Lung cancer stands as the leading cause of cancer-related deaths globally, with its prevalence casting a long and challenging shadow. The most important risk factor for lung cancer is tobacco use, a relationship strongly substantiated by data. The impact of smoking cessation to reduce lung cancer incidence is underscored by the US Preventive Services Task Force, which mandates that smoking cessation services be an integral component of lung cancer screening programs.
However, beneath the surface of this overarching concern lies a web of factors contributing to racial and ethnic disparities in smoking cessation. Cultural intricacies play a pivotal role in shaping these disparities. Despite higher instances of light or intermediate smoking, racially ethnic minority groups in the general population often face greater challenges in achieving smoking cessation, as highlighted by Bacio, et al. Adding another layer to this complex scenario is the profound impact of sustained smoking during cancer treatment. Research suggests that for individuals diagnosed with lung cancer, smoking cessation can markedly boost treatment efficacy, reduce the risk of secondary tumors, and even double the chances of survival.1
A study by Harris, et al. delving into the preferences of current smokers within a lung cancer screening setting uncovered noteworthy insights.2 White participants exhibited a fourfold greater likelihood of favoring a digital format for receiving smoking cessation information, while their Black counterparts expressed a preference for face-to-face support, phone assistance, or printed materials.
Moreover, a meta-analysis conducted by Jabari, et al. sheds light on the efficacy of culturally targeted smoking interventions.3 This comprehensive review describes a dual-level approach to tailoring smoking cessation health interventions: surface and deep. Surface adaptations encompass elements like language and imagery, which aim to enhance the acceptability of interventions within specific communities. Simultaneously, deep-tailored elements identify culturally significant factors that can fundamentally influence the behavior of the target population. The findings of this meta-analysis reveal that the integration of culturally tailored components into standard interventions significantly enhances their efficacy in facilitating smoking cessation.
In conclusion, sustained smoking cessation is a crucial element in combating the global burden of lung cancer. Recognizing the importance of individualized approaches in health care, it is imperative to tailor smoking cessation communications and interventions to diverse cultural influences and socioeconomic factors. Culturally tailored smoking cessation programs that account for nuances specific to each community have the potential to significantly enhance their effectiveness. This necessitates a shift towards individualized smoking cessation care, with a targeted focus on increasing cessation rates among racial and ethnic minority groups. In doing so, we take a step closer to a more equitable landscape in the battle against lung cancer.
Lung cancer stands as the leading cause of cancer-related deaths globally, with its prevalence casting a long and challenging shadow. The most important risk factor for lung cancer is tobacco use, a relationship strongly substantiated by data. The impact of smoking cessation to reduce lung cancer incidence is underscored by the US Preventive Services Task Force, which mandates that smoking cessation services be an integral component of lung cancer screening programs.
However, beneath the surface of this overarching concern lies a web of factors contributing to racial and ethnic disparities in smoking cessation. Cultural intricacies play a pivotal role in shaping these disparities. Despite higher instances of light or intermediate smoking, racially ethnic minority groups in the general population often face greater challenges in achieving smoking cessation, as highlighted by Bacio, et al. Adding another layer to this complex scenario is the profound impact of sustained smoking during cancer treatment. Research suggests that for individuals diagnosed with lung cancer, smoking cessation can markedly boost treatment efficacy, reduce the risk of secondary tumors, and even double the chances of survival.1
A study by Harris, et al. delving into the preferences of current smokers within a lung cancer screening setting uncovered noteworthy insights.2 White participants exhibited a fourfold greater likelihood of favoring a digital format for receiving smoking cessation information, while their Black counterparts expressed a preference for face-to-face support, phone assistance, or printed materials.
Moreover, a meta-analysis conducted by Jabari, et al. sheds light on the efficacy of culturally targeted smoking interventions.3 This comprehensive review describes a dual-level approach to tailoring smoking cessation health interventions: surface and deep. Surface adaptations encompass elements like language and imagery, which aim to enhance the acceptability of interventions within specific communities. Simultaneously, deep-tailored elements identify culturally significant factors that can fundamentally influence the behavior of the target population. The findings of this meta-analysis reveal that the integration of culturally tailored components into standard interventions significantly enhances their efficacy in facilitating smoking cessation.
In conclusion, sustained smoking cessation is a crucial element in combating the global burden of lung cancer. Recognizing the importance of individualized approaches in health care, it is imperative to tailor smoking cessation communications and interventions to diverse cultural influences and socioeconomic factors. Culturally tailored smoking cessation programs that account for nuances specific to each community have the potential to significantly enhance their effectiveness. This necessitates a shift towards individualized smoking cessation care, with a targeted focus on increasing cessation rates among racial and ethnic minority groups. In doing so, we take a step closer to a more equitable landscape in the battle against lung cancer.
References
1. Dresler et al. Lung Cancer. 2003.
2. J Cancer Educ. 2018;33[5].
3. Addiction. 2023.
Thoracic Oncology And Chest Procedures Network
Lung Cancer Section
Stella Ogake, MD, FCCP
Lung cancer stands as the leading cause of cancer-related deaths globally, with its prevalence casting a long and challenging shadow. The most important risk factor for lung cancer is tobacco use, a relationship strongly substantiated by data. The impact of smoking cessation to reduce lung cancer incidence is underscored by the US Preventive Services Task Force, which mandates that smoking cessation services be an integral component of lung cancer screening programs.
However, beneath the surface of this overarching concern lies a web of factors contributing to racial and ethnic disparities in smoking cessation. Cultural intricacies play a pivotal role in shaping these disparities. Despite higher instances of light or intermediate smoking, racially ethnic minority groups in the general population often face greater challenges in achieving smoking cessation, as highlighted by Bacio, et al. Adding another layer to this complex scenario is the profound impact of sustained smoking during cancer treatment. Research suggests that for individuals diagnosed with lung cancer, smoking cessation can markedly boost treatment efficacy, reduce the risk of secondary tumors, and even double the chances of survival.1
A study by Harris, et al. delving into the preferences of current smokers within a lung cancer screening setting uncovered noteworthy insights.2 White participants exhibited a fourfold greater likelihood of favoring a digital format for receiving smoking cessation information, while their Black counterparts expressed a preference for face-to-face support, phone assistance, or printed materials.
Moreover, a meta-analysis conducted by Jabari, et al. sheds light on the efficacy of culturally targeted smoking interventions.3 This comprehensive review describes a dual-level approach to tailoring smoking cessation health interventions: surface and deep. Surface adaptations encompass elements like language and imagery, which aim to enhance the acceptability of interventions within specific communities. Simultaneously, deep-tailored elements identify culturally significant factors that can fundamentally influence the behavior of the target population. The findings of this meta-analysis reveal that the integration of culturally tailored components into standard interventions significantly enhances their efficacy in facilitating smoking cessation.
