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COPD exacerbations associated with poor sleep quality
in an 18-month prospective study of 480 patients.
“Poor sleep quality in COPD has previously been associated with reduced health-related quality of life and reduced physical activity during the day,” wrote Matthew Shorofsky, MD, of McGill University, Montreal, and associates. Their report is in CHEST. “However, to our knowledge, this is the first population-based longitudinal study evaluating exacerbation risk in relation to subjective sleep disturbances and assessing previously diagnosed and undiagnosed COPD.”
The study included participants enrolled in the Canadian Respiratory Research Network and the Canadian Cohort Obstructive Lung Disease (CanCOLD) study who had COPD, available baseline PSQI scores, and 18 months of follow-up data. The PSQI includes 19 questions on sleep quality, latency, duration, efficiency, disturbances, use of sleep medications, and daytime dysfunction. Total score ranges between 0 and 21, and a score above 5 is considered poor sleep. Online patient surveys and quarterly phone interviews were used to track symptom-based exacerbations (at least 48 hours of increased dyspnea, sputum volume, or sputum purulence) and event-based exacerbations (a symptom-based exacerbation plus the use antibiotics or corticosteroids or health services).
At baseline, 203 patients met the PSQI threshold for poor sleep quality. During follow-up, 185 patients had at least one COPD exacerbation. Poor sleep at baseline was significantly more prevalent among patients with symptoms-based COPD exacerbations (50.3%) than among patients without symptoms-based exacerbations (37.3%; P = .01). Poor baseline sleep quality remained a significant risk factor for symptom-based exacerbations of COPD even after the researchers accounted for the effect of age, gender, body mass index, smoking, depression, angina, baseline inhaled respiratory medications, forced expiratory volume in 1 second %predicted, and modified Medical Research Council (mMRC) dyspnea scale (adjusted risk ratio, 1.09; 95% confidence interval, 1.01-1.18; P =.02).
Patients with at least one symptomatic exacerbation of COPD were significantly more likely to meet the threshold for poor sleep quality on the Pittsburgh Sleep Quality Index and have significantly higher median PSQI scores compared with patients without exacerbations (6.0 [interquartile range, 3.0 to 8.0] vs. 5.0 [2.0 to 7.0]; P = .01). Poor baseline sleep quality also was associated with event-based exacerbations and with a shorter time to symptoms-based exacerbations. Sleep disturbances, such as rising to void or experiencing respiratory issues or pain during sleep, correlated most strongly with symptoms-based exacerbations.
Several factors could explain the link between poor sleep quality and COPD exacerbations, the investigators wrote. Patients with inadequately controlled COPD have more frequent and unstable respiratory symptoms, which could disrupt sleep either directly or indirectly (secondary to medication use or anxiety, for example). Conversely, sleep disruption can impede immune function and increase systemic inflammation, which might worsen COPD control and increase exacerbation risk. Poor sleep can impair memory and cognition, “potentially fostering medication nonadherence and symptom flare-up, especially in the older COPD population.” Although the link is poorly understood, patients with COPD often have comorbid obstructive sleep apnea (OSA), which is associated with COPD exacerbations, the researchers wrote. Treating OSA is associated with improved COPD morbidity and fewer exacerbations and hospitalizations.
The researchers acknowledged limitations to their study design. “Individuals with asthma or other obstructive lung diseases could not be definitively excluded; methacholine challenges were not performed. However, analyses excluding self-reported asthma were consistent with our main results. Second, because definitions of COPD exacerbation vary among studies, comparison may be limited, but CanCOLD used a standard definition, as recommended by GOLD.”
The CanCOLD study has received funding from the Canadian Respiratory Research Network, Astra Zeneca Canada, Boehringer Ingelheim Canada, GlaxoSmithKline Canada, Novartis, Merck Nycomed, Pfizer Canada, and Theratechnologies. Dr. Shorofsky had no disclosures. Several coinvestigators reported ties to GlaxoSmithKline, Novartis, Boehringer Ingelheim, Merck, Almirall, and Theratechnologies.
SOURCE: Shorofsky M et al. CHEST. 2019 May 28. doi: 10.1016/j.chest.2019.04.132.
in an 18-month prospective study of 480 patients.
“Poor sleep quality in COPD has previously been associated with reduced health-related quality of life and reduced physical activity during the day,” wrote Matthew Shorofsky, MD, of McGill University, Montreal, and associates. Their report is in CHEST. “However, to our knowledge, this is the first population-based longitudinal study evaluating exacerbation risk in relation to subjective sleep disturbances and assessing previously diagnosed and undiagnosed COPD.”
The study included participants enrolled in the Canadian Respiratory Research Network and the Canadian Cohort Obstructive Lung Disease (CanCOLD) study who had COPD, available baseline PSQI scores, and 18 months of follow-up data. The PSQI includes 19 questions on sleep quality, latency, duration, efficiency, disturbances, use of sleep medications, and daytime dysfunction. Total score ranges between 0 and 21, and a score above 5 is considered poor sleep. Online patient surveys and quarterly phone interviews were used to track symptom-based exacerbations (at least 48 hours of increased dyspnea, sputum volume, or sputum purulence) and event-based exacerbations (a symptom-based exacerbation plus the use antibiotics or corticosteroids or health services).
At baseline, 203 patients met the PSQI threshold for poor sleep quality. During follow-up, 185 patients had at least one COPD exacerbation. Poor sleep at baseline was significantly more prevalent among patients with symptoms-based COPD exacerbations (50.3%) than among patients without symptoms-based exacerbations (37.3%; P = .01). Poor baseline sleep quality remained a significant risk factor for symptom-based exacerbations of COPD even after the researchers accounted for the effect of age, gender, body mass index, smoking, depression, angina, baseline inhaled respiratory medications, forced expiratory volume in 1 second %predicted, and modified Medical Research Council (mMRC) dyspnea scale (adjusted risk ratio, 1.09; 95% confidence interval, 1.01-1.18; P =.02).
Patients with at least one symptomatic exacerbation of COPD were significantly more likely to meet the threshold for poor sleep quality on the Pittsburgh Sleep Quality Index and have significantly higher median PSQI scores compared with patients without exacerbations (6.0 [interquartile range, 3.0 to 8.0] vs. 5.0 [2.0 to 7.0]; P = .01). Poor baseline sleep quality also was associated with event-based exacerbations and with a shorter time to symptoms-based exacerbations. Sleep disturbances, such as rising to void or experiencing respiratory issues or pain during sleep, correlated most strongly with symptoms-based exacerbations.
Several factors could explain the link between poor sleep quality and COPD exacerbations, the investigators wrote. Patients with inadequately controlled COPD have more frequent and unstable respiratory symptoms, which could disrupt sleep either directly or indirectly (secondary to medication use or anxiety, for example). Conversely, sleep disruption can impede immune function and increase systemic inflammation, which might worsen COPD control and increase exacerbation risk. Poor sleep can impair memory and cognition, “potentially fostering medication nonadherence and symptom flare-up, especially in the older COPD population.” Although the link is poorly understood, patients with COPD often have comorbid obstructive sleep apnea (OSA), which is associated with COPD exacerbations, the researchers wrote. Treating OSA is associated with improved COPD morbidity and fewer exacerbations and hospitalizations.
The researchers acknowledged limitations to their study design. “Individuals with asthma or other obstructive lung diseases could not be definitively excluded; methacholine challenges were not performed. However, analyses excluding self-reported asthma were consistent with our main results. Second, because definitions of COPD exacerbation vary among studies, comparison may be limited, but CanCOLD used a standard definition, as recommended by GOLD.”
The CanCOLD study has received funding from the Canadian Respiratory Research Network, Astra Zeneca Canada, Boehringer Ingelheim Canada, GlaxoSmithKline Canada, Novartis, Merck Nycomed, Pfizer Canada, and Theratechnologies. Dr. Shorofsky had no disclosures. Several coinvestigators reported ties to GlaxoSmithKline, Novartis, Boehringer Ingelheim, Merck, Almirall, and Theratechnologies.
SOURCE: Shorofsky M et al. CHEST. 2019 May 28. doi: 10.1016/j.chest.2019.04.132.
in an 18-month prospective study of 480 patients.
“Poor sleep quality in COPD has previously been associated with reduced health-related quality of life and reduced physical activity during the day,” wrote Matthew Shorofsky, MD, of McGill University, Montreal, and associates. Their report is in CHEST. “However, to our knowledge, this is the first population-based longitudinal study evaluating exacerbation risk in relation to subjective sleep disturbances and assessing previously diagnosed and undiagnosed COPD.”
The study included participants enrolled in the Canadian Respiratory Research Network and the Canadian Cohort Obstructive Lung Disease (CanCOLD) study who had COPD, available baseline PSQI scores, and 18 months of follow-up data. The PSQI includes 19 questions on sleep quality, latency, duration, efficiency, disturbances, use of sleep medications, and daytime dysfunction. Total score ranges between 0 and 21, and a score above 5 is considered poor sleep. Online patient surveys and quarterly phone interviews were used to track symptom-based exacerbations (at least 48 hours of increased dyspnea, sputum volume, or sputum purulence) and event-based exacerbations (a symptom-based exacerbation plus the use antibiotics or corticosteroids or health services).
At baseline, 203 patients met the PSQI threshold for poor sleep quality. During follow-up, 185 patients had at least one COPD exacerbation. Poor sleep at baseline was significantly more prevalent among patients with symptoms-based COPD exacerbations (50.3%) than among patients without symptoms-based exacerbations (37.3%; P = .01). Poor baseline sleep quality remained a significant risk factor for symptom-based exacerbations of COPD even after the researchers accounted for the effect of age, gender, body mass index, smoking, depression, angina, baseline inhaled respiratory medications, forced expiratory volume in 1 second %predicted, and modified Medical Research Council (mMRC) dyspnea scale (adjusted risk ratio, 1.09; 95% confidence interval, 1.01-1.18; P =.02).
Patients with at least one symptomatic exacerbation of COPD were significantly more likely to meet the threshold for poor sleep quality on the Pittsburgh Sleep Quality Index and have significantly higher median PSQI scores compared with patients without exacerbations (6.0 [interquartile range, 3.0 to 8.0] vs. 5.0 [2.0 to 7.0]; P = .01). Poor baseline sleep quality also was associated with event-based exacerbations and with a shorter time to symptoms-based exacerbations. Sleep disturbances, such as rising to void or experiencing respiratory issues or pain during sleep, correlated most strongly with symptoms-based exacerbations.
Several factors could explain the link between poor sleep quality and COPD exacerbations, the investigators wrote. Patients with inadequately controlled COPD have more frequent and unstable respiratory symptoms, which could disrupt sleep either directly or indirectly (secondary to medication use or anxiety, for example). Conversely, sleep disruption can impede immune function and increase systemic inflammation, which might worsen COPD control and increase exacerbation risk. Poor sleep can impair memory and cognition, “potentially fostering medication nonadherence and symptom flare-up, especially in the older COPD population.” Although the link is poorly understood, patients with COPD often have comorbid obstructive sleep apnea (OSA), which is associated with COPD exacerbations, the researchers wrote. Treating OSA is associated with improved COPD morbidity and fewer exacerbations and hospitalizations.
The researchers acknowledged limitations to their study design. “Individuals with asthma or other obstructive lung diseases could not be definitively excluded; methacholine challenges were not performed. However, analyses excluding self-reported asthma were consistent with our main results. Second, because definitions of COPD exacerbation vary among studies, comparison may be limited, but CanCOLD used a standard definition, as recommended by GOLD.”
The CanCOLD study has received funding from the Canadian Respiratory Research Network, Astra Zeneca Canada, Boehringer Ingelheim Canada, GlaxoSmithKline Canada, Novartis, Merck Nycomed, Pfizer Canada, and Theratechnologies. Dr. Shorofsky had no disclosures. Several coinvestigators reported ties to GlaxoSmithKline, Novartis, Boehringer Ingelheim, Merck, Almirall, and Theratechnologies.
