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The third surge: Are we prepared for the non-COVID crisis?
Over the last several weeks, hospitals and health systems have focused on the COVID-19 epidemic, preparing and expanding bed capacities for the surge of admissions both in intensive care and medical units. An indirect impact of this has been the reduction in outpatient staffing and resources, with the shifting of staff for inpatient care. Many areas seem to have passed the peak in the number of cases and are now seeing a plateau or downward trend in the admissions to acute care facilities.
During this period, there has been a noticeable downtrend in patients being evaluated in the ED, or admitted for decompensation of chronic conditions like heart failure, COPD and diabetes mellitus, or such acute conditions as stroke and MI. Studies from Italy and Spain, and closer to home from Atlanta and Boston, point to a significant decrease in numbers of ST-elevation myocardial infarction (STEMI) admissions.1 Duke Health saw a decrease in stroke admissions in their hospitals by 34%.2
One could argue that these patients are in fact presenting with COVID-19 or similar symptoms as is evidenced by the studies linking the severity of SARS-Co-V2 infection to chronic conditions like diabetes mellitus and obesity.2 On the other hand, the message of social isolation and avoidance of nonurgent visits could lead to delays in care resulting in patients presenting sicker and in advanced stages.3 Also, this has not been limited to the adult population. For example, reports indicate that visits to WakeMed’s pediatric emergency rooms in Wake County, N.C., were down by 60%.2
We could well be seeing a calm before the storm. While it is anticipated that there may be a second surge of COVID-19 cases, health systems would do well to be prepared for the “third surge,” consisting of patients coming in with chronic medical conditions for which they have been, so far, avoiding follow-up and managing at home, and acute medical conditions with delayed diagnoses. The impact could likely be more in the subset of patients with limited access to health care, including medications and follow-up, resulting in a disproportionate burden on safety-net hospitals.
Compounding this issue would be the economic impact of the current crisis on health systems, their staffing, and resources. Several major organizations have already proposed budget cuts and reduction of the workforce, raising significant concerns about the future of health care workers who put their lives at risk during this pandemic.4 There is no guarantee that the federal funding provided by the stimulus packages will save jobs in the health care industry. This problem needs new leadership thinking, and every organization that puts employees over profits margins will have a long-term impact on communities.
Another area of concern is a shift in resources and workflow from ambulatory to inpatient settings for the COVID-19 pandemic, and the need for revamping the ambulatory services with reshifting the workforce. As COVID-19 cases plateau, the resurgence of non-COVID–related admissions will require additional help in inpatient settings. Prioritizing the ambulatory services based on financial benefits versus patient outcomes is also a major challenge to leadership.5
Lastly, the current health care crisis has led to significant stress, both emotional and physical, among frontline caregivers, increasing the risk of burnout.6 How leadership helps health care workers to cope with these stressors, and the resources they provide, is going to play a key role in long term retention of their talent, and will reflect on the organizational culture. Though it might seem trivial, posttraumatic stress disorder related to this is already obvious, and health care leadership needs to put every effort in providing the resources to help prevent burnout, in partnership with national organizations like the Society of Hospital Medicine and the American College of Physicians.
The expansion of telemedicine has provided a unique opportunity to address several of these issues while maintaining the nonpharmacologic interventions to fight the epidemic, and keeping the cost curve as low as possible.7 Extension of these services to all ambulatory service lines, including home health and therapy, is the next big step in the new health care era. Virtual check-ins by physicians, advance practice clinicians, and home care nurses could help alleviate the concerns regarding delays in care of patients with chronic conditions, and help identify those at risk. This would also be of help with staffing shortages, and possibly provide much needed support to frontline providers.
Dr. Prasad is currently medical director of care management and a hospitalist at Advocate Aurora Health in Milwaukee. He was previously quality and utilization officer and chief of the medical staff at Aurora Sinai Medical Center. Dr. Prasad is cochair of SHM’s IT Special Interest Group, sits on the HQPS Committee, and is president of SHM’s Wisconsin Chapter. Dr. Palabindala is the medical director, utilization management and physician advisory services, at the University of Mississippi Medical Center, Jackson. He is an associate professor of medicine and academic hospitalist in the UMMC School of Medicine.
References
1. Wood S. TCTMD. 2020 Apr 2. “The mystery of the missing STEMIs during the COVID-19 pandemic.”
2. Stradling R. The News & Observer. 2020 Apr 21. “Fewer people are going to Triangle [N.C.] emergency rooms, and that could be a bad thing.”
3. Kasanagottu K. USA Today. 2020 Apr 15. “Don’t delay care for chronic illness over coronavirus. It’s bad for you and for hospitals.”
4. Snowbeck C. The Star Tribune. 2020 Apr 11. “Mayo Clinic cutting pay for more than 20,000 workers.”
5. LaPointe J. RevCycle Intelligence. 2020 Mar 31. “How much will the COVID-19 pandemic cost hospitals?”
6. Gavidia M. AJMC. 2020 Mar 31. “Sleep, physician burnout linked amid COVID-19 pandemic.”
7. Hollander JE and Carr BG. N Engl J Med. 2020 Apr 30;382(18):1679-81. “Virtually perfect? Telemedicine for COVID-19.”
Over the last several weeks, hospitals and health systems have focused on the COVID-19 epidemic, preparing and expanding bed capacities for the surge of admissions both in intensive care and medical units. An indirect impact of this has been the reduction in outpatient staffing and resources, with the shifting of staff for inpatient care. Many areas seem to have passed the peak in the number of cases and are now seeing a plateau or downward trend in the admissions to acute care facilities.
During this period, there has been a noticeable downtrend in patients being evaluated in the ED, or admitted for decompensation of chronic conditions like heart failure, COPD and diabetes mellitus, or such acute conditions as stroke and MI. Studies from Italy and Spain, and closer to home from Atlanta and Boston, point to a significant decrease in numbers of ST-elevation myocardial infarction (STEMI) admissions.1 Duke Health saw a decrease in stroke admissions in their hospitals by 34%.2
One could argue that these patients are in fact presenting with COVID-19 or similar symptoms as is evidenced by the studies linking the severity of SARS-Co-V2 infection to chronic conditions like diabetes mellitus and obesity.2 On the other hand, the message of social isolation and avoidance of nonurgent visits could lead to delays in care resulting in patients presenting sicker and in advanced stages.3 Also, this has not been limited to the adult population. For example, reports indicate that visits to WakeMed’s pediatric emergency rooms in Wake County, N.C., were down by 60%.2
We could well be seeing a calm before the storm. While it is anticipated that there may be a second surge of COVID-19 cases, health systems would do well to be prepared for the “third surge,” consisting of patients coming in with chronic medical conditions for which they have been, so far, avoiding follow-up and managing at home, and acute medical conditions with delayed diagnoses. The impact could likely be more in the subset of patients with limited access to health care, including medications and follow-up, resulting in a disproportionate burden on safety-net hospitals.
Compounding this issue would be the economic impact of the current crisis on health systems, their staffing, and resources. Several major organizations have already proposed budget cuts and reduction of the workforce, raising significant concerns about the future of health care workers who put their lives at risk during this pandemic.4 There is no guarantee that the federal funding provided by the stimulus packages will save jobs in the health care industry. This problem needs new leadership thinking, and every organization that puts employees over profits margins will have a long-term impact on communities.
Another area of concern is a shift in resources and workflow from ambulatory to inpatient settings for the COVID-19 pandemic, and the need for revamping the ambulatory services with reshifting the workforce. As COVID-19 cases plateau, the resurgence of non-COVID–related admissions will require additional help in inpatient settings. Prioritizing the ambulatory services based on financial benefits versus patient outcomes is also a major challenge to leadership.5
Lastly, the current health care crisis has led to significant stress, both emotional and physical, among frontline caregivers, increasing the risk of burnout.6 How leadership helps health care workers to cope with these stressors, and the resources they provide, is going to play a key role in long term retention of their talent, and will reflect on the organizational culture. Though it might seem trivial, posttraumatic stress disorder related to this is already obvious, and health care leadership needs to put every effort in providing the resources to help prevent burnout, in partnership with national organizations like the Society of Hospital Medicine and the American College of Physicians.
The expansion of telemedicine has provided a unique opportunity to address several of these issues while maintaining the nonpharmacologic interventions to fight the epidemic, and keeping the cost curve as low as possible.7 Extension of these services to all ambulatory service lines, including home health and therapy, is the next big step in the new health care era. Virtual check-ins by physicians, advance practice clinicians, and home care nurses could help alleviate the concerns regarding delays in care of patients with chronic conditions, and help identify those at risk. This would also be of help with staffing shortages, and possibly provide much needed support to frontline providers.
Dr. Prasad is currently medical director of care management and a hospitalist at Advocate Aurora Health in Milwaukee. He was previously quality and utilization officer and chief of the medical staff at Aurora Sinai Medical Center. Dr. Prasad is cochair of SHM’s IT Special Interest Group, sits on the HQPS Committee, and is president of SHM’s Wisconsin Chapter. Dr. Palabindala is the medical director, utilization management and physician advisory services, at the University of Mississippi Medical Center, Jackson. He is an associate professor of medicine and academic hospitalist in the UMMC School of Medicine.
References
1. Wood S. TCTMD. 2020 Apr 2. “The mystery of the missing STEMIs during the COVID-19 pandemic.”
2. Stradling R. The News & Observer. 2020 Apr 21. “Fewer people are going to Triangle [N.C.] emergency rooms, and that could be a bad thing.”
3. Kasanagottu K. USA Today. 2020 Apr 15. “Don’t delay care for chronic illness over coronavirus. It’s bad for you and for hospitals.”
4. Snowbeck C. The Star Tribune. 2020 Apr 11. “Mayo Clinic cutting pay for more than 20,000 workers.”
5. LaPointe J. RevCycle Intelligence. 2020 Mar 31. “How much will the COVID-19 pandemic cost hospitals?”
6. Gavidia M. AJMC. 2020 Mar 31. “Sleep, physician burnout linked amid COVID-19 pandemic.”
7. Hollander JE and Carr BG. N Engl J Med. 2020 Apr 30;382(18):1679-81. “Virtually perfect? Telemedicine for COVID-19.”
Over the last several weeks, hospitals and health systems have focused on the COVID-19 epidemic, preparing and expanding bed capacities for the surge of admissions both in intensive care and medical units. An indirect impact of this has been the reduction in outpatient staffing and resources, with the shifting of staff for inpatient care. Many areas seem to have passed the peak in the number of cases and are now seeing a plateau or downward trend in the admissions to acute care facilities.
During this period, there has been a noticeable downtrend in patients being evaluated in the ED, or admitted for decompensation of chronic conditions like heart failure, COPD and diabetes mellitus, or such acute conditions as stroke and MI. Studies from Italy and Spain, and closer to home from Atlanta and Boston, point to a significant decrease in numbers of ST-elevation myocardial infarction (STEMI) admissions.1 Duke Health saw a decrease in stroke admissions in their hospitals by 34%.2
One could argue that these patients are in fact presenting with COVID-19 or similar symptoms as is evidenced by the studies linking the severity of SARS-Co-V2 infection to chronic conditions like diabetes mellitus and obesity.2 On the other hand, the message of social isolation and avoidance of nonurgent visits could lead to delays in care resulting in patients presenting sicker and in advanced stages.3 Also, this has not been limited to the adult population. For example, reports indicate that visits to WakeMed’s pediatric emergency rooms in Wake County, N.C., were down by 60%.2
We could well be seeing a calm before the storm. While it is anticipated that there may be a second surge of COVID-19 cases, health systems would do well to be prepared for the “third surge,” consisting of patients coming in with chronic medical conditions for which they have been, so far, avoiding follow-up and managing at home, and acute medical conditions with delayed diagnoses. The impact could likely be more in the subset of patients with limited access to health care, including medications and follow-up, resulting in a disproportionate burden on safety-net hospitals.
Compounding this issue would be the economic impact of the current crisis on health systems, their staffing, and resources. Several major organizations have already proposed budget cuts and reduction of the workforce, raising significant concerns about the future of health care workers who put their lives at risk during this pandemic.4 There is no guarantee that the federal funding provided by the stimulus packages will save jobs in the health care industry. This problem needs new leadership thinking, and every organization that puts employees over profits margins will have a long-term impact on communities.
Another area of concern is a shift in resources and workflow from ambulatory to inpatient settings for the COVID-19 pandemic, and the need for revamping the ambulatory services with reshifting the workforce. As COVID-19 cases plateau, the resurgence of non-COVID–related admissions will require additional help in inpatient settings. Prioritizing the ambulatory services based on financial benefits versus patient outcomes is also a major challenge to leadership.5
Lastly, the current health care crisis has led to significant stress, both emotional and physical, among frontline caregivers, increasing the risk of burnout.6 How leadership helps health care workers to cope with these stressors, and the resources they provide, is going to play a key role in long term retention of their talent, and will reflect on the organizational culture. Though it might seem trivial, posttraumatic stress disorder related to this is already obvious, and health care leadership needs to put every effort in providing the resources to help prevent burnout, in partnership with national organizations like the Society of Hospital Medicine and the American College of Physicians.
The expansion of telemedicine has provided a unique opportunity to address several of these issues while maintaining the nonpharmacologic interventions to fight the epidemic, and keeping the cost curve as low as possible.7 Extension of these services to all ambulatory service lines, including home health and therapy, is the next big step in the new health care era. Virtual check-ins by physicians, advance practice clinicians, and home care nurses could help alleviate the concerns regarding delays in care of patients with chronic conditions, and help identify those at risk. This would also be of help with staffing shortages, and possibly provide much needed support to frontline providers.
Dr. Prasad is currently medical director of care management and a hospitalist at Advocate Aurora Health in Milwaukee. He was previously quality and utilization officer and chief of the medical staff at Aurora Sinai Medical Center. Dr. Prasad is cochair of SHM’s IT Special Interest Group, sits on the HQPS Committee, and is president of SHM’s Wisconsin Chapter. Dr. Palabindala is the medical director, utilization management and physician advisory services, at the University of Mississippi Medical Center, Jackson. He is an associate professor of medicine and academic hospitalist in the UMMC School of Medicine.
References
1. Wood S. TCTMD. 2020 Apr 2. “The mystery of the missing STEMIs during the COVID-19 pandemic.”
2. Stradling R. The News & Observer. 2020 Apr 21. “Fewer people are going to Triangle [N.C.] emergency rooms, and that could be a bad thing.”
