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The existing coverage criteria for home noninvasive ventilation (NIV) do not recognize the diversity of hypoventilation syndromes and advances in technologies. This document summarizes the work of the hypoventilation syndromes Technical Expert Panel working group. The most pressing current coverage barriers identified were: (1) overreliance on arterial blood gases (particularly during sleep); (2) need to perform testing on prescribed oxygen; (3) requiring a sleep study to rule out OSA as the cause of sustained hypoxemia; (4) need for spirometry; (5) need to show bilevel positive airway pressure (BPAP) without a backup rate failure to qualify for BPAP spontaneous/timed; and (6) qualifying hospitalized patients for home NIV therapy at the time of discharge. Critical evidence support for changes to current policies includes randomized controlled trial evidence and clinical practice guidelines. To decrease morbidity and mortality by achieving timely access to NIV for patients with hypoventilation, particularly those with obesity hypoventilation syndrome, we make the following key suggestions: (1) given the significant technological advances, we advise acceptance of surrogate noninvasive end-tidal and transcutaneous Pco2 and venous blood gases in lieu of arterial blood gases; (2) not requiring Pco2 measures while on prescribed oxygen; (3) not requiring a sleep study to avoid delays in care in patients being discharged from the hospital; (4) remove spirometry as a requirement; and (5) not requiring BPAP without a backup rate failure to approve BPAP spontaneous/timed. The overarching goal of the Technical Expert Panel is to establish pathways that improve clinicians' management capability to provide Medicare beneficiaries access to appropriate home NIV therapy. Adoption of these proposed suggestions would result in the right device, for the right type of patient with hypoventilation syndromes, at the right time.

This document summarizes suggestions of the central sleep apnea (CSA) Technical Expert Panel working group. This paper shares our vision for bringing the right device to the right patient at the right time. For patients with CSA, current coverage criteria do not align with guideline treatment recommendations. For example, CPAP and oxygen therapy are recommended but not covered for CSA. On the other hand, bilevel positive airway pressure (BPAP) without a backup rate may be a covered therapy for OSA, but it may worsen CSA. Narrow coverage criteria that require near elimination of obstructive breathing events on CPAP or BPAP in the spontaneous mode, even if at poorly tolerated pressure levels, may preclude therapy with BPAP with backup rate or adaptive servoventilation, even when those devices provide demonstrably better therapy. CSA is a dynamic disorder that may require different treatments over time, sometimes switching from one device to another; an example is switching from BPAP with backup rate to an adaptive servoventilation with automatic end-expiratory pressure adjustments, which may not be covered. To address these challenges, we suggest several changes to the coverage determinations, including: (1) a single simplified initial and continuing coverage definition of CSA that aligns with OSA; (2) removal of hypoventilation terminology from coverage criteria for CSA; (3) all effective therapies for CSA should be covered, including oxygen and all PAP devices with or without backup rates or servo-mechanisms; and (4) patients shown to have a suboptimal response to one PAP device should be allowed to add oxygen or change to another PAP device with different capabilities if shown to be effective with testing.

The current national coverage determinations (NCDs) for noninvasive ventilation for patients with thoracic restrictive disorders, COPD, and hypoventilation syndromes were formulated in 1998. New original research, updated formal practice guidelines, and current consensus expert opinion have accrued that are in conflict with the existing NCDs. Some inconsistencies in the NCDs have been noted, and the diagnostic and therapeutic technology has also advanced in the last quarter century. Thus, these and related NCDs relevant to bilevel positive airway pressure for the treatment of OSA and central sleep apnea need to be updated to ensure the optimal health of patients with these disorders. To that end, the American College of Chest Physicians organized a multisociety (American Thoracic Society, American Academy of Sleep Medicine, and American Association for Respiratory Care) effort to engage experts in the field to: (1) identify current barriers to optimal care; (2) highlight compelling scientific evidence that would justify changes from current policies incorporating best evidence and practice; and (3) propose suggestions that would form the basis for a revised NCD in each of these 5 areas (thoracic restrictive disorders, COPD, hypoventilation syndromes, OSA, and central sleep apnea). The expert panel met during a 2-day virtual summit in October 2020 and subsequently crafted written documents designed to achieve provision of "the right device to the right patient at the right time." These documents have been endorsed by the participating societies following peer review and publication in CHEST and will be used to inform efforts to revise the current NCDs.

