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Myocarditis is present in a small percentage of competitive athletes after COVID-19 infection, even in those without symptoms, new research suggests.

In a cohort study of 1,597 competitive collegiate athletes undergoing comprehensive cardiovascular testing in the United States, the prevalence of clinical myocarditis based on a symptom-based screening strategy was only 0.31%.

But screening with cardiac MRI increased the prevalence of clinical and subclinical myocarditis by a factor of 7.4, to 2.3%, the authors reported.

The findings are published online May 27, 2021, in JAMA Cardiology.

“It was the largest study to evaluate college athletes who have had COVID with extensive cardiac testing, including MRI, and this gave us a very objective look at the cardiac findings, as they were not purely based upon a subjective evaluation of symptoms,” lead investigator Curt J. Daniels, MD, professor at Ohio State University Wexner Medical Center, Columbus, said in an interview.

“Unfortunately, our study showed that athletes can be asymptomatic, or at least not report symptoms. This is a very subjective feature, and we don’t know if they don’t report symptoms because they didn’t want to get tested. That is why we took a very objective approach,” Dr. Daniels said.

The finding that more than half of the asymptomatic athletes had myocarditis, or as the investigators called it, “subclinical myocarditis,” was a surprise, he acknowledged.

“More than half of the athletes found to have myocarditis reported no symptoms, and yes, that was a surprise, because prior to this study, the protocols that had been published stated that you had to have symptoms to even enter into the protocol for cardiac MRI. But, as our ... paper shows, if we had followed that protocol, we only would have found about 5 cases of myocarditis, as opposed to the total of 37 we found with cardiac MRI,” Dr. Daniels said.

In October 2020, the American College of Cardiology’s Sports and Exercise Council recommended that cardiac MRI be limited to athletes who exhibited symptoms as part of their guide to ensuring a safe return to play.

As reported by this news organization the council recommended a tiered approach to screening based on the presence of symptoms, followed by electrocardiography, injury biomarkers, and echocardiography. Any abnormalities detected were to be further characterized by the selective use of cardiac MRI.

At the time, there were relatively few data to support the recommendations, and all stakeholders called for larger datasets to better drive informed recommendations in the future.

In the current study, Dr. Daniels and associates conducted comprehensive cardiac screening – including ECG, troponin testing, echocardiography, and cardiac MRI – of 1,597 college athlete survivors of COVID-19.

The athletes were part of the Big Ten athletic conference, which consists of 13 major American universities.

AlexLMX/Getty Images

Cardiac MRI revealed that 37 (2.3%) of these athletes demonstrated diagnostic criteria for COVID-19 myocarditis; of these, 20 had no cardiovascular symptoms and had normal ECGs, echocardiography, and troponin test results.

“These patients would not have been identified without CMR imaging. If we were going according to the older protocol, we would not have made this discovery. Cardiac MRI is the most sensitive and specific test for myocardial inflammation, there is no argument about that,” Dr. Daniels said.

The catch is, cardiac MRI is expensive and often difficult to access, especially in remote, rural, or other underserviced areas.

“You can’t get an MRI for every person who has had COVID, it’s just not feasible,” Dr. Daniels said. “We are not advocating that everybody get an MRI. But we do hope that our study creates awareness among clinicians and athletes themselves that if you’ve had COVID, even if you’re asymptomatic, there may be some heart changes. So be aware when you start to exercise again, if you have any symptoms, pause and seek medical care.”
 

Kudos to the sports cardiology community

In an accompanying editorial, James E. Udelson, MD, Ethan J. Rowin, MD, and Barry J. Maron, MD, from the CardioVascular Center at Tufts Medical Center, Boston, applauded the sports cardiology community for its diligence in acquiring and publishing data about the post–COVID-19 prevalence of cardiac abnormalities in competitive athletes.

“It is a real tribute to the sports cardiology community. There has been an amazing growth of information, and they not only gathered this information, they analyzed and published it, starting out with a study of 29 or 30 athletes, and now thousands,” Dr. Udelson said in an interview.

At the start of the pandemic, it appeared that 15%-20% of athletes had myocarditis, and athletic conferences were discussing canceling sports events.

However, with greater numbers comes a more accurate picture of the extent of the problem.

“Once you get thousands of subjects in these studies, you can hone in on what the real number is, so now we understand that if you screen everybody with a cardiac MRI, 1%, 2%, or 3% will have some evidence of what looks like myocarditis,” he said.

Dr. Udelson agreed that doing cardiac imaging in everyone is not feasible.

“This study looked at a very large number of people who all had an MRI, but that doesn’t mean everyone should have them. If you just do an echo, an EKG, and a troponin test, and if everything is normal, which is kind of what current recommendations are, this paper tells us that we are going to miss one or two people out of a hundred, and that might be okay,” he said. “So, if you are at a huge university that has a large medical center and you want to screen all your athletes with MRI, great. But if you’re at a high school in a remote area, you know that the alternative, not having an MRI, isn’t so bad, either.”

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

Myocarditis is present in a small percentage of competitive athletes after COVID-19 infection, even in those without symptoms, new research suggests.

In a cohort study of 1,597 competitive collegiate athletes undergoing comprehensive cardiovascular testing in the United States, the prevalence of clinical myocarditis based on a symptom-based screening strategy was only 0.31%.

But screening with cardiac MRI increased the prevalence of clinical and subclinical myocarditis by a factor of 7.4, to 2.3%, the authors reported.

The findings are published online May 27, 2021, in JAMA Cardiology.

“It was the largest study to evaluate college athletes who have had COVID with extensive cardiac testing, including MRI, and this gave us a very objective look at the cardiac findings, as they were not purely based upon a subjective evaluation of symptoms,” lead investigator Curt J. Daniels, MD, professor at Ohio State University Wexner Medical Center, Columbus, said in an interview.

“Unfortunately, our study showed that athletes can be asymptomatic, or at least not report symptoms. This is a very subjective feature, and we don’t know if they don’t report symptoms because they didn’t want to get tested. That is why we took a very objective approach,” Dr. Daniels said.

The finding that more than half of the asymptomatic athletes had myocarditis, or as the investigators called it, “subclinical myocarditis,” was a surprise, he acknowledged.

“More than half of the athletes found to have myocarditis reported no symptoms, and yes, that was a surprise, because prior to this study, the protocols that had been published stated that you had to have symptoms to even enter into the protocol for cardiac MRI. But, as our ... paper shows, if we had followed that protocol, we only would have found about 5 cases of myocarditis, as opposed to the total of 37 we found with cardiac MRI,” Dr. Daniels said.

In October 2020, the American College of Cardiology’s Sports and Exercise Council recommended that cardiac MRI be limited to athletes who exhibited symptoms as part of their guide to ensuring a safe return to play.

As reported by this news organization the council recommended a tiered approach to screening based on the presence of symptoms, followed by electrocardiography, injury biomarkers, and echocardiography. Any abnormalities detected were to be further characterized by the selective use of cardiac MRI.

At the time, there were relatively few data to support the recommendations, and all stakeholders called for larger datasets to better drive informed recommendations in the future.

In the current study, Dr. Daniels and associates conducted comprehensive cardiac screening – including ECG, troponin testing, echocardiography, and cardiac MRI – of 1,597 college athlete survivors of COVID-19.

The athletes were part of the Big Ten athletic conference, which consists of 13 major American universities.

AlexLMX/Getty Images

Cardiac MRI revealed that 37 (2.3%) of these athletes demonstrated diagnostic criteria for COVID-19 myocarditis; of these, 20 had no cardiovascular symptoms and had normal ECGs, echocardiography, and troponin test results.

“These patients would not have been identified without CMR imaging. If we were going according to the older protocol, we would not have made this discovery. Cardiac MRI is the most sensitive and specific test for myocardial inflammation, there is no argument about that,” Dr. Daniels said.

The catch is, cardiac MRI is expensive and often difficult to access, especially in remote, rural, or other underserviced areas.

“You can’t get an MRI for every person who has had COVID, it’s just not feasible,” Dr. Daniels said. “We are not advocating that everybody get an MRI. But we do hope that our study creates awareness among clinicians and athletes themselves that if you’ve had COVID, even if you’re asymptomatic, there may be some heart changes. So be aware when you start to exercise again, if you have any symptoms, pause and seek medical care.”
 

Kudos to the sports cardiology community

In an accompanying editorial, James E. Udelson, MD, Ethan J. Rowin, MD, and Barry J. Maron, MD, from the CardioVascular Center at Tufts Medical Center, Boston, applauded the sports cardiology community for its diligence in acquiring and publishing data about the post–COVID-19 prevalence of cardiac abnormalities in competitive athletes.

“It is a real tribute to the sports cardiology community. There has been an amazing growth of information, and they not only gathered this information, they analyzed and published it, starting out with a study of 29 or 30 athletes, and now thousands,” Dr. Udelson said in an interview.

At the start of the pandemic, it appeared that 15%-20% of athletes had myocarditis, and athletic conferences were discussing canceling sports events.

However, with greater numbers comes a more accurate picture of the extent of the problem.

“Once you get thousands of subjects in these studies, you can hone in on what the real number is, so now we understand that if you screen everybody with a cardiac MRI, 1%, 2%, or 3% will have some evidence of what looks like myocarditis,” he said.

Dr. Udelson agreed that doing cardiac imaging in everyone is not feasible.

“This study looked at a very large number of people who all had an MRI, but that doesn’t mean everyone should have them. If you just do an echo, an EKG, and a troponin test, and if everything is normal, which is kind of what current recommendations are, this paper tells us that we are going to miss one or two people out of a hundred, and that might be okay,” he said. “So, if you are at a huge university that has a large medical center and you want to screen all your athletes with MRI, great. But if you’re at a high school in a remote area, you know that the alternative, not having an MRI, isn’t so bad, either.”

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

Myocarditis is present in a small percentage of competitive athletes after COVID-19 infection, even in those without symptoms, new research suggests.

In a cohort study of 1,597 competitive collegiate athletes undergoing comprehensive cardiovascular testing in the United States, the prevalence of clinical myocarditis based on a symptom-based screening strategy was only 0.31%.

But screening with cardiac MRI increased the prevalence of clinical and subclinical myocarditis by a factor of 7.4, to 2.3%, the authors reported.

The findings are published online May 27, 2021, in JAMA Cardiology.

“It was the largest study to evaluate college athletes who have had COVID with extensive cardiac testing, including MRI, and this gave us a very objective look at the cardiac findings, as they were not purely based upon a subjective evaluation of symptoms,” lead investigator Curt J. Daniels, MD, professor at Ohio State University Wexner Medical Center, Columbus, said in an interview.

“Unfortunately, our study showed that athletes can be asymptomatic, or at least not report symptoms. This is a very subjective feature, and we don’t know if they don’t report symptoms because they didn’t want to get tested. That is why we took a very objective approach,” Dr. Daniels said.

The finding that more than half of the asymptomatic athletes had myocarditis, or as the investigators called it, “subclinical myocarditis,” was a surprise, he acknowledged.

“More than half of the athletes found to have myocarditis reported no symptoms, and yes, that was a surprise, because prior to this study, the protocols that had been published stated that you had to have symptoms to even enter into the protocol for cardiac MRI. But, as our ... paper shows, if we had followed that protocol, we only would have found about 5 cases of myocarditis, as opposed to the total of 37 we found with cardiac MRI,” Dr. Daniels said.

In October 2020, the American College of Cardiology’s Sports and Exercise Council recommended that cardiac MRI be limited to athletes who exhibited symptoms as part of their guide to ensuring a safe return to play.

As reported by this news organization the council recommended a tiered approach to screening based on the presence of symptoms, followed by electrocardiography, injury biomarkers, and echocardiography. Any abnormalities detected were to be further characterized by the selective use of cardiac MRI.

At the time, there were relatively few data to support the recommendations, and all stakeholders called for larger datasets to better drive informed recommendations in the future.

In the current study, Dr. Daniels and associates conducted comprehensive cardiac screening – including ECG, troponin testing, echocardiography, and cardiac MRI – of 1,597 college athlete survivors of COVID-19.

The athletes were part of the Big Ten athletic conference, which consists of 13 major American universities.

AlexLMX/Getty Images

Cardiac MRI revealed that 37 (2.3%) of these athletes demonstrated diagnostic criteria for COVID-19 myocarditis; of these, 20 had no cardiovascular symptoms and had normal ECGs, echocardiography, and troponin test results.

“These patients would not have been identified without CMR imaging. If we were going according to the older protocol, we would not have made this discovery. Cardiac MRI is the most sensitive and specific test for myocardial inflammation, there is no argument about that,” Dr. Daniels said.

The catch is, cardiac MRI is expensive and often difficult to access, especially in remote, rural, or other underserviced areas.

“You can’t get an MRI for every person who has had COVID, it’s just not feasible,” Dr. Daniels said. “We are not advocating that everybody get an MRI. But we do hope that our study creates awareness among clinicians and athletes themselves that if you’ve had COVID, even if you’re asymptomatic, there may be some heart changes. So be aware when you start to exercise again, if you have any symptoms, pause and seek medical care.”
 

Kudos to the sports cardiology community

In an accompanying editorial, James E. Udelson, MD, Ethan J. Rowin, MD, and Barry J. Maron, MD, from the CardioVascular Center at Tufts Medical Center, Boston, applauded the sports cardiology community for its diligence in acquiring and publishing data about the post–COVID-19 prevalence of cardiac abnormalities in competitive athletes.

“It is a real tribute to the sports cardiology community. There has been an amazing growth of information, and they not only gathered this information, they analyzed and published it, starting out with a study of 29 or 30 athletes, and now thousands,” Dr. Udelson said in an interview.

At the start of the pandemic, it appeared that 15%-20% of athletes had myocarditis, and athletic conferences were discussing canceling sports events.

However, with greater numbers comes a more accurate picture of the extent of the problem.