3. Kasanagottu K. USA Today. 2020 Apr 15. “Don’t delay care for chronic illness over coronavirus. It’s bad for you and for hospitals.”
4. Snowbeck C. The Star Tribune. 2020 Apr 11. “Mayo Clinic cutting pay for more than 20,000 workers.”
5. LaPointe J. RevCycle Intelligence. 2020 Mar 31. “How much will the COVID-19 pandemic cost hospitals?”
6. Gavidia M. AJMC. 2020 Mar 31. “Sleep, physician burnout linked amid COVID-19 pandemic.”
7. Hollander JE and Carr BG. N Engl J Med. 2020 Apr 30;382(18):1679-81. “Virtually perfect? Telemedicine for COVID-19.”
States vary in vulnerability to COVID-19 impact
West Virginia’s large elderly population and high rates of chronic kidney disease, cardiovascular disease, diabetes, and COPD make it the most vulnerable state to the coronavirus, according to a new analysis.
Vulnerability to the virus “isn’t just health related, though, as many people are harmed by the economic effects of the pandemic,” personal finance website WalletHub said May 12.
“It’s important for the U.S. to dedicate a large portion of its resources to providing medical support during the coronavirus pandemic, but we should also support people who don’t have adequate housing or enough money to survive the pandemic,” said WalletHub analyst Jill Gonzalez.
WalletHub graded each state on 28 measures – including share of obese adults, share of homes lacking access to basic hygienic facilities, and biggest increases in unemployment because of COVID-19 – grouped into three dimensions of vulnerability: medical (60% of the total score), housing (15%), and financial (25%).
Using those measures, Louisiana is the most vulnerable state after West Virginia, followed by Mississippi, Arkansas, and Alabama. All 5 states finished in the top 6 for medical vulnerability, and 4 were in the top 10 for financial vulnerability, but only 1 (Arkansas) was in the top 10 for housing vulnerability, WalletHub said.
Among the three vulnerability dimensions, West Virginia was first in medical, Hawaii (33rd overall) was first in housing, and Louisiana was first in financial. Utah is the least vulnerable state, overall, and the least vulnerable states in each dimension are, respectively, Colorado (50th overall), the District of Columbia (29th overall), and Iowa (45th overall), the report showed.
A look at the individual metrics WalletHub used shows some serious disparities:
- New Jersey’s unemployment recipiency rate of 57.2%, the highest in the country, is 6.1 times higher than North Carolina’s 9.3%.
- The highest uninsured rate, 17.4% in Texas, is 6.2 times higher than in Massachusetts, which is the lowest at 2.8%.
- In California, the share of the homeless population that is unsheltered (71.7%) is more than 33 times higher than in North Dakota (2.2%).
“The financial damage caused by COVID-19 is leaving many Americans without the means to pay their bills and purchase necessities. … The U.S. must continue to support its financially vulnerable populations even after the virus has subsided,” Ms. Gonzalez said.
West Virginia’s large elderly population and high rates of chronic kidney disease, cardiovascular disease, diabetes, and COPD make it the most vulnerable state to the coronavirus, according to a new analysis.
Vulnerability to the virus “isn’t just health related, though, as many people are harmed by the economic effects of the pandemic,” personal finance website WalletHub said May 12.
“It’s important for the U.S. to dedicate a large portion of its resources to providing medical support during the coronavirus pandemic, but we should also support people who don’t have adequate housing or enough money to survive the pandemic,” said WalletHub analyst Jill Gonzalez.
WalletHub graded each state on 28 measures – including share of obese adults, share of homes lacking access to basic hygienic facilities, and biggest increases in unemployment because of COVID-19 – grouped into three dimensions of vulnerability: medical (60% of the total score), housing (15%), and financial (25%).
Using those measures, Louisiana is the most vulnerable state after West Virginia, followed by Mississippi, Arkansas, and Alabama. All 5 states finished in the top 6 for medical vulnerability, and 4 were in the top 10 for financial vulnerability, but only 1 (Arkansas) was in the top 10 for housing vulnerability, WalletHub said.
Among the three vulnerability dimensions, West Virginia was first in medical, Hawaii (33rd overall) was first in housing, and Louisiana was first in financial. Utah is the least vulnerable state, overall, and the least vulnerable states in each dimension are, respectively, Colorado (50th overall), the District of Columbia (29th overall), and Iowa (45th overall), the report showed.
A look at the individual metrics WalletHub used shows some serious disparities:
- New Jersey’s unemployment recipiency rate of 57.2%, the highest in the country, is 6.1 times higher than North Carolina’s 9.3%.
- The highest uninsured rate, 17.4% in Texas, is 6.2 times higher than in Massachusetts, which is the lowest at 2.8%.
- In California, the share of the homeless population that is unsheltered (71.7%) is more than 33 times higher than in North Dakota (2.2%).
“The financial damage caused by COVID-19 is leaving many Americans without the means to pay their bills and purchase necessities. … The U.S. must continue to support its financially vulnerable populations even after the virus has subsided,” Ms. Gonzalez said.
West Virginia’s large elderly population and high rates of chronic kidney disease, cardiovascular disease, diabetes, and COPD make it the most vulnerable state to the coronavirus, according to a new analysis.
Vulnerability to the virus “isn’t just health related, though, as many people are harmed by the economic effects of the pandemic,” personal finance website WalletHub said May 12.
“It’s important for the U.S. to dedicate a large portion of its resources to providing medical support during the coronavirus pandemic, but we should also support people who don’t have adequate housing or enough money to survive the pandemic,” said WalletHub analyst Jill Gonzalez.
WalletHub graded each state on 28 measures – including share of obese adults, share of homes lacking access to basic hygienic facilities, and biggest increases in unemployment because of COVID-19 – grouped into three dimensions of vulnerability: medical (60% of the total score), housing (15%), and financial (25%).
Using those measures, Louisiana is the most vulnerable state after West Virginia, followed by Mississippi, Arkansas, and Alabama. All 5 states finished in the top 6 for medical vulnerability, and 4 were in the top 10 for financial vulnerability, but only 1 (Arkansas) was in the top 10 for housing vulnerability, WalletHub said.
Among the three vulnerability dimensions, West Virginia was first in medical, Hawaii (33rd overall) was first in housing, and Louisiana was first in financial. Utah is the least vulnerable state, overall, and the least vulnerable states in each dimension are, respectively, Colorado (50th overall), the District of Columbia (29th overall), and Iowa (45th overall), the report showed.
A look at the individual metrics WalletHub used shows some serious disparities:
- New Jersey’s unemployment recipiency rate of 57.2%, the highest in the country, is 6.1 times higher than North Carolina’s 9.3%.
- The highest uninsured rate, 17.4% in Texas, is 6.2 times higher than in Massachusetts, which is the lowest at 2.8%.
- In California, the share of the homeless population that is unsheltered (71.7%) is more than 33 times higher than in North Dakota (2.2%).
“The financial damage caused by COVID-19 is leaving many Americans without the means to pay their bills and purchase necessities. … The U.S. must continue to support its financially vulnerable populations even after the virus has subsided,” Ms. Gonzalez said.
Sleep quality may affect COPD risk in African American smokers
African American smokers who logged more total sleep time and greater sleep efficacy performed better on a functional walk test than did those with poorer sleep, based on data from 209 adults.
African American smokers tend to develop COPD sooner and also report more sleep problems, compared with white smokers, wrote Andrew J. Gangemi, MD, of Temple University Hospital, Philadelphia, and colleagues.
In addition, African Americans tend to develop COPD at a younger age and with lower levels of smoking than do non-Hispanic whites, they said. “Sleep health may be a contributing factor to the lung and cardiovascular health disparity experienced by AA smokers,” in part because data suggest that insufficient sleep may be associated with increased risk of COPD exacerbation in smokers in general, they said.
In a study published in Chest, the researchers reviewed data from 209 African American adults aged 40-65 years who had smoked at least one cigarette in the past month. The average age of the participants was 55 years, 59% were women, and the average smoking habit was nine cigarettes per day.
The researchers measured functional exercise capacity of the participants using the 6-minute walk test (6MWT). Total sleep time (TST) and sleep efficacy (SE) were measured by way of a finger-based device.
Smokers of at least 10 cigarettes per day gained an additional 0.05-0.58 meters in distance covered on the 6MWT for every added minute of total sleep time in a multivariable regression analysis. Similarly, smokers of at least 10 cigarettes per day gained an additional 0.84-6.17–meter increase in distance covered on the 6MWT for every added percentage of sleep efficacy.
The reasons for the impact of SE and TST on functional exercise capacity in smokers remain unclear, the researchers said. “Heavier smokers have higher levels of autonomic imbalance, including higher resting heart rate and heart rate variability, impaired 24-hour cardiovascular sympathetic tone, and blunted cerebrovascular autonomic regulation and baroreflex response to hypercapnia,” they said.
Also unclear is the reason for the large magnitude of the association between SE and smoking vs. the lesser association between TST and smoking on 6MWT results, the researchers wrote. “Poor sleep efficiency, outside of traditional OSA scoring, is predictive of myocardial infarction, stroke, and cardiovascular-related mortality risk. Moreover, deficits in sleep efficiency have been consistently demonstrated in smokers versus nonsmokers,” they said.
The study findings were limited by several factors including inability to extrapolate data to other demographic groups and the cross-sectional design, the researchers noted. In addition, they did not address how TST and SE may relate to lung function.
However, the results “extend current knowledge about the potential role of improved sleep health to functional exercise capacity in AA smokers,” and set the stage for future studies of how changes in sleep health may affect lung and functional exercise capacity in smokers over time, as well as effects on inflammation and autonomic imbalance, the researchers concluded.
The study was supported by the National Institute on Minority Health and Health Disparities and by the National Institute of General Medical Sciences, both part of the National Institutes Health. The researchers had no financial conflicts to disclose.
SOURCE: Gangemi A et al. Chest 2020 Apr 23. doi: 10.1016/j.chest.2020.03.070.
African American smokers who logged more total sleep time and greater sleep efficacy performed better on a functional walk test than did those with poorer sleep, based on data from 209 adults.
African American smokers tend to develop COPD sooner and also report more sleep problems, compared with white smokers, wrote Andrew J. Gangemi, MD, of Temple University Hospital, Philadelphia, and colleagues.
In addition, African Americans tend to develop COPD at a younger age and with lower levels of smoking than do non-Hispanic whites, they said. “Sleep health may be a contributing factor to the lung and cardiovascular health disparity experienced by AA smokers,” in part because data suggest that insufficient sleep may be associated with increased risk of COPD exacerbation in smokers in general, they said.
In a study published in Chest, the researchers reviewed data from 209 African American adults aged 40-65 years who had smoked at least one cigarette in the past month. The average age of the participants was 55 years, 59% were women, and the average smoking habit was nine cigarettes per day.
The researchers measured functional exercise capacity of the participants using the 6-minute walk test (6MWT). Total sleep time (TST) and sleep efficacy (SE) were measured by way of a finger-based device.
Smokers of at least 10 cigarettes per day gained an additional 0.05-0.58 meters in distance covered on the 6MWT for every added minute of total sleep time in a multivariable regression analysis. Similarly, smokers of at least 10 cigarettes per day gained an additional 0.84-6.17–meter increase in distance covered on the 6MWT for every added percentage of sleep efficacy.
The reasons for the impact of SE and TST on functional exercise capacity in smokers remain unclear, the researchers said. “Heavier smokers have higher levels of autonomic imbalance, including higher resting heart rate and heart rate variability, impaired 24-hour cardiovascular sympathetic tone, and blunted cerebrovascular autonomic regulation and baroreflex response to hypercapnia,” they said.
Also unclear is the reason for the large magnitude of the association between SE and smoking vs. the lesser association between TST and smoking on 6MWT results, the researchers wrote. “Poor sleep efficiency, outside of traditional OSA scoring, is predictive of myocardial infarction, stroke, and cardiovascular-related mortality risk. Moreover, deficits in sleep efficiency have been consistently demonstrated in smokers versus nonsmokers,” they said.
The study findings were limited by several factors including inability to extrapolate data to other demographic groups and the cross-sectional design, the researchers noted. In addition, they did not address how TST and SE may relate to lung function.
However, the results “extend current knowledge about the potential role of improved sleep health to functional exercise capacity in AA smokers,” and set the stage for future studies of how changes in sleep health may affect lung and functional exercise capacity in smokers over time, as well as effects on inflammation and autonomic imbalance, the researchers concluded.
The study was supported by the National Institute on Minority Health and Health Disparities and by the National Institute of General Medical Sciences, both part of the National Institutes Health. The researchers had no financial conflicts to disclose.
SOURCE: Gangemi A et al. Chest 2020 Apr 23. doi: 10.1016/j.chest.2020.03.070.
African American smokers who logged more total sleep time and greater sleep efficacy performed better on a functional walk test than did those with poorer sleep, based on data from 209 adults.
African American smokers tend to develop COPD sooner and also report more sleep problems, compared with white smokers, wrote Andrew J. Gangemi, MD, of Temple University Hospital, Philadelphia, and colleagues.
In addition, African Americans tend to develop COPD at a younger age and with lower levels of smoking than do non-Hispanic whites, they said. “Sleep health may be a contributing factor to the lung and cardiovascular health disparity experienced by AA smokers,” in part because data suggest that insufficient sleep may be associated with increased risk of COPD exacerbation in smokers in general, they said.
In a study published in Chest, the researchers reviewed data from 209 African American adults aged 40-65 years who had smoked at least one cigarette in the past month. The average age of the participants was 55 years, 59% were women, and the average smoking habit was nine cigarettes per day.
The researchers measured functional exercise capacity of the participants using the 6-minute walk test (6MWT). Total sleep time (TST) and sleep efficacy (SE) were measured by way of a finger-based device.
Smokers of at least 10 cigarettes per day gained an additional 0.05-0.58 meters in distance covered on the 6MWT for every added minute of total sleep time in a multivariable regression analysis. Similarly, smokers of at least 10 cigarettes per day gained an additional 0.84-6.17–meter increase in distance covered on the 6MWT for every added percentage of sleep efficacy.
The reasons for the impact of SE and TST on functional exercise capacity in smokers remain unclear, the researchers said. “Heavier smokers have higher levels of autonomic imbalance, including higher resting heart rate and heart rate variability, impaired 24-hour cardiovascular sympathetic tone, and blunted cerebrovascular autonomic regulation and baroreflex response to hypercapnia,” they said.
