CHEST Physician

Nearly 123,000 cancer deaths – or almost 30% of all cancer deaths – in the United States in 2019 were linked to cigarette smoking, a new analysis suggests.

That corresponds to more than 2 million person-years of lost life and nearly $21 billion in annual lost earnings.

“During the past few decades, smoking has substantially declined in the U.S., followed by great declines in mortality from lung cancer and some other smoking-related cancers,” said lead author Farhad Islami, MD, senior scientific director of cancer disparity research at the American Cancer Society.

AtnoYdur/Thinkstock

Despite this “remarkable progress, our results indicate that smoking is still associated with about 30% of all cancer deaths and substantial lost earnings in the U.S., and that more work should be done to further reduce smoking in the country,” he said.

The study was published online in the International Journal of Cancer.

Dr. Islami and colleagues had found that lost earnings from cancer deaths in 2015 came to nearly $95 billion. Other research showed that a substantial portion of lost earnings from cancer deaths could be traced to cigarette smoking, but estimates were more than a decade old.

To provide more recent estimates and help guide tobacco control policies, Dr. Islami and colleagues estimated person-years of life lost (PYLL) and lost earnings from cigarette smoking-related cancer deaths in 2019.

Of the 418,563 cancer deaths in adults ages 25-79 years, an estimated 122,951 could be linked to cigarette smoking. That corresponds to 29.4% of all cancer deaths and roughly 2.2 million PYLL. Translated to lost earnings, the authors estimated $20.9 billion total, with average lost earnings of $170,000 per cancer death linked to smoking.

By cancer type, lung cancer accounted for about 62%, or $12.9 billion, of the total lost earnings linked to smoking, followed by esophageal cancer (7%, or $1.5 billion), colorectal cancer (6%, or $1.2 billion), and liver cancer (5%, or $1.1 billion).

Smoking-related death rates were highest in the 13 “tobacco nation” states with weaker tobacco control policies and a higher rate of cigarette smoking. These states are Alabama, Arkansas, Indiana, Kentucky, Louisiana, Michigan, Mississippi, Missouri, Ohio, Oklahoma, South Carolina, Tennessee, and West Virginia.

The lost earnings rate in all 13 tobacco nation states combined was about 44% higher, compared with other states and the District of Columbia combined, and the annual PYLL rate was 47% higher in tobacco nation states.

The researchers estimated that if PYLL and lost earnings rates in all states matched those in Utah, which has the lowest rates, more than half of the total PYLL and lost earnings nationally would have been avoided. In other words, that would mean 1.27 million PYLL and $10.5 billion saved in 2019.

Ending the ‘scourge of tobacco’

To kick the smoking habit, health providers should “screen patients for tobacco use, document tobacco use status, advise people who smoke to quit, and assist in attempts to quit,” Dr. Islami said.

Getting more people to screen for lung cancer in the United States is also important, given that only 6.6% of eligible people in 2019 received screening.

In a statement, Lisa Lacasse, president of the American Cancer Society Cancer Action Network, said this report “further demonstrates just how critical reducing tobacco use is to ending suffering and death from cancer.”

To end the “scourge of tobacco,” local, state, and federal lawmakers need to pass proven tobacco control policies, she said.

These include regular and significant tobacco tax increases, thorough statewide smoke-free laws, and enough funding for state programs to prevent and stop smoking. It also means ensuring all Medicaid enrollees have access to all services that can help smokers quit as well as access to all FDA-approved medications that help users stop smoking.

“We have the tools to get this done, we just need lawmakers to act,” Ms. Lacasse said.

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

Nearly 123,000 cancer deaths – or almost 30% of all cancer deaths – in the United States in 2019 were linked to cigarette smoking, a new analysis suggests.

That corresponds to more than 2 million person-years of lost life and nearly $21 billion in annual lost earnings.

“During the past few decades, smoking has substantially declined in the U.S., followed by great declines in mortality from lung cancer and some other smoking-related cancers,” said lead author Farhad Islami, MD, senior scientific director of cancer disparity research at the American Cancer Society.

AtnoYdur/Thinkstock

Despite this “remarkable progress, our results indicate that smoking is still associated with about 30% of all cancer deaths and substantial lost earnings in the U.S., and that more work should be done to further reduce smoking in the country,” he said.

The study was published online in the International Journal of Cancer.

Dr. Islami and colleagues had found that lost earnings from cancer deaths in 2015 came to nearly $95 billion. Other research showed that a substantial portion of lost earnings from cancer deaths could be traced to cigarette smoking, but estimates were more than a decade old.

To provide more recent estimates and help guide tobacco control policies, Dr. Islami and colleagues estimated person-years of life lost (PYLL) and lost earnings from cigarette smoking-related cancer deaths in 2019.

Of the 418,563 cancer deaths in adults ages 25-79 years, an estimated 122,951 could be linked to cigarette smoking. That corresponds to 29.4% of all cancer deaths and roughly 2.2 million PYLL. Translated to lost earnings, the authors estimated $20.9 billion total, with average lost earnings of $170,000 per cancer death linked to smoking.

By cancer type, lung cancer accounted for about 62%, or $12.9 billion, of the total lost earnings linked to smoking, followed by esophageal cancer (7%, or $1.5 billion), colorectal cancer (6%, or $1.2 billion), and liver cancer (5%, or $1.1 billion).

Smoking-related death rates were highest in the 13 “tobacco nation” states with weaker tobacco control policies and a higher rate of cigarette smoking. These states are Alabama, Arkansas, Indiana, Kentucky, Louisiana, Michigan, Mississippi, Missouri, Ohio, Oklahoma, South Carolina, Tennessee, and West Virginia.

The lost earnings rate in all 13 tobacco nation states combined was about 44% higher, compared with other states and the District of Columbia combined, and the annual PYLL rate was 47% higher in tobacco nation states.

The researchers estimated that if PYLL and lost earnings rates in all states matched those in Utah, which has the lowest rates, more than half of the total PYLL and lost earnings nationally would have been avoided. In other words, that would mean 1.27 million PYLL and $10.5 billion saved in 2019.

Ending the ‘scourge of tobacco’

To kick the smoking habit, health providers should “screen patients for tobacco use, document tobacco use status, advise people who smoke to quit, and assist in attempts to quit,” Dr. Islami said.

Getting more people to screen for lung cancer in the United States is also important, given that only 6.6% of eligible people in 2019 received screening.

In a statement, Lisa Lacasse, president of the American Cancer Society Cancer Action Network, said this report “further demonstrates just how critical reducing tobacco use is to ending suffering and death from cancer.”

To end the “scourge of tobacco,” local, state, and federal lawmakers need to pass proven tobacco control policies, she said.

These include regular and significant tobacco tax increases, thorough statewide smoke-free laws, and enough funding for state programs to prevent and stop smoking. It also means ensuring all Medicaid enrollees have access to all services that can help smokers quit as well as access to all FDA-approved medications that help users stop smoking.

“We have the tools to get this done, we just need lawmakers to act,” Ms. Lacasse said.

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

Nearly 123,000 cancer deaths – or almost 30% of all cancer deaths – in the United States in 2019 were linked to cigarette smoking, a new analysis suggests.

That corresponds to more than 2 million person-years of lost life and nearly $21 billion in annual lost earnings.

“During the past few decades, smoking has substantially declined in the U.S., followed by great declines in mortality from lung cancer and some other smoking-related cancers,” said lead author Farhad Islami, MD, senior scientific director of cancer disparity research at the American Cancer Society.

AtnoYdur/Thinkstock

Despite this “remarkable progress, our results indicate that smoking is still associated with about 30% of all cancer deaths and substantial lost earnings in the U.S., and that more work should be done to further reduce smoking in the country,” he said.

The study was published online in the International Journal of Cancer.

Dr. Islami and colleagues had found that lost earnings from cancer deaths in 2015 came to nearly $95 billion. Other research showed that a substantial portion of lost earnings from cancer deaths could be traced to cigarette smoking, but estimates were more than a decade old.

To provide more recent estimates and help guide tobacco control policies, Dr. Islami and colleagues estimated person-years of life lost (PYLL) and lost earnings from cigarette smoking-related cancer deaths in 2019.

Of the 418,563 cancer deaths in adults ages 25-79 years, an estimated 122,951 could be linked to cigarette smoking. That corresponds to 29.4% of all cancer deaths and roughly 2.2 million PYLL. Translated to lost earnings, the authors estimated $20.9 billion total, with average lost earnings of $170,000 per cancer death linked to smoking.

By cancer type, lung cancer accounted for about 62%, or $12.9 billion, of the total lost earnings linked to smoking, followed by esophageal cancer (7%, or $1.5 billion), colorectal cancer (6%, or $1.2 billion), and liver cancer (5%, or $1.1 billion).

Smoking-related death rates were highest in the 13 “tobacco nation” states with weaker tobacco control policies and a higher rate of cigarette smoking. These states are Alabama, Arkansas, Indiana, Kentucky, Louisiana, Michigan, Mississippi, Missouri, Ohio, Oklahoma, South Carolina, Tennessee, and West Virginia.

The lost earnings rate in all 13 tobacco nation states combined was about 44% higher, compared with other states and the District of Columbia combined, and the annual PYLL rate was 47% higher in tobacco nation states.

The researchers estimated that if PYLL and lost earnings rates in all states matched those in Utah, which has the lowest rates, more than half of the total PYLL and lost earnings nationally would have been avoided. In other words, that would mean 1.27 million PYLL and $10.5 billion saved in 2019.

Ending the ‘scourge of tobacco’

To kick the smoking habit, health providers should “screen patients for tobacco use, document tobacco use status, advise people who smoke to quit, and assist in attempts to quit,” Dr. Islami said.

Getting more people to screen for lung cancer in the United States is also important, given that only 6.6% of eligible people in 2019 received screening.

In a statement, Lisa Lacasse, president of the American Cancer Society Cancer Action Network, said this report “further demonstrates just how critical reducing tobacco use is to ending suffering and death from cancer.”

To end the “scourge of tobacco,” local, state, and federal lawmakers need to pass proven tobacco control policies, she said.

These include regular and significant tobacco tax increases, thorough statewide smoke-free laws, and enough funding for state programs to prevent and stop smoking. It also means ensuring all Medicaid enrollees have access to all services that can help smokers quit as well as access to all FDA-approved medications that help users stop smoking.

“We have the tools to get this done, we just need lawmakers to act,” Ms. Lacasse said.

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

Lower levels of serum sclerostin (SOST) were significantly associated with increased risk of lung exacerbations and hospitalizations in adults with chronic obstructive pulmonary disease (COPD), based on data from 139 individuals.

COPD exacerbations contribute to poorer prognosis and diminished quality of life, but many potential triggers of these exacerbations, including serum biomarkers, have not been well studied, wrote Carlos A. Amado, MD, of Hospital Universitario Marqués de Valdecilla, Santander, Spain, and colleagues.

These biomarkers include sclerostin, which is associated with bone metabolism and may play a role in “muscle-bone crosstalk,” thereby impacting lung function, they said.

In a study published in Pulmonology, the researchers recruited 139 adult outpatients with stable COPD and normal kidney function who were treated at a single center. The patients were followed for 12 months after study enrollment and a baseline assessment of serum SOST, bone metabolism parameters, body composition, clinical characteristics, and lung function. The mean age of the participants was 65.8 years, and 71% were men. Notably, 41.7% of the participants were current smokers. Body composition was assessed using fat-free mass index (FFMI), and lung function was assessed using forced expiratory volume in the first second (FEV1) and forced vital capacity (FVC).

A total of 55 patients had SOST levels of 20 pmol/L at baseline, and 84 had SOST levels greater than 20 pmol/L. In a multivariate analysis, only age and FFMI were positively correlated with SOST levels (beta = 0.264 and beta = 1.241, respectively).

Patients in the lower tertile of SOST levels had a significantly higher risk of moderate COPD exacerbation (hazard ratio, 2.015; P = .017) and hospital admission related to COPD (HR, 5.142; P = .015), compared with the other patients. Also in a multivariate analysis, low levels of SOST were independently associated with FFMI (odds ratio, 1.936; P = .004) but not with any of the other variables.

“We can only speculate about the possible causes and effects of low SOST in COPD,” the researchers wrote in their discussion. However, “we found that SOST and FFMI were positively associated in patients with COPD; therefore, lower levels of circulating SOST might reflect sarcopenia,” they noted. Low levels of muscle mass are associated with COPD exacerbations, they added.

The study findings were limited by several factors, including the use of patients from only one center and the high prevalence of hypovitaminosis D in the study population. The study also was not designed to show causality, the researchers said.

However, the results were strengthened by their specific design and overall well-selected population, as well as the evaluation of bone metabolism, they said.

The study offers the first evidence of an association between SOST and clinical outcomes in COPD “and may have a role as a biomarker to evaluate the risk of exacerbation and hospitalization in COPD,” but more research is needed in other populations to fully evaluate the therapeutic aspects of the study findings, the researchers concluded.

The study was supported by the Instituto de Investigación Sanitaria of Cantabria. The researchers disclosed no financial conflicts.

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

Lower levels of serum sclerostin (SOST) were significantly associated with increased risk of lung exacerbations and hospitalizations in adults with chronic obstructive pulmonary disease (COPD), based on data from 139 individuals.

COPD exacerbations contribute to poorer prognosis and diminished quality of life, but many potential triggers of these exacerbations, including serum biomarkers, have not been well studied, wrote Carlos A. Amado, MD, of Hospital Universitario Marqués de Valdecilla, Santander, Spain, and colleagues.

These biomarkers include sclerostin, which is associated with bone metabolism and may play a role in “muscle-bone crosstalk,” thereby impacting lung function, they said.

In a study published in Pulmonology, the researchers recruited 139 adult outpatients with stable COPD and normal kidney function who were treated at a single center. The patients were followed for 12 months after study enrollment and a baseline assessment of serum SOST, bone metabolism parameters, body composition, clinical characteristics, and lung function. The mean age of the participants was 65.8 years, and 71% were men. Notably, 41.7% of the participants were current smokers. Body composition was assessed using fat-free mass index (FFMI), and lung function was assessed using forced expiratory volume in the first second (FEV1) and forced vital capacity (FVC).

A total of 55 patients had SOST levels of 20 pmol/L at baseline, and 84 had SOST levels greater than 20 pmol/L. In a multivariate analysis, only age and FFMI were positively correlated with SOST levels (beta = 0.264 and beta = 1.241, respectively).

Patients in the lower tertile of SOST levels had a significantly higher risk of moderate COPD exacerbation (hazard ratio, 2.015; P = .017) and hospital admission related to COPD (HR, 5.142; P = .015), compared with the other patients. Also in a multivariate analysis, low levels of SOST were independently associated with FFMI (odds ratio, 1.936; P = .004) but not with any of the other variables.

“We can only speculate about the possible causes and effects of low SOST in COPD,” the researchers wrote in their discussion. However, “we found that SOST and FFMI were positively associated in patients with COPD; therefore, lower levels of circulating SOST might reflect sarcopenia,” they noted. Low levels of muscle mass are associated with COPD exacerbations, they added.

The study findings were limited by several factors, including the use of patients from only one center and the high prevalence of hypovitaminosis D in the study population. The study also was not designed to show causality, the researchers said.

However, the results were strengthened by their specific design and overall well-selected population, as well as the evaluation of bone metabolism, they said.

The study offers the first evidence of an association between SOST and clinical outcomes in COPD “and may have a role as a biomarker to evaluate the risk of exacerbation and hospitalization in COPD,” but more research is needed in other populations to fully evaluate the therapeutic aspects of the study findings, the researchers concluded.

The study was supported by the Instituto de Investigación Sanitaria of Cantabria. The researchers disclosed no financial conflicts.

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

Lower levels of serum sclerostin (SOST) were significantly associated with increased risk of lung exacerbations and hospitalizations in adults with chronic obstructive pulmonary disease (COPD), based on data from 139 individuals.

COPD exacerbations contribute to poorer prognosis and diminished quality of life, but many potential triggers of these exacerbations, including serum biomarkers, have not been well studied, wrote Carlos A. Amado, MD, of Hospital Universitario Marqués de Valdecilla, Santander, Spain, and colleagues.

These biomarkers include sclerostin, which is associated with bone metabolism and may play a role in “muscle-bone crosstalk,” thereby impacting lung function, they said.

In a study published in Pulmonology, the researchers recruited 139 adult outpatients with stable COPD and normal kidney function who were treated at a single center. The patients were followed for 12 months after study enrollment and a baseline assessment of serum SOST, bone metabolism parameters, body composition, clinical characteristics, and lung function. The mean age of the participants was 65.8 years, and 71% were men. Notably, 41.7% of the participants were current smokers. Body composition was assessed using fat-free mass index (FFMI), and lung function was assessed using forced expiratory volume in the first second (FEV1) and forced vital capacity (FVC).

A total of 55 patients had SOST levels of 20 pmol/L at baseline, and 84 had SOST levels greater than 20 pmol/L. In a multivariate analysis, only age and FFMI were positively correlated with SOST levels (beta = 0.264 and beta = 1.241, respectively).

Patients in the lower tertile of SOST levels had a significantly higher risk of moderate COPD exacerbation (hazard ratio, 2.015; P = .017) and hospital admission related to COPD (HR, 5.142; P = .015), compared with the other patients. Also in a multivariate analysis, low levels of SOST were independently associated with FFMI (odds ratio, 1.936; P = .004) but not with any of the other variables.