“Once you get thousands of subjects in these studies, you can hone in on what the real number is, so now we understand that if you screen everybody with a cardiac MRI, 1%, 2%, or 3% will have some evidence of what looks like myocarditis,” he said.

Dr. Udelson agreed that doing cardiac imaging in everyone is not feasible.

“This study looked at a very large number of people who all had an MRI, but that doesn’t mean everyone should have them. If you just do an echo, an EKG, and a troponin test, and if everything is normal, which is kind of what current recommendations are, this paper tells us that we are going to miss one or two people out of a hundred, and that might be okay,” he said. “So, if you are at a huge university that has a large medical center and you want to screen all your athletes with MRI, great. But if you’re at a high school in a remote area, you know that the alternative, not having an MRI, isn’t so bad, either.”

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

The U.S. Department of Justice (DOJ) on May 26 announced charges against 14 defendants across the country who allegedly engaged in health care fraud schemes that exploited the COVID-19 pandemic and resulted in over $143 million in false billings to Medicare.

Among the defendants, a DOJ news release said, were a telemedicine company executive, a physician, marketers, and medical business owners.

In addition, the Centers for Medicare and Medicaid Services separately announced that it had taken “adverse administrative actions” against more than 50 providers for their involvement in fraud schemes related to COVID-19 or the abuse of CMS programs that were designed to encourage access to medical care during the pandemic.

Several of the defendants allegedly offered COVID-19 tests to Medicare beneficiaries in senior living facilities, drive-through COVID-19 testing sites, and medical offices to induce the beneficiaries to provide their personal identifying information and a saliva or a blood sample.

The DOJ charges claim the defendants then misused the information and the samples to submit claims to Medicare for unrelated, medically unnecessary, and far more expensive lab tests, including cancer genetic testing, allergy testing, and respiratory pathogen panel tests.

In some cases, it’s alleged, the lab results were not provided to the individuals in a timely fashion or were not reliable.

Other defendants are charged with exploiting temporary changes in CMS telehealth regulations that were designed to increase access to health care during the pandemic. In these cases, which the DOJ said were the first charges related to the expansion of telehealth under the COVID-19 emergency declaration, the defendants allegedly submitted false and fraudulent claims to Medicare for sham telemedicine encounters that did not occur.

“As part of these cases, medical professionals are alleged to have [been] offered and paid bribes in exchange for the medical professionals’ referral of unnecessary testing,” the DOJ news release said. However, no physicians were identified by the department.

Commenting on this aspect of the law enforcement action, FBI Director Christopher Wray said in the release: “Medical providers have been the unsung heroes for the American public throughout the pandemic. It’s disheartening that some have abused their authorities and committed COVID-19–related fraud against trusting citizens. The FBI, along with our federal law enforcement and private sector partners, are committed to continuing to combat health care fraud and protect the American people.”

The law enforcement action includes the third set of criminal charges related to the misuse of Provider Relief Fund monies, according to the release.

More than 340 individuals were charged in September 2020 with submitting $6 billion in fraudulent claims to federal health care programs and private insurers for telehealth consultations and substance abuse treatment. About $4.5 billion of that was related to telehealth, as reported by this news organization.

The new criminal charges were brought in federal district courts in Arkansas, California, Louisiana, Florida, New Jersey, and New York.
 

Case summaries

The DOJ provided several case summaries. One defendant, lab owner Billy Joe Taylor of Lavaca, Ark., was charged with participating in a scheme to defraud the government of over $42 million by filing false claims that were billed in combination with COVID-19 testing claims. He also allegedly billed for tests that were not performed.

Petros Hannesyan of Burbank, Calif., the owner of a home health agency, was charged with obtaining over $229,000 from COVID-19 relief programs under false pretenses. His firm allegedly misappropriated funds from the CARES Act Provider Relief Fund and submitted false loan applications and a false loan agreement to the Economic Injury Disaster Loan Program.

Michael Stein and Leonel Palatnik of Palm Beach County, Fla., were charged in a connection with an alleged $73 million conspiracy to defraud the government and to pay and receive health care kickbacks during the pandemic.

Mr. Stein, who owned a “purported” consulting company, and Mr. Palatnik, who owned testing labs in Texas, allegedly exploited Medicare’s waiver of telehealth restrictions “by offering telehealth providers access to Medicare beneficiaries for whom they could bill consultations. In exchange, these providers agreed to refer beneficiaries to [Mr. Palatnik’s] laboratories for expensive and medically unnecessary cancer and cardiovascular genetic testing.”
 

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

The U.S. Department of Justice (DOJ) on May 26 announced charges against 14 defendants across the country who allegedly engaged in health care fraud schemes that exploited the COVID-19 pandemic and resulted in over $143 million in false billings to Medicare.

Among the defendants, a DOJ news release said, were a telemedicine company executive, a physician, marketers, and medical business owners.

In addition, the Centers for Medicare and Medicaid Services separately announced that it had taken “adverse administrative actions” against more than 50 providers for their involvement in fraud schemes related to COVID-19 or the abuse of CMS programs that were designed to encourage access to medical care during the pandemic.

Several of the defendants allegedly offered COVID-19 tests to Medicare beneficiaries in senior living facilities, drive-through COVID-19 testing sites, and medical offices to induce the beneficiaries to provide their personal identifying information and a saliva or a blood sample.

The DOJ charges claim the defendants then misused the information and the samples to submit claims to Medicare for unrelated, medically unnecessary, and far more expensive lab tests, including cancer genetic testing, allergy testing, and respiratory pathogen panel tests.

In some cases, it’s alleged, the lab results were not provided to the individuals in a timely fashion or were not reliable.

Other defendants are charged with exploiting temporary changes in CMS telehealth regulations that were designed to increase access to health care during the pandemic. In these cases, which the DOJ said were the first charges related to the expansion of telehealth under the COVID-19 emergency declaration, the defendants allegedly submitted false and fraudulent claims to Medicare for sham telemedicine encounters that did not occur.

“As part of these cases, medical professionals are alleged to have [been] offered and paid bribes in exchange for the medical professionals’ referral of unnecessary testing,” the DOJ news release said. However, no physicians were identified by the department.

Commenting on this aspect of the law enforcement action, FBI Director Christopher Wray said in the release: “Medical providers have been the unsung heroes for the American public throughout the pandemic. It’s disheartening that some have abused their authorities and committed COVID-19–related fraud against trusting citizens. The FBI, along with our federal law enforcement and private sector partners, are committed to continuing to combat health care fraud and protect the American people.”

The law enforcement action includes the third set of criminal charges related to the misuse of Provider Relief Fund monies, according to the release.

More than 340 individuals were charged in September 2020 with submitting $6 billion in fraudulent claims to federal health care programs and private insurers for telehealth consultations and substance abuse treatment. About $4.5 billion of that was related to telehealth, as reported by this news organization.

The new criminal charges were brought in federal district courts in Arkansas, California, Louisiana, Florida, New Jersey, and New York.
 

Case summaries

The DOJ provided several case summaries. One defendant, lab owner Billy Joe Taylor of Lavaca, Ark., was charged with participating in a scheme to defraud the government of over $42 million by filing false claims that were billed in combination with COVID-19 testing claims. He also allegedly billed for tests that were not performed.

Petros Hannesyan of Burbank, Calif., the owner of a home health agency, was charged with obtaining over $229,000 from COVID-19 relief programs under false pretenses. His firm allegedly misappropriated funds from the CARES Act Provider Relief Fund and submitted false loan applications and a false loan agreement to the Economic Injury Disaster Loan Program.

Michael Stein and Leonel Palatnik of Palm Beach County, Fla., were charged in a connection with an alleged $73 million conspiracy to defraud the government and to pay and receive health care kickbacks during the pandemic.

Mr. Stein, who owned a “purported” consulting company, and Mr. Palatnik, who owned testing labs in Texas, allegedly exploited Medicare’s waiver of telehealth restrictions “by offering telehealth providers access to Medicare beneficiaries for whom they could bill consultations. In exchange, these providers agreed to refer beneficiaries to [Mr. Palatnik’s] laboratories for expensive and medically unnecessary cancer and cardiovascular genetic testing.”
 

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

The U.S. Department of Justice (DOJ) on May 26 announced charges against 14 defendants across the country who allegedly engaged in health care fraud schemes that exploited the COVID-19 pandemic and resulted in over $143 million in false billings to Medicare.

Among the defendants, a DOJ news release said, were a telemedicine company executive, a physician, marketers, and medical business owners.

In addition, the Centers for Medicare and Medicaid Services separately announced that it had taken “adverse administrative actions” against more than 50 providers for their involvement in fraud schemes related to COVID-19 or the abuse of CMS programs that were designed to encourage access to medical care during the pandemic.

Several of the defendants allegedly offered COVID-19 tests to Medicare beneficiaries in senior living facilities, drive-through COVID-19 testing sites, and medical offices to induce the beneficiaries to provide their personal identifying information and a saliva or a blood sample.

The DOJ charges claim the defendants then misused the information and the samples to submit claims to Medicare for unrelated, medically unnecessary, and far more expensive lab tests, including cancer genetic testing, allergy testing, and respiratory pathogen panel tests.

In some cases, it’s alleged, the lab results were not provided to the individuals in a timely fashion or were not reliable.

Other defendants are charged with exploiting temporary changes in CMS telehealth regulations that were designed to increase access to health care during the pandemic. In these cases, which the DOJ said were the first charges related to the expansion of telehealth under the COVID-19 emergency declaration, the defendants allegedly submitted false and fraudulent claims to Medicare for sham telemedicine encounters that did not occur.

“As part of these cases, medical professionals are alleged to have [been] offered and paid bribes in exchange for the medical professionals’ referral of unnecessary testing,” the DOJ news release said. However, no physicians were identified by the department.

Commenting on this aspect of the law enforcement action, FBI Director Christopher Wray said in the release: “Medical providers have been the unsung heroes for the American public throughout the pandemic. It’s disheartening that some have abused their authorities and committed COVID-19–related fraud against trusting citizens. The FBI, along with our federal law enforcement and private sector partners, are committed to continuing to combat health care fraud and protect the American people.”

The law enforcement action includes the third set of criminal charges related to the misuse of Provider Relief Fund monies, according to the release.

More than 340 individuals were charged in September 2020 with submitting $6 billion in fraudulent claims to federal health care programs and private insurers for telehealth consultations and substance abuse treatment. About $4.5 billion of that was related to telehealth, as reported by this news organization.

The new criminal charges were brought in federal district courts in Arkansas, California, Louisiana, Florida, New Jersey, and New York.
 

Case summaries

The DOJ provided several case summaries. One defendant, lab owner Billy Joe Taylor of Lavaca, Ark., was charged with participating in a scheme to defraud the government of over $42 million by filing false claims that were billed in combination with COVID-19 testing claims. He also allegedly billed for tests that were not performed.

Petros Hannesyan of Burbank, Calif., the owner of a home health agency, was charged with obtaining over $229,000 from COVID-19 relief programs under false pretenses. His firm allegedly misappropriated funds from the CARES Act Provider Relief Fund and submitted false loan applications and a false loan agreement to the Economic Injury Disaster Loan Program.

Michael Stein and Leonel Palatnik of Palm Beach County, Fla., were charged in a connection with an alleged $73 million conspiracy to defraud the government and to pay and receive health care kickbacks during the pandemic.

Mr. Stein, who owned a “purported” consulting company, and Mr. Palatnik, who owned testing labs in Texas, allegedly exploited Medicare’s waiver of telehealth restrictions “by offering telehealth providers access to Medicare beneficiaries for whom they could bill consultations. In exchange, these providers agreed to refer beneficiaries to [Mr. Palatnik’s] laboratories for expensive and medically unnecessary cancer and cardiovascular genetic testing.”
 

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

Rurioctocog alfa pegol prophylaxis was linked to fewer bleeding episodes in people with hemophilia A when it targeted higher levels of factor VIII (FVIII) troughs, according to a report published in Blood (2021;137[13]:1818-27).

Earlier studies demonstrated that the treatment effectively prevented bleeds with an acceptable safety profile in people with hemophilia A. The current prospective, randomized, open label PROPEL trial compared safety and efficacy of two target FVIII troughs in this population. Targeting 1%-3% and 8%-12% FVIII troughs was efficacious, with fewer bleeds in the latter arm and acceptable safety across both, according to Robert Klamroth, MD, of Vivantes Klinikum Friedrichshain, Berlin, and colleagues.

The PROPEL trial (NCT02585960) population comprised 155 patients with hepatitis A, aged 12-65 years, with severe disease and an annualized bleeding rate of at least 2 during the 12 months before enrollment in the study. All had previous FVIII treatment. Patients were randomized to 12 months’ pharmacokinetic rurioctocog alfa pegol prophylaxis targeting FVIII troughs of 1%-3% (reference arm) or 8%-12%.

The primary endpoint was absence of bleeds during the second 6-month period. A total of 95 patients completed the protocol.
 

Promising results

In the 1%-3% and 8%-12% arms, the proportions of patients who completed the protocol and had no bleeds were 40% and 67% respectively (P = .015). Serious adverse events occurred in 7 of 115 (6%) patients, including one treatment-related event in the 8%-12% arm. There were no deaths, serious thrombotic events, or adverse event-related discontinuations.

“Targeting 8% to 12% FVIII troughs resulted in a higher proportion of [patients] with no bleeds than prophylaxis that targeted 1% to 3% FVIII troughs. These results support the hypothesis that an elevated FVIII trough can benefit [patients]without changing the safety profile,” the researchers reported. Personalized treatment in this patient population should be considered, they added.
 