In conclusion, sustained smoking cessation is a crucial element in combating the global burden of lung cancer. Recognizing the importance of individualized approaches in health care, it is imperative to tailor smoking cessation communications and interventions to diverse cultural influences and socioeconomic factors. Culturally tailored smoking cessation programs that account for nuances specific to each community have the potential to significantly enhance their effectiveness. This necessitates a shift towards individualized smoking cessation care, with a targeted focus on increasing cessation rates among racial and ethnic minority groups. In doing so, we take a step closer to a more equitable landscape in the battle against lung cancer.
Q:Are there interventions that can be readily implemented to improve sleep quality for hospitalized patients?
Dr. Arora: A patient’s first night in the hospital is probably not the night to liberalize sleep; you’re still figuring out whether they’re stable. But by the second or third day, you should be questioning—do you need vitals at night? Do you need a 4 AM blood draw?
We did an intervention called SIESTA that included both staff education about batching care and system-wide, electronic health record-based interventions to remind clinicians that as patients get better, you can deintensify their care. And we’re currently doing a randomized controlled trial of educating and empowering patients to ask their teams to help them get better sleep.
Q: Does hospital sleep deprivation affect patients after discharge?
Dr. Arora: Absolutely. “Posthospital syndrome” is the idea that 30 days after discharge, you’re vulnerable to getting readmitted – not because of the disease you came in with, but something else. And people who report sleep complaints in the hospital are more likely to be readmitted.
When people are acutely sleep deprived, their blood pressure is higher. Their blood sugar is higher. Their cytokine response and immune function are blunted. And our work shows that sleep deficits from the hospital continue even when you go home. Fatigue becomes a very real issue. And when you’re super fatigued, are you going to want to do your physical therapy? Will you be able to take care of yourself? Will you be able to learn and understand your discharge instructions?
We have such a huge gap to improve sleep. It’s of interest to people, but they are struggling with how to do it. And that’s where I think empowering frontline clinicians to take the lead is a great project for people to take on.
Vineet Arora, MD, MAPP, is the Dean for Medical Education at the University of Chicago and an academic hospitalist who specializes in the quality, safety, and experience of care delivered to hospitalized adults.
Q:Are there interventions that can be readily implemented to improve sleep quality for hospitalized patients?
Dr. Arora: A patient’s first night in the hospital is probably not the night to liberalize sleep; you’re still figuring out whether they’re stable. But by the second or third day, you should be questioning—do you need vitals at night? Do you need a 4 AM blood draw?
We did an intervention called SIESTA that included both staff education about batching care and system-wide, electronic health record-based interventions to remind clinicians that as patients get better, you can deintensify their care. And we’re currently doing a randomized controlled trial of educating and empowering patients to ask their teams to help them get better sleep.
Q: Does hospital sleep deprivation affect patients after discharge?
Dr. Arora: Absolutely. “Posthospital syndrome” is the idea that 30 days after discharge, you’re vulnerable to getting readmitted – not because of the disease you came in with, but something else. And people who report sleep complaints in the hospital are more likely to be readmitted.
When people are acutely sleep deprived, their blood pressure is higher. Their blood sugar is higher. Their cytokine response and immune function are blunted. And our work shows that sleep deficits from the hospital continue even when you go home. Fatigue becomes a very real issue. And when you’re super fatigued, are you going to want to do your physical therapy? Will you be able to take care of yourself? Will you be able to learn and understand your discharge instructions?
We have such a huge gap to improve sleep. It’s of interest to people, but they are struggling with how to do it. And that’s where I think empowering frontline clinicians to take the lead is a great project for people to take on.
Vineet Arora, MD, MAPP, is the Dean for Medical Education at the University of Chicago and an academic hospitalist who specializes in the quality, safety, and experience of care delivered to hospitalized adults.
Sleep Medicine Network
Nonrespiratory Sleep Section
Dr. Vineet Arora
Q:Are there interventions that can be readily implemented to improve sleep quality for hospitalized patients?
Dr. Arora: A patient’s first night in the hospital is probably not the night to liberalize sleep; you’re still figuring out whether they’re stable. But by the second or third day, you should be questioning—do you need vitals at night? Do you need a 4 AM blood draw?
We did an intervention called SIESTA that included both staff education about batching care and system-wide, electronic health record-based interventions to remind clinicians that as patients get better, you can deintensify their care. And we’re currently doing a randomized controlled trial of educating and empowering patients to ask their teams to help them get better sleep.
Q: Does hospital sleep deprivation affect patients after discharge?
Dr. Arora: Absolutely. “Posthospital syndrome” is the idea that 30 days after discharge, you’re vulnerable to getting readmitted – not because of the disease you came in with, but something else. And people who report sleep complaints in the hospital are more likely to be readmitted.
When people are acutely sleep deprived, their blood pressure is higher. Their blood sugar is higher. Their cytokine response and immune function are blunted. And our work shows that sleep deficits from the hospital continue even when you go home. Fatigue becomes a very real issue. And when you’re super fatigued, are you going to want to do your physical therapy? Will you be able to take care of yourself? Will you be able to learn and understand your discharge instructions?
We have such a huge gap to improve sleep. It’s of interest to people, but they are struggling with how to do it. And that’s where I think empowering frontline clinicians to take the lead is a great project for people to take on.
Vineet Arora, MD, MAPP, is the Dean for Medical Education at the University of Chicago and an academic hospitalist who specializes in the quality, safety, and experience of care delivered to hospitalized adults.
For providers caring for critically ill patients, navigating death and dying in the intensive care unit (ICU) with proficiency and empathy is essential. Approximately 20% of deaths in the United States occur during or shortly after a stay in the ICU and approximately 40% of ICU deaths involve withdrawal of artificial life support (WOALS) or compassionate extubation.
This is a complex process that may involve advanced communication with family, expertise in mechanical ventilation, vasopressors, dialysis, and complex symptom management. Importantly, surrogate medical decision-making for a critically ill patient can be a challenging experience associated with anxiety and depression. How the team approaches WOALS can make a difference to both patients and decision-makers. Unfortunately, there is striking variation in practice and lack of guidance in navigating issues that arise at end-of-life in the ICU. One study of 2,814 hospitals in the US with ICU beds found that 52% had intensivists while 48% did not.2 This highlights the importance of developing resources focusing on end-of-life care in the ICU setting regardless of the providers’ educational training.
Important elements could include the role for protocol-based WOALS, use of oxygen, selection and dosing strategy of comfort-focused medications, establishing expectations, and addressing uncertainties. This would be meaningful in providing effective, ethical end-of-life care based on evidence-based strategies. While death may be unavoidable, a thoughtful approach can allow providers to bring dignity to the dying process and lessen the burden of an already difficult experience for patients and families alike.
References
1. Curtis JR, et al. Am J Respir Crit Care Med. 2012;186[7]:587-592.
2. Halpern NA, et al. Crit Care Med. 2019;47[4]:517-525.
For providers caring for critically ill patients, navigating death and dying in the intensive care unit (ICU) with proficiency and empathy is essential. Approximately 20% of deaths in the United States occur during or shortly after a stay in the ICU and approximately 40% of ICU deaths involve withdrawal of artificial life support (WOALS) or compassionate extubation.