“We can only speculate about the possible causes and effects of low SOST in COPD,” the researchers wrote in their discussion. However, “we found that SOST and FFMI were positively associated in patients with COPD; therefore, lower levels of circulating SOST might reflect sarcopenia,” they noted. Low levels of muscle mass are associated with COPD exacerbations, they added.

The study findings were limited by several factors, including the use of patients from only one center and the high prevalence of hypovitaminosis D in the study population. The study also was not designed to show causality, the researchers said.

However, the results were strengthened by their specific design and overall well-selected population, as well as the evaluation of bone metabolism, they said.

The study offers the first evidence of an association between SOST and clinical outcomes in COPD “and may have a role as a biomarker to evaluate the risk of exacerbation and hospitalization in COPD,” but more research is needed in other populations to fully evaluate the therapeutic aspects of the study findings, the researchers concluded.

The study was supported by the Instituto de Investigación Sanitaria of Cantabria. The researchers disclosed no financial conflicts.

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

Early in 2020, Anne Peters, MD, caught COVID-19. The author of Medscape’s “Peters on Diabetes” column was sick in March 2020 before state-mandated lockdowns, and well before there were any vaccines.

She remembers sitting in a small exam room with two patients who had flown to her Los Angeles office from New York. The elderly couple had hearing difficulties, so Dr. Peters sat close to them, putting on a continuous glucose monitor. “At that time, we didn’t think of COVID-19 as being in L.A.,” Dr. Peters recalled, “so I think we were not terribly consistent at mask-wearing due to the need to educate.”

“Several days later, I got COVID, but I didn’t know I had COVID per se. I felt crappy, had a terrible sore throat, lost my sense of taste and smell [which was not yet described as a COVID symptom], was completely exhausted, but had no fever or cough, which were the only criteria for getting COVID tested at the time. I didn’t know I had been exposed until 2 weeks later, when the patient’s assistant returned the sensor warning us to ‘be careful’ with it because the patient and his wife were recovering from COVID.”

That early battle with COVID-19 was just the beginning of what would become a 2-year struggle, including familial loss amid her own health problems and concerns about the under-resourced patients she cares for. Here, she shares her journey through the pandemic with this news organization.
 

Question: Thanks for talking to us. Let’s discuss your journey over these past 2.5 years.

Answer: Everybody has their own COVID story because we all went through this together. Some of us have worse COVID stories, and some of us have better ones, but all have been impacted.

I’m not a sick person. I’m a very healthy person but COVID made me so unwell for 2 years. The brain fog and fatigue were nothing compared to the autonomic neuropathy that affected my heart. It was really limiting for me. And I still don’t know the long-term implications, looking 20-30 years from now.
 

Q: When you initially had COVID, what were your symptoms? What was the impact?

A: I had all the symptoms of COVID, except for a cough and fever. I lost my sense of taste and smell. I had a horrible headache, a sore throat, and I was exhausted. I couldn’t get tested because I didn’t have the right symptoms.

Despite being sick, I never stopped working but just switched to telemedicine. I also took my regular monthly trip to our cabin in Montana. I unknowingly flew on a plane with COVID. I wore a well-fitted N95 mask, so I don’t think I gave anybody COVID. I didn’t give COVID to my partner, Eric, which is hard to believe as – at 77 – he’s older than me. He has diabetes, heart disease, and every other high-risk characteristic. If he’d gotten COVID back then, it would have been terrible, as there were no treatments, but luckily he didn’t get it.
 

Q: When were you officially diagnosed?

A: Two or 3 months after I thought I might have had COVID, I checked my antibodies, which tested strongly positive for a prior COVID infection. That was when I knew all the symptoms I’d had were due to the disease.

Q: Not only were you dealing with your own illness, but also that of those close to you. Can you talk about that?

A: In April 2020, my mother who was in her 90s and otherwise healthy except for dementia, got COVID. She could have gotten it from me. I visited often but wore a mask. She had all the horrible pulmonary symptoms. In her advance directive, she didn’t want to be hospitalized so I kept her in her home. She died from COVID in her own bed. It was fairly brutal, but at least I kept her where she felt comforted.

My 91-year-old dad was living in a different residential facility. Throughout COVID he had become very depressed because his social patterns had changed. Prior to COVID, they all ate together, but during the pandemic they were unable to. He missed his social connections, disliked being isolated in his room, hated everyone in masks.

He was a bit demented, but not so much that he couldn’t communicate with me or remember where his grandson was going to law school. I wasn’t allowed inside the facility, which was hard on him. I hadn’t told him his wife died because the hospice social workers advised me that I shouldn’t give him news that he couldn’t process readily until I could spend time with him. Unfortunately, that time never came. In December 2020, he got COVID. One of the people in that facility had gone to the hospital, came back, and tested negative, but actually had COVID and gave it to my dad. The guy who gave it to my dad didn’t die but my dad was terribly ill. He died 2 weeks short of getting his vaccine. He was coherent enough to have a conversation. I asked him: ‘Do you want to go to the hospital?’ And he said: ‘No, because it would be too scary,’ since he couldn’t be with me. I put him on hospice and held his hand as he died from pulmonary COVID, which was awful. I couldn’t give him enough morphine or valium to ease his breathing. But his last words to me were “I love you,” and at the very end he seemed peaceful, which was a blessing.

I got an autopsy, because he wanted one. Nothing else was wrong with him other than COVID. It destroyed his lungs. The rest of him was fine – no heart disease, cancer, or anything else. He died of COVID-19, the same as my mother.

That same week, my aunt, my only surviving older relative, who was in Des Moines, Iowa, died of COVID-19. All three family members died before the vaccine came out.

It was hard to lose my parents. I’m the only surviving child because my sister died in her 20s. It’s not been an easy pandemic. But what pandemic is easy? I just happened to have lost more people than most. Ironically, my grandfather was one of the legionnaires at the Bellevue-Stratford Hotel in Philadelphia in 1976 and died of Legionnaire’s disease before we knew what was causing the outbreak.
 

Q: Were you still struggling with COVID?

A: COVID impacted my whole body. I lost a lot of weight. I didn’t want to eat, and my gastrointestinal system was not happy. It took a while for my sense of taste and smell to come back. Nothing tasted good. I’m not a foodie; I don’t really care about food. We could get takeout or whatever, but none of it appealed to me. I’m not so sure it was a taste thing, I just didn’t feel like eating.

I didn’t realize I had “brain fog” per se, because I felt stressed and overwhelmed by the pandemic and my patients’ concerns. But one day, about 3 months after I had developed COVID, I woke up without the fog. Which made me aware that I hadn’t been feeling right up until that point.

The worst symptoms, however, were cardiac. I noticed also immediately that my heart rate went up very quickly with minimal exertion. My pulse has always been in the 55-60 bpm range, and suddenly just walking across a room made it go up to over 140 bpm. If I did any aerobic activity, it went up over 160 and would be associated with dyspnea and chest pain. I believed these were all post-COVID symptoms and felt validated when reports of others having similar issues were published in the literature.

Q: Did you continue seeing patients?

A: Yes, of course. Patients never needed their doctors more. In East L.A., where patients don’t have easy access to telemedicine, I kept going into clinic throughout the pandemic. In the more affluent Westside of Los Angeles, we switched to telemedicine, which was quite effective for most. However, because diabetes was associated with an increased risk of hospitalization and death from COVID, my patients were understandably afraid. I’ve never been busier, but (like all health care providers), I became more of a COVID provider than a diabetologist.

Q: Do you feel your battle with COVID impacted your work?

A: It didn’t affect me at work. If I was sitting still, I was fine. Sitting at home at a desk, I didn’t notice any symptoms. But as a habitual stair-user, I would be gasping for breath in the stairwell because I couldn’t go up the stairs to my office as I once could.

I think you empathize more with people who had COVID (when you’ve had it yourself). There was such a huge patient burden. And I think that’s been the thing that’s affected health care providers the most – no matter what specialty we’re in – that nobody has answers.
 

Q: What happened after you had your vaccine?

A: The vaccine itself was fine. I didn’t have any reaction to the first two doses. But the first booster made my cardiac issues worse.

By this point, my cardiac problems stopped me from exercising. I even went to the ER with chest pain once because I was having palpitations and chest pressure caused by simply taking my morning shower. Fortunately, I wasn’t having an MI, but I certainly wasn’t “normal.”

My measure of my fitness is the cross-country skiing trail I use in Montana. I know exactly how far I can ski. Usually I can do the loop in 35 minutes. After COVID, I lasted 10 minutes. I would be tachycardic, short of breath with chest pain radiating down my left arm. I would rest and try to keep going. But with each rest period, I only got worse. I would be laying in the snow and strangers would ask if I needed help.
 

Q: What helped you?

A: I’ve read a lot about long COVID and have tried to learn from the experts. Of course, I never went to a doctor directly, although I did ask colleagues for advice. What I learned was to never push myself. I forced myself to create an exercise schedule where I only exercised three times a week with rest days in between. When exercising, the second my heart rate went above 140 bpm, I stopped until I could get it back down. I would push against this new limit, even though my limit was low.

Additionally, I worked on my breathing patterns and did meditative breathing for 10 minutes twice daily using a commercially available app.

Although progress was slow, I did improve, and by June 2022, I seemed back to normal. I was not as fit as I was prior to COVID and needed to improve, but the tachycardic response to exercise and cardiac symptoms were gone. I felt like my normal self. Normal enough to go on a spot packing trip in the Sierras in August. (Horses carried us and a mule carried the gear over the 12,000-foot pass into the mountains, and then left my friend and me high in the Sierras for a week.) We were camped above 10,000 feet and every day hiked up to another high mountain lake where we fly-fished for trout that we ate for dinner. The hikes were a challenge, but not abnormally so. Not as they would have been while I had long COVID.
 

Q: What is the current atmosphere in your clinic?

A: COVID is much milder now in my vaccinated patients, but I feel most health care providers are exhausted. Many of my staff left when COVID hit because they didn’t want to keep working. It made practicing medicine exhausting. There’s been a shortage of nurses, a shortage of everything. We’ve been required to do a whole lot more than we ever did before. It’s much harder to be a doctor. This pandemic is the first time I’ve ever thought of quitting. Granted, I lost my whole family, or at least the older generation, but it’s just been almost overwhelming.

On the plus side, almost every one of my patients has been vaccinated, because early on, people would ask: “Do you trust this vaccine?” I would reply: “I saw my parents die from COVID when they weren’t vaccinated, so you’re getting vaccinated. This is real and the vaccines help.” It made me very good at convincing people to get vaccines because I knew what it was like to see someone dying from COVID up close.
 

Q: What advice do you have for those struggling with the COVID pandemic?

A: People need to decide what their own risk is for getting sick and how many times they want to get COVID. At this point, I want people to go out, but safely. In the beginning, when my patients said, “can I go visit my granddaughter?” I said, “no,” but that was before we had the vaccine. Now I feel it is safe to go out using common sense. I still have my patients wear masks on planes. I still have patients try to eat outside as much as possible. And I tell people to take the precautions that make sense, but I tell them to go out and do things because life is short.

I had a patient in his 70s who has many risk factors like heart disease and diabetes. His granddaughter’s Bat Mitzvah in Florida was coming up. He asked: “Can I go?” I told him “Yes,” but to be safe – to wear an N95 mask on the plane and at the event, and stay in his own hotel room, rather than with the whole family. I said, “You need to do this.” Earlier in the pandemic, I saw people who literally died from loneliness and isolation.

He and his wife flew there. He sent me a picture of himself with his granddaughter. When he returned, he showed me a handwritten note from her that said, “I love you so much. Everyone else canceled, which made me cry. You’re the only one who came. You have no idea how much this meant to me.”

He’s back in L.A., and he didn’t get COVID. He said, “It was the best thing I’ve done in years.” That’s what I need to help people with, navigating this world with COVID and assessing risks and benefits. As with all of medicine, my advice is individualized. My advice changes based on the major circulating variant and the rates of the virus in the population, as well as the risk factors of the individual.
 

Q: What are you doing now?

A: I’m trying to avoid getting COVID again, or another booster. I could get pre-exposure monoclonal antibodies but am waiting to do anything further until I see what happens over the fall and winter. I still wear a mask inside but now do a mix of in-person and telemedicine visits. I still try to go to outdoor restaurants, which is easy in California. But I’m flying to see my son in New York and plan to go to Europe this fall for a meeting. I also go to my cabin in Montana every month to get my “dose” of the wilderness. Overall, I travel for conferences and speaking engagements much less because I have learned the joy of staying home.

Thinking back on my life as a doctor, my career began as an intern at Stanford rotating through Ward 5B, the AIDS unit at San Francisco General Hospital, and will likely end with COVID. In spite of all our medical advances, my generation of physicians, much as many generations before us, has a front-row seat to the vulnerability of humans to infectious diseases and how far we still need to go to protect our patients from communicable illness.

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

Anne L. Peters, MD, is a professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts; three books on diabetes; and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations.

Early in 2020, Anne Peters, MD, caught COVID-19. The author of Medscape’s “Peters on Diabetes” column was sick in March 2020 before state-mandated lockdowns, and well before there were any vaccines.

She remembers sitting in a small exam room with two patients who had flown to her Los Angeles office from New York. The elderly couple had hearing difficulties, so Dr. Peters sat close to them, putting on a continuous glucose monitor. “At that time, we didn’t think of COVID-19 as being in L.A.,” Dr. Peters recalled, “so I think we were not terribly consistent at mask-wearing due to the need to educate.”

“Several days later, I got COVID, but I didn’t know I had COVID per se. I felt crappy, had a terrible sore throat, lost my sense of taste and smell [which was not yet described as a COVID symptom], was completely exhausted, but had no fever or cough, which were the only criteria for getting COVID tested at the time. I didn’t know I had been exposed until 2 weeks later, when the patient’s assistant returned the sensor warning us to ‘be careful’ with it because the patient and his wife were recovering from COVID.”

That early battle with COVID-19 was just the beginning of what would become a 2-year struggle, including familial loss amid her own health problems and concerns about the under-resourced patients she cares for. Here, she shares her journey through the pandemic with this news organization.
 

Question: Thanks for talking to us. Let’s discuss your journey over these past 2.5 years.

Answer: Everybody has their own COVID story because we all went through this together. Some of us have worse COVID stories, and some of us have better ones, but all have been impacted.

I’m not a sick person. I’m a very healthy person but COVID made me so unwell for 2 years. The brain fog and fatigue were nothing compared to the autonomic neuropathy that affected my heart. It was really limiting for me. And I still don’t know the long-term implications, looking 20-30 years from now.
 

Q: When you initially had COVID, what were your symptoms? What was the impact?

A: I had all the symptoms of COVID, except for a cough and fever. I lost my sense of taste and smell. I had a horrible headache, a sore throat, and I was exhausted. I couldn’t get tested because I didn’t have the right symptoms.

Despite being sick, I never stopped working but just switched to telemedicine. I also took my regular monthly trip to our cabin in Montana. I unknowingly flew on a plane with COVID. I wore a well-fitted N95 mask, so I don’t think I gave anybody COVID. I didn’t give COVID to my partner, Eric, which is hard to believe as – at 77 – he’s older than me. He has diabetes, heart disease, and every other high-risk characteristic. If he’d gotten COVID back then, it would have been terrible, as there were no treatments, but luckily he didn’t get it.
 

Q: When were you officially diagnosed?

A: Two or 3 months after I thought I might have had COVID, I checked my antibodies, which tested strongly positive for a prior COVID infection. That was when I knew all the symptoms I’d had were due to the disease.

Q: Not only were you dealing with your own illness, but also that of those close to you. Can you talk about that?

A: In April 2020, my mother who was in her 90s and otherwise healthy except for dementia, got COVID. She could have gotten it from me. I visited often but wore a mask. She had all the horrible pulmonary symptoms. In her advance directive, she didn’t want to be hospitalized so I kept her in her home. She died from COVID in her own bed. It was fairly brutal, but at least I kept her where she felt comforted.

My 91-year-old dad was living in a different residential facility. Throughout COVID he had become very depressed because his social patterns had changed. Prior to COVID, they all ate together, but during the pandemic they were unable to. He missed his social connections, disliked being isolated in his room, hated everyone in masks.

He was a bit demented, but not so much that he couldn’t communicate with me or remember where his grandson was going to law school. I wasn’t allowed inside the facility, which was hard on him. I hadn’t told him his wife died because the hospice social workers advised me that I shouldn’t give him news that he couldn’t process readily until I could spend time with him. Unfortunately, that time never came. In December 2020, he got COVID. One of the people in that facility had gone to the hospital, came back, and tested negative, but actually had COVID and gave it to my dad. The guy who gave it to my dad didn’t die but my dad was terribly ill. He died 2 weeks short of getting his vaccine. He was coherent enough to have a conversation. I asked him: ‘Do you want to go to the hospital?’ And he said: ‘No, because it would be too scary,’ since he couldn’t be with me. I put him on hospice and held his hand as he died from pulmonary COVID, which was awful. I couldn’t give him enough morphine or valium to ease his breathing. But his last words to me were “I love you,” and at the very end he seemed peaceful, which was a blessing.

I got an autopsy, because he wanted one. Nothing else was wrong with him other than COVID. It destroyed his lungs. The rest of him was fine – no heart disease, cancer, or anything else. He died of COVID-19, the same as my mother.

That same week, my aunt, my only surviving older relative, who was in Des Moines, Iowa, died of COVID-19. All three family members died before the vaccine came out.

It was hard to lose my parents. I’m the only surviving child because my sister died in her 20s. It’s not been an easy pandemic. But what pandemic is easy? I just happened to have lost more people than most. Ironically, my grandfather was one of the legionnaires at the Bellevue-Stratford Hotel in Philadelphia in 1976 and died of Legionnaire’s disease before we knew what was causing the outbreak.
 

