COPD

For smokers, deaths with a cardiovascular or cancer-related cause, or ones that can be attributed to a respiratory disease such as chronic obstructive pulmonary disease, are significantly more common than for nonsmokers. It is widely recognized that stopping smoking leads to a reduction in mortality risk. To make reliable statements on the timeline of this reduction, researchers analyzed interview data and death rates from 438,015 adult US citizens from 1997 to the end of 2019.

The analyses show that it takes 30 years for the mortality risk of ex-smokers to resemble that of people who never regularly smoked. Blake Thomson, PhD, and Fahrad Islami, MD, PhD, both members of the Department of Surveillance and Health Equity Science of the American Cancer Society in Atlanta, Georgia, published their results as a research letter in JAMA Internal Medicine.
 

After Smoking Cessation

Overall, 11,860 cardiovascular, 10,935 cancer-related, and 2,060 respiratory-related deaths were considered from over 5 million patient years. Taken from these figures, the mortality risks of continuous smokers were 2.3 times (cardiovascular), 3.4 times (cancer-related), and 13.3 times (respiratory-related) higher than those of continuous nonsmokers.

Within 10 years of stopping smoking, the following occurred:

• The cardiovascular mortality risk fell by 1.47 times, compared with nonsmokers (by 36% compared with smokers).
• The cancer-related mortality risk fell by 2.13 times, compared with nonsmokers (by 47% compared with smokers).
• The respiratory-related mortality risk fell by 6.35 times, compared with nonsmokers (by 43% compared with smokers).

In the second decade after stopping smoking, the risk dropped even further. The researchers observed the following trends:

• The cardiovascular mortality risk fell by 1.26 times.
• The cancer-related mortality risk fell by 1.59 times.
• The respiratory-related mortality risk fell by 3.63 times — each time compared with nonsmokers.

During the third decade after stopping smoking, the risk continued to decrease. The trends were as follows:

• The cardiovascular mortality risk fell by 1.07 times.
• The cancer-related mortality risk fell by 1.34 times.
• The respiratory-related mortality risk fell by 2.34 times, compared with nonsmokers.

30 Years Later

Only after more than 30 years of not smoking was the cardiovascular-related mortality risk 0.96 and, therefore, no longer significant. Compared with nonsmokers, the cancer-related mortality risk was 1.16, and the respiratory-related mortality risk was 1.31.

Therefore, former smokers can reduce their cardiovascular mortality risk by 100%, the cancer-related by 93%, and the respiratory-related mortality risk by 97%.

The result reinforces earlier analyses on the reduction in mortality risks by stopping smoking, with fewer participants. Smokers, therefore, benefit more the longer that they can refrain from using tobacco. “The earlier in life that smoking is given up, the better,” the authors wrote. But even in the first 10 years, the mortality risks examined decreased by a statistically significant 36% (cardiovascular) to 47% (cancer-related).
 

An Underestimation?

One disadvantage of the study is that the participants’ data were collected using personal questionnaires. For this reason, participants may have reported their tobacco consumption as being lower than it was, particularly because these questionnaires are often answered in hindsight, the authors pointed out.

In addition, some of the participants who reported stopping smoking completely may have only reduced their consumption. However, both circumstances would cause the results of the analysis to be even clearer, compared with reality, and therefore better.

This article was translated from the Medscape German edition.

A version of this article appeared on Medscape.com.

For smokers, deaths with a cardiovascular or cancer-related cause, or ones that can be attributed to a respiratory disease such as chronic obstructive pulmonary disease, are significantly more common than for nonsmokers. It is widely recognized that stopping smoking leads to a reduction in mortality risk. To make reliable statements on the timeline of this reduction, researchers analyzed interview data and death rates from 438,015 adult US citizens from 1997 to the end of 2019.

The analyses show that it takes 30 years for the mortality risk of ex-smokers to resemble that of people who never regularly smoked. Blake Thomson, PhD, and Fahrad Islami, MD, PhD, both members of the Department of Surveillance and Health Equity Science of the American Cancer Society in Atlanta, Georgia, published their results as a research letter in JAMA Internal Medicine.
 

After Smoking Cessation

Overall, 11,860 cardiovascular, 10,935 cancer-related, and 2,060 respiratory-related deaths were considered from over 5 million patient years. Taken from these figures, the mortality risks of continuous smokers were 2.3 times (cardiovascular), 3.4 times (cancer-related), and 13.3 times (respiratory-related) higher than those of continuous nonsmokers.

Within 10 years of stopping smoking, the following occurred:

• The cardiovascular mortality risk fell by 1.47 times, compared with nonsmokers (by 36% compared with smokers).
• The cancer-related mortality risk fell by 2.13 times, compared with nonsmokers (by 47% compared with smokers).
• The respiratory-related mortality risk fell by 6.35 times, compared with nonsmokers (by 43% compared with smokers).

In the second decade after stopping smoking, the risk dropped even further. The researchers observed the following trends:

• The cardiovascular mortality risk fell by 1.26 times.
• The cancer-related mortality risk fell by 1.59 times.
• The respiratory-related mortality risk fell by 3.63 times — each time compared with nonsmokers.

During the third decade after stopping smoking, the risk continued to decrease. The trends were as follows:

• The cardiovascular mortality risk fell by 1.07 times.
• The cancer-related mortality risk fell by 1.34 times.
• The respiratory-related mortality risk fell by 2.34 times, compared with nonsmokers.

30 Years Later

Only after more than 30 years of not smoking was the cardiovascular-related mortality risk 0.96 and, therefore, no longer significant. Compared with nonsmokers, the cancer-related mortality risk was 1.16, and the respiratory-related mortality risk was 1.31.

Therefore, former smokers can reduce their cardiovascular mortality risk by 100%, the cancer-related by 93%, and the respiratory-related mortality risk by 97%.

The result reinforces earlier analyses on the reduction in mortality risks by stopping smoking, with fewer participants. Smokers, therefore, benefit more the longer that they can refrain from using tobacco. “The earlier in life that smoking is given up, the better,” the authors wrote. But even in the first 10 years, the mortality risks examined decreased by a statistically significant 36% (cardiovascular) to 47% (cancer-related).
 

An Underestimation?

One disadvantage of the study is that the participants’ data were collected using personal questionnaires. For this reason, participants may have reported their tobacco consumption as being lower than it was, particularly because these questionnaires are often answered in hindsight, the authors pointed out.

In addition, some of the participants who reported stopping smoking completely may have only reduced their consumption. However, both circumstances would cause the results of the analysis to be even clearer, compared with reality, and therefore better.

This article was translated from the Medscape German edition.

A version of this article appeared on Medscape.com.

For smokers, deaths with a cardiovascular or cancer-related cause, or ones that can be attributed to a respiratory disease such as chronic obstructive pulmonary disease, are significantly more common than for nonsmokers. It is widely recognized that stopping smoking leads to a reduction in mortality risk. To make reliable statements on the timeline of this reduction, researchers analyzed interview data and death rates from 438,015 adult US citizens from 1997 to the end of 2019.

The analyses show that it takes 30 years for the mortality risk of ex-smokers to resemble that of people who never regularly smoked. Blake Thomson, PhD, and Fahrad Islami, MD, PhD, both members of the Department of Surveillance and Health Equity Science of the American Cancer Society in Atlanta, Georgia, published their results as a research letter in JAMA Internal Medicine.
 

After Smoking Cessation

Overall, 11,860 cardiovascular, 10,935 cancer-related, and 2,060 respiratory-related deaths were considered from over 5 million patient years. Taken from these figures, the mortality risks of continuous smokers were 2.3 times (cardiovascular), 3.4 times (cancer-related), and 13.3 times (respiratory-related) higher than those of continuous nonsmokers.

Within 10 years of stopping smoking, the following occurred:

• The cardiovascular mortality risk fell by 1.47 times, compared with nonsmokers (by 36% compared with smokers).
• The cancer-related mortality risk fell by 2.13 times, compared with nonsmokers (by 47% compared with smokers).
• The respiratory-related mortality risk fell by 6.35 times, compared with nonsmokers (by 43% compared with smokers).

In the second decade after stopping smoking, the risk dropped even further. The researchers observed the following trends:

• The cardiovascular mortality risk fell by 1.26 times.
• The cancer-related mortality risk fell by 1.59 times.
• The respiratory-related mortality risk fell by 3.63 times — each time compared with nonsmokers.

During the third decade after stopping smoking, the risk continued to decrease. The trends were as follows:

• The cardiovascular mortality risk fell by 1.07 times.
• The cancer-related mortality risk fell by 1.34 times.
• The respiratory-related mortality risk fell by 2.34 times, compared with nonsmokers.

30 Years Later

Only after more than 30 years of not smoking was the cardiovascular-related mortality risk 0.96 and, therefore, no longer significant. Compared with nonsmokers, the cancer-related mortality risk was 1.16, and the respiratory-related mortality risk was 1.31.

Therefore, former smokers can reduce their cardiovascular mortality risk by 100%, the cancer-related by 93%, and the respiratory-related mortality risk by 97%.

The result reinforces earlier analyses on the reduction in mortality risks by stopping smoking, with fewer participants. Smokers, therefore, benefit more the longer that they can refrain from using tobacco. “The earlier in life that smoking is given up, the better,” the authors wrote. But even in the first 10 years, the mortality risks examined decreased by a statistically significant 36% (cardiovascular) to 47% (cancer-related).
 

An Underestimation?

One disadvantage of the study is that the participants’ data were collected using personal questionnaires. For this reason, participants may have reported their tobacco consumption as being lower than it was, particularly because these questionnaires are often answered in hindsight, the authors pointed out.

In addition, some of the participants who reported stopping smoking completely may have only reduced their consumption. However, both circumstances would cause the results of the analysis to be even clearer, compared with reality, and therefore better.

This article was translated from the Medscape German edition.

A version of this article appeared on Medscape.com.

Continuous positive airway pressure (CPAP) is first-line therapy for sleep-related breathing disorders (SRBDs). Obstructive sleep apnea (OSA) is the major player in the SRBDs space, with a prevalence approaching 100% in adult men using current diagnostic criteria. Patients with OSA and comorbid cardiovascular disease (CVD) are diagnosed with OSA syndrome, and CPAP is prescribed. Primary care physicians and cardiologists are quick to refer patients with CVD to sleep docs to see whether CPAP can improve CVD-related outcomes.

What the Studies Show

There’s a problem though. CPAP doesn’t seem to improve CVD-related outcomes. In some cases, it’s even harmful. Let’s do a quick review. In 2005, the CANPAP study found CPAP didn’t improve a composite CVD outcome that included mortality. A post hoc analysis found that it actually increased mortality if central apneas weren’t eliminated. The post hoc analysis also found benefit when central apneas were eliminated, but for all-comers, CPAP didn’t improve outcomes. Strike one.

Enter adaptive servo-ventilation (ASV). If CANPAP showed that success depended on eliminating central apneas, why not use ASV for all patients with CVD and central apneas or Cheyne-Stokes respirations? ASV eliminates central apneas and Cheyne-Stokes. Well, that didn’t work either. The randomized, controlled SERVE-HF trial, published in 2015, showed that ASV increases all-cause and CVD-specific mortality. Oops. That’s two trials showing that CPAP and ASV can increase mortality in patients with heart failure. Strike two.

Alright. But that’s heart failure. What about hypertension or coronary artery disease (CAD)? Shouldn’t such patients be treated with CPAP to reduce CVD risk? After all, there’s all those surrogate outcomes data for CPAP — it improves vascular tone and lowers catecholamines and all that stuff. Doesn’t it lower blood pressure too? Surely CPAP benefits patients with CVD who don’t have heart failure, right?

Not really. The RICCADSA study, published in 2016, found that CPAP didn’t reduce a composite of CVD outcomes in patients with newly revascularized CAD. The SAVE trial published the same year had a similar design with similar results. CPAP did not improve CVD-related outcomes. Most recently, the ISAACC study was negative. That’s three negative randomized controlled trials in less than 5 years showing CPAP doesn’t affect CVD-related outcomes in high-risk populations with known disease. Strike three?

CPAP provides no benefit for CVD and possible harm when treating heart failure. Surely CPAP is useful for patients with hypertension. Let’s see. The American Academy of Sleep Medicine (AASM) conducted meta-analyses for the guideline it produced recommending CPAP for patients with comorbid hypertension. They note that 24-hour blood pressure measurements are best correlated with outcomes. CPAP did lead to significant 24-hour blood pressure reduction, but guess how large it was? For systolic blood pressure, it was 1.5 mm Hg; for diastolic pressure, it was 1.6 mm Hg. That’s it.

How did the AASM summarize and interpret the above data in their 2019 guidelines for prescribing CPAP? Although covered in their detailed review, both heart failure and CVD are left out of their primary recommendations . They do provide a conditional recommendation for prescribing CPAP to patients with comorbid hypertension that states, “The majority of well-informed patients would choose the intervention over no treatment.” Really? If you were told that CPAP provides less reduction in blood pressure than dietary changes and/or medications, would you choose to wear it or take a pill once a day? Remember, you have to take the pill anyway to get your blood pressure to target unless your pressure is only 1.5-1.6 mm Hg above normal. Where does one find patients who are anxious to wear a mask to bed for minimal benefit and a 20% copay? I’ve yet to meet one.