SOURCE: Shorofsky M et al. CHEST. 2019 May 28. doi: 10.1016/j.chest.2019.04.132.
FROM CHEST
Eosinophil-guided therapy reduces corticosteroid use in COPD
in terms of the number of days out of hospital and alive, new research has found.
Writing in the Lancet Respiratory Medicine, researchers reported the outcomes of a multicenter, controlled, open-label trial comparing eosinophil-guided and standard therapy with systemic corticosteroids in 318 patients with COPD.
Pradeesh Sivapalan, MD, of the respiratory medicine section of Herlev and Gentofte Hospital at the University of Copenhagen, and coauthors wrote that eosinophilic inflammation had been seen in 20%-40% of patients with acute exacerbations of COPD. Patients with higher eosinophilic blood counts were at increased risk of acute exacerbations but were also more likely to benefit from corticosteroid treatment.
In the eosinophil-guided therapy arm of the study, 159 patients received 80 mg of intravenous methylprednisolone on day 1, then from the second day were treated with 37.5 mg of prednisolone oral tablet daily – up to 4 days – only on days when their blood eosinophil count was at least 0.3 x 10⁹ cells/L. In the control arm, 159 patients also received 80 mg of intravenous methylprednisolone on day 1, followed by 37.5 mg of prednisolone tablets daily for 4 days.
After 14 days, there were no significant differences between the two groups for mean days alive and out of hospital.
There were 12 more cases of readmission with COPD, including three fatalities, in the eosinophil-guided group within the first month. However the authors said these differences were not statistically significant, but “because the study was not powered to detect differences in this absolute risk range, we cannot rule out that this was an actual harm effect from the interventional strategy.”
The eosinophil-guided therapy group did show more than a 50% reduction in the median duration of systemic corticosteroid therapy, which was 2 days in the eosinophil-guided group, compared with 5 days in the control group (P less than .0001), and the differences between the two groups remained significant at days 30 and 90.
“The tested strategy was successful in reducing the exposure to systemic corticosteroids, but we cannot exclude the possibility that a more aggressive algorithm, such as a single dose of systemic corticosteroid, might have been more effective,” the authors wrote.
At the 90-day follow-up, there were no differences in the number of infections requiring antibiotic treatment, nor in dyspepsia, ulcer complications, or initiation of new proton-pump inhibitor treatment.
The study was supported by the Danish Regions Medical Fund and the Danish Council for Independent Research. Two authors declared personal fees from pharmaceutical companies outside the submitted work. No other conflicts were declared.
SOURCE: Sivapalan P et al. Lancet Respir Med. 2019, May 20. doi: 10.1016/S2213-2600(19)30176-6.
in terms of the number of days out of hospital and alive, new research has found.
Writing in the Lancet Respiratory Medicine, researchers reported the outcomes of a multicenter, controlled, open-label trial comparing eosinophil-guided and standard therapy with systemic corticosteroids in 318 patients with COPD.
Pradeesh Sivapalan, MD, of the respiratory medicine section of Herlev and Gentofte Hospital at the University of Copenhagen, and coauthors wrote that eosinophilic inflammation had been seen in 20%-40% of patients with acute exacerbations of COPD. Patients with higher eosinophilic blood counts were at increased risk of acute exacerbations but were also more likely to benefit from corticosteroid treatment.
In the eosinophil-guided therapy arm of the study, 159 patients received 80 mg of intravenous methylprednisolone on day 1, then from the second day were treated with 37.5 mg of prednisolone oral tablet daily – up to 4 days – only on days when their blood eosinophil count was at least 0.3 x 10⁹ cells/L. In the control arm, 159 patients also received 80 mg of intravenous methylprednisolone on day 1, followed by 37.5 mg of prednisolone tablets daily for 4 days.
After 14 days, there were no significant differences between the two groups for mean days alive and out of hospital.
There were 12 more cases of readmission with COPD, including three fatalities, in the eosinophil-guided group within the first month. However the authors said these differences were not statistically significant, but “because the study was not powered to detect differences in this absolute risk range, we cannot rule out that this was an actual harm effect from the interventional strategy.”
The eosinophil-guided therapy group did show more than a 50% reduction in the median duration of systemic corticosteroid therapy, which was 2 days in the eosinophil-guided group, compared with 5 days in the control group (P less than .0001), and the differences between the two groups remained significant at days 30 and 90.
“The tested strategy was successful in reducing the exposure to systemic corticosteroids, but we cannot exclude the possibility that a more aggressive algorithm, such as a single dose of systemic corticosteroid, might have been more effective,” the authors wrote.
At the 90-day follow-up, there were no differences in the number of infections requiring antibiotic treatment, nor in dyspepsia, ulcer complications, or initiation of new proton-pump inhibitor treatment.
The study was supported by the Danish Regions Medical Fund and the Danish Council for Independent Research. Two authors declared personal fees from pharmaceutical companies outside the submitted work. No other conflicts were declared.
SOURCE: Sivapalan P et al. Lancet Respir Med. 2019, May 20. doi: 10.1016/S2213-2600(19)30176-6.
in terms of the number of days out of hospital and alive, new research has found.
Writing in the Lancet Respiratory Medicine, researchers reported the outcomes of a multicenter, controlled, open-label trial comparing eosinophil-guided and standard therapy with systemic corticosteroids in 318 patients with COPD.
Pradeesh Sivapalan, MD, of the respiratory medicine section of Herlev and Gentofte Hospital at the University of Copenhagen, and coauthors wrote that eosinophilic inflammation had been seen in 20%-40% of patients with acute exacerbations of COPD. Patients with higher eosinophilic blood counts were at increased risk of acute exacerbations but were also more likely to benefit from corticosteroid treatment.
In the eosinophil-guided therapy arm of the study, 159 patients received 80 mg of intravenous methylprednisolone on day 1, then from the second day were treated with 37.5 mg of prednisolone oral tablet daily – up to 4 days – only on days when their blood eosinophil count was at least 0.3 x 10⁹ cells/L. In the control arm, 159 patients also received 80 mg of intravenous methylprednisolone on day 1, followed by 37.5 mg of prednisolone tablets daily for 4 days.
After 14 days, there were no significant differences between the two groups for mean days alive and out of hospital.
There were 12 more cases of readmission with COPD, including three fatalities, in the eosinophil-guided group within the first month. However the authors said these differences were not statistically significant, but “because the study was not powered to detect differences in this absolute risk range, we cannot rule out that this was an actual harm effect from the interventional strategy.”
The eosinophil-guided therapy group did show more than a 50% reduction in the median duration of systemic corticosteroid therapy, which was 2 days in the eosinophil-guided group, compared with 5 days in the control group (P less than .0001), and the differences between the two groups remained significant at days 30 and 90.
“The tested strategy was successful in reducing the exposure to systemic corticosteroids, but we cannot exclude the possibility that a more aggressive algorithm, such as a single dose of systemic corticosteroid, might have been more effective,” the authors wrote.
At the 90-day follow-up, there were no differences in the number of infections requiring antibiotic treatment, nor in dyspepsia, ulcer complications, or initiation of new proton-pump inhibitor treatment.
The study was supported by the Danish Regions Medical Fund and the Danish Council for Independent Research. Two authors declared personal fees from pharmaceutical companies outside the submitted work. No other conflicts were declared.
SOURCE: Sivapalan P et al. Lancet Respir Med. 2019, May 20. doi: 10.1016/S2213-2600(19)30176-6.
FROM LANCET RESPIRATORY MEDICINE
AFib on the rise in end-stage COPD patients hospitalized for exacerbations
Atrial fibrillation is being seen with increasing frequency in patients admitted to U.S. hospitals for exacerbations of end-stage chronic obstructive pulmonary disease, based on a retrospective analysis of data from the Nationwide Inpatient Sample.
The prevalence of atrial fibrillation (AFib) among patients with end-stage chronic obstructive pulmonary disease (COPD) on home oxygen who were admitted with COPD exacerbations increased from 12.9% in 2003 to 21.3% in 2014, according to Xiaochun Xiao of the department of health statistics at Second Military Medical University in Shanghai and colleagues.
Additionally, “we found that comorbid [AFib] was associated with an increased risk of the need for mechanical ventilation, especially invasive mechanical ventilation. Moreover, comorbid [AFib] was associated with adverse clinical outcomes, including increased in-hospital death, acute respiratory failure, acute kidney injury, sepsis, and stroke,” the researchers wrote in the study published in the journal CHEST.
Patients included in the study were aged at least 18 years, were diagnosed with end-stage COPD and on home oxygen, and were hospitalized because of a COPD-related exacerbation. Based on 1,345,270 weighted hospital admissions of adults with end-stage COPD on home oxygen who met the inclusion criteria for the study, 18.2% (244,488 admissions) of patients had AFib, and the prevalence of AFib in COPD patients increased over time from 2003 (12.9%) to 2014 (21.3%; P less than .0001).
Patients with AFib, compared with patients without AFib, were older (75.5 years vs. 69.6 years; P less than .0001) and more likely to be male (50.7% vs. 59.1%; P less than .0001) and white (80.9% vs. 74.4%; P less than .0001). Patients with AFib also had higher stroke risk reflected in higher CHA2DS2-VASc scores (3.26 vs. 2.45; P less than .0001), and higher likelihood of in-hospital mortality and readmission reflected in Elixhauser scores greater than or equal to 4 (51.2% vs. 35.6%).
In addition, the prevalence of AFib increased with increasing income. Larger hospitals in terms of bed size, urban environment, and Medicare insurance status also were associated with a higher AFib prevalence.
AFib was associated with an increased cost of $1,415 and an increased length of stay of 0.6 days after adjustment for potential confounders. AFib also predicted risk for several adverse events, including stroke (odds ratio, 1.80; in-hospital death, [OR, 1.54]), invasive mechanical ventilation (OR, 1.37), sepsis (OR, 1.23), noninvasive mechanical ventilation (OR, 1.14), acute kidney injury (OR, 1.09), and acute respiratory failure (OR, 1.09).
The researchers noted the database could have potentially overinflated AFib prevalence, as they could not differentiate index admissions and readmissions. The database also does not contain information about secondary diagnoses codes present on admission, which could make it difficult to identify adverse events that occurred during hospitalization.
“Our findings should prompt further efforts to identify the reasons for increased [AFib] prevalence and provide better management strategies for end-stage COPD patients comorbid with [AFib],” the researchers concluded.
This study was funded by a grant from the Fourth Round of the Shanghai 3-year Action Plan on Public Health Discipline and Talent Program. The authors reported no relevant conflict of interest.
SOURCE: Xiao X et al. CHEST. 2019 Jan 23. doi: 10.1016/j.chest.2018.12.021.
Atrial fibrillation is being seen with increasing frequency in patients admitted to U.S. hospitals for exacerbations of end-stage chronic obstructive pulmonary disease, based on a retrospective analysis of data from the Nationwide Inpatient Sample.
The prevalence of atrial fibrillation (AFib) among patients with end-stage chronic obstructive pulmonary disease (COPD) on home oxygen who were admitted with COPD exacerbations increased from 12.9% in 2003 to 21.3% in 2014, according to Xiaochun Xiao of the department of health statistics at Second Military Medical University in Shanghai and colleagues.
Additionally, “we found that comorbid [AFib] was associated with an increased risk of the need for mechanical ventilation, especially invasive mechanical ventilation. Moreover, comorbid [AFib] was associated with adverse clinical outcomes, including increased in-hospital death, acute respiratory failure, acute kidney injury, sepsis, and stroke,” the researchers wrote in the study published in the journal CHEST.