Also unclear is the reason for the large magnitude of the association between SE and smoking vs. the lesser association between TST and smoking on 6MWT results, the researchers wrote. “Poor sleep efficiency, outside of traditional OSA scoring, is predictive of myocardial infarction, stroke, and cardiovascular-related mortality risk. Moreover, deficits in sleep efficiency have been consistently demonstrated in smokers versus nonsmokers,” they said.
The study findings were limited by several factors including inability to extrapolate data to other demographic groups and the cross-sectional design, the researchers noted. In addition, they did not address how TST and SE may relate to lung function.
However, the results “extend current knowledge about the potential role of improved sleep health to functional exercise capacity in AA smokers,” and set the stage for future studies of how changes in sleep health may affect lung and functional exercise capacity in smokers over time, as well as effects on inflammation and autonomic imbalance, the researchers concluded.
The study was supported by the National Institute on Minority Health and Health Disparities and by the National Institute of General Medical Sciences, both part of the National Institutes Health. The researchers had no financial conflicts to disclose.
SOURCE: Gangemi A et al. Chest 2020 Apr 23. doi: 10.1016/j.chest.2020.03.070.
FROM CHEST
Increased risk of lung cancer with COPD, even in never smokers
an observational cohort study has shown.
Patients with COPD who had never smoked had more than double the risk of developing lung cancer (with an adjusted hazard ratio [HR] of 2.67), compared to individuals without COPD who had never smoked.
This was slightly higher than the increased risk seen in individuals who had smoked but who did not have COPD. This group had an almost double the risk of developing lung cancer (adjusted HR, 1.97), again compared to never smokers, the investigators added.
The highest risk of lung cancer was in patients who had COPD and who had smoked; this group had a sixfold risk of developing lung cancer (adjusted HR, 6.19) compared with never smokers without COPD, they note.
“COPD was a strong independent risk factor for lung cancer incidence in never smokers,” conclude the authors, led by Hye Yun Park, MD, Samsung Medical Center, Seoul, South Korea.
“Future studies should evaluate whether COPD patients are candidates for lung cancer screening, irrespective of smoking status,” they suggest.
The study was published March 10 in the journal Thorax.
It was based on an analysis of data from the National Health Insurance (NHS) Service National Sample Cohort between January 2002 and December 2013.
“We included all men and women, 40 to 84 years of age, who underwent at least one health screening examination provided by the NHS during the study period,” Park and colleagues explain.
Overall, the cohort included 338,548 men and women. Participants were followed-up for a median of 7 years.
Over the study interval, 1834 participants developed lung cancer.
“The risk of disease [lung cancer] in never smokers with COPD was higher than that in ever smokers without COPD,” the investigators observe.
“Given that poor lung function in COPD is often a barrier to optimal lung cancer treatment due to increased risk of treatment-related morbidities, our study suggests that early detection of lung cancer in COPD patients may reduce the risk of treatment complications,” the authors write.
The study was supported by the National Research Foundation of Korea. The authors have disclosed no relevant financial relationships.
This article first appeared on Medscape.com.
an observational cohort study has shown.
Patients with COPD who had never smoked had more than double the risk of developing lung cancer (with an adjusted hazard ratio [HR] of 2.67), compared to individuals without COPD who had never smoked.
This was slightly higher than the increased risk seen in individuals who had smoked but who did not have COPD. This group had an almost double the risk of developing lung cancer (adjusted HR, 1.97), again compared to never smokers, the investigators added.
The highest risk of lung cancer was in patients who had COPD and who had smoked; this group had a sixfold risk of developing lung cancer (adjusted HR, 6.19) compared with never smokers without COPD, they note.
“COPD was a strong independent risk factor for lung cancer incidence in never smokers,” conclude the authors, led by Hye Yun Park, MD, Samsung Medical Center, Seoul, South Korea.
“Future studies should evaluate whether COPD patients are candidates for lung cancer screening, irrespective of smoking status,” they suggest.
The study was published March 10 in the journal Thorax.
It was based on an analysis of data from the National Health Insurance (NHS) Service National Sample Cohort between January 2002 and December 2013.
“We included all men and women, 40 to 84 years of age, who underwent at least one health screening examination provided by the NHS during the study period,” Park and colleagues explain.
Overall, the cohort included 338,548 men and women. Participants were followed-up for a median of 7 years.
Over the study interval, 1834 participants developed lung cancer.
“The risk of disease [lung cancer] in never smokers with COPD was higher than that in ever smokers without COPD,” the investigators observe.
“Given that poor lung function in COPD is often a barrier to optimal lung cancer treatment due to increased risk of treatment-related morbidities, our study suggests that early detection of lung cancer in COPD patients may reduce the risk of treatment complications,” the authors write.
The study was supported by the National Research Foundation of Korea. The authors have disclosed no relevant financial relationships.
This article first appeared on Medscape.com.
an observational cohort study has shown.
Patients with COPD who had never smoked had more than double the risk of developing lung cancer (with an adjusted hazard ratio [HR] of 2.67), compared to individuals without COPD who had never smoked.
This was slightly higher than the increased risk seen in individuals who had smoked but who did not have COPD. This group had an almost double the risk of developing lung cancer (adjusted HR, 1.97), again compared to never smokers, the investigators added.
The highest risk of lung cancer was in patients who had COPD and who had smoked; this group had a sixfold risk of developing lung cancer (adjusted HR, 6.19) compared with never smokers without COPD, they note.
“COPD was a strong independent risk factor for lung cancer incidence in never smokers,” conclude the authors, led by Hye Yun Park, MD, Samsung Medical Center, Seoul, South Korea.
“Future studies should evaluate whether COPD patients are candidates for lung cancer screening, irrespective of smoking status,” they suggest.
The study was published March 10 in the journal Thorax.
It was based on an analysis of data from the National Health Insurance (NHS) Service National Sample Cohort between January 2002 and December 2013.
“We included all men and women, 40 to 84 years of age, who underwent at least one health screening examination provided by the NHS during the study period,” Park and colleagues explain.
Overall, the cohort included 338,548 men and women. Participants were followed-up for a median of 7 years.
Over the study interval, 1834 participants developed lung cancer.
“The risk of disease [lung cancer] in never smokers with COPD was higher than that in ever smokers without COPD,” the investigators observe.
“Given that poor lung function in COPD is often a barrier to optimal lung cancer treatment due to increased risk of treatment-related morbidities, our study suggests that early detection of lung cancer in COPD patients may reduce the risk of treatment complications,” the authors write.
The study was supported by the National Research Foundation of Korea. The authors have disclosed no relevant financial relationships.
This article first appeared on Medscape.com.
European COVID-19 insights: Try helmet CPAP
Noninvasive ventilation with helmet continuous positive air pressure (CPAP) deserves to be embraced as an effective strategy in preventing self-induced lung injury, often a key factor in progression from the early milder expression of COVID-19 disease to classic severe acute respiratory distress syndrome, according to European physicians who have been through what they hope are the worst days of the pandemic in the Lombardy region of Northern Italy.
Helmet CPAP is a relatively inexpensive, convenient, well-tolerated intervention. It allows patients to remain conscious and responsive to commands such as “Time to roll over,” which in turn frees up nursing staff. The purpose of helmet CPAP is to curb the huge inspiratory drive that’s a defining feature of this disease and which, unchecked, can lead to self-induced lung injury (SILI), Luciano Gattinoni, MD, explained at a webinar hosted by the European Society of Anaesthesiology.
“Paranoid attention to inspiratory effort – checking it and correcting it – is something where we can make the difference between death and life. It’s extremely important,” said Dr. Gattinoni, guest professor of anesthesiology and intensive care at the University of Gottingen (Germany).
He and his fellow panelists were in accord regarding the merits of helmet CPAP as the premier method of noninvasive ventilatory assistance. They also addressed the importance of monitoring for hypercoagulation, as well as what they’ve come to see as the essential role of pronation in what they define as Type H disease, and the need to have detailed respiratory physiotherapy protocols in place.
“COVID-19 doesn’t like physiotherapy,” explained Paolo Pelosi, MD, professor of anesthesiology and intensive care medicine at the University of Genoa (Italy).
Dr. Gattinoni is credited for identification of two polar phenotypes of what he considers to be a single COVID-19 disease. Early on, many patients present with an atypical form of acute respiratory distress syndrome (ARDS), distinguished by an often-unexpected degree of hypoxia accompanied by high pulmonary compliance and surprisingly little shortness of breath. Dr. Gattinoni and colleagues call this Type L disease, which stands for low elastane, low ventilation to perfusion ratio, low lung weight on CT, and low lung recruitability, which means the patient has a high proportion of aerated lung tissue. Over time, because of either the natural history of the disease or SILI, this may shift to Type H disease, marked by high elastane, high right-to-left shunt, high lung weight, and high recruitability.
“If the pulmonary compliance is above 60 [mL/cm H2O], I’m pretty sure it’s Type L. If it’s 30 [mL/cm H2O] or less, I’m pretty sure it’s Type H. Don’t ask me about 45-55 [mL/cm H2O]; it’s a grey zone,” Dr. Gattinoni said.
Giuseppe Foti, MD, said helmet CPAP in patients with COVID-19 should be free flow, not attached to a ventilator, and the gas flow should be set high – at least 50 L/min – in order to prevent CO2 rebreathing. Although noninvasive ventilation is well accepted for patients with chronic obstructive pulmonary disease or acute cardiogenic pulmonary edema, it hasn’t been extensively studied in the setting of ARDS. A notable exception is a single-center randomized trial in which 83 patients with ARDS at the University of Chicago were assigned to noninvasive ventilation delivered by helmet or face mask (JAMA. 2016 Jun 14;315[22]:2435-41). The endotracheal intubation rate was just 18% in the helmet group, compared with 62% in the face mask group. The 90-day mortality rate was significantly lower in the helmet group as well, noted Dr. Foti, director of the department of anesthesia and intensive care at Monza University Hospital in Milan.
Christian Putensen, MD, said he views intubation for mechanical ventilation as wise in moderate or severe ARDS with an arterial oxygen partial pressure/fraction of inspired oxygen (PaO2/FiO2) ratio below 150. But in milder, Type L COVID-19 disease, he also likes helmet CPAP. It spares the patient from the traumatic compressive stress to the lung induced by mechanical ventilation, which may cause alveolar edema and SILI.
There is, however, a caveat: “Watch carefully and do not delay intubation if you see helmet CPAP is not working; that is, if the blood gas analysis doesn’t improve, the respiratory rate increases, tidal volume increases, and there is still increased respiratory drive,” advised Dr. Putensen, an anesthesiologist at the University of Bonn (Germany).
There is no agreed-upon practical quantitative measure of respiratory drive. A clinical evaluation of the patient’s depth of inspiration is the best guide, he added.
Dr. Gattinoni said that, when helmet CPAP can’t control respiratory drive in a patient with early-stage disease, he feels the only way to interrupt this destructive process is through early intubation and what he termed “gentle mechanical ventilation,” not with a positive end expiratory pressure of 20 cm H2O, but more like 4-5.
Watch for hypercoagulation
Thromboembolic complications are a common feature in COVID-19 disease.
“I’ve had occasion to see the autopsy results in more than 100 patients. It’s devastating to see the number of thromboses and microthromboses in the lungs, the liver, the kidney, and in the brain,” Dr. Gattinoni said.
“COVID-19 is a serial killer, no doubt,” Dr. Pelosi agreed. “He has no mercy for anyone. And he has two bullets: The first one is for the lung, the second is on the vascular side.”
Dr. Putensen is aggressive in utilizing prophylactic high-dose anticoagulation with heparin. He carefully monitors levels of fibrinogen, Factors V and VIII, and d-dimers. In the setting of COVID-19, he has found thromboelastography to be more reliable than partial thromboplastin time in guiding heparin titration.
Pronation
Panelists agreed that pronation is an especially valuable means of enhancing oxygenation in patients with Type H disease. Dr. Putensen tries for more than 16 hours per day. Dr. Foti is preparing a study of the impact of pronation in 50 awake, nonintubated patients, most of whom were on helmet CPAP. Seven of them couldn’t tolerate pronation for even an hour at a time; for the others, the median duration was 3.5 hours at a time.
“We saw a dramatic improvement, a nearly doubling in the PaO2/FiO2 ratio,” Dr. Foti said.
The helmet CPAP study was done outside of the ICU because, in March 2020, the Milan hospital was utterly overwhelmed by COVID-19. The university hospital ordinarily has 25 ICU beds. This was expanded to 100 ICU beds in an effort to meet the emergency, but that still wasn’t sufficient. Indeed, COVID-19 patients occupied 600 of the hospital’s 650 beds. Physicians were forced to do something formerly unthinkable: triage patients for intubation and mechanical ventilation based upon age, comorbidities, and survival prospects.
“We felt schizophrenic. I completely agree with Luciano’s idea to intubate early when we cannot control the respiratory drive that’s due to the disease. But we couldn’t do it because we had too many patients. So we had to triage,” Dr. Foti recalled, breaking off with a sob as other panelists wiped away their own tears during the webcast.
Respiratory physical therapy
Dr. Pelosi said he believes that optimal care of patients with COVID-19 disease requires a major commitment to physical therapy. He strongly recommends having thoughtfully designed separate written protocols in place for respiratory physiotherapy during mechanical ventilation, weaning, and postextubation. COVID-19 patients typically require 7-10 days of assisted ventilation before weaning, and weaning is a protracted process as well.
“I like to say COVID-19 always requires patience. You have to be very, very patient with this disease,” he emphasized. “These patients have a long and difficult weaning. If the patient isn’t improving during weaning, look at two issues: superinfection and thrombembolism, macro and micro.” The physical therapy measures routinely utilized at his hospital during mechanical ventilation include elevation of the bed head greater than 30 degrees, neuromuscular electrical stimulation, subglottic secretion suctioning, tracheal and oral aspiration, and cough assistance. Separate physical therapy menus are used during before and after extubation.
Dr. Gattinoni offered a final word: “We can do almost nothing with this disease. We try our best to keep the patient alive. What we can do is avoid excessive ventilation of the patient. Applying the typical treatment of ARDS in atypical [Type L] ARDS does not make sense and may be extremely harmful.”
