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Pulmonary rehabilitation: Similar benefit in both IPF and COPD patients
Patients with idiopathic pulmonary fibrosis (IPF) complete and respond to pulmonary rehabilitation at rates similar to patients with chronic obstructive pulmonary disease (COPD), according to results of a real-world study. The findings reported in an article published in the journal CHEST® reinforce pulmonary rehabilitation’s benefits for this population.
A progressive decline in respiratory and physical function characterizes IPF, with median survival from diagnosis of 3-5 years, according to Claire Nolan, PhD, of Harefield Hospital, Middlesex, England, and colleagues. The effects of pharmacologic therapies on IPF on symptom burden and quality of life are modest, although lung function decline may be slowed. Supporting evidence for pulmonary rehabilitation benefit in IPF is more modest than it is for COPD, for which exercise capacity, dyspnea, and health-related quality of life improvement have been demonstrated.
“We did not design a randomized, controlled trial,” Dr. Nolan said in an interview, “as it was considered unethical by the local ethics committee to withhold pulmonary rehabilitation based on clinical guidance in the United Kingdom.” She pointed out that initial pulmonary rehabilitation trials in COPD included an intervention (pulmonary rehabilitation) and a control (standard medical care) arm.
The study aims were to compare the effects of pulmonary rehabilitation with real-world data between IPF and COPD with respect to magnitude of effect and survival. The authors’ hypothesis was that IPF patients would have a blunted response to pulmonary rehabilitation with reduced completion rates, compared with a matched COPD group, and with increased mortality.
Study details
Investigators use propensity score matching of 163 IPF patients with a control group of 163 patients with COPD referred to pulmonary rehabilitation. Completion rates, responses, and survival status were recorded for 1-year following pulmonary rehabilitation discharge. The 8-week outpatient program was composed of two supervised exercise and education sessions with additional unsupervised home-based exercise each week.
While spirometry data, as expected, showed a higher proportion of IPF patients using supplemental oxygen, pulmonary rehabilitation completion rates were similar for both groups (IPF, 69%; COPD, 63%; P = .24) and there was no between group difference in the number of sessions attended (P = .39). Medical Research Council (muscle strength) (MRC), incremental shuttle walk test (ISW), and Chronic Respiratory Questionnaire total score (CRQ-T) improved significantly in both groups, again with no significant difference between groups.
Over the study course, there was progressive, significant worsening of forced vital capacity percentage, predicted, prescription supplemental oxygen, resting peripheral oxygen saturation, exercise capacity, health-related quality of life and pulmonary rehabilitation adherence across groups of responders (n = 63; 38%), nonresponders (n = 50; 31%) and noncompleters (n = 50; 31%). Among the IPF patients, 6 died before completing pulmonary rehabilitation, with 42 (27%) dying during follow-up.
Benefits of rehabilitation
Multivariable analyses showed that noncompletion and nonresponse were associated with significantly higher risk of all-cause mortality at 1-year. Also, time to all-cause mortality was shorter (P = .001) for noncompleters and nonresponders, compared with completers. A trend toward higher completion rates in the IPF group, compared with the COPD group, may be explained, the researchers explained, by fewer hospitalizations over the prior 12 months in the IPF group.
“Although many programs are designed for people with COPD,” Dr. Nolan and colleagues concluded, “our study demonstrates that people with IPF have similar clinical benefits and completion rates to those with COPD. These data reinforce the importance of referral to and engagement in pulmonary rehabilitation amongst the IPF population.”
These findings, Dr. Nolan emphasized, emerged from a single center, and validation in other settings is needed.
This study was funded by a National Institute for Health Research Doctoral Research Fellowship (2014-07-089) and a Medical Research Council New Investigator Research Grant (98576).
Patients with idiopathic pulmonary fibrosis (IPF) complete and respond to pulmonary rehabilitation at rates similar to patients with chronic obstructive pulmonary disease (COPD), according to results of a real-world study. The findings reported in an article published in the journal CHEST® reinforce pulmonary rehabilitation’s benefits for this population.
A progressive decline in respiratory and physical function characterizes IPF, with median survival from diagnosis of 3-5 years, according to Claire Nolan, PhD, of Harefield Hospital, Middlesex, England, and colleagues. The effects of pharmacologic therapies on IPF on symptom burden and quality of life are modest, although lung function decline may be slowed. Supporting evidence for pulmonary rehabilitation benefit in IPF is more modest than it is for COPD, for which exercise capacity, dyspnea, and health-related quality of life improvement have been demonstrated.
“We did not design a randomized, controlled trial,” Dr. Nolan said in an interview, “as it was considered unethical by the local ethics committee to withhold pulmonary rehabilitation based on clinical guidance in the United Kingdom.” She pointed out that initial pulmonary rehabilitation trials in COPD included an intervention (pulmonary rehabilitation) and a control (standard medical care) arm.
The study aims were to compare the effects of pulmonary rehabilitation with real-world data between IPF and COPD with respect to magnitude of effect and survival. The authors’ hypothesis was that IPF patients would have a blunted response to pulmonary rehabilitation with reduced completion rates, compared with a matched COPD group, and with increased mortality.
Study details
Investigators use propensity score matching of 163 IPF patients with a control group of 163 patients with COPD referred to pulmonary rehabilitation. Completion rates, responses, and survival status were recorded for 1-year following pulmonary rehabilitation discharge. The 8-week outpatient program was composed of two supervised exercise and education sessions with additional unsupervised home-based exercise each week.
While spirometry data, as expected, showed a higher proportion of IPF patients using supplemental oxygen, pulmonary rehabilitation completion rates were similar for both groups (IPF, 69%; COPD, 63%; P = .24) and there was no between group difference in the number of sessions attended (P = .39). Medical Research Council (muscle strength) (MRC), incremental shuttle walk test (ISW), and Chronic Respiratory Questionnaire total score (CRQ-T) improved significantly in both groups, again with no significant difference between groups.
Over the study course, there was progressive, significant worsening of forced vital capacity percentage, predicted, prescription supplemental oxygen, resting peripheral oxygen saturation, exercise capacity, health-related quality of life and pulmonary rehabilitation adherence across groups of responders (n = 63; 38%), nonresponders (n = 50; 31%) and noncompleters (n = 50; 31%). Among the IPF patients, 6 died before completing pulmonary rehabilitation, with 42 (27%) dying during follow-up.
Benefits of rehabilitation
Multivariable analyses showed that noncompletion and nonresponse were associated with significantly higher risk of all-cause mortality at 1-year. Also, time to all-cause mortality was shorter (P = .001) for noncompleters and nonresponders, compared with completers. A trend toward higher completion rates in the IPF group, compared with the COPD group, may be explained, the researchers explained, by fewer hospitalizations over the prior 12 months in the IPF group.
“Although many programs are designed for people with COPD,” Dr. Nolan and colleagues concluded, “our study demonstrates that people with IPF have similar clinical benefits and completion rates to those with COPD. These data reinforce the importance of referral to and engagement in pulmonary rehabilitation amongst the IPF population.”
These findings, Dr. Nolan emphasized, emerged from a single center, and validation in other settings is needed.
This study was funded by a National Institute for Health Research Doctoral Research Fellowship (2014-07-089) and a Medical Research Council New Investigator Research Grant (98576).
Patients with idiopathic pulmonary fibrosis (IPF) complete and respond to pulmonary rehabilitation at rates similar to patients with chronic obstructive pulmonary disease (COPD), according to results of a real-world study. The findings reported in an article published in the journal CHEST® reinforce pulmonary rehabilitation’s benefits for this population.
A progressive decline in respiratory and physical function characterizes IPF, with median survival from diagnosis of 3-5 years, according to Claire Nolan, PhD, of Harefield Hospital, Middlesex, England, and colleagues. The effects of pharmacologic therapies on IPF on symptom burden and quality of life are modest, although lung function decline may be slowed. Supporting evidence for pulmonary rehabilitation benefit in IPF is more modest than it is for COPD, for which exercise capacity, dyspnea, and health-related quality of life improvement have been demonstrated.
“We did not design a randomized, controlled trial,” Dr. Nolan said in an interview, “as it was considered unethical by the local ethics committee to withhold pulmonary rehabilitation based on clinical guidance in the United Kingdom.” She pointed out that initial pulmonary rehabilitation trials in COPD included an intervention (pulmonary rehabilitation) and a control (standard medical care) arm.
The study aims were to compare the effects of pulmonary rehabilitation with real-world data between IPF and COPD with respect to magnitude of effect and survival. The authors’ hypothesis was that IPF patients would have a blunted response to pulmonary rehabilitation with reduced completion rates, compared with a matched COPD group, and with increased mortality.
Study details
Investigators use propensity score matching of 163 IPF patients with a control group of 163 patients with COPD referred to pulmonary rehabilitation. Completion rates, responses, and survival status were recorded for 1-year following pulmonary rehabilitation discharge. The 8-week outpatient program was composed of two supervised exercise and education sessions with additional unsupervised home-based exercise each week.
While spirometry data, as expected, showed a higher proportion of IPF patients using supplemental oxygen, pulmonary rehabilitation completion rates were similar for both groups (IPF, 69%; COPD, 63%; P = .24) and there was no between group difference in the number of sessions attended (P = .39). Medical Research Council (muscle strength) (MRC), incremental shuttle walk test (ISW), and Chronic Respiratory Questionnaire total score (CRQ-T) improved significantly in both groups, again with no significant difference between groups.
Over the study course, there was progressive, significant worsening of forced vital capacity percentage, predicted, prescription supplemental oxygen, resting peripheral oxygen saturation, exercise capacity, health-related quality of life and pulmonary rehabilitation adherence across groups of responders (n = 63; 38%), nonresponders (n = 50; 31%) and noncompleters (n = 50; 31%). Among the IPF patients, 6 died before completing pulmonary rehabilitation, with 42 (27%) dying during follow-up.
Benefits of rehabilitation
Multivariable analyses showed that noncompletion and nonresponse were associated with significantly higher risk of all-cause mortality at 1-year. Also, time to all-cause mortality was shorter (P = .001) for noncompleters and nonresponders, compared with completers. A trend toward higher completion rates in the IPF group, compared with the COPD group, may be explained, the researchers explained, by fewer hospitalizations over the prior 12 months in the IPF group.
“Although many programs are designed for people with COPD,” Dr. Nolan and colleagues concluded, “our study demonstrates that people with IPF have similar clinical benefits and completion rates to those with COPD. These data reinforce the importance of referral to and engagement in pulmonary rehabilitation amongst the IPF population.”
These findings, Dr. Nolan emphasized, emerged from a single center, and validation in other settings is needed.
This study was funded by a National Institute for Health Research Doctoral Research Fellowship (2014-07-089) and a Medical Research Council New Investigator Research Grant (98576).
FROM THE JOURNAL CHEST®
Novel bronchoscopic interventions appear promising for patients with COPD
Several emerging bronchoscopic treatments have the potential to improve the quality of life for patients with chronic obstructive pulmonary disease, an investigator reported at the annual meeting of the American College of Chest Physicians.
Targeted lung denervation is one promising novel therapeutic option that is safe and may improve clinical outcomes according to investigator Christian Ghattas, MD.
Data from an ongoing phase 3 randomized controlled trial may provide new information on the efficacy of targeted lung denervation in patients with chronic obstructive pulmonary disease (COPD), said Dr. Ghattas, assistant professor of medicine and associate program director for the interventional pulmonary fellowship at The Ohio State University Medical Center in Columbus.
“Outcome data of longer follow-up on previously treated patients will provide us with more information on the durability and the effect of this treatment,” Dr. Ghattas said in an online presentation at the CHEST meeting, which was held virtually this year.
Meanwhile, a few compelling bronchoscopic treatment modalities for patients with chronic bronchitis are in earlier stages of clinical development. “Larger randomized, controlled trials are ongoing to confirm the available data and to evaluate treatment durability,” said Dr. Ghattas.
Targeted lung denervation
The targeted lung denervation system under study (dNerva®, Nuvaira Inc.) involves the use of a radiofrequency catheter to ablate the peribronchial branches of the vagus nerve, Dr. Ghattas said.
The goal of disrupting pulmonary nerve input is to achieve sustained bronchodilation and reduce mucous secretion, thereby simulating the effect of anticholinergic drugs, he added.
In pilot studies, the targeted lung denervation system demonstrated its feasibility and safety, while modifications to the system reduced the rate of serious adverse events, according to Dr. Ghattas.
In the AIRFLOW-1 study, which evaluated the safety of the latest generation version of the system, 30 patients with COPD were randomized to targeted lung denervation at one of two doses, 29 or 32 watts.
Of those 30 patients, 29 (96.7%) had procedural success, meaning the catheter was inserted, guided to its intended location, and removed intact with no reported in-hospital serious adverse events, according to results published in Respiration.
There was no difference between arms in the primary endpoint, which was the rate of adverse airway effects requiring intervention that were associated with targeted lung denervation, investigators reported. Four such events occurred, in 3 of 15 patients treated with 32 watts and 1 of 15 patients treated with 29 watts.
Procedural success, defined as device success without an in-hospital serious adverse event, was 96.7% (29/30). The rate of TLD-associated adverse airway effects requiring intervention was 3/15 in the 32 W versus 1/15 in the 29 W group (P = .6). However, serious gastric events were noted in five patients, prompting safety improvements and procedural enhancements that reduced both gastrointestinal and airway events, according to the study report.
Further data are available from AIRFLOW-2, a randomized, sham-controlled trial enrolling patients with symptomatic COPD.
In that study, targeted lung denervation plus optimal drug treatment led to fewer respiratory adverse events of interest, including hospitalizations for COPD exacerbation, according to a report on the study that appears in The American Journal of Respiratory and Critical Care Medicine.
Respiratory adverse events occurred in 32% of treated patients versus 71% of sham-treated patients in a predefined 3- to 6.5-month postprocedure window, the report says.
Currently underway is AIRFLOW-3, a randomized study of targeted lung denervation versus sham procedure in patients with COPD. The study has a primary outcome measure of moderate or severe COPD exacerbations over 12 months and is slated to enroll 480 patients.
To be eligible for AIRFLOW-3, patients must have had at least two moderate or one severe COPD exacerbation in the previous year, Dr. Ghattas said.
Metered cryospray
One novel intervention with the potential to benefit patients with chronic bronchitis is metered cryospray (RejuvenAir), which works by delivering liquid nitrogen to the tracheobronchial airways, according to Dr. Ghattas.
This targeted delivery ablates abnormal epithelium, facilitating the regeneration of healthy mucosa, according to investigators in a recently published single-arm prospective trial.
Metered cryospray was safe, feasible, and linked to clinically meaningful improvements in patient-reported outcomes among patients with COPD, according to authors of the study, which appears in the European Respiratory Journal.
In the study, 34 of 35 participants received three treatments 4-6 weeks apart.
Investigators reported that at 3 months there were significant reductions in the COPD Assessment Test that were durable to 6 months, and changes in the St. George’s Respiratory Questionnaire and the Leicester Cough Questionnaire that were durable to 9 months.
There were 14 serious adverse events, none of which were device- or procedure related, according to investigators.
An ongoing randomized study called SPRAY-CB is comparing metered cryospray to sham procedure in an anticipated 210 patients with COPD with chronic bronchitis.
Bronchial rheoplasty
Bronchial rheoplasty (RheOx, Gala Therapeutics), is another promising intervention under investigation for the treatment of chronic bronchitis, according to Dr. Ghattas.
This system delivers nonthermal pulsed electrical energy, Dr. Ghattas said, with the intention of ablating goblet cells in the airways.
“The preclinical studies have demonstrated epithelial ablation, followed by regeneration of normalized epithelium,” he said in his presentation.
In 12-month results of multicenter clinical trial, bronchial rheoplasty was technically feasible and safe, with reductions in goblet cell hyperplasia and changes in patient-reported quality of life seen following the procedure, investigators reported in The American Journal of Respiratory and Critical Care Medicine.
The mean goblet cell hyperplasia score was reduced by 39% from baseline to treatment, according to study results. Four procedure-related serious adverse events were observed through 6 months, and there were no procedure- or device-related serious adverse events over the next 6 months. Mild hemoptysis occurred in 47% of patients, investigators reported.