Patients included in the study were aged at least 18 years, were diagnosed with end-stage COPD and on home oxygen, and were hospitalized because of a COPD-related exacerbation. Based on 1,345,270 weighted hospital admissions of adults with end-stage COPD on home oxygen who met the inclusion criteria for the study, 18.2% (244,488 admissions) of patients had AFib, and the prevalence of AFib in COPD patients increased over time from 2003 (12.9%) to 2014 (21.3%; P less than .0001).
Patients with AFib, compared with patients without AFib, were older (75.5 years vs. 69.6 years; P less than .0001) and more likely to be male (50.7% vs. 59.1%; P less than .0001) and white (80.9% vs. 74.4%; P less than .0001). Patients with AFib also had higher stroke risk reflected in higher CHA2DS2-VASc scores (3.26 vs. 2.45; P less than .0001), and higher likelihood of in-hospital mortality and readmission reflected in Elixhauser scores greater than or equal to 4 (51.2% vs. 35.6%).
In addition, the prevalence of AFib increased with increasing income. Larger hospitals in terms of bed size, urban environment, and Medicare insurance status also were associated with a higher AFib prevalence.
AFib was associated with an increased cost of $1,415 and an increased length of stay of 0.6 days after adjustment for potential confounders. AFib also predicted risk for several adverse events, including stroke (odds ratio, 1.80; in-hospital death, [OR, 1.54]), invasive mechanical ventilation (OR, 1.37), sepsis (OR, 1.23), noninvasive mechanical ventilation (OR, 1.14), acute kidney injury (OR, 1.09), and acute respiratory failure (OR, 1.09).
The researchers noted the database could have potentially overinflated AFib prevalence, as they could not differentiate index admissions and readmissions. The database also does not contain information about secondary diagnoses codes present on admission, which could make it difficult to identify adverse events that occurred during hospitalization.
“Our findings should prompt further efforts to identify the reasons for increased [AFib] prevalence and provide better management strategies for end-stage COPD patients comorbid with [AFib],” the researchers concluded.
This study was funded by a grant from the Fourth Round of the Shanghai 3-year Action Plan on Public Health Discipline and Talent Program. The authors reported no relevant conflict of interest.
SOURCE: Xiao X et al. CHEST. 2019 Jan 23. doi: 10.1016/j.chest.2018.12.021.
Atrial fibrillation is being seen with increasing frequency in patients admitted to U.S. hospitals for exacerbations of end-stage chronic obstructive pulmonary disease, based on a retrospective analysis of data from the Nationwide Inpatient Sample.
The prevalence of atrial fibrillation (AFib) among patients with end-stage chronic obstructive pulmonary disease (COPD) on home oxygen who were admitted with COPD exacerbations increased from 12.9% in 2003 to 21.3% in 2014, according to Xiaochun Xiao of the department of health statistics at Second Military Medical University in Shanghai and colleagues.
Additionally, “we found that comorbid [AFib] was associated with an increased risk of the need for mechanical ventilation, especially invasive mechanical ventilation. Moreover, comorbid [AFib] was associated with adverse clinical outcomes, including increased in-hospital death, acute respiratory failure, acute kidney injury, sepsis, and stroke,” the researchers wrote in the study published in the journal CHEST.
Patients included in the study were aged at least 18 years, were diagnosed with end-stage COPD and on home oxygen, and were hospitalized because of a COPD-related exacerbation. Based on 1,345,270 weighted hospital admissions of adults with end-stage COPD on home oxygen who met the inclusion criteria for the study, 18.2% (244,488 admissions) of patients had AFib, and the prevalence of AFib in COPD patients increased over time from 2003 (12.9%) to 2014 (21.3%; P less than .0001).
Patients with AFib, compared with patients without AFib, were older (75.5 years vs. 69.6 years; P less than .0001) and more likely to be male (50.7% vs. 59.1%; P less than .0001) and white (80.9% vs. 74.4%; P less than .0001). Patients with AFib also had higher stroke risk reflected in higher CHA2DS2-VASc scores (3.26 vs. 2.45; P less than .0001), and higher likelihood of in-hospital mortality and readmission reflected in Elixhauser scores greater than or equal to 4 (51.2% vs. 35.6%).
In addition, the prevalence of AFib increased with increasing income. Larger hospitals in terms of bed size, urban environment, and Medicare insurance status also were associated with a higher AFib prevalence.
AFib was associated with an increased cost of $1,415 and an increased length of stay of 0.6 days after adjustment for potential confounders. AFib also predicted risk for several adverse events, including stroke (odds ratio, 1.80; in-hospital death, [OR, 1.54]), invasive mechanical ventilation (OR, 1.37), sepsis (OR, 1.23), noninvasive mechanical ventilation (OR, 1.14), acute kidney injury (OR, 1.09), and acute respiratory failure (OR, 1.09).
The researchers noted the database could have potentially overinflated AFib prevalence, as they could not differentiate index admissions and readmissions. The database also does not contain information about secondary diagnoses codes present on admission, which could make it difficult to identify adverse events that occurred during hospitalization.
“Our findings should prompt further efforts to identify the reasons for increased [AFib] prevalence and provide better management strategies for end-stage COPD patients comorbid with [AFib],” the researchers concluded.
This study was funded by a grant from the Fourth Round of the Shanghai 3-year Action Plan on Public Health Discipline and Talent Program. The authors reported no relevant conflict of interest.
SOURCE: Xiao X et al. CHEST. 2019 Jan 23. doi: 10.1016/j.chest.2018.12.021.
FROM CHEST
Key clinical point: Comorbid atrial fibrillation was associated with an increased risk of the need for mechanical ventilation, especially invasive mechanical ventilation, and of adverse outcomes including in-hospital death, acute respiratory failure, acute kidney injury, sepsis, and stroke.
Major finding: The prevalence of atrial fibrillation with end-stage chronic obstructive pulmonary disease increased over time from 2003 (12.9%) to 2014 (21.3%). Study details: A retrospective analysis based on 1,345,270 weighted hospital admissions of adults with end-stage chronic obstructive pulmonary disease on home oxygen from the Nationwide Impatient Sample during 2003-2014.
Disclosures: The study was funded by a grant from the Fourth Round of the Shanghai 3-Year Action Plan on Public Health Discipline and Talent Program. The authors reported no conflicts of interest.
Source: Xiao X et al. CHEST. 2019 Jan 23. doi: 10.1016/j.chest.2018.12.021.
No raised risk of cardiovascular events for COPD patients on aclidinium
, compared with placebo, in a randomized trial of more than 3,000 patients.
Aclidinium, a long-acting muscarinic antagonist (LAMA), has been shown to reduce COPD exacerbation in the short term, but long-term effectiveness has not been examined, wrote Robert A. Wise, MD, of Johns Hopkins University, Baltimore, and colleagues.
ASCENT-COPD is a multicenter, double-blind, randomized, placebo-controlled, parallel-group noninferiority study conducted at 522 sites in the United States and Canada. A paper on recent data from ASCENT-COPD, published in JAMA, supports early findings reported last year at the American Thoracic Society meeting.
The researchers randomized adults with COPD to a 400-mg dose of aclidinium bromide twice daily, or placebo. The average age of the patients was 67 years; 59% were men. The median exposure time to aclidinium or placebo was 365 days during the first year of treatment, and the median exposure overall was 495 days for aclidinium patients and 478 days for placebo patients.
Of the 2,537 patients who completed the study, 69 (3.9%) in the aclidinium group and 76 (4.2%) in the placebo group experienced a major adverse cardiovascular event (MACE, defined as a composite of cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke).
In addition, annual rates of moderate to severe COPD exacerbations were significantly lower in the aclidinium patients compared with placebo patients (0.44 vs. 0.57, P less than .001).
In a secondary analysis with a definition of MACE expanded to include heart failure, arrhythmias, or cerebrovascular disease, results remained similar between the groups; events occurred in 168 aclidinium patients (9.4%) and 160 placebo patients (8.9%). The rate of COPD exacerbations requiring hospitalization was significantly lower in aclidinium patients, compared with placebo patients (0.07 vs. 0.10, P = .006).
Overall, the most common treatment-emergent adverse events were similar in the aclidinium and placebo groups, respectively; pneumonia (6.1% vs. 5.8%), urinary tract infections (5.2% vs. 5.0%), and upper respiratory tract infections (4.8% vs. 5.6%). The most common serious adverse events (in at least 1% of patients) were pneumonia, atrial fibrillation, heart failure, and coronary artery disease. Dry mouth and urinary retention were rare, and occurred in less than 1% of patients in each group.
“No patient subgroup demonstrated a difference in efficacy except when analyzed by baseline COPD severity, in which the treatment benefit was observed only in patients with FEV1 [forced expiratory volume in 1 second] of 50% predicted or less,” the researchers noted. “This may be explained by the lower exacerbation rate seen in the placebo group in patients with moderate airway obstruction vs. severe or very severe obstruction,” they said.
“Outcomes of this trial add data to the long-standing controversy over the safety of LAMAs in COPD” and support the need for additional research, they said.
The study findings were limited by several factors including insufficient power to detect cause-specific mortality and the use of a LAMA with low risk of systemic effects, the researchers noted.
SOURCE: Wise R et al. JAMA. 2019. 321:1693-1701.
, compared with placebo, in a randomized trial of more than 3,000 patients.
Aclidinium, a long-acting muscarinic antagonist (LAMA), has been shown to reduce COPD exacerbation in the short term, but long-term effectiveness has not been examined, wrote Robert A. Wise, MD, of Johns Hopkins University, Baltimore, and colleagues.
ASCENT-COPD is a multicenter, double-blind, randomized, placebo-controlled, parallel-group noninferiority study conducted at 522 sites in the United States and Canada. A paper on recent data from ASCENT-COPD, published in JAMA, supports early findings reported last year at the American Thoracic Society meeting.
The researchers randomized adults with COPD to a 400-mg dose of aclidinium bromide twice daily, or placebo. The average age of the patients was 67 years; 59% were men. The median exposure time to aclidinium or placebo was 365 days during the first year of treatment, and the median exposure overall was 495 days for aclidinium patients and 478 days for placebo patients.
Of the 2,537 patients who completed the study, 69 (3.9%) in the aclidinium group and 76 (4.2%) in the placebo group experienced a major adverse cardiovascular event (MACE, defined as a composite of cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke).
In addition, annual rates of moderate to severe COPD exacerbations were significantly lower in the aclidinium patients compared with placebo patients (0.44 vs. 0.57, P less than .001).
In a secondary analysis with a definition of MACE expanded to include heart failure, arrhythmias, or cerebrovascular disease, results remained similar between the groups; events occurred in 168 aclidinium patients (9.4%) and 160 placebo patients (8.9%). The rate of COPD exacerbations requiring hospitalization was significantly lower in aclidinium patients, compared with placebo patients (0.07 vs. 0.10, P = .006).
Overall, the most common treatment-emergent adverse events were similar in the aclidinium and placebo groups, respectively; pneumonia (6.1% vs. 5.8%), urinary tract infections (5.2% vs. 5.0%), and upper respiratory tract infections (4.8% vs. 5.6%). The most common serious adverse events (in at least 1% of patients) were pneumonia, atrial fibrillation, heart failure, and coronary artery disease. Dry mouth and urinary retention were rare, and occurred in less than 1% of patients in each group.
“No patient subgroup demonstrated a difference in efficacy except when analyzed by baseline COPD severity, in which the treatment benefit was observed only in patients with FEV1 [forced expiratory volume in 1 second] of 50% predicted or less,” the researchers noted. “This may be explained by the lower exacerbation rate seen in the placebo group in patients with moderate airway obstruction vs. severe or very severe obstruction,” they said.
“Outcomes of this trial add data to the long-standing controversy over the safety of LAMAs in COPD” and support the need for additional research, they said.
