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Longitudinal progression of parenchymal changes on CT images — also referred to as quantitative interstitial abnormalities (QIA) – is independently associated with decreased lung function and an increased all-cause mortality risk, an analysis of two cohorts of ever-smokers indicates. And among the main risk factors for QIA progression is smoking.
“These abnormalities have gone by a few different names but fundamentally, they are high density findings of chest CT that in some cases represent early or subtle evidence of pulmonary fibrosis,” Samuel Ash, MD, MPH, assistant professor of medicine, Brigham and Women’s Hospital, Boston, told this news organization.
So when I see someone with visual evidence of this type of change on their chest CT, I make sure to emphasize that while they don’t have interstitial lung disease [ILD] yet, these findings suggest they may be susceptible to lung injury from tobacco smoke and that if they don’t stop smoking now, they are at risk for a disease like interstitial pulmonary fibrosis [IPF] which is a highly morbid disease with a high mortality risk,” he added.
The study was published online in the journal CHEST.
Ever-smoking cohorts
Analysis of QIA progression on CT chest scans was carried out on participants from the Genetic Epidemiology of COPD (COPDGene) study as well as those from the Pittsburgh Lung Screening Study (PLuSS). COPDGene was a prospective cohort of over 10,300 ever-smokers with at least a 10–pack-year smoking history between the ages of 45 and 80. Participants underwent a series of tests including chest CT scans at baseline between 2006 and 2011 and again approximately 5 years later.
Patients with a postbronchodilator forced expiratory volume in 1 second (FEV1) of 80% or more of predicted and a FEV1-to-FVC (forced vital capacity) ratio of at least 0.7 were defined to have GOLD stage 0 disease while those with a postbronchodilator FEV1 of 80% or less than predicted and a FEV1-to-FVC ratio of at least 0.7 were defined to have preserved ratio impaired spirometry (PRISm) disease.
PLuSS involved 3,642 ever-smokers between the ages of 50 years and 79 years with at least a 12.5–pack-year history with no prior history of lung cancer. Participants again underwent a series of tests including a CT scan on visit 1 between 2002 and 2005 and then a second CT scan at a second visit almost 9 years later. “In the COPDGene cohort, 4,635 participants had complete clinical data, CT scans and spirometry from visits 1 and 2 for analysis,” the authors reported.
At visit 1 almost 48% of participants were current smokers and the mean pack-year history of the cohort was 41.9 years. The mean time between visits 1 and 2 was 5.6 years. Both the mean prebronchodilator FEV1 as well as the mean FVC decreased between visits 1 and 2. For example, the mean prebronchodilator FEV1 dropped from 2.2 liters to 2.0 liters between visits 1 and 2 while the mean prebronchodilator FVC decreased from 3.2 liters to 3.0 liters between the first and second visits.
In the PLuSS cohort, 1,307 participants had complete imaging and spirometry data available for visits 1 and 2 for analysis. The mean time between visits 1 and 2 was 8.6 years. Over 59% of the cohort were current smokers with a mean pack-year history of 65. Again, the mean prebronchodilator FEV1 and FVC both dropped between visit 1 and 2, as the authors note.
The mean prebronchodilator FEV1, for example, decreased from 2.5 liters to 2.1 liters between visits 1 and 2 while the mean prebronchodilator FVC dropped from 3.6 liters to 3.2 liters during the same interval. Looking at risk factors associated with QIA progression, investigators note that each additional year of baseline age was associated with a higher annual increase in QIA by 0.01% per year (95% confidence interval, 0.01%-0.02%; P < .001) in the COPDGene cohort and a 0.02% increase (95% CI, 0.01%-0.02%; P < .001) in the PLuSS cohort.
Female sex in turn was associated with a 0.07% per year (95% CI, 0.02%-0.12%; P = .003) higher increase in the QIA, compared with men in the COPDGene cohort and a 0.14% (95% CI, 0.02%-0.26%; P = .025) per year higher increase in the QIA in the PLuSS cohort. Current smoking status was only associated with a higher rate of QIA progression in the COPDGene cohort at a rate of 0.10% per year (95% CI, 0.06%-0.15%; P < .001).
Lastly, every copy of the minor allele of the MUIC5B promoter polymorphism was associated with a 0.12% per year (95% CI, 0.07%-0.16%; P < .0001) increase in QIA in the COPDGene cohort as well.
Smoking cessation
Smoking cessation is the obvious first step for patients with evidence of QIA progression but physicians can probably do more for these patients sooner, Dr. Ash said. “If we use heart disease as an analogy, we don’t want to start treating someone until they have a heart attack or are in heart failure, we start by checking their cholesterol and blood pressure and treating them with medications to prevent progression.”