A larger randomized, double-blind prospective trial with a sham control arm is underway and will include 270 patients, according to Dr. Ghattas. “We’re going to have to wait for the results,” he said.
Dr. Ghattas reported serving as a site principal investigator for clinical trials involving the bronchoscopic interventions he discussed, including AIRFLOW-3 (evaluating the targeted lung denervation system), SPRAY-CB (metered cryospray), and RheSolve (bronchial rheoplasty).
Several emerging bronchoscopic treatments have the potential to improve the quality of life for patients with chronic obstructive pulmonary disease, an investigator reported at the annual meeting of the American College of Chest Physicians.
Targeted lung denervation is one promising novel therapeutic option that is safe and may improve clinical outcomes according to investigator Christian Ghattas, MD.
Data from an ongoing phase 3 randomized controlled trial may provide new information on the efficacy of targeted lung denervation in patients with chronic obstructive pulmonary disease (COPD), said Dr. Ghattas, assistant professor of medicine and associate program director for the interventional pulmonary fellowship at The Ohio State University Medical Center in Columbus.
“Outcome data of longer follow-up on previously treated patients will provide us with more information on the durability and the effect of this treatment,” Dr. Ghattas said in an online presentation at the CHEST meeting, which was held virtually this year.
Meanwhile, a few compelling bronchoscopic treatment modalities for patients with chronic bronchitis are in earlier stages of clinical development. “Larger randomized, controlled trials are ongoing to confirm the available data and to evaluate treatment durability,” said Dr. Ghattas.
Targeted lung denervation
The targeted lung denervation system under study (dNerva®, Nuvaira Inc.) involves the use of a radiofrequency catheter to ablate the peribronchial branches of the vagus nerve, Dr. Ghattas said.
The goal of disrupting pulmonary nerve input is to achieve sustained bronchodilation and reduce mucous secretion, thereby simulating the effect of anticholinergic drugs, he added.
In pilot studies, the targeted lung denervation system demonstrated its feasibility and safety, while modifications to the system reduced the rate of serious adverse events, according to Dr. Ghattas.
In the AIRFLOW-1 study, which evaluated the safety of the latest generation version of the system, 30 patients with COPD were randomized to targeted lung denervation at one of two doses, 29 or 32 watts.
Of those 30 patients, 29 (96.7%) had procedural success, meaning the catheter was inserted, guided to its intended location, and removed intact with no reported in-hospital serious adverse events, according to results published in Respiration.
There was no difference between arms in the primary endpoint, which was the rate of adverse airway effects requiring intervention that were associated with targeted lung denervation, investigators reported. Four such events occurred, in 3 of 15 patients treated with 32 watts and 1 of 15 patients treated with 29 watts.
Procedural success, defined as device success without an in-hospital serious adverse event, was 96.7% (29/30). The rate of TLD-associated adverse airway effects requiring intervention was 3/15 in the 32 W versus 1/15 in the 29 W group (P = .6). However, serious gastric events were noted in five patients, prompting safety improvements and procedural enhancements that reduced both gastrointestinal and airway events, according to the study report.
Further data are available from AIRFLOW-2, a randomized, sham-controlled trial enrolling patients with symptomatic COPD.
In that study, targeted lung denervation plus optimal drug treatment led to fewer respiratory adverse events of interest, including hospitalizations for COPD exacerbation, according to a report on the study that appears in The American Journal of Respiratory and Critical Care Medicine.
Respiratory adverse events occurred in 32% of treated patients versus 71% of sham-treated patients in a predefined 3- to 6.5-month postprocedure window, the report says.
Currently underway is AIRFLOW-3, a randomized study of targeted lung denervation versus sham procedure in patients with COPD. The study has a primary outcome measure of moderate or severe COPD exacerbations over 12 months and is slated to enroll 480 patients.
To be eligible for AIRFLOW-3, patients must have had at least two moderate or one severe COPD exacerbation in the previous year, Dr. Ghattas said.
Metered cryospray
One novel intervention with the potential to benefit patients with chronic bronchitis is metered cryospray (RejuvenAir), which works by delivering liquid nitrogen to the tracheobronchial airways, according to Dr. Ghattas.
This targeted delivery ablates abnormal epithelium, facilitating the regeneration of healthy mucosa, according to investigators in a recently published single-arm prospective trial.
Metered cryospray was safe, feasible, and linked to clinically meaningful improvements in patient-reported outcomes among patients with COPD, according to authors of the study, which appears in the European Respiratory Journal.
In the study, 34 of 35 participants received three treatments 4-6 weeks apart.
Investigators reported that at 3 months there were significant reductions in the COPD Assessment Test that were durable to 6 months, and changes in the St. George’s Respiratory Questionnaire and the Leicester Cough Questionnaire that were durable to 9 months.
There were 14 serious adverse events, none of which were device- or procedure related, according to investigators.
An ongoing randomized study called SPRAY-CB is comparing metered cryospray to sham procedure in an anticipated 210 patients with COPD with chronic bronchitis.
Bronchial rheoplasty
Bronchial rheoplasty (RheOx, Gala Therapeutics), is another promising intervention under investigation for the treatment of chronic bronchitis, according to Dr. Ghattas.
This system delivers nonthermal pulsed electrical energy, Dr. Ghattas said, with the intention of ablating goblet cells in the airways.
“The preclinical studies have demonstrated epithelial ablation, followed by regeneration of normalized epithelium,” he said in his presentation.
In 12-month results of multicenter clinical trial, bronchial rheoplasty was technically feasible and safe, with reductions in goblet cell hyperplasia and changes in patient-reported quality of life seen following the procedure, investigators reported in The American Journal of Respiratory and Critical Care Medicine.
The mean goblet cell hyperplasia score was reduced by 39% from baseline to treatment, according to study results. Four procedure-related serious adverse events were observed through 6 months, and there were no procedure- or device-related serious adverse events over the next 6 months. Mild hemoptysis occurred in 47% of patients, investigators reported.
A larger randomized, double-blind prospective trial with a sham control arm is underway and will include 270 patients, according to Dr. Ghattas. “We’re going to have to wait for the results,” he said.
Dr. Ghattas reported serving as a site principal investigator for clinical trials involving the bronchoscopic interventions he discussed, including AIRFLOW-3 (evaluating the targeted lung denervation system), SPRAY-CB (metered cryospray), and RheSolve (bronchial rheoplasty).
Several emerging bronchoscopic treatments have the potential to improve the quality of life for patients with chronic obstructive pulmonary disease, an investigator reported at the annual meeting of the American College of Chest Physicians.
Targeted lung denervation is one promising novel therapeutic option that is safe and may improve clinical outcomes according to investigator Christian Ghattas, MD.
Data from an ongoing phase 3 randomized controlled trial may provide new information on the efficacy of targeted lung denervation in patients with chronic obstructive pulmonary disease (COPD), said Dr. Ghattas, assistant professor of medicine and associate program director for the interventional pulmonary fellowship at The Ohio State University Medical Center in Columbus.
“Outcome data of longer follow-up on previously treated patients will provide us with more information on the durability and the effect of this treatment,” Dr. Ghattas said in an online presentation at the CHEST meeting, which was held virtually this year.
Meanwhile, a few compelling bronchoscopic treatment modalities for patients with chronic bronchitis are in earlier stages of clinical development. “Larger randomized, controlled trials are ongoing to confirm the available data and to evaluate treatment durability,” said Dr. Ghattas.
Targeted lung denervation
The targeted lung denervation system under study (dNerva®, Nuvaira Inc.) involves the use of a radiofrequency catheter to ablate the peribronchial branches of the vagus nerve, Dr. Ghattas said.
The goal of disrupting pulmonary nerve input is to achieve sustained bronchodilation and reduce mucous secretion, thereby simulating the effect of anticholinergic drugs, he added.
In pilot studies, the targeted lung denervation system demonstrated its feasibility and safety, while modifications to the system reduced the rate of serious adverse events, according to Dr. Ghattas.
In the AIRFLOW-1 study, which evaluated the safety of the latest generation version of the system, 30 patients with COPD were randomized to targeted lung denervation at one of two doses, 29 or 32 watts.
Of those 30 patients, 29 (96.7%) had procedural success, meaning the catheter was inserted, guided to its intended location, and removed intact with no reported in-hospital serious adverse events, according to results published in Respiration.
There was no difference between arms in the primary endpoint, which was the rate of adverse airway effects requiring intervention that were associated with targeted lung denervation, investigators reported. Four such events occurred, in 3 of 15 patients treated with 32 watts and 1 of 15 patients treated with 29 watts.
Procedural success, defined as device success without an in-hospital serious adverse event, was 96.7% (29/30). The rate of TLD-associated adverse airway effects requiring intervention was 3/15 in the 32 W versus 1/15 in the 29 W group (P = .6). However, serious gastric events were noted in five patients, prompting safety improvements and procedural enhancements that reduced both gastrointestinal and airway events, according to the study report.
Further data are available from AIRFLOW-2, a randomized, sham-controlled trial enrolling patients with symptomatic COPD.
In that study, targeted lung denervation plus optimal drug treatment led to fewer respiratory adverse events of interest, including hospitalizations for COPD exacerbation, according to a report on the study that appears in The American Journal of Respiratory and Critical Care Medicine.
Respiratory adverse events occurred in 32% of treated patients versus 71% of sham-treated patients in a predefined 3- to 6.5-month postprocedure window, the report says.
Currently underway is AIRFLOW-3, a randomized study of targeted lung denervation versus sham procedure in patients with COPD. The study has a primary outcome measure of moderate or severe COPD exacerbations over 12 months and is slated to enroll 480 patients.
To be eligible for AIRFLOW-3, patients must have had at least two moderate or one severe COPD exacerbation in the previous year, Dr. Ghattas said.
Metered cryospray
One novel intervention with the potential to benefit patients with chronic bronchitis is metered cryospray (RejuvenAir), which works by delivering liquid nitrogen to the tracheobronchial airways, according to Dr. Ghattas.
This targeted delivery ablates abnormal epithelium, facilitating the regeneration of healthy mucosa, according to investigators in a recently published single-arm prospective trial.
Metered cryospray was safe, feasible, and linked to clinically meaningful improvements in patient-reported outcomes among patients with COPD, according to authors of the study, which appears in the European Respiratory Journal.
In the study, 34 of 35 participants received three treatments 4-6 weeks apart.
Investigators reported that at 3 months there were significant reductions in the COPD Assessment Test that were durable to 6 months, and changes in the St. George’s Respiratory Questionnaire and the Leicester Cough Questionnaire that were durable to 9 months.
There were 14 serious adverse events, none of which were device- or procedure related, according to investigators.
An ongoing randomized study called SPRAY-CB is comparing metered cryospray to sham procedure in an anticipated 210 patients with COPD with chronic bronchitis.
Bronchial rheoplasty
Bronchial rheoplasty (RheOx, Gala Therapeutics), is another promising intervention under investigation for the treatment of chronic bronchitis, according to Dr. Ghattas.
This system delivers nonthermal pulsed electrical energy, Dr. Ghattas said, with the intention of ablating goblet cells in the airways.
“The preclinical studies have demonstrated epithelial ablation, followed by regeneration of normalized epithelium,” he said in his presentation.
In 12-month results of multicenter clinical trial, bronchial rheoplasty was technically feasible and safe, with reductions in goblet cell hyperplasia and changes in patient-reported quality of life seen following the procedure, investigators reported in The American Journal of Respiratory and Critical Care Medicine.
The mean goblet cell hyperplasia score was reduced by 39% from baseline to treatment, according to study results. Four procedure-related serious adverse events were observed through 6 months, and there were no procedure- or device-related serious adverse events over the next 6 months. Mild hemoptysis occurred in 47% of patients, investigators reported.
A larger randomized, double-blind prospective trial with a sham control arm is underway and will include 270 patients, according to Dr. Ghattas. “We’re going to have to wait for the results,” he said.
Dr. Ghattas reported serving as a site principal investigator for clinical trials involving the bronchoscopic interventions he discussed, including AIRFLOW-3 (evaluating the targeted lung denervation system), SPRAY-CB (metered cryospray), and RheSolve (bronchial rheoplasty).
FROM CHEST 2021
Sepsis multiplies in-hospital mortality risk in COPD
Although slightly fewer than 1% of hospitalizations for chronic obstructive pulmonary disease (COPD) are complicated by sepsis, this complication increases the risk for in-hospital mortality fivefold, investigators who studied a representative national sample found.
Among nearly 7 million hospitalizations in which the primary diagnosis was COPD, nearly 65,000 (0.93%) patients experienced sepsis as a complication. In all, 31% of patients with COPD and sepsis were discharged from the hospital to another care facility, and 19% of patients died in hospital, report Harshil Shah, MD, from Guthrie Corning (N.Y.) Hospital and colleagues.
“Our study highlights the need for better risk stratification in patients with COPD developing sepsis to improve the outcomes. Further studies are warranted to consider factoring some of the modifiable factors into account and to ameliorate the outcomes of sepsis during COPD hospitalizations,” Dr. Shah and colleagues write in a poster presented during the at the annual meeting of the American College of Chest Physicians, held virtually this year.
COPD has been associated with increased risk for sepsis because of the use of corticosteroids, underlying comorbidities, and, potentially, because of impaired barrier function, the authors note.
Nationwide sample
To determine the effects of sepsis and predictors of poor outcomes among patients hospitalized for COPD, the investigators used standard diagnostic codes to identify patients with a primary diagnosis of COPD from the Nationwide Inpatient Sample for the period 2007 through 2018 and sepsis from codes in secondary fields in the International Classification of Diseases (9th/10th Editions) Clinical Modification.
They identified a total of 6,940,615 hospitalizations in which the primary diagnosis was COPD; in 64,748 of those cases, sepsis was a complication.
As noted, the in-hospital death rate, one of two primary outcomes, was 19% for patients with COPD and sepsis, and the rate of discharge to other facilities was 31%.
In analysis adjusted for confounding factors, sepsis was associated with an odds ratio for mortality of 4.9 (P < .01) and an OR for discharge to a facility of 2.2 (P < .01).
With regard to trends, the investigators saw that, although the adjusted odds for in-hospital mortality remained stable over time, discharge to facilities increased significantly. In 2007, the adjusted OR was 2.2, whereas in 2018, it was 2.6 (P for trend = .02).
Predictors of in-hospital mortality among patients with sepsis included increasing age (OR, not shown), White ethnicity (OR, 1.2), treatment in the Northeast region (OR, 1.4), disseminated intravascular coagulation (OR, 3.7), pneumococcal infection (OR, 1.2), congestive heart failure (OR, 1.2), and renal failure (OR, 1.4; P < .01 for all comparisons).
Mortality risk for many patients
A COPD specialist who was not involved in the study told this news organization that sepsis is an uncommon but serious complication, not just for patients with COPD but also for those with other severe illnesses.
“Sepsis has a high risk for mortality whether a person has COPD or not,” commented David M. Mannino III MD, FCCP, FERS, professor of medicine at the University of Kentucky, Lexington, and a cofounder and co–medical director of the COPD Foundation.
“It’s not surprising that sepsis is lethal in this population; the question is, if you have COPD, are you more likely to have sepsis? And I think the answer is probably yes. The connection there is that people with COPD have a higher risk for pneumonia, and pneumonia itself is probably one of the biggest risk factors, or certainly an important risk factor, for the development of sepsis,” he said in an interview.
It would be interesting to see the relationship between sepsis and in-hospital mortality for patients with other chronic diseases or people without COPD, he said, and he would have liked to have seen more detailed information about trends over time than Dr. Shah and colleagues provided.
No funding source for the study was reported. Dr. Shah and colleagues and Dr. Mannino have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Although slightly fewer than 1% of hospitalizations for chronic obstructive pulmonary disease (COPD) are complicated by sepsis, this complication increases the risk for in-hospital mortality fivefold, investigators who studied a representative national sample found.
Among nearly 7 million hospitalizations in which the primary diagnosis was COPD, nearly 65,000 (0.93%) patients experienced sepsis as a complication. In all, 31% of patients with COPD and sepsis were discharged from the hospital to another care facility, and 19% of patients died in hospital, report Harshil Shah, MD, from Guthrie Corning (N.Y.) Hospital and colleagues.