Q: Were you still struggling with COVID?

A: COVID impacted my whole body. I lost a lot of weight. I didn’t want to eat, and my gastrointestinal system was not happy. It took a while for my sense of taste and smell to come back. Nothing tasted good. I’m not a foodie; I don’t really care about food. We could get takeout or whatever, but none of it appealed to me. I’m not so sure it was a taste thing, I just didn’t feel like eating.

I didn’t realize I had “brain fog” per se, because I felt stressed and overwhelmed by the pandemic and my patients’ concerns. But one day, about 3 months after I had developed COVID, I woke up without the fog. Which made me aware that I hadn’t been feeling right up until that point.

The worst symptoms, however, were cardiac. I noticed also immediately that my heart rate went up very quickly with minimal exertion. My pulse has always been in the 55-60 bpm range, and suddenly just walking across a room made it go up to over 140 bpm. If I did any aerobic activity, it went up over 160 and would be associated with dyspnea and chest pain. I believed these were all post-COVID symptoms and felt validated when reports of others having similar issues were published in the literature.

Q: Did you continue seeing patients?

A: Yes, of course. Patients never needed their doctors more. In East L.A., where patients don’t have easy access to telemedicine, I kept going into clinic throughout the pandemic. In the more affluent Westside of Los Angeles, we switched to telemedicine, which was quite effective for most. However, because diabetes was associated with an increased risk of hospitalization and death from COVID, my patients were understandably afraid. I’ve never been busier, but (like all health care providers), I became more of a COVID provider than a diabetologist.

Q: Do you feel your battle with COVID impacted your work?

A: It didn’t affect me at work. If I was sitting still, I was fine. Sitting at home at a desk, I didn’t notice any symptoms. But as a habitual stair-user, I would be gasping for breath in the stairwell because I couldn’t go up the stairs to my office as I once could.

I think you empathize more with people who had COVID (when you’ve had it yourself). There was such a huge patient burden. And I think that’s been the thing that’s affected health care providers the most – no matter what specialty we’re in – that nobody has answers.
 

Q: What happened after you had your vaccine?

A: The vaccine itself was fine. I didn’t have any reaction to the first two doses. But the first booster made my cardiac issues worse.

By this point, my cardiac problems stopped me from exercising. I even went to the ER with chest pain once because I was having palpitations and chest pressure caused by simply taking my morning shower. Fortunately, I wasn’t having an MI, but I certainly wasn’t “normal.”

My measure of my fitness is the cross-country skiing trail I use in Montana. I know exactly how far I can ski. Usually I can do the loop in 35 minutes. After COVID, I lasted 10 minutes. I would be tachycardic, short of breath with chest pain radiating down my left arm. I would rest and try to keep going. But with each rest period, I only got worse. I would be laying in the snow and strangers would ask if I needed help.
 

Q: What helped you?

A: I’ve read a lot about long COVID and have tried to learn from the experts. Of course, I never went to a doctor directly, although I did ask colleagues for advice. What I learned was to never push myself. I forced myself to create an exercise schedule where I only exercised three times a week with rest days in between. When exercising, the second my heart rate went above 140 bpm, I stopped until I could get it back down. I would push against this new limit, even though my limit was low.

Additionally, I worked on my breathing patterns and did meditative breathing for 10 minutes twice daily using a commercially available app.

Although progress was slow, I did improve, and by June 2022, I seemed back to normal. I was not as fit as I was prior to COVID and needed to improve, but the tachycardic response to exercise and cardiac symptoms were gone. I felt like my normal self. Normal enough to go on a spot packing trip in the Sierras in August. (Horses carried us and a mule carried the gear over the 12,000-foot pass into the mountains, and then left my friend and me high in the Sierras for a week.) We were camped above 10,000 feet and every day hiked up to another high mountain lake where we fly-fished for trout that we ate for dinner. The hikes were a challenge, but not abnormally so. Not as they would have been while I had long COVID.
 

Q: What is the current atmosphere in your clinic?

A: COVID is much milder now in my vaccinated patients, but I feel most health care providers are exhausted. Many of my staff left when COVID hit because they didn’t want to keep working. It made practicing medicine exhausting. There’s been a shortage of nurses, a shortage of everything. We’ve been required to do a whole lot more than we ever did before. It’s much harder to be a doctor. This pandemic is the first time I’ve ever thought of quitting. Granted, I lost my whole family, or at least the older generation, but it’s just been almost overwhelming.

On the plus side, almost every one of my patients has been vaccinated, because early on, people would ask: “Do you trust this vaccine?” I would reply: “I saw my parents die from COVID when they weren’t vaccinated, so you’re getting vaccinated. This is real and the vaccines help.” It made me very good at convincing people to get vaccines because I knew what it was like to see someone dying from COVID up close.
 

Q: What advice do you have for those struggling with the COVID pandemic?

A: People need to decide what their own risk is for getting sick and how many times they want to get COVID. At this point, I want people to go out, but safely. In the beginning, when my patients said, “can I go visit my granddaughter?” I said, “no,” but that was before we had the vaccine. Now I feel it is safe to go out using common sense. I still have my patients wear masks on planes. I still have patients try to eat outside as much as possible. And I tell people to take the precautions that make sense, but I tell them to go out and do things because life is short.

I had a patient in his 70s who has many risk factors like heart disease and diabetes. His granddaughter’s Bat Mitzvah in Florida was coming up. He asked: “Can I go?” I told him “Yes,” but to be safe – to wear an N95 mask on the plane and at the event, and stay in his own hotel room, rather than with the whole family. I said, “You need to do this.” Earlier in the pandemic, I saw people who literally died from loneliness and isolation.

He and his wife flew there. He sent me a picture of himself with his granddaughter. When he returned, he showed me a handwritten note from her that said, “I love you so much. Everyone else canceled, which made me cry. You’re the only one who came. You have no idea how much this meant to me.”

He’s back in L.A., and he didn’t get COVID. He said, “It was the best thing I’ve done in years.” That’s what I need to help people with, navigating this world with COVID and assessing risks and benefits. As with all of medicine, my advice is individualized. My advice changes based on the major circulating variant and the rates of the virus in the population, as well as the risk factors of the individual.
 

Q: What are you doing now?

A: I’m trying to avoid getting COVID again, or another booster. I could get pre-exposure monoclonal antibodies but am waiting to do anything further until I see what happens over the fall and winter. I still wear a mask inside but now do a mix of in-person and telemedicine visits. I still try to go to outdoor restaurants, which is easy in California. But I’m flying to see my son in New York and plan to go to Europe this fall for a meeting. I also go to my cabin in Montana every month to get my “dose” of the wilderness. Overall, I travel for conferences and speaking engagements much less because I have learned the joy of staying home.

Thinking back on my life as a doctor, my career began as an intern at Stanford rotating through Ward 5B, the AIDS unit at San Francisco General Hospital, and will likely end with COVID. In spite of all our medical advances, my generation of physicians, much as many generations before us, has a front-row seat to the vulnerability of humans to infectious diseases and how far we still need to go to protect our patients from communicable illness.

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

Anne L. Peters, MD, is a professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts; three books on diabetes; and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations.

Early in 2020, Anne Peters, MD, caught COVID-19. The author of Medscape’s “Peters on Diabetes” column was sick in March 2020 before state-mandated lockdowns, and well before there were any vaccines.

She remembers sitting in a small exam room with two patients who had flown to her Los Angeles office from New York. The elderly couple had hearing difficulties, so Dr. Peters sat close to them, putting on a continuous glucose monitor. “At that time, we didn’t think of COVID-19 as being in L.A.,” Dr. Peters recalled, “so I think we were not terribly consistent at mask-wearing due to the need to educate.”

“Several days later, I got COVID, but I didn’t know I had COVID per se. I felt crappy, had a terrible sore throat, lost my sense of taste and smell [which was not yet described as a COVID symptom], was completely exhausted, but had no fever or cough, which were the only criteria for getting COVID tested at the time. I didn’t know I had been exposed until 2 weeks later, when the patient’s assistant returned the sensor warning us to ‘be careful’ with it because the patient and his wife were recovering from COVID.”

That early battle with COVID-19 was just the beginning of what would become a 2-year struggle, including familial loss amid her own health problems and concerns about the under-resourced patients she cares for. Here, she shares her journey through the pandemic with this news organization.
 

Question: Thanks for talking to us. Let’s discuss your journey over these past 2.5 years.

Answer: Everybody has their own COVID story because we all went through this together. Some of us have worse COVID stories, and some of us have better ones, but all have been impacted.

I’m not a sick person. I’m a very healthy person but COVID made me so unwell for 2 years. The brain fog and fatigue were nothing compared to the autonomic neuropathy that affected my heart. It was really limiting for me. And I still don’t know the long-term implications, looking 20-30 years from now.
 

Q: When you initially had COVID, what were your symptoms? What was the impact?

A: I had all the symptoms of COVID, except for a cough and fever. I lost my sense of taste and smell. I had a horrible headache, a sore throat, and I was exhausted. I couldn’t get tested because I didn’t have the right symptoms.

Despite being sick, I never stopped working but just switched to telemedicine. I also took my regular monthly trip to our cabin in Montana. I unknowingly flew on a plane with COVID. I wore a well-fitted N95 mask, so I don’t think I gave anybody COVID. I didn’t give COVID to my partner, Eric, which is hard to believe as – at 77 – he’s older than me. He has diabetes, heart disease, and every other high-risk characteristic. If he’d gotten COVID back then, it would have been terrible, as there were no treatments, but luckily he didn’t get it.
 

Q: When were you officially diagnosed?

A: Two or 3 months after I thought I might have had COVID, I checked my antibodies, which tested strongly positive for a prior COVID infection. That was when I knew all the symptoms I’d had were due to the disease.

Q: Not only were you dealing with your own illness, but also that of those close to you. Can you talk about that?

A: In April 2020, my mother who was in her 90s and otherwise healthy except for dementia, got COVID. She could have gotten it from me. I visited often but wore a mask. She had all the horrible pulmonary symptoms. In her advance directive, she didn’t want to be hospitalized so I kept her in her home. She died from COVID in her own bed. It was fairly brutal, but at least I kept her where she felt comforted.

My 91-year-old dad was living in a different residential facility. Throughout COVID he had become very depressed because his social patterns had changed. Prior to COVID, they all ate together, but during the pandemic they were unable to. He missed his social connections, disliked being isolated in his room, hated everyone in masks.

He was a bit demented, but not so much that he couldn’t communicate with me or remember where his grandson was going to law school. I wasn’t allowed inside the facility, which was hard on him. I hadn’t told him his wife died because the hospice social workers advised me that I shouldn’t give him news that he couldn’t process readily until I could spend time with him. Unfortunately, that time never came. In December 2020, he got COVID. One of the people in that facility had gone to the hospital, came back, and tested negative, but actually had COVID and gave it to my dad. The guy who gave it to my dad didn’t die but my dad was terribly ill. He died 2 weeks short of getting his vaccine. He was coherent enough to have a conversation. I asked him: ‘Do you want to go to the hospital?’ And he said: ‘No, because it would be too scary,’ since he couldn’t be with me. I put him on hospice and held his hand as he died from pulmonary COVID, which was awful. I couldn’t give him enough morphine or valium to ease his breathing. But his last words to me were “I love you,” and at the very end he seemed peaceful, which was a blessing.

I got an autopsy, because he wanted one. Nothing else was wrong with him other than COVID. It destroyed his lungs. The rest of him was fine – no heart disease, cancer, or anything else. He died of COVID-19, the same as my mother.

That same week, my aunt, my only surviving older relative, who was in Des Moines, Iowa, died of COVID-19. All three family members died before the vaccine came out.

It was hard to lose my parents. I’m the only surviving child because my sister died in her 20s. It’s not been an easy pandemic. But what pandemic is easy? I just happened to have lost more people than most. Ironically, my grandfather was one of the legionnaires at the Bellevue-Stratford Hotel in Philadelphia in 1976 and died of Legionnaire’s disease before we knew what was causing the outbreak.
 

Q: Were you still struggling with COVID?

A: COVID impacted my whole body. I lost a lot of weight. I didn’t want to eat, and my gastrointestinal system was not happy. It took a while for my sense of taste and smell to come back. Nothing tasted good. I’m not a foodie; I don’t really care about food. We could get takeout or whatever, but none of it appealed to me. I’m not so sure it was a taste thing, I just didn’t feel like eating.

I didn’t realize I had “brain fog” per se, because I felt stressed and overwhelmed by the pandemic and my patients’ concerns. But one day, about 3 months after I had developed COVID, I woke up without the fog. Which made me aware that I hadn’t been feeling right up until that point.

The worst symptoms, however, were cardiac. I noticed also immediately that my heart rate went up very quickly with minimal exertion. My pulse has always been in the 55-60 bpm range, and suddenly just walking across a room made it go up to over 140 bpm. If I did any aerobic activity, it went up over 160 and would be associated with dyspnea and chest pain. I believed these were all post-COVID symptoms and felt validated when reports of others having similar issues were published in the literature.

Q: Did you continue seeing patients?

A: Yes, of course. Patients never needed their doctors more. In East L.A., where patients don’t have easy access to telemedicine, I kept going into clinic throughout the pandemic. In the more affluent Westside of Los Angeles, we switched to telemedicine, which was quite effective for most. However, because diabetes was associated with an increased risk of hospitalization and death from COVID, my patients were understandably afraid. I’ve never been busier, but (like all health care providers), I became more of a COVID provider than a diabetologist.

Q: Do you feel your battle with COVID impacted your work?

A: It didn’t affect me at work. If I was sitting still, I was fine. Sitting at home at a desk, I didn’t notice any symptoms. But as a habitual stair-user, I would be gasping for breath in the stairwell because I couldn’t go up the stairs to my office as I once could.

I think you empathize more with people who had COVID (when you’ve had it yourself). There was such a huge patient burden. And I think that’s been the thing that’s affected health care providers the most – no matter what specialty we’re in – that nobody has answers.
 

Q: What happened after you had your vaccine?

A: The vaccine itself was fine. I didn’t have any reaction to the first two doses. But the first booster made my cardiac issues worse.

By this point, my cardiac problems stopped me from exercising. I even went to the ER with chest pain once because I was having palpitations and chest pressure caused by simply taking my morning shower. Fortunately, I wasn’t having an MI, but I certainly wasn’t “normal.”

My measure of my fitness is the cross-country skiing trail I use in Montana. I know exactly how far I can ski. Usually I can do the loop in 35 minutes. After COVID, I lasted 10 minutes. I would be tachycardic, short of breath with chest pain radiating down my left arm. I would rest and try to keep going. But with each rest period, I only got worse. I would be laying in the snow and strangers would ask if I needed help.
 

Q: What helped you?

A: I’ve read a lot about long COVID and have tried to learn from the experts. Of course, I never went to a doctor directly, although I did ask colleagues for advice. What I learned was to never push myself. I forced myself to create an exercise schedule where I only exercised three times a week with rest days in between. When exercising, the second my heart rate went above 140 bpm, I stopped until I could get it back down. I would push against this new limit, even though my limit was low.

Additionally, I worked on my breathing patterns and did meditative breathing for 10 minutes twice daily using a commercially available app.

Although progress was slow, I did improve, and by June 2022, I seemed back to normal. I was not as fit as I was prior to COVID and needed to improve, but the tachycardic response to exercise and cardiac symptoms were gone. I felt like my normal self. Normal enough to go on a spot packing trip in the Sierras in August. (Horses carried us and a mule carried the gear over the 12,000-foot pass into the mountains, and then left my friend and me high in the Sierras for a week.) We were camped above 10,000 feet and every day hiked up to another high mountain lake where we fly-fished for trout that we ate for dinner. The hikes were a challenge, but not abnormally so. Not as they would have been while I had long COVID.
 

Q: What is the current atmosphere in your clinic?

A: COVID is much milder now in my vaccinated patients, but I feel most health care providers are exhausted. Many of my staff left when COVID hit because they didn’t want to keep working. It made practicing medicine exhausting. There’s been a shortage of nurses, a shortage of everything. We’ve been required to do a whole lot more than we ever did before. It’s much harder to be a doctor. This pandemic is the first time I’ve ever thought of quitting. Granted, I lost my whole family, or at least the older generation, but it’s just been almost overwhelming.

On the plus side, almost every one of my patients has been vaccinated, because early on, people would ask: “Do you trust this vaccine?” I would reply: “I saw my parents die from COVID when they weren’t vaccinated, so you’re getting vaccinated. This is real and the vaccines help.” It made me very good at convincing people to get vaccines because I knew what it was like to see someone dying from COVID up close.
 

Q: What advice do you have for those struggling with the COVID pandemic?

A: People need to decide what their own risk is for getting sick and how many times they want to get COVID. At this point, I want people to go out, but safely. In the beginning, when my patients said, “can I go visit my granddaughter?” I said, “no,” but that was before we had the vaccine. Now I feel it is safe to go out using common sense. I still have my patients wear masks on planes. I still have patients try to eat outside as much as possible. And I tell people to take the precautions that make sense, but I tell them to go out and do things because life is short.

I had a patient in his 70s who has many risk factors like heart disease and diabetes. His granddaughter’s Bat Mitzvah in Florida was coming up. He asked: “Can I go?” I told him “Yes,” but to be safe – to wear an N95 mask on the plane and at the event, and stay in his own hotel room, rather than with the whole family. I said, “You need to do this.” Earlier in the pandemic, I saw people who literally died from loneliness and isolation.