Similarly, physicians need to start thinking about IPF and other lung diseases in the same way. For IPF, medications such as pirfenidone (Esbriet) and nintedanib (Ofev) do not reverse prior lung damage but they do slow disease progression and physicians need to initiate treatment before patients are short of breath, not after. Meantime, Dr. Ash advised physicians that, if they have a patient who is getting a CT scan for whatever reason, they should keep a close eye on whether or not patients have any of these interstitial changes and, if they do, then if the changes are getting worse.
“These patients are likely to be the ones who are going to develop IPF and who may benefit from ongoing imaging surveillance,” he said. And while clinicians may not yet be ready to use a quantitative tool at the bedside, “this tool – or one like it – is coming and we have to start thinking about how to incorporate these types of devices into our clinical practice.”
Temporal changes
Asked to comment on the findings, Surya Bhatt, MD, associate professor of medicine at the University of Alabama at Birmingham, said that the study advances the community’s understanding of the relationship between temporal changes in objectively measured interstitial lung abnormalities and several important clinical outcomes, including lung function decline and mortality. “Several risk factors for progression were also identified,” he noted.
“And these results make a case for initiating clinical trials to determine whether early treatment with existing antifibrotic medications in these high risk individuals can decrease the perpetuation of these permanent lung changes,” Dr. Bhatt said.
The COPDGene study was supported in part by contributions made by an industry advisory board. Dr. Ash was supported in part by Quantitative Imaging Solutions. Dr. Bhatt declared that he has receiving consulting fees or has service on advisory boards for Boehringer Ingelheim and Sanofi/Regeneron. He ha also received fee for CME from IntegrityCE.
Longitudinal progression of parenchymal changes on CT images — also referred to as quantitative interstitial abnormalities (QIA) – is independently associated with decreased lung function and an increased all-cause mortality risk, an analysis of two cohorts of ever-smokers indicates. And among the main risk factors for QIA progression is smoking.
“These abnormalities have gone by a few different names but fundamentally, they are high density findings of chest CT that in some cases represent early or subtle evidence of pulmonary fibrosis,” Samuel Ash, MD, MPH, assistant professor of medicine, Brigham and Women’s Hospital, Boston, told this news organization.
So when I see someone with visual evidence of this type of change on their chest CT, I make sure to emphasize that while they don’t have interstitial lung disease [ILD] yet, these findings suggest they may be susceptible to lung injury from tobacco smoke and that if they don’t stop smoking now, they are at risk for a disease like interstitial pulmonary fibrosis [IPF] which is a highly morbid disease with a high mortality risk,” he added.
The study was published online in the journal CHEST.
Ever-smoking cohorts
Analysis of QIA progression on CT chest scans was carried out on participants from the Genetic Epidemiology of COPD (COPDGene) study as well as those from the Pittsburgh Lung Screening Study (PLuSS). COPDGene was a prospective cohort of over 10,300 ever-smokers with at least a 10–pack-year smoking history between the ages of 45 and 80. Participants underwent a series of tests including chest CT scans at baseline between 2006 and 2011 and again approximately 5 years later.
Patients with a postbronchodilator forced expiratory volume in 1 second (FEV1) of 80% or more of predicted and a FEV1-to-FVC (forced vital capacity) ratio of at least 0.7 were defined to have GOLD stage 0 disease while those with a postbronchodilator FEV1 of 80% or less than predicted and a FEV1-to-FVC ratio of at least 0.7 were defined to have preserved ratio impaired spirometry (PRISm) disease.
PLuSS involved 3,642 ever-smokers between the ages of 50 years and 79 years with at least a 12.5–pack-year history with no prior history of lung cancer. Participants again underwent a series of tests including a CT scan on visit 1 between 2002 and 2005 and then a second CT scan at a second visit almost 9 years later. “In the COPDGene cohort, 4,635 participants had complete clinical data, CT scans and spirometry from visits 1 and 2 for analysis,” the authors reported.
At visit 1 almost 48% of participants were current smokers and the mean pack-year history of the cohort was 41.9 years. The mean time between visits 1 and 2 was 5.6 years. Both the mean prebronchodilator FEV1 as well as the mean FVC decreased between visits 1 and 2. For example, the mean prebronchodilator FEV1 dropped from 2.2 liters to 2.0 liters between visits 1 and 2 while the mean prebronchodilator FVC decreased from 3.2 liters to 3.0 liters between the first and second visits.
In the PLuSS cohort, 1,307 participants had complete imaging and spirometry data available for visits 1 and 2 for analysis. The mean time between visits 1 and 2 was 8.6 years. Over 59% of the cohort were current smokers with a mean pack-year history of 65. Again, the mean prebronchodilator FEV1 and FVC both dropped between visit 1 and 2, as the authors note.