This is a complex process that may involve advanced communication with family, expertise in mechanical ventilation, vasopressors, dialysis, and complex symptom management. Importantly, surrogate medical decision-making for a critically ill patient can be a challenging experience associated with anxiety and depression. How the team approaches WOALS can make a difference to both patients and decision-makers. Unfortunately, there is striking variation in practice and lack of guidance in navigating issues that arise at end-of-life in the ICU. One study of 2,814 hospitals in the US with ICU beds found that 52% had intensivists while 48% did not.2 This highlights the importance of developing resources focusing on end-of-life care in the ICU setting regardless of the providers’ educational training.
Important elements could include the role for protocol-based WOALS, use of oxygen, selection and dosing strategy of comfort-focused medications, establishing expectations, and addressing uncertainties. This would be meaningful in providing effective, ethical end-of-life care based on evidence-based strategies. While death may be unavoidable, a thoughtful approach can allow providers to bring dignity to the dying process and lessen the burden of an already difficult experience for patients and families alike.
References
1. Curtis JR, et al. Am J Respir Crit Care Med. 2012;186[7]:587-592.
2. Halpern NA, et al. Crit Care Med. 2019;47[4]:517-525.
Critical Care Network
Palliative and End-of-Life Care Section
Angela Birdwell, DO, MA
For providers caring for critically ill patients, navigating death and dying in the intensive care unit (ICU) with proficiency and empathy is essential. Approximately 20% of deaths in the United States occur during or shortly after a stay in the ICU and approximately 40% of ICU deaths involve withdrawal of artificial life support (WOALS) or compassionate extubation.
This is a complex process that may involve advanced communication with family, expertise in mechanical ventilation, vasopressors, dialysis, and complex symptom management. Importantly, surrogate medical decision-making for a critically ill patient can be a challenging experience associated with anxiety and depression. How the team approaches WOALS can make a difference to both patients and decision-makers. Unfortunately, there is striking variation in practice and lack of guidance in navigating issues that arise at end-of-life in the ICU. One study of 2,814 hospitals in the US with ICU beds found that 52% had intensivists while 48% did not.2 This highlights the importance of developing resources focusing on end-of-life care in the ICU setting regardless of the providers’ educational training.
Important elements could include the role for protocol-based WOALS, use of oxygen, selection and dosing strategy of comfort-focused medications, establishing expectations, and addressing uncertainties. This would be meaningful in providing effective, ethical end-of-life care based on evidence-based strategies. While death may be unavoidable, a thoughtful approach can allow providers to bring dignity to the dying process and lessen the burden of an already difficult experience for patients and families alike.
References
1. Curtis JR, et al. Am J Respir Crit Care Med. 2012;186[7]:587-592.
2. Halpern NA, et al. Crit Care Med. 2019;47[4]:517-525.
Viral infections frequently cause acute respiratory failure requiring ICU admission. In the United States, influenza causes over 50,000 deaths annually and SARS-CoV2 resulted in 170,000 hospitalizations in December 2023 alone.1 2 RSV lacks precise incidence data due to inconsistent testing but is increasingly implicated in respiratory failure.
Patients with underlying pulmonary comorbidities are at increased risk of severe infection. RSV induces bronchospasm and increases the risk for severe infection in patients with obstructive lung disease.3 Additionally, COPD patients with viral respiratory infections have higher rates of ICU admission, mechanical ventilation, and death compared with similar patients admitted for other etiologies.4
Diagnosis typically is achieved with nasopharyngeal PCR swabs. Positive viral swabs correlate with higher ICU admission and ventilation rates in patients with COPD.4 Coinfection with multiple respiratory viruses leads to higher mortality rates and bacterial and fungal coinfection further increases morbidity and mortality.5
Treatment includes respiratory support with noninvasive ventilation and high-flow nasal cannula, reducing the need for mechanical ventilation.6 Inhaled bronchodilators are particularly beneficial in patients with RSV infection.5 Oseltamivir reduces mortality in severe influenza cases, while remdesivir shows efficacy in SARS-CoV2 infection not requiring invasive ventilation.7 Severe SARS-CoV2 infection can be treated with immunomodulators. However, their availability is limited. Corticosteroids reduce mortality and mechanical ventilation in patients with SARS-CoV2; however, their use is associated with worse outcomes in influenza and RSV.7 8
Vaccination remains crucial for prevention of severe disease. RSV vaccination, in addition to influenza and SARS-CoV2 immunization, presents an opportunity to reduce morbidity and mortality.
References
1. Troeger C, et al. Lancet Infect Dis. 2018;18[11]:1191-1210.
2. WHO COVID-19 Epidemiological Update, 2024.
3. Coussement J, et al. Chest. 2022;161[6]:1475-1484.
4. Mulpuru S, et al. Influenza Other Respir Viruses. 2022;16[6]:1172-1182.
5. Saura O, et al. Expert Rev Anti Infect Ther. 2022;20[12]:1537-1550.
6. Inglis R, Ayebale E, Schultz MJ. Curr Opin Crit Care. 2019;25[1]:45-53.
7. O’Driscoll LS, Martin-Loeches I. Semin Respir Crit Care Med. 2021;42[6]:771-787.
Viral infections frequently cause acute respiratory failure requiring ICU admission. In the United States, influenza causes over 50,000 deaths annually and SARS-CoV2 resulted in 170,000 hospitalizations in December 2023 alone.1 2 RSV lacks precise incidence data due to inconsistent testing but is increasingly implicated in respiratory failure.
Patients with underlying pulmonary comorbidities are at increased risk of severe infection. RSV induces bronchospasm and increases the risk for severe infection in patients with obstructive lung disease.3 Additionally, COPD patients with viral respiratory infections have higher rates of ICU admission, mechanical ventilation, and death compared with similar patients admitted for other etiologies.4
Diagnosis typically is achieved with nasopharyngeal PCR swabs. Positive viral swabs correlate with higher ICU admission and ventilation rates in patients with COPD.4 Coinfection with multiple respiratory viruses leads to higher mortality rates and bacterial and fungal coinfection further increases morbidity and mortality.5
Treatment includes respiratory support with noninvasive ventilation and high-flow nasal cannula, reducing the need for mechanical ventilation.6 Inhaled bronchodilators are particularly beneficial in patients with RSV infection.5 Oseltamivir reduces mortality in severe influenza cases, while remdesivir shows efficacy in SARS-CoV2 infection not requiring invasive ventilation.7 Severe SARS-CoV2 infection can be treated with immunomodulators. However, their availability is limited. Corticosteroids reduce mortality and mechanical ventilation in patients with SARS-CoV2; however, their use is associated with worse outcomes in influenza and RSV.7 8
Vaccination remains crucial for prevention of severe disease. RSV vaccination, in addition to influenza and SARS-CoV2 immunization, presents an opportunity to reduce morbidity and mortality.