Noninvasive ventilation with helmet continuous positive air pressure (CPAP) deserves to be embraced as an effective strategy in preventing self-induced lung injury, often a key factor in progression from the early milder expression of COVID-19 disease to classic severe acute respiratory distress syndrome, according to European physicians who have been through what they hope are the worst days of the pandemic in the Lombardy region of Northern Italy.
Helmet CPAP is a relatively inexpensive, convenient, well-tolerated intervention. It allows patients to remain conscious and responsive to commands such as “Time to roll over,” which in turn frees up nursing staff. The purpose of helmet CPAP is to curb the huge inspiratory drive that’s a defining feature of this disease and which, unchecked, can lead to self-induced lung injury (SILI), Luciano Gattinoni, MD, explained at a webinar hosted by the European Society of Anaesthesiology.
“Paranoid attention to inspiratory effort – checking it and correcting it – is something where we can make the difference between death and life. It’s extremely important,” said Dr. Gattinoni, guest professor of anesthesiology and intensive care at the University of Gottingen (Germany).
He and his fellow panelists were in accord regarding the merits of helmet CPAP as the premier method of noninvasive ventilatory assistance. They also addressed the importance of monitoring for hypercoagulation, as well as what they’ve come to see as the essential role of pronation in what they define as Type H disease, and the need to have detailed respiratory physiotherapy protocols in place.
“COVID-19 doesn’t like physiotherapy,” explained Paolo Pelosi, MD, professor of anesthesiology and intensive care medicine at the University of Genoa (Italy).
Dr. Gattinoni is credited for identification of two polar phenotypes of what he considers to be a single COVID-19 disease. Early on, many patients present with an atypical form of acute respiratory distress syndrome (ARDS), distinguished by an often-unexpected degree of hypoxia accompanied by high pulmonary compliance and surprisingly little shortness of breath. Dr. Gattinoni and colleagues call this Type L disease, which stands for low elastane, low ventilation to perfusion ratio, low lung weight on CT, and low lung recruitability, which means the patient has a high proportion of aerated lung tissue. Over time, because of either the natural history of the disease or SILI, this may shift to Type H disease, marked by high elastane, high right-to-left shunt, high lung weight, and high recruitability.
“If the pulmonary compliance is above 60 [mL/cm H2O], I’m pretty sure it’s Type L. If it’s 30 [mL/cm H2O] or less, I’m pretty sure it’s Type H. Don’t ask me about 45-55 [mL/cm H2O]; it’s a grey zone,” Dr. Gattinoni said.
Giuseppe Foti, MD, said helmet CPAP in patients with COVID-19 should be free flow, not attached to a ventilator, and the gas flow should be set high – at least 50 L/min – in order to prevent CO2 rebreathing. Although noninvasive ventilation is well accepted for patients with chronic obstructive pulmonary disease or acute cardiogenic pulmonary edema, it hasn’t been extensively studied in the setting of ARDS. A notable exception is a single-center randomized trial in which 83 patients with ARDS at the University of Chicago were assigned to noninvasive ventilation delivered by helmet or face mask (JAMA. 2016 Jun 14;315[22]:2435-41). The endotracheal intubation rate was just 18% in the helmet group, compared with 62% in the face mask group. The 90-day mortality rate was significantly lower in the helmet group as well, noted Dr. Foti, director of the department of anesthesia and intensive care at Monza University Hospital in Milan.
Christian Putensen, MD, said he views intubation for mechanical ventilation as wise in moderate or severe ARDS with an arterial oxygen partial pressure/fraction of inspired oxygen (PaO2/FiO2) ratio below 150. But in milder, Type L COVID-19 disease, he also likes helmet CPAP. It spares the patient from the traumatic compressive stress to the lung induced by mechanical ventilation, which may cause alveolar edema and SILI.
There is, however, a caveat: “Watch carefully and do not delay intubation if you see helmet CPAP is not working; that is, if the blood gas analysis doesn’t improve, the respiratory rate increases, tidal volume increases, and there is still increased respiratory drive,” advised Dr. Putensen, an anesthesiologist at the University of Bonn (Germany).
There is no agreed-upon practical quantitative measure of respiratory drive. A clinical evaluation of the patient’s depth of inspiration is the best guide, he added.
Dr. Gattinoni said that, when helmet CPAP can’t control respiratory drive in a patient with early-stage disease, he feels the only way to interrupt this destructive process is through early intubation and what he termed “gentle mechanical ventilation,” not with a positive end expiratory pressure of 20 cm H2O, but more like 4-5.
Watch for hypercoagulation
Thromboembolic complications are a common feature in COVID-19 disease.
“I’ve had occasion to see the autopsy results in more than 100 patients. It’s devastating to see the number of thromboses and microthromboses in the lungs, the liver, the kidney, and in the brain,” Dr. Gattinoni said.
“COVID-19 is a serial killer, no doubt,” Dr. Pelosi agreed. “He has no mercy for anyone. And he has two bullets: The first one is for the lung, the second is on the vascular side.”
Dr. Putensen is aggressive in utilizing prophylactic high-dose anticoagulation with heparin. He carefully monitors levels of fibrinogen, Factors V and VIII, and d-dimers. In the setting of COVID-19, he has found thromboelastography to be more reliable than partial thromboplastin time in guiding heparin titration.
Pronation
Panelists agreed that pronation is an especially valuable means of enhancing oxygenation in patients with Type H disease. Dr. Putensen tries for more than 16 hours per day. Dr. Foti is preparing a study of the impact of pronation in 50 awake, nonintubated patients, most of whom were on helmet CPAP. Seven of them couldn’t tolerate pronation for even an hour at a time; for the others, the median duration was 3.5 hours at a time.
“We saw a dramatic improvement, a nearly doubling in the PaO2/FiO2 ratio,” Dr. Foti said.
The helmet CPAP study was done outside of the ICU because, in March 2020, the Milan hospital was utterly overwhelmed by COVID-19. The university hospital ordinarily has 25 ICU beds. This was expanded to 100 ICU beds in an effort to meet the emergency, but that still wasn’t sufficient. Indeed, COVID-19 patients occupied 600 of the hospital’s 650 beds. Physicians were forced to do something formerly unthinkable: triage patients for intubation and mechanical ventilation based upon age, comorbidities, and survival prospects.
“We felt schizophrenic. I completely agree with Luciano’s idea to intubate early when we cannot control the respiratory drive that’s due to the disease. But we couldn’t do it because we had too many patients. So we had to triage,” Dr. Foti recalled, breaking off with a sob as other panelists wiped away their own tears during the webcast.
Respiratory physical therapy
Dr. Pelosi said he believes that optimal care of patients with COVID-19 disease requires a major commitment to physical therapy. He strongly recommends having thoughtfully designed separate written protocols in place for respiratory physiotherapy during mechanical ventilation, weaning, and postextubation. COVID-19 patients typically require 7-10 days of assisted ventilation before weaning, and weaning is a protracted process as well.
“I like to say COVID-19 always requires patience. You have to be very, very patient with this disease,” he emphasized. “These patients have a long and difficult weaning. If the patient isn’t improving during weaning, look at two issues: superinfection and thrombembolism, macro and micro.” The physical therapy measures routinely utilized at his hospital during mechanical ventilation include elevation of the bed head greater than 30 degrees, neuromuscular electrical stimulation, subglottic secretion suctioning, tracheal and oral aspiration, and cough assistance. Separate physical therapy menus are used during before and after extubation.
Dr. Gattinoni offered a final word: “We can do almost nothing with this disease. We try our best to keep the patient alive. What we can do is avoid excessive ventilation of the patient. Applying the typical treatment of ARDS in atypical [Type L] ARDS does not make sense and may be extremely harmful.”
Noninvasive ventilation with helmet continuous positive air pressure (CPAP) deserves to be embraced as an effective strategy in preventing self-induced lung injury, often a key factor in progression from the early milder expression of COVID-19 disease to classic severe acute respiratory distress syndrome, according to European physicians who have been through what they hope are the worst days of the pandemic in the Lombardy region of Northern Italy.
Helmet CPAP is a relatively inexpensive, convenient, well-tolerated intervention. It allows patients to remain conscious and responsive to commands such as “Time to roll over,” which in turn frees up nursing staff. The purpose of helmet CPAP is to curb the huge inspiratory drive that’s a defining feature of this disease and which, unchecked, can lead to self-induced lung injury (SILI), Luciano Gattinoni, MD, explained at a webinar hosted by the European Society of Anaesthesiology.
“Paranoid attention to inspiratory effort – checking it and correcting it – is something where we can make the difference between death and life. It’s extremely important,” said Dr. Gattinoni, guest professor of anesthesiology and intensive care at the University of Gottingen (Germany).
He and his fellow panelists were in accord regarding the merits of helmet CPAP as the premier method of noninvasive ventilatory assistance. They also addressed the importance of monitoring for hypercoagulation, as well as what they’ve come to see as the essential role of pronation in what they define as Type H disease, and the need to have detailed respiratory physiotherapy protocols in place.
“COVID-19 doesn’t like physiotherapy,” explained Paolo Pelosi, MD, professor of anesthesiology and intensive care medicine at the University of Genoa (Italy).
Dr. Gattinoni is credited for identification of two polar phenotypes of what he considers to be a single COVID-19 disease. Early on, many patients present with an atypical form of acute respiratory distress syndrome (ARDS), distinguished by an often-unexpected degree of hypoxia accompanied by high pulmonary compliance and surprisingly little shortness of breath. Dr. Gattinoni and colleagues call this Type L disease, which stands for low elastane, low ventilation to perfusion ratio, low lung weight on CT, and low lung recruitability, which means the patient has a high proportion of aerated lung tissue. Over time, because of either the natural history of the disease or SILI, this may shift to Type H disease, marked by high elastane, high right-to-left shunt, high lung weight, and high recruitability.
“If the pulmonary compliance is above 60 [mL/cm H2O], I’m pretty sure it’s Type L. If it’s 30 [mL/cm H2O] or less, I’m pretty sure it’s Type H. Don’t ask me about 45-55 [mL/cm H2O]; it’s a grey zone,” Dr. Gattinoni said.
Giuseppe Foti, MD, said helmet CPAP in patients with COVID-19 should be free flow, not attached to a ventilator, and the gas flow should be set high – at least 50 L/min – in order to prevent CO2 rebreathing. Although noninvasive ventilation is well accepted for patients with chronic obstructive pulmonary disease or acute cardiogenic pulmonary edema, it hasn’t been extensively studied in the setting of ARDS. A notable exception is a single-center randomized trial in which 83 patients with ARDS at the University of Chicago were assigned to noninvasive ventilation delivered by helmet or face mask (JAMA. 2016 Jun 14;315[22]:2435-41). The endotracheal intubation rate was just 18% in the helmet group, compared with 62% in the face mask group. The 90-day mortality rate was significantly lower in the helmet group as well, noted Dr. Foti, director of the department of anesthesia and intensive care at Monza University Hospital in Milan.
Christian Putensen, MD, said he views intubation for mechanical ventilation as wise in moderate or severe ARDS with an arterial oxygen partial pressure/fraction of inspired oxygen (PaO2/FiO2) ratio below 150. But in milder, Type L COVID-19 disease, he also likes helmet CPAP. It spares the patient from the traumatic compressive stress to the lung induced by mechanical ventilation, which may cause alveolar edema and SILI.
There is, however, a caveat: “Watch carefully and do not delay intubation if you see helmet CPAP is not working; that is, if the blood gas analysis doesn’t improve, the respiratory rate increases, tidal volume increases, and there is still increased respiratory drive,” advised Dr. Putensen, an anesthesiologist at the University of Bonn (Germany).
There is no agreed-upon practical quantitative measure of respiratory drive. A clinical evaluation of the patient’s depth of inspiration is the best guide, he added.
Dr. Gattinoni said that, when helmet CPAP can’t control respiratory drive in a patient with early-stage disease, he feels the only way to interrupt this destructive process is through early intubation and what he termed “gentle mechanical ventilation,” not with a positive end expiratory pressure of 20 cm H2O, but more like 4-5.
Watch for hypercoagulation
Thromboembolic complications are a common feature in COVID-19 disease.
“I’ve had occasion to see the autopsy results in more than 100 patients. It’s devastating to see the number of thromboses and microthromboses in the lungs, the liver, the kidney, and in the brain,” Dr. Gattinoni said.
“COVID-19 is a serial killer, no doubt,” Dr. Pelosi agreed. “He has no mercy for anyone. And he has two bullets: The first one is for the lung, the second is on the vascular side.”
Dr. Putensen is aggressive in utilizing prophylactic high-dose anticoagulation with heparin. He carefully monitors levels of fibrinogen, Factors V and VIII, and d-dimers. In the setting of COVID-19, he has found thromboelastography to be more reliable than partial thromboplastin time in guiding heparin titration.
Pronation
Panelists agreed that pronation is an especially valuable means of enhancing oxygenation in patients with Type H disease. Dr. Putensen tries for more than 16 hours per day. Dr. Foti is preparing a study of the impact of pronation in 50 awake, nonintubated patients, most of whom were on helmet CPAP. Seven of them couldn’t tolerate pronation for even an hour at a time; for the others, the median duration was 3.5 hours at a time.
“We saw a dramatic improvement, a nearly doubling in the PaO2/FiO2 ratio,” Dr. Foti said.
The helmet CPAP study was done outside of the ICU because, in March 2020, the Milan hospital was utterly overwhelmed by COVID-19. The university hospital ordinarily has 25 ICU beds. This was expanded to 100 ICU beds in an effort to meet the emergency, but that still wasn’t sufficient. Indeed, COVID-19 patients occupied 600 of the hospital’s 650 beds. Physicians were forced to do something formerly unthinkable: triage patients for intubation and mechanical ventilation based upon age, comorbidities, and survival prospects.
“We felt schizophrenic. I completely agree with Luciano’s idea to intubate early when we cannot control the respiratory drive that’s due to the disease. But we couldn’t do it because we had too many patients. So we had to triage,” Dr. Foti recalled, breaking off with a sob as other panelists wiped away their own tears during the webcast.
Respiratory physical therapy
Dr. Pelosi said he believes that optimal care of patients with COVID-19 disease requires a major commitment to physical therapy. He strongly recommends having thoughtfully designed separate written protocols in place for respiratory physiotherapy during mechanical ventilation, weaning, and postextubation. COVID-19 patients typically require 7-10 days of assisted ventilation before weaning, and weaning is a protracted process as well.