As always, the pressure pushers are undeterred by inconvenient evidence. A secondary analysis of adherent patients in RICCADSA resorts to the “bait and switch” that’s propped up CPAP enthusiasts for decades: Compare adherent patients versus those who are not (or those who refuse treatment) to prove benefit. The flaws to this approach are obvious. First, performing a post hoc analysis that reintroduces all of the confounding that plagues existing CPAP data negates the benefits of randomization, fancy statistics notwithstanding. Second, it belies the reality that in well-controlled, well-conducted randomized trials where patients get far more support than those in the community (and sometimes are preselected for adherence), a majority simply won’t use CPAP . Excluding the nonadherent or comparing them with the adherent is the epitome of selection bias.

The editorial accompanying the ISAACC study is a tour de force in CPAP apologies. The apnea-hypopnea index (AHI) isn’t the right metric — this one’s invoked often. Never mind that the very premise that OSA causes CVD is from observational data based on the AHI. If you abandon the AHI, don’t you lose your justification for prospective trials targeting CVD with CPAP?

Even better, in an argument fit for a Twitter ban, the author suggests that patients in ISAACC, SAVE, and RICCADSA couldn’t benefit because they already have CVD. The very concept, refuted by decades of secondary prevention research in cardiology, implies that CPAP should be used for primary prevention. Only a sleep researcher could spin a negative study into an expansion of CPAP indications. Others in the AASM have made similar proposals.

Final Thoughts

The sleep field lacks unblinded realists capable of choosing wisely. A little therapeutic underconfidence is warranted. Diseases and therapies will always have champions. Prudence and restraint? Not so much. The AASM could summarize the CPAP literature in a single recommendation: “If your patient is sleepy, CPAP might help them feel better if their disease is moderate or severe.” All other indications are soft.

A version of this article first appeared on Medscape.com.

Aaron B. Holley, MD, is a professor of medicine at Uniformed Services University in Bethesda, Maryland, and a pulmonary/sleep and critical care medicine physician at MedStar Washington Hospital Center in Washington, DC. He covers a  wide range of topics in pulmonary, critical care, and sleep medicine .

Continuous positive airway pressure (CPAP) is first-line therapy for sleep-related breathing disorders (SRBDs). Obstructive sleep apnea (OSA) is the major player in the SRBDs space, with a prevalence approaching 100% in adult men using current diagnostic criteria. Patients with OSA and comorbid cardiovascular disease (CVD) are diagnosed with OSA syndrome, and CPAP is prescribed. Primary care physicians and cardiologists are quick to refer patients with CVD to sleep docs to see whether CPAP can improve CVD-related outcomes.

What the Studies Show

There’s a problem though. CPAP doesn’t seem to improve CVD-related outcomes. In some cases, it’s even harmful. Let’s do a quick review. In 2005, the CANPAP study found CPAP didn’t improve a composite CVD outcome that included mortality. A post hoc analysis found that it actually increased mortality if central apneas weren’t eliminated. The post hoc analysis also found benefit when central apneas were eliminated, but for all-comers, CPAP didn’t improve outcomes. Strike one.

Enter adaptive servo-ventilation (ASV). If CANPAP showed that success depended on eliminating central apneas, why not use ASV for all patients with CVD and central apneas or Cheyne-Stokes respirations? ASV eliminates central apneas and Cheyne-Stokes. Well, that didn’t work either. The randomized, controlled SERVE-HF trial, published in 2015, showed that ASV increases all-cause and CVD-specific mortality. Oops. That’s two trials showing that CPAP and ASV can increase mortality in patients with heart failure. Strike two.

Alright. But that’s heart failure. What about hypertension or coronary artery disease (CAD)? Shouldn’t such patients be treated with CPAP to reduce CVD risk? After all, there’s all those surrogate outcomes data for CPAP — it improves vascular tone and lowers catecholamines and all that stuff. Doesn’t it lower blood pressure too? Surely CPAP benefits patients with CVD who don’t have heart failure, right?

Not really. The RICCADSA study, published in 2016, found that CPAP didn’t reduce a composite of CVD outcomes in patients with newly revascularized CAD. The SAVE trial published the same year had a similar design with similar results. CPAP did not improve CVD-related outcomes. Most recently, the ISAACC study was negative. That’s three negative randomized controlled trials in less than 5 years showing CPAP doesn’t affect CVD-related outcomes in high-risk populations with known disease. Strike three?

CPAP provides no benefit for CVD and possible harm when treating heart failure. Surely CPAP is useful for patients with hypertension. Let’s see. The American Academy of Sleep Medicine (AASM) conducted meta-analyses for the guideline it produced recommending CPAP for patients with comorbid hypertension. They note that 24-hour blood pressure measurements are best correlated with outcomes. CPAP did lead to significant 24-hour blood pressure reduction, but guess how large it was? For systolic blood pressure, it was 1.5 mm Hg; for diastolic pressure, it was 1.6 mm Hg. That’s it.

How did the AASM summarize and interpret the above data in their 2019 guidelines for prescribing CPAP? Although covered in their detailed review, both heart failure and CVD are left out of their primary recommendations . They do provide a conditional recommendation for prescribing CPAP to patients with comorbid hypertension that states, “The majority of well-informed patients would choose the intervention over no treatment.” Really? If you were told that CPAP provides less reduction in blood pressure than dietary changes and/or medications, would you choose to wear it or take a pill once a day? Remember, you have to take the pill anyway to get your blood pressure to target unless your pressure is only 1.5-1.6 mm Hg above normal. Where does one find patients who are anxious to wear a mask to bed for minimal benefit and a 20% copay? I’ve yet to meet one.

As always, the pressure pushers are undeterred by inconvenient evidence. A secondary analysis of adherent patients in RICCADSA resorts to the “bait and switch” that’s propped up CPAP enthusiasts for decades: Compare adherent patients versus those who are not (or those who refuse treatment) to prove benefit. The flaws to this approach are obvious. First, performing a post hoc analysis that reintroduces all of the confounding that plagues existing CPAP data negates the benefits of randomization, fancy statistics notwithstanding. Second, it belies the reality that in well-controlled, well-conducted randomized trials where patients get far more support than those in the community (and sometimes are preselected for adherence), a majority simply won’t use CPAP . Excluding the nonadherent or comparing them with the adherent is the epitome of selection bias.

The editorial accompanying the ISAACC study is a tour de force in CPAP apologies. The apnea-hypopnea index (AHI) isn’t the right metric — this one’s invoked often. Never mind that the very premise that OSA causes CVD is from observational data based on the AHI. If you abandon the AHI, don’t you lose your justification for prospective trials targeting CVD with CPAP?

Even better, in an argument fit for a Twitter ban, the author suggests that patients in ISAACC, SAVE, and RICCADSA couldn’t benefit because they already have CVD. The very concept, refuted by decades of secondary prevention research in cardiology, implies that CPAP should be used for primary prevention. Only a sleep researcher could spin a negative study into an expansion of CPAP indications. Others in the AASM have made similar proposals.

Final Thoughts

The sleep field lacks unblinded realists capable of choosing wisely. A little therapeutic underconfidence is warranted. Diseases and therapies will always have champions. Prudence and restraint? Not so much. The AASM could summarize the CPAP literature in a single recommendation: “If your patient is sleepy, CPAP might help them feel better if their disease is moderate or severe.” All other indications are soft.

A version of this article first appeared on Medscape.com.

Aaron B. Holley, MD, is a professor of medicine at Uniformed Services University in Bethesda, Maryland, and a pulmonary/sleep and critical care medicine physician at MedStar Washington Hospital Center in Washington, DC. He covers a  wide range of topics in pulmonary, critical care, and sleep medicine .

Continuous positive airway pressure (CPAP) is first-line therapy for sleep-related breathing disorders (SRBDs). Obstructive sleep apnea (OSA) is the major player in the SRBDs space, with a prevalence approaching 100% in adult men using current diagnostic criteria. Patients with OSA and comorbid cardiovascular disease (CVD) are diagnosed with OSA syndrome, and CPAP is prescribed. Primary care physicians and cardiologists are quick to refer patients with CVD to sleep docs to see whether CPAP can improve CVD-related outcomes.

What the Studies Show

There’s a problem though. CPAP doesn’t seem to improve CVD-related outcomes. In some cases, it’s even harmful. Let’s do a quick review. In 2005, the CANPAP study found CPAP didn’t improve a composite CVD outcome that included mortality. A post hoc analysis found that it actually increased mortality if central apneas weren’t eliminated. The post hoc analysis also found benefit when central apneas were eliminated, but for all-comers, CPAP didn’t improve outcomes. Strike one.

Enter adaptive servo-ventilation (ASV). If CANPAP showed that success depended on eliminating central apneas, why not use ASV for all patients with CVD and central apneas or Cheyne-Stokes respirations? ASV eliminates central apneas and Cheyne-Stokes. Well, that didn’t work either. The randomized, controlled SERVE-HF trial, published in 2015, showed that ASV increases all-cause and CVD-specific mortality. Oops. That’s two trials showing that CPAP and ASV can increase mortality in patients with heart failure. Strike two.

Alright. But that’s heart failure. What about hypertension or coronary artery disease (CAD)? Shouldn’t such patients be treated with CPAP to reduce CVD risk? After all, there’s all those surrogate outcomes data for CPAP — it improves vascular tone and lowers catecholamines and all that stuff. Doesn’t it lower blood pressure too? Surely CPAP benefits patients with CVD who don’t have heart failure, right?

Not really. The RICCADSA study, published in 2016, found that CPAP didn’t reduce a composite of CVD outcomes in patients with newly revascularized CAD. The SAVE trial published the same year had a similar design with similar results. CPAP did not improve CVD-related outcomes. Most recently, the ISAACC study was negative. That’s three negative randomized controlled trials in less than 5 years showing CPAP doesn’t affect CVD-related outcomes in high-risk populations with known disease. Strike three?

CPAP provides no benefit for CVD and possible harm when treating heart failure. Surely CPAP is useful for patients with hypertension. Let’s see. The American Academy of Sleep Medicine (AASM) conducted meta-analyses for the guideline it produced recommending CPAP for patients with comorbid hypertension. They note that 24-hour blood pressure measurements are best correlated with outcomes. CPAP did lead to significant 24-hour blood pressure reduction, but guess how large it was? For systolic blood pressure, it was 1.5 mm Hg; for diastolic pressure, it was 1.6 mm Hg. That’s it.

How did the AASM summarize and interpret the above data in their 2019 guidelines for prescribing CPAP? Although covered in their detailed review, both heart failure and CVD are left out of their primary recommendations . They do provide a conditional recommendation for prescribing CPAP to patients with comorbid hypertension that states, “The majority of well-informed patients would choose the intervention over no treatment.” Really? If you were told that CPAP provides less reduction in blood pressure than dietary changes and/or medications, would you choose to wear it or take a pill once a day? Remember, you have to take the pill anyway to get your blood pressure to target unless your pressure is only 1.5-1.6 mm Hg above normal. Where does one find patients who are anxious to wear a mask to bed for minimal benefit and a 20% copay? I’ve yet to meet one.

As always, the pressure pushers are undeterred by inconvenient evidence. A secondary analysis of adherent patients in RICCADSA resorts to the “bait and switch” that’s propped up CPAP enthusiasts for decades: Compare adherent patients versus those who are not (or those who refuse treatment) to prove benefit. The flaws to this approach are obvious. First, performing a post hoc analysis that reintroduces all of the confounding that plagues existing CPAP data negates the benefits of randomization, fancy statistics notwithstanding. Second, it belies the reality that in well-controlled, well-conducted randomized trials where patients get far more support than those in the community (and sometimes are preselected for adherence), a majority simply won’t use CPAP . Excluding the nonadherent or comparing them with the adherent is the epitome of selection bias.

The editorial accompanying the ISAACC study is a tour de force in CPAP apologies. The apnea-hypopnea index (AHI) isn’t the right metric — this one’s invoked often. Never mind that the very premise that OSA causes CVD is from observational data based on the AHI. If you abandon the AHI, don’t you lose your justification for prospective trials targeting CVD with CPAP?

Even better, in an argument fit for a Twitter ban, the author suggests that patients in ISAACC, SAVE, and RICCADSA couldn’t benefit because they already have CVD. The very concept, refuted by decades of secondary prevention research in cardiology, implies that CPAP should be used for primary prevention. Only a sleep researcher could spin a negative study into an expansion of CPAP indications. Others in the AASM have made similar proposals.

Final Thoughts

The sleep field lacks unblinded realists capable of choosing wisely. A little therapeutic underconfidence is warranted. Diseases and therapies will always have champions. Prudence and restraint? Not so much. The AASM could summarize the CPAP literature in a single recommendation: “If your patient is sleepy, CPAP might help them feel better if their disease is moderate or severe.” All other indications are soft.

A version of this article first appeared on Medscape.com.

Aaron B. Holley, MD, is a professor of medicine at Uniformed Services University in Bethesda, Maryland, and a pulmonary/sleep and critical care medicine physician at MedStar Washington Hospital Center in Washington, DC. He covers a  wide range of topics in pulmonary, critical care, and sleep medicine .