References
1. Troeger C, et al. Lancet Infect Dis. 2018;18[11]:1191-1210.
2. WHO COVID-19 Epidemiological Update, 2024.
3. Coussement J, et al. Chest. 2022;161[6]:1475-1484.
4. Mulpuru S, et al. Influenza Other Respir Viruses. 2022;16[6]:1172-1182.
5. Saura O, et al. Expert Rev Anti Infect Ther. 2022;20[12]:1537-1550.
6. Inglis R, Ayebale E, Schultz MJ. Curr Opin Crit Care. 2019;25[1]:45-53.
7. O’Driscoll LS, Martin-Loeches I. Semin Respir Crit Care Med. 2021;42[6]:771-787.
8. Bhimraj, A et al. Clin Inf Dis. 2022.
Chest Infections and Disaster Response Network
Disaster Response and Global Health Section
Zein Kattih, MD
Kathryn Hughes, MD
Brian Tran, MD
Viral infections frequently cause acute respiratory failure requiring ICU admission. In the United States, influenza causes over 50,000 deaths annually and SARS-CoV2 resulted in 170,000 hospitalizations in December 2023 alone.1 2 RSV lacks precise incidence data due to inconsistent testing but is increasingly implicated in respiratory failure.
Patients with underlying pulmonary comorbidities are at increased risk of severe infection. RSV induces bronchospasm and increases the risk for severe infection in patients with obstructive lung disease.3 Additionally, COPD patients with viral respiratory infections have higher rates of ICU admission, mechanical ventilation, and death compared with similar patients admitted for other etiologies.4
Diagnosis typically is achieved with nasopharyngeal PCR swabs. Positive viral swabs correlate with higher ICU admission and ventilation rates in patients with COPD.4 Coinfection with multiple respiratory viruses leads to higher mortality rates and bacterial and fungal coinfection further increases morbidity and mortality.5
Treatment includes respiratory support with noninvasive ventilation and high-flow nasal cannula, reducing the need for mechanical ventilation.6 Inhaled bronchodilators are particularly beneficial in patients with RSV infection.5 Oseltamivir reduces mortality in severe influenza cases, while remdesivir shows efficacy in SARS-CoV2 infection not requiring invasive ventilation.7 Severe SARS-CoV2 infection can be treated with immunomodulators. However, their availability is limited. Corticosteroids reduce mortality and mechanical ventilation in patients with SARS-CoV2; however, their use is associated with worse outcomes in influenza and RSV.7 8
Vaccination remains crucial for prevention of severe disease. RSV vaccination, in addition to influenza and SARS-CoV2 immunization, presents an opportunity to reduce morbidity and mortality.
References
1. Troeger C, et al. Lancet Infect Dis. 2018;18[11]:1191-1210.
2. WHO COVID-19 Epidemiological Update, 2024.
3. Coussement J, et al. Chest. 2022;161[6]:1475-1484.
4. Mulpuru S, et al. Influenza Other Respir Viruses. 2022;16[6]:1172-1182.
5. Saura O, et al. Expert Rev Anti Infect Ther. 2022;20[12]:1537-1550.
6. Inglis R, Ayebale E, Schultz MJ. Curr Opin Crit Care. 2019;25[1]:45-53.
7. O’Driscoll LS, Martin-Loeches I. Semin Respir Crit Care Med. 2021;42[6]:771-787.
Remodeling of airways and destruction of parenchyma by immune and inflammatory mechanisms are the leading cause of lung function decline in patients with COPD. Type 2 inflammation has been recognized as an important phenotypic pathway in asthma. However, its role in COPD has been much less clear, which had been largely associated with innate immune response.1
Activation of Interleukin (IL)-25, IL-33, thymic stromal lymphopoietin (TSLP) produces type 2 cytokines IL-4, IL-5, and IL-13, either by binding to ILC2 or by direct Th2 cells resulting in elevated eosinophils in sputum, lungs, and blood, as well as fractional exhaled nitric oxide.2 The combined inflammation from this pathway underpins the pathological changes seen in airway mucosa, causing mucous hypersecretion and hyperresponsiveness.
Prior trials delineating the role of biologics, such as mepolizumab and benralizumab, showed variable results with possible benefit of add-on biologics on the annual COPD exacerbations among patients with eosinophilic phenotype of COPD.3
More recently, the BOREAS trial evaluated the role of dupilumab as an add-on therapy for patients with type 2 inflammation-driven COPD established using blood eosinophil count of at least 300/mL at initial screening.4 Dupilumab is a human monoclonal antibody that blocks combined IL-4 and IL-13 pathways with a broader effect on the type 2 inflammation. It included patients with moderate to severe exacerbations despite maximal triple inhaler therapy with blood eosinophilia. Patients with asthma were excluded. This 52-week trial showed reduction in annual moderate to severe COPD exacerbations, sustained lung function improvement as measured by prebronchodilator FEV1, and improvement in patient-reported respiratory symptoms.4 Evaluation of sustainability of these results with therapy step-down approaches should be explored.
Remodeling of airways and destruction of parenchyma by immune and inflammatory mechanisms are the leading cause of lung function decline in patients with COPD. Type 2 inflammation has been recognized as an important phenotypic pathway in asthma. However, its role in COPD has been much less clear, which had been largely associated with innate immune response.1
Activation of Interleukin (IL)-25, IL-33, thymic stromal lymphopoietin (TSLP) produces type 2 cytokines IL-4, IL-5, and IL-13, either by binding to ILC2 or by direct Th2 cells resulting in elevated eosinophils in sputum, lungs, and blood, as well as fractional exhaled nitric oxide.2 The combined inflammation from this pathway underpins the pathological changes seen in airway mucosa, causing mucous hypersecretion and hyperresponsiveness.
Prior trials delineating the role of biologics, such as mepolizumab and benralizumab, showed variable results with possible benefit of add-on biologics on the annual COPD exacerbations among patients with eosinophilic phenotype of COPD.3
More recently, the BOREAS trial evaluated the role of dupilumab as an add-on therapy for patients with type 2 inflammation-driven COPD established using blood eosinophil count of at least 300/mL at initial screening.4 Dupilumab is a human monoclonal antibody that blocks combined IL-4 and IL-13 pathways with a broader effect on the type 2 inflammation. It included patients with moderate to severe exacerbations despite maximal triple inhaler therapy with blood eosinophilia. Patients with asthma were excluded. This 52-week trial showed reduction in annual moderate to severe COPD exacerbations, sustained lung function improvement as measured by prebronchodilator FEV1, and improvement in patient-reported respiratory symptoms.4 Evaluation of sustainability of these results with therapy step-down approaches should be explored.