“I like to say COVID-19 always requires patience. You have to be very, very patient with this disease,” he emphasized. “These patients have a long and difficult weaning. If the patient isn’t improving during weaning, look at two issues: superinfection and thrombembolism, macro and micro.” The physical therapy measures routinely utilized at his hospital during mechanical ventilation include elevation of the bed head greater than 30 degrees, neuromuscular electrical stimulation, subglottic secretion suctioning, tracheal and oral aspiration, and cough assistance. Separate physical therapy menus are used during before and after extubation.
Dr. Gattinoni offered a final word: “We can do almost nothing with this disease. We try our best to keep the patient alive. What we can do is avoid excessive ventilation of the patient. Applying the typical treatment of ARDS in atypical [Type L] ARDS does not make sense and may be extremely harmful.”
DLCO found to predict outcomes in subset of COPD patients
Use of diffusing capacity of the lung for carbon monoxide may be a useful prognostic tool in patients with chronic pulmonary disease who develop pulmonary hypertension, results from a single-center retrospective cohort study found.
“Historically, COPD-PH was thought to develop as the severity of airflow obstruction, measured by Forced Expiratory Volume in one second (FEV1), and subsequent chronic hypoxemia progressed,” authors led by Aparna Balasubramanian, MD, wrote in a study published online in CHEST. “However, airflow obstruction has increasingly been noted to be insufficient in predicting clinical outcomes in the general COPD population.”
Dr. Balasubramanian of the Johns Hopkins University Division of Pulmonary and Critical Care, Baltimore, and colleagues went on to note that, while studies in COPD-PH have identified hemodynamic measures as better predictors of prognosis, these metrics require right-heart catheterization (RHC), an invasive procedure that carries its own risks. “An alternative noninvasive measure of interest is diffusing capacity of the lung for carbon monoxide (DLCO). DLCO is a measure of gas exchange reflective of the complex interactions occurring at the alveolar-capillary interface, including morphologic changes in the pulmonary vasculature,” they wrote. “Recent work by our group in a large COPD cohort has demonstrated that DLCO is an indicator of disease morbidity beyond that represented by airflow obstruction or by CT evidence of emphysema alone. This may be particularly relevant for those with COPD-PH.”
The study population consisted of 71 patients enrolled in the Johns Hopkins Pulmonary Hypertension Registry between January 2000 and January 2018, all of whom had right-heart catheterization (RHC)–proven PH and pulmonary function testing (PFT) data within 1 year of diagnostic RHC. The researchers calculated transplant-free survival from index RHC and used Cox proportional hazard methods to determine transplant-free survival with age, pulmonary vascular resistance, FEV1, oxygen use, and N-terminal pro-brain natriuretic peptide included as covariates.
The average age of patients was 65 years, 66% were female, their average body mass index was 28.3 kg/m2, and the mean number of pack-years smoked was 44. On unadjusted analysis, the transplant-free survival was 87% at 1 year, 60% at 3 years, and 51% at 5 years. Survival was associated with reduced DLCO across the observed range of pulmonary artery pressures and pulmonary vascular resistance. The researchers found that severe DLCO impairment was associated with poorer survival (P less than .001), and when they adjusted for covariates, they found that mortality increased by 4% for every percent predicted decrease in DLCO (hazard ratio, 1.04).
“This study demonstrates that DLCO, a readily available, inexpensive, noninvasive measurement, is a strong independent predictor of mortality in COPD patients with PH,” the authors concluded. “The presented findings suggest that DLCO should be considered for inclusion in prognostic tools for COPD-PH.”
Dr. Balasubramanian and associates acknowledged certain limitations of the study, including its modest sample size and single-center design and the fact that the cohort underwent subspecialty referral and invasive testing, thereby limiting its generalizability to the larger COPD population. “The findings do, however, offer insight into clinical and physiologic characteristics at one extreme of the pulmonary vascular disease spectrum among COPD patients, and generate hypotheses regarding measures that warrant further exploration in the larger COPD population,” they wrote.
The study was supported by National Heart, Lung and Blood Institute. One of the study authors has served as a consultant to GlaxoSmithKline and Celgene and receives royalties from UpToDate for authorship. Another study author has served as a consultant for Arena, Actelion, Liquidia, and United Therapeutics, and has served on the Scientific Leadership Council of the Pulmonary Hypertension Association. He also serves on the Rare Disease Advisory Panel of the Patient Centered Outcomes Research Institute. The other study authors reported having no disclosures.
SOURCE: Balasubramanian A et al. CHEST. 2020 Mar 14. doi: 10.1016/j.chest.2020.02.047.
Use of diffusing capacity of the lung for carbon monoxide may be a useful prognostic tool in patients with chronic pulmonary disease who develop pulmonary hypertension, results from a single-center retrospective cohort study found.
“Historically, COPD-PH was thought to develop as the severity of airflow obstruction, measured by Forced Expiratory Volume in one second (FEV1), and subsequent chronic hypoxemia progressed,” authors led by Aparna Balasubramanian, MD, wrote in a study published online in CHEST. “However, airflow obstruction has increasingly been noted to be insufficient in predicting clinical outcomes in the general COPD population.”
Dr. Balasubramanian of the Johns Hopkins University Division of Pulmonary and Critical Care, Baltimore, and colleagues went on to note that, while studies in COPD-PH have identified hemodynamic measures as better predictors of prognosis, these metrics require right-heart catheterization (RHC), an invasive procedure that carries its own risks. “An alternative noninvasive measure of interest is diffusing capacity of the lung for carbon monoxide (DLCO). DLCO is a measure of gas exchange reflective of the complex interactions occurring at the alveolar-capillary interface, including morphologic changes in the pulmonary vasculature,” they wrote. “Recent work by our group in a large COPD cohort has demonstrated that DLCO is an indicator of disease morbidity beyond that represented by airflow obstruction or by CT evidence of emphysema alone. This may be particularly relevant for those with COPD-PH.”
The study population consisted of 71 patients enrolled in the Johns Hopkins Pulmonary Hypertension Registry between January 2000 and January 2018, all of whom had right-heart catheterization (RHC)–proven PH and pulmonary function testing (PFT) data within 1 year of diagnostic RHC. The researchers calculated transplant-free survival from index RHC and used Cox proportional hazard methods to determine transplant-free survival with age, pulmonary vascular resistance, FEV1, oxygen use, and N-terminal pro-brain natriuretic peptide included as covariates.
The average age of patients was 65 years, 66% were female, their average body mass index was 28.3 kg/m2, and the mean number of pack-years smoked was 44. On unadjusted analysis, the transplant-free survival was 87% at 1 year, 60% at 3 years, and 51% at 5 years. Survival was associated with reduced DLCO across the observed range of pulmonary artery pressures and pulmonary vascular resistance. The researchers found that severe DLCO impairment was associated with poorer survival (P less than .001), and when they adjusted for covariates, they found that mortality increased by 4% for every percent predicted decrease in DLCO (hazard ratio, 1.04).
“This study demonstrates that DLCO, a readily available, inexpensive, noninvasive measurement, is a strong independent predictor of mortality in COPD patients with PH,” the authors concluded. “The presented findings suggest that DLCO should be considered for inclusion in prognostic tools for COPD-PH.”
Dr. Balasubramanian and associates acknowledged certain limitations of the study, including its modest sample size and single-center design and the fact that the cohort underwent subspecialty referral and invasive testing, thereby limiting its generalizability to the larger COPD population. “The findings do, however, offer insight into clinical and physiologic characteristics at one extreme of the pulmonary vascular disease spectrum among COPD patients, and generate hypotheses regarding measures that warrant further exploration in the larger COPD population,” they wrote.
The study was supported by National Heart, Lung and Blood Institute. One of the study authors has served as a consultant to GlaxoSmithKline and Celgene and receives royalties from UpToDate for authorship. Another study author has served as a consultant for Arena, Actelion, Liquidia, and United Therapeutics, and has served on the Scientific Leadership Council of the Pulmonary Hypertension Association. He also serves on the Rare Disease Advisory Panel of the Patient Centered Outcomes Research Institute. The other study authors reported having no disclosures.
SOURCE: Balasubramanian A et al. CHEST. 2020 Mar 14. doi: 10.1016/j.chest.2020.02.047.
Use of diffusing capacity of the lung for carbon monoxide may be a useful prognostic tool in patients with chronic pulmonary disease who develop pulmonary hypertension, results from a single-center retrospective cohort study found.
“Historically, COPD-PH was thought to develop as the severity of airflow obstruction, measured by Forced Expiratory Volume in one second (FEV1), and subsequent chronic hypoxemia progressed,” authors led by Aparna Balasubramanian, MD, wrote in a study published online in CHEST. “However, airflow obstruction has increasingly been noted to be insufficient in predicting clinical outcomes in the general COPD population.”
Dr. Balasubramanian of the Johns Hopkins University Division of Pulmonary and Critical Care, Baltimore, and colleagues went on to note that, while studies in COPD-PH have identified hemodynamic measures as better predictors of prognosis, these metrics require right-heart catheterization (RHC), an invasive procedure that carries its own risks. “An alternative noninvasive measure of interest is diffusing capacity of the lung for carbon monoxide (DLCO). DLCO is a measure of gas exchange reflective of the complex interactions occurring at the alveolar-capillary interface, including morphologic changes in the pulmonary vasculature,” they wrote. “Recent work by our group in a large COPD cohort has demonstrated that DLCO is an indicator of disease morbidity beyond that represented by airflow obstruction or by CT evidence of emphysema alone. This may be particularly relevant for those with COPD-PH.”
The study population consisted of 71 patients enrolled in the Johns Hopkins Pulmonary Hypertension Registry between January 2000 and January 2018, all of whom had right-heart catheterization (RHC)–proven PH and pulmonary function testing (PFT) data within 1 year of diagnostic RHC. The researchers calculated transplant-free survival from index RHC and used Cox proportional hazard methods to determine transplant-free survival with age, pulmonary vascular resistance, FEV1, oxygen use, and N-terminal pro-brain natriuretic peptide included as covariates.
The average age of patients was 65 years, 66% were female, their average body mass index was 28.3 kg/m2, and the mean number of pack-years smoked was 44. On unadjusted analysis, the transplant-free survival was 87% at 1 year, 60% at 3 years, and 51% at 5 years. Survival was associated with reduced DLCO across the observed range of pulmonary artery pressures and pulmonary vascular resistance. The researchers found that severe DLCO impairment was associated with poorer survival (P less than .001), and when they adjusted for covariates, they found that mortality increased by 4% for every percent predicted decrease in DLCO (hazard ratio, 1.04).
“This study demonstrates that DLCO, a readily available, inexpensive, noninvasive measurement, is a strong independent predictor of mortality in COPD patients with PH,” the authors concluded. “The presented findings suggest that DLCO should be considered for inclusion in prognostic tools for COPD-PH.”
Dr. Balasubramanian and associates acknowledged certain limitations of the study, including its modest sample size and single-center design and the fact that the cohort underwent subspecialty referral and invasive testing, thereby limiting its generalizability to the larger COPD population. “The findings do, however, offer insight into clinical and physiologic characteristics at one extreme of the pulmonary vascular disease spectrum among COPD patients, and generate hypotheses regarding measures that warrant further exploration in the larger COPD population,” they wrote.
The study was supported by National Heart, Lung and Blood Institute. One of the study authors has served as a consultant to GlaxoSmithKline and Celgene and receives royalties from UpToDate for authorship. Another study author has served as a consultant for Arena, Actelion, Liquidia, and United Therapeutics, and has served on the Scientific Leadership Council of the Pulmonary Hypertension Association. He also serves on the Rare Disease Advisory Panel of the Patient Centered Outcomes Research Institute. The other study authors reported having no disclosures.
SOURCE: Balasubramanian A et al. CHEST. 2020 Mar 14. doi: 10.1016/j.chest.2020.02.047.
FROM CHEST
Researchers investigate impact of smoking on COVID-19 risk
but quitting smoking is likely to lower the risk of developing more severe or fatal cases of the infection, according to research from several recent papers.
Interest in how tobacco use affects COVID-19 infection rates stems from research showing that men at the epicenter of the outbreak in China having a higher early mortality rate. Early reports from China showed a case fatality rate of 4.7% for men, compared with 2.8% for women, according to the World Health Organization. The virus that causes COVID-19, severe acute respiratory syndrome coronavirus 2, is suspected to enter a cell using the ACE2 receptor. Since smoking up-regulates this receptor, one popular theory is that smoking can increase the risk of COVID-19 or exacerbate symptoms of an existing infection (Eur Respir J. 2020 Apr 8. doi: 10.1183/13993003.00688-2020). In China, about half of men are active smokers, compared with 2.7% of women (Transl Lung Cancer Res. 2019;8[Suppl 1]:S21-30), so this association would explain the severe cases and increased mortality in this group. In response to potential risk for public health, the World Health Organization, Centers for Disease Control and Prevention, the Attorney General of Massachusetts, and other organizations have warned that smoking may increase one’s risk of transmitting and developing COVID-19 or may worsen the infection.
“While it is easy to jump to the conclusion that more ACE2 means more susceptibility to severe infection, there is no evidence to support this,” Brandon Michael Henry, MD, of the cardiac intensive care unit and the Heart Institute at Cincinnati Children’s Hospital Medical Center, said in an interview. “Moreover, some would argue (including myself) that increased ACE2 may in fact be protective, as ACE2 decreases the levels of angiotensin-2 which likely plays a significant role in the pathophysiology of ARDS.”
Some researchers have examined the limited evidence of smoking on COVID-19 risk and come to preliminary conclusions. In a letter to the editor recently published in the European Journal of Internal Medicine, Dr. Henry and Giuseppe Lippi, MD, of the section of clinical biochemistry in the department of neuroscience, biomedicine, and movement at the University of Verona (Italy), performed a meta-analysis of papers examining smoking and COVID-19 up to March 9, 2020 and identified five articles with 1,399 COVID-19 cases (Eur J Intern Med. 2020 Mar 16. doi: 10.1016/j.ejim.2020.03.014).
“Given the fact that COVID-19 is a primarily respiratory illness, smoking was one of first risk factors we examined,” Dr. Henry said.