Systematically biased artificial intelligence (AI) models did not improve clinicians’ accuracy in diagnosing hospitalized patients, based on data from more than 450 clinicians.

“Artificial Intelligence (AI) could support clinicians in their diagnostic decisions of hospitalized patients but could also be biased and cause potential harm,” said Sarah Jabbour, MSE, a PhD candidate in computer science and engineering at the University of Michigan, Ann Arbor, in an interview.

“Regulatory guidance has suggested that the use of AI explanations could mitigate these harms, but the effectiveness of using AI explanations has not been established,” she said.

To examine whether AI explanations can be effective in mitigating the potential harms of systemic bias in AI models, Ms. Jabbour and colleagues conducted a randomized clinical vignette survey study. The survey was administered between April 2022 and January 2023 across 13 states, and the study population included hospitalist physicians, nurse practitioners, and physician assistants. The results were published in JAMA.

Participants were randomized to AI predictions with AI explanations (226 clinicians) or without AI explanations (231 clinicians).

The primary outcome was diagnostic accuracy for pneumonia, heart failure, and chronic obstructive pulmonary disease, defined as the number of correct diagnoses over the total number of assessments, the researchers wrote.

The clinicians viewed nine clinical vignettes of patients hospitalized with acute respiratory failure, including their presenting symptoms, physical examination, laboratory results, and chest radiographs. Clinicians viewed two vignettes with no AI model input to establish baseline diagnostic accuracy. They made three assessments in each vignette, one for each diagnosis. The order of the vignettes was two without AI predictions (to establish baseline diagnostic accuracy), six with AI predictions, and one with a clinical consultation by a hypothetical colleague. The vignettes included standard and systematically biased AI models.

The baseline diagnostic accuracy was 73% for the diagnoses of pneumonia, heart failure, and chronic obstructive pulmonary disease. Clinicians’ accuracy increased by 2.9% when they viewed a standard diagnostic AI model without explanations and by 4.4% when they viewed models with AI explanations.

However, clinicians’ accuracy decreased by 11.3% after viewing systematically biased AI model predictions without explanations compared with baseline, and biased AI model predictions with explanations decreased accuracy by 9.1%.

The decrease in accuracy with systematically biased AI predictions without explanations was mainly attributable to a decrease in the participants’ diagnostic specificity, the researchers noted, but the addition of explanations did little to improve it, the researchers said.

Potentially Useful but Still Imperfect

The findings were limited by several factors including the use of a web-based survey, which differs from surveys in a clinical setting, the researchers wrote. Other limitations included the younger than average study population, and the focus on the clinicians making treatment decisions, vs other clinicians who might have a better understanding of the AI explanations.

“In our study, explanations were presented in a way that were considered to be obvious, where the AI model was completely focused on areas of the chest X-rays unrelated to the clinical condition,” Ms. Jabbour told this news organization. “We hypothesized that if presented with such explanations, the participants in our study would notice that the model was behaving incorrectly and not rely on its predictions. This was surprisingly not the case, and the explanations when presented alongside biased AI predictions had seemingly no effect in mitigating clinicians’ overreliance on biased AI,” she said.

“AI is being developed at an extraordinary rate, and our study shows that it has the potential to improve clinical decision-making. At the same time, it could harm clinical decision-making when biased,” Ms. Jabbour said. “We must be thoughtful about how to carefully integrate AI into clinical workflows, with the goal of improving clinical care while not introducing systematic errors or harming patients,” she added.

Looking ahead, “There are several potential research areas that could be explored,” said Ms. Jabbour. “Researchers should focus on careful validation of AI models to identify biased model behavior prior to deployment. AI researchers should also continue including and communicating with clinicians during the development of AI tools to better understand clinicians’ needs and how they interact with AI,” she said. “This is not an exhaustive list of research directions, and it will take much discussion between experts across disciplines such as AI, human computer interaction, and medicine to ultimately deploy AI safely into clinical care.”

Don’t Overestimate AI

“With the increasing use of artificial intelligence and machine learning in other spheres, there has been an increase in interest in exploring how they can be utilized to improve clinical outcomes,” said Suman Pal, MD, assistant professor in the division of hospital medicine at the University of New Mexico, Albuquerque, in an interview. “However, concerns remain regarding the possible harms and ways to mitigate them,” said Dr. Pal, who was not involved in the current study.

In the current study, “It was interesting to note that explanations did not significantly mitigate the decrease in clinician accuracy from systematically biased AI model predictions,” Dr. Pal said.

“For the clinician, the findings of this study caution against overreliance on AI in clinical decision-making, especially because of the risk of exacerbating existing health disparities due to systemic inequities in existing literature,” Dr. Pal told this news organization.

“Additional research is needed to explore how clinicians can be better trained in identifying both the utility and the limitations of AI and into methods of validation and continuous quality checks with integration of AI into clinical workflows,” he noted.

The study was funded by the National Heart, Lung, and Blood Institute. The researchers had no financial conflicts to disclose. Dr. Pal had no financial conflicts to disclose.

A version of this article first appeared on Medscape.com.

Systematically biased artificial intelligence (AI) models did not improve clinicians’ accuracy in diagnosing hospitalized patients, based on data from more than 450 clinicians.

“Artificial Intelligence (AI) could support clinicians in their diagnostic decisions of hospitalized patients but could also be biased and cause potential harm,” said Sarah Jabbour, MSE, a PhD candidate in computer science and engineering at the University of Michigan, Ann Arbor, in an interview.

“Regulatory guidance has suggested that the use of AI explanations could mitigate these harms, but the effectiveness of using AI explanations has not been established,” she said.

To examine whether AI explanations can be effective in mitigating the potential harms of systemic bias in AI models, Ms. Jabbour and colleagues conducted a randomized clinical vignette survey study. The survey was administered between April 2022 and January 2023 across 13 states, and the study population included hospitalist physicians, nurse practitioners, and physician assistants. The results were published in JAMA.

Participants were randomized to AI predictions with AI explanations (226 clinicians) or without AI explanations (231 clinicians).

The primary outcome was diagnostic accuracy for pneumonia, heart failure, and chronic obstructive pulmonary disease, defined as the number of correct diagnoses over the total number of assessments, the researchers wrote.

The clinicians viewed nine clinical vignettes of patients hospitalized with acute respiratory failure, including their presenting symptoms, physical examination, laboratory results, and chest radiographs. Clinicians viewed two vignettes with no AI model input to establish baseline diagnostic accuracy. They made three assessments in each vignette, one for each diagnosis. The order of the vignettes was two without AI predictions (to establish baseline diagnostic accuracy), six with AI predictions, and one with a clinical consultation by a hypothetical colleague. The vignettes included standard and systematically biased AI models.

The baseline diagnostic accuracy was 73% for the diagnoses of pneumonia, heart failure, and chronic obstructive pulmonary disease. Clinicians’ accuracy increased by 2.9% when they viewed a standard diagnostic AI model without explanations and by 4.4% when they viewed models with AI explanations.

However, clinicians’ accuracy decreased by 11.3% after viewing systematically biased AI model predictions without explanations compared with baseline, and biased AI model predictions with explanations decreased accuracy by 9.1%.

The decrease in accuracy with systematically biased AI predictions without explanations was mainly attributable to a decrease in the participants’ diagnostic specificity, the researchers noted, but the addition of explanations did little to improve it, the researchers said.

Potentially Useful but Still Imperfect

The findings were limited by several factors including the use of a web-based survey, which differs from surveys in a clinical setting, the researchers wrote. Other limitations included the younger than average study population, and the focus on the clinicians making treatment decisions, vs other clinicians who might have a better understanding of the AI explanations.

“In our study, explanations were presented in a way that were considered to be obvious, where the AI model was completely focused on areas of the chest X-rays unrelated to the clinical condition,” Ms. Jabbour told this news organization. “We hypothesized that if presented with such explanations, the participants in our study would notice that the model was behaving incorrectly and not rely on its predictions. This was surprisingly not the case, and the explanations when presented alongside biased AI predictions had seemingly no effect in mitigating clinicians’ overreliance on biased AI,” she said.

“AI is being developed at an extraordinary rate, and our study shows that it has the potential to improve clinical decision-making. At the same time, it could harm clinical decision-making when biased,” Ms. Jabbour said. “We must be thoughtful about how to carefully integrate AI into clinical workflows, with the goal of improving clinical care while not introducing systematic errors or harming patients,” she added.

Looking ahead, “There are several potential research areas that could be explored,” said Ms. Jabbour. “Researchers should focus on careful validation of AI models to identify biased model behavior prior to deployment. AI researchers should also continue including and communicating with clinicians during the development of AI tools to better understand clinicians’ needs and how they interact with AI,” she said. “This is not an exhaustive list of research directions, and it will take much discussion between experts across disciplines such as AI, human computer interaction, and medicine to ultimately deploy AI safely into clinical care.”

Don’t Overestimate AI

“With the increasing use of artificial intelligence and machine learning in other spheres, there has been an increase in interest in exploring how they can be utilized to improve clinical outcomes,” said Suman Pal, MD, assistant professor in the division of hospital medicine at the University of New Mexico, Albuquerque, in an interview. “However, concerns remain regarding the possible harms and ways to mitigate them,” said Dr. Pal, who was not involved in the current study.

In the current study, “It was interesting to note that explanations did not significantly mitigate the decrease in clinician accuracy from systematically biased AI model predictions,” Dr. Pal said.

“For the clinician, the findings of this study caution against overreliance on AI in clinical decision-making, especially because of the risk of exacerbating existing health disparities due to systemic inequities in existing literature,” Dr. Pal told this news organization.

“Additional research is needed to explore how clinicians can be better trained in identifying both the utility and the limitations of AI and into methods of validation and continuous quality checks with integration of AI into clinical workflows,” he noted.

The study was funded by the National Heart, Lung, and Blood Institute. The researchers had no financial conflicts to disclose. Dr. Pal had no financial conflicts to disclose.

A version of this article first appeared on Medscape.com.

Systematically biased artificial intelligence (AI) models did not improve clinicians’ accuracy in diagnosing hospitalized patients, based on data from more than 450 clinicians.

“Artificial Intelligence (AI) could support clinicians in their diagnostic decisions of hospitalized patients but could also be biased and cause potential harm,” said Sarah Jabbour, MSE, a PhD candidate in computer science and engineering at the University of Michigan, Ann Arbor, in an interview.

“Regulatory guidance has suggested that the use of AI explanations could mitigate these harms, but the effectiveness of using AI explanations has not been established,” she said.

To examine whether AI explanations can be effective in mitigating the potential harms of systemic bias in AI models, Ms. Jabbour and colleagues conducted a randomized clinical vignette survey study. The survey was administered between April 2022 and January 2023 across 13 states, and the study population included hospitalist physicians, nurse practitioners, and physician assistants. The results were published in JAMA.

Participants were randomized to AI predictions with AI explanations (226 clinicians) or without AI explanations (231 clinicians).

The primary outcome was diagnostic accuracy for pneumonia, heart failure, and chronic obstructive pulmonary disease, defined as the number of correct diagnoses over the total number of assessments, the researchers wrote.

The clinicians viewed nine clinical vignettes of patients hospitalized with acute respiratory failure, including their presenting symptoms, physical examination, laboratory results, and chest radiographs. Clinicians viewed two vignettes with no AI model input to establish baseline diagnostic accuracy. They made three assessments in each vignette, one for each diagnosis. The order of the vignettes was two without AI predictions (to establish baseline diagnostic accuracy), six with AI predictions, and one with a clinical consultation by a hypothetical colleague. The vignettes included standard and systematically biased AI models.

The baseline diagnostic accuracy was 73% for the diagnoses of pneumonia, heart failure, and chronic obstructive pulmonary disease. Clinicians’ accuracy increased by 2.9% when they viewed a standard diagnostic AI model without explanations and by 4.4% when they viewed models with AI explanations.

However, clinicians’ accuracy decreased by 11.3% after viewing systematically biased AI model predictions without explanations compared with baseline, and biased AI model predictions with explanations decreased accuracy by 9.1%.

The decrease in accuracy with systematically biased AI predictions without explanations was mainly attributable to a decrease in the participants’ diagnostic specificity, the researchers noted, but the addition of explanations did little to improve it, the researchers said.

Potentially Useful but Still Imperfect

The findings were limited by several factors including the use of a web-based survey, which differs from surveys in a clinical setting, the researchers wrote. Other limitations included the younger than average study population, and the focus on the clinicians making treatment decisions, vs other clinicians who might have a better understanding of the AI explanations.

“In our study, explanations were presented in a way that were considered to be obvious, where the AI model was completely focused on areas of the chest X-rays unrelated to the clinical condition,” Ms. Jabbour told this news organization. “We hypothesized that if presented with such explanations, the participants in our study would notice that the model was behaving incorrectly and not rely on its predictions. This was surprisingly not the case, and the explanations when presented alongside biased AI predictions had seemingly no effect in mitigating clinicians’ overreliance on biased AI,” she said.