He and his wife flew there. He sent me a picture of himself with his granddaughter. When he returned, he showed me a handwritten note from her that said, “I love you so much. Everyone else canceled, which made me cry. You’re the only one who came. You have no idea how much this meant to me.”

He’s back in L.A., and he didn’t get COVID. He said, “It was the best thing I’ve done in years.” That’s what I need to help people with, navigating this world with COVID and assessing risks and benefits. As with all of medicine, my advice is individualized. My advice changes based on the major circulating variant and the rates of the virus in the population, as well as the risk factors of the individual.
 

Q: What are you doing now?

A: I’m trying to avoid getting COVID again, or another booster. I could get pre-exposure monoclonal antibodies but am waiting to do anything further until I see what happens over the fall and winter. I still wear a mask inside but now do a mix of in-person and telemedicine visits. I still try to go to outdoor restaurants, which is easy in California. But I’m flying to see my son in New York and plan to go to Europe this fall for a meeting. I also go to my cabin in Montana every month to get my “dose” of the wilderness. Overall, I travel for conferences and speaking engagements much less because I have learned the joy of staying home.

Thinking back on my life as a doctor, my career began as an intern at Stanford rotating through Ward 5B, the AIDS unit at San Francisco General Hospital, and will likely end with COVID. In spite of all our medical advances, my generation of physicians, much as many generations before us, has a front-row seat to the vulnerability of humans to infectious diseases and how far we still need to go to protect our patients from communicable illness.

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

Anne L. Peters, MD, is a professor of medicine at the University of Southern California, Los Angeles, and director of the USC clinical diabetes programs. She has published more than 200 articles, reviews, and abstracts; three books on diabetes; and has been an investigator for more than 40 research studies. She has spoken internationally at over 400 programs and serves on many committees of several professional organizations.

A home-based strength training program does not improve dyspnea in patients with chronic obstructive lung disease (COPD), but it does improve some functional capacity and helps patients feel better, a 12-month long HOMEX exercise program shows. 

“Home-based programs became increasingly popular in the last years and complement traditional center-based inpatient and outpatient PR (pulmonary rehabilitation),” Anja Frei, PhD, University of Zurich, Switzerland, and colleagues reported.

“Our study showed that the HOMEX strength training program had no effect on dyspnea after 12 months in persons with COPD who completed PR, [but] the program improved functional exercise capacity ... and many participants reported having perceived positive effects that they attributed to the training,” investigators add.

The study was published online  in the journal CHEST.
 

Intervention or controls

A total of 123 patients (mean age, 67 years) with COPD were randomly assigned to the intervention group or to the control group. The mean forced expiratory volume in 1 second (FEV1) was 39.3% of predicted. Three-quarters of participants had severe or very severe COPD.

A total of 104 patients completed the 12-month study. “The primary outcome was change in dyspnea (Chronic Respiratory Questionnaire, CRQ) from baseline to 12 months,” investigators note. Secondary outcomes included change in exercise capacity as assessed by the 1-minute-sit-to-stand test (1-min-STST); the 6-minute walk test (6MWT); health-related quality of life, exacerbations, and symptoms.

The HOMEX program was a structured, home-based strength training program developed for patients with COPD that could be done following the pulmonary rehabilitation program, with the intention of maintaining the training benefits gained during pulmonary rehabilitation.

“We deliberately focused on the strength component of exercise training due to the fact that skeletal muscle dysfunction is prevalent in COPD and [is] associated with lower daily physical activity and poor prognosis,” the authors explain. Patients had completed pulmonary rehabilitation no longer than 1 month prior to starting the training program. The program required a chair and a set of resistance bands and consisted of trunk, upper limb, and lower limb exercises done at different intensity levels.

Participants were instructed to do the exercises 6 days per week for about 20 minutes per day over the 12-month study interval. The dyspnea score dropped from 4.65 to 4.42 from baseline to 12 months in the intervention group, compared with a drop from 4.61 to 4.06 in the control group, the investigators reported. “There was no evidence for a difference between the two groups in change in the 6MWT distance after 12 months ... but moderate evidence for a between-group difference in the change of repetitions in the 1-min-STST favoring the IG (intervention group),” they also noted, at an adjusted mean difference of 2.6 (95% confidence interval, 0.22-5.03, P = .033).

In all other outcomes, no differences were observed between the two groups. Importantly, 70% of participants carried on with the HOMEX training program until study endpoint and at least 79% of them persevered for at least 10 months. Based on results from a satisfaction survey, 81% of participants randomly assigned to the intervention group indicated that they “liked” or “very much liked” participating in the program, and 79% of them reported that they experienced positive effects that they felt were attributed to the training.

“The program was safe and the majority of the multimorbid and severely ill study participants adhered to the training during the study year,” the authors write. And while the program had no effect on functional exercise capacity as measured by the 6MWT, it did improve the strength and intramuscular coordination of the lower leg muscles because the program had repetitive sit-to-stand exercises as a component of the training. “Adherence to this long-term training program was surprisingly high,” the authors say. “It was well accepted by COPD patients and may facilitate continued training at home.”

One limitation of the study was that some participants did not travel to the rehabilitation clinic for a follow-up assessment.

The authors reported no relevant financial relationships.

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

A home-based strength training program does not improve dyspnea in patients with chronic obstructive lung disease (COPD), but it does improve some functional capacity and helps patients feel better, a 12-month long HOMEX exercise program shows. 

“Home-based programs became increasingly popular in the last years and complement traditional center-based inpatient and outpatient PR (pulmonary rehabilitation),” Anja Frei, PhD, University of Zurich, Switzerland, and colleagues reported.

“Our study showed that the HOMEX strength training program had no effect on dyspnea after 12 months in persons with COPD who completed PR, [but] the program improved functional exercise capacity ... and many participants reported having perceived positive effects that they attributed to the training,” investigators add.

The study was published online  in the journal CHEST.
 

Intervention or controls

A total of 123 patients (mean age, 67 years) with COPD were randomly assigned to the intervention group or to the control group. The mean forced expiratory volume in 1 second (FEV1) was 39.3% of predicted. Three-quarters of participants had severe or very severe COPD.

A total of 104 patients completed the 12-month study. “The primary outcome was change in dyspnea (Chronic Respiratory Questionnaire, CRQ) from baseline to 12 months,” investigators note. Secondary outcomes included change in exercise capacity as assessed by the 1-minute-sit-to-stand test (1-min-STST); the 6-minute walk test (6MWT); health-related quality of life, exacerbations, and symptoms.

The HOMEX program was a structured, home-based strength training program developed for patients with COPD that could be done following the pulmonary rehabilitation program, with the intention of maintaining the training benefits gained during pulmonary rehabilitation.

“We deliberately focused on the strength component of exercise training due to the fact that skeletal muscle dysfunction is prevalent in COPD and [is] associated with lower daily physical activity and poor prognosis,” the authors explain. Patients had completed pulmonary rehabilitation no longer than 1 month prior to starting the training program. The program required a chair and a set of resistance bands and consisted of trunk, upper limb, and lower limb exercises done at different intensity levels.

Participants were instructed to do the exercises 6 days per week for about 20 minutes per day over the 12-month study interval. The dyspnea score dropped from 4.65 to 4.42 from baseline to 12 months in the intervention group, compared with a drop from 4.61 to 4.06 in the control group, the investigators reported. “There was no evidence for a difference between the two groups in change in the 6MWT distance after 12 months ... but moderate evidence for a between-group difference in the change of repetitions in the 1-min-STST favoring the IG (intervention group),” they also noted, at an adjusted mean difference of 2.6 (95% confidence interval, 0.22-5.03, P = .033).

In all other outcomes, no differences were observed between the two groups. Importantly, 70% of participants carried on with the HOMEX training program until study endpoint and at least 79% of them persevered for at least 10 months. Based on results from a satisfaction survey, 81% of participants randomly assigned to the intervention group indicated that they “liked” or “very much liked” participating in the program, and 79% of them reported that they experienced positive effects that they felt were attributed to the training.

“The program was safe and the majority of the multimorbid and severely ill study participants adhered to the training during the study year,” the authors write. And while the program had no effect on functional exercise capacity as measured by the 6MWT, it did improve the strength and intramuscular coordination of the lower leg muscles because the program had repetitive sit-to-stand exercises as a component of the training. “Adherence to this long-term training program was surprisingly high,” the authors say. “It was well accepted by COPD patients and may facilitate continued training at home.”

One limitation of the study was that some participants did not travel to the rehabilitation clinic for a follow-up assessment.

The authors reported no relevant financial relationships.

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

A home-based strength training program does not improve dyspnea in patients with chronic obstructive lung disease (COPD), but it does improve some functional capacity and helps patients feel better, a 12-month long HOMEX exercise program shows. 

“Home-based programs became increasingly popular in the last years and complement traditional center-based inpatient and outpatient PR (pulmonary rehabilitation),” Anja Frei, PhD, University of Zurich, Switzerland, and colleagues reported.

“Our study showed that the HOMEX strength training program had no effect on dyspnea after 12 months in persons with COPD who completed PR, [but] the program improved functional exercise capacity ... and many participants reported having perceived positive effects that they attributed to the training,” investigators add.

The study was published online  in the journal CHEST.
 

Intervention or controls

A total of 123 patients (mean age, 67 years) with COPD were randomly assigned to the intervention group or to the control group. The mean forced expiratory volume in 1 second (FEV1) was 39.3% of predicted. Three-quarters of participants had severe or very severe COPD.

A total of 104 patients completed the 12-month study. “The primary outcome was change in dyspnea (Chronic Respiratory Questionnaire, CRQ) from baseline to 12 months,” investigators note. Secondary outcomes included change in exercise capacity as assessed by the 1-minute-sit-to-stand test (1-min-STST); the 6-minute walk test (6MWT); health-related quality of life, exacerbations, and symptoms.

The HOMEX program was a structured, home-based strength training program developed for patients with COPD that could be done following the pulmonary rehabilitation program, with the intention of maintaining the training benefits gained during pulmonary rehabilitation.

“We deliberately focused on the strength component of exercise training due to the fact that skeletal muscle dysfunction is prevalent in COPD and [is] associated with lower daily physical activity and poor prognosis,” the authors explain. Patients had completed pulmonary rehabilitation no longer than 1 month prior to starting the training program. The program required a chair and a set of resistance bands and consisted of trunk, upper limb, and lower limb exercises done at different intensity levels.

Participants were instructed to do the exercises 6 days per week for about 20 minutes per day over the 12-month study interval. The dyspnea score dropped from 4.65 to 4.42 from baseline to 12 months in the intervention group, compared with a drop from 4.61 to 4.06 in the control group, the investigators reported. “There was no evidence for a difference between the two groups in change in the 6MWT distance after 12 months ... but moderate evidence for a between-group difference in the change of repetitions in the 1-min-STST favoring the IG (intervention group),” they also noted, at an adjusted mean difference of 2.6 (95% confidence interval, 0.22-5.03, P = .033).

In all other outcomes, no differences were observed between the two groups. Importantly, 70% of participants carried on with the HOMEX training program until study endpoint and at least 79% of them persevered for at least 10 months. Based on results from a satisfaction survey, 81% of participants randomly assigned to the intervention group indicated that they “liked” or “very much liked” participating in the program, and 79% of them reported that they experienced positive effects that they felt were attributed to the training.

“The program was safe and the majority of the multimorbid and severely ill study participants adhered to the training during the study year,” the authors write. And while the program had no effect on functional exercise capacity as measured by the 6MWT, it did improve the strength and intramuscular coordination of the lower leg muscles because the program had repetitive sit-to-stand exercises as a component of the training. “Adherence to this long-term training program was surprisingly high,” the authors say. “It was well accepted by COPD patients and may facilitate continued training at home.”

One limitation of the study was that some participants did not travel to the rehabilitation clinic for a follow-up assessment.

The authors reported no relevant financial relationships.

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

The antiviral drug Paxlovid appears to reduce the risk of dying from COVID-19 by 79% and decrease hospitalizations by 73% in at-risk patients who are ages 65 and older, according to a new study published in The New England Journal of Medicine.

The pill, which is a combination of the drugs nirmatrelvir and ritonavir, received FDA emergency use authorization in December 2021 to treat mild to moderate disease in ages 12 and older who face high risks for having severe COVID-19, hospitalization, and death.

“The results of the study show unequivocally that treatment with Paxlovid significantly reduces the risk of hospitalization and death from COVID-19,” Doron Netzer, MD, the senior study author and a researcher with Clalit Health Services, Tel Aviv, told The Jerusalem Post.

“We are the country’s leader in the provision of giving Paxlovid to relevant patients,” he said. “It was given to patients all over the country, with medical teams monitoring the patients who took the pills.”

The research is considered one of the most thorough studies published to date about how well Paxlovid works, the news outlet reported. The research team analyzed information from Clalit’s electronic medical records. The health care organization covers about 52% of the Israeli population and almost two-thirds of older adults. More than 30,000 COVID-19 patients in Israel have been treated with the drug so far.

Dr. Netzer and colleagues looked at hospitalization and death data for at-risk COVID-19 patients ages 40 and older between Jan. 9 and March 31, when the original Omicron variant was the dominant strain in Israel. During that time, more than 1.1 million Clalit patients were infected with COVID-19, 109,000 patients were considered at-risk, and 3,900 patients received the drug.

The average age of the patients was 60, and 39% of the patients were 65 and older. Overall, 78% of the patients had previous COVID-19 immunity due to vaccination, prior infection, or both.

Among ages 65 and older, the rate of COVID-19 hospitalization was 14.7 cases per 100,000 person-days among treated patients, compared with 58.9 cases per 100,000 person-days among untreated patients. This represented a 73% lower chance of being hospitalized.

Among ages 40-64, the rate of hospitalization due to COVID-19 was 15.2 cases per 100,000 person-days among treated patients, compared with 15.8 cases per 100,000 person-days among untreated patients. The risk of hospitalization wasn’t significantly lower for this age group.

Among ages 65 and older, there were two deaths from COVID-19 in 2,484 treated patients, compared with 158 in the 40,337 untreated patients. This represented a 79% lower chance of dying from COVID-19.

Among ages 40-64, there was one death from COVID-19 in 1,418 treated patients, compared with 16 in the 65,015 untreated patients. The risk of death wasn’t significantly lower for this age group.

For both age groups, a lack of previous COVID-19 immunity and a previous hospitalization were most strongly linked to high rates of hospitalization during the Omicron wave.

The researchers noted that they didn’t break down the data on ages 40-64 who had cancer and other severe conditions that weaken the immune system. These patients may be more likely to benefit from Paxlovid, they said, though future studies will need to analyze the data.

The study didn’t receive any financial or in-kind support, the authors said.

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

The antiviral drug Paxlovid appears to reduce the risk of dying from COVID-19 by 79% and decrease hospitalizations by 73% in at-risk patients who are ages 65 and older, according to a new study published in The New England Journal of Medicine.

The pill, which is a combination of the drugs nirmatrelvir and ritonavir, received FDA emergency use authorization in December 2021 to treat mild to moderate disease in ages 12 and older who face high risks for having severe COVID-19, hospitalization, and death.

“The results of the study show unequivocally that treatment with Paxlovid significantly reduces the risk of hospitalization and death from COVID-19,” Doron Netzer, MD, the senior study author and a researcher with Clalit Health Services, Tel Aviv, told The Jerusalem Post.

“We are the country’s leader in the provision of giving Paxlovid to relevant patients,” he said. “It was given to patients all over the country, with medical teams monitoring the patients who took the pills.”

The research is considered one of the most thorough studies published to date about how well Paxlovid works, the news outlet reported. The research team analyzed information from Clalit’s electronic medical records. The health care organization covers about 52% of the Israeli population and almost two-thirds of older adults. More than 30,000 COVID-19 patients in Israel have been treated with the drug so far.

Dr. Netzer and colleagues looked at hospitalization and death data for at-risk COVID-19 patients ages 40 and older between Jan. 9 and March 31, when the original Omicron variant was the dominant strain in Israel. During that time, more than 1.1 million Clalit patients were infected with COVID-19, 109,000 patients were considered at-risk, and 3,900 patients received the drug.

The average age of the patients was 60, and 39% of the patients were 65 and older. Overall, 78% of the patients had previous COVID-19 immunity due to vaccination, prior infection, or both.

Among ages 65 and older, the rate of COVID-19 hospitalization was 14.7 cases per 100,000 person-days among treated patients, compared with 58.9 cases per 100,000 person-days among untreated patients. This represented a 73% lower chance of being hospitalized.

Among ages 40-64, the rate of hospitalization due to COVID-19 was 15.2 cases per 100,000 person-days among treated patients, compared with 15.8 cases per 100,000 person-days among untreated patients. The risk of hospitalization wasn’t significantly lower for this age group.

Among ages 65 and older, there were two deaths from COVID-19 in 2,484 treated patients, compared with 158 in the 40,337 untreated patients. This represented a 79% lower chance of dying from COVID-19.

Among ages 40-64, there was one death from COVID-19 in 1,418 treated patients, compared with 16 in the 65,015 untreated patients. The risk of death wasn’t significantly lower for this age group.

For both age groups, a lack of previous COVID-19 immunity and a previous hospitalization were most strongly linked to high rates of hospitalization during the Omicron wave.

The researchers noted that they didn’t break down the data on ages 40-64 who had cancer and other severe conditions that weaken the immune system. These patients may be more likely to benefit from Paxlovid, they said, though future studies will need to analyze the data.

The study didn’t receive any financial or in-kind support, the authors said.