References
1. Scanlon & McKenzie, 2012.
2. Brusselle et al, 2013.
3. Pavord et al, 2017.
4. Bhatt et al, 2023.
Airways Disorders Network
Asthma and COPD Section
Maria Azhar, MD
Abdullah Alismail, PhD, RRT, FCCP
Raghav Gupta, MD, FCCP
Remodeling of airways and destruction of parenchyma by immune and inflammatory mechanisms are the leading cause of lung function decline in patients with COPD. Type 2 inflammation has been recognized as an important phenotypic pathway in asthma. However, its role in COPD has been much less clear, which had been largely associated with innate immune response.1
Activation of Interleukin (IL)-25, IL-33, thymic stromal lymphopoietin (TSLP) produces type 2 cytokines IL-4, IL-5, and IL-13, either by binding to ILC2 or by direct Th2 cells resulting in elevated eosinophils in sputum, lungs, and blood, as well as fractional exhaled nitric oxide.2 The combined inflammation from this pathway underpins the pathological changes seen in airway mucosa, causing mucous hypersecretion and hyperresponsiveness.
Prior trials delineating the role of biologics, such as mepolizumab and benralizumab, showed variable results with possible benefit of add-on biologics on the annual COPD exacerbations among patients with eosinophilic phenotype of COPD.3
More recently, the BOREAS trial evaluated the role of dupilumab as an add-on therapy for patients with type 2 inflammation-driven COPD established using blood eosinophil count of at least 300/mL at initial screening.4 Dupilumab is a human monoclonal antibody that blocks combined IL-4 and IL-13 pathways with a broader effect on the type 2 inflammation. It included patients with moderate to severe exacerbations despite maximal triple inhaler therapy with blood eosinophilia. Patients with asthma were excluded. This 52-week trial showed reduction in annual moderate to severe COPD exacerbations, sustained lung function improvement as measured by prebronchodilator FEV1, and improvement in patient-reported respiratory symptoms.4 Evaluation of sustainability of these results with therapy step-down approaches should be explored.
During the last decade, the explosion of technological advancements in the field of interventional pulmonary (IP) has afforded patients the opportunity to undergo novel, minimally invasive diagnostic and therapeutic procedures. However, these unprecedented technological advances have often been introduced without the support of high-quality research on safety and efficacy, and without evaluating their impact on meaningful patient outcomes. Encouraging and participating in high-quality IP research should remain a top priority for those practicing in the field.
CHEST
Dr. Jennifer D. Duke
Structured research networks, such as the UK Pleural Society and more recently the Interventional Pulmonary Outcome Group, have facilitated the transition of IP research from observational case series and single-center experiences to multicenter, randomized controlled trials to generate level I evidence and inform patient care (Laskawiec-Szkonter M, et al. Br J Hosp Med (Lond). 2019 Apr 2;80[4]:186-7) (Maldonado F, et al. J Bronchology Interv Pulmonol. 2019 Jul;26(3):150-2). In the bronchoscopy space, important investigator-initiated clinical trial results anticipated in 2024 include VERITAS (NCT04250194), FROSTBITE2 (NCT05751278), and RELIANT (NCT05705544), among others. These research efforts complement industry-sponsored clinical trials (such as RheSolve, NCT04677465) and aim to emulate the extraordinary track record achieved in the field of pleural disease that has led to recently updated evidence-based guidelines for the management of challenging diseases like malignant pleural effusions, pleural space infections, and pneumothorax (Davies HE, et a l. JAMA. 2012 Jun 13;307[22]:2383-9, Mishra EK, et al. Am JRespir Crit Care Med. 2018 Feb 15;197[4]:502-8) (Rahman NM, et al. N Engl J Med. 2011 Aug 11;365[6]:518-26) (Hallifax RJ, et al. Lancet. 2020 Jul 4;396[10243]:39-49).
Ultimately, the rapidly evolving technological advancements in interventional pulmonology must be supported by research based on high-quality clinical trials, which will be contingent on appropriate trial funding requiring partnership with industry and federal funding agencies. Only through such collaboration can researchers design robust clinical trials based on complex methodology, which will advance patient care and lead to improved patient outcomes.
During the last decade, the explosion of technological advancements in the field of interventional pulmonary (IP) has afforded patients the opportunity to undergo novel, minimally invasive diagnostic and therapeutic procedures. However, these unprecedented technological advances have often been introduced without the support of high-quality research on safety and efficacy, and without evaluating their impact on meaningful patient outcomes. Encouraging and participating in high-quality IP research should remain a top priority for those practicing in the field.
CHEST
Dr. Jennifer D. Duke
Structured research networks, such as the UK Pleural Society and more recently the Interventional Pulmonary Outcome Group, have facilitated the transition of IP research from observational case series and single-center experiences to multicenter, randomized controlled trials to generate level I evidence and inform patient care (Laskawiec-Szkonter M, et al. Br J Hosp Med (Lond). 2019 Apr 2;80[4]:186-7) (Maldonado F, et al. J Bronchology Interv Pulmonol. 2019 Jul;26(3):150-2). In the bronchoscopy space, important investigator-initiated clinical trial results anticipated in 2024 include VERITAS (NCT04250194), FROSTBITE2 (NCT05751278), and RELIANT (NCT05705544), among others. These research efforts complement industry-sponsored clinical trials (such as RheSolve, NCT04677465) and aim to emulate the extraordinary track record achieved in the field of pleural disease that has led to recently updated evidence-based guidelines for the management of challenging diseases like malignant pleural effusions, pleural space infections, and pneumothorax (Davies HE, et a l. JAMA. 2012 Jun 13;307[22]:2383-9, Mishra EK, et al. Am JRespir Crit Care Med. 2018 Feb 15;197[4]:502-8) (Rahman NM, et al. N Engl J Med. 2011 Aug 11;365[6]:518-26) (Hallifax RJ, et al. Lancet. 2020 Jul 4;396[10243]:39-49).
Ultimately, the rapidly evolving technological advancements in interventional pulmonology must be supported by research based on high-quality clinical trials, which will be contingent on appropriate trial funding requiring partnership with industry and federal funding agencies. Only through such collaboration can researchers design robust clinical trials based on complex methodology, which will advance patient care and lead to improved patient outcomes.
– Jennifer D. Duke, MD
Section Fellow-in-Training
– Fabien Maldonado, MD, MSc, FCCP
Section Member
THORACIC ONCOLOGY AND CHEST PROCEDURES NETWORK
Interventional Procedures Section
During the last decade, the explosion of technological advancements in the field of interventional pulmonary (IP) has afforded patients the opportunity to undergo novel, minimally invasive diagnostic and therapeutic procedures. However, these unprecedented technological advances have often been introduced without the support of high-quality research on safety and efficacy, and without evaluating their impact on meaningful patient outcomes. Encouraging and participating in high-quality IP research should remain a top priority for those practicing in the field.