They noted that a study by Liu et al. in the Chinese Medical Journal was the only paper that showed a significant association between smoking status and COVID-19 case severity (Chin Med J [Engl]. 2020 Feb 28. doi: 10.1097/CM9.0000000000000775), while the four other studies showed no significant association. The pooled data of all five studies showed an association that was not statistically significant (odds ratio, 1.69; 95% confidence interval, 0.41-6.92; P = .254). When Dr. Lippi and Dr. Henry performed the analysis again after removing a paper by Guan et al. (N Engl J Med. 2020 Feb 28. doi: 10.1056/NEJMoa2002032) comprising 89.5% of patients in the pooled analysis, there was no significant association (OR, 4.35; 95% CI, 0.86-21.86; P = .129).
Constantine I. Vardavas, MD, FCCP, of the department of oral health policy and epidemiology at Harvard School of Dental Medicine, Boston, and Katerina Nikitara, of the University of Crete in Heraklion, Greece, also published a systematic review in Tobacco Induced Diseases of five studies evaluating smoking and COVID-19 (Tob Induc Dis. 2020. doi: 10.18332/tid/119324). Of the studies chosen for the review, four were shared with the paper by Dr. Lippi and Dr. Henry. They found “a higher percentage of smokers” made up severe COVID-19 cases, but acknowledged the majority of these were from the largest study by Guan et al. Overall, they calculated smokers carried a risk ratio of 1.4 (95% CI, 0.98-2.00) for developing severe COVID-19 symptoms, and were over twice as likely to be admitted to an ICU, require a mechanical ventilator, or die from COVID-19, compared with patients who did not smoke (RR, 2.4; 95% CI, 1.43-4.04).
“Although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19,” Dr. Vardavas and Ms. Nikitara concluded.
However, the association between smoking and severe disease was not significant, and it is not immediately clear how the analysis was performed based on the details in the editorial. “Both of our reports were limited by a lack of data adjusted for age, sex, and comorbidities which may influence any analysis on smoking,” Dr. Henry said.
Some researchers have proposed collecting information on smoking status and conducting further research on whether vaping devices like e-cigarettes also impact COVID-19 cases. An editorial by Samuel Brake and colleagues published in the Journal of Clinical Medicine proposed the ACE2-receptor binding site as an area of interest for COVID-19 and as a potential therapeutic target (J Clin Med. 2020 Mar 20. doi: 10.3390/jcm9030841).
Ultimately, whether smoking itself is associated with COVID-19 is still an open question. Nonetheless, encouraging patients to quit smoking should be a priority because long-term sequelae of smoking have been linked to worsened or fatal COVID-19 cases, said Dr. Henry.
“There is a lack of definitive data on smoking to date. Nonetheless, we do know that many illnesses associated with smoking, such as [chronic obstructive pulmonary disease, hypertension, and heart disease are all strong risk factors for severe and fatal COVID-19,” he said. “Thus, absolutely we should encourage the public to quit smoking, especially for older individuals and those with comorbidities.”
The papers by Lippi et al., Vardavas et al., and Brake et al. had no funding source, and the authors reported no relevant conflicts of interest.
but quitting smoking is likely to lower the risk of developing more severe or fatal cases of the infection, according to research from several recent papers.
Interest in how tobacco use affects COVID-19 infection rates stems from research showing that men at the epicenter of the outbreak in China having a higher early mortality rate. Early reports from China showed a case fatality rate of 4.7% for men, compared with 2.8% for women, according to the World Health Organization. The virus that causes COVID-19, severe acute respiratory syndrome coronavirus 2, is suspected to enter a cell using the ACE2 receptor. Since smoking up-regulates this receptor, one popular theory is that smoking can increase the risk of COVID-19 or exacerbate symptoms of an existing infection (Eur Respir J. 2020 Apr 8. doi: 10.1183/13993003.00688-2020). In China, about half of men are active smokers, compared with 2.7% of women (Transl Lung Cancer Res. 2019;8[Suppl 1]:S21-30), so this association would explain the severe cases and increased mortality in this group. In response to potential risk for public health, the World Health Organization, Centers for Disease Control and Prevention, the Attorney General of Massachusetts, and other organizations have warned that smoking may increase one’s risk of transmitting and developing COVID-19 or may worsen the infection.
“While it is easy to jump to the conclusion that more ACE2 means more susceptibility to severe infection, there is no evidence to support this,” Brandon Michael Henry, MD, of the cardiac intensive care unit and the Heart Institute at Cincinnati Children’s Hospital Medical Center, said in an interview. “Moreover, some would argue (including myself) that increased ACE2 may in fact be protective, as ACE2 decreases the levels of angiotensin-2 which likely plays a significant role in the pathophysiology of ARDS.”
Some researchers have examined the limited evidence of smoking on COVID-19 risk and come to preliminary conclusions. In a letter to the editor recently published in the European Journal of Internal Medicine, Dr. Henry and Giuseppe Lippi, MD, of the section of clinical biochemistry in the department of neuroscience, biomedicine, and movement at the University of Verona (Italy), performed a meta-analysis of papers examining smoking and COVID-19 up to March 9, 2020 and identified five articles with 1,399 COVID-19 cases (Eur J Intern Med. 2020 Mar 16. doi: 10.1016/j.ejim.2020.03.014).
“Given the fact that COVID-19 is a primarily respiratory illness, smoking was one of first risk factors we examined,” Dr. Henry said.
They noted that a study by Liu et al. in the Chinese Medical Journal was the only paper that showed a significant association between smoking status and COVID-19 case severity (Chin Med J [Engl]. 2020 Feb 28. doi: 10.1097/CM9.0000000000000775), while the four other studies showed no significant association. The pooled data of all five studies showed an association that was not statistically significant (odds ratio, 1.69; 95% confidence interval, 0.41-6.92; P = .254). When Dr. Lippi and Dr. Henry performed the analysis again after removing a paper by Guan et al. (N Engl J Med. 2020 Feb 28. doi: 10.1056/NEJMoa2002032) comprising 89.5% of patients in the pooled analysis, there was no significant association (OR, 4.35; 95% CI, 0.86-21.86; P = .129).
Constantine I. Vardavas, MD, FCCP, of the department of oral health policy and epidemiology at Harvard School of Dental Medicine, Boston, and Katerina Nikitara, of the University of Crete in Heraklion, Greece, also published a systematic review in Tobacco Induced Diseases of five studies evaluating smoking and COVID-19 (Tob Induc Dis. 2020. doi: 10.18332/tid/119324). Of the studies chosen for the review, four were shared with the paper by Dr. Lippi and Dr. Henry. They found “a higher percentage of smokers” made up severe COVID-19 cases, but acknowledged the majority of these were from the largest study by Guan et al. Overall, they calculated smokers carried a risk ratio of 1.4 (95% CI, 0.98-2.00) for developing severe COVID-19 symptoms, and were over twice as likely to be admitted to an ICU, require a mechanical ventilator, or die from COVID-19, compared with patients who did not smoke (RR, 2.4; 95% CI, 1.43-4.04).
“Although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19,” Dr. Vardavas and Ms. Nikitara concluded.
However, the association between smoking and severe disease was not significant, and it is not immediately clear how the analysis was performed based on the details in the editorial. “Both of our reports were limited by a lack of data adjusted for age, sex, and comorbidities which may influence any analysis on smoking,” Dr. Henry said.
Some researchers have proposed collecting information on smoking status and conducting further research on whether vaping devices like e-cigarettes also impact COVID-19 cases. An editorial by Samuel Brake and colleagues published in the Journal of Clinical Medicine proposed the ACE2-receptor binding site as an area of interest for COVID-19 and as a potential therapeutic target (J Clin Med. 2020 Mar 20. doi: 10.3390/jcm9030841).
Ultimately, whether smoking itself is associated with COVID-19 is still an open question. Nonetheless, encouraging patients to quit smoking should be a priority because long-term sequelae of smoking have been linked to worsened or fatal COVID-19 cases, said Dr. Henry.
“There is a lack of definitive data on smoking to date. Nonetheless, we do know that many illnesses associated with smoking, such as [chronic obstructive pulmonary disease, hypertension, and heart disease are all strong risk factors for severe and fatal COVID-19,” he said. “Thus, absolutely we should encourage the public to quit smoking, especially for older individuals and those with comorbidities.”
The papers by Lippi et al., Vardavas et al., and Brake et al. had no funding source, and the authors reported no relevant conflicts of interest.
but quitting smoking is likely to lower the risk of developing more severe or fatal cases of the infection, according to research from several recent papers.
Interest in how tobacco use affects COVID-19 infection rates stems from research showing that men at the epicenter of the outbreak in China having a higher early mortality rate. Early reports from China showed a case fatality rate of 4.7% for men, compared with 2.8% for women, according to the World Health Organization. The virus that causes COVID-19, severe acute respiratory syndrome coronavirus 2, is suspected to enter a cell using the ACE2 receptor. Since smoking up-regulates this receptor, one popular theory is that smoking can increase the risk of COVID-19 or exacerbate symptoms of an existing infection (Eur Respir J. 2020 Apr 8. doi: 10.1183/13993003.00688-2020). In China, about half of men are active smokers, compared with 2.7% of women (Transl Lung Cancer Res. 2019;8[Suppl 1]:S21-30), so this association would explain the severe cases and increased mortality in this group. In response to potential risk for public health, the World Health Organization, Centers for Disease Control and Prevention, the Attorney General of Massachusetts, and other organizations have warned that smoking may increase one’s risk of transmitting and developing COVID-19 or may worsen the infection.
“While it is easy to jump to the conclusion that more ACE2 means more susceptibility to severe infection, there is no evidence to support this,” Brandon Michael Henry, MD, of the cardiac intensive care unit and the Heart Institute at Cincinnati Children’s Hospital Medical Center, said in an interview. “Moreover, some would argue (including myself) that increased ACE2 may in fact be protective, as ACE2 decreases the levels of angiotensin-2 which likely plays a significant role in the pathophysiology of ARDS.”
Some researchers have examined the limited evidence of smoking on COVID-19 risk and come to preliminary conclusions. In a letter to the editor recently published in the European Journal of Internal Medicine, Dr. Henry and Giuseppe Lippi, MD, of the section of clinical biochemistry in the department of neuroscience, biomedicine, and movement at the University of Verona (Italy), performed a meta-analysis of papers examining smoking and COVID-19 up to March 9, 2020 and identified five articles with 1,399 COVID-19 cases (Eur J Intern Med. 2020 Mar 16. doi: 10.1016/j.ejim.2020.03.014).
“Given the fact that COVID-19 is a primarily respiratory illness, smoking was one of first risk factors we examined,” Dr. Henry said.
They noted that a study by Liu et al. in the Chinese Medical Journal was the only paper that showed a significant association between smoking status and COVID-19 case severity (Chin Med J [Engl]. 2020 Feb 28. doi: 10.1097/CM9.0000000000000775), while the four other studies showed no significant association. The pooled data of all five studies showed an association that was not statistically significant (odds ratio, 1.69; 95% confidence interval, 0.41-6.92; P = .254). When Dr. Lippi and Dr. Henry performed the analysis again after removing a paper by Guan et al. (N Engl J Med. 2020 Feb 28. doi: 10.1056/NEJMoa2002032) comprising 89.5% of patients in the pooled analysis, there was no significant association (OR, 4.35; 95% CI, 0.86-21.86; P = .129).
Constantine I. Vardavas, MD, FCCP, of the department of oral health policy and epidemiology at Harvard School of Dental Medicine, Boston, and Katerina Nikitara, of the University of Crete in Heraklion, Greece, also published a systematic review in Tobacco Induced Diseases of five studies evaluating smoking and COVID-19 (Tob Induc Dis. 2020. doi: 10.18332/tid/119324). Of the studies chosen for the review, four were shared with the paper by Dr. Lippi and Dr. Henry. They found “a higher percentage of smokers” made up severe COVID-19 cases, but acknowledged the majority of these were from the largest study by Guan et al. Overall, they calculated smokers carried a risk ratio of 1.4 (95% CI, 0.98-2.00) for developing severe COVID-19 symptoms, and were over twice as likely to be admitted to an ICU, require a mechanical ventilator, or die from COVID-19, compared with patients who did not smoke (RR, 2.4; 95% CI, 1.43-4.04).
“Although further research is warranted as the weight of the evidence increases, with the limited available data, and although the above results are unadjusted for other factors that may impact disease progression, smoking is most likely associated with the negative progression and adverse outcomes of COVID-19,” Dr. Vardavas and Ms. Nikitara concluded.
However, the association between smoking and severe disease was not significant, and it is not immediately clear how the analysis was performed based on the details in the editorial. “Both of our reports were limited by a lack of data adjusted for age, sex, and comorbidities which may influence any analysis on smoking,” Dr. Henry said.
Some researchers have proposed collecting information on smoking status and conducting further research on whether vaping devices like e-cigarettes also impact COVID-19 cases. An editorial by Samuel Brake and colleagues published in the Journal of Clinical Medicine proposed the ACE2-receptor binding site as an area of interest for COVID-19 and as a potential therapeutic target (J Clin Med. 2020 Mar 20. doi: 10.3390/jcm9030841).
Ultimately, whether smoking itself is associated with COVID-19 is still an open question. Nonetheless, encouraging patients to quit smoking should be a priority because long-term sequelae of smoking have been linked to worsened or fatal COVID-19 cases, said Dr. Henry.
“There is a lack of definitive data on smoking to date. Nonetheless, we do know that many illnesses associated with smoking, such as [chronic obstructive pulmonary disease, hypertension, and heart disease are all strong risk factors for severe and fatal COVID-19,” he said. “Thus, absolutely we should encourage the public to quit smoking, especially for older individuals and those with comorbidities.”
The papers by Lippi et al., Vardavas et al., and Brake et al. had no funding source, and the authors reported no relevant conflicts of interest.
COPD, smoking independently associated with developing depression
People with chronic obstructive pulmonary disorder (COPD) and those who smoke are at an increased risk of developing depression, results of a population-based cohort study of more than 3 million patients show.
Using data from the Veterans Affairs Corporate Data Warehouse, Natalie B. Riblet, MD, MPH, and colleagues conducted the study on 3,284,496 patients who accessed VA health care during 2004-2014 and had a negative depression screen. About 95% of this population was male, 83.4% were white, and the average age was 61.3 years. Just under 40,000 people were patients with COPD, reported Dr. Riblet, of the Veterans Affairs Medical Center in White River Junction, Vt., and the Geisel School of Medicine at Dartmouth, Hanover, N.H. The study was published in General Hospital Psychiatry.
The investigators found that current, former, and never smokers were split fairly evenly at 32.1%, 32.4%, and 30.3% of the total study population, respectively. Of those with COPD, 53.6% were current smokers, 27% were former smokers, and 11.6% were never smokers.