“Our study highlights the need for better risk stratification in patients with COPD developing sepsis to improve the outcomes. Further studies are warranted to consider factoring some of the modifiable factors into account and to ameliorate the outcomes of sepsis during COPD hospitalizations,” Dr. Shah and colleagues write in a poster presented during the at the annual meeting of the American College of Chest Physicians, held virtually this year.
COPD has been associated with increased risk for sepsis because of the use of corticosteroids, underlying comorbidities, and, potentially, because of impaired barrier function, the authors note.
Nationwide sample
To determine the effects of sepsis and predictors of poor outcomes among patients hospitalized for COPD, the investigators used standard diagnostic codes to identify patients with a primary diagnosis of COPD from the Nationwide Inpatient Sample for the period 2007 through 2018 and sepsis from codes in secondary fields in the International Classification of Diseases (9th/10th Editions) Clinical Modification.
They identified a total of 6,940,615 hospitalizations in which the primary diagnosis was COPD; in 64,748 of those cases, sepsis was a complication.
As noted, the in-hospital death rate, one of two primary outcomes, was 19% for patients with COPD and sepsis, and the rate of discharge to other facilities was 31%.
In analysis adjusted for confounding factors, sepsis was associated with an odds ratio for mortality of 4.9 (P < .01) and an OR for discharge to a facility of 2.2 (P < .01).
With regard to trends, the investigators saw that, although the adjusted odds for in-hospital mortality remained stable over time, discharge to facilities increased significantly. In 2007, the adjusted OR was 2.2, whereas in 2018, it was 2.6 (P for trend = .02).
Predictors of in-hospital mortality among patients with sepsis included increasing age (OR, not shown), White ethnicity (OR, 1.2), treatment in the Northeast region (OR, 1.4), disseminated intravascular coagulation (OR, 3.7), pneumococcal infection (OR, 1.2), congestive heart failure (OR, 1.2), and renal failure (OR, 1.4; P < .01 for all comparisons).
Mortality risk for many patients
A COPD specialist who was not involved in the study told this news organization that sepsis is an uncommon but serious complication, not just for patients with COPD but also for those with other severe illnesses.
“Sepsis has a high risk for mortality whether a person has COPD or not,” commented David M. Mannino III MD, FCCP, FERS, professor of medicine at the University of Kentucky, Lexington, and a cofounder and co–medical director of the COPD Foundation.
“It’s not surprising that sepsis is lethal in this population; the question is, if you have COPD, are you more likely to have sepsis? And I think the answer is probably yes. The connection there is that people with COPD have a higher risk for pneumonia, and pneumonia itself is probably one of the biggest risk factors, or certainly an important risk factor, for the development of sepsis,” he said in an interview.
It would be interesting to see the relationship between sepsis and in-hospital mortality for patients with other chronic diseases or people without COPD, he said, and he would have liked to have seen more detailed information about trends over time than Dr. Shah and colleagues provided.
No funding source for the study was reported. Dr. Shah and colleagues and Dr. Mannino have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Although slightly fewer than 1% of hospitalizations for chronic obstructive pulmonary disease (COPD) are complicated by sepsis, this complication increases the risk for in-hospital mortality fivefold, investigators who studied a representative national sample found.
Among nearly 7 million hospitalizations in which the primary diagnosis was COPD, nearly 65,000 (0.93%) patients experienced sepsis as a complication. In all, 31% of patients with COPD and sepsis were discharged from the hospital to another care facility, and 19% of patients died in hospital, report Harshil Shah, MD, from Guthrie Corning (N.Y.) Hospital and colleagues.
“Our study highlights the need for better risk stratification in patients with COPD developing sepsis to improve the outcomes. Further studies are warranted to consider factoring some of the modifiable factors into account and to ameliorate the outcomes of sepsis during COPD hospitalizations,” Dr. Shah and colleagues write in a poster presented during the at the annual meeting of the American College of Chest Physicians, held virtually this year.
COPD has been associated with increased risk for sepsis because of the use of corticosteroids, underlying comorbidities, and, potentially, because of impaired barrier function, the authors note.
Nationwide sample
To determine the effects of sepsis and predictors of poor outcomes among patients hospitalized for COPD, the investigators used standard diagnostic codes to identify patients with a primary diagnosis of COPD from the Nationwide Inpatient Sample for the period 2007 through 2018 and sepsis from codes in secondary fields in the International Classification of Diseases (9th/10th Editions) Clinical Modification.
They identified a total of 6,940,615 hospitalizations in which the primary diagnosis was COPD; in 64,748 of those cases, sepsis was a complication.
As noted, the in-hospital death rate, one of two primary outcomes, was 19% for patients with COPD and sepsis, and the rate of discharge to other facilities was 31%.
In analysis adjusted for confounding factors, sepsis was associated with an odds ratio for mortality of 4.9 (P < .01) and an OR for discharge to a facility of 2.2 (P < .01).
With regard to trends, the investigators saw that, although the adjusted odds for in-hospital mortality remained stable over time, discharge to facilities increased significantly. In 2007, the adjusted OR was 2.2, whereas in 2018, it was 2.6 (P for trend = .02).
Predictors of in-hospital mortality among patients with sepsis included increasing age (OR, not shown), White ethnicity (OR, 1.2), treatment in the Northeast region (OR, 1.4), disseminated intravascular coagulation (OR, 3.7), pneumococcal infection (OR, 1.2), congestive heart failure (OR, 1.2), and renal failure (OR, 1.4; P < .01 for all comparisons).
Mortality risk for many patients
A COPD specialist who was not involved in the study told this news organization that sepsis is an uncommon but serious complication, not just for patients with COPD but also for those with other severe illnesses.
“Sepsis has a high risk for mortality whether a person has COPD or not,” commented David M. Mannino III MD, FCCP, FERS, professor of medicine at the University of Kentucky, Lexington, and a cofounder and co–medical director of the COPD Foundation.
“It’s not surprising that sepsis is lethal in this population; the question is, if you have COPD, are you more likely to have sepsis? And I think the answer is probably yes. The connection there is that people with COPD have a higher risk for pneumonia, and pneumonia itself is probably one of the biggest risk factors, or certainly an important risk factor, for the development of sepsis,” he said in an interview.
It would be interesting to see the relationship between sepsis and in-hospital mortality for patients with other chronic diseases or people without COPD, he said, and he would have liked to have seen more detailed information about trends over time than Dr. Shah and colleagues provided.
No funding source for the study was reported. Dr. Shah and colleagues and Dr. Mannino have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Life-threatening paradoxical bronchospasm may escape recognition in patients with COPD or asthma
according to a researcher who reviewed spirometry test results from U.S. military veterans.
Nearly 1.5% of the tests met the criteria for paradoxical bronchospasm, which refers to airway constriction that may rapidly occur after inhalation of a short-acting beta2 agonist (SABA) such as albuterol.
However, none of those reports alluded to paradoxical bronchospasm, said investigator Malvika Kaul, MD, fellow in the department of pulmonary and critical care at the University of Illinois at Chicago and the Jesse Brown Veterans Affairs Medical Center, also in Chicago.
“Paradoxical bronchospasm was neither recognized nor reported in any spirometry test results,” Dr. Kaul said in an online poster presentation at the annual meeting of the American College of Chest Physicians, held virtually this year.
By recognizing paradoxical bronchospasm, health care providers could address its clinical implications and identify potential alternative management options, according to Dr. Kaul.
“We hope in the future, education of clinicians about this phenomena is emphasized,” Dr. Kaul said in her presentation.
Recognizing paradoxical bronchospasm
In an interview, Dr. Kaul said she began researching paradoxical bronchospasm after encountering a patient who had an acute reaction to albuterol during a pulmonary function test.
“I was not taught about it, and I wasn’t recognizing that pattern very frequently in my patients,” she said.
Prescribing information for Food and Drug Administration–approved SABAs include a warning that life-threatening paradoxical bronchospasm may occur, said Dr. Kaul.
If paradoxical bronchospasm occurs, the patient should discontinue the medication immediately and start on alternative therapy, according to the available prescribing information for albuterol sulfate.
Paradoxical bronchospasm has been linked to worsened respiratory outcomes, including more frequent exacerbations, in patients with obstructive lung diseases, according to Dr. Kaul.
Two previous large studies pegged the prevalence of paradoxical bronchospasm at around 4.5% in patients with COPD or asthma, but “it has not been reported or addressed in high-risk population, such as veterans who have high prevalence of obstructive lung diseases like COPD,” Dr. Kaul said.
Latest study results
Dr. Kaul described a retrospective analysis of 1,150 pre- and postbronchodilator spirometry tests conducted in patients with COPD or asthma at the Jesse Brown VA Medical Center between 2017 and 2020.
A positive paradoxical bronchodilator response was defined as a decrease of least 12% and 200 mL in forced expiratory volume in 1 second and forced vital capacity from baseline after four puffs of albuterol were inhaled, Dr. Kaul said.
Out of 18 reviewed spirometry results that met the criteria, none of the test results reported or recognized paradoxical bronchospasm, according to Dr. Kaul.
Those meeting the criteria were predominantly COPD patients, according to Dr. Kaul, who said 12 had an underlying diagnosis COPD, 4 had asthma, and 2 had COPD and asthma.
Of the 18 patients, 13 were African American, and all but 1 of the 18 patients had a current or past smoking history, according to reported data.
A history of obstructive sleep apnea was reported in nine patients, and history of gastroesophageal reflux disease was also reported in nine patients. Eleven patients had emphysema.
Greater awareness needed
Results of this study emphasize the need to recognize potential cases paradoxical bronchospasm in clinical practice, as well as a need for more research, according to Allen J. Blaivas, DO, FCCP, chair of the CHEST Airway Disorders NetWork.
“It’s something to be on the alert for, and certainly be aware that, if your patient is telling you that they feel worse, we shouldn’t just pooh-pooh it,” said Dr. Blaivas, who is medical director of the intensive care unit at the East Orange campus of the VA New Jersey Health Care System.
Further research could focus on breaking down whether patients with suspected paradoxical bronchospasm are using metered-dose inhalers or nebulizers, whether or not they are also taking inhaled corticosteroids, and whether prospective testing can confirm paradoxical bronchospasm in patients who report tightness after using a SABA, he said in an interview.
Dr. Kaul and coauthor Israel Rubinstein, MD had no relevant relationships to disclose. Dr. Blaivas had no relevant relationships to disclose.
according to a researcher who reviewed spirometry test results from U.S. military veterans.
Nearly 1.5% of the tests met the criteria for paradoxical bronchospasm, which refers to airway constriction that may rapidly occur after inhalation of a short-acting beta2 agonist (SABA) such as albuterol.
However, none of those reports alluded to paradoxical bronchospasm, said investigator Malvika Kaul, MD, fellow in the department of pulmonary and critical care at the University of Illinois at Chicago and the Jesse Brown Veterans Affairs Medical Center, also in Chicago.
“Paradoxical bronchospasm was neither recognized nor reported in any spirometry test results,” Dr. Kaul said in an online poster presentation at the annual meeting of the American College of Chest Physicians, held virtually this year.
By recognizing paradoxical bronchospasm, health care providers could address its clinical implications and identify potential alternative management options, according to Dr. Kaul.
“We hope in the future, education of clinicians about this phenomena is emphasized,” Dr. Kaul said in her presentation.
Recognizing paradoxical bronchospasm
In an interview, Dr. Kaul said she began researching paradoxical bronchospasm after encountering a patient who had an acute reaction to albuterol during a pulmonary function test.
“I was not taught about it, and I wasn’t recognizing that pattern very frequently in my patients,” she said.
Prescribing information for Food and Drug Administration–approved SABAs include a warning that life-threatening paradoxical bronchospasm may occur, said Dr. Kaul.
If paradoxical bronchospasm occurs, the patient should discontinue the medication immediately and start on alternative therapy, according to the available prescribing information for albuterol sulfate.
Paradoxical bronchospasm has been linked to worsened respiratory outcomes, including more frequent exacerbations, in patients with obstructive lung diseases, according to Dr. Kaul.
Two previous large studies pegged the prevalence of paradoxical bronchospasm at around 4.5% in patients with COPD or asthma, but “it has not been reported or addressed in high-risk population, such as veterans who have high prevalence of obstructive lung diseases like COPD,” Dr. Kaul said.
Latest study results
Dr. Kaul described a retrospective analysis of 1,150 pre- and postbronchodilator spirometry tests conducted in patients with COPD or asthma at the Jesse Brown VA Medical Center between 2017 and 2020.
A positive paradoxical bronchodilator response was defined as a decrease of least 12% and 200 mL in forced expiratory volume in 1 second and forced vital capacity from baseline after four puffs of albuterol were inhaled, Dr. Kaul said.
Out of 18 reviewed spirometry results that met the criteria, none of the test results reported or recognized paradoxical bronchospasm, according to Dr. Kaul.
Those meeting the criteria were predominantly COPD patients, according to Dr. Kaul, who said 12 had an underlying diagnosis COPD, 4 had asthma, and 2 had COPD and asthma.
Of the 18 patients, 13 were African American, and all but 1 of the 18 patients had a current or past smoking history, according to reported data.
A history of obstructive sleep apnea was reported in nine patients, and history of gastroesophageal reflux disease was also reported in nine patients. Eleven patients had emphysema.
Greater awareness needed
Results of this study emphasize the need to recognize potential cases paradoxical bronchospasm in clinical practice, as well as a need for more research, according to Allen J. Blaivas, DO, FCCP, chair of the CHEST Airway Disorders NetWork.
“It’s something to be on the alert for, and certainly be aware that, if your patient is telling you that they feel worse, we shouldn’t just pooh-pooh it,” said Dr. Blaivas, who is medical director of the intensive care unit at the East Orange campus of the VA New Jersey Health Care System.
Further research could focus on breaking down whether patients with suspected paradoxical bronchospasm are using metered-dose inhalers or nebulizers, whether or not they are also taking inhaled corticosteroids, and whether prospective testing can confirm paradoxical bronchospasm in patients who report tightness after using a SABA, he said in an interview.
Dr. Kaul and coauthor Israel Rubinstein, MD had no relevant relationships to disclose. Dr. Blaivas had no relevant relationships to disclose.
according to a researcher who reviewed spirometry test results from U.S. military veterans.
Nearly 1.5% of the tests met the criteria for paradoxical bronchospasm, which refers to airway constriction that may rapidly occur after inhalation of a short-acting beta2 agonist (SABA) such as albuterol.
However, none of those reports alluded to paradoxical bronchospasm, said investigator Malvika Kaul, MD, fellow in the department of pulmonary and critical care at the University of Illinois at Chicago and the Jesse Brown Veterans Affairs Medical Center, also in Chicago.
“Paradoxical bronchospasm was neither recognized nor reported in any spirometry test results,” Dr. Kaul said in an online poster presentation at the annual meeting of the American College of Chest Physicians, held virtually this year.
By recognizing paradoxical bronchospasm, health care providers could address its clinical implications and identify potential alternative management options, according to Dr. Kaul.
“We hope in the future, education of clinicians about this phenomena is emphasized,” Dr. Kaul said in her presentation.
Recognizing paradoxical bronchospasm
In an interview, Dr. Kaul said she began researching paradoxical bronchospasm after encountering a patient who had an acute reaction to albuterol during a pulmonary function test.
“I was not taught about it, and I wasn’t recognizing that pattern very frequently in my patients,” she said.
Prescribing information for Food and Drug Administration–approved SABAs include a warning that life-threatening paradoxical bronchospasm may occur, said Dr. Kaul.
If paradoxical bronchospasm occurs, the patient should discontinue the medication immediately and start on alternative therapy, according to the available prescribing information for albuterol sulfate.
Paradoxical bronchospasm has been linked to worsened respiratory outcomes, including more frequent exacerbations, in patients with obstructive lung diseases, according to Dr. Kaul.
Two previous large studies pegged the prevalence of paradoxical bronchospasm at around 4.5% in patients with COPD or asthma, but “it has not been reported or addressed in high-risk population, such as veterans who have high prevalence of obstructive lung diseases like COPD,” Dr. Kaul said.
Latest study results
Dr. Kaul described a retrospective analysis of 1,150 pre- and postbronchodilator spirometry tests conducted in patients with COPD or asthma at the Jesse Brown VA Medical Center between 2017 and 2020.