Problems remain

In an invited commentary, Christine L. Kempton, MD, of Emory University, Atlanta, pointed out that the study did not answer the question of what trough level is best, and that the target trough level may be up to a patient’s individual clinician to decide. “Many participants (42%) treated with the target trough level of 1% to 3% had no bleeding events during the study period, but some (38%) continued to have bleeding events despite higher target trough levels,” Dr. Kempton wrote. She added that, beyond this concern, the presence of subclinical bleeding is difficult to study and quantify, but its presence is supported in the literature by magnetic resonance imaging that demonstrated joint damage despite a lack of clinically evident bleeding.

“Thus, targeting zero clinical bleeding events does not mean that all joint disease, dysfunction, and pain will be eliminated. This reality underscores the need for better, not just more convenient, therapies,” she concluded.

The authors reported numerous relationships with a variety of pharmaceutical companies including grants, honoraria, and participation in speakers bureaus. Dr. Kempton reported honoraria from Takeda, Spark, Octapharma, and Pfizer, and research grants from Novo Nordisk.

mlesney@mdedge.com

Rurioctocog alfa pegol prophylaxis was linked to fewer bleeding episodes in people with hemophilia A when it targeted higher levels of factor VIII (FVIII) troughs, according to a report published in Blood (2021;137[13]:1818-27).

Earlier studies demonstrated that the treatment effectively prevented bleeds with an acceptable safety profile in people with hemophilia A. The current prospective, randomized, open label PROPEL trial compared safety and efficacy of two target FVIII troughs in this population. Targeting 1%-3% and 8%-12% FVIII troughs was efficacious, with fewer bleeds in the latter arm and acceptable safety across both, according to Robert Klamroth, MD, of Vivantes Klinikum Friedrichshain, Berlin, and colleagues.

The PROPEL trial (NCT02585960) population comprised 155 patients with hepatitis A, aged 12-65 years, with severe disease and an annualized bleeding rate of at least 2 during the 12 months before enrollment in the study. All had previous FVIII treatment. Patients were randomized to 12 months’ pharmacokinetic rurioctocog alfa pegol prophylaxis targeting FVIII troughs of 1%-3% (reference arm) or 8%-12%.

The primary endpoint was absence of bleeds during the second 6-month period. A total of 95 patients completed the protocol.
 

Promising results

In the 1%-3% and 8%-12% arms, the proportions of patients who completed the protocol and had no bleeds were 40% and 67% respectively (P = .015). Serious adverse events occurred in 7 of 115 (6%) patients, including one treatment-related event in the 8%-12% arm. There were no deaths, serious thrombotic events, or adverse event-related discontinuations.

“Targeting 8% to 12% FVIII troughs resulted in a higher proportion of [patients] with no bleeds than prophylaxis that targeted 1% to 3% FVIII troughs. These results support the hypothesis that an elevated FVIII trough can benefit [patients]without changing the safety profile,” the researchers reported. Personalized treatment in this patient population should be considered, they added.
 

Problems remain

In an invited commentary, Christine L. Kempton, MD, of Emory University, Atlanta, pointed out that the study did not answer the question of what trough level is best, and that the target trough level may be up to a patient’s individual clinician to decide. “Many participants (42%) treated with the target trough level of 1% to 3% had no bleeding events during the study period, but some (38%) continued to have bleeding events despite higher target trough levels,” Dr. Kempton wrote. She added that, beyond this concern, the presence of subclinical bleeding is difficult to study and quantify, but its presence is supported in the literature by magnetic resonance imaging that demonstrated joint damage despite a lack of clinically evident bleeding.

“Thus, targeting zero clinical bleeding events does not mean that all joint disease, dysfunction, and pain will be eliminated. This reality underscores the need for better, not just more convenient, therapies,” she concluded.

The authors reported numerous relationships with a variety of pharmaceutical companies including grants, honoraria, and participation in speakers bureaus. Dr. Kempton reported honoraria from Takeda, Spark, Octapharma, and Pfizer, and research grants from Novo Nordisk.

mlesney@mdedge.com

Rurioctocog alfa pegol prophylaxis was linked to fewer bleeding episodes in people with hemophilia A when it targeted higher levels of factor VIII (FVIII) troughs, according to a report published in Blood (2021;137[13]:1818-27).

Earlier studies demonstrated that the treatment effectively prevented bleeds with an acceptable safety profile in people with hemophilia A. The current prospective, randomized, open label PROPEL trial compared safety and efficacy of two target FVIII troughs in this population. Targeting 1%-3% and 8%-12% FVIII troughs was efficacious, with fewer bleeds in the latter arm and acceptable safety across both, according to Robert Klamroth, MD, of Vivantes Klinikum Friedrichshain, Berlin, and colleagues.

The PROPEL trial (NCT02585960) population comprised 155 patients with hepatitis A, aged 12-65 years, with severe disease and an annualized bleeding rate of at least 2 during the 12 months before enrollment in the study. All had previous FVIII treatment. Patients were randomized to 12 months’ pharmacokinetic rurioctocog alfa pegol prophylaxis targeting FVIII troughs of 1%-3% (reference arm) or 8%-12%.

The primary endpoint was absence of bleeds during the second 6-month period. A total of 95 patients completed the protocol.
 

Promising results

In the 1%-3% and 8%-12% arms, the proportions of patients who completed the protocol and had no bleeds were 40% and 67% respectively (P = .015). Serious adverse events occurred in 7 of 115 (6%) patients, including one treatment-related event in the 8%-12% arm. There were no deaths, serious thrombotic events, or adverse event-related discontinuations.

“Targeting 8% to 12% FVIII troughs resulted in a higher proportion of [patients] with no bleeds than prophylaxis that targeted 1% to 3% FVIII troughs. These results support the hypothesis that an elevated FVIII trough can benefit [patients]without changing the safety profile,” the researchers reported. Personalized treatment in this patient population should be considered, they added.
 

Problems remain

In an invited commentary, Christine L. Kempton, MD, of Emory University, Atlanta, pointed out that the study did not answer the question of what trough level is best, and that the target trough level may be up to a patient’s individual clinician to decide. “Many participants (42%) treated with the target trough level of 1% to 3% had no bleeding events during the study period, but some (38%) continued to have bleeding events despite higher target trough levels,” Dr. Kempton wrote. She added that, beyond this concern, the presence of subclinical bleeding is difficult to study and quantify, but its presence is supported in the literature by magnetic resonance imaging that demonstrated joint damage despite a lack of clinically evident bleeding.

“Thus, targeting zero clinical bleeding events does not mean that all joint disease, dysfunction, and pain will be eliminated. This reality underscores the need for better, not just more convenient, therapies,” she concluded.

The authors reported numerous relationships with a variety of pharmaceutical companies including grants, honoraria, and participation in speakers bureaus. Dr. Kempton reported honoraria from Takeda, Spark, Octapharma, and Pfizer, and research grants from Novo Nordisk.

mlesney@mdedge.com

More children aged 12-15 years already have received at least one dose of a COVID-19 vaccine than have 16- and 17-year-olds, based on data from the Centers for Disease Control and Prevention.

As of May 30, almost 2.89 million children aged 12-15 years had received at least one dose, compared with nearly 2.73 million children aged 16-17, with those figures representing increases of 31.6% and 6.6% in the past week, respectively. Since the overall size of the 12-15 population is much larger, however, the proportion vaccinated is still smaller: 19.5% to 36.4%, according to the CDC’s COVID Data Tracker.

A look at full vaccination status shows that only 0.7% of those aged 12-15 years have received both doses of a two-dose vaccine or one dose of the single-shot variety, compared with 24% of those aged 16-17. For the country as a whole, 50.5% of all ages have received at least one dose and 40.7% are fully vaccinated, the CDC said.

Children aged 12-15 represent the largest share of the U.S. population (23.4%) initiating vaccination in the 14 days ending May 30, while children aged 16-17 made up just 4.5% of those getting their first dose. The younger group’s later entry into the vaccination pool shows up again when looking at completion rates, though, representing just 0.4% of all Americans who reached full vaccination during that same 14-day period, compared with 4.6% of the older children, the CDC data show.

Not all states are reporting data such as age for vaccine recipients, the CDC noted, and there are other variables that affect data collection. “Demographic data ... might differ by populations prioritized within each state or jurisdiction’s vaccination phase. Every geographic area has a different racial and ethnic composition, and not all are in the same vaccination phase,” the CDC said.

rfranki@mdedge.com

More children aged 12-15 years already have received at least one dose of a COVID-19 vaccine than have 16- and 17-year-olds, based on data from the Centers for Disease Control and Prevention.

As of May 30, almost 2.89 million children aged 12-15 years had received at least one dose, compared with nearly 2.73 million children aged 16-17, with those figures representing increases of 31.6% and 6.6% in the past week, respectively. Since the overall size of the 12-15 population is much larger, however, the proportion vaccinated is still smaller: 19.5% to 36.4%, according to the CDC’s COVID Data Tracker.

A look at full vaccination status shows that only 0.7% of those aged 12-15 years have received both doses of a two-dose vaccine or one dose of the single-shot variety, compared with 24% of those aged 16-17. For the country as a whole, 50.5% of all ages have received at least one dose and 40.7% are fully vaccinated, the CDC said.

Children aged 12-15 represent the largest share of the U.S. population (23.4%) initiating vaccination in the 14 days ending May 30, while children aged 16-17 made up just 4.5% of those getting their first dose. The younger group’s later entry into the vaccination pool shows up again when looking at completion rates, though, representing just 0.4% of all Americans who reached full vaccination during that same 14-day period, compared with 4.6% of the older children, the CDC data show.

Not all states are reporting data such as age for vaccine recipients, the CDC noted, and there are other variables that affect data collection. “Demographic data ... might differ by populations prioritized within each state or jurisdiction’s vaccination phase. Every geographic area has a different racial and ethnic composition, and not all are in the same vaccination phase,” the CDC said.

rfranki@mdedge.com

More children aged 12-15 years already have received at least one dose of a COVID-19 vaccine than have 16- and 17-year-olds, based on data from the Centers for Disease Control and Prevention.

As of May 30, almost 2.89 million children aged 12-15 years had received at least one dose, compared with nearly 2.73 million children aged 16-17, with those figures representing increases of 31.6% and 6.6% in the past week, respectively. Since the overall size of the 12-15 population is much larger, however, the proportion vaccinated is still smaller: 19.5% to 36.4%, according to the CDC’s COVID Data Tracker.

A look at full vaccination status shows that only 0.7% of those aged 12-15 years have received both doses of a two-dose vaccine or one dose of the single-shot variety, compared with 24% of those aged 16-17. For the country as a whole, 50.5% of all ages have received at least one dose and 40.7% are fully vaccinated, the CDC said.

Children aged 12-15 represent the largest share of the U.S. population (23.4%) initiating vaccination in the 14 days ending May 30, while children aged 16-17 made up just 4.5% of those getting their first dose. The younger group’s later entry into the vaccination pool shows up again when looking at completion rates, though, representing just 0.4% of all Americans who reached full vaccination during that same 14-day period, compared with 4.6% of the older children, the CDC data show.

Not all states are reporting data such as age for vaccine recipients, the CDC noted, and there are other variables that affect data collection. “Demographic data ... might differ by populations prioritized within each state or jurisdiction’s vaccination phase. Every geographic area has a different racial and ethnic composition, and not all are in the same vaccination phase,” the CDC said.

rfranki@mdedge.com

Cancer surgery is filled with moments of fear, even for doctors. Our cameras follow as an oncologist confronts this anxiety in the second episode of our video series The Oncologists.

Medscape Oncology © 2021 WebMD, LLC

Any views expressed above are the author's own and do not necessarily reflect the views of WebMD or Medscape.

Cite this: A Pivotal Moment in Cancer Surgery, Captured on Film - Medscape - Feb 18, 2021.

Cancer surgery is filled with moments of fear, even for doctors. Our cameras follow as an oncologist confronts this anxiety in the second episode of our video series The Oncologists.

Medscape Oncology © 2021 WebMD, LLC

Any views expressed above are the author's own and do not necessarily reflect the views of WebMD or Medscape.

Cite this: A Pivotal Moment in Cancer Surgery, Captured on Film - Medscape - Feb 18, 2021.

Cancer surgery is filled with moments of fear, even for doctors. Our cameras follow as an oncologist confronts this anxiety in the second episode of our video series The Oncologists.

Medscape Oncology © 2021 WebMD, LLC

Any views expressed above are the author's own and do not necessarily reflect the views of WebMD or Medscape.

Cite this: A Pivotal Moment in Cancer Surgery, Captured on Film - Medscape - Feb 18, 2021.

Health workers already know that indoor air quality can be as important to human health as clean water and uncontaminated food. But before the COVID-19 pandemic, its importance in the prevention of respiratory illnesses outside of health circles was only whispered about.

Now, a team of nearly 40 scientists from 14 countries is calling for “a paradigm shift,” so that improvements in indoor air quality are viewed as essential to curb respiratory infections.

Most countries do not have indoor air-quality standards, the scientists point out in their recent report, and those that do often fall short in scope and enforcement.

“We expect everywhere in the world to have clean water flowing from our taps. In most parts of the developed world, it is happening and we take it completely for granted,” said lead investigator Lidia Morawska, PhD, of the International Laboratory for Air Quality and Health at the Queensland University of Technology in Brisbane, Australia.

But bacteria and viruses can circulate freely in the air, and “no one thinks about this, whatsoever, apart from health care facilities,” she said.

A first step is to recognize the risk posed by airborne pathogens, something not yet universally acknowledged. The investigators also want the World Health Organization to extend its guidelines to cover airborne pathogens, and for ventilation standards to include higher airflow and filtration rates.

Germany has been at the forefront of air-quality measures, Dr. Morawska said. Years ago, she observed a monitor showing the carbon dioxide level and relative humidity in the room where she was attending a meeting. The screen was accompanied by red, yellow, and green signals to communicate risk. Such indicators are also commonly displayed in German schools so teachers know when to open the windows or adjust the ventilation.
 