The study findings were limited by several factors including insufficient power to detect cause-specific mortality and the use of a LAMA with low risk of systemic effects, the researchers noted.
SOURCE: Wise R et al. JAMA. 2019. 321:1693-1701.
, compared with placebo, in a randomized trial of more than 3,000 patients.
Aclidinium, a long-acting muscarinic antagonist (LAMA), has been shown to reduce COPD exacerbation in the short term, but long-term effectiveness has not been examined, wrote Robert A. Wise, MD, of Johns Hopkins University, Baltimore, and colleagues.
ASCENT-COPD is a multicenter, double-blind, randomized, placebo-controlled, parallel-group noninferiority study conducted at 522 sites in the United States and Canada. A paper on recent data from ASCENT-COPD, published in JAMA, supports early findings reported last year at the American Thoracic Society meeting.
The researchers randomized adults with COPD to a 400-mg dose of aclidinium bromide twice daily, or placebo. The average age of the patients was 67 years; 59% were men. The median exposure time to aclidinium or placebo was 365 days during the first year of treatment, and the median exposure overall was 495 days for aclidinium patients and 478 days for placebo patients.
Of the 2,537 patients who completed the study, 69 (3.9%) in the aclidinium group and 76 (4.2%) in the placebo group experienced a major adverse cardiovascular event (MACE, defined as a composite of cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke).
In addition, annual rates of moderate to severe COPD exacerbations were significantly lower in the aclidinium patients compared with placebo patients (0.44 vs. 0.57, P less than .001).
In a secondary analysis with a definition of MACE expanded to include heart failure, arrhythmias, or cerebrovascular disease, results remained similar between the groups; events occurred in 168 aclidinium patients (9.4%) and 160 placebo patients (8.9%). The rate of COPD exacerbations requiring hospitalization was significantly lower in aclidinium patients, compared with placebo patients (0.07 vs. 0.10, P = .006).
Overall, the most common treatment-emergent adverse events were similar in the aclidinium and placebo groups, respectively; pneumonia (6.1% vs. 5.8%), urinary tract infections (5.2% vs. 5.0%), and upper respiratory tract infections (4.8% vs. 5.6%). The most common serious adverse events (in at least 1% of patients) were pneumonia, atrial fibrillation, heart failure, and coronary artery disease. Dry mouth and urinary retention were rare, and occurred in less than 1% of patients in each group.
“No patient subgroup demonstrated a difference in efficacy except when analyzed by baseline COPD severity, in which the treatment benefit was observed only in patients with FEV1 [forced expiratory volume in 1 second] of 50% predicted or less,” the researchers noted. “This may be explained by the lower exacerbation rate seen in the placebo group in patients with moderate airway obstruction vs. severe or very severe obstruction,” they said.
“Outcomes of this trial add data to the long-standing controversy over the safety of LAMAs in COPD” and support the need for additional research, they said.
The study findings were limited by several factors including insufficient power to detect cause-specific mortality and the use of a LAMA with low risk of systemic effects, the researchers noted.
SOURCE: Wise R et al. JAMA. 2019. 321:1693-1701.
FROM JAMA
Respiratory effects may account for worse survival in women undergoing DTA and TAAA repair
Women undergoing open descending thoracic aortic aneurysm (DTA) and open thoracoabdominal aortic aneurysm (TAAA) repair are not at greater risk for operative mortality than their male counterparts. However, they are at significantly greater risk for major adverse events and have significantly lower 5-year survival, according to the results of a single institution database review of 738 surgery patients.
From May 1997 to June 2017, there were 462 men (59%) and 321 women (41%) who underwent open repair of DTA or TAAA, according to Leonard N. Girardi, MD, and colleagues from Weill Cornell Medicine, New York, who performed the study published in the Journal of Vascular Surgery. The researchers used logistic regression and Cox regression analyses to assess the effect of sex on perioperative and long-term outcomes.
Demographically, women were significantly older (67.6 years vs. 62.6 years), with a significantly higher incidence of chronic obstructive pulmonary disease (47.0% vs. 35.7%) and a significantly greater percentage of patients with a forced expiratory volume in 1 second less than 50% (28.3% vs 18.2%). Degenerative aneurysms were significantly more common in women (61.7% vs. 41.6%), whereas chronic dissections significantly predominated in men (42.4% vs. 23.1%). Operative mortality was not significantly different between women and men (5.6% vs. 6.2%); however, women were significantly more likely to require a tracheostomy after surgery (10.6% vs. 5.0%).
Logistic regression found that being a woman was an independent risk factor for a composite of major adverse events (odds ratio, 2.68) and need for tracheostomy (OR, 3.73). In addition, women had significantly worse 5-year survival than men undergoing DTA or TAAA repair (59.7% vs. 66.2%, P =.025). There was no difference in overall survival between 1997-2007 and 2008-2017.
“Women and men undergoing TAAA repair have significant and consistent differences in preoperative characteristics. Despite these differences, operative mortality is similar between the two groups. However, women are at significantly increased risk of [major adverse events], especially respiratory failure, because of those differences in risk factors, including age, pulmonary function, and aneurysm etiology,” the researchers concluded.
The authors reported that they had no conflicts of interest.
SOURCE: Girardi LN et al. J Vasc Surg 2019;69:1028-35.
Women undergoing open descending thoracic aortic aneurysm (DTA) and open thoracoabdominal aortic aneurysm (TAAA) repair are not at greater risk for operative mortality than their male counterparts. However, they are at significantly greater risk for major adverse events and have significantly lower 5-year survival, according to the results of a single institution database review of 738 surgery patients.
From May 1997 to June 2017, there were 462 men (59%) and 321 women (41%) who underwent open repair of DTA or TAAA, according to Leonard N. Girardi, MD, and colleagues from Weill Cornell Medicine, New York, who performed the study published in the Journal of Vascular Surgery. The researchers used logistic regression and Cox regression analyses to assess the effect of sex on perioperative and long-term outcomes.
Demographically, women were significantly older (67.6 years vs. 62.6 years), with a significantly higher incidence of chronic obstructive pulmonary disease (47.0% vs. 35.7%) and a significantly greater percentage of patients with a forced expiratory volume in 1 second less than 50% (28.3% vs 18.2%). Degenerative aneurysms were significantly more common in women (61.7% vs. 41.6%), whereas chronic dissections significantly predominated in men (42.4% vs. 23.1%). Operative mortality was not significantly different between women and men (5.6% vs. 6.2%); however, women were significantly more likely to require a tracheostomy after surgery (10.6% vs. 5.0%).
Logistic regression found that being a woman was an independent risk factor for a composite of major adverse events (odds ratio, 2.68) and need for tracheostomy (OR, 3.73). In addition, women had significantly worse 5-year survival than men undergoing DTA or TAAA repair (59.7% vs. 66.2%, P =.025). There was no difference in overall survival between 1997-2007 and 2008-2017.
“Women and men undergoing TAAA repair have significant and consistent differences in preoperative characteristics. Despite these differences, operative mortality is similar between the two groups. However, women are at significantly increased risk of [major adverse events], especially respiratory failure, because of those differences in risk factors, including age, pulmonary function, and aneurysm etiology,” the researchers concluded.
The authors reported that they had no conflicts of interest.
SOURCE: Girardi LN et al. J Vasc Surg 2019;69:1028-35.
Women undergoing open descending thoracic aortic aneurysm (DTA) and open thoracoabdominal aortic aneurysm (TAAA) repair are not at greater risk for operative mortality than their male counterparts. However, they are at significantly greater risk for major adverse events and have significantly lower 5-year survival, according to the results of a single institution database review of 738 surgery patients.
From May 1997 to June 2017, there were 462 men (59%) and 321 women (41%) who underwent open repair of DTA or TAAA, according to Leonard N. Girardi, MD, and colleagues from Weill Cornell Medicine, New York, who performed the study published in the Journal of Vascular Surgery. The researchers used logistic regression and Cox regression analyses to assess the effect of sex on perioperative and long-term outcomes.
Demographically, women were significantly older (67.6 years vs. 62.6 years), with a significantly higher incidence of chronic obstructive pulmonary disease (47.0% vs. 35.7%) and a significantly greater percentage of patients with a forced expiratory volume in 1 second less than 50% (28.3% vs 18.2%). Degenerative aneurysms were significantly more common in women (61.7% vs. 41.6%), whereas chronic dissections significantly predominated in men (42.4% vs. 23.1%). Operative mortality was not significantly different between women and men (5.6% vs. 6.2%); however, women were significantly more likely to require a tracheostomy after surgery (10.6% vs. 5.0%).
Logistic regression found that being a woman was an independent risk factor for a composite of major adverse events (odds ratio, 2.68) and need for tracheostomy (OR, 3.73). In addition, women had significantly worse 5-year survival than men undergoing DTA or TAAA repair (59.7% vs. 66.2%, P =.025). There was no difference in overall survival between 1997-2007 and 2008-2017.
“Women and men undergoing TAAA repair have significant and consistent differences in preoperative characteristics. Despite these differences, operative mortality is similar between the two groups. However, women are at significantly increased risk of [major adverse events], especially respiratory failure, because of those differences in risk factors, including age, pulmonary function, and aneurysm etiology,” the researchers concluded.
The authors reported that they had no conflicts of interest.
SOURCE: Girardi LN et al. J Vasc Surg 2019;69:1028-35.
FROM THE JOURNAL OF VASCULAR SURGERY
Pulmonologist: In COPD, try dual therapy before adding corticosteroid
PHILADELPHIA – While triple therapy is effective for patients with chronic obstructive pulmonary disease (COPD), not all patients actually need the inhaled corticosteroid component to reduce exacerbations, a Mayo Clinic pulmonologist said at the annual meeting of the American College of Physicians.
“When you’re increasing therapy, we can go to a dual-bronchodilator combination before adding corticosteroids,” Megan Dulohery Scrodin, MD, of Mayo Clinic, Rochester, Minn., noted in a well-attended session.
That approach came as news to many internists, at least going by results of an audience poll in which 76% of attendees picked triple therapy for a 65-year-old male with COPD and frequent exacerbations despite having used a long-acting muscarinic antagonist (LAMA). Only 10% picked what Dr. Dulohery Scrodin said was optimal: to keep the patient on the LAMA, and add a long-acting beta-agonist (LABA).
“I would encourage you to do this as a stepwise process,” Dr. Dulohery Scrodin told attendees after seeing those poll results.
For a patient with minimal symptoms and few exacerbations, the best approach is a short-acting bronchodilator plus smoking cessation, avoidance of environmental triggers, and keeping up to date with vaccinations, she said.
For patients with more severe symptoms or frequent exacerbations, adding a LAMA or LABA would be warranted, along with considering pulmonary rehabilitation.
“There’s been studies comparing long-acting muscarinic antagonists to long-acting beta agonists, and the long-acting muscarinic antagonists like tiotropium seem to be superior,” she said. “So I always do a LAMA inhaler first.”
For patients still having exacerbations despite one long-acting bronchodilator, the best approach would be to add the second bronchodilator, and if that still doesn’t work, she said, add an inhaled corticosteroid and consider a pulmonary consultation for advanced therapy.
“If the patient doesn’t need an inhaled corticosteroid, we try to avoid it and use dual bronchodilator therapy,” said Dr. Dulohery Scrodin, noting that inhaled corticosteroids are associated with increased risk of pneumonia, along with other complications such as dysphonia and oral candidiasis.
In studies, single-inhaler triple therapy with fluticasone furoate, umeclidinium, and vilanterol does seem to reduce exacerbations more than LABA/LAMA combination therapy or LABA/inhaled corticosteroid treatment, but that doesn’t necessarily mean it should be automatically chosen over dual therapy, the presenter noted.
“Similar to asthma, I would do the least amount of therapy that your patient gets under control,” she told the audience.