A positive paradoxical bronchodilator response was defined as a decrease of least 12% and 200 mL in forced expiratory volume in 1 second and forced vital capacity from baseline after four puffs of albuterol were inhaled, Dr. Kaul said.
Out of 18 reviewed spirometry results that met the criteria, none of the test results reported or recognized paradoxical bronchospasm, according to Dr. Kaul.
Those meeting the criteria were predominantly COPD patients, according to Dr. Kaul, who said 12 had an underlying diagnosis COPD, 4 had asthma, and 2 had COPD and asthma.
Of the 18 patients, 13 were African American, and all but 1 of the 18 patients had a current or past smoking history, according to reported data.
A history of obstructive sleep apnea was reported in nine patients, and history of gastroesophageal reflux disease was also reported in nine patients. Eleven patients had emphysema.
Greater awareness needed
Results of this study emphasize the need to recognize potential cases paradoxical bronchospasm in clinical practice, as well as a need for more research, according to Allen J. Blaivas, DO, FCCP, chair of the CHEST Airway Disorders NetWork.
“It’s something to be on the alert for, and certainly be aware that, if your patient is telling you that they feel worse, we shouldn’t just pooh-pooh it,” said Dr. Blaivas, who is medical director of the intensive care unit at the East Orange campus of the VA New Jersey Health Care System.
Further research could focus on breaking down whether patients with suspected paradoxical bronchospasm are using metered-dose inhalers or nebulizers, whether or not they are also taking inhaled corticosteroids, and whether prospective testing can confirm paradoxical bronchospasm in patients who report tightness after using a SABA, he said in an interview.
Dr. Kaul and coauthor Israel Rubinstein, MD had no relevant relationships to disclose. Dr. Blaivas had no relevant relationships to disclose.
FROM CHEST 2021
COPD: Higher mortality with low baseline CO diffusing capacity
Patients with a baseline DLCO (diffusing capacity for carbon monoxide) of < 60% of predicted have more severe disease clinical expression with higher mortality risk, according to a long-term observational study of Global Initiative for Obstructive Lung Disease (GOLD) I chronic obstructive pulmonary disease (COPD) patients. Clarifying mechanisms of low DLCO may help clinicians direct interventions toward ameliorating the low capacity, Juan Pablo de Torres, MD, and colleagues wrote in the journal CHEST®.
Defining increased risk
“Can a DLCO threshold help define an increased risk of death and a different clinical presentation in GOLD I patients?” the researchers questioned. For evaluation of COPD, the GOLD does not currently promote the use of DLCO, and the clinical and prognostic utility of a low DLCO has not been studied, the authors noted.
Several COPD studies, however, have shown associations between low DLCO values and reduced exercise capacity, increased symptoms, risk of severe exacerbations, and mortality. The patients included in these studies, however, have generally had moderate to severe airflow limitation, and have not had postbronchodilator forced expiratory volume in 1 second/forced vital capacity (FEV1/FVC) < 0.70 and an FEV1 ≥ 80%, defined by GOLD as COPD spirometric stage I. These mild obstruction GOLD I patients, in large epidemiological studies, do have increased risk of death. But it is often assumed, Dr. de Torres and colleagues noted, that “mild” suggests a good prognosis. They propose that a simple DLCO measurement could help identify those GOLD I patients with “worse overall COPD compromise and an increased risk of death.” Importantly, GOLD I represents the largest percentage of patients with airflow limitation that epidemiological studies have identified.
The researchers enrolled 360 GOLD stage I COPD patients, recording their age, sex, pack-years’ history, body mass index, dyspnea, lung function measurements, exercise capacity, BODE (body mass index, airflow obstruction, dyspnea, and exercise capacity) index, and history of exacerbations, and followed them for a mean of 109 months. They identified a cutoff DLCO value for all-cause mortality, compared the clinical and physiological characteristics of patients above and below the threshold, and explored the predictive power of that cutoff value.
All-cause mortality difference
The mean age in the overall population studied was 63 years (31% were women), with 43% active smokers, and pack-years history of 45. Overall mortality was 11% during the follow-up period. The predominantly male population was mildly overweight, had few comorbidities, normal FEV1 values, mild dyspnea, normal 6-minute walk distance, and very few exacerbations.
Analysis showed a DLCO cutoff value of < 60% was associated with a significant all-cause mortality differential (DLCO ≥ 60%: 9% vs. DLCO < 60%: 23%, P = .01). At a same FEV1% predicted and Charlson score, patients with DLCO < 60% had lower BMI, more dyspnea, lower inspiratory capacity (IC)/total lung capacity (TLC) ratio, lower 6-minute walk distance, and higher BODE index. Adjusted Cox multiple regression analysis confirmed that a DLCO < 60% was associated with an all-cause mortality hazard ratio [HR] of 3.37, (95% confidence interval, 1.35-8.39; P = .009).
Multiorgan loss of tissue
The researchers found that patients with baseline DLCO < 60% were more likely to be women (46% versus 28%), and to have a lower BMI (25 vs. 27), higher pack-year history (54 vs. 43), the same spirometric values but lower IC/TLC ratio (.37 vs. .40), a lower walk distance (443 vs. 485 meters), higher dyspnea (MRC score 1.1 vs. .7), similar exacerbation rate, higher BODE index (.5 vs. .2) and higher mortality than patients with higher DLCO % predicted values. This group, Dr. de Torres and colleagues suggest, represents a multiorgan loss of tissue, a phenotype associated with worse clinical outcomes and prognosis.
“Low DLCO in these patients,” Dr. de Torres said in an interview, “could mainly be secondary to coexistent emphysema, which is the most common cause of low DLCO in this population. Also possible, but less likely, is coexistent pulmonary hypertension.” He noted further that “This study opens the door to research specifically testing if such is the case, and if it is, for clinicians to use available therapies to prevent adverse outcomes.”
Comorbidity burden
Patients with GOLD I COPD die more often of cardiovascular disease instead of underlying lung disease, according to Richard H. Zou, MD, and Jessica Bon, MD, of the University of Pittsburgh, in an accompanying editorial in the journal CHEST.
Increased mortality rates, they suggest, may be related to higher comorbidity burden, particularly comorbidities associated with cardiovascular-related health. Subclinical cardiovascular disease is a common comorbidity in COPD, and concomitant endothelial dysfunction has been associated with both cardiovascular disease and early emphysema in smokers. They may have disproportionately reduced DLCO levels because of parenchymal destruction.
“This study suggests that DLCO can be used to identify patients with GOLD I COPD at increased death risk and that individuals with mild airflow obstruction with DLCO <60% predicted are a clinical phenotype distinct from those with higher DLCO levels,” Dr. Zhou and Dr. Bon concluded.
The researchers and the editorialists declared that they had no disclosures. One of the three cohorts assessed in the current study (CHAIN cohort in Spain) received funding from AstraZeneca.
Patients with a baseline DLCO (diffusing capacity for carbon monoxide) of < 60% of predicted have more severe disease clinical expression with higher mortality risk, according to a long-term observational study of Global Initiative for Obstructive Lung Disease (GOLD) I chronic obstructive pulmonary disease (COPD) patients. Clarifying mechanisms of low DLCO may help clinicians direct interventions toward ameliorating the low capacity, Juan Pablo de Torres, MD, and colleagues wrote in the journal CHEST®.
Defining increased risk
“Can a DLCO threshold help define an increased risk of death and a different clinical presentation in GOLD I patients?” the researchers questioned. For evaluation of COPD, the GOLD does not currently promote the use of DLCO, and the clinical and prognostic utility of a low DLCO has not been studied, the authors noted.
Several COPD studies, however, have shown associations between low DLCO values and reduced exercise capacity, increased symptoms, risk of severe exacerbations, and mortality. The patients included in these studies, however, have generally had moderate to severe airflow limitation, and have not had postbronchodilator forced expiratory volume in 1 second/forced vital capacity (FEV1/FVC) < 0.70 and an FEV1 ≥ 80%, defined by GOLD as COPD spirometric stage I. These mild obstruction GOLD I patients, in large epidemiological studies, do have increased risk of death. But it is often assumed, Dr. de Torres and colleagues noted, that “mild” suggests a good prognosis. They propose that a simple DLCO measurement could help identify those GOLD I patients with “worse overall COPD compromise and an increased risk of death.” Importantly, GOLD I represents the largest percentage of patients with airflow limitation that epidemiological studies have identified.
The researchers enrolled 360 GOLD stage I COPD patients, recording their age, sex, pack-years’ history, body mass index, dyspnea, lung function measurements, exercise capacity, BODE (body mass index, airflow obstruction, dyspnea, and exercise capacity) index, and history of exacerbations, and followed them for a mean of 109 months. They identified a cutoff DLCO value for all-cause mortality, compared the clinical and physiological characteristics of patients above and below the threshold, and explored the predictive power of that cutoff value.
All-cause mortality difference
The mean age in the overall population studied was 63 years (31% were women), with 43% active smokers, and pack-years history of 45. Overall mortality was 11% during the follow-up period. The predominantly male population was mildly overweight, had few comorbidities, normal FEV1 values, mild dyspnea, normal 6-minute walk distance, and very few exacerbations.
Analysis showed a DLCO cutoff value of < 60% was associated with a significant all-cause mortality differential (DLCO ≥ 60%: 9% vs. DLCO < 60%: 23%, P = .01). At a same FEV1% predicted and Charlson score, patients with DLCO < 60% had lower BMI, more dyspnea, lower inspiratory capacity (IC)/total lung capacity (TLC) ratio, lower 6-minute walk distance, and higher BODE index. Adjusted Cox multiple regression analysis confirmed that a DLCO < 60% was associated with an all-cause mortality hazard ratio [HR] of 3.37, (95% confidence interval, 1.35-8.39; P = .009).
Multiorgan loss of tissue
The researchers found that patients with baseline DLCO < 60% were more likely to be women (46% versus 28%), and to have a lower BMI (25 vs. 27), higher pack-year history (54 vs. 43), the same spirometric values but lower IC/TLC ratio (.37 vs. .40), a lower walk distance (443 vs. 485 meters), higher dyspnea (MRC score 1.1 vs. .7), similar exacerbation rate, higher BODE index (.5 vs. .2) and higher mortality than patients with higher DLCO % predicted values. This group, Dr. de Torres and colleagues suggest, represents a multiorgan loss of tissue, a phenotype associated with worse clinical outcomes and prognosis.
“Low DLCO in these patients,” Dr. de Torres said in an interview, “could mainly be secondary to coexistent emphysema, which is the most common cause of low DLCO in this population. Also possible, but less likely, is coexistent pulmonary hypertension.” He noted further that “This study opens the door to research specifically testing if such is the case, and if it is, for clinicians to use available therapies to prevent adverse outcomes.”
Comorbidity burden
Patients with GOLD I COPD die more often of cardiovascular disease instead of underlying lung disease, according to Richard H. Zou, MD, and Jessica Bon, MD, of the University of Pittsburgh, in an accompanying editorial in the journal CHEST.
Increased mortality rates, they suggest, may be related to higher comorbidity burden, particularly comorbidities associated with cardiovascular-related health. Subclinical cardiovascular disease is a common comorbidity in COPD, and concomitant endothelial dysfunction has been associated with both cardiovascular disease and early emphysema in smokers. They may have disproportionately reduced DLCO levels because of parenchymal destruction.
“This study suggests that DLCO can be used to identify patients with GOLD I COPD at increased death risk and that individuals with mild airflow obstruction with DLCO <60% predicted are a clinical phenotype distinct from those with higher DLCO levels,” Dr. Zhou and Dr. Bon concluded.
The researchers and the editorialists declared that they had no disclosures. One of the three cohorts assessed in the current study (CHAIN cohort in Spain) received funding from AstraZeneca.
Patients with a baseline DLCO (diffusing capacity for carbon monoxide) of < 60% of predicted have more severe disease clinical expression with higher mortality risk, according to a long-term observational study of Global Initiative for Obstructive Lung Disease (GOLD) I chronic obstructive pulmonary disease (COPD) patients. Clarifying mechanisms of low DLCO may help clinicians direct interventions toward ameliorating the low capacity, Juan Pablo de Torres, MD, and colleagues wrote in the journal CHEST®.
Defining increased risk
“Can a DLCO threshold help define an increased risk of death and a different clinical presentation in GOLD I patients?” the researchers questioned. For evaluation of COPD, the GOLD does not currently promote the use of DLCO, and the clinical and prognostic utility of a low DLCO has not been studied, the authors noted.
Several COPD studies, however, have shown associations between low DLCO values and reduced exercise capacity, increased symptoms, risk of severe exacerbations, and mortality. The patients included in these studies, however, have generally had moderate to severe airflow limitation, and have not had postbronchodilator forced expiratory volume in 1 second/forced vital capacity (FEV1/FVC) < 0.70 and an FEV1 ≥ 80%, defined by GOLD as COPD spirometric stage I. These mild obstruction GOLD I patients, in large epidemiological studies, do have increased risk of death. But it is often assumed, Dr. de Torres and colleagues noted, that “mild” suggests a good prognosis. They propose that a simple DLCO measurement could help identify those GOLD I patients with “worse overall COPD compromise and an increased risk of death.” Importantly, GOLD I represents the largest percentage of patients with airflow limitation that epidemiological studies have identified.
The researchers enrolled 360 GOLD stage I COPD patients, recording their age, sex, pack-years’ history, body mass index, dyspnea, lung function measurements, exercise capacity, BODE (body mass index, airflow obstruction, dyspnea, and exercise capacity) index, and history of exacerbations, and followed them for a mean of 109 months. They identified a cutoff DLCO value for all-cause mortality, compared the clinical and physiological characteristics of patients above and below the threshold, and explored the predictive power of that cutoff value.
All-cause mortality difference
The mean age in the overall population studied was 63 years (31% were women), with 43% active smokers, and pack-years history of 45. Overall mortality was 11% during the follow-up period. The predominantly male population was mildly overweight, had few comorbidities, normal FEV1 values, mild dyspnea, normal 6-minute walk distance, and very few exacerbations.
Analysis showed a DLCO cutoff value of < 60% was associated with a significant all-cause mortality differential (DLCO ≥ 60%: 9% vs. DLCO < 60%: 23%, P = .01). At a same FEV1% predicted and Charlson score, patients with DLCO < 60% had lower BMI, more dyspnea, lower inspiratory capacity (IC)/total lung capacity (TLC) ratio, lower 6-minute walk distance, and higher BODE index. Adjusted Cox multiple regression analysis confirmed that a DLCO < 60% was associated with an all-cause mortality hazard ratio [HR] of 3.37, (95% confidence interval, 1.35-8.39; P = .009).
Multiorgan loss of tissue
The researchers found that patients with baseline DLCO < 60% were more likely to be women (46% versus 28%), and to have a lower BMI (25 vs. 27), higher pack-year history (54 vs. 43), the same spirometric values but lower IC/TLC ratio (.37 vs. .40), a lower walk distance (443 vs. 485 meters), higher dyspnea (MRC score 1.1 vs. .7), similar exacerbation rate, higher BODE index (.5 vs. .2) and higher mortality than patients with higher DLCO % predicted values. This group, Dr. de Torres and colleagues suggest, represents a multiorgan loss of tissue, a phenotype associated with worse clinical outcomes and prognosis.
“Low DLCO in these patients,” Dr. de Torres said in an interview, “could mainly be secondary to coexistent emphysema, which is the most common cause of low DLCO in this population. Also possible, but less likely, is coexistent pulmonary hypertension.” He noted further that “This study opens the door to research specifically testing if such is the case, and if it is, for clinicians to use available therapies to prevent adverse outcomes.”
Comorbidity burden
Patients with GOLD I COPD die more often of cardiovascular disease instead of underlying lung disease, according to Richard H. Zou, MD, and Jessica Bon, MD, of the University of Pittsburgh, in an accompanying editorial in the journal CHEST.
Increased mortality rates, they suggest, may be related to higher comorbidity burden, particularly comorbidities associated with cardiovascular-related health. Subclinical cardiovascular disease is a common comorbidity in COPD, and concomitant endothelial dysfunction has been associated with both cardiovascular disease and early emphysema in smokers. They may have disproportionately reduced DLCO levels because of parenchymal destruction.