The mean prebronchodilator FEV1, for example, decreased from 2.5 liters to 2.1 liters between visits 1 and 2 while the mean prebronchodilator FVC dropped from 3.6 liters to 3.2 liters during the same interval. Looking at risk factors associated with QIA progression, investigators note that each additional year of baseline age was associated with a higher annual increase in QIA by 0.01% per year (95% confidence interval, 0.01%-0.02%; P < .001) in the COPDGene cohort and a 0.02% increase (95% CI, 0.01%-0.02%; P < .001) in the PLuSS cohort.
Female sex in turn was associated with a 0.07% per year (95% CI, 0.02%-0.12%; P = .003) higher increase in the QIA, compared with men in the COPDGene cohort and a 0.14% (95% CI, 0.02%-0.26%; P = .025) per year higher increase in the QIA in the PLuSS cohort. Current smoking status was only associated with a higher rate of QIA progression in the COPDGene cohort at a rate of 0.10% per year (95% CI, 0.06%-0.15%; P < .001).
Lastly, every copy of the minor allele of the MUIC5B promoter polymorphism was associated with a 0.12% per year (95% CI, 0.07%-0.16%; P < .0001) increase in QIA in the COPDGene cohort as well.
Smoking cessation
Smoking cessation is the obvious first step for patients with evidence of QIA progression but physicians can probably do more for these patients sooner, Dr. Ash said. “If we use heart disease as an analogy, we don’t want to start treating someone until they have a heart attack or are in heart failure, we start by checking their cholesterol and blood pressure and treating them with medications to prevent progression.”
Similarly, physicians need to start thinking about IPF and other lung diseases in the same way. For IPF, medications such as pirfenidone (Esbriet) and nintedanib (Ofev) do not reverse prior lung damage but they do slow disease progression and physicians need to initiate treatment before patients are short of breath, not after. Meantime, Dr. Ash advised physicians that, if they have a patient who is getting a CT scan for whatever reason, they should keep a close eye on whether or not patients have any of these interstitial changes and, if they do, then if the changes are getting worse.
“These patients are likely to be the ones who are going to develop IPF and who may benefit from ongoing imaging surveillance,” he said. And while clinicians may not yet be ready to use a quantitative tool at the bedside, “this tool – or one like it – is coming and we have to start thinking about how to incorporate these types of devices into our clinical practice.”
Temporal changes
Asked to comment on the findings, Surya Bhatt, MD, associate professor of medicine at the University of Alabama at Birmingham, said that the study advances the community’s understanding of the relationship between temporal changes in objectively measured interstitial lung abnormalities and several important clinical outcomes, including lung function decline and mortality. “Several risk factors for progression were also identified,” he noted.
“And these results make a case for initiating clinical trials to determine whether early treatment with existing antifibrotic medications in these high risk individuals can decrease the perpetuation of these permanent lung changes,” Dr. Bhatt said.
The COPDGene study was supported in part by contributions made by an industry advisory board. Dr. Ash was supported in part by Quantitative Imaging Solutions. Dr. Bhatt declared that he has receiving consulting fees or has service on advisory boards for Boehringer Ingelheim and Sanofi/Regeneron. He ha also received fee for CME from IntegrityCE.
Longitudinal progression of parenchymal changes on CT images — also referred to as quantitative interstitial abnormalities (QIA) – is independently associated with decreased lung function and an increased all-cause mortality risk, an analysis of two cohorts of ever-smokers indicates. And among the main risk factors for QIA progression is smoking.
“These abnormalities have gone by a few different names but fundamentally, they are high density findings of chest CT that in some cases represent early or subtle evidence of pulmonary fibrosis,” Samuel Ash, MD, MPH, assistant professor of medicine, Brigham and Women’s Hospital, Boston, told this news organization.
So when I see someone with visual evidence of this type of change on their chest CT, I make sure to emphasize that while they don’t have interstitial lung disease [ILD] yet, these findings suggest they may be susceptible to lung injury from tobacco smoke and that if they don’t stop smoking now, they are at risk for a disease like interstitial pulmonary fibrosis [IPF] which is a highly morbid disease with a high mortality risk,” he added.
The study was published online in the journal CHEST.
Ever-smoking cohorts
Analysis of QIA progression on CT chest scans was carried out on participants from the Genetic Epidemiology of COPD (COPDGene) study as well as those from the Pittsburgh Lung Screening Study (PLuSS). COPDGene was a prospective cohort of over 10,300 ever-smokers with at least a 10–pack-year smoking history between the ages of 45 and 80. Participants underwent a series of tests including chest CT scans at baseline between 2006 and 2011 and again approximately 5 years later.