This document summarizes the work of the CPAP and bilevel PAP therapy for OSA Technical Expert Panel working group. For positive airway pressure (PAP) therapy, the most pressing current coverage barriers identified were: an insufficient symptom list describing all potential symptoms in patients with mild OSA; the 4 h per night of PAP usage requirement to keep the device; the additional sleep studies requirement to re-qualify for PAP or supplemental oxygen; and the inability to use telehealth visits for follow-up visits. Critical evidence supports changes to current policies and includes: symptom list inadequate to cover all scenarios based on updated clinical practice guidelines; published evidence that 2 h per night of PAP use can result in benefit to quality of life and other metrics; the costs of another sleep study not justified for all nonadherent patients or for supplemental oxygen due to other types of assessment currently available; and the remarkable success and acceptance of telehealth visits. To achieve optimal access for patients on PAP therapy, we make the following key suggestions: removing symptom criteria for mild OSA; reduce continued coverage criteria to > 2 h per night; eliminate the need for a sleep study to re-qualify if nonadherent or for new Centers for Medicare & Medicaid Services beneficiaries already on and adherent to PAP therapy; allow telehealth visits for documenting benefit and adherence; and allow PAP reports and domiciliary oximetry to qualify for supplemental oxygen with PAP if needed. This paper shares our best vision for bringing the right device to the right patient at the right time.

This document summarizes the work of the COPD Technical Expert Panel working group. For patients with COPD, the most pressing current coverage barriers identified were onerous diagnostic requirements focused on oxygenation (rather than ventilation) and difficulty obtaining bilevel devices with backup rate capabilities. Because of these difficulties, many patients with COPD were instead sometimes prescribed home mechanical ventilators. Critical evidence supports changes to current policies, including randomized controlled trial evidence suggesting a mortality benefit from bilevel positive airway pressure with backup rate and updated clinical practice guidelines from the American Thoracic Society as well as the European Respiratory Society. To achieve optimal access to noninvasive ventilation for patients with COPD, we make the following key recommendations: (1) removal of the need for overnight oximetry testing; (2) the ability to initiate therapy using bilevel devices with backup rate capability; and (3) increased duration of time to meet adherence criteria (ie, a second 90-day trial period) in those patients actively engaged in their care. Clear guidelines based on medical necessity are also included for patients who require initiation of or switch to a home mechanical ventilator. Adoption of these proposed recommendations would result in the right device, for the right type of patient with COPD, at the right time. Finally, we emphasize the need for adequate clinical support during initiation and maintenance of home noninvasive ventilation in such patients.

The existing coverage criteria for noninvasive ventilation (NIV) do not recognize the benefits of early initiation of NIV for those with thoracic restrictive disorders and do not address the unique needs for daytime support as the patients progress to ventilator dependence. This document summarizes the work of the thoracic restrictive disorder Technical Expert Panel working group. The most pressing current coverage barriers identified were: (1) delays in implementing NIV treatment; (2) lack of coverage for many nonprogressive neuromuscular diseases; and (3) lack of clear policy indications for home mechanical ventilation (HMV) support in thoracic restrictive disorders. To best address these issues, we make the following key recommendations: (1) given the need to encourage early initiation of NIV with bilevel positive airway pressure devices, we recommend that symptoms be considered as a reason to initiate therapy even at mildly reduced FVCs; (2) broaden CO2 measurements to include surrogates such as transcutaneous, end-tidal, or venous blood gas; (3) expand the diagnostic category to include phrenic nerve injuries and disorders of central drive; (4) allow a bilevel positive airway pressure device to be advanced to an HMV when the vital capacity is < 30% or to address severe daytime respiratory symptoms; and (5) provide additional HMV when the patient is ventilator dependent with use > 18 h per day. Adoption of these proposed recommendations would result in the right device, at the right time, for the right type of patients with thoracic restrictive disorders.