“This study suggests that DLCO can be used to identify patients with GOLD I COPD at increased death risk and that individuals with mild airflow obstruction with DLCO <60% predicted are a clinical phenotype distinct from those with higher DLCO levels,” Dr. Zhou and Dr. Bon concluded.
The researchers and the editorialists declared that they had no disclosures. One of the three cohorts assessed in the current study (CHAIN cohort in Spain) received funding from AstraZeneca.
FROM THE JOURNAL CHEST®
Earliest 9/11 responders have higher COPD rates
The earliest responders to reach the site of the destroyed twin towers of the World Trade Center on Sept. 11, 2001, are at highest risk for chronic obstructive pulmonary disease and asthma/COPD overlap (ACO) among all those who worked at the site. The 9/11 attack was the deadliest terrorist attack on American soil.
The findings come from a case-control study that included nearly 18,000 emergency responders and volunteers. The investigators found that those who arrived at the site within 48 hours had an approximately 30% higher risk of developing COPD than those who arrived later, after adjustment for smoking and obesity, reported Rafael E de la Hoz, MD, a professor of environmental medicine, public health, and medicine at Mount Sinai Medical Center, New York, and colleagues.
“In this largest World Trade Center occupational cohort, spirometrically defined COPD and ACO were both modestly but significantly associated with World Trade Center exposure intensity, but the association seemed driven by the overlap,” he said in a narrated poster presentation during the European Respiratory Society 2021 International Congress.
“Around the world, we rely on our emergency workers to help when disasters occur,” commented Arzu Yorgancıoğlu, MD, professor and head of the department of pulmonology at Celal Bayar University, Manisa, Turkey, who was not involved in the study.
“This study shows how important it is to keep monitoring the health of workers, like those who attended the World Trade Center site 20 years ago, as occupational exposure to pollutants can lead to COPD. What we can learn from research like this is not only how best to care for emergency workers who operate in dangerous conditions but also how we can protect them in their work in the future,” she said.
Inconsistent findings
Fire and police personnel, emergency medical workers, construction workers, and others who labored amid the lingering pall of toxic dust and smoke at the World Trade Center site have developed asthma and other lower respiratory tract diseases over the ensuing decades.
“As the occupational cohorts age, there are concerns about chronic, longer latency, and disabling respiratory disease,” Dr. de la Hoz and colleagues wrote.
There have been inconsistent reports about the potential associations between COPD and ACO and the intensity of occupational exposure at the World Trade Center site. This prompted the investigators to further explore these associations using spirometry-defined disease.
They assessed data on 17,996 former World Trade Center site workers who had undergone at least two good-quality spirometric evaluations from 2002 to 2018.
To be classified as having COPD, workers had to have fixed airway obstruction. Those in the ACO subgroup were also required to have prebronchodilator obstruction with forced expiratory volume in 1 second of more than 400 mL in response to bronchodilation.
The patients were matched for sex and height within 5 cm using a 1:4 nested case-control design. Missing data were imputed.
Earliest arrivals paid the highest penalty
Of the total cohort, 85.4% were men, and 85.6% were overweight or obese. A total of 586 workers (3.3%) met the case definition for having COPD; 258 (1.4%) met the definition for having ACO.
The investigators found that the prevalence of self-reported ACO was six times higher than the prevalence of spirometry-confirmed disease. Among those who reported an onset date, 56.7% reported having asthma before COPD; the remainder reported having COPD first.
In analyses adjusted for age, sex, cohort entry period, smoking status, body mass index, metabolic syndrome parameters, and eosinophil levels, both COPD and ACO were significantly associated with early arrival at the World Trade Center site, with an adjusted odds ratio for COPD of 1.3 (95% confidence interval, 1.03-1.64), and an OR for ACO of 1.66 (95% CI, 1.1-2.49).
There was no significant interaction between early site arrival and smoking status.
The association between early exposure and COPD was no longer significant when those with ACO were excluded, the authors noted.
“We also observed that COPD more often followed asthma in these workers than the reverse, suggesting that asthma may have been on the path to COPD in most workers affected by the inhaled toxicants at the disaster site,” Dr. de la Hoz and colleagues wrote.
In addition, “our data suggest that self-reported physician diagnoses of COPD, asthma, and ACO are poorly correlated with objective data in this cohort,” they concluded.
The study was supported by the Centers for Disease Control and Prevention and the National Institute for Occupational Safety and Health. The authors and Dr. Yorgancıoğlu disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The earliest responders to reach the site of the destroyed twin towers of the World Trade Center on Sept. 11, 2001, are at highest risk for chronic obstructive pulmonary disease and asthma/COPD overlap (ACO) among all those who worked at the site. The 9/11 attack was the deadliest terrorist attack on American soil.
The findings come from a case-control study that included nearly 18,000 emergency responders and volunteers. The investigators found that those who arrived at the site within 48 hours had an approximately 30% higher risk of developing COPD than those who arrived later, after adjustment for smoking and obesity, reported Rafael E de la Hoz, MD, a professor of environmental medicine, public health, and medicine at Mount Sinai Medical Center, New York, and colleagues.
“In this largest World Trade Center occupational cohort, spirometrically defined COPD and ACO were both modestly but significantly associated with World Trade Center exposure intensity, but the association seemed driven by the overlap,” he said in a narrated poster presentation during the European Respiratory Society 2021 International Congress.
“Around the world, we rely on our emergency workers to help when disasters occur,” commented Arzu Yorgancıoğlu, MD, professor and head of the department of pulmonology at Celal Bayar University, Manisa, Turkey, who was not involved in the study.
“This study shows how important it is to keep monitoring the health of workers, like those who attended the World Trade Center site 20 years ago, as occupational exposure to pollutants can lead to COPD. What we can learn from research like this is not only how best to care for emergency workers who operate in dangerous conditions but also how we can protect them in their work in the future,” she said.
Inconsistent findings
Fire and police personnel, emergency medical workers, construction workers, and others who labored amid the lingering pall of toxic dust and smoke at the World Trade Center site have developed asthma and other lower respiratory tract diseases over the ensuing decades.
“As the occupational cohorts age, there are concerns about chronic, longer latency, and disabling respiratory disease,” Dr. de la Hoz and colleagues wrote.
There have been inconsistent reports about the potential associations between COPD and ACO and the intensity of occupational exposure at the World Trade Center site. This prompted the investigators to further explore these associations using spirometry-defined disease.
They assessed data on 17,996 former World Trade Center site workers who had undergone at least two good-quality spirometric evaluations from 2002 to 2018.
To be classified as having COPD, workers had to have fixed airway obstruction. Those in the ACO subgroup were also required to have prebronchodilator obstruction with forced expiratory volume in 1 second of more than 400 mL in response to bronchodilation.
The patients were matched for sex and height within 5 cm using a 1:4 nested case-control design. Missing data were imputed.
Earliest arrivals paid the highest penalty
Of the total cohort, 85.4% were men, and 85.6% were overweight or obese. A total of 586 workers (3.3%) met the case definition for having COPD; 258 (1.4%) met the definition for having ACO.
The investigators found that the prevalence of self-reported ACO was six times higher than the prevalence of spirometry-confirmed disease. Among those who reported an onset date, 56.7% reported having asthma before COPD; the remainder reported having COPD first.
In analyses adjusted for age, sex, cohort entry period, smoking status, body mass index, metabolic syndrome parameters, and eosinophil levels, both COPD and ACO were significantly associated with early arrival at the World Trade Center site, with an adjusted odds ratio for COPD of 1.3 (95% confidence interval, 1.03-1.64), and an OR for ACO of 1.66 (95% CI, 1.1-2.49).
There was no significant interaction between early site arrival and smoking status.
The association between early exposure and COPD was no longer significant when those with ACO were excluded, the authors noted.
“We also observed that COPD more often followed asthma in these workers than the reverse, suggesting that asthma may have been on the path to COPD in most workers affected by the inhaled toxicants at the disaster site,” Dr. de la Hoz and colleagues wrote.
In addition, “our data suggest that self-reported physician diagnoses of COPD, asthma, and ACO are poorly correlated with objective data in this cohort,” they concluded.
The study was supported by the Centers for Disease Control and Prevention and the National Institute for Occupational Safety and Health. The authors and Dr. Yorgancıoğlu disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
The earliest responders to reach the site of the destroyed twin towers of the World Trade Center on Sept. 11, 2001, are at highest risk for chronic obstructive pulmonary disease and asthma/COPD overlap (ACO) among all those who worked at the site. The 9/11 attack was the deadliest terrorist attack on American soil.
The findings come from a case-control study that included nearly 18,000 emergency responders and volunteers. The investigators found that those who arrived at the site within 48 hours had an approximately 30% higher risk of developing COPD than those who arrived later, after adjustment for smoking and obesity, reported Rafael E de la Hoz, MD, a professor of environmental medicine, public health, and medicine at Mount Sinai Medical Center, New York, and colleagues.
“In this largest World Trade Center occupational cohort, spirometrically defined COPD and ACO were both modestly but significantly associated with World Trade Center exposure intensity, but the association seemed driven by the overlap,” he said in a narrated poster presentation during the European Respiratory Society 2021 International Congress.
“Around the world, we rely on our emergency workers to help when disasters occur,” commented Arzu Yorgancıoğlu, MD, professor and head of the department of pulmonology at Celal Bayar University, Manisa, Turkey, who was not involved in the study.
“This study shows how important it is to keep monitoring the health of workers, like those who attended the World Trade Center site 20 years ago, as occupational exposure to pollutants can lead to COPD. What we can learn from research like this is not only how best to care for emergency workers who operate in dangerous conditions but also how we can protect them in their work in the future,” she said.
Inconsistent findings
Fire and police personnel, emergency medical workers, construction workers, and others who labored amid the lingering pall of toxic dust and smoke at the World Trade Center site have developed asthma and other lower respiratory tract diseases over the ensuing decades.
“As the occupational cohorts age, there are concerns about chronic, longer latency, and disabling respiratory disease,” Dr. de la Hoz and colleagues wrote.
There have been inconsistent reports about the potential associations between COPD and ACO and the intensity of occupational exposure at the World Trade Center site. This prompted the investigators to further explore these associations using spirometry-defined disease.
They assessed data on 17,996 former World Trade Center site workers who had undergone at least two good-quality spirometric evaluations from 2002 to 2018.
To be classified as having COPD, workers had to have fixed airway obstruction. Those in the ACO subgroup were also required to have prebronchodilator obstruction with forced expiratory volume in 1 second of more than 400 mL in response to bronchodilation.
The patients were matched for sex and height within 5 cm using a 1:4 nested case-control design. Missing data were imputed.
Earliest arrivals paid the highest penalty
Of the total cohort, 85.4% were men, and 85.6% were overweight or obese. A total of 586 workers (3.3%) met the case definition for having COPD; 258 (1.4%) met the definition for having ACO.
The investigators found that the prevalence of self-reported ACO was six times higher than the prevalence of spirometry-confirmed disease. Among those who reported an onset date, 56.7% reported having asthma before COPD; the remainder reported having COPD first.
In analyses adjusted for age, sex, cohort entry period, smoking status, body mass index, metabolic syndrome parameters, and eosinophil levels, both COPD and ACO were significantly associated with early arrival at the World Trade Center site, with an adjusted odds ratio for COPD of 1.3 (95% confidence interval, 1.03-1.64), and an OR for ACO of 1.66 (95% CI, 1.1-2.49).
There was no significant interaction between early site arrival and smoking status.
The association between early exposure and COPD was no longer significant when those with ACO were excluded, the authors noted.
“We also observed that COPD more often followed asthma in these workers than the reverse, suggesting that asthma may have been on the path to COPD in most workers affected by the inhaled toxicants at the disaster site,” Dr. de la Hoz and colleagues wrote.
In addition, “our data suggest that self-reported physician diagnoses of COPD, asthma, and ACO are poorly correlated with objective data in this cohort,” they concluded.
The study was supported by the Centers for Disease Control and Prevention and the National Institute for Occupational Safety and Health. The authors and Dr. Yorgancıoğlu disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Should magnesium be used for COPD exacerbations?
Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are a major driver of disease-related morbidity. Their prevention and treatment are a focus of COPD management. Antibiotics, corticosteroids, and nebulized bronchodilators are all given to patients with AECOPD, and while the supporting data aren’t perfect, there’s little debate surrounding their use. These medications are well known to most physicians; we’re comfortable with their efficacy and aware of their side effects. They are nothing if not familiar.
What about magnesium (Mg), though? Apparently, in the emergency room (ER) it is part of the standard AECOPD cocktail. I would argue that Mg is familiar to most too; every internal medicine trainee in the United States is taught to infuse 2 g of Mg intravenously for any inpatient (ICU or otherwise) with a serum level <2.0 mg/dL. In fact, “electrolyte protocols” are part of the order sets at most hospitals where I’ve worked. Mg is infused reflexively when it drops below certain levels.
I’m less familiar with using Mg in the setting of an AECOPD, though. A recent online post by an academic ER physician (Richard Pescatore, DO) urged caution in this setting. He argues that too many in the ER are embracing the “Dutch Hypothesis” and treating asthma and COPD as the same disease. Dr. Pescatore believes that Mg works for asthma exacerbations because asthma is a disease of smooth muscle and large airways, while COPD is not. COPD, he says, is a disease of the small airways, largely resulting from parenchymal distortions due to emphysema. Therefore, Mg, which is thought to act on the smooth muscle surrounding the large airways, won’t be beneficial for AECOPD and may even cause harm.
Data are lacking
What data exist for using Mg for AECOPD? The best randomized controlled trial (RCT) I could find was published in 1995 and is cited in the reader’s rebuttal. The trial found a significant improvement in peak expiratory flow rate (PEFR) with Mg and a nonsignificant reduction in hospitalizations.
A poorly done systematic review of RCTs using Mg for AECOPD was published in 2014, and in 2020 the Agency for Healthcare Research and Quality (AHRQ) included Mg in its well-executed meta-analysis of pharmacologic treatments for AECOPD. Data across the four to five Mg RCTs included in each of the reviews (study inclusion criteria were slightly different) could not be combined. All RCTs were small, and only soft outcomes like PEFR and forced expiratory volume in 1 second (FEV1) seemed to improve with Mg. No adverse events were noted, but this should be interpreted with caution given that many studies did not report on adverse events at all.
A small RCT published this year (after both systematic reviews were completed) showed that using intravenous magnesium sulfate had no significant effect on FEV1, vital signs, or symptoms.
In summary, the data aren’t great. Mg doesn’t show up at all as a treatment option in the Global Initiative for Chronic Obstructive Lung Disease (GOLD) Report on COPD, and the authors of the AHRQ review concluded that large, high-quality RCTs are needed to assess the impact of Mg in AECOPD. Although I didn’t do an extensive review of Mg for asthma exacerbations, it’s not clear that the data here are much better. Mg gets an honorable mention (add for severe exacerbations when there’s inadequate response to standard treatments) in both the 2007 National Heart, Lung, and Blood Institute (NHLBI) guideline and the 2019 Global Initiative for Asthma (GINA) guide. The 2020 update to the 2007 NHLBI guideline is more targeted in its review and does not cover Mg as a treatment option. On the basis of my anecdotal clinical experience and on networking with airway experts, I do think Mg is used more often for asthma than for AECOPD.
Final thoughts on using Mg for AECOPD
All that being said, is it reasonable to use Mg for AECOPD? I think so. I’d stick to using it for severe cases where conventional treatments have failed, just like the NHLBI and GINA advise for asthma. I’d also limit it to 2-3 g, which is the dosing range employed by several of the existing AECOPD RCTs. The assertion that Mg may be harmful in AECOPD because COPD affects the small airways, and asthma does not, is misguided. Both affect the small airways. Furthermore, none of our inhaled therapies reach the small airways, so one can’t argue against using Mg because it only targets larger airways without abandoning albuterol and ipratropium as well. I don’t think anyone would advise that. Given what we now know about asthma and COPD phenotypes and asthma-COPD overlap, I’d caution against pedantic theories about response to therapies.
Aaron B. Holley, MD, is an associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center. He has received research grants from Fisher-Paykel and has received payments from the American College of Chest Physicians.