Monitors show carbon dioxide levels

But this is not yet being done in most other countries, Dr. Morawska said. Levels of carbon dioxide are one measure of indoor air quality, but they serve as a proxy for ventilation, she pointed out. Although the technology is available, sensors that can test a variety of components in a building in real time are not yet affordable.

Dr. Morawska envisions a future where the air quality numbers of the places people frequent are displayed so they know the risk for airborne transmission of respiratory illnesses. And people can begin to expect clean indoor air when they enter a business, office, or entertainment space and request changes when the air quality dips and improvement is needed, she said.

It is a daunting challenge to clean indoor air for several reasons. Air is not containable in the same way water is, which makes it difficult to trace contaminants. And infections transmitted through dirty water and food are usually evident immediately, whereas infections transmitted through airborne pathogens can take days to develop. Plus, the necessary infrastructure changes will be expensive.

However, the initial cost required to change the flow and quality of indoor air might be less than the cost of infections, the scientists pointed out. It is estimated that the global harm caused by COVID-19 alone costs $1 trillion each month.

“In the United States, the yearly cost – direct and indirect – of influenza has been calculated at $11.2 billion. For respiratory infections other than influenza, the yearly cost stood at $40 billion,” the team noted.

“If even half of this was caused by inhalation, we are still talking about massive costs,” said Dr. Morawska.
 

Bigger is not always better

It is tempting to see the solution as increased ventilation, said Ehsan Mousavi, PhD, assistant professor of construction science and management at Clemson (S.C.) University, who studies indoor air quality and ventilation in hospitals.

“We are ventilating the heck out of hospitals,” he said in an interview. But there is much debate about how much ventilation is the right amount. Too much and “you can blow pathogens into an open wound,” he explained. “Bigger is not always better.”

And there is still debate about the best mix of outside and recirculated air. An increase in the intake of outdoor air can refresh indoor air if it is clean, but that depends on where you live, he pointed out.

The mix used in most standard office buildings is 15% outside air and 85% recirculated air, Dr. Mousavi said. Boosting the percentage of outside air increases costs and energy use.

In fact, it can take five times more energy to ventilate hospital spaces than office spaces, he reported.

Engineers searching for clean-air solutions need to know what particulates are in the air and whether they are harmful to humans, but the sensors currently available can’t identify whether a virus is present in real time.

Samples have to be taken to a lab and, “by the time you know a virus was in the space, the moment is gone,” Dr. Mousavi explained.

More research is needed. “We need a reasonable answer that looks at the problem holistically, not just from the infectious disease perspective,” he said.
 

Hydrating indoor air

Research is making it clear that health care environments can play a significant role in patient recovery, according to Stephanie Taylor, MD. Dr. Taylor is president of Building4Health, which she founded to help businesses assess the quality of air in their buildings and find solutions. The company uses an algorithm to arrive at a health assessment score.

Air hydration is the most important aspect to target, she said.

Since the 1980s, research has shown that a relative humidity of 40%-60% is healthy for humans, she said. Currently, in an office building in a winter climate, the humidity level is more like 20%.

Canada is the first country to officially recommend the 40%-60% range for senior citizen centers and residential homes.

“Properly hydrated air supports our immune system and prevents skin problems and respiratory problems. It also inactivates many bacteria and viruses,” Dr. Taylor explained. Inhaling dry air compromises the ability of the body to restrict influenza virus infection, researchers showed in a 2019 study.

In the case of COVID-19, as virus particles attach to water molecules, they get bigger and heavier and eventually drop out of the breathing zone and onto surfaces where they can be wiped away, she explained.

But when the particles “are very small – like 5 microns in diameter – and you inhale them, they can lodge deep in the lungs,” she said.

In properly hydrated air, particles will be larger – about 10-20 microns when they attach to the water vapor – so they will get stuck in the nose or the back of the throat, where they can be washed away by mucous and not travel to the lungs.

“Indoor air metrics” can support our health or contribute to disease, “not just over time, but quickly, within minutes or hours,” she said.

No one expects the world’s building stock to suddenly upgrade to the ideal air quality. “But that doesn’t mean we shouldn’t move in that direction,” Dr. Taylor said. Changes can start small and gradually increase.
 

New research targets indoor air

Humidity is one of the key areas for current research, said Karl Rockne, PhD, director of the environmental engineering program at the National Science Foundation.

“When a virus comes out, it’s not just a naked virus, which is exceptionally small. It’s a virus encapsulated in liquid. And that’s why the humidity is so key. The degree of humidity can determine how fast the water evaporates from the particle,” he said in an interview.

In the wake of COVID-19, his institution is funding more cross-disciplinary research in biology, building science, architecture, and physics, he pointed out.

One such effort involved the development of a sensor that can capture live COVID-19 virus. This so-called “smoking gun,” which proved that the virus can spread through the air, took the combined expertise of professionals in medicine, engineering, and several other disciplines.

Currently, investigators are examining indoor air quality and water supplies in offices that have been left empty during the pandemic, and the effect they will have on human health. And others are looking at the way outside air quality affects indoor air quality, particularly where outdoor air quality is poor, such as in areas experiencing wildfires.

So will COVID-19 be the catalyst that finally drives changes to building design, regulation, and public expectations of air quality in the spaces where we spend close to 90% of our time?

“If not COVID, what else? It affected every country, every sector,” Dr. Morawska said. “There’s enough momentum now to do something about this. And enough realization there is a problem.”
 

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

Health workers already know that indoor air quality can be as important to human health as clean water and uncontaminated food. But before the COVID-19 pandemic, its importance in the prevention of respiratory illnesses outside of health circles was only whispered about.

Now, a team of nearly 40 scientists from 14 countries is calling for “a paradigm shift,” so that improvements in indoor air quality are viewed as essential to curb respiratory infections.

Most countries do not have indoor air-quality standards, the scientists point out in their recent report, and those that do often fall short in scope and enforcement.

“We expect everywhere in the world to have clean water flowing from our taps. In most parts of the developed world, it is happening and we take it completely for granted,” said lead investigator Lidia Morawska, PhD, of the International Laboratory for Air Quality and Health at the Queensland University of Technology in Brisbane, Australia.

But bacteria and viruses can circulate freely in the air, and “no one thinks about this, whatsoever, apart from health care facilities,” she said.

A first step is to recognize the risk posed by airborne pathogens, something not yet universally acknowledged. The investigators also want the World Health Organization to extend its guidelines to cover airborne pathogens, and for ventilation standards to include higher airflow and filtration rates.

Germany has been at the forefront of air-quality measures, Dr. Morawska said. Years ago, she observed a monitor showing the carbon dioxide level and relative humidity in the room where she was attending a meeting. The screen was accompanied by red, yellow, and green signals to communicate risk. Such indicators are also commonly displayed in German schools so teachers know when to open the windows or adjust the ventilation.
 

Monitors show carbon dioxide levels

But this is not yet being done in most other countries, Dr. Morawska said. Levels of carbon dioxide are one measure of indoor air quality, but they serve as a proxy for ventilation, she pointed out. Although the technology is available, sensors that can test a variety of components in a building in real time are not yet affordable.

Dr. Morawska envisions a future where the air quality numbers of the places people frequent are displayed so they know the risk for airborne transmission of respiratory illnesses. And people can begin to expect clean indoor air when they enter a business, office, or entertainment space and request changes when the air quality dips and improvement is needed, she said.

It is a daunting challenge to clean indoor air for several reasons. Air is not containable in the same way water is, which makes it difficult to trace contaminants. And infections transmitted through dirty water and food are usually evident immediately, whereas infections transmitted through airborne pathogens can take days to develop. Plus, the necessary infrastructure changes will be expensive.

However, the initial cost required to change the flow and quality of indoor air might be less than the cost of infections, the scientists pointed out. It is estimated that the global harm caused by COVID-19 alone costs $1 trillion each month.

“In the United States, the yearly cost – direct and indirect – of influenza has been calculated at $11.2 billion. For respiratory infections other than influenza, the yearly cost stood at $40 billion,” the team noted.

“If even half of this was caused by inhalation, we are still talking about massive costs,” said Dr. Morawska.
 

Bigger is not always better

It is tempting to see the solution as increased ventilation, said Ehsan Mousavi, PhD, assistant professor of construction science and management at Clemson (S.C.) University, who studies indoor air quality and ventilation in hospitals.

“We are ventilating the heck out of hospitals,” he said in an interview. But there is much debate about how much ventilation is the right amount. Too much and “you can blow pathogens into an open wound,” he explained. “Bigger is not always better.”

And there is still debate about the best mix of outside and recirculated air. An increase in the intake of outdoor air can refresh indoor air if it is clean, but that depends on where you live, he pointed out.

The mix used in most standard office buildings is 15% outside air and 85% recirculated air, Dr. Mousavi said. Boosting the percentage of outside air increases costs and energy use.

In fact, it can take five times more energy to ventilate hospital spaces than office spaces, he reported.

Engineers searching for clean-air solutions need to know what particulates are in the air and whether they are harmful to humans, but the sensors currently available can’t identify whether a virus is present in real time.

Samples have to be taken to a lab and, “by the time you know a virus was in the space, the moment is gone,” Dr. Mousavi explained.

More research is needed. “We need a reasonable answer that looks at the problem holistically, not just from the infectious disease perspective,” he said.
 

Hydrating indoor air

Research is making it clear that health care environments can play a significant role in patient recovery, according to Stephanie Taylor, MD. Dr. Taylor is president of Building4Health, which she founded to help businesses assess the quality of air in their buildings and find solutions. The company uses an algorithm to arrive at a health assessment score.

Air hydration is the most important aspect to target, she said.

Since the 1980s, research has shown that a relative humidity of 40%-60% is healthy for humans, she said. Currently, in an office building in a winter climate, the humidity level is more like 20%.

Canada is the first country to officially recommend the 40%-60% range for senior citizen centers and residential homes.

“Properly hydrated air supports our immune system and prevents skin problems and respiratory problems. It also inactivates many bacteria and viruses,” Dr. Taylor explained. Inhaling dry air compromises the ability of the body to restrict influenza virus infection, researchers showed in a 2019 study.

In the case of COVID-19, as virus particles attach to water molecules, they get bigger and heavier and eventually drop out of the breathing zone and onto surfaces where they can be wiped away, she explained.

But when the particles “are very small – like 5 microns in diameter – and you inhale them, they can lodge deep in the lungs,” she said.

In properly hydrated air, particles will be larger – about 10-20 microns when they attach to the water vapor – so they will get stuck in the nose or the back of the throat, where they can be washed away by mucous and not travel to the lungs.

“Indoor air metrics” can support our health or contribute to disease, “not just over time, but quickly, within minutes or hours,” she said.

No one expects the world’s building stock to suddenly upgrade to the ideal air quality. “But that doesn’t mean we shouldn’t move in that direction,” Dr. Taylor said. Changes can start small and gradually increase.
 

New research targets indoor air

Humidity is one of the key areas for current research, said Karl Rockne, PhD, director of the environmental engineering program at the National Science Foundation.

“When a virus comes out, it’s not just a naked virus, which is exceptionally small. It’s a virus encapsulated in liquid. And that’s why the humidity is so key. The degree of humidity can determine how fast the water evaporates from the particle,” he said in an interview.

In the wake of COVID-19, his institution is funding more cross-disciplinary research in biology, building science, architecture, and physics, he pointed out.

One such effort involved the development of a sensor that can capture live COVID-19 virus. This so-called “smoking gun,” which proved that the virus can spread through the air, took the combined expertise of professionals in medicine, engineering, and several other disciplines.

Currently, investigators are examining indoor air quality and water supplies in offices that have been left empty during the pandemic, and the effect they will have on human health. And others are looking at the way outside air quality affects indoor air quality, particularly where outdoor air quality is poor, such as in areas experiencing wildfires.

So will COVID-19 be the catalyst that finally drives changes to building design, regulation, and public expectations of air quality in the spaces where we spend close to 90% of our time?

“If not COVID, what else? It affected every country, every sector,” Dr. Morawska said. “There’s enough momentum now to do something about this. And enough realization there is a problem.”
 

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

Health workers already know that indoor air quality can be as important to human health as clean water and uncontaminated food. But before the COVID-19 pandemic, its importance in the prevention of respiratory illnesses outside of health circles was only whispered about.

Now, a team of nearly 40 scientists from 14 countries is calling for “a paradigm shift,” so that improvements in indoor air quality are viewed as essential to curb respiratory infections.

Most countries do not have indoor air-quality standards, the scientists point out in their recent report, and those that do often fall short in scope and enforcement.

“We expect everywhere in the world to have clean water flowing from our taps. In most parts of the developed world, it is happening and we take it completely for granted,” said lead investigator Lidia Morawska, PhD, of the International Laboratory for Air Quality and Health at the Queensland University of Technology in Brisbane, Australia.

But bacteria and viruses can circulate freely in the air, and “no one thinks about this, whatsoever, apart from health care facilities,” she said.

A first step is to recognize the risk posed by airborne pathogens, something not yet universally acknowledged. The investigators also want the World Health Organization to extend its guidelines to cover airborne pathogens, and for ventilation standards to include higher airflow and filtration rates.

Germany has been at the forefront of air-quality measures, Dr. Morawska said. Years ago, she observed a monitor showing the carbon dioxide level and relative humidity in the room where she was attending a meeting. The screen was accompanied by red, yellow, and green signals to communicate risk. Such indicators are also commonly displayed in German schools so teachers know when to open the windows or adjust the ventilation.
 

Monitors show carbon dioxide levels

But this is not yet being done in most other countries, Dr. Morawska said. Levels of carbon dioxide are one measure of indoor air quality, but they serve as a proxy for ventilation, she pointed out. Although the technology is available, sensors that can test a variety of components in a building in real time are not yet affordable.