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

The antiviral drug Paxlovid appears to reduce the risk of dying from COVID-19 by 79% and decrease hospitalizations by 73% in at-risk patients who are ages 65 and older, according to a new study published in The New England Journal of Medicine.

The pill, which is a combination of the drugs nirmatrelvir and ritonavir, received FDA emergency use authorization in December 2021 to treat mild to moderate disease in ages 12 and older who face high risks for having severe COVID-19, hospitalization, and death.

“The results of the study show unequivocally that treatment with Paxlovid significantly reduces the risk of hospitalization and death from COVID-19,” Doron Netzer, MD, the senior study author and a researcher with Clalit Health Services, Tel Aviv, told The Jerusalem Post.

“We are the country’s leader in the provision of giving Paxlovid to relevant patients,” he said. “It was given to patients all over the country, with medical teams monitoring the patients who took the pills.”

The research is considered one of the most thorough studies published to date about how well Paxlovid works, the news outlet reported. The research team analyzed information from Clalit’s electronic medical records. The health care organization covers about 52% of the Israeli population and almost two-thirds of older adults. More than 30,000 COVID-19 patients in Israel have been treated with the drug so far.

Dr. Netzer and colleagues looked at hospitalization and death data for at-risk COVID-19 patients ages 40 and older between Jan. 9 and March 31, when the original Omicron variant was the dominant strain in Israel. During that time, more than 1.1 million Clalit patients were infected with COVID-19, 109,000 patients were considered at-risk, and 3,900 patients received the drug.

The average age of the patients was 60, and 39% of the patients were 65 and older. Overall, 78% of the patients had previous COVID-19 immunity due to vaccination, prior infection, or both.

Among ages 65 and older, the rate of COVID-19 hospitalization was 14.7 cases per 100,000 person-days among treated patients, compared with 58.9 cases per 100,000 person-days among untreated patients. This represented a 73% lower chance of being hospitalized.

Among ages 40-64, the rate of hospitalization due to COVID-19 was 15.2 cases per 100,000 person-days among treated patients, compared with 15.8 cases per 100,000 person-days among untreated patients. The risk of hospitalization wasn’t significantly lower for this age group.

Among ages 65 and older, there were two deaths from COVID-19 in 2,484 treated patients, compared with 158 in the 40,337 untreated patients. This represented a 79% lower chance of dying from COVID-19.

Among ages 40-64, there was one death from COVID-19 in 1,418 treated patients, compared with 16 in the 65,015 untreated patients. The risk of death wasn’t significantly lower for this age group.

For both age groups, a lack of previous COVID-19 immunity and a previous hospitalization were most strongly linked to high rates of hospitalization during the Omicron wave.

The researchers noted that they didn’t break down the data on ages 40-64 who had cancer and other severe conditions that weaken the immune system. These patients may be more likely to benefit from Paxlovid, they said, though future studies will need to analyze the data.

The study didn’t receive any financial or in-kind support, the authors said.

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

Respiratory syncytial virus (RSV) is the leading cause of U.S. infant hospitalizations overall and across population subgroups, new data published in the Journal of Infectious Diseases confirm.

Acute bronchiolitis caused by RSV accounted for 9.6% (95% confidence interval, 9.4%-9.9%) and 9.3% (95% CI, 9.0%-9.6%) of total infant hospitalizations from January 2009 to September 2015 and October 2015 to December 2019, respectively.
 

Journal issue includes 14 RSV studies

The latest issue of the journal includes a special section with results from 14 studies related to the widespread, easy-to-catch virus, highlighting the urgency of finding a solution for all infants.

In one study, authors led by Mina Suh, MPH, with EpidStrategies, a division of ToxStrategies in Rockville, Md., reported that, in children under the age of 5 years in the United States, RSV caused 58,000 annual hospitalizations and from 100 to 500 annual deaths from 2009 to 2019 (the latest year data were available).

Globally, in 2015, among infants younger than 6 months, an estimated 1.4 million hospital admissions and 27,300 in-hospital deaths were attributed to RSV lower respiratory tract infection (LRTI).

The researchers used the largest publicly available, all-payer database in the United States – the National (Nationwide) Inpatient Sample – to describe the leading causes of infant hospitalizations.

The authors noted that, because clinicians don’t routinely perform lab tests for RSV, the true health care burden is likely higher and its public health impact greater than these numbers show.

Immunization candidates advance

There are no preventative options currently available to substantially cut RSV infections in all infants, though immunization candidates are advancing, showing safety and efficacy in clinical trials.

Palivizumab is currently the only available option in the United States to prevent RSV and is recommended only for a small group of infants with particular forms of heart or lung disease and those born prematurely at 29 weeks’ gestational age. Further, palivizumab has to be given monthly throughout the RSV season.

Another of the studies in the journal supplement concluded that a universal immunization strategy with one of the candidates, nirsevimab (Sanofi, AstraZeneca), an investigational long-acting monoclonal antibody, could substantially reduce the health burden and economic burden for U.S. infants in their first RSV season.

The researchers, led by Alexia Kieffer, MSc, MPH, with Sanofi, used static decision-analytic modeling for the estimates. Modeled RSV-related outcomes included primary care and ED visits, hospitalizations, including ICU admission and mechanical ventilations, and RSV-related deaths.

“The results of this model suggested that the use of nirsevimab in all infants could reduce health events by 55% and the overall costs to the payer by 49%,” the authors of the study wrote.

According to the study, universal immunization of all infants with nirsevimab is expected to reduce 290,174 RSV-related medically attended LRTI (MALRTI), 24,986 hospitalizations, and cut $612 million in costs to the health care system.

The authors wrote: “While this reduction would be driven by term infants, who account for most of the RSV-MALRTI burden; all infants, including palivizumab-eligible and preterm infants who suffer from significantly higher rates of disease, would benefit from this immunization strategy.”
 

Excitement for another option

Jörn-Hendrik Weitkamp, MD, professor of pediatrics and director for patient-oriented research at Monroe Carell Jr. Children’s Hospital at Vanderbilt University, Nashville, Tenn., said in an interview there is much excitement in the field for nirsevimab as it has significant advantages over palivizumab.

RSV “is a huge burden to the children, the families, the hospitals, and the medical system,” he said.

Ideally there would be a vaccine to offer the best protection, he noted.

“People have spent their lives, their careers trying to develop a vaccine for RSV,” he said, but that has been elusive for more than 60 years. Therefore, passive immunization is the best of the current options, he says, and nirsevimab “seems to be very effective.”

What’s not clear, Dr. Weitkamp said, is how much nirsevimab will cost as it is not yet approved by the Food and Drug Administration. However, it has the great advantage of being given only once before the season starts instead of monthly (as required for palivizumab) through the season, “which is painful, inconvenient, and traumatizing. We limit that one to the children at highest risk.”

Rolling out an infant nirsevimab program would likely vary by geographic region, Ms. Kieffer and colleagues said, to help ensure infants are protected during the peak of their region’s RSV season.

The journal’s RSV supplement was supported by Sanofi and AstraZeneca. The studies by Ms. Suh and colleagues and Ms. Kieffer and colleagues were supported by AstraZeneca and Sanofi. Ms. Suh and several coauthors are employees of EpidStrategies. One coauthor is an employee of Sanofi and may hold shares and/or stock options in the company. Ms. Kieffer and several coauthors are employees of Sanofi and may hold shares and/or stock options in the company. Dr. Weitkamp reported no relevant financial relationships.

Respiratory syncytial virus (RSV) is the leading cause of U.S. infant hospitalizations overall and across population subgroups, new data published in the Journal of Infectious Diseases confirm.

Acute bronchiolitis caused by RSV accounted for 9.6% (95% confidence interval, 9.4%-9.9%) and 9.3% (95% CI, 9.0%-9.6%) of total infant hospitalizations from January 2009 to September 2015 and October 2015 to December 2019, respectively.
 

Journal issue includes 14 RSV studies

The latest issue of the journal includes a special section with results from 14 studies related to the widespread, easy-to-catch virus, highlighting the urgency of finding a solution for all infants.

In one study, authors led by Mina Suh, MPH, with EpidStrategies, a division of ToxStrategies in Rockville, Md., reported that, in children under the age of 5 years in the United States, RSV caused 58,000 annual hospitalizations and from 100 to 500 annual deaths from 2009 to 2019 (the latest year data were available).

Globally, in 2015, among infants younger than 6 months, an estimated 1.4 million hospital admissions and 27,300 in-hospital deaths were attributed to RSV lower respiratory tract infection (LRTI).

The researchers used the largest publicly available, all-payer database in the United States – the National (Nationwide) Inpatient Sample – to describe the leading causes of infant hospitalizations.

The authors noted that, because clinicians don’t routinely perform lab tests for RSV, the true health care burden is likely higher and its public health impact greater than these numbers show.

Immunization candidates advance

There are no preventative options currently available to substantially cut RSV infections in all infants, though immunization candidates are advancing, showing safety and efficacy in clinical trials.

Palivizumab is currently the only available option in the United States to prevent RSV and is recommended only for a small group of infants with particular forms of heart or lung disease and those born prematurely at 29 weeks’ gestational age. Further, palivizumab has to be given monthly throughout the RSV season.

Another of the studies in the journal supplement concluded that a universal immunization strategy with one of the candidates, nirsevimab (Sanofi, AstraZeneca), an investigational long-acting monoclonal antibody, could substantially reduce the health burden and economic burden for U.S. infants in their first RSV season.

The researchers, led by Alexia Kieffer, MSc, MPH, with Sanofi, used static decision-analytic modeling for the estimates. Modeled RSV-related outcomes included primary care and ED visits, hospitalizations, including ICU admission and mechanical ventilations, and RSV-related deaths.

“The results of this model suggested that the use of nirsevimab in all infants could reduce health events by 55% and the overall costs to the payer by 49%,” the authors of the study wrote.

According to the study, universal immunization of all infants with nirsevimab is expected to reduce 290,174 RSV-related medically attended LRTI (MALRTI), 24,986 hospitalizations, and cut $612 million in costs to the health care system.

The authors wrote: “While this reduction would be driven by term infants, who account for most of the RSV-MALRTI burden; all infants, including palivizumab-eligible and preterm infants who suffer from significantly higher rates of disease, would benefit from this immunization strategy.”
 

Excitement for another option

Jörn-Hendrik Weitkamp, MD, professor of pediatrics and director for patient-oriented research at Monroe Carell Jr. Children’s Hospital at Vanderbilt University, Nashville, Tenn., said in an interview there is much excitement in the field for nirsevimab as it has significant advantages over palivizumab.

RSV “is a huge burden to the children, the families, the hospitals, and the medical system,” he said.

Ideally there would be a vaccine to offer the best protection, he noted.

“People have spent their lives, their careers trying to develop a vaccine for RSV,” he said, but that has been elusive for more than 60 years. Therefore, passive immunization is the best of the current options, he says, and nirsevimab “seems to be very effective.”

What’s not clear, Dr. Weitkamp said, is how much nirsevimab will cost as it is not yet approved by the Food and Drug Administration. However, it has the great advantage of being given only once before the season starts instead of monthly (as required for palivizumab) through the season, “which is painful, inconvenient, and traumatizing. We limit that one to the children at highest risk.”

Rolling out an infant nirsevimab program would likely vary by geographic region, Ms. Kieffer and colleagues said, to help ensure infants are protected during the peak of their region’s RSV season.

The journal’s RSV supplement was supported by Sanofi and AstraZeneca. The studies by Ms. Suh and colleagues and Ms. Kieffer and colleagues were supported by AstraZeneca and Sanofi. Ms. Suh and several coauthors are employees of EpidStrategies. One coauthor is an employee of Sanofi and may hold shares and/or stock options in the company. Ms. Kieffer and several coauthors are employees of Sanofi and may hold shares and/or stock options in the company. Dr. Weitkamp reported no relevant financial relationships.

Respiratory syncytial virus (RSV) is the leading cause of U.S. infant hospitalizations overall and across population subgroups, new data published in the Journal of Infectious Diseases confirm.

Acute bronchiolitis caused by RSV accounted for 9.6% (95% confidence interval, 9.4%-9.9%) and 9.3% (95% CI, 9.0%-9.6%) of total infant hospitalizations from January 2009 to September 2015 and October 2015 to December 2019, respectively.
 

Journal issue includes 14 RSV studies

The latest issue of the journal includes a special section with results from 14 studies related to the widespread, easy-to-catch virus, highlighting the urgency of finding a solution for all infants.

In one study, authors led by Mina Suh, MPH, with EpidStrategies, a division of ToxStrategies in Rockville, Md., reported that, in children under the age of 5 years in the United States, RSV caused 58,000 annual hospitalizations and from 100 to 500 annual deaths from 2009 to 2019 (the latest year data were available).

Globally, in 2015, among infants younger than 6 months, an estimated 1.4 million hospital admissions and 27,300 in-hospital deaths were attributed to RSV lower respiratory tract infection (LRTI).

The researchers used the largest publicly available, all-payer database in the United States – the National (Nationwide) Inpatient Sample – to describe the leading causes of infant hospitalizations.

The authors noted that, because clinicians don’t routinely perform lab tests for RSV, the true health care burden is likely higher and its public health impact greater than these numbers show.

Immunization candidates advance

There are no preventative options currently available to substantially cut RSV infections in all infants, though immunization candidates are advancing, showing safety and efficacy in clinical trials.

Palivizumab is currently the only available option in the United States to prevent RSV and is recommended only for a small group of infants with particular forms of heart or lung disease and those born prematurely at 29 weeks’ gestational age. Further, palivizumab has to be given monthly throughout the RSV season.

Another of the studies in the journal supplement concluded that a universal immunization strategy with one of the candidates, nirsevimab (Sanofi, AstraZeneca), an investigational long-acting monoclonal antibody, could substantially reduce the health burden and economic burden for U.S. infants in their first RSV season.

The researchers, led by Alexia Kieffer, MSc, MPH, with Sanofi, used static decision-analytic modeling for the estimates. Modeled RSV-related outcomes included primary care and ED visits, hospitalizations, including ICU admission and mechanical ventilations, and RSV-related deaths.

“The results of this model suggested that the use of nirsevimab in all infants could reduce health events by 55% and the overall costs to the payer by 49%,” the authors of the study wrote.

According to the study, universal immunization of all infants with nirsevimab is expected to reduce 290,174 RSV-related medically attended LRTI (MALRTI), 24,986 hospitalizations, and cut $612 million in costs to the health care system.

The authors wrote: “While this reduction would be driven by term infants, who account for most of the RSV-MALRTI burden; all infants, including palivizumab-eligible and preterm infants who suffer from significantly higher rates of disease, would benefit from this immunization strategy.”
 

Excitement for another option

Jörn-Hendrik Weitkamp, MD, professor of pediatrics and director for patient-oriented research at Monroe Carell Jr. Children’s Hospital at Vanderbilt University, Nashville, Tenn., said in an interview there is much excitement in the field for nirsevimab as it has significant advantages over palivizumab.

RSV “is a huge burden to the children, the families, the hospitals, and the medical system,” he said.

Ideally there would be a vaccine to offer the best protection, he noted.

“People have spent their lives, their careers trying to develop a vaccine for RSV,” he said, but that has been elusive for more than 60 years. Therefore, passive immunization is the best of the current options, he says, and nirsevimab “seems to be very effective.”

What’s not clear, Dr. Weitkamp said, is how much nirsevimab will cost as it is not yet approved by the Food and Drug Administration. However, it has the great advantage of being given only once before the season starts instead of monthly (as required for palivizumab) through the season, “which is painful, inconvenient, and traumatizing. We limit that one to the children at highest risk.”

Rolling out an infant nirsevimab program would likely vary by geographic region, Ms. Kieffer and colleagues said, to help ensure infants are protected during the peak of their region’s RSV season.

The journal’s RSV supplement was supported by Sanofi and AstraZeneca. The studies by Ms. Suh and colleagues and Ms. Kieffer and colleagues were supported by AstraZeneca and Sanofi. Ms. Suh and several coauthors are employees of EpidStrategies. One coauthor is an employee of Sanofi and may hold shares and/or stock options in the company. Ms. Kieffer and several coauthors are employees of Sanofi and may hold shares and/or stock options in the company. Dr. Weitkamp reported no relevant financial relationships.

Patients with heart failure (HF) who received two doses of COVID mRNA vaccines were not more likely to have worsening disease, venous thromboembolism, or myocarditis within 90 days than similar unvaccinated patients, in a case-control study in Denmark.

Moreover, in the 90 days after receiving the second shot, vaccinated patients were less likely to die of any cause, compared with unvaccinated patients during a similar 90-day period.

Caroline Sindet-Pedersen, PhD, Herlev and Gentofte Hospital, Hellerup, Denmark, and colleagues presented these findings at the annual congress of the European Society of Cardiology.
 

Major risk is not receiving vaccine

These results “confirm that the major risk for patients with HF is not receiving vaccination for COVID-19,” Marco Metra, MD, who was not involved with this research, said in an interview.

Dr. Metra was coauthor of an ESC guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic, published online ahead of print November 2021 in the European Heart Journal.

The guidance explains that patients with HF are at increased risk for hospitalization, need for mechanical ventilation, and death because of COVID-19, and that vaccination reduces the risk for serious illness from COVID-19, Dr. Sindet-Pedersen and colleagues explained in a press release from the ESC.

However, “concerns remain,” they added, “about the safety of the SARS-CoV-2 mRNA vaccines in heart failure patients, due to a perceived increased risk of cardiovascular side effects.”