Dr. Dulohery Scrodin reported that she had no relevant disclosures.
PHILADELPHIA – While triple therapy is effective for patients with chronic obstructive pulmonary disease (COPD), not all patients actually need the inhaled corticosteroid component to reduce exacerbations, a Mayo Clinic pulmonologist said at the annual meeting of the American College of Physicians.
“When you’re increasing therapy, we can go to a dual-bronchodilator combination before adding corticosteroids,” Megan Dulohery Scrodin, MD, of Mayo Clinic, Rochester, Minn., noted in a well-attended session.
That approach came as news to many internists, at least going by results of an audience poll in which 76% of attendees picked triple therapy for a 65-year-old male with COPD and frequent exacerbations despite having used a long-acting muscarinic antagonist (LAMA). Only 10% picked what Dr. Dulohery Scrodin said was optimal: to keep the patient on the LAMA, and add a long-acting beta-agonist (LABA).
“I would encourage you to do this as a stepwise process,” Dr. Dulohery Scrodin told attendees after seeing those poll results.
For a patient with minimal symptoms and few exacerbations, the best approach is a short-acting bronchodilator plus smoking cessation, avoidance of environmental triggers, and keeping up to date with vaccinations, she said.
For patients with more severe symptoms or frequent exacerbations, adding a LAMA or LABA would be warranted, along with considering pulmonary rehabilitation.
“There’s been studies comparing long-acting muscarinic antagonists to long-acting beta agonists, and the long-acting muscarinic antagonists like tiotropium seem to be superior,” she said. “So I always do a LAMA inhaler first.”
For patients still having exacerbations despite one long-acting bronchodilator, the best approach would be to add the second bronchodilator, and if that still doesn’t work, she said, add an inhaled corticosteroid and consider a pulmonary consultation for advanced therapy.
“If the patient doesn’t need an inhaled corticosteroid, we try to avoid it and use dual bronchodilator therapy,” said Dr. Dulohery Scrodin, noting that inhaled corticosteroids are associated with increased risk of pneumonia, along with other complications such as dysphonia and oral candidiasis.
In studies, single-inhaler triple therapy with fluticasone furoate, umeclidinium, and vilanterol does seem to reduce exacerbations more than LABA/LAMA combination therapy or LABA/inhaled corticosteroid treatment, but that doesn’t necessarily mean it should be automatically chosen over dual therapy, the presenter noted.
“Similar to asthma, I would do the least amount of therapy that your patient gets under control,” she told the audience.
Dr. Dulohery Scrodin reported that she had no relevant disclosures.
PHILADELPHIA – While triple therapy is effective for patients with chronic obstructive pulmonary disease (COPD), not all patients actually need the inhaled corticosteroid component to reduce exacerbations, a Mayo Clinic pulmonologist said at the annual meeting of the American College of Physicians.
“When you’re increasing therapy, we can go to a dual-bronchodilator combination before adding corticosteroids,” Megan Dulohery Scrodin, MD, of Mayo Clinic, Rochester, Minn., noted in a well-attended session.
That approach came as news to many internists, at least going by results of an audience poll in which 76% of attendees picked triple therapy for a 65-year-old male with COPD and frequent exacerbations despite having used a long-acting muscarinic antagonist (LAMA). Only 10% picked what Dr. Dulohery Scrodin said was optimal: to keep the patient on the LAMA, and add a long-acting beta-agonist (LABA).
“I would encourage you to do this as a stepwise process,” Dr. Dulohery Scrodin told attendees after seeing those poll results.
For a patient with minimal symptoms and few exacerbations, the best approach is a short-acting bronchodilator plus smoking cessation, avoidance of environmental triggers, and keeping up to date with vaccinations, she said.
For patients with more severe symptoms or frequent exacerbations, adding a LAMA or LABA would be warranted, along with considering pulmonary rehabilitation.
“There’s been studies comparing long-acting muscarinic antagonists to long-acting beta agonists, and the long-acting muscarinic antagonists like tiotropium seem to be superior,” she said. “So I always do a LAMA inhaler first.”
For patients still having exacerbations despite one long-acting bronchodilator, the best approach would be to add the second bronchodilator, and if that still doesn’t work, she said, add an inhaled corticosteroid and consider a pulmonary consultation for advanced therapy.
“If the patient doesn’t need an inhaled corticosteroid, we try to avoid it and use dual bronchodilator therapy,” said Dr. Dulohery Scrodin, noting that inhaled corticosteroids are associated with increased risk of pneumonia, along with other complications such as dysphonia and oral candidiasis.
In studies, single-inhaler triple therapy with fluticasone furoate, umeclidinium, and vilanterol does seem to reduce exacerbations more than LABA/LAMA combination therapy or LABA/inhaled corticosteroid treatment, but that doesn’t necessarily mean it should be automatically chosen over dual therapy, the presenter noted.
“Similar to asthma, I would do the least amount of therapy that your patient gets under control,” she told the audience.
Dr. Dulohery Scrodin reported that she had no relevant disclosures.
REPORTING FROM INTERNAL MEDICINE 2019
Abatacept appears safe for RA patients with COPD
Concerns about abatacept (Orencia)-related lung disease in patients with rheumatoid arthritis appear to be unfounded, a large U.S. database review has determined.
Safety signals seen in a small subset of patients in the 2006 ASSURE study likely arose from chance, Samy Suissa, PhD, and his colleagues wrote in Seminars in Arthritis & Rheumatism. Patients in that study with preexisting chronic obstructive pulmonary disease (COPD) were 84% more likely to develop an exacerbation or other lung disorder than were those taking a placebo comparator.
The new database study contradicted that finding.
“Our study suggests that these numerical differences in ASSURE are expected results of random variation and thus compatible with chance,” Dr. Suissa of Jewish General Hospital and McGill University, both in Montreal, and his coauthors wrote. “Moreover, our findings are consistent with two studies of the safety of abatacept in the context of interstitial lung disease, albeit a different respiratory disease than COPD.”
The year-long ASSURE trial reported on the safety of abatacept in 959 patients versus 482 assigned to placebo. The safety signal arose in a subgroup of 54 patients with COPD, 37 of whom were assigned to abatacept and 17 to placebo. Among these were four serious respiratory adverse events (COPD exacerbation, worsening of COPD, bronchitis, and pneumonia) in four patients taking abatacept and none in the placebo arm.
“It is useful to note that this difference of 11% versus 0% rate is compatible with chance [exact P = .31], while the exact 95% confidence interval for the odds ratio is wide and includes unity ... The trial also reported more mild-moderate respiratory events with abatacept than with placebo [43.2% vs. 23.5%], including cough, rhonchi, COPD exacerbation, COPD, dyspnea, and nasal congestion. This difference resulted in an odds ration of 1.84,” with a wide confidence interval that included unity (0.48-8.63).
Nevertheless, these findings led to the addition of a warning in the prescribing insert: “Adult COPD patients treated with Orencia developed adverse events more frequently than those treated with placebo, including COPD exacerbations, cough, rhonchi, and dyspnea. Use of Orencia in patients with RA and COPD should be undertaken with caution and such patients should be monitored for worsening of their respiratory status.”
Dr. Suissa’s team used the U.S. MarketScan prescribing database to asses the risk of respiratory adverse events associated with abatacept, compared with other biologic disease-modifying antirheumatic drugs (DMARDs) in a real-world setting.
The cohort comprised 1,807 patients with rheumatoid arthritis and COPD who started a new prescription for abatacept, matched in time to 3,547 who initiated another biologic DMARD. The primary endpoint was the combined risk of hospitalization for COPD exacerbation, bronchitis, and hospitalized pneumonia or influenza.
The most common comparator biologic DMARDs were etanercept, adalimumab, rituximab, and infliximab.
For patients with COPD and comparator patients, the incidence rates for COPD exacerbation were 1.2 per 100 person-years with abatacept and 2.1 per 100 person-years with a different biologic DMARD; for bronchitis, the respective rates were 4.2 and 5.3; for hospitalized pneumonia or influenza, 3.6 and 2.6; and for outpatient pneumonia or flu, 14.7 and 14.4. For the combined endpoint, the incidence rate was 8.7 per 100 person-years with abatacept and 9.9 per 100 person-years with other biologic DMARDs.
The adjusted hazard ratio of the combined endpoint with abatacept versus that with other biologic DMARDs was a nonsignificant risk of 0.87. The hazard ratio with abatacept was 0.60 for hospitalized COPD; 0.80 for bronchitis; 1.39 for hospitalized pneumonia and flu; and 1.05 for outpatient pneumonia and flu. None of these associations was statistically significant.
“One exception was the risk of hospitalization for pneumonia or influenza, which was higher with abatacept among patients with more severe COPD,” at 6.99, than it was with other biologic DMARDs, the authors noted.
Dr. Suissa disclosed relationships with AstraZeneca, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, and Novartis.
SOURCE: Suissa S et al. Semin Arthritis Rheum. 2019 Mar 16. doi: 10.1016j.semarthrit.2019.03.007.
Concerns about abatacept (Orencia)-related lung disease in patients with rheumatoid arthritis appear to be unfounded, a large U.S. database review has determined.
Safety signals seen in a small subset of patients in the 2006 ASSURE study likely arose from chance, Samy Suissa, PhD, and his colleagues wrote in Seminars in Arthritis & Rheumatism. Patients in that study with preexisting chronic obstructive pulmonary disease (COPD) were 84% more likely to develop an exacerbation or other lung disorder than were those taking a placebo comparator.
The new database study contradicted that finding.
“Our study suggests that these numerical differences in ASSURE are expected results of random variation and thus compatible with chance,” Dr. Suissa of Jewish General Hospital and McGill University, both in Montreal, and his coauthors wrote. “Moreover, our findings are consistent with two studies of the safety of abatacept in the context of interstitial lung disease, albeit a different respiratory disease than COPD.”
The year-long ASSURE trial reported on the safety of abatacept in 959 patients versus 482 assigned to placebo. The safety signal arose in a subgroup of 54 patients with COPD, 37 of whom were assigned to abatacept and 17 to placebo. Among these were four serious respiratory adverse events (COPD exacerbation, worsening of COPD, bronchitis, and pneumonia) in four patients taking abatacept and none in the placebo arm.
“It is useful to note that this difference of 11% versus 0% rate is compatible with chance [exact P = .31], while the exact 95% confidence interval for the odds ratio is wide and includes unity ... The trial also reported more mild-moderate respiratory events with abatacept than with placebo [43.2% vs. 23.5%], including cough, rhonchi, COPD exacerbation, COPD, dyspnea, and nasal congestion. This difference resulted in an odds ration of 1.84,” with a wide confidence interval that included unity (0.48-8.63).
Nevertheless, these findings led to the addition of a warning in the prescribing insert: “Adult COPD patients treated with Orencia developed adverse events more frequently than those treated with placebo, including COPD exacerbations, cough, rhonchi, and dyspnea. Use of Orencia in patients with RA and COPD should be undertaken with caution and such patients should be monitored for worsening of their respiratory status.”
Dr. Suissa’s team used the U.S. MarketScan prescribing database to asses the risk of respiratory adverse events associated with abatacept, compared with other biologic disease-modifying antirheumatic drugs (DMARDs) in a real-world setting.
The cohort comprised 1,807 patients with rheumatoid arthritis and COPD who started a new prescription for abatacept, matched in time to 3,547 who initiated another biologic DMARD. The primary endpoint was the combined risk of hospitalization for COPD exacerbation, bronchitis, and hospitalized pneumonia or influenza.
The most common comparator biologic DMARDs were etanercept, adalimumab, rituximab, and infliximab.