“AI is being developed at an extraordinary rate, and our study shows that it has the potential to improve clinical decision-making. At the same time, it could harm clinical decision-making when biased,” Ms. Jabbour said. “We must be thoughtful about how to carefully integrate AI into clinical workflows, with the goal of improving clinical care while not introducing systematic errors or harming patients,” she added.

Looking ahead, “There are several potential research areas that could be explored,” said Ms. Jabbour. “Researchers should focus on careful validation of AI models to identify biased model behavior prior to deployment. AI researchers should also continue including and communicating with clinicians during the development of AI tools to better understand clinicians’ needs and how they interact with AI,” she said. “This is not an exhaustive list of research directions, and it will take much discussion between experts across disciplines such as AI, human computer interaction, and medicine to ultimately deploy AI safely into clinical care.”

Don’t Overestimate AI

“With the increasing use of artificial intelligence and machine learning in other spheres, there has been an increase in interest in exploring how they can be utilized to improve clinical outcomes,” said Suman Pal, MD, assistant professor in the division of hospital medicine at the University of New Mexico, Albuquerque, in an interview. “However, concerns remain regarding the possible harms and ways to mitigate them,” said Dr. Pal, who was not involved in the current study.

In the current study, “It was interesting to note that explanations did not significantly mitigate the decrease in clinician accuracy from systematically biased AI model predictions,” Dr. Pal said.

“For the clinician, the findings of this study caution against overreliance on AI in clinical decision-making, especially because of the risk of exacerbating existing health disparities due to systemic inequities in existing literature,” Dr. Pal told this news organization.

“Additional research is needed to explore how clinicians can be better trained in identifying both the utility and the limitations of AI and into methods of validation and continuous quality checks with integration of AI into clinical workflows,” he noted.

The study was funded by the National Heart, Lung, and Blood Institute. The researchers had no financial conflicts to disclose. Dr. Pal had no financial conflicts to disclose.

A version of this article first appeared on Medscape.com.

TOPLINE:

Both blood eosinophil-directed treatment (BET) and standard care treatment (ST) similarly reduced treatment failure following acute exacerbations in chronic obstructive pulmonary disease (COPD).

METHODOLOGY:

• The researchers randomized 152 adults with a mean age of 70 years to BET or a placebo (if eosinophil counts were less than 2%) or to standard care treatment regardless of baseline eosinophil counts; the final population available for analysis included 47 patients in the blood eosinophil group and 46 in the primary care group, with 73 and 71 exacerbations, respectively.
• Participants were assessed at baseline and at day 14, day 30, and day 90 after exacerbation; the primary outcome was the rate of treatment failure at 30 days post exacerbation, defined as any need for retreatment with antibiotics or steroids, hospitalization, or death; secondary outcomes included health-related quality of life, forced expiratory volume in 1 second, and visual analogue score respiratory symptoms.
• Participants were recruited from 14 general practices between November 6, 2017, and April 30, 2020; the study was terminated on April 30, 2023, because of the COVID-19 pandemic.

TAKEAWAY:

• BET was noninferior to ST in a noninferiority analysis.
• At 30 days post exacerbation, 14 treatment failures had occurred in the BET group and 23 in the ST group; the relative risk was 0.60 (P = .070).
• The frequency of adverse events was similar between the groups; the most common adverse events were glycosuria and hospital admission for COPD exacerbation (2% in the BET group and 1% in the ST group for both event types), and no deaths occurred during the study period.
• Subgroup analysis showed the greatest benefit in both groups was to patients with higher eosinophil counts who received prednisolone.

IN PRACTICE: 

“There was improvement of lung function, quality of life, and symptoms in exacerbations with low eosinophil count independent of whether placebo or prednisolone was prescribed,” the authors wrote in their discussion.

SOURCE:

The lead author on the study was Sanjay Ramakrishnan, MBBS, University of Oxford, United Kingdom. The study was published online in Lancet Respiratory Medicine .

LIMITATIONS:

A key limitation was an error in the randomization code that prevented the trial’s completion as a superiority study; other limitations included the relatively low number of exacerbations associated with low eosinophil counts and reduction in the recommended length of treatment with prednisolone during the study period.

DISCLOSURES:

The study was supported by the National Institute for Health and Care Research. Dr. Ramakrishnan disclosed personal salary support from the National Institute for Health and Care Research, an unrestricted research grant from AstraZeneca to his institution, and speaker fees and conference travel support from AstraZeneca, all unrelated to the current study.

A version of this article first appeared on Medscape.com.

TOPLINE:

Both blood eosinophil-directed treatment (BET) and standard care treatment (ST) similarly reduced treatment failure following acute exacerbations in chronic obstructive pulmonary disease (COPD).

METHODOLOGY:

• The researchers randomized 152 adults with a mean age of 70 years to BET or a placebo (if eosinophil counts were less than 2%) or to standard care treatment regardless of baseline eosinophil counts; the final population available for analysis included 47 patients in the blood eosinophil group and 46 in the primary care group, with 73 and 71 exacerbations, respectively.
• Participants were assessed at baseline and at day 14, day 30, and day 90 after exacerbation; the primary outcome was the rate of treatment failure at 30 days post exacerbation, defined as any need for retreatment with antibiotics or steroids, hospitalization, or death; secondary outcomes included health-related quality of life, forced expiratory volume in 1 second, and visual analogue score respiratory symptoms.
• Participants were recruited from 14 general practices between November 6, 2017, and April 30, 2020; the study was terminated on April 30, 2023, because of the COVID-19 pandemic.

TAKEAWAY:

• BET was noninferior to ST in a noninferiority analysis.
• At 30 days post exacerbation, 14 treatment failures had occurred in the BET group and 23 in the ST group; the relative risk was 0.60 (P = .070).
• The frequency of adverse events was similar between the groups; the most common adverse events were glycosuria and hospital admission for COPD exacerbation (2% in the BET group and 1% in the ST group for both event types), and no deaths occurred during the study period.
• Subgroup analysis showed the greatest benefit in both groups was to patients with higher eosinophil counts who received prednisolone.

IN PRACTICE: 

“There was improvement of lung function, quality of life, and symptoms in exacerbations with low eosinophil count independent of whether placebo or prednisolone was prescribed,” the authors wrote in their discussion.

SOURCE:

The lead author on the study was Sanjay Ramakrishnan, MBBS, University of Oxford, United Kingdom. The study was published online in Lancet Respiratory Medicine .

LIMITATIONS:

A key limitation was an error in the randomization code that prevented the trial’s completion as a superiority study; other limitations included the relatively low number of exacerbations associated with low eosinophil counts and reduction in the recommended length of treatment with prednisolone during the study period.

DISCLOSURES:

The study was supported by the National Institute for Health and Care Research. Dr. Ramakrishnan disclosed personal salary support from the National Institute for Health and Care Research, an unrestricted research grant from AstraZeneca to his institution, and speaker fees and conference travel support from AstraZeneca, all unrelated to the current study.

A version of this article first appeared on Medscape.com.

TOPLINE:

Both blood eosinophil-directed treatment (BET) and standard care treatment (ST) similarly reduced treatment failure following acute exacerbations in chronic obstructive pulmonary disease (COPD).

METHODOLOGY:

• The researchers randomized 152 adults with a mean age of 70 years to BET or a placebo (if eosinophil counts were less than 2%) or to standard care treatment regardless of baseline eosinophil counts; the final population available for analysis included 47 patients in the blood eosinophil group and 46 in the primary care group, with 73 and 71 exacerbations, respectively.
• Participants were assessed at baseline and at day 14, day 30, and day 90 after exacerbation; the primary outcome was the rate of treatment failure at 30 days post exacerbation, defined as any need for retreatment with antibiotics or steroids, hospitalization, or death; secondary outcomes included health-related quality of life, forced expiratory volume in 1 second, and visual analogue score respiratory symptoms.
• Participants were recruited from 14 general practices between November 6, 2017, and April 30, 2020; the study was terminated on April 30, 2023, because of the COVID-19 pandemic.

TAKEAWAY:

• BET was noninferior to ST in a noninferiority analysis.
• At 30 days post exacerbation, 14 treatment failures had occurred in the BET group and 23 in the ST group; the relative risk was 0.60 (P = .070).
• The frequency of adverse events was similar between the groups; the most common adverse events were glycosuria and hospital admission for COPD exacerbation (2% in the BET group and 1% in the ST group for both event types), and no deaths occurred during the study period.
• Subgroup analysis showed the greatest benefit in both groups was to patients with higher eosinophil counts who received prednisolone.

IN PRACTICE: 

“There was improvement of lung function, quality of life, and symptoms in exacerbations with low eosinophil count independent of whether placebo or prednisolone was prescribed,” the authors wrote in their discussion.

SOURCE:

The lead author on the study was Sanjay Ramakrishnan, MBBS, University of Oxford, United Kingdom. The study was published online in Lancet Respiratory Medicine .

LIMITATIONS:

A key limitation was an error in the randomization code that prevented the trial’s completion as a superiority study; other limitations included the relatively low number of exacerbations associated with low eosinophil counts and reduction in the recommended length of treatment with prednisolone during the study period.

DISCLOSURES:

The study was supported by the National Institute for Health and Care Research. Dr. Ramakrishnan disclosed personal salary support from the National Institute for Health and Care Research, an unrestricted research grant from AstraZeneca to his institution, and speaker fees and conference travel support from AstraZeneca, all unrelated to the current study.

A version of this article first appeared on Medscape.com.

Reducing exposure to tobacco smoke may reduce the burden of chronic obstructive pulmonary disease, and public health measures are needed, according to a new Tobacco Knowledge Summary from the World Health Organization.

“Smoking is a major risk factor for COPD and leads to airway inflammation and remodeling associated with lung destruction,” and contributes to approximately 70% of COPD cases worldwide, according to the statement.

Types of tobacco exposure include not only traditional smoked tobacco products (cigarettes, cigars, pipes, water pipes, kreteks, and bidis), but also smokeless tobacco, heated tobacco products, and electronic nicotine delivery systems; the addition of chemicals and flavors can increase the appeal of tobacco products and promote addiction, the authors wrote. Hookahs and water pipes “are at least as detrimental to lung health as smoking cigarettes and should not be considered as a safe alternative,” they added.

The risk of COPD extends to new e-cigarette products, the authors noted. A study in the American Journal of Preventive Medicine showed that current users of e-cigarettes had a 75% increased risk of developing COPD compared with individuals who have never used e-cigarettes.

Individuals with COPD also face an increased risk of cardiovascular disease and type 2 diabetes, and smokers with COPD who quit not only improve their COPD but also reduce their risk of developing these conditions, the authors said.
 

Mechanism of action explored

The authors noted how tobacco smoking may cause COPD when inhaled particles are deposited through the airway.

Growing evidence suggests that extracellular vesicles may play a role in the development of lung disorders such as COPD, and cigarette smoke can have an impact through this channel. A study published in the American Journal of Respiratory and Critical Care Medicine offered evidence of a potential link between exposure to cigarette smoke and the generation of a unique extracellular vesicle population that could promote the development of lung damage. In the study, Matthew C. Madison, MD, of the University of Alabama, Birmingham, and colleagues examined activity in extracellular vesicles from the bronchoalveolar lavage (BAL) fluid of smoke-exposed mice and human smokers who were otherwise healthy.

The researchers found that airway extracellular vesicles in mice or humans exposed to cigarette smoke had the ability to cause rapid lung damage when transferred into naive recipient mice. The results provide a new model that can inform preclinical COPD research, they wrote.
 

Public health action needed

“In recognition of COPD and Lung Cancer Awareness Month, the World Health Organization (WHO) emphasizes the impact of various forms of tobacco use on COPD,” Dharani K. Narendra, MD, of Baylor College of Medicine, Houston, said in an interview.

“This article focuses on the different types of tobacco exposure, the health care burden associated with COPD, and the risk of developing lung cancer. It also addresses the high-risk groups, especially youth, underscoring the importance of public education and the implementation of restrictions on tobacco use to combat these growing concerns,” she said.

“Education, awareness, and targeted interventions are essential for smoking cessation and COPD management,” said Dr. Narendra. “These elements are key to informing the public about smoking risks, encouraging behavioral change, and ultimately reducing the incidence of smoking-related diseases,” she emphasized.

The WHO statement called for population-level interventions including brief advice to tobacco users, toll-free quit lines, pharmacological interventions, use of messaging and chatbots to provide quit support, and the WHO quit tobacco mobile app.

“It is imperative that all tobacco users, particularly those living in low- to middle-income countries, have access to comprehensive cessation support aligned with WHO recommendations,” the authors wrote.

Finally, the authors emphasized the need to protect children and teens from the dangers of tobacco use through product regulation and to expose the tobacco industry’s marketing tactics.

“The article offers a comprehensive look at different types of tobacco exposure and their contribution to the development of COPD,” Dr. Narendra told this news organization. “Notably, it presents groundbreaking evidence of a strong association between the use of electronic nicotine delivery systems (ENDS) and heated tobacco products to development of COPD; additionally, it provides valuable guidance on smoking cessation resources for physicians to help patients quit smoking,” she said.

Looking ahead, more research is needed on “developing and sustaining state-specific or population-specific interventions for effective smoking cessation programs, and reducing the burden of COPD,” Dr. Narendra said.