A version of this article first appeared on Medscape.com.
Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are a major driver of disease-related morbidity. Their prevention and treatment are a focus of COPD management. Antibiotics, corticosteroids, and nebulized bronchodilators are all given to patients with AECOPD, and while the supporting data aren’t perfect, there’s little debate surrounding their use. These medications are well known to most physicians; we’re comfortable with their efficacy and aware of their side effects. They are nothing if not familiar.
What about magnesium (Mg), though? Apparently, in the emergency room (ER) it is part of the standard AECOPD cocktail. I would argue that Mg is familiar to most too; every internal medicine trainee in the United States is taught to infuse 2 g of Mg intravenously for any inpatient (ICU or otherwise) with a serum level <2.0 mg/dL. In fact, “electrolyte protocols” are part of the order sets at most hospitals where I’ve worked. Mg is infused reflexively when it drops below certain levels.
I’m less familiar with using Mg in the setting of an AECOPD, though. A recent online post by an academic ER physician (Richard Pescatore, DO) urged caution in this setting. He argues that too many in the ER are embracing the “Dutch Hypothesis” and treating asthma and COPD as the same disease. Dr. Pescatore believes that Mg works for asthma exacerbations because asthma is a disease of smooth muscle and large airways, while COPD is not. COPD, he says, is a disease of the small airways, largely resulting from parenchymal distortions due to emphysema. Therefore, Mg, which is thought to act on the smooth muscle surrounding the large airways, won’t be beneficial for AECOPD and may even cause harm.
Data are lacking
What data exist for using Mg for AECOPD? The best randomized controlled trial (RCT) I could find was published in 1995 and is cited in the reader’s rebuttal. The trial found a significant improvement in peak expiratory flow rate (PEFR) with Mg and a nonsignificant reduction in hospitalizations.
A poorly done systematic review of RCTs using Mg for AECOPD was published in 2014, and in 2020 the Agency for Healthcare Research and Quality (AHRQ) included Mg in its well-executed meta-analysis of pharmacologic treatments for AECOPD. Data across the four to five Mg RCTs included in each of the reviews (study inclusion criteria were slightly different) could not be combined. All RCTs were small, and only soft outcomes like PEFR and forced expiratory volume in 1 second (FEV1) seemed to improve with Mg. No adverse events were noted, but this should be interpreted with caution given that many studies did not report on adverse events at all.
A small RCT published this year (after both systematic reviews were completed) showed that using intravenous magnesium sulfate had no significant effect on FEV1, vital signs, or symptoms.
In summary, the data aren’t great. Mg doesn’t show up at all as a treatment option in the Global Initiative for Chronic Obstructive Lung Disease (GOLD) Report on COPD, and the authors of the AHRQ review concluded that large, high-quality RCTs are needed to assess the impact of Mg in AECOPD. Although I didn’t do an extensive review of Mg for asthma exacerbations, it’s not clear that the data here are much better. Mg gets an honorable mention (add for severe exacerbations when there’s inadequate response to standard treatments) in both the 2007 National Heart, Lung, and Blood Institute (NHLBI) guideline and the 2019 Global Initiative for Asthma (GINA) guide. The 2020 update to the 2007 NHLBI guideline is more targeted in its review and does not cover Mg as a treatment option. On the basis of my anecdotal clinical experience and on networking with airway experts, I do think Mg is used more often for asthma than for AECOPD.
Final thoughts on using Mg for AECOPD
All that being said, is it reasonable to use Mg for AECOPD? I think so. I’d stick to using it for severe cases where conventional treatments have failed, just like the NHLBI and GINA advise for asthma. I’d also limit it to 2-3 g, which is the dosing range employed by several of the existing AECOPD RCTs. The assertion that Mg may be harmful in AECOPD because COPD affects the small airways, and asthma does not, is misguided. Both affect the small airways. Furthermore, none of our inhaled therapies reach the small airways, so one can’t argue against using Mg because it only targets larger airways without abandoning albuterol and ipratropium as well. I don’t think anyone would advise that. Given what we now know about asthma and COPD phenotypes and asthma-COPD overlap, I’d caution against pedantic theories about response to therapies.
Aaron B. Holley, MD, is an associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center. He has received research grants from Fisher-Paykel and has received payments from the American College of Chest Physicians.
A version of this article first appeared on Medscape.com.
Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are a major driver of disease-related morbidity. Their prevention and treatment are a focus of COPD management. Antibiotics, corticosteroids, and nebulized bronchodilators are all given to patients with AECOPD, and while the supporting data aren’t perfect, there’s little debate surrounding their use. These medications are well known to most physicians; we’re comfortable with their efficacy and aware of their side effects. They are nothing if not familiar.
What about magnesium (Mg), though? Apparently, in the emergency room (ER) it is part of the standard AECOPD cocktail. I would argue that Mg is familiar to most too; every internal medicine trainee in the United States is taught to infuse 2 g of Mg intravenously for any inpatient (ICU or otherwise) with a serum level <2.0 mg/dL. In fact, “electrolyte protocols” are part of the order sets at most hospitals where I’ve worked. Mg is infused reflexively when it drops below certain levels.
I’m less familiar with using Mg in the setting of an AECOPD, though. A recent online post by an academic ER physician (Richard Pescatore, DO) urged caution in this setting. He argues that too many in the ER are embracing the “Dutch Hypothesis” and treating asthma and COPD as the same disease. Dr. Pescatore believes that Mg works for asthma exacerbations because asthma is a disease of smooth muscle and large airways, while COPD is not. COPD, he says, is a disease of the small airways, largely resulting from parenchymal distortions due to emphysema. Therefore, Mg, which is thought to act on the smooth muscle surrounding the large airways, won’t be beneficial for AECOPD and may even cause harm.
Data are lacking
What data exist for using Mg for AECOPD? The best randomized controlled trial (RCT) I could find was published in 1995 and is cited in the reader’s rebuttal. The trial found a significant improvement in peak expiratory flow rate (PEFR) with Mg and a nonsignificant reduction in hospitalizations.
A poorly done systematic review of RCTs using Mg for AECOPD was published in 2014, and in 2020 the Agency for Healthcare Research and Quality (AHRQ) included Mg in its well-executed meta-analysis of pharmacologic treatments for AECOPD. Data across the four to five Mg RCTs included in each of the reviews (study inclusion criteria were slightly different) could not be combined. All RCTs were small, and only soft outcomes like PEFR and forced expiratory volume in 1 second (FEV1) seemed to improve with Mg. No adverse events were noted, but this should be interpreted with caution given that many studies did not report on adverse events at all.
A small RCT published this year (after both systematic reviews were completed) showed that using intravenous magnesium sulfate had no significant effect on FEV1, vital signs, or symptoms.
In summary, the data aren’t great. Mg doesn’t show up at all as a treatment option in the Global Initiative for Chronic Obstructive Lung Disease (GOLD) Report on COPD, and the authors of the AHRQ review concluded that large, high-quality RCTs are needed to assess the impact of Mg in AECOPD. Although I didn’t do an extensive review of Mg for asthma exacerbations, it’s not clear that the data here are much better. Mg gets an honorable mention (add for severe exacerbations when there’s inadequate response to standard treatments) in both the 2007 National Heart, Lung, and Blood Institute (NHLBI) guideline and the 2019 Global Initiative for Asthma (GINA) guide. The 2020 update to the 2007 NHLBI guideline is more targeted in its review and does not cover Mg as a treatment option. On the basis of my anecdotal clinical experience and on networking with airway experts, I do think Mg is used more often for asthma than for AECOPD.
Final thoughts on using Mg for AECOPD
All that being said, is it reasonable to use Mg for AECOPD? I think so. I’d stick to using it for severe cases where conventional treatments have failed, just like the NHLBI and GINA advise for asthma. I’d also limit it to 2-3 g, which is the dosing range employed by several of the existing AECOPD RCTs. The assertion that Mg may be harmful in AECOPD because COPD affects the small airways, and asthma does not, is misguided. Both affect the small airways. Furthermore, none of our inhaled therapies reach the small airways, so one can’t argue against using Mg because it only targets larger airways without abandoning albuterol and ipratropium as well. I don’t think anyone would advise that. Given what we now know about asthma and COPD phenotypes and asthma-COPD overlap, I’d caution against pedantic theories about response to therapies.
Aaron B. Holley, MD, is an associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center. He has received research grants from Fisher-Paykel and has received payments from the American College of Chest Physicians.
A version of this article first appeared on Medscape.com.
Some patients with more severe PH in COPD may respond to treatment
Patients with pulmonary hypertension (PH) as a complication of chronic obstructive pulmonary disease (COPD) have worse functional impairment and higher mortality, compared with patients who have idiopathic pulmonary arterial hypertension (IPAH).
Despite these factors, some patients with more severe PH in COPD may respond to treatment and show clinical improvement after treatment, according to recent research published in the journal CHEST®.
Carmine Dario Vizza, MD, of the pulmonary hypertension unit, department of cardiovascular and respiratory diseases at Sapienza University of Rome, and colleagues evaluated patients in the Comparative, Prospective Registry of Newly Initiated Therapies for Pulmonary Hypertension (COMPERA) database, enrolled up to August 2020, identifying 68 patients with moderate PH and COPD and 307 patients with severe PH and COPD. The researchers compared the PH and COPD groups with 307 patients who had idiopathic pulmonary arterial hypertension.
Overall, mostly older men made up the group of patients with moderate (50%; mean, 68.5 years) and severe PH in COPD (61%; mean 68.4 years), compared with those who had IPAH (37%; mean 61.7 years. Oral monotherapy for patients with PH and COPD was the main treatment, consisting of phosphodiesterase-5 inhibitors, while most patients with IPAH received endothelin receptor antagonists.
On functional tests, patients in the PH and COPD group tended to perform poorer on the 6-minute walking distance (6MWD) and World Health Organization functional class (WHO FC) than patients with IPAH. Specifically, among 42.7% of patients in both group for whom follow-up data were available, there was a similar frequency of improvement for 6MWD of 30 meters or more from baseline for both PH and COPD and IPAH groups (46.9% vs. 52.6%; P = .294), but there were significant differences between 6MWD between patients with moderate and severe PH and COPD (51.6% vs. 31.6%; P = .04). There was a nonsignificant improvement in WHO FC improvement of one or more classes for 65.6% of patients with PH and COPD and 58.3% of patients with IPAH with follow-up data available, with 28.5% of patients with PH in COPD improving compared with 35.8% of patients with IPAH (P = .078) and nonsignificant differences between moderate and severe PH and COPD (19.0% vs. 30.4%; P = .188).
Comparing outcomes
Follow-up data were available for 84% of patients with IPAH and 94% of patients with PH and COPD. Dr. Dario Vizza and colleagues found 45.7% of patients in the PH and COPD group and 24.9% of patients in the IPAH group died during follow-up, while 1.1% in the PH and COPD group and 1.5% of patients in the IPAH group underwent lung transplantations. For patients with moderate PH and COPD, 31.3% died and none underwent lung transplantation, while 49.0% of patients in the severe PH and COPD group died and 1.4% underwent lung transplantations.
Patients in the moderate PH and COPD group were more likely to discontinue treatment (10.9%), compared with patients with IPAH (6.6%) and patients with severe PH and COPD (5.2%). The most common reasons for discontinuations were tolerability and efficacy failure; the IPAH group had 63% of patients discontinue because of tolerability and 7% for efficacy failure, 47% of patients in the severe PH and COPD group discontinued because of tolerability and efficacy, and 29% discontinued treatment for tolerability and 57% for efficacy failure in the moderate and COPD group.
The researchers said male sex, low 6MWD, and high pulmonary vascular resistance at baseline were predictive of poorer outcomes for PH and COPD, but patients with more severe PH and COPD had better outcomes if they improved by 30 meters or more in 6MWD, or improved in WHO FC after receiving medical therapy. For patients with IPAH response to therapy was better among patients who were younger, had higher WHO FC, had high diffusing capacity of the lung for carbon monoxide, had high mean pulmonary artery pressure, and had low PCO2.
“Our data suggest that PH-targeted drug therapy in patients with COPD and severe PH may improve exercise tolerance and WHO FC in a subgroup of patients and that patients with COPD and PH who respond to therapy may have a better prognosis than patients who do not show clinical improvement. These findings need to be explored further in prospective, randomized controlled clinical studies,” the authors concluded.
More research needed
In a related editorial, James R. Klinger, MD, a pulmonologist with Brown University, Providence, R.I., and the director of the Rhode Island Hospital Pulmonary Hypertension Center in East Providence, said there is a “keen interest” in treating PH in COPD despite a lack of consistency on whether treatment is effective in this patient population. About 80% of PH centers in the United States treat PH in COPD when they treat conditions like lung disease with PAH medication, he pointed out. However, he questioned whether current medications designed for PAH could improve pulmonary hemodynamics for PH in COPD.
“Reasons that the pathobiologic condition of PH-COPD may differ from PAH include the likely exposure of the pulmonary circulation to greater degrees of hypoxia and hypercapnia and the greater loss of alveolar capillaries associated with emphysema,” he said.
The study by Dr. Dario Vizza and colleagues is an attempt to evaluate treatment response for patients with PH and COPD “in a way that allows comparison with patients who have been treated with similar drugs for PAH,” Dr. Klinger said. He noted the study’s retrospective nature, lack of control group, and lack of information on lung disease severity could limit the findings.
“These limitations preclude recommendations for the routine treatment of patients with PH-COPD, but the findings suggest that, despite greater morbidity at baseline, patients with PH-COPD may be nearly as likely to benefit from PAH medications as patients with IPAH,” he said.
“What is needed now is well-designed randomized controlled studies to determine whether improved outcomes can be achieved in this population and which patients are most likely to benefit,” he concluded. “Simply put: How bad does PH need to be in patients with COPD before treatment is helpful, and how severe does COPD need to be before PH treatment is futile?”
The authors reported personal and institutional relationships in the form of grants, consultancies, advisory board memberships, speakers bureau appointments, honoraria, patents, grant and research funding, lectures, travel compensation, and steering committee positions for a variety of pharmaceutical companies, agencies, societies, journals, medical publishing companies, and other organizations. Dr. Klinger reported his institution receives grant support from Acceleron and United Therapeutics in the area of PH, and he has been an unpaid consultant for Bayer.
Patients with pulmonary hypertension (PH) as a complication of chronic obstructive pulmonary disease (COPD) have worse functional impairment and higher mortality, compared with patients who have idiopathic pulmonary arterial hypertension (IPAH).
Despite these factors, some patients with more severe PH in COPD may respond to treatment and show clinical improvement after treatment, according to recent research published in the journal CHEST®.
Carmine Dario Vizza, MD, of the pulmonary hypertension unit, department of cardiovascular and respiratory diseases at Sapienza University of Rome, and colleagues evaluated patients in the Comparative, Prospective Registry of Newly Initiated Therapies for Pulmonary Hypertension (COMPERA) database, enrolled up to August 2020, identifying 68 patients with moderate PH and COPD and 307 patients with severe PH and COPD. The researchers compared the PH and COPD groups with 307 patients who had idiopathic pulmonary arterial hypertension.
Overall, mostly older men made up the group of patients with moderate (50%; mean, 68.5 years) and severe PH in COPD (61%; mean 68.4 years), compared with those who had IPAH (37%; mean 61.7 years. Oral monotherapy for patients with PH and COPD was the main treatment, consisting of phosphodiesterase-5 inhibitors, while most patients with IPAH received endothelin receptor antagonists.
On functional tests, patients in the PH and COPD group tended to perform poorer on the 6-minute walking distance (6MWD) and World Health Organization functional class (WHO FC) than patients with IPAH. Specifically, among 42.7% of patients in both group for whom follow-up data were available, there was a similar frequency of improvement for 6MWD of 30 meters or more from baseline for both PH and COPD and IPAH groups (46.9% vs. 52.6%; P = .294), but there were significant differences between 6MWD between patients with moderate and severe PH and COPD (51.6% vs. 31.6%; P = .04). There was a nonsignificant improvement in WHO FC improvement of one or more classes for 65.6% of patients with PH and COPD and 58.3% of patients with IPAH with follow-up data available, with 28.5% of patients with PH in COPD improving compared with 35.8% of patients with IPAH (P = .078) and nonsignificant differences between moderate and severe PH and COPD (19.0% vs. 30.4%; P = .188).