For patients with COPD and comparator patients, the incidence rates for COPD exacerbation were 1.2 per 100 person-years with abatacept and 2.1 per 100 person-years with a different biologic DMARD; for bronchitis, the respective rates were 4.2 and 5.3; for hospitalized pneumonia or influenza, 3.6 and 2.6; and for outpatient pneumonia or flu, 14.7 and 14.4. For the combined endpoint, the incidence rate was 8.7 per 100 person-years with abatacept and 9.9 per 100 person-years with other biologic DMARDs.
The adjusted hazard ratio of the combined endpoint with abatacept versus that with other biologic DMARDs was a nonsignificant risk of 0.87. The hazard ratio with abatacept was 0.60 for hospitalized COPD; 0.80 for bronchitis; 1.39 for hospitalized pneumonia and flu; and 1.05 for outpatient pneumonia and flu. None of these associations was statistically significant.
“One exception was the risk of hospitalization for pneumonia or influenza, which was higher with abatacept among patients with more severe COPD,” at 6.99, than it was with other biologic DMARDs, the authors noted.
Dr. Suissa disclosed relationships with AstraZeneca, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, and Novartis.
SOURCE: Suissa S et al. Semin Arthritis Rheum. 2019 Mar 16. doi: 10.1016j.semarthrit.2019.03.007.
Concerns about abatacept (Orencia)-related lung disease in patients with rheumatoid arthritis appear to be unfounded, a large U.S. database review has determined.
Safety signals seen in a small subset of patients in the 2006 ASSURE study likely arose from chance, Samy Suissa, PhD, and his colleagues wrote in Seminars in Arthritis & Rheumatism. Patients in that study with preexisting chronic obstructive pulmonary disease (COPD) were 84% more likely to develop an exacerbation or other lung disorder than were those taking a placebo comparator.
The new database study contradicted that finding.
“Our study suggests that these numerical differences in ASSURE are expected results of random variation and thus compatible with chance,” Dr. Suissa of Jewish General Hospital and McGill University, both in Montreal, and his coauthors wrote. “Moreover, our findings are consistent with two studies of the safety of abatacept in the context of interstitial lung disease, albeit a different respiratory disease than COPD.”
The year-long ASSURE trial reported on the safety of abatacept in 959 patients versus 482 assigned to placebo. The safety signal arose in a subgroup of 54 patients with COPD, 37 of whom were assigned to abatacept and 17 to placebo. Among these were four serious respiratory adverse events (COPD exacerbation, worsening of COPD, bronchitis, and pneumonia) in four patients taking abatacept and none in the placebo arm.
“It is useful to note that this difference of 11% versus 0% rate is compatible with chance [exact P = .31], while the exact 95% confidence interval for the odds ratio is wide and includes unity ... The trial also reported more mild-moderate respiratory events with abatacept than with placebo [43.2% vs. 23.5%], including cough, rhonchi, COPD exacerbation, COPD, dyspnea, and nasal congestion. This difference resulted in an odds ration of 1.84,” with a wide confidence interval that included unity (0.48-8.63).
Nevertheless, these findings led to the addition of a warning in the prescribing insert: “Adult COPD patients treated with Orencia developed adverse events more frequently than those treated with placebo, including COPD exacerbations, cough, rhonchi, and dyspnea. Use of Orencia in patients with RA and COPD should be undertaken with caution and such patients should be monitored for worsening of their respiratory status.”
Dr. Suissa’s team used the U.S. MarketScan prescribing database to asses the risk of respiratory adverse events associated with abatacept, compared with other biologic disease-modifying antirheumatic drugs (DMARDs) in a real-world setting.
The cohort comprised 1,807 patients with rheumatoid arthritis and COPD who started a new prescription for abatacept, matched in time to 3,547 who initiated another biologic DMARD. The primary endpoint was the combined risk of hospitalization for COPD exacerbation, bronchitis, and hospitalized pneumonia or influenza.
The most common comparator biologic DMARDs were etanercept, adalimumab, rituximab, and infliximab.
For patients with COPD and comparator patients, the incidence rates for COPD exacerbation were 1.2 per 100 person-years with abatacept and 2.1 per 100 person-years with a different biologic DMARD; for bronchitis, the respective rates were 4.2 and 5.3; for hospitalized pneumonia or influenza, 3.6 and 2.6; and for outpatient pneumonia or flu, 14.7 and 14.4. For the combined endpoint, the incidence rate was 8.7 per 100 person-years with abatacept and 9.9 per 100 person-years with other biologic DMARDs.
The adjusted hazard ratio of the combined endpoint with abatacept versus that with other biologic DMARDs was a nonsignificant risk of 0.87. The hazard ratio with abatacept was 0.60 for hospitalized COPD; 0.80 for bronchitis; 1.39 for hospitalized pneumonia and flu; and 1.05 for outpatient pneumonia and flu. None of these associations was statistically significant.
“One exception was the risk of hospitalization for pneumonia or influenza, which was higher with abatacept among patients with more severe COPD,” at 6.99, than it was with other biologic DMARDs, the authors noted.
Dr. Suissa disclosed relationships with AstraZeneca, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, and Novartis.
SOURCE: Suissa S et al. Semin Arthritis Rheum. 2019 Mar 16. doi: 10.1016j.semarthrit.2019.03.007.
FROM SEMINARS IN ARTHRITIS & RHEUMATISM
Daily aspirin associated with lower risk of COPD flareup
Daily aspirin use could reduce the risk of acute exacerbations of chronic obstructive pulmonary disease, new data suggest.
Researchers reported the outcomes of an observational cohort study of 1,698 individuals with COPD, 45% of whom said they were taking daily aspirin at baseline. Their findings were published in Chest.
After a median follow up of 2.7 years, aspirin users had an overall 22% lower incidence of acute COPD exacerbations compared with nonusers. This was largely accounted for by a 25% reduction in moderate exacerbations, but there was no significant difference between aspirin users and nonusers in severe exacerbations.
A similar pattern was seen after just 1 year of follow-up, with an overall 30% reduction in the incidence of exacerbations, a 37% reduction in moderate exacerbations, but no significant reduction in severe exacerbations.
“Though aspirin use has previously been linked with reduced mortality risk in patients with COPD, to our knowledge, this is the first study to investigate the association of daily aspirin use with respiratory morbidity in COPD,” wrote Ashraf Fawzy, MD, of the division of pulmonary and critical care medicine at Johns Hopkins University, Baltimore, and his coauthors.
The association between aspirin use and reduced incidence of exacerbations was stronger among individuals with chronic bronchitis, which prompted the authors to suggest that future studies of aspirin in COPD should focus on participants with chronic bronchitis.
However, the association was not affected by COPD severity, emphysema presence or severity, or cardiometabolic phenotype.
Aspirin users reported better respiratory-specific quality of life than that of nonusers, including 34% lower odds of reporting moderate to severe dyspnea, and better baseline COPD health status.
“Findings of this study add to the existing literature by highlighting that aspirin use is also associated with reduced respiratory morbidity across several domains – including exacerbation risk, quality of life, and dyspnea – factors related to patient well-being and healthcare utilization,” the authors wrote.
Aspirin users were more likely to be white, male, and obese, and less likely to be smokers. They had better lung function but more cardiovascular comorbidities at baseline, although the aspirin users and nonusers were matched on baseline characteristics.
Speculating on the mechanisms by which aspirin might impact COPD exacerbations, the authors noted that the drug has both systemic and local pulmonary mechanisms of action.
For example, a pathway that results in elevated levels of a urinary metabolite in patients with COPD is irreversibly blocked by aspirin. Aspirin also attenuates the elevation of inflammatory markers interleukin-6 and C-reactive protein, which are part of the inflammatory phenotype of COPD. Aspirin has been shown to reduce proinflammatory cytokines in the lung.
The authors did note that aspirin use was self-reported, so they did not have data on dosage or duration of use.
The National Institutes of Health funded the study. Six authors declared advisory board positions, research support, and other funding from the pharmaceutical sector. One author was also a founder of a company commercializing lung image analysis software. No other conflicts of interest were declared.
SOURCE: Fawzy A et al. Chest. 2019 Mar;155(3): 519-27. doi: 10.1016/j.chest.2018.11.028.
Daily aspirin use could reduce the risk of acute exacerbations of chronic obstructive pulmonary disease, new data suggest.
Researchers reported the outcomes of an observational cohort study of 1,698 individuals with COPD, 45% of whom said they were taking daily aspirin at baseline. Their findings were published in Chest.
After a median follow up of 2.7 years, aspirin users had an overall 22% lower incidence of acute COPD exacerbations compared with nonusers. This was largely accounted for by a 25% reduction in moderate exacerbations, but there was no significant difference between aspirin users and nonusers in severe exacerbations.
A similar pattern was seen after just 1 year of follow-up, with an overall 30% reduction in the incidence of exacerbations, a 37% reduction in moderate exacerbations, but no significant reduction in severe exacerbations.
“Though aspirin use has previously been linked with reduced mortality risk in patients with COPD, to our knowledge, this is the first study to investigate the association of daily aspirin use with respiratory morbidity in COPD,” wrote Ashraf Fawzy, MD, of the division of pulmonary and critical care medicine at Johns Hopkins University, Baltimore, and his coauthors.
The association between aspirin use and reduced incidence of exacerbations was stronger among individuals with chronic bronchitis, which prompted the authors to suggest that future studies of aspirin in COPD should focus on participants with chronic bronchitis.
However, the association was not affected by COPD severity, emphysema presence or severity, or cardiometabolic phenotype.
Aspirin users reported better respiratory-specific quality of life than that of nonusers, including 34% lower odds of reporting moderate to severe dyspnea, and better baseline COPD health status.
“Findings of this study add to the existing literature by highlighting that aspirin use is also associated with reduced respiratory morbidity across several domains – including exacerbation risk, quality of life, and dyspnea – factors related to patient well-being and healthcare utilization,” the authors wrote.
Aspirin users were more likely to be white, male, and obese, and less likely to be smokers. They had better lung function but more cardiovascular comorbidities at baseline, although the aspirin users and nonusers were matched on baseline characteristics.
Speculating on the mechanisms by which aspirin might impact COPD exacerbations, the authors noted that the drug has both systemic and local pulmonary mechanisms of action.
For example, a pathway that results in elevated levels of a urinary metabolite in patients with COPD is irreversibly blocked by aspirin. Aspirin also attenuates the elevation of inflammatory markers interleukin-6 and C-reactive protein, which are part of the inflammatory phenotype of COPD. Aspirin has been shown to reduce proinflammatory cytokines in the lung.
The authors did note that aspirin use was self-reported, so they did not have data on dosage or duration of use.
The National Institutes of Health funded the study. Six authors declared advisory board positions, research support, and other funding from the pharmaceutical sector. One author was also a founder of a company commercializing lung image analysis software. No other conflicts of interest were declared.
SOURCE: Fawzy A et al. Chest. 2019 Mar;155(3): 519-27. doi: 10.1016/j.chest.2018.11.028.
Daily aspirin use could reduce the risk of acute exacerbations of chronic obstructive pulmonary disease, new data suggest.
Researchers reported the outcomes of an observational cohort study of 1,698 individuals with COPD, 45% of whom said they were taking daily aspirin at baseline. Their findings were published in Chest.
After a median follow up of 2.7 years, aspirin users had an overall 22% lower incidence of acute COPD exacerbations compared with nonusers. This was largely accounted for by a 25% reduction in moderate exacerbations, but there was no significant difference between aspirin users and nonusers in severe exacerbations.
A similar pattern was seen after just 1 year of follow-up, with an overall 30% reduction in the incidence of exacerbations, a 37% reduction in moderate exacerbations, but no significant reduction in severe exacerbations.
“Though aspirin use has previously been linked with reduced mortality risk in patients with COPD, to our knowledge, this is the first study to investigate the association of daily aspirin use with respiratory morbidity in COPD,” wrote Ashraf Fawzy, MD, of the division of pulmonary and critical care medicine at Johns Hopkins University, Baltimore, and his coauthors.