The study findings suggest that “there should be no concern about cardiovascular side effects from mRNA vaccines in heart failure patients,” Dr. Sindet-Pedersen and colleagues summarized.

The results also “point to a beneficial effect of vaccination on mortality” and “indicate that patients with HF should be prioritized for COVID-19 vaccinations and boosters,” they added.

“There are ongoing concerns about the safety of COVID-19 vaccination in fragile patients and patients with heart failure,” said Dr. Metra, professor of cardiology and director of the Institute of Cardiology of the Civil Hospital and University of Brescia (Italy).

“These concerns are not based on evidence but just on reports of rare side effects (namely, myocarditis and pericarditis) in vaccinated people,” he added.

Dr. Metra also coauthored a position paper on COVID-19 vaccination in patients with HF from the Heart Failure Association of the ESC, which was published online October 2021 in the European Journal of Heart Failure.

“The current study,” he summarized, “shows a lower risk of mortality among patients vaccinated, compared with those not vaccinated.

“It has limitations,” he cautioned, “as it is not a prospective randomized study, but [rather] an observational one with comparison between vaccinated and not vaccinated patients with similar characteristics.

“However, it was done in a large population,” he noted, “and its results confirm that the major risk for patients with HF is not receiving vaccination for COVID-19.”

95% of patients with HF in Denmark double vaccinated

The group did not analyze the types of all-cause death in their study, Dr. Sindet-Pedersen clarified in an interview.

Other studies have shown that vaccines are associated with improved survival, she noted. For example, bacillus Calmette-Guérin vaccines and the measles vaccines have been linked with a decreased risk for nonspecific mortality in children, and influenza vaccines are associated with decreased all-cause mortality in patients with HF.

The rates of vaccination in this study were much higher than those for patients with HF in the United States.

In a study of 7,094 patients with HF seen at the Mount Sinai Health System between January 2021 and January 2022, 31% of patients were fully vaccinated with two doses and 14.8% had also received a booster, as per Centers for Disease Control and Prevention guidance. However, another 9.1% of patients were only partially vaccinated with one dose, and 45% remained unvaccinated by January 2022,

In the current study, “the uptake was very high,” Dr. Sindet-Pedersen noted, that is, “95% of the prevalent heart failure patients in 2021 received a vaccine.”

“It might be that the last 5% of the patients that did not receive a vaccine were too ill [terminal] to receive the vaccine,” she speculated, “or that was due to personal reasons.”

The researchers identified 50,893 patients with HF who were double vaccinated in 2021 and they matched them with 50,893 unvaccinated patients with HF in 2019 (prepandemic), with the same age, sex, HF duration, use of HF medications, ischemic heart disease, cancer, diabetes, atrial fibrillation, and admission with HF within 90 days.

Almost all patients in the vaccinated group received the Pfizer/BioNTech mRNA vaccine (92%) and the rest received the Moderna mRNA vaccine (8%), in 2021.

The patients had a mean age of 74, and 64% were men. They had HF for a median of 4.1 years.

During the 90-day follow-up, 1,311 patients in the unvaccinated cohort (2.56%) and 1,113 patients in the vaccinated cohort (2.23%) died; there was a significantly lower risk for all-cause death in the vaccinated cohort versus the unvaccinated cohort (–0.33 percentage points; 95% CI, –0.52 to –0.15 percentage points).

The risk for worsening heart failure was 1.1% in each group; myocarditis and venous thromboembolism were extremely rare, and risks for these conditions were not significantly different in the two groups.

The researchers and Dr. Metra declared they have no relevant financial disclosures. Dr. Metra is editor-in-chief of the European Journal of Heart Failure and senior consulting editor of the European Heart Journal.

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

Patients with heart failure (HF) who received two doses of COVID mRNA vaccines were not more likely to have worsening disease, venous thromboembolism, or myocarditis within 90 days than similar unvaccinated patients, in a case-control study in Denmark.

Moreover, in the 90 days after receiving the second shot, vaccinated patients were less likely to die of any cause, compared with unvaccinated patients during a similar 90-day period.

Caroline Sindet-Pedersen, PhD, Herlev and Gentofte Hospital, Hellerup, Denmark, and colleagues presented these findings at the annual congress of the European Society of Cardiology.
 

Major risk is not receiving vaccine

These results “confirm that the major risk for patients with HF is not receiving vaccination for COVID-19,” Marco Metra, MD, who was not involved with this research, said in an interview.

Dr. Metra was coauthor of an ESC guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic, published online ahead of print November 2021 in the European Heart Journal.

The guidance explains that patients with HF are at increased risk for hospitalization, need for mechanical ventilation, and death because of COVID-19, and that vaccination reduces the risk for serious illness from COVID-19, Dr. Sindet-Pedersen and colleagues explained in a press release from the ESC.

However, “concerns remain,” they added, “about the safety of the SARS-CoV-2 mRNA vaccines in heart failure patients, due to a perceived increased risk of cardiovascular side effects.”

The study findings suggest that “there should be no concern about cardiovascular side effects from mRNA vaccines in heart failure patients,” Dr. Sindet-Pedersen and colleagues summarized.

The results also “point to a beneficial effect of vaccination on mortality” and “indicate that patients with HF should be prioritized for COVID-19 vaccinations and boosters,” they added.

“There are ongoing concerns about the safety of COVID-19 vaccination in fragile patients and patients with heart failure,” said Dr. Metra, professor of cardiology and director of the Institute of Cardiology of the Civil Hospital and University of Brescia (Italy).

“These concerns are not based on evidence but just on reports of rare side effects (namely, myocarditis and pericarditis) in vaccinated people,” he added.

Dr. Metra also coauthored a position paper on COVID-19 vaccination in patients with HF from the Heart Failure Association of the ESC, which was published online October 2021 in the European Journal of Heart Failure.

“The current study,” he summarized, “shows a lower risk of mortality among patients vaccinated, compared with those not vaccinated.

“It has limitations,” he cautioned, “as it is not a prospective randomized study, but [rather] an observational one with comparison between vaccinated and not vaccinated patients with similar characteristics.

“However, it was done in a large population,” he noted, “and its results confirm that the major risk for patients with HF is not receiving vaccination for COVID-19.”

95% of patients with HF in Denmark double vaccinated

The group did not analyze the types of all-cause death in their study, Dr. Sindet-Pedersen clarified in an interview.

Other studies have shown that vaccines are associated with improved survival, she noted. For example, bacillus Calmette-Guérin vaccines and the measles vaccines have been linked with a decreased risk for nonspecific mortality in children, and influenza vaccines are associated with decreased all-cause mortality in patients with HF.

The rates of vaccination in this study were much higher than those for patients with HF in the United States.

In a study of 7,094 patients with HF seen at the Mount Sinai Health System between January 2021 and January 2022, 31% of patients were fully vaccinated with two doses and 14.8% had also received a booster, as per Centers for Disease Control and Prevention guidance. However, another 9.1% of patients were only partially vaccinated with one dose, and 45% remained unvaccinated by January 2022,

In the current study, “the uptake was very high,” Dr. Sindet-Pedersen noted, that is, “95% of the prevalent heart failure patients in 2021 received a vaccine.”

“It might be that the last 5% of the patients that did not receive a vaccine were too ill [terminal] to receive the vaccine,” she speculated, “or that was due to personal reasons.”

The researchers identified 50,893 patients with HF who were double vaccinated in 2021 and they matched them with 50,893 unvaccinated patients with HF in 2019 (prepandemic), with the same age, sex, HF duration, use of HF medications, ischemic heart disease, cancer, diabetes, atrial fibrillation, and admission with HF within 90 days.

Almost all patients in the vaccinated group received the Pfizer/BioNTech mRNA vaccine (92%) and the rest received the Moderna mRNA vaccine (8%), in 2021.

The patients had a mean age of 74, and 64% were men. They had HF for a median of 4.1 years.

During the 90-day follow-up, 1,311 patients in the unvaccinated cohort (2.56%) and 1,113 patients in the vaccinated cohort (2.23%) died; there was a significantly lower risk for all-cause death in the vaccinated cohort versus the unvaccinated cohort (–0.33 percentage points; 95% CI, –0.52 to –0.15 percentage points).

The risk for worsening heart failure was 1.1% in each group; myocarditis and venous thromboembolism were extremely rare, and risks for these conditions were not significantly different in the two groups.

The researchers and Dr. Metra declared they have no relevant financial disclosures. Dr. Metra is editor-in-chief of the European Journal of Heart Failure and senior consulting editor of the European Heart Journal.

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

Patients with heart failure (HF) who received two doses of COVID mRNA vaccines were not more likely to have worsening disease, venous thromboembolism, or myocarditis within 90 days than similar unvaccinated patients, in a case-control study in Denmark.

Moreover, in the 90 days after receiving the second shot, vaccinated patients were less likely to die of any cause, compared with unvaccinated patients during a similar 90-day period.

Caroline Sindet-Pedersen, PhD, Herlev and Gentofte Hospital, Hellerup, Denmark, and colleagues presented these findings at the annual congress of the European Society of Cardiology.
 

Major risk is not receiving vaccine

These results “confirm that the major risk for patients with HF is not receiving vaccination for COVID-19,” Marco Metra, MD, who was not involved with this research, said in an interview.

Dr. Metra was coauthor of an ESC guidance for the diagnosis and management of cardiovascular disease during the COVID-19 pandemic, published online ahead of print November 2021 in the European Heart Journal.

The guidance explains that patients with HF are at increased risk for hospitalization, need for mechanical ventilation, and death because of COVID-19, and that vaccination reduces the risk for serious illness from COVID-19, Dr. Sindet-Pedersen and colleagues explained in a press release from the ESC.

However, “concerns remain,” they added, “about the safety of the SARS-CoV-2 mRNA vaccines in heart failure patients, due to a perceived increased risk of cardiovascular side effects.”

The study findings suggest that “there should be no concern about cardiovascular side effects from mRNA vaccines in heart failure patients,” Dr. Sindet-Pedersen and colleagues summarized.

The results also “point to a beneficial effect of vaccination on mortality” and “indicate that patients with HF should be prioritized for COVID-19 vaccinations and boosters,” they added.

“There are ongoing concerns about the safety of COVID-19 vaccination in fragile patients and patients with heart failure,” said Dr. Metra, professor of cardiology and director of the Institute of Cardiology of the Civil Hospital and University of Brescia (Italy).

“These concerns are not based on evidence but just on reports of rare side effects (namely, myocarditis and pericarditis) in vaccinated people,” he added.

Dr. Metra also coauthored a position paper on COVID-19 vaccination in patients with HF from the Heart Failure Association of the ESC, which was published online October 2021 in the European Journal of Heart Failure.

“The current study,” he summarized, “shows a lower risk of mortality among patients vaccinated, compared with those not vaccinated.

“It has limitations,” he cautioned, “as it is not a prospective randomized study, but [rather] an observational one with comparison between vaccinated and not vaccinated patients with similar characteristics.

“However, it was done in a large population,” he noted, “and its results confirm that the major risk for patients with HF is not receiving vaccination for COVID-19.”

95% of patients with HF in Denmark double vaccinated

The group did not analyze the types of all-cause death in their study, Dr. Sindet-Pedersen clarified in an interview.

Other studies have shown that vaccines are associated with improved survival, she noted. For example, bacillus Calmette-Guérin vaccines and the measles vaccines have been linked with a decreased risk for nonspecific mortality in children, and influenza vaccines are associated with decreased all-cause mortality in patients with HF.

The rates of vaccination in this study were much higher than those for patients with HF in the United States.

In a study of 7,094 patients with HF seen at the Mount Sinai Health System between January 2021 and January 2022, 31% of patients were fully vaccinated with two doses and 14.8% had also received a booster, as per Centers for Disease Control and Prevention guidance. However, another 9.1% of patients were only partially vaccinated with one dose, and 45% remained unvaccinated by January 2022,

In the current study, “the uptake was very high,” Dr. Sindet-Pedersen noted, that is, “95% of the prevalent heart failure patients in 2021 received a vaccine.”

“It might be that the last 5% of the patients that did not receive a vaccine were too ill [terminal] to receive the vaccine,” she speculated, “or that was due to personal reasons.”

The researchers identified 50,893 patients with HF who were double vaccinated in 2021 and they matched them with 50,893 unvaccinated patients with HF in 2019 (prepandemic), with the same age, sex, HF duration, use of HF medications, ischemic heart disease, cancer, diabetes, atrial fibrillation, and admission with HF within 90 days.

Almost all patients in the vaccinated group received the Pfizer/BioNTech mRNA vaccine (92%) and the rest received the Moderna mRNA vaccine (8%), in 2021.

The patients had a mean age of 74, and 64% were men. They had HF for a median of 4.1 years.

During the 90-day follow-up, 1,311 patients in the unvaccinated cohort (2.56%) and 1,113 patients in the vaccinated cohort (2.23%) died; there was a significantly lower risk for all-cause death in the vaccinated cohort versus the unvaccinated cohort (–0.33 percentage points; 95% CI, –0.52 to –0.15 percentage points).

The risk for worsening heart failure was 1.1% in each group; myocarditis and venous thromboembolism were extremely rare, and risks for these conditions were not significantly different in the two groups.

The researchers and Dr. Metra declared they have no relevant financial disclosures. Dr. Metra is editor-in-chief of the European Journal of Heart Failure and senior consulting editor of the European Heart Journal.

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

When Jaime Seltzer first heard about a new virus that was spreading globally early in 2020, she was on full alert. As an advocate for the post-viral condition known as myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), she worried about a new wave of people having long-term disabilities.

“The hair on my arms stood on end,” said Ms. Seltzer, director of scientific and medical outreach at the advocacy group MEAction and a consultant researcher at Stanford University.

If the percentage of people with COVID-19 who go on to have long-term symptoms “similar to what has been seen for other pathogens, then we’re looking at a mass disabling event,” Ms. Seltzer, who has had ME/CFS herself, said she wondered.

Sure enough, later in 2020, reports began emerging about people with extreme fatigue, postexertion crashes, brain fog, unrefreshing sleep, and dizziness when standing up months after a bout with the then-new viral illness. Those same symptoms had been designated as “core criteria” of ME/CFS by the National Academy of Medicine in a 2015 report.

Now, advocates like Ms. Seltzer are hoping the research and medical communities will give ME/CFS and other postviral illnesses the same attention they have increasingly focused on long COVID.

The emergence of long COVID was no surprise to researchers who study ME/CFS, because the same set of symptoms has arisen after many other viruses.

“This for all the world looks like ME/CFS. We think they are frighteningly similar, if not identical,” said David M. Systrom, MD, a pulmonary and critical care medicine specialist at Brigham and Women’s Hospital in Boston, who studies people with both diagnoses.

The actual numbers are hard to determine, since many people who meet ME/CFS criteria aren’t formally diagnosed. But a combined analysis of data from several studies published in March found that about one in three people had fatigue and about one in five reported having a hard time with thinking and memory 12 or more weeks after they had COVID-19.

According to some estimates, about half of people with long COVID will meet the criteria for ME/CFS, whether they’re given that specific diagnosis or not.

Other conditions that often exist with ME/CFS are also being seen in people with long COVID, including postural orthostatic tachycardia syndrome, which causes people to feel dizzy when they stand, along with other symptoms; other problems with the autonomic nervous system, which controls body systems such as heart rate, blood pressure, and digestion, known together as dysautonomia; and a condition related to allergies called mast cell activation disorder.

Post–acute infection syndromes have been linked to a long list of viruses, including Ebola, the 2003-2004 SARS virus, and Epstein-Barr – the virus most commonly associated with ME/CFS.

The problem in clinical medicine is that once an infection has cleared, the teaching has been that the person should no longer feel sick, said Nancy G. Klimas, MD, director of the Institute for Neuro-Immune Medicine at Nova Southeastern University in Miami. “I was taught that there has to be an antigen [such as a viral protein] in the system to drive the immune system to make it create sickness, and the immune system should shut off when it’s done,” she said.

Thus, if virus is gone and other routine lab tests come up negative, doctors often deem the person’s reported symptoms to be psychological, which can upset patients, Anthony Komaroff, MD, of Brigham and Women’s Hospital in Boston, wrote in July 2021.

Only recently have doctors started to appreciate the idea that the immune system may be overreacting long term, Dr. Klimas said.

Now, long COVID appears to be speeding up that recognition. Dr. Systrom said he has “absolutely” seen a change in attitude among fellow doctors who had been skeptical of ME/CFS as a “real” illness because there’s no test for it.

“I’m very keenly aware of a large group of health care professionals who really had not bought into the concept of ME/CFS as a real disease who have had an epiphany of sorts with long COVID and now, in a backwards way, have applied that same thinking to their very same patients with ME/CFS,” he said.
 

Science showing ‘frighteningly similar’ symptoms

Dr. Systrom has spent several years researching how ME/CFS patients cannot tolerate exercise and now is doing similar studies in people with long COVID. “Several months into the pandemic, we began receiving reports of patients who had survived COVID and maybe even had a relatively mild disease ... and as the summer of 2020 moved into the fall, it became apparent that there was a subset of patients who for all the world appeared to meet ME/CFS clinical criteria,” he said.

Using bicycle exercise tests on long COVID patients with catheters placed in their veins, Dr. Systrom and associates have shown a lack of exercise capacity that isn’t caused by heart or lung disease but instead is related to abnormal nerves and blood vessels, just as they’d shown previously in ME/CFS patient.

Avindra Nath, MD, senior investigator and clinical director of intramural research at the National Institute of Neurological Disorders and Stroke, Bethesda, Md., was doing a deep-dive scientific study on ME/CFS when the COVID-19 pandemic hit. Since then, he›s begun another study using the same protocol and sophisticated laboratory measurement to evaluate people with long COVID.