The odds of developing depression in a year were 2.3%, 1.5%, and 1.4% in current, former, and never smokers without COPD, respectively; for those with COPD, the odds were 2.9%, 2.2%, and 2% for current, former, and never smokers, respectively. Overall, the odds ratio of patients with COPD developing depression, compared with those without COPD, was 1.57 (95% confidence interval, 1.54-1.61). Current smokers also were at an increased risk, compared with never smokers (OR, 1.83; 95% CI, 1.81-1.85), though the effect was somewhat mitigated after adjusting for confounders (OR, 1.56; 95% CI, 1.55-1.58).
as this may guide the development and implementation of new treatments for depression in the COPD population,” the investigators concluded. “If COPD-related depression is due, at least in part, to adverse physiological effects related to chronic hypoxia, these patients may require new or more tailored interventions.”
No disclosures or conflicts of interest were reported.
SOURCE: Riblet NB et al. Gen Hosp Psychiatry. 2020 May-Jun;64:72-9.
People with chronic obstructive pulmonary disorder (COPD) and those who smoke are at an increased risk of developing depression, results of a population-based cohort study of more than 3 million patients show.
Using data from the Veterans Affairs Corporate Data Warehouse, Natalie B. Riblet, MD, MPH, and colleagues conducted the study on 3,284,496 patients who accessed VA health care during 2004-2014 and had a negative depression screen. About 95% of this population was male, 83.4% were white, and the average age was 61.3 years. Just under 40,000 people were patients with COPD, reported Dr. Riblet, of the Veterans Affairs Medical Center in White River Junction, Vt., and the Geisel School of Medicine at Dartmouth, Hanover, N.H. The study was published in General Hospital Psychiatry.
The investigators found that current, former, and never smokers were split fairly evenly at 32.1%, 32.4%, and 30.3% of the total study population, respectively. Of those with COPD, 53.6% were current smokers, 27% were former smokers, and 11.6% were never smokers.
The odds of developing depression in a year were 2.3%, 1.5%, and 1.4% in current, former, and never smokers without COPD, respectively; for those with COPD, the odds were 2.9%, 2.2%, and 2% for current, former, and never smokers, respectively. Overall, the odds ratio of patients with COPD developing depression, compared with those without COPD, was 1.57 (95% confidence interval, 1.54-1.61). Current smokers also were at an increased risk, compared with never smokers (OR, 1.83; 95% CI, 1.81-1.85), though the effect was somewhat mitigated after adjusting for confounders (OR, 1.56; 95% CI, 1.55-1.58).
as this may guide the development and implementation of new treatments for depression in the COPD population,” the investigators concluded. “If COPD-related depression is due, at least in part, to adverse physiological effects related to chronic hypoxia, these patients may require new or more tailored interventions.”
No disclosures or conflicts of interest were reported.
SOURCE: Riblet NB et al. Gen Hosp Psychiatry. 2020 May-Jun;64:72-9.
People with chronic obstructive pulmonary disorder (COPD) and those who smoke are at an increased risk of developing depression, results of a population-based cohort study of more than 3 million patients show.
Using data from the Veterans Affairs Corporate Data Warehouse, Natalie B. Riblet, MD, MPH, and colleagues conducted the study on 3,284,496 patients who accessed VA health care during 2004-2014 and had a negative depression screen. About 95% of this population was male, 83.4% were white, and the average age was 61.3 years. Just under 40,000 people were patients with COPD, reported Dr. Riblet, of the Veterans Affairs Medical Center in White River Junction, Vt., and the Geisel School of Medicine at Dartmouth, Hanover, N.H. The study was published in General Hospital Psychiatry.
The investigators found that current, former, and never smokers were split fairly evenly at 32.1%, 32.4%, and 30.3% of the total study population, respectively. Of those with COPD, 53.6% were current smokers, 27% were former smokers, and 11.6% were never smokers.
The odds of developing depression in a year were 2.3%, 1.5%, and 1.4% in current, former, and never smokers without COPD, respectively; for those with COPD, the odds were 2.9%, 2.2%, and 2% for current, former, and never smokers, respectively. Overall, the odds ratio of patients with COPD developing depression, compared with those without COPD, was 1.57 (95% confidence interval, 1.54-1.61). Current smokers also were at an increased risk, compared with never smokers (OR, 1.83; 95% CI, 1.81-1.85), though the effect was somewhat mitigated after adjusting for confounders (OR, 1.56; 95% CI, 1.55-1.58).
as this may guide the development and implementation of new treatments for depression in the COPD population,” the investigators concluded. “If COPD-related depression is due, at least in part, to adverse physiological effects related to chronic hypoxia, these patients may require new or more tailored interventions.”
No disclosures or conflicts of interest were reported.
SOURCE: Riblet NB et al. Gen Hosp Psychiatry. 2020 May-Jun;64:72-9.
FROM GENERAL HOSPITAL PSYCHIATRY
OSA increases odds of hospital readmission after COPD exacerbation
more than threefold, according to results from a single-center study published in CHEST.
Mario Naranjo, MD, and colleagues retrospectively examined data from Albert Einstein Medical Center in Philadelphia to assess the impact of OSA on hospital readmission within 30 days of discharge after treatment for a COPD exacerbation. Dr. Naranjo is affiliated with Johns Hopkins Medicine, Baltimore.
The researchers analyzed data from 238 patients admitted for COPD exacerbation between May 2017 and July 2018 who were screened for previously unrecognized and untreated OSA and underwent a high-resolution pulse-oximetry or portable sleep monitoring study. In all, 111 (46.6%) had OSA; 28.6% had mild OSA, 9.7% had moderate OSA, and 8.4% had severe OSA.
Most baseline characteristics were similar among patients with and without OSA, but patients with OSA had a greater mean body mass index (33.9 vs. 30.3 kg/m2) and were more likely to have comorbid heart failure (19.8% vs. 7.1%), compared with patients without OSA. In addition, the proportion of male patients was greater in the cohort with OSA (60.4% vs. 49.6%).
For patients with mild OSA (oxygen desaturation index [ODI] ≥ 5 and < 15/hour), the odds of 30-day readmission were 2.05 times higher, compared with patients without OSA (32.4% vs. 18.9%). With moderate OSA (ODI ≥ 15 and < 30/hour), the odds of 30-day readmission were 6.68 times higher (60.9% vs. 18.9%). For severe OSA (ODI ≥ 30/hour), the odds were 10.01 times higher (70.0% vs. 18.9%). “For combined OSA severity categories, the odds of 30-day readmission were 3.5 times higher,” said Dr. Naranjo and colleagues. In addition, 90- and 180-day readmission rates and 6-month mortality rates were higher among patients with OSA.
“These findings have important implications for the evaluation and care of patients admitted to the hospital for COPD exacerbations,” Dr. Naranjo and colleagues said. “Although the combination of COPD and OSA (also known as the “overlap syndrome”) in ambulatory settings has been shown to have worse outcomes in terms of COPD exacerbations and mortality, these findings have not been reported previously for hospitalized COPD patients.”
Greater degrees of nocturnal hypoxemia and hypercapnia, worse functional status, and daytime sleepiness and fatigue may contribute to the relationship between OSA and the likelihood of hospital readmission, according to the authors. A multicenter study is warranted to confirm the results, they said.
Dr. Naranjo had no conflicts of interest. Coauthors have received grants from ResMed, Dayzz, and the National Institutes of Health and consulted for Jazz Pharmaceuticals, Best Doctors, and ResMed. One author is a committee chair for the American Academy of Sleep Medicine.
SOURCE: Naranjo M et al. Chest. 2020 Apr 2. doi: 10.1016/j.chest.2020.03.036.
more than threefold, according to results from a single-center study published in CHEST.
Mario Naranjo, MD, and colleagues retrospectively examined data from Albert Einstein Medical Center in Philadelphia to assess the impact of OSA on hospital readmission within 30 days of discharge after treatment for a COPD exacerbation. Dr. Naranjo is affiliated with Johns Hopkins Medicine, Baltimore.
The researchers analyzed data from 238 patients admitted for COPD exacerbation between May 2017 and July 2018 who were screened for previously unrecognized and untreated OSA and underwent a high-resolution pulse-oximetry or portable sleep monitoring study. In all, 111 (46.6%) had OSA; 28.6% had mild OSA, 9.7% had moderate OSA, and 8.4% had severe OSA.
Most baseline characteristics were similar among patients with and without OSA, but patients with OSA had a greater mean body mass index (33.9 vs. 30.3 kg/m2) and were more likely to have comorbid heart failure (19.8% vs. 7.1%), compared with patients without OSA. In addition, the proportion of male patients was greater in the cohort with OSA (60.4% vs. 49.6%).
For patients with mild OSA (oxygen desaturation index [ODI] ≥ 5 and < 15/hour), the odds of 30-day readmission were 2.05 times higher, compared with patients without OSA (32.4% vs. 18.9%). With moderate OSA (ODI ≥ 15 and < 30/hour), the odds of 30-day readmission were 6.68 times higher (60.9% vs. 18.9%). For severe OSA (ODI ≥ 30/hour), the odds were 10.01 times higher (70.0% vs. 18.9%). “For combined OSA severity categories, the odds of 30-day readmission were 3.5 times higher,” said Dr. Naranjo and colleagues. In addition, 90- and 180-day readmission rates and 6-month mortality rates were higher among patients with OSA.
“These findings have important implications for the evaluation and care of patients admitted to the hospital for COPD exacerbations,” Dr. Naranjo and colleagues said. “Although the combination of COPD and OSA (also known as the “overlap syndrome”) in ambulatory settings has been shown to have worse outcomes in terms of COPD exacerbations and mortality, these findings have not been reported previously for hospitalized COPD patients.”
Greater degrees of nocturnal hypoxemia and hypercapnia, worse functional status, and daytime sleepiness and fatigue may contribute to the relationship between OSA and the likelihood of hospital readmission, according to the authors. A multicenter study is warranted to confirm the results, they said.
Dr. Naranjo had no conflicts of interest. Coauthors have received grants from ResMed, Dayzz, and the National Institutes of Health and consulted for Jazz Pharmaceuticals, Best Doctors, and ResMed. One author is a committee chair for the American Academy of Sleep Medicine.
SOURCE: Naranjo M et al. Chest. 2020 Apr 2. doi: 10.1016/j.chest.2020.03.036.
more than threefold, according to results from a single-center study published in CHEST.
Mario Naranjo, MD, and colleagues retrospectively examined data from Albert Einstein Medical Center in Philadelphia to assess the impact of OSA on hospital readmission within 30 days of discharge after treatment for a COPD exacerbation. Dr. Naranjo is affiliated with Johns Hopkins Medicine, Baltimore.
The researchers analyzed data from 238 patients admitted for COPD exacerbation between May 2017 and July 2018 who were screened for previously unrecognized and untreated OSA and underwent a high-resolution pulse-oximetry or portable sleep monitoring study. In all, 111 (46.6%) had OSA; 28.6% had mild OSA, 9.7% had moderate OSA, and 8.4% had severe OSA.
Most baseline characteristics were similar among patients with and without OSA, but patients with OSA had a greater mean body mass index (33.9 vs. 30.3 kg/m2) and were more likely to have comorbid heart failure (19.8% vs. 7.1%), compared with patients without OSA. In addition, the proportion of male patients was greater in the cohort with OSA (60.4% vs. 49.6%).
For patients with mild OSA (oxygen desaturation index [ODI] ≥ 5 and < 15/hour), the odds of 30-day readmission were 2.05 times higher, compared with patients without OSA (32.4% vs. 18.9%). With moderate OSA (ODI ≥ 15 and < 30/hour), the odds of 30-day readmission were 6.68 times higher (60.9% vs. 18.9%). For severe OSA (ODI ≥ 30/hour), the odds were 10.01 times higher (70.0% vs. 18.9%). “For combined OSA severity categories, the odds of 30-day readmission were 3.5 times higher,” said Dr. Naranjo and colleagues. In addition, 90- and 180-day readmission rates and 6-month mortality rates were higher among patients with OSA.
“These findings have important implications for the evaluation and care of patients admitted to the hospital for COPD exacerbations,” Dr. Naranjo and colleagues said. “Although the combination of COPD and OSA (also known as the “overlap syndrome”) in ambulatory settings has been shown to have worse outcomes in terms of COPD exacerbations and mortality, these findings have not been reported previously for hospitalized COPD patients.”
Greater degrees of nocturnal hypoxemia and hypercapnia, worse functional status, and daytime sleepiness and fatigue may contribute to the relationship between OSA and the likelihood of hospital readmission, according to the authors. A multicenter study is warranted to confirm the results, they said.
Dr. Naranjo had no conflicts of interest. Coauthors have received grants from ResMed, Dayzz, and the National Institutes of Health and consulted for Jazz Pharmaceuticals, Best Doctors, and ResMed. One author is a committee chair for the American Academy of Sleep Medicine.
SOURCE: Naranjo M et al. Chest. 2020 Apr 2. doi: 10.1016/j.chest.2020.03.036.
FROM CHEST
Stronger links forged between RA and asthma, COPD
Asthma and chronic obstructive pulmonary disease were both linked to an increased risk of rheumatoid arthritis in a recent large, prospective cohort study, researchers have reported, which adds to a growing body of evidence that airway inflammation is implicated in the development of this disease.
RA risk was increased by about 50% among asthma patients, even when excluding those who had ever smoked, according to the study’s results, which were based on more than 200,000 women in the Nurses’ Health Study I and II.
Risk of RA nearly doubled among those with chronic obstructive pulmonary disease (COPD), with an even stronger association seen in older ever-smokers, according to authors of the study.
The findings not only strengthen the case for the potential role of obstructive lung diseases in RA development, according to the study’s authors, but also suggest that health care providers need to lower the bar for evaluation of patients with lung diseases and inflammatory joint symptoms.
“If these patients develop arthralgias, then the clinicians taking care of them should have a low threshold to consider RA, and perhaps refer, or check these patients with a diagnostic test for RA,” said researcher Jeffrey A. Sparks, MD, of Brigham and Women’s Hospital and Harvard Medical School in Boston.
What’s perhaps not as clear now is whether screening obstructive lung disease patients in the absence of early RA signs would be warranted: “I don’t know if we’re quite at the point where we would need to screen these patients if they’re not symptomatic,” Dr. Sparks said in an interview.