Dr. Morawska envisions a future where the air quality numbers of the places people frequent are displayed so they know the risk for airborne transmission of respiratory illnesses. And people can begin to expect clean indoor air when they enter a business, office, or entertainment space and request changes when the air quality dips and improvement is needed, she said.

It is a daunting challenge to clean indoor air for several reasons. Air is not containable in the same way water is, which makes it difficult to trace contaminants. And infections transmitted through dirty water and food are usually evident immediately, whereas infections transmitted through airborne pathogens can take days to develop. Plus, the necessary infrastructure changes will be expensive.

However, the initial cost required to change the flow and quality of indoor air might be less than the cost of infections, the scientists pointed out. It is estimated that the global harm caused by COVID-19 alone costs $1 trillion each month.

“In the United States, the yearly cost – direct and indirect – of influenza has been calculated at $11.2 billion. For respiratory infections other than influenza, the yearly cost stood at $40 billion,” the team noted.

“If even half of this was caused by inhalation, we are still talking about massive costs,” said Dr. Morawska.
 

Bigger is not always better

It is tempting to see the solution as increased ventilation, said Ehsan Mousavi, PhD, assistant professor of construction science and management at Clemson (S.C.) University, who studies indoor air quality and ventilation in hospitals.

“We are ventilating the heck out of hospitals,” he said in an interview. But there is much debate about how much ventilation is the right amount. Too much and “you can blow pathogens into an open wound,” he explained. “Bigger is not always better.”

And there is still debate about the best mix of outside and recirculated air. An increase in the intake of outdoor air can refresh indoor air if it is clean, but that depends on where you live, he pointed out.

The mix used in most standard office buildings is 15% outside air and 85% recirculated air, Dr. Mousavi said. Boosting the percentage of outside air increases costs and energy use.

In fact, it can take five times more energy to ventilate hospital spaces than office spaces, he reported.

Engineers searching for clean-air solutions need to know what particulates are in the air and whether they are harmful to humans, but the sensors currently available can’t identify whether a virus is present in real time.

Samples have to be taken to a lab and, “by the time you know a virus was in the space, the moment is gone,” Dr. Mousavi explained.

More research is needed. “We need a reasonable answer that looks at the problem holistically, not just from the infectious disease perspective,” he said.
 

Hydrating indoor air

Research is making it clear that health care environments can play a significant role in patient recovery, according to Stephanie Taylor, MD. Dr. Taylor is president of Building4Health, which she founded to help businesses assess the quality of air in their buildings and find solutions. The company uses an algorithm to arrive at a health assessment score.

Air hydration is the most important aspect to target, she said.

Since the 1980s, research has shown that a relative humidity of 40%-60% is healthy for humans, she said. Currently, in an office building in a winter climate, the humidity level is more like 20%.

Canada is the first country to officially recommend the 40%-60% range for senior citizen centers and residential homes.

“Properly hydrated air supports our immune system and prevents skin problems and respiratory problems. It also inactivates many bacteria and viruses,” Dr. Taylor explained. Inhaling dry air compromises the ability of the body to restrict influenza virus infection, researchers showed in a 2019 study.

In the case of COVID-19, as virus particles attach to water molecules, they get bigger and heavier and eventually drop out of the breathing zone and onto surfaces where they can be wiped away, she explained.

But when the particles “are very small – like 5 microns in diameter – and you inhale them, they can lodge deep in the lungs,” she said.

In properly hydrated air, particles will be larger – about 10-20 microns when they attach to the water vapor – so they will get stuck in the nose or the back of the throat, where they can be washed away by mucous and not travel to the lungs.

“Indoor air metrics” can support our health or contribute to disease, “not just over time, but quickly, within minutes or hours,” she said.

No one expects the world’s building stock to suddenly upgrade to the ideal air quality. “But that doesn’t mean we shouldn’t move in that direction,” Dr. Taylor said. Changes can start small and gradually increase.
 

New research targets indoor air

Humidity is one of the key areas for current research, said Karl Rockne, PhD, director of the environmental engineering program at the National Science Foundation.

“When a virus comes out, it’s not just a naked virus, which is exceptionally small. It’s a virus encapsulated in liquid. And that’s why the humidity is so key. The degree of humidity can determine how fast the water evaporates from the particle,” he said in an interview.

In the wake of COVID-19, his institution is funding more cross-disciplinary research in biology, building science, architecture, and physics, he pointed out.

One such effort involved the development of a sensor that can capture live COVID-19 virus. This so-called “smoking gun,” which proved that the virus can spread through the air, took the combined expertise of professionals in medicine, engineering, and several other disciplines.

Currently, investigators are examining indoor air quality and water supplies in offices that have been left empty during the pandemic, and the effect they will have on human health. And others are looking at the way outside air quality affects indoor air quality, particularly where outdoor air quality is poor, such as in areas experiencing wildfires.

So will COVID-19 be the catalyst that finally drives changes to building design, regulation, and public expectations of air quality in the spaces where we spend close to 90% of our time?

“If not COVID, what else? It affected every country, every sector,” Dr. Morawska said. “There’s enough momentum now to do something about this. And enough realization there is a problem.”
 

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

Greater severity of obstructive sleep apnea (OSA) is associated with a higher risk of contracting COVID-19, and positive airway pressure (PAP) treatment may counter that risk, according to a retrospective analysis from the records of Kaiser Permanente Southern California.

OSA patients often worry that PAP therapy might increase risk of severe COVID-19, said Dennis Hwang, MD, who presented the study at the American Thoracic Society’s virtual international conference (Abstract A1108). But the findings should be reassuring. “If you have obstructive sleep apnea, and you’re supposed to be using PAP, we recommend that you continue using PAP. It’s good for your overall wellness and reducing the risk of cardiovascular disease, but as it relates to COVID-19, it’s possible that it could protect. And there doesn’t appear to be any risk of increased severity of illness (with use of PAP),” Dr. Hwang said in an interview. He is medical director of sleep medicine for Kaiser Permanente San Bernardino County and cochair of sleep medicine for Kaiser Southern California.

He noted that the retrospective nature of the study makes it difficult to pin down whether PAP therapy is truly protective, “but I think there’s enough that we’ve been able conceptually to understand, to suggest that a direct causative relationship is possible,” said Dr. Hwang.

The results may imply that OSA patients should pay special attention to their OSA when there’s concern about exposure to an infectious agent like SARS-CoV-2. “The intermittent hypoxia at night, which can linger over to the day as increased sympathetic activity, increased heart rate. All of these are stresses to the body. So if you’re going to get infected, you want to start at a healthier level. You want to eliminate your sleep apnea to help reduce your risk of morbidity,” said Esra Tasali, MD, who was asked to comment on the study. Dr. Tasali is associate professor of medicine at the University of Chicago, and director of the Sleep Research Center there.

During the Q&A session after the talk, audience members asked about the timing of PAP use during COVID-19 infection, for example how often it was used during the asymptomatic phase of infection and if PAP has a positive effect. The data were not available, but “I think that the way to go is to understand this chronology,” said Dr. Tasali.

The researchers examined records between 2015 and 2020, using sleep study data, remotely collected daily PAP data, and electronic health records, all from Kaiser Permanente Southern California. Included subjects were adults who had enrolled before Feb. 1, 2020, and had sleep diagnostic or PAP data on record by March 1, 2020. The researchers analyzed PAP adherence between March 1, 2020, and the time of COVID-19 diagnosis, or until the study ended on July 31, 2020.

Patients were defined as being untreated (< 2 hours/night PAP), moderately treated (2-3.9 hours/night), or well treated (4 or more hours/night). Apnea hypopnea index (AHI) was used to determine severity. The analysis included 81,932 patients (39.8% were women, mean age was 54.0 years, 9.9% were Black, and 34.5% were Hispanic). A total of 1.7% of subjects without OSA experienced COVID-19 infection, compared to 1.8% with OSA; 0.3% with OSA were hospitalized and 0.07% underwent intensive care or died.

There were some differences between the two groups. The non-USA population was younger (mean age 47.0 vs. 54.5 years), was less likely to be men (44% vs. 60.3%), had a lower mean body mass index (30.4 vs. 34.3), had fewer comorbidities according to the Charleston Comorbidity Index (1.3 vs. 2.0), and were less likely to have hypertension (5.6% vs. 12.4%; P < .0001 for all).

Infection rates were higher in patients with more severe OSA. The rates in untreated mild, moderate, and severe OSA were 2%, 2%, and 2.4% respectively. The rate among all treated patients was 1.4% (P < .0001). Infection rates also dropped among patients with better treatment: untreated, 2.1%; moderately treated, 1.7%; and well treated, 1.3% (P < .0001).

Not having OSA was associated with a lower infection risk than was having OSA (odds ratio [OR], 0.82; 95% confidence interval, 0.70-0.96). Compared to untreated patients, there was lower infection risk in the moderately treated (OR, 0.82; 95% CI, 0.65-1.03) and well treated (OR, 0.68; 95% CI, 0.59-0.79) groups. Higher infection rates were associated with obesity, higher Charlson Comorbidity score (> 2; OR, 1.29; 95% CI, 1.09-1.53), Black (OR, 1.51; 95% CI, 1.24-1.84) and Hispanic ethnicities (OR, 2.23; 95% CI, 1.96-2.54), and Medicaid enrollment. Increasing age was associated with lower risk of infection, with each 5-year increment linked to reduced risk (OR, 0.88; 95% CI, 0.86-0.90). Dr. Hwang suggested that the age association may be because older individuals were more likely to follow social distancing and other precautions.

A multivariate analysis found that OSA was associated with infection risk according to OSA severity, including mild (OR, 1.21; 95% CI, 1.01-1.44), and moderate to severe (OR, 1.27; 95% CI, 1.07-1.51). There was no association between hospitalization rate or ICU admission/death and presence of OSA or PAP adherence in the data presented, but Dr. Hwang said that an updated analysis suggests that OSA may be associated with a risk of greater COVID-19 severity.

The control group was composed of individuals who had undergone sleep testing, but found to not have OSA. Still, they aren’t necessarily representative of the general population, since symptoms likely drove them to testing. A high percentage were also obese, and the average BMI was 30. “It’s certainly not a ‘normal population,’ but the advantage of what we did in terms of using this control group is that they underwent sleep testing, so they were proven to have no obstructive sleep apnea, whereas if we used a general population, we just don’t know,” said Dr. Hwang.

The study received technical and data support from Somnoware, and was funded by Kaiser Permanente. Dr. Tasali has no relevant financial disclosures.
 

Greater severity of obstructive sleep apnea (OSA) is associated with a higher risk of contracting COVID-19, and positive airway pressure (PAP) treatment may counter that risk, according to a retrospective analysis from the records of Kaiser Permanente Southern California.

OSA patients often worry that PAP therapy might increase risk of severe COVID-19, said Dennis Hwang, MD, who presented the study at the American Thoracic Society’s virtual international conference (Abstract A1108). But the findings should be reassuring. “If you have obstructive sleep apnea, and you’re supposed to be using PAP, we recommend that you continue using PAP. It’s good for your overall wellness and reducing the risk of cardiovascular disease, but as it relates to COVID-19, it’s possible that it could protect. And there doesn’t appear to be any risk of increased severity of illness (with use of PAP),” Dr. Hwang said in an interview. He is medical director of sleep medicine for Kaiser Permanente San Bernardino County and cochair of sleep medicine for Kaiser Southern California.

He noted that the retrospective nature of the study makes it difficult to pin down whether PAP therapy is truly protective, “but I think there’s enough that we’ve been able conceptually to understand, to suggest that a direct causative relationship is possible,” said Dr. Hwang.

The results may imply that OSA patients should pay special attention to their OSA when there’s concern about exposure to an infectious agent like SARS-CoV-2. “The intermittent hypoxia at night, which can linger over to the day as increased sympathetic activity, increased heart rate. All of these are stresses to the body. So if you’re going to get infected, you want to start at a healthier level. You want to eliminate your sleep apnea to help reduce your risk of morbidity,” said Esra Tasali, MD, who was asked to comment on the study. Dr. Tasali is associate professor of medicine at the University of Chicago, and director of the Sleep Research Center there.

During the Q&A session after the talk, audience members asked about the timing of PAP use during COVID-19 infection, for example how often it was used during the asymptomatic phase of infection and if PAP has a positive effect. The data were not available, but “I think that the way to go is to understand this chronology,” said Dr. Tasali.

The researchers examined records between 2015 and 2020, using sleep study data, remotely collected daily PAP data, and electronic health records, all from Kaiser Permanente Southern California. Included subjects were adults who had enrolled before Feb. 1, 2020, and had sleep diagnostic or PAP data on record by March 1, 2020. The researchers analyzed PAP adherence between March 1, 2020, and the time of COVID-19 diagnosis, or until the study ended on July 31, 2020.

Patients were defined as being untreated (< 2 hours/night PAP), moderately treated (2-3.9 hours/night), or well treated (4 or more hours/night). Apnea hypopnea index (AHI) was used to determine severity. The analysis included 81,932 patients (39.8% were women, mean age was 54.0 years, 9.9% were Black, and 34.5% were Hispanic). A total of 1.7% of subjects without OSA experienced COVID-19 infection, compared to 1.8% with OSA; 0.3% with OSA were hospitalized and 0.07% underwent intensive care or died.

There were some differences between the two groups. The non-USA population was younger (mean age 47.0 vs. 54.5 years), was less likely to be men (44% vs. 60.3%), had a lower mean body mass index (30.4 vs. 34.3), had fewer comorbidities according to the Charleston Comorbidity Index (1.3 vs. 2.0), and were less likely to have hypertension (5.6% vs. 12.4%; P < .0001 for all).