CHEST
Dr. Jennifer D. Duke
Structured research networks, such as the UK Pleural Society and more recently the Interventional Pulmonary Outcome Group, have facilitated the transition of IP research from observational case series and single-center experiences to multicenter, randomized controlled trials to generate level I evidence and inform patient care (Laskawiec-Szkonter M, et al. Br J Hosp Med (Lond). 2019 Apr 2;80[4]:186-7) (Maldonado F, et al. J Bronchology Interv Pulmonol. 2019 Jul;26(3):150-2). In the bronchoscopy space, important investigator-initiated clinical trial results anticipated in 2024 include VERITAS (NCT04250194), FROSTBITE2 (NCT05751278), and RELIANT (NCT05705544), among others. These research efforts complement industry-sponsored clinical trials (such as RheSolve, NCT04677465) and aim to emulate the extraordinary track record achieved in the field of pleural disease that has led to recently updated evidence-based guidelines for the management of challenging diseases like malignant pleural effusions, pleural space infections, and pneumothorax (Davies HE, et a l. JAMA. 2012 Jun 13;307[22]:2383-9, Mishra EK, et al. Am JRespir Crit Care Med. 2018 Feb 15;197[4]:502-8) (Rahman NM, et al. N Engl J Med. 2011 Aug 11;365[6]:518-26) (Hallifax RJ, et al. Lancet. 2020 Jul 4;396[10243]:39-49).
Ultimately, the rapidly evolving technological advancements in interventional pulmonology must be supported by research based on high-quality clinical trials, which will be contingent on appropriate trial funding requiring partnership with industry and federal funding agencies. Only through such collaboration can researchers design robust clinical trials based on complex methodology, which will advance patient care and lead to improved patient outcomes.
Interstitial lung diseases (ILD) are a heterogeneous group of fibro-inflammatory disorders that can be progressive despite available therapies. The cornerstones of pharmacologic therapy include immunosuppression and antifibrotics.
CHEST
Dr. Tessy K. Paul
Data on the use of rituximab, a B-lymphocyte-depleting monoclonal antibody, often utilized as rescue therapy in progressive and severe ILD, was limited until recently. The RECITAL trial reported the first randomized controlled trial investigating rituximab in severe or progressive autoimmune ILD. Though rituximab was not superior to cyclophosphamide, both agents improved forced vital capacity (FVC) at 24 weeks and respiratory-related quality of life. Rituximab was associated with less adverse events and lower corticosteroid exposure (Maher et al. Lancet Respir Med. 2023;11:45-54). In the DESIRES trial, patients with systemic sclerosis-associated ILD treated with rituximab had preservation of FVC at 24 and 48 weeks compared to placebo (Ebata et al. Lancet Rheumatol. 2021;3:e489-97; Lancet Rheumatol. 2022;4:e546-55). The EVER-ILD investigators compared mycophenolate mofetil (MMF) alone vs addition of rituximab in patients with autoimmune and idiopathic nonspecific interstitial pneumonia (NSIP). Combination therapy was superior to MMF alone in improving FVC and progression-free survival. Combination regimen was well tolerated though nonserious viral and bacterial infections were more frequent (Mankikian et al. Eur Respir J. 2023;61[6]:2202071).
These findings, primarily in autoimmune ILD, are promising and provide clinicians with evidence for utilizing rituximab in patients with severe and progressive ILD. Nonetheless, they highlight the need for additional research and standardized guidance regarding the target population who stands to most benefit from rituximab.
Interstitial lung diseases (ILD) are a heterogeneous group of fibro-inflammatory disorders that can be progressive despite available therapies. The cornerstones of pharmacologic therapy include immunosuppression and antifibrotics.
CHEST
Dr. Tessy K. Paul
Data on the use of rituximab, a B-lymphocyte-depleting monoclonal antibody, often utilized as rescue therapy in progressive and severe ILD, was limited until recently. The RECITAL trial reported the first randomized controlled trial investigating rituximab in severe or progressive autoimmune ILD. Though rituximab was not superior to cyclophosphamide, both agents improved forced vital capacity (FVC) at 24 weeks and respiratory-related quality of life. Rituximab was associated with less adverse events and lower corticosteroid exposure (Maher et al. Lancet Respir Med. 2023;11:45-54). In the DESIRES trial, patients with systemic sclerosis-associated ILD treated with rituximab had preservation of FVC at 24 and 48 weeks compared to placebo (Ebata et al. Lancet Rheumatol. 2021;3:e489-97; Lancet Rheumatol. 2022;4:e546-55). The EVER-ILD investigators compared mycophenolate mofetil (MMF) alone vs addition of rituximab in patients with autoimmune and idiopathic nonspecific interstitial pneumonia (NSIP). Combination therapy was superior to MMF alone in improving FVC and progression-free survival. Combination regimen was well tolerated though nonserious viral and bacterial infections were more frequent (Mankikian et al. Eur Respir J. 2023;61[6]:2202071).
These findings, primarily in autoimmune ILD, are promising and provide clinicians with evidence for utilizing rituximab in patients with severe and progressive ILD. Nonetheless, they highlight the need for additional research and standardized guidance regarding the target population who stands to most benefit from rituximab.
–Tessy K. Paul, MD
Section Member-at-Large
–Tejaswini Kulkarni, MD, MBBS, FCCP
Section Chair
DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK
Interstitial Lung Disease Section
Interstitial lung diseases (ILD) are a heterogeneous group of fibro-inflammatory disorders that can be progressive despite available therapies. The cornerstones of pharmacologic therapy include immunosuppression and antifibrotics.
CHEST
Dr. Tessy K. Paul
Data on the use of rituximab, a B-lymphocyte-depleting monoclonal antibody, often utilized as rescue therapy in progressive and severe ILD, was limited until recently. The RECITAL trial reported the first randomized controlled trial investigating rituximab in severe or progressive autoimmune ILD. Though rituximab was not superior to cyclophosphamide, both agents improved forced vital capacity (FVC) at 24 weeks and respiratory-related quality of life. Rituximab was associated with less adverse events and lower corticosteroid exposure (Maher et al. Lancet Respir Med. 2023;11:45-54). In the DESIRES trial, patients with systemic sclerosis-associated ILD treated with rituximab had preservation of FVC at 24 and 48 weeks compared to placebo (Ebata et al. Lancet Rheumatol. 2021;3:e489-97; Lancet Rheumatol. 2022;4:e546-55). The EVER-ILD investigators compared mycophenolate mofetil (MMF) alone vs addition of rituximab in patients with autoimmune and idiopathic nonspecific interstitial pneumonia (NSIP). Combination therapy was superior to MMF alone in improving FVC and progression-free survival. Combination regimen was well tolerated though nonserious viral and bacterial infections were more frequent (Mankikian et al. Eur Respir J. 2023;61[6]:2202071).
These findings, primarily in autoimmune ILD, are promising and provide clinicians with evidence for utilizing rituximab in patients with severe and progressive ILD. Nonetheless, they highlight the need for additional research and standardized guidance regarding the target population who stands to most benefit from rituximab.
CHEST 2023 in Honolulu kicked off for Network Leadership during the Council of Networks meeting. Leadership from the seven Networks presented their plans for CHEST 2023, participation in proposed guidelines, CHEST projects completed over the past year, and other accomplishments.