“As terrible as [long COVID] is, it’s kind of a blessing in disguise for ME/CFS because there’s just so much overlap between the two and they could very well be in many ways one in the same thing. The problem with studying ME/CFS is oftentimes you didn’t know what the trigger was. You see patients many years later, then try to backtrack and find out what happened,” said Dr. Nath, a neuroimmunologist.

With long COVID, on the other hand, “we know when they got infected and when their symptoms actually started, so it becomes much more uniform. ... It gives us an opportunity to maybe solve certain things in a much more well-defined population and try to find answers.”

Advocacy groups want to see more.

In February 2021, Solve M.E. launched the Long COVID Alliance, made up of several organizations, companies, and people with a goal to influence policy and speed up research into a range of postviral illnesses.

Solve M.E. has also pushed for inclusion of language regarding ME/CFS and related conditions into congressional bills addressing long COVID, including those that call for funding of research and clinical care.

“On the political front, we’ve really capitalized on a moment in time in which we have the spotlight,” said Emily Taylor, vice president of advocacy and engagement for Solve M.E.

“One of the hardest parts about ME/CFS is how to show that it’s real when it’s invisible. Most people agree that COVID is real and therefore if somebody gets ME/CFS after COVID, it’s real,” she said.

The advocacy groups are now pushing for non-COVID postinfection illnesses to be included in efforts aimed at helping people with long COVID, with mixed results. For example, the RECOVER Initiative, established in February 2021 with $1.5 billion in funding from Congress to the National Institutes of Health, is specifically for studying long COVID and does not fund research into other postinfection illnesses, although representatives from the ME/CFS community are advisers.

Language addressing ME/CFS and other postinfectious chronic illnesses has been included in several long COVID bills now pending in Congress, including the Care for Long COVID Act in the Senate and its companion COVID-19 Long Haulers Act in the House. “Our goal is to push for passage of a long COVID bill by the end of the year,” Ms. Taylor said.

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

When Jaime Seltzer first heard about a new virus that was spreading globally early in 2020, she was on full alert. As an advocate for the post-viral condition known as myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), she worried about a new wave of people having long-term disabilities.

“The hair on my arms stood on end,” said Ms. Seltzer, director of scientific and medical outreach at the advocacy group MEAction and a consultant researcher at Stanford University.

If the percentage of people with COVID-19 who go on to have long-term symptoms “similar to what has been seen for other pathogens, then we’re looking at a mass disabling event,” Ms. Seltzer, who has had ME/CFS herself, said she wondered.

Sure enough, later in 2020, reports began emerging about people with extreme fatigue, postexertion crashes, brain fog, unrefreshing sleep, and dizziness when standing up months after a bout with the then-new viral illness. Those same symptoms had been designated as “core criteria” of ME/CFS by the National Academy of Medicine in a 2015 report.

Now, advocates like Ms. Seltzer are hoping the research and medical communities will give ME/CFS and other postviral illnesses the same attention they have increasingly focused on long COVID.

The emergence of long COVID was no surprise to researchers who study ME/CFS, because the same set of symptoms has arisen after many other viruses.

“This for all the world looks like ME/CFS. We think they are frighteningly similar, if not identical,” said David M. Systrom, MD, a pulmonary and critical care medicine specialist at Brigham and Women’s Hospital in Boston, who studies people with both diagnoses.

The actual numbers are hard to determine, since many people who meet ME/CFS criteria aren’t formally diagnosed. But a combined analysis of data from several studies published in March found that about one in three people had fatigue and about one in five reported having a hard time with thinking and memory 12 or more weeks after they had COVID-19.

According to some estimates, about half of people with long COVID will meet the criteria for ME/CFS, whether they’re given that specific diagnosis or not.

Other conditions that often exist with ME/CFS are also being seen in people with long COVID, including postural orthostatic tachycardia syndrome, which causes people to feel dizzy when they stand, along with other symptoms; other problems with the autonomic nervous system, which controls body systems such as heart rate, blood pressure, and digestion, known together as dysautonomia; and a condition related to allergies called mast cell activation disorder.

Post–acute infection syndromes have been linked to a long list of viruses, including Ebola, the 2003-2004 SARS virus, and Epstein-Barr – the virus most commonly associated with ME/CFS.

The problem in clinical medicine is that once an infection has cleared, the teaching has been that the person should no longer feel sick, said Nancy G. Klimas, MD, director of the Institute for Neuro-Immune Medicine at Nova Southeastern University in Miami. “I was taught that there has to be an antigen [such as a viral protein] in the system to drive the immune system to make it create sickness, and the immune system should shut off when it’s done,” she said.

Thus, if virus is gone and other routine lab tests come up negative, doctors often deem the person’s reported symptoms to be psychological, which can upset patients, Anthony Komaroff, MD, of Brigham and Women’s Hospital in Boston, wrote in July 2021.

Only recently have doctors started to appreciate the idea that the immune system may be overreacting long term, Dr. Klimas said.

Now, long COVID appears to be speeding up that recognition. Dr. Systrom said he has “absolutely” seen a change in attitude among fellow doctors who had been skeptical of ME/CFS as a “real” illness because there’s no test for it.

“I’m very keenly aware of a large group of health care professionals who really had not bought into the concept of ME/CFS as a real disease who have had an epiphany of sorts with long COVID and now, in a backwards way, have applied that same thinking to their very same patients with ME/CFS,” he said.
 

Science showing ‘frighteningly similar’ symptoms

Dr. Systrom has spent several years researching how ME/CFS patients cannot tolerate exercise and now is doing similar studies in people with long COVID. “Several months into the pandemic, we began receiving reports of patients who had survived COVID and maybe even had a relatively mild disease ... and as the summer of 2020 moved into the fall, it became apparent that there was a subset of patients who for all the world appeared to meet ME/CFS clinical criteria,” he said.

Using bicycle exercise tests on long COVID patients with catheters placed in their veins, Dr. Systrom and associates have shown a lack of exercise capacity that isn’t caused by heart or lung disease but instead is related to abnormal nerves and blood vessels, just as they’d shown previously in ME/CFS patient.

Avindra Nath, MD, senior investigator and clinical director of intramural research at the National Institute of Neurological Disorders and Stroke, Bethesda, Md., was doing a deep-dive scientific study on ME/CFS when the COVID-19 pandemic hit. Since then, he›s begun another study using the same protocol and sophisticated laboratory measurement to evaluate people with long COVID.

“As terrible as [long COVID] is, it’s kind of a blessing in disguise for ME/CFS because there’s just so much overlap between the two and they could very well be in many ways one in the same thing. The problem with studying ME/CFS is oftentimes you didn’t know what the trigger was. You see patients many years later, then try to backtrack and find out what happened,” said Dr. Nath, a neuroimmunologist.

With long COVID, on the other hand, “we know when they got infected and when their symptoms actually started, so it becomes much more uniform. ... It gives us an opportunity to maybe solve certain things in a much more well-defined population and try to find answers.”

Advocacy groups want to see more.

In February 2021, Solve M.E. launched the Long COVID Alliance, made up of several organizations, companies, and people with a goal to influence policy and speed up research into a range of postviral illnesses.

Solve M.E. has also pushed for inclusion of language regarding ME/CFS and related conditions into congressional bills addressing long COVID, including those that call for funding of research and clinical care.

“On the political front, we’ve really capitalized on a moment in time in which we have the spotlight,” said Emily Taylor, vice president of advocacy and engagement for Solve M.E.

“One of the hardest parts about ME/CFS is how to show that it’s real when it’s invisible. Most people agree that COVID is real and therefore if somebody gets ME/CFS after COVID, it’s real,” she said.

The advocacy groups are now pushing for non-COVID postinfection illnesses to be included in efforts aimed at helping people with long COVID, with mixed results. For example, the RECOVER Initiative, established in February 2021 with $1.5 billion in funding from Congress to the National Institutes of Health, is specifically for studying long COVID and does not fund research into other postinfection illnesses, although representatives from the ME/CFS community are advisers.

Language addressing ME/CFS and other postinfectious chronic illnesses has been included in several long COVID bills now pending in Congress, including the Care for Long COVID Act in the Senate and its companion COVID-19 Long Haulers Act in the House. “Our goal is to push for passage of a long COVID bill by the end of the year,” Ms. Taylor said.

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

When Jaime Seltzer first heard about a new virus that was spreading globally early in 2020, she was on full alert. As an advocate for the post-viral condition known as myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), she worried about a new wave of people having long-term disabilities.

“The hair on my arms stood on end,” said Ms. Seltzer, director of scientific and medical outreach at the advocacy group MEAction and a consultant researcher at Stanford University.

If the percentage of people with COVID-19 who go on to have long-term symptoms “similar to what has been seen for other pathogens, then we’re looking at a mass disabling event,” Ms. Seltzer, who has had ME/CFS herself, said she wondered.

Sure enough, later in 2020, reports began emerging about people with extreme fatigue, postexertion crashes, brain fog, unrefreshing sleep, and dizziness when standing up months after a bout with the then-new viral illness. Those same symptoms had been designated as “core criteria” of ME/CFS by the National Academy of Medicine in a 2015 report.

Now, advocates like Ms. Seltzer are hoping the research and medical communities will give ME/CFS and other postviral illnesses the same attention they have increasingly focused on long COVID.

The emergence of long COVID was no surprise to researchers who study ME/CFS, because the same set of symptoms has arisen after many other viruses.

“This for all the world looks like ME/CFS. We think they are frighteningly similar, if not identical,” said David M. Systrom, MD, a pulmonary and critical care medicine specialist at Brigham and Women’s Hospital in Boston, who studies people with both diagnoses.

The actual numbers are hard to determine, since many people who meet ME/CFS criteria aren’t formally diagnosed. But a combined analysis of data from several studies published in March found that about one in three people had fatigue and about one in five reported having a hard time with thinking and memory 12 or more weeks after they had COVID-19.

According to some estimates, about half of people with long COVID will meet the criteria for ME/CFS, whether they’re given that specific diagnosis or not.

Other conditions that often exist with ME/CFS are also being seen in people with long COVID, including postural orthostatic tachycardia syndrome, which causes people to feel dizzy when they stand, along with other symptoms; other problems with the autonomic nervous system, which controls body systems such as heart rate, blood pressure, and digestion, known together as dysautonomia; and a condition related to allergies called mast cell activation disorder.

Post–acute infection syndromes have been linked to a long list of viruses, including Ebola, the 2003-2004 SARS virus, and Epstein-Barr – the virus most commonly associated with ME/CFS.

The problem in clinical medicine is that once an infection has cleared, the teaching has been that the person should no longer feel sick, said Nancy G. Klimas, MD, director of the Institute for Neuro-Immune Medicine at Nova Southeastern University in Miami. “I was taught that there has to be an antigen [such as a viral protein] in the system to drive the immune system to make it create sickness, and the immune system should shut off when it’s done,” she said.

Thus, if virus is gone and other routine lab tests come up negative, doctors often deem the person’s reported symptoms to be psychological, which can upset patients, Anthony Komaroff, MD, of Brigham and Women’s Hospital in Boston, wrote in July 2021.

Only recently have doctors started to appreciate the idea that the immune system may be overreacting long term, Dr. Klimas said.

Now, long COVID appears to be speeding up that recognition. Dr. Systrom said he has “absolutely” seen a change in attitude among fellow doctors who had been skeptical of ME/CFS as a “real” illness because there’s no test for it.

“I’m very keenly aware of a large group of health care professionals who really had not bought into the concept of ME/CFS as a real disease who have had an epiphany of sorts with long COVID and now, in a backwards way, have applied that same thinking to their very same patients with ME/CFS,” he said.
 

Science showing ‘frighteningly similar’ symptoms

Dr. Systrom has spent several years researching how ME/CFS patients cannot tolerate exercise and now is doing similar studies in people with long COVID. “Several months into the pandemic, we began receiving reports of patients who had survived COVID and maybe even had a relatively mild disease ... and as the summer of 2020 moved into the fall, it became apparent that there was a subset of patients who for all the world appeared to meet ME/CFS clinical criteria,” he said.

Using bicycle exercise tests on long COVID patients with catheters placed in their veins, Dr. Systrom and associates have shown a lack of exercise capacity that isn’t caused by heart or lung disease but instead is related to abnormal nerves and blood vessels, just as they’d shown previously in ME/CFS patient.

Avindra Nath, MD, senior investigator and clinical director of intramural research at the National Institute of Neurological Disorders and Stroke, Bethesda, Md., was doing a deep-dive scientific study on ME/CFS when the COVID-19 pandemic hit. Since then, he›s begun another study using the same protocol and sophisticated laboratory measurement to evaluate people with long COVID.

“As terrible as [long COVID] is, it’s kind of a blessing in disguise for ME/CFS because there’s just so much overlap between the two and they could very well be in many ways one in the same thing. The problem with studying ME/CFS is oftentimes you didn’t know what the trigger was. You see patients many years later, then try to backtrack and find out what happened,” said Dr. Nath, a neuroimmunologist.

With long COVID, on the other hand, “we know when they got infected and when their symptoms actually started, so it becomes much more uniform. ... It gives us an opportunity to maybe solve certain things in a much more well-defined population and try to find answers.”

Advocacy groups want to see more.

In February 2021, Solve M.E. launched the Long COVID Alliance, made up of several organizations, companies, and people with a goal to influence policy and speed up research into a range of postviral illnesses.

Solve M.E. has also pushed for inclusion of language regarding ME/CFS and related conditions into congressional bills addressing long COVID, including those that call for funding of research and clinical care.

“On the political front, we’ve really capitalized on a moment in time in which we have the spotlight,” said Emily Taylor, vice president of advocacy and engagement for Solve M.E.

“One of the hardest parts about ME/CFS is how to show that it’s real when it’s invisible. Most people agree that COVID is real and therefore if somebody gets ME/CFS after COVID, it’s real,” she said.

The advocacy groups are now pushing for non-COVID postinfection illnesses to be included in efforts aimed at helping people with long COVID, with mixed results. For example, the RECOVER Initiative, established in February 2021 with $1.5 billion in funding from Congress to the National Institutes of Health, is specifically for studying long COVID and does not fund research into other postinfection illnesses, although representatives from the ME/CFS community are advisers.

Language addressing ME/CFS and other postinfectious chronic illnesses has been included in several long COVID bills now pending in Congress, including the Care for Long COVID Act in the Senate and its companion COVID-19 Long Haulers Act in the House. “Our goal is to push for passage of a long COVID bill by the end of the year,” Ms. Taylor said.

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

The Spanish Society of Pulmonology and Thoracic Surgery (SEPAR) has issued a new international consensus document (ICD) on obstructive sleep apnea (OSA). The objective is to improve the diagnosis and treatment of one of the most prevalent sleep disorders.

The ICD represents a collaboration of experts from 17 scientific societies and 56 specialists from various countries. It provides a series of clinical guidelines to help health care professionals make the best decisions for adult patients with OSA. Notably, the authors propose changing the name from sleep apnea syndrome. In recommending the term OSA, they reintroduce the term “obstructive” – to differentiate the disorder from central sleep apnea – and remove the outdated word “syndrome.”

“The definition has also been changed, as it was a bit vague and difficult to understand. And there are significant changes to the treatment and to the diagnostic algorithms – one for primary care and another for sleep units,” Olga Mediano, MD, said in an interview. She is a SEPAR pulmonologist, first author of the ICD, and the coordinator of SEPAR 2022 Year of Intermediate Respiratory Care Units.
 

Diagnosis in primary care

The ICD indicates that all levels of care must be involved in the management of OSA, a condition in which complete or partial upper airway blockage occurs during sleep, causing the individual to stop breathing for a few seconds. These pauses, which produce hypoxia and sleep fragmentation, increase the risk of workplace and traffic accidents, affect cardiovascular health, and contribute to uncontrolled or resistant hypertension.

The recommendations in the ICD aim at increasing the role of primary care physicians so as to reduce underdiagnosis of OSA in primary care. “The vast majority of patients with OSA haven’t been diagnosed. In fact, those whom we have diagnosed are the patients with the most severe cases – in other words, patients who present with the most symptoms,” said Dr. Mediano. She explained that many patients with OSA don’t consider it a medical condition, so they do not go to the doctor.

“The other big problem is that, before, there was a preconceived notion of the typical OSA patient: A middle-aged obese man who’s fallen asleep in the waiting room. However, there are many other profiles: thin build, women. ... Sleep has a heterogeneous profile, and all profiles need to be known,” said Dr. Mediano. The difficulties in carrying out a sleep study with the various patients are an added problem that the new consensus document also seeks to resolve. “The step we’ve taken is to involve the primary care physician in super-simplified studies to reach more people,” she said. For this, the primary care site must work in coordination with a sleep unit.

“In the super-simplified study, the patient is given a machine to use at home; they hook themselves up to it when they go to sleep. This machine records the number of apnea episodes the patient experiences during the night, as well as the oxygen level. The next day, the patient returns the machine. The data are downloaded to a computer. The software analyzes the breathing pauses that the patient had during the night and automatically gives a series of values that, if very pronounced, as the document indicates, would lead to a diagnosis of OSA. Once diagnosed by a primary care physician, the patient is referred to a sleep unit where treatment can then be assessed,” explained Dr. Mediano.
 

