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• W2790521281 abstract "Sleep-disordered breathing is common in the community and associated with significant cardiovascular and neurocognitive complications, particularly in vulnerable populations with coexisting morbid conditions. Newer management paradigms are being increasingly implemented to cope with high demand and limited specialist sleep services. These pathways have been primarily used in patients with high clinical risk for obstructive sleep apnoea (OSA), but also need to be extended to other clinical populations including those with co-morbidities. It is increasingly recognized that while continuous positive airway pressure (CPAP) is very effective in correcting OSA and improving sleepiness, reductions in cardiovascular complications and mortality have not been demonstrated. Poor acceptance and suboptimal use of CPAP undoubtedly contribute to this. Emerging technologies, including device connectivity and web-based applications, are allowing patients to more fully engage in their health care and could be leveraged to enhance adherence. Phenotyping patients based on the predominant pathogenic mechanism/s responsible for upper airway collapse is also providing opportunities to provide more targeted non-CPAP therapies and develop newer therapeutic strategies. This personalization of care needs to extend to those with chronic hypoventilation syndromes as well. Significant advances in interstitial lung disease have occurred over the past year and further work will be key in moving closer towards finding effective treatments. The diagnostic criteria for idiopathic pulmonary fibrosis (IPF) will require regular revision and an international consensus on diagnostic criteria for entities such as hypersensitivity pneumonitis (HP) is urgently needed. The introduction of new anti-fibrotic agents is welcomed. However, these agents only reduce disease progression with inter-individual differences in clinical response. This highlights the need to develop and implement more personalized treatment approaches for IPF. The integration of clinical and imaging characteristics with genomic/molecular data to aid in diagnosis, prognosis and treatment response classification will be key, ideally occurring in parallel with ongoing clinical and preclinical studies of novel treatments for progressive fibrotic lung diseases. Management of pulmonary arterial hypertension (PAH) has improved significantly over the past decade, resulting in increased survival and improved quality of life. Nevertheless, disability and premature mortality are still major issues. The identification of simple, non-invasive methods for the early detection and progression of disease are important for prognostication and monitoring response to therapy. Understanding the pathogenic mechanisms underpinning the vascular remodelling in PAH will advance our attempts in developing targeted therapies for this condition. The high mortality of patients with pulmonary embolism (PE) admitted to intensive care unit (ICU) and requiring mechanical ventilation is sobering, especially in light of a failure to improve outcomes over the past decade. New strategies to manage this high-risk group are needed. OSA has been generally considered a disorder of upper airway closure associated with excessive daytime sleepiness, diagnosed by polysomnogram (PSG) and treated with CPAP. A more granular view of OSA has emerged recently, recognizing the complexity of this disorder, the heterogeneity in mechanisms contributing to airway closure and variable responses to non-CPAP therapies. One of the major themes we saw in 2017 was the value of phenotyping patients particularly with respect to pathogenic mechanisms leading to OSA in order to provide more target therapy options. OSA is prevalent in the general population1 and associated with cardiovascular and neurocognitive consequences.2-4 Nevertheless, underdiagnosis remains a significant problem.5 Portable monitoring (PM) offers an opportunity to increase diagnostic capacity but needs to be accurate across a range of disease severity and clinical situations.6-9 Underestimation of disease severity can occur as analysis is based on recording period not sleep time.10 Newer approaches to monitoring such as mandibular movements (MM) may address this issue by distinguishing wake from quite sleep.11-13 Although automatic scoring of PM is currently not recommended,14, 15 improving technology and algorithms are moving us closer to this becoming possible.16, 17 While ageing is associated with increasing OSA,18 the clinical relevance of this in asymptomatic otherwise healthy elderly is not clear, and may represent physiological rather than pathological processes,19 with implications for intervention.20 Phenotyping may be based on clinical or polysomnographic features,21-24 or according to physiological factors contributing to upper airway obstruction.25, 26 In addition to anatomical traits such as craniofacial restriction and obesity, non-anatomical factors including upper airway muscle responsiveness, ventilatory control (loop gain) and respiratory arousal threshold contribute to and modify the tendency for airway closure.25-27 Notwithstanding the small but significant changes in ventilatory control stability with changes in body position, for most individuals