Rationale: Body mass index (BMI) is associated with chronic obstructive pulmonary disease (COPD) mortality, but the underlying mechanisms are unclear. The effect of genetic variants aggregated into a polygenic score may elucidate the causal mechanisms and predict risk. Objectives: To examine the associations of genetically predicted BMI with all-cause and cause-specific mortality in COPD. Methods: We developed a polygenic score (PGS) for BMI (PGSBMI) and tested for associations of the PGSBMI with all-cause, respiratory, and cardiovascular mortality in participants with COPD from the COPDGene (Genetic Epidemiology of COPD), ECLIPSE (Evaluation of COPD Longitudinally to Identify Predictive Surrogate End-points), and Framingham Heart studies. We calculated the difference between measured BMI and PGS-predicted BMI (BMIdiff) and categorized participants into groups of discordantly low (BMIdiff <20th percentile), concordant (BMIdiff between the 20th and 80th percentiles), and discordantly high (BMIdiff >80th percentile) BMI. We applied Cox models, examined potential nonlinear associations of the PGSBMI and BMIdiff with mortality, and summarized results with meta-analysis. Measurements and Main Results: We observed significant nonlinear associations of measured BMI and BMIdiff, but not PGSBMI, with all-cause mortality. In meta-analyses, a one–standard deviation increase in the PGSBMI was associated with an increased hazard for cardiovascular mortality (hazard ratio [HR], 1.29; 95% confidence interval [CI], 1.12–1.49), but not for respiratory or all-cause mortality. Compared with participants with concordant measured and genetically predicted BMI, those with discordantly low BMI had higher risks for all-cause mortality (HR, 1.57; 95% CI, 1.41–1.74) and respiratory death (HR, 2.01; 95% CI, 1.61–2.51). Conclusions: In people with COPD, a higher genetically predicted BMI is associated with higher cardiovascular mortality but not respiratory mortality. Individuals with a discordantly low BMI have higher all-cause and respiratory mortality rates than those with a concordant BMI. [ABSTRACT FROM AUTHOR]

ImportanceInterstitial lung abnormalities have been associated with lower 6-minute walk distance, diffusion capacity for carbon monoxide, and total lung capacity. However, to our knowledge, an association with mortality has not been previously investigated.ObjectiveTo investigate whether interstitial lung abnormalities are associated with increased mortality.Design, setting, and populationProspective cohort studies of 2633 participants from the FHS (Framingham Heart Study; computed tomographic [CT] scans obtained September 2008-March 2011), 5320 from the AGES-Reykjavik Study (Age Gene/Environment Susceptibility; recruited January 2002-February 2006), 2068 from the COPDGene Study (Chronic Obstructive Pulmonary Disease; recruited November 2007-April 2010), and 1670 from ECLIPSE (Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints; between December 2005-December 2006).ExposuresInterstitial lung abnormality status as determined by chest CT evaluation.Main outcomes and measuresAll-cause mortality over an approximate 3- to 9-year median follow-up time. Cause-of-death information was also examined in the AGES-Reykjavik cohort.ResultsInterstitial lung abnormalities were present in 177 (7%) of the 2633 participants from FHS, 378 (7%) of 5320 from AGES-Reykjavik, 156 (8%) of 2068 from COPDGene, and in 157 (9%) of 1670 from ECLIPSE. Over median follow-up times of approximately 3 to 9 years, there were more deaths (and a greater absolute rate of mortality) among participants with interstitial lung abnormalities when compared with those who did not have interstitial lung abnormalities in the following cohorts: 7% vs 1% in FHS (6% difference [95% CI, 2% to 10%]), 56% vs 33% in AGES-Reykjavik (23% difference [95% CI, 18% to 28%]), and 11% vs 5% in ECLIPSE (6% difference [95% CI, 1% to 11%]). After adjustment for covariates, interstitial lung abnormalities were associated with a higher risk of death in the FHS (hazard ratio [HR], 2.7 [95% CI, 1.1 to 6.5]; P = .03), AGES-Reykjavik (HR, 1.3 [95% CI, 1.2 to 1.4]; P

RationaleMuscle wasting in chronic obstructive pulmonary disease (COPD) is associated with a poor prognosis and is not readily assessed by measures of body mass index (BMI). BMI does not discriminate between relative proportions of adipose tissue and lean muscle and may be insensitive to early pathologic changes in body composition. Computed tomography (CT)-based assessments of the pectoralis muscles may provide insight into the clinical significance of skeletal muscles in smokers.ObjectivesWe hypothesized that objective assessment of the pectoralis muscle area on chest CT scans provides information that is clinically relevant and independent of BMI.MethodsData from the ECLIPSE (Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints) Study (n = 73) were used to assess the relationship between pectoralis muscle area and fat-free mass. We then used data in a subset (n = 966) of a larger cohort, the COPDGene (COPD Genetic Epidemiology) Study, to explore the relationship between pectoralis muscle area and COPD-related traits.Measurements and main resultsWe first investigated the correlation between pectoralis muscle area and fat-free mass, using data from a subset of participants in the ECLIPSE Study. We then further investigated pectoralis muscle area in COPDGene Study participants and found that higher pectoralis muscle area values were associated with greater height, male sex, and younger age. On subsequent clinical correlation, compared with BMI, pectoralis muscle area was more significantly associated with COPD-related traits, including spirometric measures, dyspnea, and 6-minute-walk distance (6MWD). For example, on average, each 10-cm(2) increase in pectoralis muscle area was associated with a 0.8-unit decrease in the BODE (Body mass index, Obstruction, Dyspnea, Exercise) index (95% confidence interval, -1.0 to -0.6; P < 0.001). Furthermore, statistically significant associations between pectoralis muscle area and COPD-related traits remained even after adjustment for BMI.ConclusionsCT-derived pectoralis muscle area provides relevant indices of COPD morbidity that may be more predictive of important COPD-related traits than BMI. However, the relationship with clinically relevant outcomes such as hospitalization and death requires additional investigation. Pectoralis muscle area is a convenient measure that can be collected in the clinical setting in addition to BMI.