Infection rates were higher in patients with more severe OSA. The rates in untreated mild, moderate, and severe OSA were 2%, 2%, and 2.4% respectively. The rate among all treated patients was 1.4% (P < .0001). Infection rates also dropped among patients with better treatment: untreated, 2.1%; moderately treated, 1.7%; and well treated, 1.3% (P < .0001).

Not having OSA was associated with a lower infection risk than was having OSA (odds ratio [OR], 0.82; 95% confidence interval, 0.70-0.96). Compared to untreated patients, there was lower infection risk in the moderately treated (OR, 0.82; 95% CI, 0.65-1.03) and well treated (OR, 0.68; 95% CI, 0.59-0.79) groups. Higher infection rates were associated with obesity, higher Charlson Comorbidity score (> 2; OR, 1.29; 95% CI, 1.09-1.53), Black (OR, 1.51; 95% CI, 1.24-1.84) and Hispanic ethnicities (OR, 2.23; 95% CI, 1.96-2.54), and Medicaid enrollment. Increasing age was associated with lower risk of infection, with each 5-year increment linked to reduced risk (OR, 0.88; 95% CI, 0.86-0.90). Dr. Hwang suggested that the age association may be because older individuals were more likely to follow social distancing and other precautions.

A multivariate analysis found that OSA was associated with infection risk according to OSA severity, including mild (OR, 1.21; 95% CI, 1.01-1.44), and moderate to severe (OR, 1.27; 95% CI, 1.07-1.51). There was no association between hospitalization rate or ICU admission/death and presence of OSA or PAP adherence in the data presented, but Dr. Hwang said that an updated analysis suggests that OSA may be associated with a risk of greater COVID-19 severity.

The control group was composed of individuals who had undergone sleep testing, but found to not have OSA. Still, they aren’t necessarily representative of the general population, since symptoms likely drove them to testing. A high percentage were also obese, and the average BMI was 30. “It’s certainly not a ‘normal population,’ but the advantage of what we did in terms of using this control group is that they underwent sleep testing, so they were proven to have no obstructive sleep apnea, whereas if we used a general population, we just don’t know,” said Dr. Hwang.

The study received technical and data support from Somnoware, and was funded by Kaiser Permanente. Dr. Tasali has no relevant financial disclosures.
 

Greater severity of obstructive sleep apnea (OSA) is associated with a higher risk of contracting COVID-19, and positive airway pressure (PAP) treatment may counter that risk, according to a retrospective analysis from the records of Kaiser Permanente Southern California.

OSA patients often worry that PAP therapy might increase risk of severe COVID-19, said Dennis Hwang, MD, who presented the study at the American Thoracic Society’s virtual international conference (Abstract A1108). But the findings should be reassuring. “If you have obstructive sleep apnea, and you’re supposed to be using PAP, we recommend that you continue using PAP. It’s good for your overall wellness and reducing the risk of cardiovascular disease, but as it relates to COVID-19, it’s possible that it could protect. And there doesn’t appear to be any risk of increased severity of illness (with use of PAP),” Dr. Hwang said in an interview. He is medical director of sleep medicine for Kaiser Permanente San Bernardino County and cochair of sleep medicine for Kaiser Southern California.

He noted that the retrospective nature of the study makes it difficult to pin down whether PAP therapy is truly protective, “but I think there’s enough that we’ve been able conceptually to understand, to suggest that a direct causative relationship is possible,” said Dr. Hwang.

The results may imply that OSA patients should pay special attention to their OSA when there’s concern about exposure to an infectious agent like SARS-CoV-2. “The intermittent hypoxia at night, which can linger over to the day as increased sympathetic activity, increased heart rate. All of these are stresses to the body. So if you’re going to get infected, you want to start at a healthier level. You want to eliminate your sleep apnea to help reduce your risk of morbidity,” said Esra Tasali, MD, who was asked to comment on the study. Dr. Tasali is associate professor of medicine at the University of Chicago, and director of the Sleep Research Center there.

During the Q&A session after the talk, audience members asked about the timing of PAP use during COVID-19 infection, for example how often it was used during the asymptomatic phase of infection and if PAP has a positive effect. The data were not available, but “I think that the way to go is to understand this chronology,” said Dr. Tasali.

The researchers examined records between 2015 and 2020, using sleep study data, remotely collected daily PAP data, and electronic health records, all from Kaiser Permanente Southern California. Included subjects were adults who had enrolled before Feb. 1, 2020, and had sleep diagnostic or PAP data on record by March 1, 2020. The researchers analyzed PAP adherence between March 1, 2020, and the time of COVID-19 diagnosis, or until the study ended on July 31, 2020.

Patients were defined as being untreated (< 2 hours/night PAP), moderately treated (2-3.9 hours/night), or well treated (4 or more hours/night). Apnea hypopnea index (AHI) was used to determine severity. The analysis included 81,932 patients (39.8% were women, mean age was 54.0 years, 9.9% were Black, and 34.5% were Hispanic). A total of 1.7% of subjects without OSA experienced COVID-19 infection, compared to 1.8% with OSA; 0.3% with OSA were hospitalized and 0.07% underwent intensive care or died.

There were some differences between the two groups. The non-USA population was younger (mean age 47.0 vs. 54.5 years), was less likely to be men (44% vs. 60.3%), had a lower mean body mass index (30.4 vs. 34.3), had fewer comorbidities according to the Charleston Comorbidity Index (1.3 vs. 2.0), and were less likely to have hypertension (5.6% vs. 12.4%; P < .0001 for all).

Infection rates were higher in patients with more severe OSA. The rates in untreated mild, moderate, and severe OSA were 2%, 2%, and 2.4% respectively. The rate among all treated patients was 1.4% (P < .0001). Infection rates also dropped among patients with better treatment: untreated, 2.1%; moderately treated, 1.7%; and well treated, 1.3% (P < .0001).

Not having OSA was associated with a lower infection risk than was having OSA (odds ratio [OR], 0.82; 95% confidence interval, 0.70-0.96). Compared to untreated patients, there was lower infection risk in the moderately treated (OR, 0.82; 95% CI, 0.65-1.03) and well treated (OR, 0.68; 95% CI, 0.59-0.79) groups. Higher infection rates were associated with obesity, higher Charlson Comorbidity score (> 2; OR, 1.29; 95% CI, 1.09-1.53), Black (OR, 1.51; 95% CI, 1.24-1.84) and Hispanic ethnicities (OR, 2.23; 95% CI, 1.96-2.54), and Medicaid enrollment. Increasing age was associated with lower risk of infection, with each 5-year increment linked to reduced risk (OR, 0.88; 95% CI, 0.86-0.90). Dr. Hwang suggested that the age association may be because older individuals were more likely to follow social distancing and other precautions.

A multivariate analysis found that OSA was associated with infection risk according to OSA severity, including mild (OR, 1.21; 95% CI, 1.01-1.44), and moderate to severe (OR, 1.27; 95% CI, 1.07-1.51). There was no association between hospitalization rate or ICU admission/death and presence of OSA or PAP adherence in the data presented, but Dr. Hwang said that an updated analysis suggests that OSA may be associated with a risk of greater COVID-19 severity.

The control group was composed of individuals who had undergone sleep testing, but found to not have OSA. Still, they aren’t necessarily representative of the general population, since symptoms likely drove them to testing. A high percentage were also obese, and the average BMI was 30. “It’s certainly not a ‘normal population,’ but the advantage of what we did in terms of using this control group is that they underwent sleep testing, so they were proven to have no obstructive sleep apnea, whereas if we used a general population, we just don’t know,” said Dr. Hwang.

The study received technical and data support from Somnoware, and was funded by Kaiser Permanente. Dr. Tasali has no relevant financial disclosures.
 

Some nonsleepy patients with coronary artery disease and obstructive sleep apnea (OSA) may receive cardiovascular benefit from continuous positive airway pressure (CPAP) therapy, according to a post hoc analysis of the RICCADSA clinical trial. That study found no benefit among patients overall, but the new analysis found that patients whose heart rate increases (delta heart rate, or dHR) more than average during apnea or hypopnea experienced fewer cardiovascular or cerebrovascular events during apnea or hypopnea when treated with CPAP.

Although RICCADSA showed no benefit, an analysis of the Multi-Ethnic Study of Atherosclerosis (MESA) and the Sleep Heart Health Study (SHHS) cohorts found that elevated pulse rate response to respiratory events was associated with greater risk of cardiovascular disease (CVD) morbidity and mortality. But the effect was seen only in nonsleepy patients. “We hypothesized that pulse rate response to apneas would predict which patients with OSA may most benefit from CPAP treatment. Now, our study suggests that there is, in fact, a subgroup of nonsleepy patients with OSA for whom CPAP could provide a reduction in risk, specifically those with a higher pulse rate response to their respiratory events,” Ali Azarbarzin, PhD, said in an interview.

Dr. Azarbarzin presented the study at the American Thoracic Society’s virtual international conference (Abstract A1103). He is in the division of sleep and circadian disorders at Brigham and Women’s Hospital, and is assistant professor of medicine at Harvard Medical School, both in Boston.

The study is in line with recent efforts to subgroup OSA patients to determine which are at higher risk of cardiovascular events and other complications, and which are most likely to respond to treatment, according to Esra Tasali, MD, of the University of Chicago, who moderated the session where the study was presented. “The field is really urgently in need of coming up with new methods, and I think this study is getting a handle on that,” said Dr. Tasali in an interview.

“I think that this is really pointing toward a new area that the whole (sleep field) is moving toward, which is better phenotyping of sleep apnea so that we can come up with more personalized treatments,” said Dr. Tasali.

The patients who appeared to gain a cardiovascular benefit from CPAP represented about 16% of trial participants. Dr. Azarbarzin refrained from making clinical recommendations, citing the need for more data. The team next plans to reproduce the findings in additional, larger trials such as the SAVE and ISAACC trials. “Ultimately, our goal is to confirm our findings in a future randomized controlled trial of CPAP by enrolling participants based on their pulse rate response,” said Dr. Azarbarzin.

The RICCADSA study was a single center randomized, controlled trial with 226 patients with coronary artery disease and OSA who were randomized to CPAP or no CPAP treatment. In the overall population, CPAP treatment was not associated with a statistically significant change in repeat revascularization, myocardial infarction, stroke, or cardiovascular mortality (hazard ratio [HR], 0.79; P = .435). That study assumed that the effect of OSA on CVD is similar across all subgroups of dHR.

The mean increase in heart rate was 7.1 beats per minute (BPM; standard deviation, 3.7). Each standard deviation increase in dHR was linked to greater CVD risk (HR, 1.45; P = .029). For each standard deviation decrease in dHR, treatment with CPAP decreased the CVD risk (HR, 0.54; P = .043).

For patients with a low dHR of 4 BPM, the hazard ratio for CVD was 0.8 with no CPAP treatment and 1.2 for CPAP treatment. For those at the mean value of 7 BPM, the HRs were 1.1 and 0.9 respectively. For those with a high dHR, (10 BPM), the hazard ratio was 1.6 without treatment and 0.7 with CPAP.

“We modeled delta heart rate interaction with CPAP, which was significant. What this means is that for someone with a mean delta heart rate of 7 beats per minute, the risk reduction (with CPAP) is similar to what RICCADSA reported. But if you look at those with high delta heart rate, the risk reduction was significantly larger. It was actually a more than 50% reduction of risk with CPAP treatment,” said Dr. Azarbarzin.

Dr. Azarbarzin has consulted for Somnifix and Apnimed and has received grants from Somnifix. Dr. Tasali has no relevant financial disclosures.

Some nonsleepy patients with coronary artery disease and obstructive sleep apnea (OSA) may receive cardiovascular benefit from continuous positive airway pressure (CPAP) therapy, according to a post hoc analysis of the RICCADSA clinical trial. That study found no benefit among patients overall, but the new analysis found that patients whose heart rate increases (delta heart rate, or dHR) more than average during apnea or hypopnea experienced fewer cardiovascular or cerebrovascular events during apnea or hypopnea when treated with CPAP.

Although RICCADSA showed no benefit, an analysis of the Multi-Ethnic Study of Atherosclerosis (MESA) and the Sleep Heart Health Study (SHHS) cohorts found that elevated pulse rate response to respiratory events was associated with greater risk of cardiovascular disease (CVD) morbidity and mortality. But the effect was seen only in nonsleepy patients. “We hypothesized that pulse rate response to apneas would predict which patients with OSA may most benefit from CPAP treatment. Now, our study suggests that there is, in fact, a subgroup of nonsleepy patients with OSA for whom CPAP could provide a reduction in risk, specifically those with a higher pulse rate response to their respiratory events,” Ali Azarbarzin, PhD, said in an interview.

Dr. Azarbarzin presented the study at the American Thoracic Society’s virtual international conference (Abstract A1103). He is in the division of sleep and circadian disorders at Brigham and Women’s Hospital, and is assistant professor of medicine at Harvard Medical School, both in Boston.

The study is in line with recent efforts to subgroup OSA patients to determine which are at higher risk of cardiovascular events and other complications, and which are most likely to respond to treatment, according to Esra Tasali, MD, of the University of Chicago, who moderated the session where the study was presented. “The field is really urgently in need of coming up with new methods, and I think this study is getting a handle on that,” said Dr. Tasali in an interview.

“I think that this is really pointing toward a new area that the whole (sleep field) is moving toward, which is better phenotyping of sleep apnea so that we can come up with more personalized treatments,” said Dr. Tasali.

The patients who appeared to gain a cardiovascular benefit from CPAP represented about 16% of trial participants. Dr. Azarbarzin refrained from making clinical recommendations, citing the need for more data. The team next plans to reproduce the findings in additional, larger trials such as the SAVE and ISAACC trials. “Ultimately, our goal is to confirm our findings in a future randomized controlled trial of CPAP by enrolling participants based on their pulse rate response,” said Dr. Azarbarzin.