The association between aspirin use and reduced incidence of exacerbations was stronger among individuals with chronic bronchitis, which prompted the authors to suggest that future studies of aspirin in COPD should focus on participants with chronic bronchitis.
However, the association was not affected by COPD severity, emphysema presence or severity, or cardiometabolic phenotype.
Aspirin users reported better respiratory-specific quality of life than that of nonusers, including 34% lower odds of reporting moderate to severe dyspnea, and better baseline COPD health status.
“Findings of this study add to the existing literature by highlighting that aspirin use is also associated with reduced respiratory morbidity across several domains – including exacerbation risk, quality of life, and dyspnea – factors related to patient well-being and healthcare utilization,” the authors wrote.
Aspirin users were more likely to be white, male, and obese, and less likely to be smokers. They had better lung function but more cardiovascular comorbidities at baseline, although the aspirin users and nonusers were matched on baseline characteristics.
Speculating on the mechanisms by which aspirin might impact COPD exacerbations, the authors noted that the drug has both systemic and local pulmonary mechanisms of action.
For example, a pathway that results in elevated levels of a urinary metabolite in patients with COPD is irreversibly blocked by aspirin. Aspirin also attenuates the elevation of inflammatory markers interleukin-6 and C-reactive protein, which are part of the inflammatory phenotype of COPD. Aspirin has been shown to reduce proinflammatory cytokines in the lung.
The authors did note that aspirin use was self-reported, so they did not have data on dosage or duration of use.
The National Institutes of Health funded the study. Six authors declared advisory board positions, research support, and other funding from the pharmaceutical sector. One author was also a founder of a company commercializing lung image analysis software. No other conflicts of interest were declared.
SOURCE: Fawzy A et al. Chest. 2019 Mar;155(3): 519-27. doi: 10.1016/j.chest.2018.11.028.
FROM CHEST
Poor COPD management might increase MI risk in HIV
SEATTLE – Chronic obstructive pulmonary disease is independently associated with an increased risk of myocardial infarction in people with HIV, according to a report at the Conference on Retroviruses and Opportunistic Infections.
Chronic obstructive pulmonary disease (COPD) is known to increase the risk of myocardial infarction (MI) in the general population, but hadn’t been shown until now to do the same in HIV. The study raises the question of whether COPD is being managed adequately in patients with the virus, according to study lead Kristina Crothers, MD, associate professor in the division of pulmonary, critical care & sleep medicine at the University of Washington, Seattle.
The investigators reviewed 25,509 HIV patients in the Center for AIDS Research Network of Integrated Clinical Systems cohort, a large electronic database of HIV-infected people. They defined COPD by diagnostic codes and inhaler prescriptions. MIs were adjudicated by review.
The team identified 423 subjects with moderate to severe COPD, and 698 who had MIs, including 339 type 1 MIs (T1MI) from a ruptured plaque (54%), and 294 (46%) type 2 heart attacks (T2MI) from a supply-demand mismatch due to sepsis or some other problem. In general, T2MIs are far more common in people with HIV.
COPD was associated with a greater than twofold increased risk of MI after adjustment for age, sex, viral load, nadir CD4 count, hypertension, and other confounders. The risk dropped slightly when smoking – both current smoking and pack years – was added to the model (adjusted hazard ratio 1.88, 95% confidence interval, 1.34-2.63).
The association was particularly strong for T2MI, especially in the setting of bacteremia and sepsis, and unlike T1MI, it remained significant after adjustment for smoking.
The study establishes a link between COPD and MI in HIV, but it could not answer what’s going on. Chronic inflammation from the virus could be at play, but the team also found hints of inadequate COPD management.
“About 60% of patients were on inhalers ... but only about 25% of them were on long-acting inhalers. 75% were only on short-acting.” That’s a problem because long-acting inhalers are needed to control exacerbations, Dr. Crothers said.
The study didn’t capture exacerbation rates, but increased rates could help explain the MI risk. Increased rates of pneumonia could as well, since pneumonia is a common cause of sepsis.
“We need to better manage complications of COPD in this population. I think optimizing long-term COPD management could have many beneficial effects,” Dr. Crothers said.
The National Institutes of Health funded the work. Dr. Crothers had no disclosures.
SOURCE: Crothers K et al. CROI 2019, Abstract 31.
SEATTLE – Chronic obstructive pulmonary disease is independently associated with an increased risk of myocardial infarction in people with HIV, according to a report at the Conference on Retroviruses and Opportunistic Infections.
Chronic obstructive pulmonary disease (COPD) is known to increase the risk of myocardial infarction (MI) in the general population, but hadn’t been shown until now to do the same in HIV. The study raises the question of whether COPD is being managed adequately in patients with the virus, according to study lead Kristina Crothers, MD, associate professor in the division of pulmonary, critical care & sleep medicine at the University of Washington, Seattle.
The investigators reviewed 25,509 HIV patients in the Center for AIDS Research Network of Integrated Clinical Systems cohort, a large electronic database of HIV-infected people. They defined COPD by diagnostic codes and inhaler prescriptions. MIs were adjudicated by review.
The team identified 423 subjects with moderate to severe COPD, and 698 who had MIs, including 339 type 1 MIs (T1MI) from a ruptured plaque (54%), and 294 (46%) type 2 heart attacks (T2MI) from a supply-demand mismatch due to sepsis or some other problem. In general, T2MIs are far more common in people with HIV.
COPD was associated with a greater than twofold increased risk of MI after adjustment for age, sex, viral load, nadir CD4 count, hypertension, and other confounders. The risk dropped slightly when smoking – both current smoking and pack years – was added to the model (adjusted hazard ratio 1.88, 95% confidence interval, 1.34-2.63).
The association was particularly strong for T2MI, especially in the setting of bacteremia and sepsis, and unlike T1MI, it remained significant after adjustment for smoking.
The study establishes a link between COPD and MI in HIV, but it could not answer what’s going on. Chronic inflammation from the virus could be at play, but the team also found hints of inadequate COPD management.
“About 60% of patients were on inhalers ... but only about 25% of them were on long-acting inhalers. 75% were only on short-acting.” That’s a problem because long-acting inhalers are needed to control exacerbations, Dr. Crothers said.
The study didn’t capture exacerbation rates, but increased rates could help explain the MI risk. Increased rates of pneumonia could as well, since pneumonia is a common cause of sepsis.
“We need to better manage complications of COPD in this population. I think optimizing long-term COPD management could have many beneficial effects,” Dr. Crothers said.
The National Institutes of Health funded the work. Dr. Crothers had no disclosures.
SOURCE: Crothers K et al. CROI 2019, Abstract 31.
SEATTLE – Chronic obstructive pulmonary disease is independently associated with an increased risk of myocardial infarction in people with HIV, according to a report at the Conference on Retroviruses and Opportunistic Infections.
Chronic obstructive pulmonary disease (COPD) is known to increase the risk of myocardial infarction (MI) in the general population, but hadn’t been shown until now to do the same in HIV. The study raises the question of whether COPD is being managed adequately in patients with the virus, according to study lead Kristina Crothers, MD, associate professor in the division of pulmonary, critical care & sleep medicine at the University of Washington, Seattle.
The investigators reviewed 25,509 HIV patients in the Center for AIDS Research Network of Integrated Clinical Systems cohort, a large electronic database of HIV-infected people. They defined COPD by diagnostic codes and inhaler prescriptions. MIs were adjudicated by review.
The team identified 423 subjects with moderate to severe COPD, and 698 who had MIs, including 339 type 1 MIs (T1MI) from a ruptured plaque (54%), and 294 (46%) type 2 heart attacks (T2MI) from a supply-demand mismatch due to sepsis or some other problem. In general, T2MIs are far more common in people with HIV.
COPD was associated with a greater than twofold increased risk of MI after adjustment for age, sex, viral load, nadir CD4 count, hypertension, and other confounders. The risk dropped slightly when smoking – both current smoking and pack years – was added to the model (adjusted hazard ratio 1.88, 95% confidence interval, 1.34-2.63).
The association was particularly strong for T2MI, especially in the setting of bacteremia and sepsis, and unlike T1MI, it remained significant after adjustment for smoking.
The study establishes a link between COPD and MI in HIV, but it could not answer what’s going on. Chronic inflammation from the virus could be at play, but the team also found hints of inadequate COPD management.
“About 60% of patients were on inhalers ... but only about 25% of them were on long-acting inhalers. 75% were only on short-acting.” That’s a problem because long-acting inhalers are needed to control exacerbations, Dr. Crothers said.
The study didn’t capture exacerbation rates, but increased rates could help explain the MI risk. Increased rates of pneumonia could as well, since pneumonia is a common cause of sepsis.
“We need to better manage complications of COPD in this population. I think optimizing long-term COPD management could have many beneficial effects,” Dr. Crothers said.
The National Institutes of Health funded the work. Dr. Crothers had no disclosures.
SOURCE: Crothers K et al. CROI 2019, Abstract 31.
REPORTING FROM CROI 2019
E-cigarettes beat nicotine patch for smoking cessation
E-cigarettes might be more effective for smoking cessation than nicotine replacement therapy, results of a randomized study of almost 900 adults suggest.
Rates of abstinence at 1 year were 18% for adults who used refillable e-cigarettes to wean themselves off smoking, according to the reported results, compared with about 10% for those who tried nicotine replacement therapies.
“This is particularly noteworthy given that nicotine replacement was used under expert guidance, with access to the full range of nicotine replacement products, and with 88.1% of participants using combination treatments,” said investigator Peter Hajek, PhD, of Queen Mary University of London, and his coauthors in the New England Journal of Medicine.
The findings contrast with those of earlier studies, which showed a lesser effect of e-cigarettes as a stop-smoking strategy, Dr. Hajek and coauthors wrote.
In previous studies, participants used first-generation cartridge-based e-cigarettes, while in the present study, they were given second-generation refillable e-cigarettes and free choice of e-liquids, the authors noted. Moreover, those previous studies provided limited face-to-face support, they said, but
The randomized study by Dr. Hajek and his colleagues included 886 adults in the United Kingdom attending stop-smoking services provided by the U.K. National Health Service. They were randomized to receive either an e-cigarette starter pack and one bottle of nicotine-containing e-liquid, or 3 months’ worth of nicotine replacement products of their own choosing. At the 52-week validation visits, the study participants received about the equivalence of about $26 U.S. dollars for their travel and time.
Abstinence from smoking at 52 weeks, which was verified by measuring expired carbon monoxide levels, was achieved in 18.0% of the e-cigarette group and 9.9% of the nicotine replacement group (relative risk, 1.83; 95% confidence interval, 1.30-2.58; P less than .001), according to the report.
However, the rate of continued e-cigarette use was “fairly high,” investigators wrote. Eighty percent of the e-cigarette group was still using their assigned product at 52 weeks, compared with just 9% in the nicotine replacement group.
“This can be seen as problematic if e-cigarette use for a year signals long-term use, which may pose as-yet-unknown health risks,” they said.
Tobacco withdrawal symptoms were less severe and satisfaction ratings were higher with e-cigarettes versus nicotine replacement therapy, similar to what had been observed in previous studies, investigators said.
They cited several limitations. For example, product assignments were not blinded. However, the investigators said they tried to “limit expectation effects by recruiting only participants with no strong product preference.”
Dr. Hajek reported grants and fees from Pfizer unrelated to the present study. Coauthors reported disclosures related to Pfizer and Johnson and Johnson, along with grants from the U.K. National Institute for Health Research.
SOURCE: Hajek P et al. N Engl J Med. 2019;380:629-37. doi: 10.1056/NEJMoa1808779.
Any smoking cessation benefit of e-cigarettes needs to be balanced against short- and long-term safety risks of using these products, according to authors of an editorial.