We congratulated our Network leaders – Margaret Pisani, Council of Networks Vice-chair, who was awarded the Roger C. Bone Memorial Lecture in Critical Care; and Jean Elwing, Chair of the Pulmonary Vascular & Cardiovascular Network, for being awarded the Distinguished Scientist Honor Lecture in Cardiopulmonary Physiology. CHEST 2023 included excellent educational content by the Networks, including two Network highlights per each of the seven Networks, as well as an Experience CHEST submission from each of the 22 sections.
We also had the opportunity to meet face-to-face at the Network Open Forums, the Network Mixer, and the inaugural Fellow-in-Training Mixer in the Trainee Lounge. We saw a lot of familiar faces at these events, and 182 new individuals also signed up to become Network members.
There will be one final Council of Networks leadership meeting in December prior to our leadership transition in January.
We thank outgoing Network chairs, Dr. Marcos Restrepo of the Chest Infections & Disaster Response Network, Dr. Christopher Carroll of the Critical Care Network, Dr. Debbie Levine of the Diffuse Lung Disease & Lung Transplant Network, and Dr. Carolyn D’Ambrosio of the Sleep Medicine Network, for their leadership and hard work dedicated to the Networks that have greatly benefited from their service.
Cassie Kennedy, MD, FCCP – Chair, Council of Networks
Margaret Pisani, MD, MPH, FCCP – Vice-Chair, Council of Networks
CHEST 2023 in Honolulu kicked off for Network Leadership during the Council of Networks meeting. Leadership from the seven Networks presented their plans for CHEST 2023, participation in proposed guidelines, CHEST projects completed over the past year, and other accomplishments.
We congratulated our Network leaders – Margaret Pisani, Council of Networks Vice-chair, who was awarded the Roger C. Bone Memorial Lecture in Critical Care; and Jean Elwing, Chair of the Pulmonary Vascular & Cardiovascular Network, for being awarded the Distinguished Scientist Honor Lecture in Cardiopulmonary Physiology. CHEST 2023 included excellent educational content by the Networks, including two Network highlights per each of the seven Networks, as well as an Experience CHEST submission from each of the 22 sections.
We also had the opportunity to meet face-to-face at the Network Open Forums, the Network Mixer, and the inaugural Fellow-in-Training Mixer in the Trainee Lounge. We saw a lot of familiar faces at these events, and 182 new individuals also signed up to become Network members.
There will be one final Council of Networks leadership meeting in December prior to our leadership transition in January.
We thank outgoing Network chairs, Dr. Marcos Restrepo of the Chest Infections & Disaster Response Network, Dr. Christopher Carroll of the Critical Care Network, Dr. Debbie Levine of the Diffuse Lung Disease & Lung Transplant Network, and Dr. Carolyn D’Ambrosio of the Sleep Medicine Network, for their leadership and hard work dedicated to the Networks that have greatly benefited from their service.
Cassie Kennedy, MD, FCCP – Chair, Council of Networks
Margaret Pisani, MD, MPH, FCCP – Vice-Chair, Council of Networks
CHEST 2023 in Honolulu kicked off for Network Leadership during the Council of Networks meeting. Leadership from the seven Networks presented their plans for CHEST 2023, participation in proposed guidelines, CHEST projects completed over the past year, and other accomplishments.
We congratulated our Network leaders – Margaret Pisani, Council of Networks Vice-chair, who was awarded the Roger C. Bone Memorial Lecture in Critical Care; and Jean Elwing, Chair of the Pulmonary Vascular & Cardiovascular Network, for being awarded the Distinguished Scientist Honor Lecture in Cardiopulmonary Physiology. CHEST 2023 included excellent educational content by the Networks, including two Network highlights per each of the seven Networks, as well as an Experience CHEST submission from each of the 22 sections.
We also had the opportunity to meet face-to-face at the Network Open Forums, the Network Mixer, and the inaugural Fellow-in-Training Mixer in the Trainee Lounge. We saw a lot of familiar faces at these events, and 182 new individuals also signed up to become Network members.
There will be one final Council of Networks leadership meeting in December prior to our leadership transition in January.
We thank outgoing Network chairs, Dr. Marcos Restrepo of the Chest Infections & Disaster Response Network, Dr. Christopher Carroll of the Critical Care Network, Dr. Debbie Levine of the Diffuse Lung Disease & Lung Transplant Network, and Dr. Carolyn D’Ambrosio of the Sleep Medicine Network, for their leadership and hard work dedicated to the Networks that have greatly benefited from their service.
Cassie Kennedy, MD, FCCP – Chair, Council of Networks
Margaret Pisani, MD, MPH, FCCP – Vice-Chair, Council of Networks
Thoracic ultrasound (TUS) is standard of care for the detection of pleural effusion and guidance of pleural procedures. Recent advancements have further expanded the utility of TUS. TUS has better diagnostic performance than CT scan or chest radiograph for predicting complicated parapneumonic effusion (Svigals PZ, et al. Thorax. 2017;72[1]:94-5). This is likely because of better visualization of septation, but there are still limitations. In a study of 300 pleural ultrasounds, TUS was found to be inadequately reliable in the diagnosis of transudative pleural effusion as 56% of anechoic effusions were exudative, but complex appearing pleural effusion on TUS was found to have high predictive value for the diagnosis of exudative pleural effusion (Shkolnik B, et al. Chest. 2020;158[2]:692-7).
TUS may diagnose nonexpendable lung prior to drainage in malignant pleural effusions. Using M-mode to assess lung motion and speckled tracking for the assessment of lung stain, blunted cardio-phasic response of the lung was highly specific for the diagnosis of nonexpandable lung (Salamonsen MR, et al. Chest. 2014;146[5]:1286-93). TUS can also be used to assess the success of pleurodesis as measured by the adherence score (abolishment of pleural sliding). TUS guided pleurodesis approach was shown to decrease the hospital length of stay in patients undergoing pleurodesis for malignant pleural effusion (Psallidas I, et al. Lancet Respir Med. 2022;10[2]:139-48). Point-of-care TUS is evolving, and adapted use focusing on patient-centered outcomes will further enhance the utility of this indispensable tool.
Thoracic ultrasound (TUS) is standard of care for the detection of pleural effusion and guidance of pleural procedures. Recent advancements have further expanded the utility of TUS. TUS has better diagnostic performance than CT scan or chest radiograph for predicting complicated parapneumonic effusion (Svigals PZ, et al. Thorax. 2017;72[1]:94-5). This is likely because of better visualization of septation, but there are still limitations. In a study of 300 pleural ultrasounds, TUS was found to be inadequately reliable in the diagnosis of transudative pleural effusion as 56% of anechoic effusions were exudative, but complex appearing pleural effusion on TUS was found to have high predictive value for the diagnosis of exudative pleural effusion (Shkolnik B, et al. Chest. 2020;158[2]:692-7).