The study by Madison and colleagues was supported by the National Heart, Lung, and Blood Institute, the National Institute of General Medical Science, the U.S. Veterans Affairs Administration, the Cystic Fibrosis Foundation Research Development Program, and the Veterans Affairs Merit grant.

Additional financial support came from Imperial College London, a Wellcome Trust Senior Research Fellowship, and Rosetrees Trust/The Stoneygate Trust.

Dr. Narendra had no financial conflicts to disclose but serves as a member of the editorial board of CHEST Physician.

Reducing exposure to tobacco smoke may reduce the burden of chronic obstructive pulmonary disease, and public health measures are needed, according to a new Tobacco Knowledge Summary from the World Health Organization.

“Smoking is a major risk factor for COPD and leads to airway inflammation and remodeling associated with lung destruction,” and contributes to approximately 70% of COPD cases worldwide, according to the statement.

Types of tobacco exposure include not only traditional smoked tobacco products (cigarettes, cigars, pipes, water pipes, kreteks, and bidis), but also smokeless tobacco, heated tobacco products, and electronic nicotine delivery systems; the addition of chemicals and flavors can increase the appeal of tobacco products and promote addiction, the authors wrote. Hookahs and water pipes “are at least as detrimental to lung health as smoking cigarettes and should not be considered as a safe alternative,” they added.

The risk of COPD extends to new e-cigarette products, the authors noted. A study in the American Journal of Preventive Medicine showed that current users of e-cigarettes had a 75% increased risk of developing COPD compared with individuals who have never used e-cigarettes.

Individuals with COPD also face an increased risk of cardiovascular disease and type 2 diabetes, and smokers with COPD who quit not only improve their COPD but also reduce their risk of developing these conditions, the authors said.
 

Mechanism of action explored

The authors noted how tobacco smoking may cause COPD when inhaled particles are deposited through the airway.

Growing evidence suggests that extracellular vesicles may play a role in the development of lung disorders such as COPD, and cigarette smoke can have an impact through this channel. A study published in the American Journal of Respiratory and Critical Care Medicine offered evidence of a potential link between exposure to cigarette smoke and the generation of a unique extracellular vesicle population that could promote the development of lung damage. In the study, Matthew C. Madison, MD, of the University of Alabama, Birmingham, and colleagues examined activity in extracellular vesicles from the bronchoalveolar lavage (BAL) fluid of smoke-exposed mice and human smokers who were otherwise healthy.

The researchers found that airway extracellular vesicles in mice or humans exposed to cigarette smoke had the ability to cause rapid lung damage when transferred into naive recipient mice. The results provide a new model that can inform preclinical COPD research, they wrote.
 

Public health action needed

“In recognition of COPD and Lung Cancer Awareness Month, the World Health Organization (WHO) emphasizes the impact of various forms of tobacco use on COPD,” Dharani K. Narendra, MD, of Baylor College of Medicine, Houston, said in an interview.

“This article focuses on the different types of tobacco exposure, the health care burden associated with COPD, and the risk of developing lung cancer. It also addresses the high-risk groups, especially youth, underscoring the importance of public education and the implementation of restrictions on tobacco use to combat these growing concerns,” she said.

“Education, awareness, and targeted interventions are essential for smoking cessation and COPD management,” said Dr. Narendra. “These elements are key to informing the public about smoking risks, encouraging behavioral change, and ultimately reducing the incidence of smoking-related diseases,” she emphasized.

The WHO statement called for population-level interventions including brief advice to tobacco users, toll-free quit lines, pharmacological interventions, use of messaging and chatbots to provide quit support, and the WHO quit tobacco mobile app.

“It is imperative that all tobacco users, particularly those living in low- to middle-income countries, have access to comprehensive cessation support aligned with WHO recommendations,” the authors wrote.

Finally, the authors emphasized the need to protect children and teens from the dangers of tobacco use through product regulation and to expose the tobacco industry’s marketing tactics.

“The article offers a comprehensive look at different types of tobacco exposure and their contribution to the development of COPD,” Dr. Narendra told this news organization. “Notably, it presents groundbreaking evidence of a strong association between the use of electronic nicotine delivery systems (ENDS) and heated tobacco products to development of COPD; additionally, it provides valuable guidance on smoking cessation resources for physicians to help patients quit smoking,” she said.

Looking ahead, more research is needed on “developing and sustaining state-specific or population-specific interventions for effective smoking cessation programs, and reducing the burden of COPD,” Dr. Narendra said.

The study by Madison and colleagues was supported by the National Heart, Lung, and Blood Institute, the National Institute of General Medical Science, the U.S. Veterans Affairs Administration, the Cystic Fibrosis Foundation Research Development Program, and the Veterans Affairs Merit grant.

Additional financial support came from Imperial College London, a Wellcome Trust Senior Research Fellowship, and Rosetrees Trust/The Stoneygate Trust.

Dr. Narendra had no financial conflicts to disclose but serves as a member of the editorial board of CHEST Physician.

Reducing exposure to tobacco smoke may reduce the burden of chronic obstructive pulmonary disease, and public health measures are needed, according to a new Tobacco Knowledge Summary from the World Health Organization.

“Smoking is a major risk factor for COPD and leads to airway inflammation and remodeling associated with lung destruction,” and contributes to approximately 70% of COPD cases worldwide, according to the statement.

Types of tobacco exposure include not only traditional smoked tobacco products (cigarettes, cigars, pipes, water pipes, kreteks, and bidis), but also smokeless tobacco, heated tobacco products, and electronic nicotine delivery systems; the addition of chemicals and flavors can increase the appeal of tobacco products and promote addiction, the authors wrote. Hookahs and water pipes “are at least as detrimental to lung health as smoking cigarettes and should not be considered as a safe alternative,” they added.

The risk of COPD extends to new e-cigarette products, the authors noted. A study in the American Journal of Preventive Medicine showed that current users of e-cigarettes had a 75% increased risk of developing COPD compared with individuals who have never used e-cigarettes.

Individuals with COPD also face an increased risk of cardiovascular disease and type 2 diabetes, and smokers with COPD who quit not only improve their COPD but also reduce their risk of developing these conditions, the authors said.
 

Mechanism of action explored

The authors noted how tobacco smoking may cause COPD when inhaled particles are deposited through the airway.

Growing evidence suggests that extracellular vesicles may play a role in the development of lung disorders such as COPD, and cigarette smoke can have an impact through this channel. A study published in the American Journal of Respiratory and Critical Care Medicine offered evidence of a potential link between exposure to cigarette smoke and the generation of a unique extracellular vesicle population that could promote the development of lung damage. In the study, Matthew C. Madison, MD, of the University of Alabama, Birmingham, and colleagues examined activity in extracellular vesicles from the bronchoalveolar lavage (BAL) fluid of smoke-exposed mice and human smokers who were otherwise healthy.

The researchers found that airway extracellular vesicles in mice or humans exposed to cigarette smoke had the ability to cause rapid lung damage when transferred into naive recipient mice. The results provide a new model that can inform preclinical COPD research, they wrote.
 

Public health action needed

“In recognition of COPD and Lung Cancer Awareness Month, the World Health Organization (WHO) emphasizes the impact of various forms of tobacco use on COPD,” Dharani K. Narendra, MD, of Baylor College of Medicine, Houston, said in an interview.

“This article focuses on the different types of tobacco exposure, the health care burden associated with COPD, and the risk of developing lung cancer. It also addresses the high-risk groups, especially youth, underscoring the importance of public education and the implementation of restrictions on tobacco use to combat these growing concerns,” she said.

“Education, awareness, and targeted interventions are essential for smoking cessation and COPD management,” said Dr. Narendra. “These elements are key to informing the public about smoking risks, encouraging behavioral change, and ultimately reducing the incidence of smoking-related diseases,” she emphasized.

The WHO statement called for population-level interventions including brief advice to tobacco users, toll-free quit lines, pharmacological interventions, use of messaging and chatbots to provide quit support, and the WHO quit tobacco mobile app.

“It is imperative that all tobacco users, particularly those living in low- to middle-income countries, have access to comprehensive cessation support aligned with WHO recommendations,” the authors wrote.

Finally, the authors emphasized the need to protect children and teens from the dangers of tobacco use through product regulation and to expose the tobacco industry’s marketing tactics.

“The article offers a comprehensive look at different types of tobacco exposure and their contribution to the development of COPD,” Dr. Narendra told this news organization. “Notably, it presents groundbreaking evidence of a strong association between the use of electronic nicotine delivery systems (ENDS) and heated tobacco products to development of COPD; additionally, it provides valuable guidance on smoking cessation resources for physicians to help patients quit smoking,” she said.

Looking ahead, more research is needed on “developing and sustaining state-specific or population-specific interventions for effective smoking cessation programs, and reducing the burden of COPD,” Dr. Narendra said.

The study by Madison and colleagues was supported by the National Heart, Lung, and Blood Institute, the National Institute of General Medical Science, the U.S. Veterans Affairs Administration, the Cystic Fibrosis Foundation Research Development Program, and the Veterans Affairs Merit grant.

Additional financial support came from Imperial College London, a Wellcome Trust Senior Research Fellowship, and Rosetrees Trust/The Stoneygate Trust.

Dr. Narendra had no financial conflicts to disclose but serves as a member of the editorial board of CHEST Physician.

An investigation into associations between serum phosphate levels and in-hospital mortality risk among patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD) found significantly higher in-hospital mortality among AECOPD patients with high serum phosphate levels. The finding, according to Siqi Li et al. in a preproof HELIYON article, suggests that hyperphosphatemia may be a high-risk factor for AECOPD-related in-hospital mortality.

Phosphorus is key to several physiological processes, among them energy metabolism, bone mineralization, membrane transport, and intracellular signaling. Li et al. pointed out that in patients with multiple diseases, hyperphosphatemia is associated with increased mortality. In the development of COPD specifically, acute exacerbations have been shown in several recent studies to be an important adverse event conferring heightened mortality risk. Despite many efforts, AECOPD mortality rates remain high, making identification of potential factors, Li et al. stated, crucial for improving outcomes in high-risk patients.

The electronic Intensive Care Unit Collaborative Research Database (eICU-CRD) holds data associated with over 200,000 patient stays, providing a large sample size for research studies. To determine the relationship between serum phosphate and in-hospital mortality in AECOPD patients, investigators analyzed data from a total of 1,199 AECOPD patients (mean age, 68 years; ~55% female) enrolled in eICU-CRD and divided them into three groups according to serum phosphate level tertiles: lowest tertile (serum phosphate ≤ 3.0 mg/dL, n = 445), median tertile (serum phosphate > 3.0 mg/dL and ≤ 4.0 mg/dL, n = 378), and highest tertile (serum phosphate > 4.0 mg/dL, n = 376). The Li et al. study’s primary outcome was all-cause in-hospital mortality, defined as survival to hospital discharge. Secondary outcomes included length of stay (LOS) in the intensive care unit (ICU), LOS in the hospital, and all-cause ICU mortality.

The Li et al. analysis of patient characteristics showed that patients in the highest tertile of serum phosphate had significantly higher body mass index (BMI) (P < .001), lower temperature (P < .001), lower heart rate (P < .001), lower mean arterial blood pressure (P = .011), higher creatinine (P < .001), higher potassium (P < .001), higher sequential organ failure assessment (SOFA) (P < .001), higher acute physiology and chronic health evaluation (APACHE IV) (P < .001), and higher ICU mortality (P < .001). Also, patients with higher serum phosphate levels were more likely to receive renal replacement therapy (RRT) (P < .001) and vasoactive drugs (P = .003) than those in the lower serum phosphate group. Such differences were also observed for age (P = .021), calcium level (P = .023), sodium level (P = .039), hypertension (P = .014), coronary artery disease (P = .004), diabetes (P = .017), and chronic kidney disease (P < .001). No significant differences were observed for gender, respiration rate, SpO₂, white blood cell count, hemoglobin, platelets, cirrhosis, stroke, ventilation, LOS in ICU, and LOS in hospital (P > .05).

A univariate logistic regression analysis performed to determine the relationship between serum phosphate level and risk of in-hospital mortality revealed that higher serum phosphate level correlated with increased in-hospital mortality (odds ratio, 1.30; 95% confidence interval, 1.16-1.46; P < .001).

Li et al. posited that several mechanisms may explain increased mortality at higher serum phosphate levels in AECOPD patients: increased serum phosphate induces vascular calcification and endothelial dysfunction, leading to organ dysfunction; hyperphosphatemia causes oxidative stress, cell apoptosis, and inflammation, all of which are involved in the pathogenesis of AECOPD, and a higher phosphate diet exacerbates aging and lung emphysema phenotypes; restriction of phosphate intake and absorption relieves these phenotypes and alveolar destruction, which might contribute to the development of AECOPD.

Li et al. concluded: “Reducing serum phosphate levels may be a therapeutic strategy to improve prognosis of AECOPD patients.”