The RICCADSA study was a single center randomized, controlled trial with 226 patients with coronary artery disease and OSA who were randomized to CPAP or no CPAP treatment. In the overall population, CPAP treatment was not associated with a statistically significant change in repeat revascularization, myocardial infarction, stroke, or cardiovascular mortality (hazard ratio [HR], 0.79; P = .435). That study assumed that the effect of OSA on CVD is similar across all subgroups of dHR.

The mean increase in heart rate was 7.1 beats per minute (BPM; standard deviation, 3.7). Each standard deviation increase in dHR was linked to greater CVD risk (HR, 1.45; P = .029). For each standard deviation decrease in dHR, treatment with CPAP decreased the CVD risk (HR, 0.54; P = .043).

For patients with a low dHR of 4 BPM, the hazard ratio for CVD was 0.8 with no CPAP treatment and 1.2 for CPAP treatment. For those at the mean value of 7 BPM, the HRs were 1.1 and 0.9 respectively. For those with a high dHR, (10 BPM), the hazard ratio was 1.6 without treatment and 0.7 with CPAP.

“We modeled delta heart rate interaction with CPAP, which was significant. What this means is that for someone with a mean delta heart rate of 7 beats per minute, the risk reduction (with CPAP) is similar to what RICCADSA reported. But if you look at those with high delta heart rate, the risk reduction was significantly larger. It was actually a more than 50% reduction of risk with CPAP treatment,” said Dr. Azarbarzin.

Dr. Azarbarzin has consulted for Somnifix and Apnimed and has received grants from Somnifix. Dr. Tasali has no relevant financial disclosures.

Some nonsleepy patients with coronary artery disease and obstructive sleep apnea (OSA) may receive cardiovascular benefit from continuous positive airway pressure (CPAP) therapy, according to a post hoc analysis of the RICCADSA clinical trial. That study found no benefit among patients overall, but the new analysis found that patients whose heart rate increases (delta heart rate, or dHR) more than average during apnea or hypopnea experienced fewer cardiovascular or cerebrovascular events during apnea or hypopnea when treated with CPAP.

Although RICCADSA showed no benefit, an analysis of the Multi-Ethnic Study of Atherosclerosis (MESA) and the Sleep Heart Health Study (SHHS) cohorts found that elevated pulse rate response to respiratory events was associated with greater risk of cardiovascular disease (CVD) morbidity and mortality. But the effect was seen only in nonsleepy patients. “We hypothesized that pulse rate response to apneas would predict which patients with OSA may most benefit from CPAP treatment. Now, our study suggests that there is, in fact, a subgroup of nonsleepy patients with OSA for whom CPAP could provide a reduction in risk, specifically those with a higher pulse rate response to their respiratory events,” Ali Azarbarzin, PhD, said in an interview.

Dr. Azarbarzin presented the study at the American Thoracic Society’s virtual international conference (Abstract A1103). He is in the division of sleep and circadian disorders at Brigham and Women’s Hospital, and is assistant professor of medicine at Harvard Medical School, both in Boston.

The study is in line with recent efforts to subgroup OSA patients to determine which are at higher risk of cardiovascular events and other complications, and which are most likely to respond to treatment, according to Esra Tasali, MD, of the University of Chicago, who moderated the session where the study was presented. “The field is really urgently in need of coming up with new methods, and I think this study is getting a handle on that,” said Dr. Tasali in an interview.

“I think that this is really pointing toward a new area that the whole (sleep field) is moving toward, which is better phenotyping of sleep apnea so that we can come up with more personalized treatments,” said Dr. Tasali.

The patients who appeared to gain a cardiovascular benefit from CPAP represented about 16% of trial participants. Dr. Azarbarzin refrained from making clinical recommendations, citing the need for more data. The team next plans to reproduce the findings in additional, larger trials such as the SAVE and ISAACC trials. “Ultimately, our goal is to confirm our findings in a future randomized controlled trial of CPAP by enrolling participants based on their pulse rate response,” said Dr. Azarbarzin.

The RICCADSA study was a single center randomized, controlled trial with 226 patients with coronary artery disease and OSA who were randomized to CPAP or no CPAP treatment. In the overall population, CPAP treatment was not associated with a statistically significant change in repeat revascularization, myocardial infarction, stroke, or cardiovascular mortality (hazard ratio [HR], 0.79; P = .435). That study assumed that the effect of OSA on CVD is similar across all subgroups of dHR.

The mean increase in heart rate was 7.1 beats per minute (BPM; standard deviation, 3.7). Each standard deviation increase in dHR was linked to greater CVD risk (HR, 1.45; P = .029). For each standard deviation decrease in dHR, treatment with CPAP decreased the CVD risk (HR, 0.54; P = .043).

For patients with a low dHR of 4 BPM, the hazard ratio for CVD was 0.8 with no CPAP treatment and 1.2 for CPAP treatment. For those at the mean value of 7 BPM, the HRs were 1.1 and 0.9 respectively. For those with a high dHR, (10 BPM), the hazard ratio was 1.6 without treatment and 0.7 with CPAP.

“We modeled delta heart rate interaction with CPAP, which was significant. What this means is that for someone with a mean delta heart rate of 7 beats per minute, the risk reduction (with CPAP) is similar to what RICCADSA reported. But if you look at those with high delta heart rate, the risk reduction was significantly larger. It was actually a more than 50% reduction of risk with CPAP treatment,” said Dr. Azarbarzin.

Dr. Azarbarzin has consulted for Somnifix and Apnimed and has received grants from Somnifix. Dr. Tasali has no relevant financial disclosures.

Results from the NAVIGATOR study of tezepelumab showed that treatment of adults and adolescents with severe, uncontrolled asthma with the new biologic led to a large reduction in exacerbations requiring hospital stays and ED visits.

Tezepelumab, codeveloped by Amgen and AstraZeneca, has a novel mechanism of action. It blocks thymic stromal lymphopoietin (TSLP), which is a cytokine produced by epithelial cells. TSLP levels correlate with airway obstruction, severity of disease, and glucocorticoid resistance. TSLP is involved in T2 inflammation within the airway, but also plays a role in the interactions between airway cells and immune cells, which doesn’t rely only solely on T2 inflammation. That broad mechanism of action distinguishes tezepelumab from most other biologics for the treatment of asthma, which are more targeted.

“By working at the top of the cascade, tezepelumab helps stop inflammation at a key source. Clinical trials with tezepelumab showed a clinical benefit in patients irrespective of their baseline biomarker level, including patients with low eosinophil levels at baseline,” said Jean-Pierre Llanos-Ackert, MD, who is executive medical director and global medical affairs lead for tezepelumab at Amgen.

The primary endpoint data look robust, according to Praveen Akuthota, MD, who is an associate professor of medicine at the University of California, San Diego, and comoderated the session at the American Thoracic Society’s virtual international conference, where the research was presented. The study was also published on May 13, 2021, in the New England Journal of Medicine. The conference session included updated results.

The drug holds promise, but more study is needed. “The question really will be, how is this drug different from the existing biologics? How much better is this drug in patients who have borderline T2 biomarkers, or even low T2. The study does show some efficacy in patients whose T2 signals may not be as robust. We’ll have to see with ongoing longitudinal data, how this drug positions, compared to the other agents. It’s obviously exciting, though, to have another option, given that we know what our current armamentarium of agents there are still nonresponders,” said Dr. Akuthota in an interview.

The other comoderator in the session, Laura Crotty Alexander, MD, commented: “It seems like it might work possibly even better than some that are directly covering one pathway only. Hopefully, this agent will be efficacious in a broader population than some of the more targeted biologics.” Dr. Alexander is an associate professor of medicine at the University of California, San Diego, and section chief of pulmonary critical care at the Veterans Affairs San Diego Healthcare System.

She pointed out that physicians often think of asthma patients in broad brush terms, as high or low T2, or T2 high and Th1 or neutrophilic or obese, but many patients present a more complicated picture. “There is some overlap across those phenotypes, such that an agent that works really well for one group doesn’t mean that it won’t have an impact, especially clinically, on some of these other phenotypes,” said Dr. Alexander.

Dr. Akuthota agreed. “Having options for patients whose biomarkers are not maybe as clear is, I think, important.”
 

Promising results

The study included 1,059 patients aged 12-80 who received 210 mg tezepelumab or placebo. Over 52 weeks, the treatment group had a 79% reduction in exacerbations requiring hospitalization or an ED visit, compared with placebo (rate ratio, 0.21; 95% confidence interval, 0.12-0.37), and an 85% reduction in exacerbations requiring hospitalization (RR, 0.15; 95% CI, 0.07-0.33). The drug increased the time to first exacerbation requiring hospitalization that required hospitalization or an ED visit, reducing risk by 65% (hazard ratio, 0.35; 95% CI, 0.22-0.56).

Fewer patients in the treatment group than placebo used asthma-related health care resources, including: ED visits (32 vs. 94), unscheduled visit to a specialist (285 vs. 406), telephone calls to a health care provider (234 vs. 599), ambulance transport (5 vs. 22), and home visits from a health care provider (18 vs. 22). Fewer patients in the tezepelumab group had hospital stays (3.2% vs. 7.0%), and they had a lower total number of hospital days (108 vs. 497) and days in the ICU (0 vs. 31).

The study was funded by Amgen and AstraZeneca. Dr. Llanos-Ackert is an employee of Amgen. Dr. Alexander has no relevant financial disclosures. Dr. Akuthota has consulted for AstraZeneca and participated in their clinical trials.

Results from the NAVIGATOR study of tezepelumab showed that treatment of adults and adolescents with severe, uncontrolled asthma with the new biologic led to a large reduction in exacerbations requiring hospital stays and ED visits.

Tezepelumab, codeveloped by Amgen and AstraZeneca, has a novel mechanism of action. It blocks thymic stromal lymphopoietin (TSLP), which is a cytokine produced by epithelial cells. TSLP levels correlate with airway obstruction, severity of disease, and glucocorticoid resistance. TSLP is involved in T2 inflammation within the airway, but also plays a role in the interactions between airway cells and immune cells, which doesn’t rely only solely on T2 inflammation. That broad mechanism of action distinguishes tezepelumab from most other biologics for the treatment of asthma, which are more targeted.

“By working at the top of the cascade, tezepelumab helps stop inflammation at a key source. Clinical trials with tezepelumab showed a clinical benefit in patients irrespective of their baseline biomarker level, including patients with low eosinophil levels at baseline,” said Jean-Pierre Llanos-Ackert, MD, who is executive medical director and global medical affairs lead for tezepelumab at Amgen.

The primary endpoint data look robust, according to Praveen Akuthota, MD, who is an associate professor of medicine at the University of California, San Diego, and comoderated the session at the American Thoracic Society’s virtual international conference, where the research was presented. The study was also published on May 13, 2021, in the New England Journal of Medicine. The conference session included updated results.

The drug holds promise, but more study is needed. “The question really will be, how is this drug different from the existing biologics? How much better is this drug in patients who have borderline T2 biomarkers, or even low T2. The study does show some efficacy in patients whose T2 signals may not be as robust. We’ll have to see with ongoing longitudinal data, how this drug positions, compared to the other agents. It’s obviously exciting, though, to have another option, given that we know what our current armamentarium of agents there are still nonresponders,” said Dr. Akuthota in an interview.

The other comoderator in the session, Laura Crotty Alexander, MD, commented: “It seems like it might work possibly even better than some that are directly covering one pathway only. Hopefully, this agent will be efficacious in a broader population than some of the more targeted biologics.” Dr. Alexander is an associate professor of medicine at the University of California, San Diego, and section chief of pulmonary critical care at the Veterans Affairs San Diego Healthcare System.

She pointed out that physicians often think of asthma patients in broad brush terms, as high or low T2, or T2 high and Th1 or neutrophilic or obese, but many patients present a more complicated picture. “There is some overlap across those phenotypes, such that an agent that works really well for one group doesn’t mean that it won’t have an impact, especially clinically, on some of these other phenotypes,” said Dr. Alexander.

Dr. Akuthota agreed. “Having options for patients whose biomarkers are not maybe as clear is, I think, important.”
 

Promising results

The study included 1,059 patients aged 12-80 who received 210 mg tezepelumab or placebo. Over 52 weeks, the treatment group had a 79% reduction in exacerbations requiring hospitalization or an ED visit, compared with placebo (rate ratio, 0.21; 95% confidence interval, 0.12-0.37), and an 85% reduction in exacerbations requiring hospitalization (RR, 0.15; 95% CI, 0.07-0.33). The drug increased the time to first exacerbation requiring hospitalization that required hospitalization or an ED visit, reducing risk by 65% (hazard ratio, 0.35; 95% CI, 0.22-0.56).

Fewer patients in the treatment group than placebo used asthma-related health care resources, including: ED visits (32 vs. 94), unscheduled visit to a specialist (285 vs. 406), telephone calls to a health care provider (234 vs. 599), ambulance transport (5 vs. 22), and home visits from a health care provider (18 vs. 22). Fewer patients in the tezepelumab group had hospital stays (3.2% vs. 7.0%), and they had a lower total number of hospital days (108 vs. 497) and days in the ICU (0 vs. 31).

The study was funded by Amgen and AstraZeneca. Dr. Llanos-Ackert is an employee of Amgen. Dr. Alexander has no relevant financial disclosures. Dr. Akuthota has consulted for AstraZeneca and participated in their clinical trials.

Results from the NAVIGATOR study of tezepelumab showed that treatment of adults and adolescents with severe, uncontrolled asthma with the new biologic led to a large reduction in exacerbations requiring hospital stays and ED visits.

Tezepelumab, codeveloped by Amgen and AstraZeneca, has a novel mechanism of action. It blocks thymic stromal lymphopoietin (TSLP), which is a cytokine produced by epithelial cells. TSLP levels correlate with airway obstruction, severity of disease, and glucocorticoid resistance. TSLP is involved in T2 inflammation within the airway, but also plays a role in the interactions between airway cells and immune cells, which doesn’t rely only solely on T2 inflammation. That broad mechanism of action distinguishes tezepelumab from most other biologics for the treatment of asthma, which are more targeted.