anatomical factors are the major cause of worsening OSA when supine.28 Ethnicity may also influence phenotypic traits.29 Chinese patients with moderate-severe OSA are less likely to have a low arousal threshold compared with Caucasians,30 supporting previous work suggesting OSA severity in Chinese populations is primarily related to anatomical traits.31, 32 High loop gain is thought to be an important contributor to OSA in those with mild-moderate disease33 and plays a key role in the pathogenesis of central and complex sleep apnoea,34 including those patients with heart failure.35 A greater understanding of the various phenotypes within an individual provides an opportunity to tailor therapy and improve outcomes.36-39 Acceptance and long-term adherence to CPAP are suboptimal40 despite being highly efficacious. Various non-CPAP options are available,41-45 although the clinical responses to these are mixed and not easily predictable.46 Phenotyping an individual aids in determining whether a therapy is likely to be effective and opens the way for developing newer targeted therapies.27 This is particularly relevant for pharmacological approaches to OSA47 which, to date, have been uniformly unsuccessful.48 However, some promising results using phenotyping-based pharmacotherapy are emerging.49-51 Nonetheless, for physiological phenotyping to be clinically feasible, simple non-invasive methods are needed with validity across a range of clinical populations.47, 52, 53 Some progress has been made in this area with surrogate measures of physiological traits discernible from awake breathing measures,54 PSG data55-57 and therapeutic CPAP levels.58 Similarly, breathing regularity during CPAP acclimation is predictive of subsequent CPAP adherence.59 This phenotypic approach to OSA holds the possibility of altering our assessment and treatment paradigm27 and fits in well with the P4 approach to personalized health care (Fig. 1).47, 53, 60 Associations between OSA and cardiovascular61 and metabolic disorders62, 63 are well established. However, the biological pathways linking these are less clear.3 Systemic inflammation and endothelial dysfunction are believed to play key roles in the development of the cardiovascular complications of OSA,3, 64 but whether this is due to intermittent hypoxia, the confounding effects of obesity or other interacting factors is not clear.3 The impact of CPAP on reversing blood biomarkers or other cardiovascular risk factors such as endothelial dysfunction or carotid intima-media thickness has been variable,65-69 and often negative.68, 70 Several recent randomized trials have similarly failed to show a benefit of CPAP on cardiovascular disease or mortality.71-75 Whether this is a failure of CPAP or a failure of sufficient CPAP is not clear, although optimal adherence may be associated with better outcomes.76, 77 Mounting evidence demonstrates the complex interactions between OSA and other co-morbid conditions.2, 78, 79 These co-morbidities affect healthcare utilization80 and are associated with poorer clinical outcomes.62 The concurrence of OSA with various neurocognitive78 and mental health issues2 can worsen outcomes compared with experiencing either condition in isolation.4 Similar worsening of outcomes has been reported with the overlap of OSA and obstructive lung disease (overlap syndrome).79 Improved cognition function with CPAP has been reported, particularly in vulnerable populations,81, 82 while its use in overlap syndrome is associated with quality of life improvements,83 reduced hospitalizations84 and lower mortality.85 Self-management is one of the pillars of the P4 approach to personalized medicine,53 and newer CPAP monitoring technologies appear to be useful in promoting this.86 While wireless connectivity is making it increasingly easier for clinicians to monitor CPAP adherence and troubleshoot problems rapidly,87 it is not clear if usage or outcomes are improved over standard care alone.88, 89 In contrast, web-based technology encouraging patient engagement in care appears to be promising.90, 91 Recommendations for commencing NIV for sleep hypoventilation are based on symptoms, gas exchange and lung function parameters.92, 93 While venous bicarbonate sampling may be used to screen for sleep hypoventilation particularly for obesity hypoventilation syndrome,94, 95 raised levels may also reflect multimorbidity in this population.96 As shown by O’Donoghue et al.,97 the development of awake hypercapnia and sleepiness in patients with myotonic dystrophy is not necessarily a consequence simply of sleep-disordered breathing, raising issues of disease-specific guidelines for NIV timing, modes of ventilation98 and expected outcomes.99 Mask fitting is critical in minimizing complications and improving NIV efficacy. Real-time visual feedback during a mask fitting procedure reduced leak and improved mask seal, independent of the health professionals’ NIV experience.100 Whether this reduces complications over time is unknown.101 Nevertheless, strategies to optimize mask fitting, particularly for staff with limited skills in the area, are welcome. ILD include a varied group of conditions, with significant overlap in clinical and radiological features, but often distinct natural history and response to treatment. Following the widespread licensing of anti-fibrotic