“This large retrospective analysis on eICU database in the U.S. revealed elevated serum phosphate levels with increased in-hospital mortality among patients experiencing acute exacerbation of COPD,” commented Dharani Narendra, MD, assistant professor in medicine, at Baylor College of Medicine, Houston. “This association, previously observed in various chronic conditions including COPD, particularly in men, is now noted to apply to both genders, irrespective of chronic kidney disease. The study also hints at potential mechanisms for elevated phosphate levels, such as inflammation, oxidative stress, and cell apoptosis in AECOPD, as well as a high-phosphate diet.”

She told this news organization also, “It remains imperative to ascertain whether treating hyperphosphatemia or implementing dietary phosphate restrictions can reduce mortality or prevent AECOPD episodes. These demand additional clinical trials to establish a definitive cause-and-effect relationship and to guide potential treatment and prevention strategies.”

Noting study limitations, Li et al. stated that many variables, such as smoking, exacerbation frequency, severity, PH, PaO₂, PaCO₂, and lactate, were not included in this study owing to more than 20% missing values.

This work was supported by the National Natural Science Foundation of China, Scientific Research Fund of Hunan Provincial Education Department, Hunan Provincial Natural Science Foundation, and Special fund for rehabilitation medicine of the National Clinical Research Center for Geriatric Disorders Clinical Research Fund. The authors declare no competing interests.
 

An investigation into associations between serum phosphate levels and in-hospital mortality risk among patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD) found significantly higher in-hospital mortality among AECOPD patients with high serum phosphate levels. The finding, according to Siqi Li et al. in a preproof HELIYON article, suggests that hyperphosphatemia may be a high-risk factor for AECOPD-related in-hospital mortality.

Phosphorus is key to several physiological processes, among them energy metabolism, bone mineralization, membrane transport, and intracellular signaling. Li et al. pointed out that in patients with multiple diseases, hyperphosphatemia is associated with increased mortality. In the development of COPD specifically, acute exacerbations have been shown in several recent studies to be an important adverse event conferring heightened mortality risk. Despite many efforts, AECOPD mortality rates remain high, making identification of potential factors, Li et al. stated, crucial for improving outcomes in high-risk patients.

The electronic Intensive Care Unit Collaborative Research Database (eICU-CRD) holds data associated with over 200,000 patient stays, providing a large sample size for research studies. To determine the relationship between serum phosphate and in-hospital mortality in AECOPD patients, investigators analyzed data from a total of 1,199 AECOPD patients (mean age, 68 years; ~55% female) enrolled in eICU-CRD and divided them into three groups according to serum phosphate level tertiles: lowest tertile (serum phosphate ≤ 3.0 mg/dL, n = 445), median tertile (serum phosphate > 3.0 mg/dL and ≤ 4.0 mg/dL, n = 378), and highest tertile (serum phosphate > 4.0 mg/dL, n = 376). The Li et al. study’s primary outcome was all-cause in-hospital mortality, defined as survival to hospital discharge. Secondary outcomes included length of stay (LOS) in the intensive care unit (ICU), LOS in the hospital, and all-cause ICU mortality.

The Li et al. analysis of patient characteristics showed that patients in the highest tertile of serum phosphate had significantly higher body mass index (BMI) (P < .001), lower temperature (P < .001), lower heart rate (P < .001), lower mean arterial blood pressure (P = .011), higher creatinine (P < .001), higher potassium (P < .001), higher sequential organ failure assessment (SOFA) (P < .001), higher acute physiology and chronic health evaluation (APACHE IV) (P < .001), and higher ICU mortality (P < .001). Also, patients with higher serum phosphate levels were more likely to receive renal replacement therapy (RRT) (P < .001) and vasoactive drugs (P = .003) than those in the lower serum phosphate group. Such differences were also observed for age (P = .021), calcium level (P = .023), sodium level (P = .039), hypertension (P = .014), coronary artery disease (P = .004), diabetes (P = .017), and chronic kidney disease (P < .001). No significant differences were observed for gender, respiration rate, SpO₂, white blood cell count, hemoglobin, platelets, cirrhosis, stroke, ventilation, LOS in ICU, and LOS in hospital (P > .05).

A univariate logistic regression analysis performed to determine the relationship between serum phosphate level and risk of in-hospital mortality revealed that higher serum phosphate level correlated with increased in-hospital mortality (odds ratio, 1.30; 95% confidence interval, 1.16-1.46; P < .001).

Li et al. posited that several mechanisms may explain increased mortality at higher serum phosphate levels in AECOPD patients: increased serum phosphate induces vascular calcification and endothelial dysfunction, leading to organ dysfunction; hyperphosphatemia causes oxidative stress, cell apoptosis, and inflammation, all of which are involved in the pathogenesis of AECOPD, and a higher phosphate diet exacerbates aging and lung emphysema phenotypes; restriction of phosphate intake and absorption relieves these phenotypes and alveolar destruction, which might contribute to the development of AECOPD.

Li et al. concluded: “Reducing serum phosphate levels may be a therapeutic strategy to improve prognosis of AECOPD patients.”

“This large retrospective analysis on eICU database in the U.S. revealed elevated serum phosphate levels with increased in-hospital mortality among patients experiencing acute exacerbation of COPD,” commented Dharani Narendra, MD, assistant professor in medicine, at Baylor College of Medicine, Houston. “This association, previously observed in various chronic conditions including COPD, particularly in men, is now noted to apply to both genders, irrespective of chronic kidney disease. The study also hints at potential mechanisms for elevated phosphate levels, such as inflammation, oxidative stress, and cell apoptosis in AECOPD, as well as a high-phosphate diet.”

She told this news organization also, “It remains imperative to ascertain whether treating hyperphosphatemia or implementing dietary phosphate restrictions can reduce mortality or prevent AECOPD episodes. These demand additional clinical trials to establish a definitive cause-and-effect relationship and to guide potential treatment and prevention strategies.”

Noting study limitations, Li et al. stated that many variables, such as smoking, exacerbation frequency, severity, PH, PaO₂, PaCO₂, and lactate, were not included in this study owing to more than 20% missing values.

This work was supported by the National Natural Science Foundation of China, Scientific Research Fund of Hunan Provincial Education Department, Hunan Provincial Natural Science Foundation, and Special fund for rehabilitation medicine of the National Clinical Research Center for Geriatric Disorders Clinical Research Fund. The authors declare no competing interests.
 

An investigation into associations between serum phosphate levels and in-hospital mortality risk among patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD) found significantly higher in-hospital mortality among AECOPD patients with high serum phosphate levels. The finding, according to Siqi Li et al. in a preproof HELIYON article, suggests that hyperphosphatemia may be a high-risk factor for AECOPD-related in-hospital mortality.

Phosphorus is key to several physiological processes, among them energy metabolism, bone mineralization, membrane transport, and intracellular signaling. Li et al. pointed out that in patients with multiple diseases, hyperphosphatemia is associated with increased mortality. In the development of COPD specifically, acute exacerbations have been shown in several recent studies to be an important adverse event conferring heightened mortality risk. Despite many efforts, AECOPD mortality rates remain high, making identification of potential factors, Li et al. stated, crucial for improving outcomes in high-risk patients.

The electronic Intensive Care Unit Collaborative Research Database (eICU-CRD) holds data associated with over 200,000 patient stays, providing a large sample size for research studies. To determine the relationship between serum phosphate and in-hospital mortality in AECOPD patients, investigators analyzed data from a total of 1,199 AECOPD patients (mean age, 68 years; ~55% female) enrolled in eICU-CRD and divided them into three groups according to serum phosphate level tertiles: lowest tertile (serum phosphate ≤ 3.0 mg/dL, n = 445), median tertile (serum phosphate > 3.0 mg/dL and ≤ 4.0 mg/dL, n = 378), and highest tertile (serum phosphate > 4.0 mg/dL, n = 376). The Li et al. study’s primary outcome was all-cause in-hospital mortality, defined as survival to hospital discharge. Secondary outcomes included length of stay (LOS) in the intensive care unit (ICU), LOS in the hospital, and all-cause ICU mortality.

The Li et al. analysis of patient characteristics showed that patients in the highest tertile of serum phosphate had significantly higher body mass index (BMI) (P < .001), lower temperature (P < .001), lower heart rate (P < .001), lower mean arterial blood pressure (P = .011), higher creatinine (P < .001), higher potassium (P < .001), higher sequential organ failure assessment (SOFA) (P < .001), higher acute physiology and chronic health evaluation (APACHE IV) (P < .001), and higher ICU mortality (P < .001). Also, patients with higher serum phosphate levels were more likely to receive renal replacement therapy (RRT) (P < .001) and vasoactive drugs (P = .003) than those in the lower serum phosphate group. Such differences were also observed for age (P = .021), calcium level (P = .023), sodium level (P = .039), hypertension (P = .014), coronary artery disease (P = .004), diabetes (P = .017), and chronic kidney disease (P < .001). No significant differences were observed for gender, respiration rate, SpO₂, white blood cell count, hemoglobin, platelets, cirrhosis, stroke, ventilation, LOS in ICU, and LOS in hospital (P > .05).

A univariate logistic regression analysis performed to determine the relationship between serum phosphate level and risk of in-hospital mortality revealed that higher serum phosphate level correlated with increased in-hospital mortality (odds ratio, 1.30; 95% confidence interval, 1.16-1.46; P < .001).

Li et al. posited that several mechanisms may explain increased mortality at higher serum phosphate levels in AECOPD patients: increased serum phosphate induces vascular calcification and endothelial dysfunction, leading to organ dysfunction; hyperphosphatemia causes oxidative stress, cell apoptosis, and inflammation, all of which are involved in the pathogenesis of AECOPD, and a higher phosphate diet exacerbates aging and lung emphysema phenotypes; restriction of phosphate intake and absorption relieves these phenotypes and alveolar destruction, which might contribute to the development of AECOPD.

Li et al. concluded: “Reducing serum phosphate levels may be a therapeutic strategy to improve prognosis of AECOPD patients.”

“This large retrospective analysis on eICU database in the U.S. revealed elevated serum phosphate levels with increased in-hospital mortality among patients experiencing acute exacerbation of COPD,” commented Dharani Narendra, MD, assistant professor in medicine, at Baylor College of Medicine, Houston. “This association, previously observed in various chronic conditions including COPD, particularly in men, is now noted to apply to both genders, irrespective of chronic kidney disease. The study also hints at potential mechanisms for elevated phosphate levels, such as inflammation, oxidative stress, and cell apoptosis in AECOPD, as well as a high-phosphate diet.”

She told this news organization also, “It remains imperative to ascertain whether treating hyperphosphatemia or implementing dietary phosphate restrictions can reduce mortality or prevent AECOPD episodes. These demand additional clinical trials to establish a definitive cause-and-effect relationship and to guide potential treatment and prevention strategies.”

Noting study limitations, Li et al. stated that many variables, such as smoking, exacerbation frequency, severity, PH, PaO₂, PaCO₂, and lactate, were not included in this study owing to more than 20% missing values.

This work was supported by the National Natural Science Foundation of China, Scientific Research Fund of Hunan Provincial Education Department, Hunan Provincial Natural Science Foundation, and Special fund for rehabilitation medicine of the National Clinical Research Center for Geriatric Disorders Clinical Research Fund. The authors declare no competing interests.
 

Inhalers, nebulizers, antibiotics, and steroids – these are some of the most common tools in our pulmonary arsenal that we deploy on a daily basis. But, there is no treatment more fundamental to a pulmonary practitioner than oxygen. So how is it that something that naturally occurs and comprises 21% of ambient air has become so medicalized?

It is difficult (perhaps impossible) to find a pulmonologist or a hospitalist who has not included the phrase “obtain ambulatory saturation to qualify the patient for home oxygen” in at least one of their progress notes on a daily basis. Chronic obstructive pulmonary disease (COPD) is the most common reason for the prescription of long-term oxygen therapy (LTOT), a large industry tightly regulated by the Centers for Medicare & Medicaid Services (CMS).

The evidence for the use of LTOT in patients with COPD dates back to two seminal papers published in 1980 and 1981. The British Medical Research Council Working Party conducted the BMRC trial, in which 87 patients with a Pao2 of 40 mm Hg to 60 mm Hg, CO2 retention, and a history of congestive heart failure were randomized to treatment with 15 hours per day of home oxygen therapy, starting at 2 L and titrating to Pao2 of 60 mm Hg vs. standard therapy without oxygen (Lancet. 1981;1[8222]:681-6). There was an impressive 22% mortality benefit at 3 years.

Another study published around the same time, the Continuous or nocturnal oxygen therapy in hypoxemic chronic obstructive lung disease (NOTT) trial (Ann Intern Med. 1980;93[3]:391-8) directly compared continuous 24-hour to nocturnal home oxygen therapy in patients with COPD and severe hypoxemia with a Pao2 less than 55 mm Hg. Again, there was an impressive mortality benefit in favor of continuous home oxygen with a 9% and 18% mortality difference at 1 and 2 years of enrollment, respectively.