The study by Dr. Sparks and colleagues is, by far, not the first study to implicate asthma or other lung conditions in RA development. However, most previous studies are retrospective, and interpretation of the findings has been subject to limitations such as inadequate power to detect an increased risk or lack of adjustment for important confounding factors, such as smoking.
As such, the study by Dr. Sparks and colleagues is believed to be the first-ever prospective study to evaluate asthma and COPD as risk factors for RA, study authors reported in Arthritis & Rheumatology.
Researchers were able to identify 1,060 incident RA cases that developed in 15,148 women with asthma and 3,573 with COPD in the study with more than 4 million person-years of follow-up.
The association between asthma and increased RA risk was seen not only for the asthma population as a whole (hazard ratio, 1.53; 95% confidence interval, 1.24-1.88), but also for the subset of women who had never smoked, to a similar degree (HR, 1.53; 95% CI, 1.14-2.05), the report shows.
COPD’s association with RA risk was apparent overall (HR, 1.89; 95% CI, 1.31-2.75) and even more so in the subgroup of ever-smokers 55 years of age and older (HR, 2.20; 95% CI, 1.38-3.51), the data further show.
Findings of studies looking at the inflammation of airways and other mucosal sites are “critically important to understand” when it comes to trying to prevent RA, said Kevin Deane, MD, of the University of Colorado at Denver at Aurora.
“If we indeed are trying to prevent rheumatoid arthritis in terms of the joint disease, we may need to look at these mucosal sites in individuals who don’t yet have joint disease as potential sites to target for prevention, or at least areas to study to understand how prevention may work,” said Dr. Deane, principal investigator on the National Institutes of Health–funded Strategy for the Prevention of RA (StopRA) trial.
With that in mind, it’s conceivable targeting a lung process might prevent joint disease in a patient with asthma or airway inflammation and blood markers that indicate a risk of RA, Dr. Deane said in an interview.
Blood markers of RA have been evaluated in some recent studies, with findings that provide further evidence of a link between lung diseases and RA, and vice versa.
In particular, anti–citrullinated protein antibodies (ACPA) are clearly central to RA pathogenesis. And while asthma is increasingly linked to RA risk, there have been relatively little data on any potential links between ACPA and asthma.
That research gap led to a case-control study of the Nurses’ Health Study I and II (on which Dr. Sparks was senior author) showing that asthma was strongly linked to elevated ACPA in blood drawn from patients prior to a diagnosis of RA.
Results, published last year in Arthritis Research & Therapy, showed a significant association between asthma and pre-RA ACPA elevation (odds ratio, 3.57; 95% CI, 1.58-8.04), after adjustment for smoking and other potentially confounding factors. Investigators said the findings provided evidence that chronic mucosal airway inflammation is a factor in the development of ACPA and in the pathogenesis of RA.
In a follow-up study published more recently in Arthritis Care & Research, investigators showed that, among women in the Nurses Health Study I and II, pre-RA ACPA elevation was linked to increased risk of COPD, compared with controls (HR, 3.04; 95% CI, 1.33-7.00), while the risk for development of asthma was similar in women with or without elevated pre-RA ACPA.
That study was in part an attempt to establish a “timeline” related to antibodies, lung diseases, and RA onset, Dr. Sparks said in the interview.
“We think that probably the asthma is more important in developing the antibody, but that once you have the antibody, if you didn’t have asthma by then, you’re unlikely to develop it,” he said. “So asthma seems to be something that could happen before the antibody production, whereas COPD seems to happen after – but ACPA seems to be the common link in both of these obstructive lung diseases.”
The study in Arthritis & Rheumatology linking asthma and COPD to risk of incident RA was supported by the National Institutes of Health. Dr. Sparks reported grant support from Amgen and Bristol Myers Squibb and consulting fees from Inova and Optum. Coauthors provided disclosures related to GlaxoSmithKline, AstraZeneca, Merck, Neutrolis, and Genentech.
SOURCE: Ford JA et al. Arthritis Rheumatol. 2020 Mar 4. doi: 10.1002/art.41194.
Asthma and chronic obstructive pulmonary disease were both linked to an increased risk of rheumatoid arthritis in a recent large, prospective cohort study, researchers have reported, which adds to a growing body of evidence that airway inflammation is implicated in the development of this disease.
RA risk was increased by about 50% among asthma patients, even when excluding those who had ever smoked, according to the study’s results, which were based on more than 200,000 women in the Nurses’ Health Study I and II.
Risk of RA nearly doubled among those with chronic obstructive pulmonary disease (COPD), with an even stronger association seen in older ever-smokers, according to authors of the study.
The findings not only strengthen the case for the potential role of obstructive lung diseases in RA development, according to the study’s authors, but also suggest that health care providers need to lower the bar for evaluation of patients with lung diseases and inflammatory joint symptoms.
“If these patients develop arthralgias, then the clinicians taking care of them should have a low threshold to consider RA, and perhaps refer, or check these patients with a diagnostic test for RA,” said researcher Jeffrey A. Sparks, MD, of Brigham and Women’s Hospital and Harvard Medical School in Boston.
What’s perhaps not as clear now is whether screening obstructive lung disease patients in the absence of early RA signs would be warranted: “I don’t know if we’re quite at the point where we would need to screen these patients if they’re not symptomatic,” Dr. Sparks said in an interview.
The study by Dr. Sparks and colleagues is, by far, not the first study to implicate asthma or other lung conditions in RA development. However, most previous studies are retrospective, and interpretation of the findings has been subject to limitations such as inadequate power to detect an increased risk or lack of adjustment for important confounding factors, such as smoking.
As such, the study by Dr. Sparks and colleagues is believed to be the first-ever prospective study to evaluate asthma and COPD as risk factors for RA, study authors reported in Arthritis & Rheumatology.
Researchers were able to identify 1,060 incident RA cases that developed in 15,148 women with asthma and 3,573 with COPD in the study with more than 4 million person-years of follow-up.
The association between asthma and increased RA risk was seen not only for the asthma population as a whole (hazard ratio, 1.53; 95% confidence interval, 1.24-1.88), but also for the subset of women who had never smoked, to a similar degree (HR, 1.53; 95% CI, 1.14-2.05), the report shows.
COPD’s association with RA risk was apparent overall (HR, 1.89; 95% CI, 1.31-2.75) and even more so in the subgroup of ever-smokers 55 years of age and older (HR, 2.20; 95% CI, 1.38-3.51), the data further show.
Findings of studies looking at the inflammation of airways and other mucosal sites are “critically important to understand” when it comes to trying to prevent RA, said Kevin Deane, MD, of the University of Colorado at Denver at Aurora.
“If we indeed are trying to prevent rheumatoid arthritis in terms of the joint disease, we may need to look at these mucosal sites in individuals who don’t yet have joint disease as potential sites to target for prevention, or at least areas to study to understand how prevention may work,” said Dr. Deane, principal investigator on the National Institutes of Health–funded Strategy for the Prevention of RA (StopRA) trial.
With that in mind, it’s conceivable targeting a lung process might prevent joint disease in a patient with asthma or airway inflammation and blood markers that indicate a risk of RA, Dr. Deane said in an interview.
Blood markers of RA have been evaluated in some recent studies, with findings that provide further evidence of a link between lung diseases and RA, and vice versa.
In particular, anti–citrullinated protein antibodies (ACPA) are clearly central to RA pathogenesis. And while asthma is increasingly linked to RA risk, there have been relatively little data on any potential links between ACPA and asthma.
That research gap led to a case-control study of the Nurses’ Health Study I and II (on which Dr. Sparks was senior author) showing that asthma was strongly linked to elevated ACPA in blood drawn from patients prior to a diagnosis of RA.
Results, published last year in Arthritis Research & Therapy, showed a significant association between asthma and pre-RA ACPA elevation (odds ratio, 3.57; 95% CI, 1.58-8.04), after adjustment for smoking and other potentially confounding factors. Investigators said the findings provided evidence that chronic mucosal airway inflammation is a factor in the development of ACPA and in the pathogenesis of RA.
In a follow-up study published more recently in Arthritis Care & Research, investigators showed that, among women in the Nurses Health Study I and II, pre-RA ACPA elevation was linked to increased risk of COPD, compared with controls (HR, 3.04; 95% CI, 1.33-7.00), while the risk for development of asthma was similar in women with or without elevated pre-RA ACPA.
That study was in part an attempt to establish a “timeline” related to antibodies, lung diseases, and RA onset, Dr. Sparks said in the interview.
“We think that probably the asthma is more important in developing the antibody, but that once you have the antibody, if you didn’t have asthma by then, you’re unlikely to develop it,” he said. “So asthma seems to be something that could happen before the antibody production, whereas COPD seems to happen after – but ACPA seems to be the common link in both of these obstructive lung diseases.”
The study in Arthritis & Rheumatology linking asthma and COPD to risk of incident RA was supported by the National Institutes of Health. Dr. Sparks reported grant support from Amgen and Bristol Myers Squibb and consulting fees from Inova and Optum. Coauthors provided disclosures related to GlaxoSmithKline, AstraZeneca, Merck, Neutrolis, and Genentech.
SOURCE: Ford JA et al. Arthritis Rheumatol. 2020 Mar 4. doi: 10.1002/art.41194.
Asthma and chronic obstructive pulmonary disease were both linked to an increased risk of rheumatoid arthritis in a recent large, prospective cohort study, researchers have reported, which adds to a growing body of evidence that airway inflammation is implicated in the development of this disease.
RA risk was increased by about 50% among asthma patients, even when excluding those who had ever smoked, according to the study’s results, which were based on more than 200,000 women in the Nurses’ Health Study I and II.
Risk of RA nearly doubled among those with chronic obstructive pulmonary disease (COPD), with an even stronger association seen in older ever-smokers, according to authors of the study.
The findings not only strengthen the case for the potential role of obstructive lung diseases in RA development, according to the study’s authors, but also suggest that health care providers need to lower the bar for evaluation of patients with lung diseases and inflammatory joint symptoms.
“If these patients develop arthralgias, then the clinicians taking care of them should have a low threshold to consider RA, and perhaps refer, or check these patients with a diagnostic test for RA,” said researcher Jeffrey A. Sparks, MD, of Brigham and Women’s Hospital and Harvard Medical School in Boston.
What’s perhaps not as clear now is whether screening obstructive lung disease patients in the absence of early RA signs would be warranted: “I don’t know if we’re quite at the point where we would need to screen these patients if they’re not symptomatic,” Dr. Sparks said in an interview.
The study by Dr. Sparks and colleagues is, by far, not the first study to implicate asthma or other lung conditions in RA development. However, most previous studies are retrospective, and interpretation of the findings has been subject to limitations such as inadequate power to detect an increased risk or lack of adjustment for important confounding factors, such as smoking.
As such, the study by Dr. Sparks and colleagues is believed to be the first-ever prospective study to evaluate asthma and COPD as risk factors for RA, study authors reported in Arthritis & Rheumatology.
Researchers were able to identify 1,060 incident RA cases that developed in 15,148 women with asthma and 3,573 with COPD in the study with more than 4 million person-years of follow-up.
The association between asthma and increased RA risk was seen not only for the asthma population as a whole (hazard ratio, 1.53; 95% confidence interval, 1.24-1.88), but also for the subset of women who had never smoked, to a similar degree (HR, 1.53; 95% CI, 1.14-2.05), the report shows.
COPD’s association with RA risk was apparent overall (HR, 1.89; 95% CI, 1.31-2.75) and even more so in the subgroup of ever-smokers 55 years of age and older (HR, 2.20; 95% CI, 1.38-3.51), the data further show.
Findings of studies looking at the inflammation of airways and other mucosal sites are “critically important to understand” when it comes to trying to prevent RA, said Kevin Deane, MD, of the University of Colorado at Denver at Aurora.
“If we indeed are trying to prevent rheumatoid arthritis in terms of the joint disease, we may need to look at these mucosal sites in individuals who don’t yet have joint disease as potential sites to target for prevention, or at least areas to study to understand how prevention may work,” said Dr. Deane, principal investigator on the National Institutes of Health–funded Strategy for the Prevention of RA (StopRA) trial.
With that in mind, it’s conceivable targeting a lung process might prevent joint disease in a patient with asthma or airway inflammation and blood markers that indicate a risk of RA, Dr. Deane said in an interview.
Blood markers of RA have been evaluated in some recent studies, with findings that provide further evidence of a link between lung diseases and RA, and vice versa.
In particular, anti–citrullinated protein antibodies (ACPA) are clearly central to RA pathogenesis. And while asthma is increasingly linked to RA risk, there have been relatively little data on any potential links between ACPA and asthma.
That research gap led to a case-control study of the Nurses’ Health Study I and II (on which Dr. Sparks was senior author) showing that asthma was strongly linked to elevated ACPA in blood drawn from patients prior to a diagnosis of RA.
Results, published last year in Arthritis Research & Therapy, showed a significant association between asthma and pre-RA ACPA elevation (odds ratio, 3.57; 95% CI, 1.58-8.04), after adjustment for smoking and other potentially confounding factors. Investigators said the findings provided evidence that chronic mucosal airway inflammation is a factor in the development of ACPA and in the pathogenesis of RA.
In a follow-up study published more recently in Arthritis Care & Research, investigators showed that, among women in the Nurses Health Study I and II, pre-RA ACPA elevation was linked to increased risk of COPD, compared with controls (HR, 3.04; 95% CI, 1.33-7.00), while the risk for development of asthma was similar in women with or without elevated pre-RA ACPA.
That study was in part an attempt to establish a “timeline” related to antibodies, lung diseases, and RA onset, Dr. Sparks said in the interview.
“We think that probably the asthma is more important in developing the antibody, but that once you have the antibody, if you didn’t have asthma by then, you’re unlikely to develop it,” he said. “So asthma seems to be something that could happen before the antibody production, whereas COPD seems to happen after – but ACPA seems to be the common link in both of these obstructive lung diseases.”
The study in Arthritis & Rheumatology linking asthma and COPD to risk of incident RA was supported by the National Institutes of Health. Dr. Sparks reported grant support from Amgen and Bristol Myers Squibb and consulting fees from Inova and Optum. Coauthors provided disclosures related to GlaxoSmithKline, AstraZeneca, Merck, Neutrolis, and Genentech.
SOURCE: Ford JA et al. Arthritis Rheumatol. 2020 Mar 4. doi: 10.1002/art.41194.
FROM ARTHRITIS & RHEUMATOLOGY