treatments for IPF, there has been a surge in clinical, translation and basic science research in the field (Table 1).118, 119 RELIEF-trial102 RCT, double-blind, placebo-controlled, phase II Oral pirfenidone (1:1 ratio) PF-ILD trial103 RCT, double-blind, placebo-controlled, phase III NCT02999178 Oral nintedanib (1:1 ratio) AmbOx trial104 RCT, controlled crossover RECITAL105 RCT, double-blind NCT02821689 Oral pirfenidone (2:1 ratio) LOTUSS trial108 Randomized, open label Diagnosis of SSc-ILD (duration < 7 years) Stable background MMF dose allowed Oral nintedanib (1:1 ratio) 250 Patients Oral pirfenidone (1:1 ratio) Oral pirfenidone (2:1 ratio) SSc Lung Study III112 RCT, double-blind, placebo-controlled, phase II Oral pirfenidone plus MMF versus placebo plus MMF (1:1 ratio) Oral pirfenidone (1:1 ratio) April Study, open-label, phase II115 EvER-ILD study, RCT, parallel group116 The diagnostic criteria for IPF have been updated recently,120 advocating an increase in the scope of a non-invasive IPF diagnosis if the computed tomography (CT) shows a ‘probable’ usual interstitial pneumonia (UIP) pattern in the correct clinical setting. The crucial role of the multidisciplinary team (MDT) meeting across a range of scenarios, including establishing a working diagnosis of IPF, and the importance of documenting diagnostic uncertainty are among the highlighted issues.121-123 Recognizing current challenges, the position statement by the Thoracic Society of Australia and New Zealand (TSANZ) in association with the Lung Foundation of Australia (LFA) on the MDT in ILD diagnosis, is timely. It provides guidelines on MDT composition, requirements and governance, so as to promote increased standardization across disparate areas with differing access to ILD expertise.124, 125 ILD remains unclassifiable in at least 10% of cases across series. Hyldgaard et al. describe the clinical characteristics of a cohort of 105 (24% of the total ILD referrals) patients with unclassifiable ILD, with intermediate survival rates between IPF and non-IPF ILD,126 in keeping with previous reports.127 Interestingly, the gender age physiology (GAP) severity score and the disease behaviour classification were both independently predictive of outcome, an observation of practical utility in this patient group, where uncertainty can paralyse management. The long-term safety of the two anti-fibrotic regimens has been evaluated in open-label extensions of placebo-controlled trials of pirfenidone and nintedanib, respectively.128-130 Among ‘real–life’ study cohorts, Galli et al. reported similar safety profiles for pirfenidone and nintedanib, despite more severe pulmonary fibrosis and more frequent co-morbidities than in the placebo-controlled clinical trials,131, 132 also reported in other real-world studies.133-135 Among issues highlighted by the TSANZ/LFA position statement on IPF treatment is the need for a holistic approach, with particular focus on co-morbidities and non-pharmacological treatments and on the challenges due to geographical differences as well as funding criteria restrictions.136 Position statements from number of countries have also been published over the last years.137-142 Although licensed anti-fibrotic agents represent a major breakthrough in IPF treatment, they do not halt/reverse the scarring process, and have limited symptomatic benefit. While clinical trials and preclinical research on novel therapeutic targets are ongoing,119 increasing attention is also focused on measuring and improving quality of life.143, 144 In a study of 516 patients from the Australian IPF Registry, dyspnoea was the strongest determinant of HRQoL.145 Interestingly, HRQoL scores correlate poorly with lung function parameters.146, 147 Furthermore, Milne et al. found that a frailty index in patients with IPF was independently linked to dyspnoea but not to lung function, also suggesting that the determinants of patients’ well-being are complex.148 Among non-pharmacological treatments, early referral to pulmonary rehabilitation is recommended,136 in view of its demonstrated effect on exercise capacity, dyspnoea and quality of life.149-151 Although ambulatory oxygen is used empirically in patients who desaturate on exertion, surprisingly little data and no guidelines exist on its use in ILD. A crossover trial comparing the efficacy of two portable oxygen concentrators with traditionally used compressed oxygen cylinders showed no significant differences in either the desaturation rate or 6-min walk test (6MWT) distance.152 The complete results of the AmbOx study, a multicentre, prospective, randomized controlled crossover trial of ambulatory oxygen in patients with ILD, are eagerly anticipated (NCT02286063).104 The difficulty in predicting disease behaviour and response to treatment across ILD entities has driven the search for improved prognostic tools. Matrix metalloproteinase 7 (MMP7) has perhaps been the most studied single serum marker in IPF.153-156 Tzouvelekis et al. confirmed a previously published threshold of 12.1 ng/mL for serum MMP7 as predictive of all-cause mortality, in an independent cohort of IPF patients.155, 157 Interestingly, in two discovery and validation prospective cohorts of treatment-naive patients with IPF, high serum MMP7 was associated with poorer survival, but was less informative than other serum