Afterward, it became universally accepted dogma that patients with COPD and severe hypoxemia stood to substantially benefit from LTOT. For years, it was the only therapy associated with a mortality reduction. The LOTT study (Albert RK, et al. N Engl J Med. 2016;375[17]:1617-27) included 768 patients with stable COPD and a resting or nocturnal Spo2 of 89% to93%, as well as patients with moderate exercise-induced desaturation (Spo2 of greater than or equal to 80% and less than 90% for greater than or equal to 10 seconds during the 6-minute walk test). Half of these patients received oxygen for 24 hours per day, during sleep, or during exercise (depending on when desaturation would occur) and half received no oxygen. There was no difference in time to death or first hospitalization or in rates of hospitalization or exacerbation. There was also no difference between groups in quality of life, lung function, or distance walked in 6 minutes.

The INOX (Lacasse Y, et al. N Engl J Med. 2020;383[12]:1129-38) trial, in which 243 patients with oxygen saturation less than 90% for at least 30% of the night were assigned to receive nocturnal vs sham oxygen, found similar results. There was no difference in the composite outcome of all-cause mortality and progression to 24-7 oxygen requirement (according to the criteria originally defined by NOTT). A 2022 systematic review and meta-analysis including six studies designed to assess the role of LTOT in patients with COPD and moderate desaturation, including LOTT and INOX, found no benefit to providing LTOT (Lacasse Y, et al. Lancet Respir Med. 2022;10[11]:1029-37).

Based on these studies, a resting Spo2 of 88% seems to be the threshold below which LTOT improves outcomes. CMS lists four classes of patients eligible for LTOT: (1) Patients with Pao2 < 55 mm Hg or pulse oximetry less than or equal to 88% at rest or (2) during sleep or (3) during exercise, and (4) patients with Pao2 > 55 mm Hg but less than or equal to 59 mm Hg or pulse oximetry of 89% who have lower extremity edema, evidence of pulmonary hypertension, or erythrocythemia (Centers for Medicare & Medicaid Services. Medicare Coverage Database. 2021;100-103:240.2. These criteria reflect the inclusion criteria of the BMRC trial and NOTT.

COPD management has changed significantly in the 40 years since NOTT was published. In the early 1980s, standard of care included an inhaled beta-agonist and oral theophylline. We now prescribe a regimen of modern-day inhaler combinations, which can lead to a mortality benefit in the correct population. Additionally, rates of smoking are markedly lower now than they were in 1980. In the Minnesota Heart Survey, the prevalence of being an ever-smoking man or woman in 1980 compared with 2009 dropped from 71.6% and 54.7% to 44.2% and 39.6%, respectively (Filion KB, et al. Am J Public Health. 2012;102[4]:705-13). Treatment of common comorbid conditions has also dramatically improved.

A report containing all fee-for-service data published in 2021 by CMS reported oxygen therapy accounted for 9.8% of all DME costs covered by CMS and totaled approximately $800,000,000 (Centers for Medicare & Medicaid Services. FFS Data. 2021. This represents a significant financial burden to our health system and government.

Two of the eligible groups per CMS (those with isolated ambulatory or nocturnal hypoxemia) do not benefit from LTOT in RCTs. The other two groups are eligible based on trial data from a small number of patients who were studied more than 40 years ago. These facts raise serious questions about the cost-efficacy of LTOT.

So where does this leave us?

There are significant barriers to repeating large randomized oxygen trials. Due to broad inclusion criteria for LTOT by CMS, there are undoubtedly many people prescribed LTOT for whom there is minimal to no benefit. Patients often feel restricted in their mobility and may feel isolated being tethered to medical equipment. It is good practice to think about LTOT the same way we do any other therapy we provide - as a medicine with associated risks, benefits, and costs.

Despite its ubiquity, oxygen remains an important therapeutic tool. Still, choosing wisely means recognizing that not all patients who qualify for LTOT by CMS criteria will benefit.

Drs. Kreisel and Sonti are with the Division of Pulmonary, Critical Care, and Sleep Medicine, MedStar Georgetown University Hospital, Washington, DC.

Inhalers, nebulizers, antibiotics, and steroids – these are some of the most common tools in our pulmonary arsenal that we deploy on a daily basis. But, there is no treatment more fundamental to a pulmonary practitioner than oxygen. So how is it that something that naturally occurs and comprises 21% of ambient air has become so medicalized?

It is difficult (perhaps impossible) to find a pulmonologist or a hospitalist who has not included the phrase “obtain ambulatory saturation to qualify the patient for home oxygen” in at least one of their progress notes on a daily basis. Chronic obstructive pulmonary disease (COPD) is the most common reason for the prescription of long-term oxygen therapy (LTOT), a large industry tightly regulated by the Centers for Medicare & Medicaid Services (CMS).

The evidence for the use of LTOT in patients with COPD dates back to two seminal papers published in 1980 and 1981. The British Medical Research Council Working Party conducted the BMRC trial, in which 87 patients with a Pao2 of 40 mm Hg to 60 mm Hg, CO2 retention, and a history of congestive heart failure were randomized to treatment with 15 hours per day of home oxygen therapy, starting at 2 L and titrating to Pao2 of 60 mm Hg vs. standard therapy without oxygen (Lancet. 1981;1[8222]:681-6). There was an impressive 22% mortality benefit at 3 years.

Another study published around the same time, the Continuous or nocturnal oxygen therapy in hypoxemic chronic obstructive lung disease (NOTT) trial (Ann Intern Med. 1980;93[3]:391-8) directly compared continuous 24-hour to nocturnal home oxygen therapy in patients with COPD and severe hypoxemia with a Pao2 less than 55 mm Hg. Again, there was an impressive mortality benefit in favor of continuous home oxygen with a 9% and 18% mortality difference at 1 and 2 years of enrollment, respectively.

Afterward, it became universally accepted dogma that patients with COPD and severe hypoxemia stood to substantially benefit from LTOT. For years, it was the only therapy associated with a mortality reduction. The LOTT study (Albert RK, et al. N Engl J Med. 2016;375[17]:1617-27) included 768 patients with stable COPD and a resting or nocturnal Spo2 of 89% to93%, as well as patients with moderate exercise-induced desaturation (Spo2 of greater than or equal to 80% and less than 90% for greater than or equal to 10 seconds during the 6-minute walk test). Half of these patients received oxygen for 24 hours per day, during sleep, or during exercise (depending on when desaturation would occur) and half received no oxygen. There was no difference in time to death or first hospitalization or in rates of hospitalization or exacerbation. There was also no difference between groups in quality of life, lung function, or distance walked in 6 minutes.

The INOX (Lacasse Y, et al. N Engl J Med. 2020;383[12]:1129-38) trial, in which 243 patients with oxygen saturation less than 90% for at least 30% of the night were assigned to receive nocturnal vs sham oxygen, found similar results. There was no difference in the composite outcome of all-cause mortality and progression to 24-7 oxygen requirement (according to the criteria originally defined by NOTT). A 2022 systematic review and meta-analysis including six studies designed to assess the role of LTOT in patients with COPD and moderate desaturation, including LOTT and INOX, found no benefit to providing LTOT (Lacasse Y, et al. Lancet Respir Med. 2022;10[11]:1029-37).

Based on these studies, a resting Spo2 of 88% seems to be the threshold below which LTOT improves outcomes. CMS lists four classes of patients eligible for LTOT: (1) Patients with Pao2 < 55 mm Hg or pulse oximetry less than or equal to 88% at rest or (2) during sleep or (3) during exercise, and (4) patients with Pao2 > 55 mm Hg but less than or equal to 59 mm Hg or pulse oximetry of 89% who have lower extremity edema, evidence of pulmonary hypertension, or erythrocythemia (Centers for Medicare & Medicaid Services. Medicare Coverage Database. 2021;100-103:240.2. These criteria reflect the inclusion criteria of the BMRC trial and NOTT.

COPD management has changed significantly in the 40 years since NOTT was published. In the early 1980s, standard of care included an inhaled beta-agonist and oral theophylline. We now prescribe a regimen of modern-day inhaler combinations, which can lead to a mortality benefit in the correct population. Additionally, rates of smoking are markedly lower now than they were in 1980. In the Minnesota Heart Survey, the prevalence of being an ever-smoking man or woman in 1980 compared with 2009 dropped from 71.6% and 54.7% to 44.2% and 39.6%, respectively (Filion KB, et al. Am J Public Health. 2012;102[4]:705-13). Treatment of common comorbid conditions has also dramatically improved.

A report containing all fee-for-service data published in 2021 by CMS reported oxygen therapy accounted for 9.8% of all DME costs covered by CMS and totaled approximately $800,000,000 (Centers for Medicare & Medicaid Services. FFS Data. 2021. This represents a significant financial burden to our health system and government.

Two of the eligible groups per CMS (those with isolated ambulatory or nocturnal hypoxemia) do not benefit from LTOT in RCTs. The other two groups are eligible based on trial data from a small number of patients who were studied more than 40 years ago. These facts raise serious questions about the cost-efficacy of LTOT.

So where does this leave us?

There are significant barriers to repeating large randomized oxygen trials. Due to broad inclusion criteria for LTOT by CMS, there are undoubtedly many people prescribed LTOT for whom there is minimal to no benefit. Patients often feel restricted in their mobility and may feel isolated being tethered to medical equipment. It is good practice to think about LTOT the same way we do any other therapy we provide - as a medicine with associated risks, benefits, and costs.

Despite its ubiquity, oxygen remains an important therapeutic tool. Still, choosing wisely means recognizing that not all patients who qualify for LTOT by CMS criteria will benefit.

Drs. Kreisel and Sonti are with the Division of Pulmonary, Critical Care, and Sleep Medicine, MedStar Georgetown University Hospital, Washington, DC.

Inhalers, nebulizers, antibiotics, and steroids – these are some of the most common tools in our pulmonary arsenal that we deploy on a daily basis. But, there is no treatment more fundamental to a pulmonary practitioner than oxygen. So how is it that something that naturally occurs and comprises 21% of ambient air has become so medicalized?

It is difficult (perhaps impossible) to find a pulmonologist or a hospitalist who has not included the phrase “obtain ambulatory saturation to qualify the patient for home oxygen” in at least one of their progress notes on a daily basis. Chronic obstructive pulmonary disease (COPD) is the most common reason for the prescription of long-term oxygen therapy (LTOT), a large industry tightly regulated by the Centers for Medicare & Medicaid Services (CMS).

The evidence for the use of LTOT in patients with COPD dates back to two seminal papers published in 1980 and 1981. The British Medical Research Council Working Party conducted the BMRC trial, in which 87 patients with a Pao2 of 40 mm Hg to 60 mm Hg, CO2 retention, and a history of congestive heart failure were randomized to treatment with 15 hours per day of home oxygen therapy, starting at 2 L and titrating to Pao2 of 60 mm Hg vs. standard therapy without oxygen (Lancet. 1981;1[8222]:681-6). There was an impressive 22% mortality benefit at 3 years.

Another study published around the same time, the Continuous or nocturnal oxygen therapy in hypoxemic chronic obstructive lung disease (NOTT) trial (Ann Intern Med. 1980;93[3]:391-8) directly compared continuous 24-hour to nocturnal home oxygen therapy in patients with COPD and severe hypoxemia with a Pao2 less than 55 mm Hg. Again, there was an impressive mortality benefit in favor of continuous home oxygen with a 9% and 18% mortality difference at 1 and 2 years of enrollment, respectively.

Afterward, it became universally accepted dogma that patients with COPD and severe hypoxemia stood to substantially benefit from LTOT. For years, it was the only therapy associated with a mortality reduction. The LOTT study (Albert RK, et al. N Engl J Med. 2016;375[17]:1617-27) included 768 patients with stable COPD and a resting or nocturnal Spo2 of 89% to93%, as well as patients with moderate exercise-induced desaturation (Spo2 of greater than or equal to 80% and less than 90% for greater than or equal to 10 seconds during the 6-minute walk test). Half of these patients received oxygen for 24 hours per day, during sleep, or during exercise (depending on when desaturation would occur) and half received no oxygen. There was no difference in time to death or first hospitalization or in rates of hospitalization or exacerbation. There was also no difference between groups in quality of life, lung function, or distance walked in 6 minutes.

The INOX (Lacasse Y, et al. N Engl J Med. 2020;383[12]:1129-38) trial, in which 243 patients with oxygen saturation less than 90% for at least 30% of the night were assigned to receive nocturnal vs sham oxygen, found similar results. There was no difference in the composite outcome of all-cause mortality and progression to 24-7 oxygen requirement (according to the criteria originally defined by NOTT). A 2022 systematic review and meta-analysis including six studies designed to assess the role of LTOT in patients with COPD and moderate desaturation, including LOTT and INOX, found no benefit to providing LTOT (Lacasse Y, et al. Lancet Respir Med. 2022;10[11]:1029-37).

Based on these studies, a resting Spo2 of 88% seems to be the threshold below which LTOT improves outcomes. CMS lists four classes of patients eligible for LTOT: (1) Patients with Pao2 < 55 mm Hg or pulse oximetry less than or equal to 88% at rest or (2) during sleep or (3) during exercise, and (4) patients with Pao2 > 55 mm Hg but less than or equal to 59 mm Hg or pulse oximetry of 89% who have lower extremity edema, evidence of pulmonary hypertension, or erythrocythemia (Centers for Medicare & Medicaid Services. Medicare Coverage Database. 2021;100-103:240.2. These criteria reflect the inclusion criteria of the BMRC trial and NOTT.