Patients with a postbronchodilator forced expiratory volume in 1 second (FEV1) of 80% or more of predicted and a FEV1-to-FVC (forced vital capacity) ratio of at least 0.7 were defined to have GOLD stage 0 disease while those with a postbronchodilator FEV1 of 80% or less than predicted and a FEV1-to-FVC ratio of at least 0.7 were defined to have preserved ratio impaired spirometry (PRISm) disease.
PLuSS involved 3,642 ever-smokers between the ages of 50 years and 79 years with at least a 12.5–pack-year history with no prior history of lung cancer. Participants again underwent a series of tests including a CT scan on visit 1 between 2002 and 2005 and then a second CT scan at a second visit almost 9 years later. “In the COPDGene cohort, 4,635 participants had complete clinical data, CT scans and spirometry from visits 1 and 2 for analysis,” the authors reported.
At visit 1 almost 48% of participants were current smokers and the mean pack-year history of the cohort was 41.9 years. The mean time between visits 1 and 2 was 5.6 years. Both the mean prebronchodilator FEV1 as well as the mean FVC decreased between visits 1 and 2. For example, the mean prebronchodilator FEV1 dropped from 2.2 liters to 2.0 liters between visits 1 and 2 while the mean prebronchodilator FVC decreased from 3.2 liters to 3.0 liters between the first and second visits.
In the PLuSS cohort, 1,307 participants had complete imaging and spirometry data available for visits 1 and 2 for analysis. The mean time between visits 1 and 2 was 8.6 years. Over 59% of the cohort were current smokers with a mean pack-year history of 65. Again, the mean prebronchodilator FEV1 and FVC both dropped between visit 1 and 2, as the authors note.
The mean prebronchodilator FEV1, for example, decreased from 2.5 liters to 2.1 liters between visits 1 and 2 while the mean prebronchodilator FVC dropped from 3.6 liters to 3.2 liters during the same interval. Looking at risk factors associated with QIA progression, investigators note that each additional year of baseline age was associated with a higher annual increase in QIA by 0.01% per year (95% confidence interval, 0.01%-0.02%; P < .001) in the COPDGene cohort and a 0.02% increase (95% CI, 0.01%-0.02%; P < .001) in the PLuSS cohort.
Female sex in turn was associated with a 0.07% per year (95% CI, 0.02%-0.12%; P = .003) higher increase in the QIA, compared with men in the COPDGene cohort and a 0.14% (95% CI, 0.02%-0.26%; P = .025) per year higher increase in the QIA in the PLuSS cohort. Current smoking status was only associated with a higher rate of QIA progression in the COPDGene cohort at a rate of 0.10% per year (95% CI, 0.06%-0.15%; P < .001).
Lastly, every copy of the minor allele of the MUIC5B promoter polymorphism was associated with a 0.12% per year (95% CI, 0.07%-0.16%; P < .0001) increase in QIA in the COPDGene cohort as well.
Smoking cessation
Smoking cessation is the obvious first step for patients with evidence of QIA progression but physicians can probably do more for these patients sooner, Dr. Ash said. “If we use heart disease as an analogy, we don’t want to start treating someone until they have a heart attack or are in heart failure, we start by checking their cholesterol and blood pressure and treating them with medications to prevent progression.”
Similarly, physicians need to start thinking about IPF and other lung diseases in the same way. For IPF, medications such as pirfenidone (Esbriet) and nintedanib (Ofev) do not reverse prior lung damage but they do slow disease progression and physicians need to initiate treatment before patients are short of breath, not after. Meantime, Dr. Ash advised physicians that, if they have a patient who is getting a CT scan for whatever reason, they should keep a close eye on whether or not patients have any of these interstitial changes and, if they do, then if the changes are getting worse.
“These patients are likely to be the ones who are going to develop IPF and who may benefit from ongoing imaging surveillance,” he said. And while clinicians may not yet be ready to use a quantitative tool at the bedside, “this tool – or one like it – is coming and we have to start thinking about how to incorporate these types of devices into our clinical practice.”
Temporal changes
Asked to comment on the findings, Surya Bhatt, MD, associate professor of medicine at the University of Alabama at Birmingham, said that the study advances the community’s understanding of the relationship between temporal changes in objectively measured interstitial lung abnormalities and several important clinical outcomes, including lung function decline and mortality. “Several risk factors for progression were also identified,” he noted.
“And these results make a case for initiating clinical trials to determine whether early treatment with existing antifibrotic medications in these high risk individuals can decrease the perpetuation of these permanent lung changes,” Dr. Bhatt said.
The COPDGene study was supported in part by contributions made by an industry advisory board. Dr. Ash was supported in part by Quantitative Imaging Solutions. Dr. Bhatt declared that he has receiving consulting fees or has service on advisory boards for Boehringer Ingelheim and Sanofi/Regeneron. He ha also received fee for CME from IntegrityCE.
FROM CHEST