markers, including surfactant protein D for diagnosis, CA19-9 for progressive disease and CA-125 for dynamic changes.153 A peripheral blood 52 gene expression signature added prognostic information to the GAP severity score in six independent IPF cohorts, although a control reference set will need to be developed before the signature can be applied to clinical practice.158, 159 Other studied biomarkers include serum receptor for advanced glycation end product (AGER) associated with worse survival in IPF,160 and, in pulmonary alveolar proteinosis, serum and bronchoalveolar lavage (BAL) levels of YKL-40 associated with disease progression.161 Automated characterization of HRCT findings across ILD represents a rapidly growing area of research. In a large group of patients with HP, computer-based quantification of CT findings was better correlated with lung function test parameters than visual CT scoring and an automated quantification of vascular volume predicted HP patients with poor outcome.162, 163 Similar superiority in automated quantification of disease extent compared with visual CT scoring was reported for IPF162 and for scleroderma-associated ILD (SSc-ILD),164 suggesting its potential as an outcome marker. Guerrero Zuniga et al. report on ultrasonic pneumography as a potential biomarker of small airway abnormalities in HP.165 Among clinical/physical prognostic markers, a fat-free mass index (FFMI) > 16 kg/m2 was predictive of a better survival in a study of 44 patients with moderate IPF,166 while short-term changes in the Medical Research Council (MRC) dyspnoea score were predictive of survival across fibrotic ILD.167 Following the recent update on acute exacerbation (AEx) of IPF,168 there have been a number of further publications on the subject.169-176 Bronchoscopy assessment of AEx in a retrospective cohort of patients with varied ILD diagnoses did not provide benefit,177, 178 with a positive yield of 13%, and a change in management in only 4 of 106 patients, while ICU transfer as a result of the procedure occurred in more than half of the patients.177 From a treatment perspective, maintenance of high prednisolone dose (≥0.6 mg/kg) after 1gr × 3 consecutive days intravenous methylprednisolone was associated with improved survival in patients with AEx of idiopathic interstitial pneumonia, but only in patients not requiring positive pressure ventilation and after adjustment for other prognostic determinants.169 Inhibition of endotoxins and/or other proinflammatory signals through polymyxin B columns in patients with AEx and a variety of ILDs was beneficial only in patients with dermatomyositis.171 In patients with drug-induced acute lung injury, BAL thrombomodulin levels were independently predictive of respiratory failure,179 while inhibition of neutrophil elastase and chemotaxis was beneficial in acute respiratory distress syndrome (ARDS) in humans and in a mouse model, respectively.180, 181 Acute lung injury following household chemical inhalation was associated with a permanent restrictive defect in half of the patients.182 Pulmonary hypertension (PH) has negative prognostic implications across ILD, although its detection is hampered by the invasive nature of right heart catheterization (RHC) on one hand, and the high degree of misclassification by echocardiography on the other hand.183 In a cohort of IPF patients, a main pulmonary artery (PA) to ascending aorta ratio > 0.9 on CT was predictive of a mean pulmonary pressure of >20 mm Hg on RHC and associated with worse prognosis.184 On follow-up, a drop in the lowest oxygen saturation during a 6MWT was predictive of worsening mean PA pressure (mPAP) on RHC in a retrospective cohort of 95 IPF patients.185 In contrast to IPF, immunosuppressive treatment stabilizes progressive ILD in the context of connective tissue disease (CTD) in most cases,186-188 with more novel approaches currently under study.105 Cough was associated with severity of both ILD and gastro-oesophageal reflux in the study by Tashkin et al. on SSc-ILD,187 and was partially improved by immunosuppressive treatment. By contrast, Cheng et al. did not observe a correlation with gastro-oesophageal reflux in SSc-ILD, suggesting the need for further studies in this area, to assess the determinants of cough and identify effective treatments.189, 190 Sarcoidosis is a multisystem disorder of unknown origin characterized by significant heterogeneity in presentation, organ involvement and disease behaviour with current treatment approaches recently reviewed.191-193 A study of 306 newly diagnosed sarcoidosis patients in Japan between 2000 and 2009, with mainly stage I and II diseases at presentation, found lower than expected resolution rates (only 29.9% at 5 years) compared with previous surveys, possibly as a result of a shift to older age of onset, itself associated with chronicity.194 Wilsher et al. describe the high frequency of skin and ocular manifestations on sarcoidosis organ involvement.195 Perret et al. offers an interesting but concerning update on the recent increase in diagnosis of coal workers’ pneumoconiosis and the suggested action in terms of monitoring and research into this highly preventable, but potentially lethal disease.196 An enlarged main PA is usually a trigger to consider the presence of PH defined as an mPAP of ≥25 mm Hg at rest. Although studies