“By working at the top of the cascade, tezepelumab helps stop inflammation at a key source. Clinical trials with tezepelumab showed a clinical benefit in patients irrespective of their baseline biomarker level, including patients with low eosinophil levels at baseline,” said Jean-Pierre Llanos-Ackert, MD, who is executive medical director and global medical affairs lead for tezepelumab at Amgen.

The primary endpoint data look robust, according to Praveen Akuthota, MD, who is an associate professor of medicine at the University of California, San Diego, and comoderated the session at the American Thoracic Society’s virtual international conference, where the research was presented. The study was also published on May 13, 2021, in the New England Journal of Medicine. The conference session included updated results.

The drug holds promise, but more study is needed. “The question really will be, how is this drug different from the existing biologics? How much better is this drug in patients who have borderline T2 biomarkers, or even low T2. The study does show some efficacy in patients whose T2 signals may not be as robust. We’ll have to see with ongoing longitudinal data, how this drug positions, compared to the other agents. It’s obviously exciting, though, to have another option, given that we know what our current armamentarium of agents there are still nonresponders,” said Dr. Akuthota in an interview.

The other comoderator in the session, Laura Crotty Alexander, MD, commented: “It seems like it might work possibly even better than some that are directly covering one pathway only. Hopefully, this agent will be efficacious in a broader population than some of the more targeted biologics.” Dr. Alexander is an associate professor of medicine at the University of California, San Diego, and section chief of pulmonary critical care at the Veterans Affairs San Diego Healthcare System.

She pointed out that physicians often think of asthma patients in broad brush terms, as high or low T2, or T2 high and Th1 or neutrophilic or obese, but many patients present a more complicated picture. “There is some overlap across those phenotypes, such that an agent that works really well for one group doesn’t mean that it won’t have an impact, especially clinically, on some of these other phenotypes,” said Dr. Alexander.

Dr. Akuthota agreed. “Having options for patients whose biomarkers are not maybe as clear is, I think, important.”
 

Promising results

The study included 1,059 patients aged 12-80 who received 210 mg tezepelumab or placebo. Over 52 weeks, the treatment group had a 79% reduction in exacerbations requiring hospitalization or an ED visit, compared with placebo (rate ratio, 0.21; 95% confidence interval, 0.12-0.37), and an 85% reduction in exacerbations requiring hospitalization (RR, 0.15; 95% CI, 0.07-0.33). The drug increased the time to first exacerbation requiring hospitalization that required hospitalization or an ED visit, reducing risk by 65% (hazard ratio, 0.35; 95% CI, 0.22-0.56).

Fewer patients in the treatment group than placebo used asthma-related health care resources, including: ED visits (32 vs. 94), unscheduled visit to a specialist (285 vs. 406), telephone calls to a health care provider (234 vs. 599), ambulance transport (5 vs. 22), and home visits from a health care provider (18 vs. 22). Fewer patients in the tezepelumab group had hospital stays (3.2% vs. 7.0%), and they had a lower total number of hospital days (108 vs. 497) and days in the ICU (0 vs. 31).

The study was funded by Amgen and AstraZeneca. Dr. Llanos-Ackert is an employee of Amgen. Dr. Alexander has no relevant financial disclosures. Dr. Akuthota has consulted for AstraZeneca and participated in their clinical trials.

Adults in their 30s, 40s and 50s with chronic obstructive pulmonary disease (COPD) experience significant morbidity and excess mortality from the disease, results of a population-based study show.

Among adults aged 35-55 years with COPD in Ontario in a longitudinal population cohort study, the overall mortality rate was fivefold higher, compared with other adults in the same age range without COPD.

In contrast, the mortality rate among adults 65 years and older with COPD was 2.5-fold higher than that of their peers without COPD, reported Alina J. Blazer, MSc, MD, a clinical and research fellow at the University of Toronto.

“Overall, our study has shown that younger adults with COPD experience significant morbidity, as evidence by their elevated rates of health care use and excess mortality from their disease. This study provides further evidence that so-called ‘early’ COPD is not a benign disease, and suggests that we should focus clinical efforts on identifying COPD in younger patients, in the hopes that earlier intervention may improve their current health, reduce resource utilization, and prevent further disease progression,” she said during a minisymposium at the American Thoracic Society’s virtual international conference (Abstract A1131).

COPD is widely regarded as a disease affecting only older adults, but it can also occur in those younger than 65, and although it is commonly assumed that COPD diagnosed earlier in life will be milder in severity, this assumption has not been fully explored in real-world settings, Dr. Blazer said.

She and her colleagues conducted a study to examine disease burden as measured by health services utilization and mortality among younger adults with COPD, and compared the rates with those of older adults with COPD.

The sample for this study included 194,759 adults with COPD aged 35-55 years in Ontario in 2016. COPD was identified from health administrative data for three or more outpatient claims or one or more hospitalization claims for COPD over a 2-year period.

For context, the data were compared with those for 496,2113 COPD patients aged 65 years and older.

They found that, compared with their peers without the disease, younger adults had a 3.1-fold higher rate of hospitalization for any cause, a 2.2-fold higher rate of all-cause ED visits, and a 1.7-fold higher rate of outpatient visits for any cause.

In contrast, the comparative rates for seniors with versus without COPD were 2.1-fold, 1.8-fold, and 1.4-fold, respectively.

As noted before, the mortality rate for younger adults with COPD was 5-fold higher than for those without COPD, compared with 2.5-fold among older adults with COPD versus those without.
 

Earlier diagnosis, follow-up

“A very important talk,” commented session comoderator Valerie Press, MD, MPH, from the University of Chicago. “I know that there’s a lot of work to be done in earlier diagnosis in general, and I think starting with the younger population is a really important area.”

She asked Dr. Blazer about the possibility of asthma codiagnosis or misdiagnosis in the younger patients.

“We use a very specific, validated case definition in the study that our group has used before, and the specificity is over 96% for physician-diagnosed COPD, at the expense of sensitivity, so if anything we probably underestimated the rate of COPD in our study,” Dr. Blazer said.

Audience member Sherry Rogers, MD, an allergist and immunologist in private practice in Syracuse, N.Y., asked whether the investigators could determine what proportion of the excess mortality they saw was attributable to COPD.

“This was looking at all-cause mortality, so we don’t know that it’s necessarily all attributable to COPD per se but perhaps also to COPD-attributable comorbidities,” Dr. Blazer said. “It would be important to piece out the actual causes of mortality that are contributing to that elevated [morality] in that population.”

She added that the next step could include examining rates of specialty referrals and pharmacotherapy to see whether younger patients with COPD are receiving appropriate care, and to ascertain how they are being followed.

The study was supported by the University of Toronto and Sunnybrook Research Institute. Dr. Blazer reported no conflicts of interest to disclose.

Adults in their 30s, 40s and 50s with chronic obstructive pulmonary disease (COPD) experience significant morbidity and excess mortality from the disease, results of a population-based study show.

Among adults aged 35-55 years with COPD in Ontario in a longitudinal population cohort study, the overall mortality rate was fivefold higher, compared with other adults in the same age range without COPD.

In contrast, the mortality rate among adults 65 years and older with COPD was 2.5-fold higher than that of their peers without COPD, reported Alina J. Blazer, MSc, MD, a clinical and research fellow at the University of Toronto.

“Overall, our study has shown that younger adults with COPD experience significant morbidity, as evidence by their elevated rates of health care use and excess mortality from their disease. This study provides further evidence that so-called ‘early’ COPD is not a benign disease, and suggests that we should focus clinical efforts on identifying COPD in younger patients, in the hopes that earlier intervention may improve their current health, reduce resource utilization, and prevent further disease progression,” she said during a minisymposium at the American Thoracic Society’s virtual international conference (Abstract A1131).

COPD is widely regarded as a disease affecting only older adults, but it can also occur in those younger than 65, and although it is commonly assumed that COPD diagnosed earlier in life will be milder in severity, this assumption has not been fully explored in real-world settings, Dr. Blazer said.

She and her colleagues conducted a study to examine disease burden as measured by health services utilization and mortality among younger adults with COPD, and compared the rates with those of older adults with COPD.

The sample for this study included 194,759 adults with COPD aged 35-55 years in Ontario in 2016. COPD was identified from health administrative data for three or more outpatient claims or one or more hospitalization claims for COPD over a 2-year period.

For context, the data were compared with those for 496,2113 COPD patients aged 65 years and older.

They found that, compared with their peers without the disease, younger adults had a 3.1-fold higher rate of hospitalization for any cause, a 2.2-fold higher rate of all-cause ED visits, and a 1.7-fold higher rate of outpatient visits for any cause.

In contrast, the comparative rates for seniors with versus without COPD were 2.1-fold, 1.8-fold, and 1.4-fold, respectively.

As noted before, the mortality rate for younger adults with COPD was 5-fold higher than for those without COPD, compared with 2.5-fold among older adults with COPD versus those without.
 

Earlier diagnosis, follow-up

“A very important talk,” commented session comoderator Valerie Press, MD, MPH, from the University of Chicago. “I know that there’s a lot of work to be done in earlier diagnosis in general, and I think starting with the younger population is a really important area.”

She asked Dr. Blazer about the possibility of asthma codiagnosis or misdiagnosis in the younger patients.

“We use a very specific, validated case definition in the study that our group has used before, and the specificity is over 96% for physician-diagnosed COPD, at the expense of sensitivity, so if anything we probably underestimated the rate of COPD in our study,” Dr. Blazer said.

Audience member Sherry Rogers, MD, an allergist and immunologist in private practice in Syracuse, N.Y., asked whether the investigators could determine what proportion of the excess mortality they saw was attributable to COPD.

“This was looking at all-cause mortality, so we don’t know that it’s necessarily all attributable to COPD per se but perhaps also to COPD-attributable comorbidities,” Dr. Blazer said. “It would be important to piece out the actual causes of mortality that are contributing to that elevated [morality] in that population.”

She added that the next step could include examining rates of specialty referrals and pharmacotherapy to see whether younger patients with COPD are receiving appropriate care, and to ascertain how they are being followed.

The study was supported by the University of Toronto and Sunnybrook Research Institute. Dr. Blazer reported no conflicts of interest to disclose.

Adults in their 30s, 40s and 50s with chronic obstructive pulmonary disease (COPD) experience significant morbidity and excess mortality from the disease, results of a population-based study show.

Among adults aged 35-55 years with COPD in Ontario in a longitudinal population cohort study, the overall mortality rate was fivefold higher, compared with other adults in the same age range without COPD.

In contrast, the mortality rate among adults 65 years and older with COPD was 2.5-fold higher than that of their peers without COPD, reported Alina J. Blazer, MSc, MD, a clinical and research fellow at the University of Toronto.

“Overall, our study has shown that younger adults with COPD experience significant morbidity, as evidence by their elevated rates of health care use and excess mortality from their disease. This study provides further evidence that so-called ‘early’ COPD is not a benign disease, and suggests that we should focus clinical efforts on identifying COPD in younger patients, in the hopes that earlier intervention may improve their current health, reduce resource utilization, and prevent further disease progression,” she said during a minisymposium at the American Thoracic Society’s virtual international conference (Abstract A1131).

COPD is widely regarded as a disease affecting only older adults, but it can also occur in those younger than 65, and although it is commonly assumed that COPD diagnosed earlier in life will be milder in severity, this assumption has not been fully explored in real-world settings, Dr. Blazer said.

She and her colleagues conducted a study to examine disease burden as measured by health services utilization and mortality among younger adults with COPD, and compared the rates with those of older adults with COPD.

The sample for this study included 194,759 adults with COPD aged 35-55 years in Ontario in 2016. COPD was identified from health administrative data for three or more outpatient claims or one or more hospitalization claims for COPD over a 2-year period.

For context, the data were compared with those for 496,2113 COPD patients aged 65 years and older.

They found that, compared with their peers without the disease, younger adults had a 3.1-fold higher rate of hospitalization for any cause, a 2.2-fold higher rate of all-cause ED visits, and a 1.7-fold higher rate of outpatient visits for any cause.

In contrast, the comparative rates for seniors with versus without COPD were 2.1-fold, 1.8-fold, and 1.4-fold, respectively.

As noted before, the mortality rate for younger adults with COPD was 5-fold higher than for those without COPD, compared with 2.5-fold among older adults with COPD versus those without.
 

Earlier diagnosis, follow-up

“A very important talk,” commented session comoderator Valerie Press, MD, MPH, from the University of Chicago. “I know that there’s a lot of work to be done in earlier diagnosis in general, and I think starting with the younger population is a really important area.”

She asked Dr. Blazer about the possibility of asthma codiagnosis or misdiagnosis in the younger patients.

“We use a very specific, validated case definition in the study that our group has used before, and the specificity is over 96% for physician-diagnosed COPD, at the expense of sensitivity, so if anything we probably underestimated the rate of COPD in our study,” Dr. Blazer said.

Audience member Sherry Rogers, MD, an allergist and immunologist in private practice in Syracuse, N.Y., asked whether the investigators could determine what proportion of the excess mortality they saw was attributable to COPD.

“This was looking at all-cause mortality, so we don’t know that it’s necessarily all attributable to COPD per se but perhaps also to COPD-attributable comorbidities,” Dr. Blazer said. “It would be important to piece out the actual causes of mortality that are contributing to that elevated [morality] in that population.”

She added that the next step could include examining rates of specialty referrals and pharmacotherapy to see whether younger patients with COPD are receiving appropriate care, and to ascertain how they are being followed.

The study was supported by the University of Toronto and Sunnybrook Research Institute. Dr. Blazer reported no conflicts of interest to disclose.