AbstractBackgroundThe changes in inspiratory capacity (IC) over time in chronic obstructive pulmonary disease (COPD) patients are unknown. The Understanding Potential Long-term Impacts on Function with Tiotropium (UPLIFT®) trial included IC measurements.MethodsIC analysis from UPLIFT® (N = 5992) was performed at 1 and 6 months, and every 6 months through 4 years. Annualized rate of decline in pre- and post-bronchodilator IC and mean differences at each time point were analyzed by mixed-effects models. The relationships between baseline IC and exacerbation rate and mortality were explored using Cox regression analysis.ResultsBaseline characteristics: age, 65 years; 75% men; post-bronchodilator forced expiratory volume in 1 second, 1.32 L (48% predicted); pre- and post-bronchodilator IC, 2.03 and 2.33 L. Mean IC rate of decline (mL/year) was 34 ± 2 (1.7% of baseline) and 50 ± 3 (2.1% of baseline) pre- and post-bronchodilator, respectively, without significant between-group differences. Morning pre-bronchodilator (trough) IC improved with tiotropium versus placebo: 124 mL (1 month), 103 mL (1 year), 107 mL (2 years), 98 mL (3 years), and 97 mL (4 years) (all p

The letter to the editor responds to an article titled "Can We Use Lung Function Thresholds and Respiratory Symptoms to Identify Pre-Chronic Obstructive Pulmonary Disease? A Prospective, Population-based Cohort Study." The authors of the letter provide constructive feedback on certain points in the study. They suggest that previous studies have already explored and demonstrated similar findings, making the claim of being the first inaccurate. They also mention their own research on the sensitivity and specificity of applying clinical, physiological, and radiological abnormalities to define pre-COPD. Additionally, they express reservations about the optimistic values in the study's analysis and suggest that incorporating variables from their own work may yield more meaningful results. [Extracted from the article]

Chronic obstructive pulmonary disease (COPD) is a complex, heterogeneous, progressive inflammatory airway disease associated with a significant impact on patients' lives, including morbidity and mortality, and significant healthcare costs. Current pharmacologic strategies, including first- and second-line therapies such as long-acting β2-agonists, long-acting muscarinic antagonists, inhaled corticosteroids, phosphodiesterase-4 inhibitors, and macrolides, provide relief to patients with COPD. However, many patients remain symptomatic, with persistent symptoms and/or acute exacerbations and progressive lung function loss. Although neutrophilic inflammation is the most common type of inflammation in COPD, 20-40% of patients with COPD exhibit type 2 inflammation, with roles for CD4+ (cluster of differentiation 4) T-helper cell type 1 cells, type 2 innate lymphoid cells, eosinophils, and alternatively activated macrophages. On the basis of the current limitations of available therapies, a significant unmet need exists in COPD management, including the need for targeted therapies to address the underlying pathophysiology leading to disease progression, such as type 2 inflammation, as well as biomarkers to help select the patients who would most benefit from the new therapies. Significant progress is being made, with evolving understanding of the pathobiology of COPD leading to novel therapeutic targets including epithelial alarmins. In this review, we describe the current therapeutic landscape in COPD, discuss unmet treatment needs, review the current knowledge of type 2 inflammation and epithelial alarmins in COPD, explore potential biomarkers of type 2 inflammation in COPD, and finally provide a rationale for incorporating therapies targeting type 2 inflammation and epithelial alarmins in COPD. [ABSTRACT FROM AUTHOR]