DK, Butler JE, Gandevia SC. Respiratory muscle function and activation in chronic obstructive pulmonary disease. J. Appl. Physiol. (1985) 2009; 107: 621–9. 10 McNicholas WT, Verbraecken J, Marin JM. Sleep disorders in COPD: the forgotten dimension. Eur. Respir. Rev. 2013; 22: 365–75. 11 Hukins CA, Hillman DR. Daytime predictors of sleep hypoventilation in Duchenne muscular dystrophy. Am. J. Respir. Crit. Care Med. 2000; 161: 166–70. 12 Jaoude P, Kufel T, El-Solh AA. Survival benefit of CPAP favors hypercapnic patients with the overlap syndrome. Lung 2014; 192: 251–8. 13 Marin JM, Soriano JB, Carrizo SJ, Boldova A, Celli BR. Outcomes in patients with chronic obstructive pulmonary disease and obstructive sleep apnea: the overlap syndrome. Am. J. Respir. Crit. Care Med. 2010; 182: 325–31. 14 Ram FSF, Picot J, Lightowler J, Wedzicha JA. Non-invasive positive pressure ventilation for treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst. Rev. 2004; (3): CD004104. 15 McEvoy RD, Pierce RJ, Hillman D, Esterman A, Ellis EE, Catcheside PG, O’Donoghue FJ, Barnes DJ, Grunstein RR; Australian trial of non-invasive Ventilation in Chronic Airflow Limitation (AVCAL) Study Group. Nocturnal non-invasive nasal ventilation in stable hypercapnic COPD: a randomised controlled trial. Thorax 2009; 64: 561–6. 16 Casanova C, Celli BR, Tost L, Soriano E, Abreu J, Velasco V, Santolaria F. Long-term controlled trial of nocturnal nasal positive pressure ventilation in patients with severe COPD. Chest 2000; 118: 1582–90. 17 Clini E, Sturani C, Rossi A, Viaggi S, Corrado A, Donner CF, Ambrosino N; Rehabilitation and Chronic Care Study Group, Italian Association of Hospital Pulmonologists (AIPO). The Italian multicentre study on noninvasive ventilation in chronic obstructive pulmonary disease patients. Eur. Respir. J. 2002; 20: 529–38. 18 Dreher M, Storre JH, Schmoor C, Windisch W. High-intensity versus low-intensity non-invasive ventilation in patients with stable hypercapnic COPD: a randomised crossover trial. Thorax 2010; 65: 303–8. 19 Elliott MW. Domiciliary non-invasive ventilation in stable COPD? Thorax 2009; 64: 553–6. 20 Ora J, Laveneziana P, Ofir D, Deesomchok A, Webb KA, O’Donnell DE. Combined effects of obesity and chronic obstructive pulmonary disease on dyspnea and exercise tolerance. Am. J. Respir. Crit. Care Med. 2009; 180: 964–71. 21 Sanders MH, Newman AB, Haggerty CL, Redline S, Lebowitz M, Samet J, O’Connor GT, Punjabi NM, Shahar E; Sleep Heart Health Study. Sleep and sleep-disordered breathing in adults with predominantly mild obstructive airway disease. Am. J. Respir. Crit. Care Med. 2003; 167: 7–14. 22 O’Donoghue FJ, Catcheside PG, Ellis EE, Grunstein RR, Pierce RJ, Rowland LS, Collins ER, Rochford SE, McEvoy RD; Australian trial of Noninvasive Ventilation in Chronic Airflow Limitation investigators. Sleep hypoventilation in hypercapnic chronic obstructive pulmonary disease: prevalence and associated factors. Eur. Respir. J. 2003; 21: 977–84. 23 Ballard RD, Clover CW, Suh BY. Influence of sleep on respiratory function in emphysema. Am. J. Respir. Crit. Care Med. 1995; 151: 945–51. 24 Hudgel DW, Martin RJ, Capehart M, Johnson B, Hill P. Contribution of hypoventilation to sleep oxygen desaturation in chronic obstructive pulmonary disease. J. Appl. Physiol. Respir. Environ. Exerc. Physiol. 1983; 55: 669–77. 25 O’Donoghue FJ, Catcheside PG, Eckert DJ, McEvoy RD. Changes in respiration in NREM sleep in hypercapnic chronic obstructive pulmonary disease. J. Physiol. 2004; 559(Pt 2): 663–73. 26 Cao C, Wang R, Wang J, Bunjhoo H, Xu Y, Xiong W. Body mass index and mortality in chronic obstructive pulmonary disease: a meta-analysis. PLoS ONE 2012; 7: e43892. © 2014 Asian Pacific Society of Respirology
Editorial 27 Jordan JG Jr, Mann JR. Obesity and mortality in persons with obstructive lung disease using data from the NHANES III. South. Med. J. 2010; 103: 323–30. 28 Global Initiative for Chronic Obstructive Lung Disease (GOLD). 2014. Available from URL: http://www.goldcopd.org/uploads/ users/files/GOLD_Report2014_Feb07.pdf 29 McKim DA, Road J, Avendano M, Abdool S, Cote F, Duguid N, Fraser J, Maltais F, Morrison DL, O’Connell C et al. Home mechanical ventilation: a Canadian Thoracic Society clinical practice guideline. Can. Respir. J. 2011; 18: 197–215. 30 Garner DJ, Berlowitz DJ, Douglas J, Harkness N, Howard M, McArdle N, Naughton MT, Neill A, Piper A, Yeo A et al. Home mechanical ventilation in Australia and New Zealand. Eur. Respir. J. 2013; 41: 39–45. 31 Jones SE, Packham S, Hebden M, Smith AP. Domiciliary nocturnal intermittent positive pressure ventilation in patients with
© 2014 Asian Pacific Society of Respirology
779 respiratory failure due to severe COPD: long-term follow up and effect on survival. Thorax 1998; 53: 495–8. 32 Meecham Jones DJ, Paul EA, Jones PW, Wedzicha JA. Nasal pressure support ventilation plus oxygen compared with oxygen therapy alone in hypercapnic COPD. Am. J. Respir. Crit. Care Med. 1995; 152: 538–44. 33 Borel J-C, Pepin J-L, Pison C, Vesin A, Gonzalez-Bermejo J, Court-Fortune I, Timsit J-F. Long-term adherence with noninvasive ventilation improves prognosis in obese COPD patients. Respirology 2014; 19: 857–65 34 Budweiser S, Jorres RA, Riedl T, Heinemann F, Hitzl AP, Windisch W, Pfeifer M. Predictors of survival in COPD patients with chronic hypercapnic respiratory failure receiving noninvasive home ventilation. Chest 2007; 131: 1650–8.
Respirology (2014) 19, 777–779