In the study by Hajek et al., the 1-year abstinence rate of 18% in the e-cigarette group compares favorably to what has been reported for Food and Drug Administration–approved smoking cessation treatments, according to Belinda Borelli, PhD, and George T. O’Connor, MD.
The short-term safety data in the trial are “reassuring,” with a low incidence of oropharyngeal irritation, no excess wheezing or dyspnea, and greater declines in cough and phlegm production versus the nicotine replacement group, Dr. Borelli and Dr. O’Connor said.
However, a notable finding was that 80% of participants in the e-cigarette group were still using the product at 1 year, versus just 9% in the nicotine replacement group. “This differential pattern of long-term use raises concerns about the health consequences of long-term e-cigarette use,” they said.
E-cigarette vapor generally has lower levels of toxins and fewer biologic effects than does tobacco smoke, but it has produced adverse biologic effects in animal models and human cells in vitro, according to the authors.
“These findings argue against complacency in accepting the transition from tobacco smoking to indefinite e-cigarette use as a completely successful smoking cessation outcome,” they wrote. Policy analysts need to be careful and do their due diligence to ensure all consequences of the policy options are fully understood, especially as pharmaceuticals account for greater costs in the Medicare program. Future policy analyses must account for changes to Medicare costs as well as beneficiary costs to understand the overall effects of policy changes.
Dr. Borelli is with the Center for Behavioral Science Research, department of health policy and health services research at the Henry M. Goldman School of Dental Medicine, Boston University. Dr. O’Connor is with the Pulmonary Center at Boston University and with the division of pulmonary, allergy, sleep, and critical care medicine at Boston Medical Center. Dr. Borelli had no disclosures; Dr. O’Connor reported disclosures with AstraZeneca and Janssen Pharmaceuticals. They made these comments in an accompanying editorial (N Eng J Med. 2019. doi: 10.1056/NEJMe1816406).
Any smoking cessation benefit of e-cigarettes needs to be balanced against short- and long-term safety risks of using these products, according to authors of an editorial.
In the study by Hajek et al., the 1-year abstinence rate of 18% in the e-cigarette group compares favorably to what has been reported for Food and Drug Administration–approved smoking cessation treatments, according to Belinda Borelli, PhD, and George T. O’Connor, MD.
The short-term safety data in the trial are “reassuring,” with a low incidence of oropharyngeal irritation, no excess wheezing or dyspnea, and greater declines in cough and phlegm production versus the nicotine replacement group, Dr. Borelli and Dr. O’Connor said.
However, a notable finding was that 80% of participants in the e-cigarette group were still using the product at 1 year, versus just 9% in the nicotine replacement group. “This differential pattern of long-term use raises concerns about the health consequences of long-term e-cigarette use,” they said.
E-cigarette vapor generally has lower levels of toxins and fewer biologic effects than does tobacco smoke, but it has produced adverse biologic effects in animal models and human cells in vitro, according to the authors.
“These findings argue against complacency in accepting the transition from tobacco smoking to indefinite e-cigarette use as a completely successful smoking cessation outcome,” they wrote. Policy analysts need to be careful and do their due diligence to ensure all consequences of the policy options are fully understood, especially as pharmaceuticals account for greater costs in the Medicare program. Future policy analyses must account for changes to Medicare costs as well as beneficiary costs to understand the overall effects of policy changes.
Dr. Borelli is with the Center for Behavioral Science Research, department of health policy and health services research at the Henry M. Goldman School of Dental Medicine, Boston University. Dr. O’Connor is with the Pulmonary Center at Boston University and with the division of pulmonary, allergy, sleep, and critical care medicine at Boston Medical Center. Dr. Borelli had no disclosures; Dr. O’Connor reported disclosures with AstraZeneca and Janssen Pharmaceuticals. They made these comments in an accompanying editorial (N Eng J Med. 2019. doi: 10.1056/NEJMe1816406).
Any smoking cessation benefit of e-cigarettes needs to be balanced against short- and long-term safety risks of using these products, according to authors of an editorial.
In the study by Hajek et al., the 1-year abstinence rate of 18% in the e-cigarette group compares favorably to what has been reported for Food and Drug Administration–approved smoking cessation treatments, according to Belinda Borelli, PhD, and George T. O’Connor, MD.
The short-term safety data in the trial are “reassuring,” with a low incidence of oropharyngeal irritation, no excess wheezing or dyspnea, and greater declines in cough and phlegm production versus the nicotine replacement group, Dr. Borelli and Dr. O’Connor said.
However, a notable finding was that 80% of participants in the e-cigarette group were still using the product at 1 year, versus just 9% in the nicotine replacement group. “This differential pattern of long-term use raises concerns about the health consequences of long-term e-cigarette use,” they said.
E-cigarette vapor generally has lower levels of toxins and fewer biologic effects than does tobacco smoke, but it has produced adverse biologic effects in animal models and human cells in vitro, according to the authors.
“These findings argue against complacency in accepting the transition from tobacco smoking to indefinite e-cigarette use as a completely successful smoking cessation outcome,” they wrote. Policy analysts need to be careful and do their due diligence to ensure all consequences of the policy options are fully understood, especially as pharmaceuticals account for greater costs in the Medicare program. Future policy analyses must account for changes to Medicare costs as well as beneficiary costs to understand the overall effects of policy changes.
Dr. Borelli is with the Center for Behavioral Science Research, department of health policy and health services research at the Henry M. Goldman School of Dental Medicine, Boston University. Dr. O’Connor is with the Pulmonary Center at Boston University and with the division of pulmonary, allergy, sleep, and critical care medicine at Boston Medical Center. Dr. Borelli had no disclosures; Dr. O’Connor reported disclosures with AstraZeneca and Janssen Pharmaceuticals. They made these comments in an accompanying editorial (N Eng J Med. 2019. doi: 10.1056/NEJMe1816406).
E-cigarettes might be more effective for smoking cessation than nicotine replacement therapy, results of a randomized study of almost 900 adults suggest.
Rates of abstinence at 1 year were 18% for adults who used refillable e-cigarettes to wean themselves off smoking, according to the reported results, compared with about 10% for those who tried nicotine replacement therapies.
“This is particularly noteworthy given that nicotine replacement was used under expert guidance, with access to the full range of nicotine replacement products, and with 88.1% of participants using combination treatments,” said investigator Peter Hajek, PhD, of Queen Mary University of London, and his coauthors in the New England Journal of Medicine.
The findings contrast with those of earlier studies, which showed a lesser effect of e-cigarettes as a stop-smoking strategy, Dr. Hajek and coauthors wrote.
In previous studies, participants used first-generation cartridge-based e-cigarettes, while in the present study, they were given second-generation refillable e-cigarettes and free choice of e-liquids, the authors noted. Moreover, those previous studies provided limited face-to-face support, they said, but
The randomized study by Dr. Hajek and his colleagues included 886 adults in the United Kingdom attending stop-smoking services provided by the U.K. National Health Service. They were randomized to receive either an e-cigarette starter pack and one bottle of nicotine-containing e-liquid, or 3 months’ worth of nicotine replacement products of their own choosing. At the 52-week validation visits, the study participants received about the equivalence of about $26 U.S. dollars for their travel and time.
Abstinence from smoking at 52 weeks, which was verified by measuring expired carbon monoxide levels, was achieved in 18.0% of the e-cigarette group and 9.9% of the nicotine replacement group (relative risk, 1.83; 95% confidence interval, 1.30-2.58; P less than .001), according to the report.
However, the rate of continued e-cigarette use was “fairly high,” investigators wrote. Eighty percent of the e-cigarette group was still using their assigned product at 52 weeks, compared with just 9% in the nicotine replacement group.
“This can be seen as problematic if e-cigarette use for a year signals long-term use, which may pose as-yet-unknown health risks,” they said.
Tobacco withdrawal symptoms were less severe and satisfaction ratings were higher with e-cigarettes versus nicotine replacement therapy, similar to what had been observed in previous studies, investigators said.
They cited several limitations. For example, product assignments were not blinded. However, the investigators said they tried to “limit expectation effects by recruiting only participants with no strong product preference.”
Dr. Hajek reported grants and fees from Pfizer unrelated to the present study. Coauthors reported disclosures related to Pfizer and Johnson and Johnson, along with grants from the U.K. National Institute for Health Research.
SOURCE: Hajek P et al. N Engl J Med. 2019;380:629-37. doi: 10.1056/NEJMoa1808779.
E-cigarettes might be more effective for smoking cessation than nicotine replacement therapy, results of a randomized study of almost 900 adults suggest.
Rates of abstinence at 1 year were 18% for adults who used refillable e-cigarettes to wean themselves off smoking, according to the reported results, compared with about 10% for those who tried nicotine replacement therapies.
“This is particularly noteworthy given that nicotine replacement was used under expert guidance, with access to the full range of nicotine replacement products, and with 88.1% of participants using combination treatments,” said investigator Peter Hajek, PhD, of Queen Mary University of London, and his coauthors in the New England Journal of Medicine.
The findings contrast with those of earlier studies, which showed a lesser effect of e-cigarettes as a stop-smoking strategy, Dr. Hajek and coauthors wrote.
In previous studies, participants used first-generation cartridge-based e-cigarettes, while in the present study, they were given second-generation refillable e-cigarettes and free choice of e-liquids, the authors noted. Moreover, those previous studies provided limited face-to-face support, they said, but
The randomized study by Dr. Hajek and his colleagues included 886 adults in the United Kingdom attending stop-smoking services provided by the U.K. National Health Service. They were randomized to receive either an e-cigarette starter pack and one bottle of nicotine-containing e-liquid, or 3 months’ worth of nicotine replacement products of their own choosing. At the 52-week validation visits, the study participants received about the equivalence of about $26 U.S. dollars for their travel and time.
Abstinence from smoking at 52 weeks, which was verified by measuring expired carbon monoxide levels, was achieved in 18.0% of the e-cigarette group and 9.9% of the nicotine replacement group (relative risk, 1.83; 95% confidence interval, 1.30-2.58; P less than .001), according to the report.
However, the rate of continued e-cigarette use was “fairly high,” investigators wrote. Eighty percent of the e-cigarette group was still using their assigned product at 52 weeks, compared with just 9% in the nicotine replacement group.
“This can be seen as problematic if e-cigarette use for a year signals long-term use, which may pose as-yet-unknown health risks,” they said.
Tobacco withdrawal symptoms were less severe and satisfaction ratings were higher with e-cigarettes versus nicotine replacement therapy, similar to what had been observed in previous studies, investigators said.
They cited several limitations. For example, product assignments were not blinded. However, the investigators said they tried to “limit expectation effects by recruiting only participants with no strong product preference.”
Dr. Hajek reported grants and fees from Pfizer unrelated to the present study. Coauthors reported disclosures related to Pfizer and Johnson and Johnson, along with grants from the U.K. National Institute for Health Research.
SOURCE: Hajek P et al. N Engl J Med. 2019;380:629-37. doi: 10.1056/NEJMoa1808779.
FROM THE NEW ENGLAND JOURNAL OF MEDICINE
Key clinical point: The rate of smokers who continued to use e-cigarettes after 1 year was “fairly high,” which might be problematic.
Major finding: Abstinence from smoking at 52 weeks was achieved in 18.0% of the e-cigarette group and 9.9% of the nicotine replacement group (relative risk, 1.83; 95% confidence interval, 1.30-2.58; P less than .001).
Study details: Randomized study of 886 adults in the United Kingdom attending stop-smoking services provided by the U.K. National Health Service.
Disclosures: Dr. Hajek reported grants and fees from Pfizer unrelated to the present study.The coauthors reported disclosures related to Pfizer, and Johnson and Johnson, along with grants from the U.K. National Institute for Health Research.
Source: Hajek P et al. N Engl J Med. 2019;380:629-37. doi: 10.1056/NEJMoa1808779.