COPD management has changed significantly in the 40 years since NOTT was published. In the early 1980s, standard of care included an inhaled beta-agonist and oral theophylline. We now prescribe a regimen of modern-day inhaler combinations, which can lead to a mortality benefit in the correct population. Additionally, rates of smoking are markedly lower now than they were in 1980. In the Minnesota Heart Survey, the prevalence of being an ever-smoking man or woman in 1980 compared with 2009 dropped from 71.6% and 54.7% to 44.2% and 39.6%, respectively (Filion KB, et al. Am J Public Health. 2012;102[4]:705-13). Treatment of common comorbid conditions has also dramatically improved.

A report containing all fee-for-service data published in 2021 by CMS reported oxygen therapy accounted for 9.8% of all DME costs covered by CMS and totaled approximately $800,000,000 (Centers for Medicare & Medicaid Services. FFS Data. 2021. This represents a significant financial burden to our health system and government.

Two of the eligible groups per CMS (those with isolated ambulatory or nocturnal hypoxemia) do not benefit from LTOT in RCTs. The other two groups are eligible based on trial data from a small number of patients who were studied more than 40 years ago. These facts raise serious questions about the cost-efficacy of LTOT.

So where does this leave us?

There are significant barriers to repeating large randomized oxygen trials. Due to broad inclusion criteria for LTOT by CMS, there are undoubtedly many people prescribed LTOT for whom there is minimal to no benefit. Patients often feel restricted in their mobility and may feel isolated being tethered to medical equipment. It is good practice to think about LTOT the same way we do any other therapy we provide - as a medicine with associated risks, benefits, and costs.

Despite its ubiquity, oxygen remains an important therapeutic tool. Still, choosing wisely means recognizing that not all patients who qualify for LTOT by CMS criteria will benefit.

Drs. Kreisel and Sonti are with the Division of Pulmonary, Critical Care, and Sleep Medicine, MedStar Georgetown University Hospital, Washington, DC.

HONOLULU – Among patients hospitalized with chronic obstructive pulmonary disease (COPD) exacerbations, treatment with a combination of long-acting bronchodilators was similar in safety and efficacy to a short-acting combination of albuterol and ipratropium.

The 2023 Gold Report on prevention, management, and diagnosis of COPD recommended switching to long-acting bronchodilators despite a lack of clinical evidence showing safety in patients hospitalized for COPD exacerbation, according to Rajiv Dhand, MD, who presented the new study at the annual meeting of the American College of Chest Physicians (CHEST).

“We wanted to establish the safety, because long-acting agents are approved only for use in nonhospitalized patients. We established that it was safe and that it was comparably effective, but you could give 30% lower doses. Patients don’t have to be woken up to get the medication, and there’s a better chance that all the doses will be administered to these patients. So I think that it provides convenience with similar efficacy and safety,” said Dr. Dhand, a pulmonologist and professor of medicine at the University of Tennessee, Knoxville.

The researchers randomized 60 patients to receive nebulized albuterol (2.5 mg) and ipratropium (0.5 mg) every 6 hours (short-acting group) or nebulized formoterol (20 mcg) every 12 hours and revefenacin (175 mcg) every 24 hours (long-acting group). The mean age was 63.2 years, 58.3% were male, and 65% were current smokers.

The median decrease between day 1 and day 3 in the Modified Borg Dyspnea score was 4.0 in the long-acting group (P < .001), and 2.0 in the short-acting group, though the latter was not statistically significant (P = .134). Both groups had a decrease in supplemental oxygen requirement, with no difference between the two groups. There was also no difference in the number of respiratory visits for rescue therapy.

Respiratory therapists in the audience welcomed the new evidence. “As a respiratory therapist, I feel that we should move away from giving good short acting [therapies] ... the new guidelines state that we should move away from them, but I think that physicians in general have not gone that way. The way that we’re working, giving short acting every four hours – I don’t see that it’s a benefit to our patients,” said Sharon Armstead, who attended the session and was asked to comment on the study. She is a respiratory therapist at Ascension Health and an instructor at Concordia University, Austin, Texas. Ms. Armstead has asthma, and has first-hand experience as a patient when respiratory therapists are unable to attend to the patient every 4 hours.

She suggested that continued use of short-acting therapies may be due to inertia. “It’s easier [for a physician] to click a button on [a computer screen] than to actually slow down and write the order. If we need a rescue, then we’ll call for a rescue,” Ms. Armstead said.

She anticipates that long-acting therapies will ultimately lead to better outcomes because they will increase the time that respiratory therapists can spend with patients. “That’s what we really want to do. We want to spend time with our patients and stay there and watch our patients. But if you’re just telling us to [administer a therapy] every 4 hours, it’s not really giving the patient what they need.”

Specifically, there were concerns about cardiovascular safety, but the researchers found no between-group differences.

Asked for comment, session co-moderator Brittany Duchene, MD remarked: “It’s super interesting, but I worry about the cost. From a practical perspective, it’s challenging to get those drugs placed on an outpatient basis. They are very expensive, and they’re newer [drugs], but I think overall it’s good to give less,” said Dr. Duchene, a pulmonary critical care physician at Northeastern Vermont Regional Hospital, St. Johnsbury.

A potential concern raised by one audience member is that some patients are used to frequent treatment and may grow anxious with less frequent therapy. “I think we just need some reeducation that this is like a long-acting medicine. It also decreases the burden on our respiratory therapists, which is very good,” said Dr. Duchene.

The study was funded by Mylan/Theravance Biopharma. Dr. Dhand has received research support from Theravance, Mylan, and Viatris. He has received honoraria from Teva and UpToDate. Ms. Armstead and Dr. Duchene have no relevant financial disclosures.

HONOLULU – Among patients hospitalized with chronic obstructive pulmonary disease (COPD) exacerbations, treatment with a combination of long-acting bronchodilators was similar in safety and efficacy to a short-acting combination of albuterol and ipratropium.

The 2023 Gold Report on prevention, management, and diagnosis of COPD recommended switching to long-acting bronchodilators despite a lack of clinical evidence showing safety in patients hospitalized for COPD exacerbation, according to Rajiv Dhand, MD, who presented the new study at the annual meeting of the American College of Chest Physicians (CHEST).

“We wanted to establish the safety, because long-acting agents are approved only for use in nonhospitalized patients. We established that it was safe and that it was comparably effective, but you could give 30% lower doses. Patients don’t have to be woken up to get the medication, and there’s a better chance that all the doses will be administered to these patients. So I think that it provides convenience with similar efficacy and safety,” said Dr. Dhand, a pulmonologist and professor of medicine at the University of Tennessee, Knoxville.

The researchers randomized 60 patients to receive nebulized albuterol (2.5 mg) and ipratropium (0.5 mg) every 6 hours (short-acting group) or nebulized formoterol (20 mcg) every 12 hours and revefenacin (175 mcg) every 24 hours (long-acting group). The mean age was 63.2 years, 58.3% were male, and 65% were current smokers.

The median decrease between day 1 and day 3 in the Modified Borg Dyspnea score was 4.0 in the long-acting group (P < .001), and 2.0 in the short-acting group, though the latter was not statistically significant (P = .134). Both groups had a decrease in supplemental oxygen requirement, with no difference between the two groups. There was also no difference in the number of respiratory visits for rescue therapy.

Respiratory therapists in the audience welcomed the new evidence. “As a respiratory therapist, I feel that we should move away from giving good short acting [therapies] ... the new guidelines state that we should move away from them, but I think that physicians in general have not gone that way. The way that we’re working, giving short acting every four hours – I don’t see that it’s a benefit to our patients,” said Sharon Armstead, who attended the session and was asked to comment on the study. She is a respiratory therapist at Ascension Health and an instructor at Concordia University, Austin, Texas. Ms. Armstead has asthma, and has first-hand experience as a patient when respiratory therapists are unable to attend to the patient every 4 hours.

She suggested that continued use of short-acting therapies may be due to inertia. “It’s easier [for a physician] to click a button on [a computer screen] than to actually slow down and write the order. If we need a rescue, then we’ll call for a rescue,” Ms. Armstead said.

She anticipates that long-acting therapies will ultimately lead to better outcomes because they will increase the time that respiratory therapists can spend with patients. “That’s what we really want to do. We want to spend time with our patients and stay there and watch our patients. But if you’re just telling us to [administer a therapy] every 4 hours, it’s not really giving the patient what they need.”

Specifically, there were concerns about cardiovascular safety, but the researchers found no between-group differences.

Asked for comment, session co-moderator Brittany Duchene, MD remarked: “It’s super interesting, but I worry about the cost. From a practical perspective, it’s challenging to get those drugs placed on an outpatient basis. They are very expensive, and they’re newer [drugs], but I think overall it’s good to give less,” said Dr. Duchene, a pulmonary critical care physician at Northeastern Vermont Regional Hospital, St. Johnsbury.

A potential concern raised by one audience member is that some patients are used to frequent treatment and may grow anxious with less frequent therapy. “I think we just need some reeducation that this is like a long-acting medicine. It also decreases the burden on our respiratory therapists, which is very good,” said Dr. Duchene.

The study was funded by Mylan/Theravance Biopharma. Dr. Dhand has received research support from Theravance, Mylan, and Viatris. He has received honoraria from Teva and UpToDate. Ms. Armstead and Dr. Duchene have no relevant financial disclosures.

HONOLULU – Among patients hospitalized with chronic obstructive pulmonary disease (COPD) exacerbations, treatment with a combination of long-acting bronchodilators was similar in safety and efficacy to a short-acting combination of albuterol and ipratropium.

The 2023 Gold Report on prevention, management, and diagnosis of COPD recommended switching to long-acting bronchodilators despite a lack of clinical evidence showing safety in patients hospitalized for COPD exacerbation, according to Rajiv Dhand, MD, who presented the new study at the annual meeting of the American College of Chest Physicians (CHEST).

“We wanted to establish the safety, because long-acting agents are approved only for use in nonhospitalized patients. We established that it was safe and that it was comparably effective, but you could give 30% lower doses. Patients don’t have to be woken up to get the medication, and there’s a better chance that all the doses will be administered to these patients. So I think that it provides convenience with similar efficacy and safety,” said Dr. Dhand, a pulmonologist and professor of medicine at the University of Tennessee, Knoxville.

The researchers randomized 60 patients to receive nebulized albuterol (2.5 mg) and ipratropium (0.5 mg) every 6 hours (short-acting group) or nebulized formoterol (20 mcg) every 12 hours and revefenacin (175 mcg) every 24 hours (long-acting group). The mean age was 63.2 years, 58.3% were male, and 65% were current smokers.

The median decrease between day 1 and day 3 in the Modified Borg Dyspnea score was 4.0 in the long-acting group (P < .001), and 2.0 in the short-acting group, though the latter was not statistically significant (P = .134). Both groups had a decrease in supplemental oxygen requirement, with no difference between the two groups. There was also no difference in the number of respiratory visits for rescue therapy.

Respiratory therapists in the audience welcomed the new evidence. “As a respiratory therapist, I feel that we should move away from giving good short acting [therapies] ... the new guidelines state that we should move away from them, but I think that physicians in general have not gone that way. The way that we’re working, giving short acting every four hours – I don’t see that it’s a benefit to our patients,” said Sharon Armstead, who attended the session and was asked to comment on the study. She is a respiratory therapist at Ascension Health and an instructor at Concordia University, Austin, Texas. Ms. Armstead has asthma, and has first-hand experience as a patient when respiratory therapists are unable to attend to the patient every 4 hours.

She suggested that continued use of short-acting therapies may be due to inertia. “It’s easier [for a physician] to click a button on [a computer screen] than to actually slow down and write the order. If we need a rescue, then we’ll call for a rescue,” Ms. Armstead said.

She anticipates that long-acting therapies will ultimately lead to better outcomes because they will increase the time that respiratory therapists can spend with patients. “That’s what we really want to do. We want to spend time with our patients and stay there and watch our patients. But if you’re just telling us to [administer a therapy] every 4 hours, it’s not really giving the patient what they need.”

Specifically, there were concerns about cardiovascular safety, but the researchers found no between-group differences.

Asked for comment, session co-moderator Brittany Duchene, MD remarked: “It’s super interesting, but I worry about the cost. From a practical perspective, it’s challenging to get those drugs placed on an outpatient basis. They are very expensive, and they’re newer [drugs], but I think overall it’s good to give less,” said Dr. Duchene, a pulmonary critical care physician at Northeastern Vermont Regional Hospital, St. Johnsbury.

A potential concern raised by one audience member is that some patients are used to frequent treatment and may grow anxious with less frequent therapy. “I think we just need some reeducation that this is like a long-acting medicine. It also decreases the burden on our respiratory therapists, which is very good,” said Dr. Duchene.

The study was funded by Mylan/Theravance Biopharma. Dr. Dhand has received research support from Theravance, Mylan, and Viatris. He has received honoraria from Teva and UpToDate. Ms. Armstead and Dr. Duchene have no relevant financial disclosures.

Click to read more from Pulmonology Data Trends 2023.

Click to read more from Pulmonology Data Trends 2023.

Click to read more from Pulmonology Data Trends 2023.