TUS may diagnose nonexpendable lung prior to drainage in malignant pleural effusions. Using M-mode to assess lung motion and speckled tracking for the assessment of lung stain, blunted cardio-phasic response of the lung was highly specific for the diagnosis of nonexpandable lung (Salamonsen MR, et al. Chest. 2014;146[5]:1286-93). TUS can also be used to assess the success of pleurodesis as measured by the adherence score (abolishment of pleural sliding). TUS guided pleurodesis approach was shown to decrease the hospital length of stay in patients undergoing pleurodesis for malignant pleural effusion (Psallidas I, et al. Lancet Respir Med. 2022;10[2]:139-48). Point-of-care TUS is evolving, and adapted use focusing on patient-centered outcomes will further enhance the utility of this indispensable tool.
Amit Chopra, MD, FCCP
Nicholas Villalobos, MD
Thoracic Oncology Network
Ultrasound & Chest Imaging Section
Thoracic ultrasound (TUS) is standard of care for the detection of pleural effusion and guidance of pleural procedures. Recent advancements have further expanded the utility of TUS. TUS has better diagnostic performance than CT scan or chest radiograph for predicting complicated parapneumonic effusion (Svigals PZ, et al. Thorax. 2017;72[1]:94-5). This is likely because of better visualization of septation, but there are still limitations. In a study of 300 pleural ultrasounds, TUS was found to be inadequately reliable in the diagnosis of transudative pleural effusion as 56% of anechoic effusions were exudative, but complex appearing pleural effusion on TUS was found to have high predictive value for the diagnosis of exudative pleural effusion (Shkolnik B, et al. Chest. 2020;158[2]:692-7).
TUS may diagnose nonexpendable lung prior to drainage in malignant pleural effusions. Using M-mode to assess lung motion and speckled tracking for the assessment of lung stain, blunted cardio-phasic response of the lung was highly specific for the diagnosis of nonexpandable lung (Salamonsen MR, et al. Chest. 2014;146[5]:1286-93). TUS can also be used to assess the success of pleurodesis as measured by the adherence score (abolishment of pleural sliding). TUS guided pleurodesis approach was shown to decrease the hospital length of stay in patients undergoing pleurodesis for malignant pleural effusion (Psallidas I, et al. Lancet Respir Med. 2022;10[2]:139-48). Point-of-care TUS is evolving, and adapted use focusing on patient-centered outcomes will further enhance the utility of this indispensable tool.
Do you feel like you sleep worse in the spring and have more difficulty keeping your schedule on track? There are new data to support the way you feel based on our deeper understanding of seasonal variations in sleep architecture.
Patients in a recent study had 43 minutes less total sleep time and approximately 30 less minutes of REM sleep in the late spring when compared with the winter (Seidler A, et al. Front Neurosci. 2023 Feb 17:17:1105233). Accumulation of decreased sleep time and quality can lead to the sensation of ‘running-on-empty’ by early spring.
Experts believe these seasonal variations in sleep architecture are mainly secondary to circadian shifts. Our social synchronization overrides our natural alignment with daylight patterns and can lead to known consequences of circadian misalignment. Common consequences of poor circadian alignment include worsening sleep disturbances, cognitive impairments, occupational mistakes, and metabolic and mental health disturbances (Schmal C, et al. Front Physiol. 2020 Apr 28:11:334; Boivin D, et al. J Biol Rhythms. 2022 Feb;37[1]:3-28).
The effects of circadian misalignment can be particularly dramatic in children receiving less than their age-appropriate hours of sleep. Children with sleep deprivation are at increased risk of attention, behavior, and learning problems (Paruthi S, et al. J Clinl Sleep Med. 2016;12[6]:785-6).
To improve circadian alignment in spring, it is recommended to achieve morning bright light exposure and perform regular exercise. The elimination of daylight savings time to a consensus of permanent standard time will optimize circadian alignment.
Do you feel like you sleep worse in the spring and have more difficulty keeping your schedule on track? There are new data to support the way you feel based on our deeper understanding of seasonal variations in sleep architecture.
Patients in a recent study had 43 minutes less total sleep time and approximately 30 less minutes of REM sleep in the late spring when compared with the winter (Seidler A, et al. Front Neurosci. 2023 Feb 17:17:1105233). Accumulation of decreased sleep time and quality can lead to the sensation of ‘running-on-empty’ by early spring.
Experts believe these seasonal variations in sleep architecture are mainly secondary to circadian shifts. Our social synchronization overrides our natural alignment with daylight patterns and can lead to known consequences of circadian misalignment. Common consequences of poor circadian alignment include worsening sleep disturbances, cognitive impairments, occupational mistakes, and metabolic and mental health disturbances (Schmal C, et al. Front Physiol. 2020 Apr 28:11:334; Boivin D, et al. J Biol Rhythms. 2022 Feb;37[1]:3-28).
The effects of circadian misalignment can be particularly dramatic in children receiving less than their age-appropriate hours of sleep. Children with sleep deprivation are at increased risk of attention, behavior, and learning problems (Paruthi S, et al. J Clinl Sleep Med. 2016;12[6]:785-6).
To improve circadian alignment in spring, it is recommended to achieve morning bright light exposure and perform regular exercise. The elimination of daylight savings time to a consensus of permanent standard time will optimize circadian alignment.
Christopher Izzo, DO – Section Fellow-in-Training
William Healy, MD – Section Member-at-Large
Mariam Louis, MD – Section Chair
Sleep Network
Non-Respiratory Sleep Section
Do you feel like you sleep worse in the spring and have more difficulty keeping your schedule on track? There are new data to support the way you feel based on our deeper understanding of seasonal variations in sleep architecture.
Patients in a recent study had 43 minutes less total sleep time and approximately 30 less minutes of REM sleep in the late spring when compared with the winter (Seidler A, et al. Front Neurosci. 2023 Feb 17:17:1105233). Accumulation of decreased sleep time and quality can lead to the sensation of ‘running-on-empty’ by early spring.
Experts believe these seasonal variations in sleep architecture are mainly secondary to circadian shifts. Our social synchronization overrides our natural alignment with daylight patterns and can lead to known consequences of circadian misalignment. Common consequences of poor circadian alignment include worsening sleep disturbances, cognitive impairments, occupational mistakes, and metabolic and mental health disturbances (Schmal C, et al. Front Physiol. 2020 Apr 28:11:334; Boivin D, et al. J Biol Rhythms. 2022 Feb;37[1]:3-28).
The effects of circadian misalignment can be particularly dramatic in children receiving less than their age-appropriate hours of sleep. Children with sleep deprivation are at increased risk of attention, behavior, and learning problems (Paruthi S, et al. J Clinl Sleep Med. 2016;12[6]:785-6).
To improve circadian alignment in spring, it is recommended to achieve morning bright light exposure and perform regular exercise. The elimination of daylight savings time to a consensus of permanent standard time will optimize circadian alignment.