Different treatments

The new ICD’s approach incorporates therapeutic alternatives as well. Until now, many consensus documents and clinical guidelines have focused on continuous positive airway pressure therapy, in which a machine delivers continuous airflow to help keep the patient’s airway open and unobstructed during sleep. Some guidelines recommend its use, and others do not. “However, in this new document, management of the patient is much more multidisciplinary. What changes, with respect to the treatment, is the philosophy. It’s not one single type of treatment; rather, other therapeutic options are kept in mind,” said Dr. Mediano.

First, treatment of reversible causes of OSA must be offered. The conditions that lead to OSA and that can be reversed are addressed. These include overweight and obesity; heavy drinking; tonsillar hypertrophy, or severe dental or facial alterations, for which surgery can be considered; and gastroesophageal reflux or hypothyroidism, both of which can be treated. “For example, the leading cause of sleep apnea is obesity. If we can get the patient to lose weight, that can end up making the OSA go away. What does the document say? Well, you have to try to implement intensive strategies regarding diet, exercise, etc. And if that’s not enough, you need to consider using drugs or even bariatric surgery,” said Dr. Mediano.

“If there’s no one definitive treatment, we highly recommend that all patients implement hygienic-dietary measures and then assess all the therapeutic options. In some cases, several can be in place at the same time,” she said. Various medical specialists can play a role in the treatment of OSA, said Dr. Mediano. They include otolaryngologists, maxillofacial surgeons, dentists, cardiologists, and neurophysiologists, to mention a few.

A website has been created to explain the ICD. There, visitors will be able to find the most up-to-date version of the ICD as well as related information, news, and materials.

A version of this article appeared on Medscape.com. This article was translated from Univadis Spain.

The Spanish Society of Pulmonology and Thoracic Surgery (SEPAR) has issued a new international consensus document (ICD) on obstructive sleep apnea (OSA). The objective is to improve the diagnosis and treatment of one of the most prevalent sleep disorders.

The ICD represents a collaboration of experts from 17 scientific societies and 56 specialists from various countries. It provides a series of clinical guidelines to help health care professionals make the best decisions for adult patients with OSA. Notably, the authors propose changing the name from sleep apnea syndrome. In recommending the term OSA, they reintroduce the term “obstructive” – to differentiate the disorder from central sleep apnea – and remove the outdated word “syndrome.”

“The definition has also been changed, as it was a bit vague and difficult to understand. And there are significant changes to the treatment and to the diagnostic algorithms – one for primary care and another for sleep units,” Olga Mediano, MD, said in an interview. She is a SEPAR pulmonologist, first author of the ICD, and the coordinator of SEPAR 2022 Year of Intermediate Respiratory Care Units.
 

Diagnosis in primary care

The ICD indicates that all levels of care must be involved in the management of OSA, a condition in which complete or partial upper airway blockage occurs during sleep, causing the individual to stop breathing for a few seconds. These pauses, which produce hypoxia and sleep fragmentation, increase the risk of workplace and traffic accidents, affect cardiovascular health, and contribute to uncontrolled or resistant hypertension.

The recommendations in the ICD aim at increasing the role of primary care physicians so as to reduce underdiagnosis of OSA in primary care. “The vast majority of patients with OSA haven’t been diagnosed. In fact, those whom we have diagnosed are the patients with the most severe cases – in other words, patients who present with the most symptoms,” said Dr. Mediano. She explained that many patients with OSA don’t consider it a medical condition, so they do not go to the doctor.

“The other big problem is that, before, there was a preconceived notion of the typical OSA patient: A middle-aged obese man who’s fallen asleep in the waiting room. However, there are many other profiles: thin build, women. ... Sleep has a heterogeneous profile, and all profiles need to be known,” said Dr. Mediano. The difficulties in carrying out a sleep study with the various patients are an added problem that the new consensus document also seeks to resolve. “The step we’ve taken is to involve the primary care physician in super-simplified studies to reach more people,” she said. For this, the primary care site must work in coordination with a sleep unit.

“In the super-simplified study, the patient is given a machine to use at home; they hook themselves up to it when they go to sleep. This machine records the number of apnea episodes the patient experiences during the night, as well as the oxygen level. The next day, the patient returns the machine. The data are downloaded to a computer. The software analyzes the breathing pauses that the patient had during the night and automatically gives a series of values that, if very pronounced, as the document indicates, would lead to a diagnosis of OSA. Once diagnosed by a primary care physician, the patient is referred to a sleep unit where treatment can then be assessed,” explained Dr. Mediano.
 

Different treatments

The new ICD’s approach incorporates therapeutic alternatives as well. Until now, many consensus documents and clinical guidelines have focused on continuous positive airway pressure therapy, in which a machine delivers continuous airflow to help keep the patient’s airway open and unobstructed during sleep. Some guidelines recommend its use, and others do not. “However, in this new document, management of the patient is much more multidisciplinary. What changes, with respect to the treatment, is the philosophy. It’s not one single type of treatment; rather, other therapeutic options are kept in mind,” said Dr. Mediano.

First, treatment of reversible causes of OSA must be offered. The conditions that lead to OSA and that can be reversed are addressed. These include overweight and obesity; heavy drinking; tonsillar hypertrophy, or severe dental or facial alterations, for which surgery can be considered; and gastroesophageal reflux or hypothyroidism, both of which can be treated. “For example, the leading cause of sleep apnea is obesity. If we can get the patient to lose weight, that can end up making the OSA go away. What does the document say? Well, you have to try to implement intensive strategies regarding diet, exercise, etc. And if that’s not enough, you need to consider using drugs or even bariatric surgery,” said Dr. Mediano.

“If there’s no one definitive treatment, we highly recommend that all patients implement hygienic-dietary measures and then assess all the therapeutic options. In some cases, several can be in place at the same time,” she said. Various medical specialists can play a role in the treatment of OSA, said Dr. Mediano. They include otolaryngologists, maxillofacial surgeons, dentists, cardiologists, and neurophysiologists, to mention a few.

A website has been created to explain the ICD. There, visitors will be able to find the most up-to-date version of the ICD as well as related information, news, and materials.

A version of this article appeared on Medscape.com. This article was translated from Univadis Spain.

The Spanish Society of Pulmonology and Thoracic Surgery (SEPAR) has issued a new international consensus document (ICD) on obstructive sleep apnea (OSA). The objective is to improve the diagnosis and treatment of one of the most prevalent sleep disorders.

The ICD represents a collaboration of experts from 17 scientific societies and 56 specialists from various countries. It provides a series of clinical guidelines to help health care professionals make the best decisions for adult patients with OSA. Notably, the authors propose changing the name from sleep apnea syndrome. In recommending the term OSA, they reintroduce the term “obstructive” – to differentiate the disorder from central sleep apnea – and remove the outdated word “syndrome.”

“The definition has also been changed, as it was a bit vague and difficult to understand. And there are significant changes to the treatment and to the diagnostic algorithms – one for primary care and another for sleep units,” Olga Mediano, MD, said in an interview. She is a SEPAR pulmonologist, first author of the ICD, and the coordinator of SEPAR 2022 Year of Intermediate Respiratory Care Units.
 

Diagnosis in primary care

The ICD indicates that all levels of care must be involved in the management of OSA, a condition in which complete or partial upper airway blockage occurs during sleep, causing the individual to stop breathing for a few seconds. These pauses, which produce hypoxia and sleep fragmentation, increase the risk of workplace and traffic accidents, affect cardiovascular health, and contribute to uncontrolled or resistant hypertension.

The recommendations in the ICD aim at increasing the role of primary care physicians so as to reduce underdiagnosis of OSA in primary care. “The vast majority of patients with OSA haven’t been diagnosed. In fact, those whom we have diagnosed are the patients with the most severe cases – in other words, patients who present with the most symptoms,” said Dr. Mediano. She explained that many patients with OSA don’t consider it a medical condition, so they do not go to the doctor.

“The other big problem is that, before, there was a preconceived notion of the typical OSA patient: A middle-aged obese man who’s fallen asleep in the waiting room. However, there are many other profiles: thin build, women. ... Sleep has a heterogeneous profile, and all profiles need to be known,” said Dr. Mediano. The difficulties in carrying out a sleep study with the various patients are an added problem that the new consensus document also seeks to resolve. “The step we’ve taken is to involve the primary care physician in super-simplified studies to reach more people,” she said. For this, the primary care site must work in coordination with a sleep unit.

“In the super-simplified study, the patient is given a machine to use at home; they hook themselves up to it when they go to sleep. This machine records the number of apnea episodes the patient experiences during the night, as well as the oxygen level. The next day, the patient returns the machine. The data are downloaded to a computer. The software analyzes the breathing pauses that the patient had during the night and automatically gives a series of values that, if very pronounced, as the document indicates, would lead to a diagnosis of OSA. Once diagnosed by a primary care physician, the patient is referred to a sleep unit where treatment can then be assessed,” explained Dr. Mediano.
 

Different treatments

The new ICD’s approach incorporates therapeutic alternatives as well. Until now, many consensus documents and clinical guidelines have focused on continuous positive airway pressure therapy, in which a machine delivers continuous airflow to help keep the patient’s airway open and unobstructed during sleep. Some guidelines recommend its use, and others do not. “However, in this new document, management of the patient is much more multidisciplinary. What changes, with respect to the treatment, is the philosophy. It’s not one single type of treatment; rather, other therapeutic options are kept in mind,” said Dr. Mediano.

First, treatment of reversible causes of OSA must be offered. The conditions that lead to OSA and that can be reversed are addressed. These include overweight and obesity; heavy drinking; tonsillar hypertrophy, or severe dental or facial alterations, for which surgery can be considered; and gastroesophageal reflux or hypothyroidism, both of which can be treated. “For example, the leading cause of sleep apnea is obesity. If we can get the patient to lose weight, that can end up making the OSA go away. What does the document say? Well, you have to try to implement intensive strategies regarding diet, exercise, etc. And if that’s not enough, you need to consider using drugs or even bariatric surgery,” said Dr. Mediano.

“If there’s no one definitive treatment, we highly recommend that all patients implement hygienic-dietary measures and then assess all the therapeutic options. In some cases, several can be in place at the same time,” she said. Various medical specialists can play a role in the treatment of OSA, said Dr. Mediano. They include otolaryngologists, maxillofacial surgeons, dentists, cardiologists, and neurophysiologists, to mention a few.

A website has been created to explain the ICD. There, visitors will be able to find the most up-to-date version of the ICD as well as related information, news, and materials.

A version of this article appeared on Medscape.com. This article was translated from Univadis Spain.

A former Kentucky nurse was charged with murder stemming from an incident in which she gave “something special” to a 97-year-old patient who died 5 days later, according to multiple sources, including police and nursing records.

Eyvette Hunter, 52, who had been a registered nurse and previously a licensed practical nurse, was arrested Aug. 23 and charged in connection with the death of James A. Morris, a veteran of World War II and the Korean War, who was being treated at Baptist Health Lexington after a slip-and-fall injury. Ms. Hunter allegedly gave lorazepam, typically used for anxiety, to Mr. Morris on April 30. He subsequently developed pneumonia and died on May 5.

Ms. Hunter “intentionally performed actions of medical maltreatment,” according to the Lexington Police Department’s report.

A Baptist Health Lexington spokeswoman told this news organization that the nurse who was charged hasn’t worked at the hospital since the April incident. “We have learned that a former nurse at our hospital has been arrested yesterday on criminal charges,” spokeswoman Ruth Ann Childers stated. “The hospital has fully cooperated with the police investigation. Patient care and safety are always our top priorities. Out of respect for the patient’s family and because this is criminal matter, we are not able to talk about the investigation.”

According to the Kentucky Board of Nursing, which suspended Ms. Hunter’s RN license on a temporary basis on Aug. 22, she allegedly asked the on-duty physician and a nurse practitioner separately for a medication order to calm Mr. Morris, who had become agitated and aggressive. They denied Ms. Hunter’s request, so she withdrew lorazepam intended for another patient and administered it to Mr. Morris, the nursing board suspension order states. “When asked what was administered, she replied ‘something special,’ “ the order states.

Another RN found the patient with labored breathing and “it was determined that respondent had disarmed/lowered the oxygen monitoring system several times as to not set off an alarm at the bedside,” the order continued. “The RN discussed with charge nurse that the patient had been given something intravenously that was causing his decline.”

When the charge nurse entered the room later, she found the patient in “respiratory distress with labored breathing and poor oxygen saturation. ... X-rays would show that the aspiration from the substances ingested by the patient while in his condition caused the patient to develop aspirational pneumonia,” the order continues.

“Despite the rapidly declining condition of the patient, respondent never called for rapid response nor acted with any sense of urgency. Respondent did however edit documentation of administration of Ativan on ‘patient B’ to state ‘not given.’ ”

Mr. Morris’ condition never improved. He was taken to hospice care on May 3 and died 2 days later, the order states.

Ms. Hunter was being held in the Lexington Jail on $100,000 bond, according to jail records.

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

A former Kentucky nurse was charged with murder stemming from an incident in which she gave “something special” to a 97-year-old patient who died 5 days later, according to multiple sources, including police and nursing records.

Eyvette Hunter, 52, who had been a registered nurse and previously a licensed practical nurse, was arrested Aug. 23 and charged in connection with the death of James A. Morris, a veteran of World War II and the Korean War, who was being treated at Baptist Health Lexington after a slip-and-fall injury. Ms. Hunter allegedly gave lorazepam, typically used for anxiety, to Mr. Morris on April 30. He subsequently developed pneumonia and died on May 5.

Ms. Hunter “intentionally performed actions of medical maltreatment,” according to the Lexington Police Department’s report.

A Baptist Health Lexington spokeswoman told this news organization that the nurse who was charged hasn’t worked at the hospital since the April incident. “We have learned that a former nurse at our hospital has been arrested yesterday on criminal charges,” spokeswoman Ruth Ann Childers stated. “The hospital has fully cooperated with the police investigation. Patient care and safety are always our top priorities. Out of respect for the patient’s family and because this is criminal matter, we are not able to talk about the investigation.”

According to the Kentucky Board of Nursing, which suspended Ms. Hunter’s RN license on a temporary basis on Aug. 22, she allegedly asked the on-duty physician and a nurse practitioner separately for a medication order to calm Mr. Morris, who had become agitated and aggressive. They denied Ms. Hunter’s request, so she withdrew lorazepam intended for another patient and administered it to Mr. Morris, the nursing board suspension order states. “When asked what was administered, she replied ‘something special,’ “ the order states.

Another RN found the patient with labored breathing and “it was determined that respondent had disarmed/lowered the oxygen monitoring system several times as to not set off an alarm at the bedside,” the order continued. “The RN discussed with charge nurse that the patient had been given something intravenously that was causing his decline.”

When the charge nurse entered the room later, she found the patient in “respiratory distress with labored breathing and poor oxygen saturation. ... X-rays would show that the aspiration from the substances ingested by the patient while in his condition caused the patient to develop aspirational pneumonia,” the order continues.

“Despite the rapidly declining condition of the patient, respondent never called for rapid response nor acted with any sense of urgency. Respondent did however edit documentation of administration of Ativan on ‘patient B’ to state ‘not given.’ ”

Mr. Morris’ condition never improved. He was taken to hospice care on May 3 and died 2 days later, the order states.

Ms. Hunter was being held in the Lexington Jail on $100,000 bond, according to jail records.

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

A former Kentucky nurse was charged with murder stemming from an incident in which she gave “something special” to a 97-year-old patient who died 5 days later, according to multiple sources, including police and nursing records.

Eyvette Hunter, 52, who had been a registered nurse and previously a licensed practical nurse, was arrested Aug. 23 and charged in connection with the death of James A. Morris, a veteran of World War II and the Korean War, who was being treated at Baptist Health Lexington after a slip-and-fall injury. Ms. Hunter allegedly gave lorazepam, typically used for anxiety, to Mr. Morris on April 30. He subsequently developed pneumonia and died on May 5.

Ms. Hunter “intentionally performed actions of medical maltreatment,” according to the Lexington Police Department’s report.

A Baptist Health Lexington spokeswoman told this news organization that the nurse who was charged hasn’t worked at the hospital since the April incident. “We have learned that a former nurse at our hospital has been arrested yesterday on criminal charges,” spokeswoman Ruth Ann Childers stated. “The hospital has fully cooperated with the police investigation. Patient care and safety are always our top priorities. Out of respect for the patient’s family and because this is criminal matter, we are not able to talk about the investigation.”

According to the Kentucky Board of Nursing, which suspended Ms. Hunter’s RN license on a temporary basis on Aug. 22, she allegedly asked the on-duty physician and a nurse practitioner separately for a medication order to calm Mr. Morris, who had become agitated and aggressive. They denied Ms. Hunter’s request, so she withdrew lorazepam intended for another patient and administered it to Mr. Morris, the nursing board suspension order states. “When asked what was administered, she replied ‘something special,’ “ the order states.

Another RN found the patient with labored breathing and “it was determined that respondent had disarmed/lowered the oxygen monitoring system several times as to not set off an alarm at the bedside,” the order continued. “The RN discussed with charge nurse that the patient had been given something intravenously that was causing his decline.”

When the charge nurse entered the room later, she found the patient in “respiratory distress with labored breathing and poor oxygen saturation. ... X-rays would show that the aspiration from the substances ingested by the patient while in his condition caused the patient to develop aspirational pneumonia,” the order continues.

“Despite the rapidly declining condition of the patient, respondent never called for rapid response nor acted with any sense of urgency. Respondent did however edit documentation of administration of Ativan on ‘patient B’ to state ‘not given.’ ”

Mr. Morris’ condition never improved. He was taken to hospice care on May 3 and died 2 days later, the order states.

Ms. Hunter was being held in the Lexington Jail on $100,000 bond, according to jail records.

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