Comparing outcomes
Follow-up data were available for 84% of patients with IPAH and 94% of patients with PH and COPD. Dr. Dario Vizza and colleagues found 45.7% of patients in the PH and COPD group and 24.9% of patients in the IPAH group died during follow-up, while 1.1% in the PH and COPD group and 1.5% of patients in the IPAH group underwent lung transplantations. For patients with moderate PH and COPD, 31.3% died and none underwent lung transplantation, while 49.0% of patients in the severe PH and COPD group died and 1.4% underwent lung transplantations.
Patients in the moderate PH and COPD group were more likely to discontinue treatment (10.9%), compared with patients with IPAH (6.6%) and patients with severe PH and COPD (5.2%). The most common reasons for discontinuations were tolerability and efficacy failure; the IPAH group had 63% of patients discontinue because of tolerability and 7% for efficacy failure, 47% of patients in the severe PH and COPD group discontinued because of tolerability and efficacy, and 29% discontinued treatment for tolerability and 57% for efficacy failure in the moderate and COPD group.
The researchers said male sex, low 6MWD, and high pulmonary vascular resistance at baseline were predictive of poorer outcomes for PH and COPD, but patients with more severe PH and COPD had better outcomes if they improved by 30 meters or more in 6MWD, or improved in WHO FC after receiving medical therapy. For patients with IPAH response to therapy was better among patients who were younger, had higher WHO FC, had high diffusing capacity of the lung for carbon monoxide, had high mean pulmonary artery pressure, and had low PCO2.
“Our data suggest that PH-targeted drug therapy in patients with COPD and severe PH may improve exercise tolerance and WHO FC in a subgroup of patients and that patients with COPD and PH who respond to therapy may have a better prognosis than patients who do not show clinical improvement. These findings need to be explored further in prospective, randomized controlled clinical studies,” the authors concluded.
More research needed
In a related editorial, James R. Klinger, MD, a pulmonologist with Brown University, Providence, R.I., and the director of the Rhode Island Hospital Pulmonary Hypertension Center in East Providence, said there is a “keen interest” in treating PH in COPD despite a lack of consistency on whether treatment is effective in this patient population. About 80% of PH centers in the United States treat PH in COPD when they treat conditions like lung disease with PAH medication, he pointed out. However, he questioned whether current medications designed for PAH could improve pulmonary hemodynamics for PH in COPD.
“Reasons that the pathobiologic condition of PH-COPD may differ from PAH include the likely exposure of the pulmonary circulation to greater degrees of hypoxia and hypercapnia and the greater loss of alveolar capillaries associated with emphysema,” he said.
The study by Dr. Dario Vizza and colleagues is an attempt to evaluate treatment response for patients with PH and COPD “in a way that allows comparison with patients who have been treated with similar drugs for PAH,” Dr. Klinger said. He noted the study’s retrospective nature, lack of control group, and lack of information on lung disease severity could limit the findings.
“These limitations preclude recommendations for the routine treatment of patients with PH-COPD, but the findings suggest that, despite greater morbidity at baseline, patients with PH-COPD may be nearly as likely to benefit from PAH medications as patients with IPAH,” he said.
“What is needed now is well-designed randomized controlled studies to determine whether improved outcomes can be achieved in this population and which patients are most likely to benefit,” he concluded. “Simply put: How bad does PH need to be in patients with COPD before treatment is helpful, and how severe does COPD need to be before PH treatment is futile?”
The authors reported personal and institutional relationships in the form of grants, consultancies, advisory board memberships, speakers bureau appointments, honoraria, patents, grant and research funding, lectures, travel compensation, and steering committee positions for a variety of pharmaceutical companies, agencies, societies, journals, medical publishing companies, and other organizations. Dr. Klinger reported his institution receives grant support from Acceleron and United Therapeutics in the area of PH, and he has been an unpaid consultant for Bayer.
Patients with pulmonary hypertension (PH) as a complication of chronic obstructive pulmonary disease (COPD) have worse functional impairment and higher mortality, compared with patients who have idiopathic pulmonary arterial hypertension (IPAH).
Despite these factors, some patients with more severe PH in COPD may respond to treatment and show clinical improvement after treatment, according to recent research published in the journal CHEST®.
Carmine Dario Vizza, MD, of the pulmonary hypertension unit, department of cardiovascular and respiratory diseases at Sapienza University of Rome, and colleagues evaluated patients in the Comparative, Prospective Registry of Newly Initiated Therapies for Pulmonary Hypertension (COMPERA) database, enrolled up to August 2020, identifying 68 patients with moderate PH and COPD and 307 patients with severe PH and COPD. The researchers compared the PH and COPD groups with 307 patients who had idiopathic pulmonary arterial hypertension.
Overall, mostly older men made up the group of patients with moderate (50%; mean, 68.5 years) and severe PH in COPD (61%; mean 68.4 years), compared with those who had IPAH (37%; mean 61.7 years. Oral monotherapy for patients with PH and COPD was the main treatment, consisting of phosphodiesterase-5 inhibitors, while most patients with IPAH received endothelin receptor antagonists.
On functional tests, patients in the PH and COPD group tended to perform poorer on the 6-minute walking distance (6MWD) and World Health Organization functional class (WHO FC) than patients with IPAH. Specifically, among 42.7% of patients in both group for whom follow-up data were available, there was a similar frequency of improvement for 6MWD of 30 meters or more from baseline for both PH and COPD and IPAH groups (46.9% vs. 52.6%; P = .294), but there were significant differences between 6MWD between patients with moderate and severe PH and COPD (51.6% vs. 31.6%; P = .04). There was a nonsignificant improvement in WHO FC improvement of one or more classes for 65.6% of patients with PH and COPD and 58.3% of patients with IPAH with follow-up data available, with 28.5% of patients with PH in COPD improving compared with 35.8% of patients with IPAH (P = .078) and nonsignificant differences between moderate and severe PH and COPD (19.0% vs. 30.4%; P = .188).
Comparing outcomes
Follow-up data were available for 84% of patients with IPAH and 94% of patients with PH and COPD. Dr. Dario Vizza and colleagues found 45.7% of patients in the PH and COPD group and 24.9% of patients in the IPAH group died during follow-up, while 1.1% in the PH and COPD group and 1.5% of patients in the IPAH group underwent lung transplantations. For patients with moderate PH and COPD, 31.3% died and none underwent lung transplantation, while 49.0% of patients in the severe PH and COPD group died and 1.4% underwent lung transplantations.
Patients in the moderate PH and COPD group were more likely to discontinue treatment (10.9%), compared with patients with IPAH (6.6%) and patients with severe PH and COPD (5.2%). The most common reasons for discontinuations were tolerability and efficacy failure; the IPAH group had 63% of patients discontinue because of tolerability and 7% for efficacy failure, 47% of patients in the severe PH and COPD group discontinued because of tolerability and efficacy, and 29% discontinued treatment for tolerability and 57% for efficacy failure in the moderate and COPD group.
The researchers said male sex, low 6MWD, and high pulmonary vascular resistance at baseline were predictive of poorer outcomes for PH and COPD, but patients with more severe PH and COPD had better outcomes if they improved by 30 meters or more in 6MWD, or improved in WHO FC after receiving medical therapy. For patients with IPAH response to therapy was better among patients who were younger, had higher WHO FC, had high diffusing capacity of the lung for carbon monoxide, had high mean pulmonary artery pressure, and had low PCO2.
“Our data suggest that PH-targeted drug therapy in patients with COPD and severe PH may improve exercise tolerance and WHO FC in a subgroup of patients and that patients with COPD and PH who respond to therapy may have a better prognosis than patients who do not show clinical improvement. These findings need to be explored further in prospective, randomized controlled clinical studies,” the authors concluded.
More research needed
In a related editorial, James R. Klinger, MD, a pulmonologist with Brown University, Providence, R.I., and the director of the Rhode Island Hospital Pulmonary Hypertension Center in East Providence, said there is a “keen interest” in treating PH in COPD despite a lack of consistency on whether treatment is effective in this patient population. About 80% of PH centers in the United States treat PH in COPD when they treat conditions like lung disease with PAH medication, he pointed out. However, he questioned whether current medications designed for PAH could improve pulmonary hemodynamics for PH in COPD.
“Reasons that the pathobiologic condition of PH-COPD may differ from PAH include the likely exposure of the pulmonary circulation to greater degrees of hypoxia and hypercapnia and the greater loss of alveolar capillaries associated with emphysema,” he said.
The study by Dr. Dario Vizza and colleagues is an attempt to evaluate treatment response for patients with PH and COPD “in a way that allows comparison with patients who have been treated with similar drugs for PAH,” Dr. Klinger said. He noted the study’s retrospective nature, lack of control group, and lack of information on lung disease severity could limit the findings.
“These limitations preclude recommendations for the routine treatment of patients with PH-COPD, but the findings suggest that, despite greater morbidity at baseline, patients with PH-COPD may be nearly as likely to benefit from PAH medications as patients with IPAH,” he said.
“What is needed now is well-designed randomized controlled studies to determine whether improved outcomes can be achieved in this population and which patients are most likely to benefit,” he concluded. “Simply put: How bad does PH need to be in patients with COPD before treatment is helpful, and how severe does COPD need to be before PH treatment is futile?”
The authors reported personal and institutional relationships in the form of grants, consultancies, advisory board memberships, speakers bureau appointments, honoraria, patents, grant and research funding, lectures, travel compensation, and steering committee positions for a variety of pharmaceutical companies, agencies, societies, journals, medical publishing companies, and other organizations. Dr. Klinger reported his institution receives grant support from Acceleron and United Therapeutics in the area of PH, and he has been an unpaid consultant for Bayer.
FROM THE JOURNAL CHEST®
Obesity hypoventilation: Moving the needle on underrecognition
Obesity hypoventilation syndrome (OHS) is bound to be increasing because of the rising obesity epidemic but is underrecognized and “frequently underdiagnosed,” Saiprakash B. Venkateshiah, MD, said at the virtual annual meeting of the Associated Professional Sleep Societies.
The condition, which can cause significant morbidity and mortality, is defined by the combination of obesity and awake alveolar hypoventilation (PaCO2 ≥45 mm Hg), with the exclusion of alternate causes of hypoventilation. Sleep-disordered breathing (SDB) is almost universally present, with approximately 90% of individuals with OHS also having obstructive sleep apnea (OSA), most often severe, and approximately 10% having sleep-related hypoventilation, or a “pure hypoventilation subtype, if you will,” said Dr. Venkateshiah, assistant professor of medicine at Emory University, Atlanta.
The prevalence of OHS in the general population is unknown, but its prevalence in patients who present for the evaluation of SDB has ranged from 8%-20% across multiple studies, he said. Up to 40% of patients with OHS present for the first time with acute hypercapnic respiratory failure, which has an in-hospital mortality of 18%.
Postmenopausal women appear to have a higher prevalence, compared with premenopausal women and men, he noted, and women appear to be more likely than men to present with the clinical phenotype of OHS without associated OSA.
The arterial blood gas measurement needed to document alveolar hypoventilation and definitively diagnosis OHA is a “simple and economical test,” he said, “but it is logistically very difficult to obtain [these measurements] routinely in all patients in the clinic ... and is one of the reasons why OSH is underdiagnosed.”
Guideline advice
A practice guideline published in 2019 by the American Thoracic Society suggests that, for obese patients with SDB and a low to moderate probability of having OSH, a serum bicarbonate level be measured first. “In patients with serum bicarbonate less than 27 mmol/L, clinicians might forgo measuring PaCO2, as the diagnosis in them is very unlikely,” Dr. Venkateshiah said, referring to the guideline. “In patients with a serum bicarbonate greater than 27, you might need to measure PaCO2 to confirm or rule out the diagnosis of OHS.”
(Patients strongly suspected of having OHS, with more than a low to moderate probability – those in whom arterial blood gases should be measured – are “usually severely obese with typical signs and symptoms such as dyspnea, nocturia, lower-extremity edema, excessive daytime sleepiness, fatigue, loud disruptive snoring, witnessed apneas, as well as mild hypoxemia during wake and/or significant hypoxemia during sleep,” the ATS guideline says.)
The guideline panel considered the use of oxygen saturation measured with pulse oximetry during wakefulness to screen for OHS and decided to advise against it because of the paucity of evidence-based literature, Dr. Venkateshiah noted. (In making its five conditional recommendations, the guideline panel cited an overall very low quality of evidence.)
Symptoms of OHS overlap with those of OSA (for example, daytime hypersomnolence, witnessed apneas, loud snoring, and morning headaches), so “symptoms alone cannot be used to discriminate between the two disorders,” he advised. Signs of OHS commonly seen in clinical exams, however, are low resting daytime oxygen saturations and lower-extremity edema. A sleep study, he added, is needed to document and characterize SDB in patients with OHS.
Positive airway pressure therapy is the first-line treatment for OHS, and long-term outcomes of patients with OHS on PAP treatment are significantly better, compared with untreated individuals. There is no strong evidence to recommend one form of PAP therapy over another for patients with OHS and concomitant severe OSA, he said, but “the bottom line” from both short- and long-term randomized clinical trials comparing CPAP with noninvasive ventilation “is that CPAP is equivalent to noninvasive ventilation as far as outcomes are concerned.”
The ATS guideline panel recommends continuous positive airway pressure therapy for patients with OHS and severe OSA. And for OHS with nonsevere OSA, bilevel PAP is traditionally used – including pure hypoventilators, Dr. Venkateshiah said.
Weight-loss interventions are paramount, since “the primary driver of OHS is obesity,” he said at the meeting. There are only a few studies that have looked at bariatric surgery in patients with OHS, he said, “but they did note significant improvements in gas exchange, sleep apnea, lung volumes and pulmonary hypertension.”
The ATS guideline suggests weight-loss interventions that produce sustained weight loss of 25%-30% of the actual body weight. Such interventions are “most likely required to achieve resolution of hypoventilation,” Dr. Venkateshiah said.
OHS vs. COPD
In a separate presentation on OHS, Michelle Cao, DO, clinical associate professor at Stanford (Calif.) University, emphasized the importance of distinguishing the patient with OHS from the patient with hypercapnic chronic obstructive pulmonary disease (COPD). Spirometry and the flow volume curve can help rule out hypercapnic COPD and other conditions that cause daytime hypoventilation.
A study published in 2016 of 600 hospitalized patients determined to have unequivocal OHS found that 43% had been misdiagnosed as having COPD and none had been previously diagnosed with OHS, Dr. Cao noted. Patients in the study had a mean age of 58 and a mean body mass index of 48.2 kg/m2; 64% were women.
Dr. Venkateshiah and Dr. Cao had no relevant disclosures.
Obesity hypoventilation syndrome (OHS) is bound to be increasing because of the rising obesity epidemic but is underrecognized and “frequently underdiagnosed,” Saiprakash B. Venkateshiah, MD, said at the virtual annual meeting of the Associated Professional Sleep Societies.
The condition, which can cause significant morbidity and mortality, is defined by the combination of obesity and awake alveolar hypoventilation (PaCO2 ≥45 mm Hg), with the exclusion of alternate causes of hypoventilation. Sleep-disordered breathing (SDB) is almost universally present, with approximately 90% of individuals with OHS also having obstructive sleep apnea (OSA), most often severe, and approximately 10% having sleep-related hypoventilation, or a “pure hypoventilation subtype, if you will,” said Dr. Venkateshiah, assistant professor of medicine at Emory University, Atlanta.
The prevalence of OHS in the general population is unknown, but its prevalence in patients who present for the evaluation of SDB has ranged from 8%-20% across multiple studies, he said. Up to 40% of patients with OHS present for the first time with acute hypercapnic respiratory failure, which has an in-hospital mortality of 18%.
Postmenopausal women appear to have a higher prevalence, compared with premenopausal women and men, he noted, and women appear to be more likely than men to present with the clinical phenotype of OHS without associated OSA.
The arterial blood gas measurement needed to document alveolar hypoventilation and definitively diagnosis OHA is a “simple and economical test,” he said, “but it is logistically very difficult to obtain [these measurements] routinely in all patients in the clinic ... and is one of the reasons why OSH is underdiagnosed.”