have shown a moderate correlation to invasively measured mPAP,197 there does appear to be an important prognostic component to having an enlarged PA for those patients with PAH and chronic thromboembolic PH (CTEPH).198 Furthermore, in COPD, an enlarged PA is a predictor of AEx.199 In this journal, Tonelli et al. reported CT measurements of main PA diameter in a retrospective cohort of patients with mixed aetiology of PAH.200 Not only did they confirm the relationship between baseline haemodynamics and size of PA, they were also able to demonstrate that serial enlargement of PA was associated with higher mortality. As pointed out in an accompanying editorial by MacDonald, the use of serial measurement of CT-derived PA size warrants further investigation especially in patients with chronic respiratory disease where repeated RHC is not practical.201 PE is an important cardiovascular cause of death. It is also associated with considerable morbidity such as chest pain and dyspnoea. Dyspnoea associated with PE is poorly characterized. In a prospective study of 90, non-obese patients with PE, Sanchez et al. investigated the relationship of dyspnoea to measures of vascular obstruction and non-vascular components such as age, anxiety levels and psychological trait.202 Although impact measures of dyspnoea (using the MRC scale) were related to vascular obstruction (and sequelae such as PH), the sensory component was also related to age, depression and breathing variability. In international registries, although a steady increase in incidence of PE is observed, mortality and complications such as bleeding from anticoagulation appear to be decreasing.203 Despite this, little is known about those patients with PE requiring ICU admission. Winterton et al. report the results of the Australia and New Zealand Intensive Care Society (ANZICS) Centre for Outcome and Resource Evaluation (CORE) Adult Patient Database (APD), which included over 90% of admissions to respective ICUs.204 Over a 9-year period, they found that mortality remains very high especially for mechanically ventilated patients (41%) and that this does not appear to have improved over time. As discussed in an accompanying editorial by Proud, there does not exist at present a robust method of determining which patients are at highest risk and therefore require ICU/high dependency unit admission.205 A rare, later complication of PE is CTEPH. Suda et al. investigated the prognostic role of diffusing lung capacity for carbon monoxide (DLCO) in patients with CTEPH.206 The authors found that medically treated CTEPH patients with a DLCO/alveolar volume (Va) < 80% predicted fared worse than those with normal values. Similarly, a low DLCO/Va predicted a worse outcome after pulmonary endarterectomy, likely indicating a more distal, microvascular component. PH is a recognized complication in patients with scleroderma. Due to its multisystemic nature, scleroderma can modify both pre- and post-capillary haemodynamics. Lammi et al. reported the outcomes of 59 patients recruited from the PHAROS study with post-capillary PH (a wedge pressure of >15 mm Hg), most of which had left ventricular diastolic dysfunction; 36% had combined pre-and post-capillary PH, whereas 64% had pure post-capillary PH.207 Interestingly, the survival curve between the two groups was very similar despite more patients receiving pulmonary vasodilators in the combined group. Non-invasive, early detection of right ventricular dysfunction is important for managing patients with PAH. Using MRI, Li et al. found that RV time to peak ejection rate (TPER) and TPER/time of cardiac cycle reflected early RV dysfunction in idiopathic PAH patients and therefore may be a useful technique of identifying at-risk individuals.208 Other, non-invasive tests such as cardiopulmonary exercise test (CPET) may also add value to the management of PAH patients. Morris et al. found that addition of CPET to 6MWT allowed a better correlation to disease severity than 6MWT alone. However, practical, routine use of CPET would require portable apparatus.209 Finally, endothelial cell inflammation and proliferation are important in the pathogenesis of PAH. Mumby et al. found that key enzymes integral in epigenetic regulation are dysfunctional in PAH patients.210 Furthermore, drugs targeting epigenetic pathways could inhibit inflammation and may therefore provide novel therapeutic options for this devastating condition. A.J.P. has received honoraria from ResMed and Philips for lectures and workshops. She has also been involved in a COPD clinical advisory panel for Philips. E.A.R. has received lecture fees from Boehringer Ingelheim and Roche. S.J.W. has received honoraria from Bayer Healthcare, Actelion and GlaxoSmithKline. He also reports grant support from Bayer Healthcare and Actelion. V.K. has no competing interests to declare." @default.
• W2790521281 created "2018-03-29" @default.
• W2790521281 creator A5010568573 @default.
• W2790521281 creator A5019516193 @default.
• W2790521281 creator A5021739200 @default.
• W2790521281 creator A5082411522 @default.
• W2790521281 date "2018-02-22" @default.
• W2790521281 modified "2023-09-23" @default.
• W2790521281 title "Year in review 2017: Interstitial lung disease, pulmonary vascular disease and sleep" @default.
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