Guideline advice
A practice guideline published in 2019 by the American Thoracic Society suggests that, for obese patients with SDB and a low to moderate probability of having OSH, a serum bicarbonate level be measured first. “In patients with serum bicarbonate less than 27 mmol/L, clinicians might forgo measuring PaCO2, as the diagnosis in them is very unlikely,” Dr. Venkateshiah said, referring to the guideline. “In patients with a serum bicarbonate greater than 27, you might need to measure PaCO2 to confirm or rule out the diagnosis of OHS.”
(Patients strongly suspected of having OHS, with more than a low to moderate probability – those in whom arterial blood gases should be measured – are “usually severely obese with typical signs and symptoms such as dyspnea, nocturia, lower-extremity edema, excessive daytime sleepiness, fatigue, loud disruptive snoring, witnessed apneas, as well as mild hypoxemia during wake and/or significant hypoxemia during sleep,” the ATS guideline says.)
The guideline panel considered the use of oxygen saturation measured with pulse oximetry during wakefulness to screen for OHS and decided to advise against it because of the paucity of evidence-based literature, Dr. Venkateshiah noted. (In making its five conditional recommendations, the guideline panel cited an overall very low quality of evidence.)
Symptoms of OHS overlap with those of OSA (for example, daytime hypersomnolence, witnessed apneas, loud snoring, and morning headaches), so “symptoms alone cannot be used to discriminate between the two disorders,” he advised. Signs of OHS commonly seen in clinical exams, however, are low resting daytime oxygen saturations and lower-extremity edema. A sleep study, he added, is needed to document and characterize SDB in patients with OHS.
Positive airway pressure therapy is the first-line treatment for OHS, and long-term outcomes of patients with OHS on PAP treatment are significantly better, compared with untreated individuals. There is no strong evidence to recommend one form of PAP therapy over another for patients with OHS and concomitant severe OSA, he said, but “the bottom line” from both short- and long-term randomized clinical trials comparing CPAP with noninvasive ventilation “is that CPAP is equivalent to noninvasive ventilation as far as outcomes are concerned.”
The ATS guideline panel recommends continuous positive airway pressure therapy for patients with OHS and severe OSA. And for OHS with nonsevere OSA, bilevel PAP is traditionally used – including pure hypoventilators, Dr. Venkateshiah said.
Weight-loss interventions are paramount, since “the primary driver of OHS is obesity,” he said at the meeting. There are only a few studies that have looked at bariatric surgery in patients with OHS, he said, “but they did note significant improvements in gas exchange, sleep apnea, lung volumes and pulmonary hypertension.”
The ATS guideline suggests weight-loss interventions that produce sustained weight loss of 25%-30% of the actual body weight. Such interventions are “most likely required to achieve resolution of hypoventilation,” Dr. Venkateshiah said.
OHS vs. COPD
In a separate presentation on OHS, Michelle Cao, DO, clinical associate professor at Stanford (Calif.) University, emphasized the importance of distinguishing the patient with OHS from the patient with hypercapnic chronic obstructive pulmonary disease (COPD). Spirometry and the flow volume curve can help rule out hypercapnic COPD and other conditions that cause daytime hypoventilation.
A study published in 2016 of 600 hospitalized patients determined to have unequivocal OHS found that 43% had been misdiagnosed as having COPD and none had been previously diagnosed with OHS, Dr. Cao noted. Patients in the study had a mean age of 58 and a mean body mass index of 48.2 kg/m2; 64% were women.
Dr. Venkateshiah and Dr. Cao had no relevant disclosures.
Obesity hypoventilation syndrome (OHS) is bound to be increasing because of the rising obesity epidemic but is underrecognized and “frequently underdiagnosed,” Saiprakash B. Venkateshiah, MD, said at the virtual annual meeting of the Associated Professional Sleep Societies.
The condition, which can cause significant morbidity and mortality, is defined by the combination of obesity and awake alveolar hypoventilation (PaCO2 ≥45 mm Hg), with the exclusion of alternate causes of hypoventilation. Sleep-disordered breathing (SDB) is almost universally present, with approximately 90% of individuals with OHS also having obstructive sleep apnea (OSA), most often severe, and approximately 10% having sleep-related hypoventilation, or a “pure hypoventilation subtype, if you will,” said Dr. Venkateshiah, assistant professor of medicine at Emory University, Atlanta.
The prevalence of OHS in the general population is unknown, but its prevalence in patients who present for the evaluation of SDB has ranged from 8%-20% across multiple studies, he said. Up to 40% of patients with OHS present for the first time with acute hypercapnic respiratory failure, which has an in-hospital mortality of 18%.
Postmenopausal women appear to have a higher prevalence, compared with premenopausal women and men, he noted, and women appear to be more likely than men to present with the clinical phenotype of OHS without associated OSA.
The arterial blood gas measurement needed to document alveolar hypoventilation and definitively diagnosis OHA is a “simple and economical test,” he said, “but it is logistically very difficult to obtain [these measurements] routinely in all patients in the clinic ... and is one of the reasons why OSH is underdiagnosed.”
Guideline advice
A practice guideline published in 2019 by the American Thoracic Society suggests that, for obese patients with SDB and a low to moderate probability of having OSH, a serum bicarbonate level be measured first. “In patients with serum bicarbonate less than 27 mmol/L, clinicians might forgo measuring PaCO2, as the diagnosis in them is very unlikely,” Dr. Venkateshiah said, referring to the guideline. “In patients with a serum bicarbonate greater than 27, you might need to measure PaCO2 to confirm or rule out the diagnosis of OHS.”
(Patients strongly suspected of having OHS, with more than a low to moderate probability – those in whom arterial blood gases should be measured – are “usually severely obese with typical signs and symptoms such as dyspnea, nocturia, lower-extremity edema, excessive daytime sleepiness, fatigue, loud disruptive snoring, witnessed apneas, as well as mild hypoxemia during wake and/or significant hypoxemia during sleep,” the ATS guideline says.)
The guideline panel considered the use of oxygen saturation measured with pulse oximetry during wakefulness to screen for OHS and decided to advise against it because of the paucity of evidence-based literature, Dr. Venkateshiah noted. (In making its five conditional recommendations, the guideline panel cited an overall very low quality of evidence.)
Symptoms of OHS overlap with those of OSA (for example, daytime hypersomnolence, witnessed apneas, loud snoring, and morning headaches), so “symptoms alone cannot be used to discriminate between the two disorders,” he advised. Signs of OHS commonly seen in clinical exams, however, are low resting daytime oxygen saturations and lower-extremity edema. A sleep study, he added, is needed to document and characterize SDB in patients with OHS.
Positive airway pressure therapy is the first-line treatment for OHS, and long-term outcomes of patients with OHS on PAP treatment are significantly better, compared with untreated individuals. There is no strong evidence to recommend one form of PAP therapy over another for patients with OHS and concomitant severe OSA, he said, but “the bottom line” from both short- and long-term randomized clinical trials comparing CPAP with noninvasive ventilation “is that CPAP is equivalent to noninvasive ventilation as far as outcomes are concerned.”
The ATS guideline panel recommends continuous positive airway pressure therapy for patients with OHS and severe OSA. And for OHS with nonsevere OSA, bilevel PAP is traditionally used – including pure hypoventilators, Dr. Venkateshiah said.
Weight-loss interventions are paramount, since “the primary driver of OHS is obesity,” he said at the meeting. There are only a few studies that have looked at bariatric surgery in patients with OHS, he said, “but they did note significant improvements in gas exchange, sleep apnea, lung volumes and pulmonary hypertension.”
The ATS guideline suggests weight-loss interventions that produce sustained weight loss of 25%-30% of the actual body weight. Such interventions are “most likely required to achieve resolution of hypoventilation,” Dr. Venkateshiah said.
OHS vs. COPD
In a separate presentation on OHS, Michelle Cao, DO, clinical associate professor at Stanford (Calif.) University, emphasized the importance of distinguishing the patient with OHS from the patient with hypercapnic chronic obstructive pulmonary disease (COPD). Spirometry and the flow volume curve can help rule out hypercapnic COPD and other conditions that cause daytime hypoventilation.
A study published in 2016 of 600 hospitalized patients determined to have unequivocal OHS found that 43% had been misdiagnosed as having COPD and none had been previously diagnosed with OHS, Dr. Cao noted. Patients in the study had a mean age of 58 and a mean body mass index of 48.2 kg/m2; 64% were women.
Dr. Venkateshiah and Dr. Cao had no relevant disclosures.
FROM SLEEP 2021
Fewer dangerous COPD flare-ups during COVID-19
Public health precautions meant to reduce the spread of COVID-19 may have had an unintended but happy side effect.
They may also have benefited individuals who have chronic obstructive pulmonary disease (COPD), according to a new study.
During the pandemic, admissions for COPD flare-ups dropped dramatically – by 53% – at University of Maryland Medical System hospitals.
Researchers at the university suspect this was the result of a drop in circulating seasonal respiratory viruses, such as influenza. They theorized that stay-at-home orders, social distancing, mask mandates, and strict limits on large gatherings reduced exposure not only to COVID but also to other respiratory infections.
“Our study shows there’s a silver lining to the behavior changes beyond protecting against COVID-19,” said senior author Robert Reed, MD, a pulmonologist and professor of medicine.
COPD is a group of lung diseases that worsen over time and make it hard to breathe. Before the pandemic, they were the fourth-leading cause of death worldwide, commonly triggered by tobacco smoke and dirty air. Nearly half of flare-ups are caused by seasonal respiratory viruses.
For the study, the researchers analyzed data from 13 UMMS hospitals, comparing weekly admissions for COPD in 2018 and 2019, with admissions after April 1, 2020, when COVID-19 public health measures were introduced. Investigators chose the same six-month period in each year for comparison – April 1 to Sept. 30.
The findings were matched against U.S. federal data on respiratory viral trends between Jan. 1, 2018, and Oct. 1, 2020.
As significant as was the system’s 53% drop in COPD admissions during the pandemic, there was also a 36% decline in weekly admissions for such serious conditions as congestive heart failure, diabetes and heart attack, said co–lead author Jennifer So, MD. She’s an assistant professor of medicine and COPD specialist.
The researchers warned that a full return to normal may again expose COPD patients to the familiar seasonal triggers.
“If we completely eliminate masks and distancing during cold and flu season, we’ll allow all those viruses that have been effectively suppressed to come raging back,” Dr. Reed said in a university news release. “There could be a lot of illness.”
He noted that the study did not assess which measures tamed seasonal viruses. But, Dr. Reed added, “a simple thing like wearing a mask while riding on public transit or working from home when you’re sick with a cold could go a long way to reduce virus exposure.”
Dr. So said it is a cultural norm in her native South Korea to wear masks during the winter.
“The COVID-19 pandemic has helped a lot of people around the world become more aware of the role of masking and social distancing to reduce the spread of disease,” she said in the release.
The findings were recently published in the preprint server medRxiv and have not yet been peer reviewed.
The U.S. Centers for Disease Control and Prevention has more information on COVID-19 and chronic lung diseases.
A version of this article first appeared on WebMD.com.
Public health precautions meant to reduce the spread of COVID-19 may have had an unintended but happy side effect.
They may also have benefited individuals who have chronic obstructive pulmonary disease (COPD), according to a new study.
During the pandemic, admissions for COPD flare-ups dropped dramatically – by 53% – at University of Maryland Medical System hospitals.
Researchers at the university suspect this was the result of a drop in circulating seasonal respiratory viruses, such as influenza. They theorized that stay-at-home orders, social distancing, mask mandates, and strict limits on large gatherings reduced exposure not only to COVID but also to other respiratory infections.
“Our study shows there’s a silver lining to the behavior changes beyond protecting against COVID-19,” said senior author Robert Reed, MD, a pulmonologist and professor of medicine.
COPD is a group of lung diseases that worsen over time and make it hard to breathe. Before the pandemic, they were the fourth-leading cause of death worldwide, commonly triggered by tobacco smoke and dirty air. Nearly half of flare-ups are caused by seasonal respiratory viruses.
For the study, the researchers analyzed data from 13 UMMS hospitals, comparing weekly admissions for COPD in 2018 and 2019, with admissions after April 1, 2020, when COVID-19 public health measures were introduced. Investigators chose the same six-month period in each year for comparison – April 1 to Sept. 30.
The findings were matched against U.S. federal data on respiratory viral trends between Jan. 1, 2018, and Oct. 1, 2020.
As significant as was the system’s 53% drop in COPD admissions during the pandemic, there was also a 36% decline in weekly admissions for such serious conditions as congestive heart failure, diabetes and heart attack, said co–lead author Jennifer So, MD. She’s an assistant professor of medicine and COPD specialist.
The researchers warned that a full return to normal may again expose COPD patients to the familiar seasonal triggers.
“If we completely eliminate masks and distancing during cold and flu season, we’ll allow all those viruses that have been effectively suppressed to come raging back,” Dr. Reed said in a university news release. “There could be a lot of illness.”
He noted that the study did not assess which measures tamed seasonal viruses. But, Dr. Reed added, “a simple thing like wearing a mask while riding on public transit or working from home when you’re sick with a cold could go a long way to reduce virus exposure.”
Dr. So said it is a cultural norm in her native South Korea to wear masks during the winter.
“The COVID-19 pandemic has helped a lot of people around the world become more aware of the role of masking and social distancing to reduce the spread of disease,” she said in the release.
The findings were recently published in the preprint server medRxiv and have not yet been peer reviewed.
The U.S. Centers for Disease Control and Prevention has more information on COVID-19 and chronic lung diseases.
A version of this article first appeared on WebMD.com.
Public health precautions meant to reduce the spread of COVID-19 may have had an unintended but happy side effect.
They may also have benefited individuals who have chronic obstructive pulmonary disease (COPD), according to a new study.
During the pandemic, admissions for COPD flare-ups dropped dramatically – by 53% – at University of Maryland Medical System hospitals.
Researchers at the university suspect this was the result of a drop in circulating seasonal respiratory viruses, such as influenza. They theorized that stay-at-home orders, social distancing, mask mandates, and strict limits on large gatherings reduced exposure not only to COVID but also to other respiratory infections.
“Our study shows there’s a silver lining to the behavior changes beyond protecting against COVID-19,” said senior author Robert Reed, MD, a pulmonologist and professor of medicine.
COPD is a group of lung diseases that worsen over time and make it hard to breathe. Before the pandemic, they were the fourth-leading cause of death worldwide, commonly triggered by tobacco smoke and dirty air. Nearly half of flare-ups are caused by seasonal respiratory viruses.
For the study, the researchers analyzed data from 13 UMMS hospitals, comparing weekly admissions for COPD in 2018 and 2019, with admissions after April 1, 2020, when COVID-19 public health measures were introduced. Investigators chose the same six-month period in each year for comparison – April 1 to Sept. 30.
The findings were matched against U.S. federal data on respiratory viral trends between Jan. 1, 2018, and Oct. 1, 2020.
As significant as was the system’s 53% drop in COPD admissions during the pandemic, there was also a 36% decline in weekly admissions for such serious conditions as congestive heart failure, diabetes and heart attack, said co–lead author Jennifer So, MD. She’s an assistant professor of medicine and COPD specialist.
The researchers warned that a full return to normal may again expose COPD patients to the familiar seasonal triggers.
“If we completely eliminate masks and distancing during cold and flu season, we’ll allow all those viruses that have been effectively suppressed to come raging back,” Dr. Reed said in a university news release. “There could be a lot of illness.”
He noted that the study did not assess which measures tamed seasonal viruses. But, Dr. Reed added, “a simple thing like wearing a mask while riding on public transit or working from home when you’re sick with a cold could go a long way to reduce virus exposure.”
Dr. So said it is a cultural norm in her native South Korea to wear masks during the winter.
“The COVID-19 pandemic has helped a lot of people around the world become more aware of the role of masking and social distancing to reduce the spread of disease,” she said in the release.
The findings were recently published in the preprint server medRxiv and have not yet been peer reviewed.
The U.S. Centers for Disease Control and Prevention has more information on COVID-19 and chronic lung diseases.
A version of this article first appeared on WebMD.com.