More than three years after the start of the pandemic, many Covid survivors continue to struggle. Some, especially those who became so severely ill that they were hospitalized and unable to breathe on their own, face lasting lung damage.

To better understand the long-term impact of Covid’s assault on the lungs, The New York Times spoke with three patients who were hospitalized during the pandemic’s early waves, interviewed doctors who treated them and reviewed C.T. scans of their lungs over time.

One patient spent time connected to a ventilator; the other two were so debilitated they required months on a heart-lung bypass machine called ECMO. These patients were not yet vaccinated — for two, vaccines weren’t available, and the third had planned to get vaccinated but was infected before he could.

The Times analyzed hundreds of millions of data points from the patients’ scans to reconstruct their lungs in 3-D. The resulting visualization offers a vivid, visceral picture of damage that can linger years after infection and irrevocably alter everyday life.

Two and a half years after her infection, Ms. Rodríguez can accomplish most daily activities, but she becomes breathless and wheezes when she carries her toddler daughter or does chores such as mopping the floor. She uses an albuterol inhaler for tiring tasks like climbing stairs.

“She doesn’t have a lot of lung to give,” Dr. Sayah said. “She’s certainly at risk for ending up in more trouble if she does have additional respiratory issues in the future.”


Explore the graphic below using your device’s motion.
Tap to enable



A 3-D visualization comparing a healthy set of lungs with Ms. Rodríguez’s lungs 14 months after her infection. While the healthy lungs are filled with orderly airways that look like tree branches, Ms. Rodríguez’s are scarred and disorganized.

Healthy airways look like tree branches.

Ms. Rodríguez’s lungs are erratically scarred.

Tilt your device to rotate lungs


Healthy lungs are filled with millions of tiny air sacs called alveoli. Covid patients can develop scar tissue and permanent changes to the alveolar walls that limit airflow even after the inflammation and fluid of an active infection has cleared.


An illustration comparing different types of lung tissue. Healthy lung tissue has many open pockets where air can easily flow in and out. Lung tissue during an infection has areas filled with fluid and inflammation that inhibits airflow. Lung tissue with chronic damage shows scarred, thickened areas and collapsed sections with reduced airflow.

Many patients who experienced such severe lung damage early in the pandemic did not recover. Many died from a combination of direct injury by the virus and storms of inflammation incited by the immune system’s attempts to battle the infection. These three patients have been able to regain lung function to varying degrees, but the differences in their experiences reflect how unpredictable Covid’s impact can be.

Effects vary by how healthy people were before infection and how their immune systems responded to the virus. Ms. Rodríguez has come closer to recovering, most likely helped by her youth and previous good health.

Ms. Rodríguez shows her young son the fist-sized biosensor she wears below her neck to monitor her heart. The sensor is white with four nodes branching off it.

Marlene Rodríguez, who has three young children, is wearing a temporary monitor to check her heart rhythm. She has made significant progress toward recovery, but said, “I don’t feel the same as how I used to.”

Meridith Kohut for The New York Times

Mr. Kennedy was overweight, had diabetes and had suffered a heart attack six weeks before his infection, factors that increased his risk for a serious outcome.

“Had I taken better care of my health before Covid,” he said, “Covid would probably have not done to me what it did.”

Mr. Muñoz was very healthy and had intended to get vaccinated, but had not managed to do so before becoming infected in the summer of 2021. Dr. Huang said that because his immune system was not primed by a vaccine to recognize the invading virus, it most likely reacted overzealously, causing an inflammation surge that made his illness worse.

All three patients were listed as candidates for lung transplants, an option doctors hope to avoid because patients require immunosuppressive drugs and often die within five to 10 years after transplant. Now, doctors say Mr. Kennedy and Ms. Rodríguez probably won’t need transplants, but Mr. Muñoz may need one eventually.

Andy Muñoz sits at a table and helps his two young sons paint and color.

Andy Muñoz has been unable to return to work as a welding inspector and requires round-the-clock oxygen.

Meridith Kohut for The New York Times

In some ways, these patients have made better progress than doctors would have predicted. “We’re seeing examples where people do improve, even though they started out with a terrible-looking C.T.,” Dr. Huang said. But they’re unlikely to recover fully. “I don’t think anybody gets off completely scot-free if they’re that sick with Covid,” he said.

In addition to lung scans, doctors use several measures to evaluate respiratory function. A six-minute walk test evaluates patients’ cardiovascular health and fitness, tracking the distance patients walk and the way their lungs and heart respond. In March 2022, Mr. Muñoz walked 656 feet, slightly more than one-tenth of a mile, in six minutes. A year later, he walked over 1,443 feet.

Mr. Kennedy’s six-minute walk distance had increased to 2,024 feet in April 2023, from 1,489 feet in May 2021. But his oxygen levels still dipped after walking for several minutes in the April test.


A chart showing Mr. Kennedy’s blood oxygen saturation as he walks for six minutes. Although his oxygen levels begin above 95 percent, they quickly drop below 90 percent.





100% blood oxygen

saturation

100% blood oxygen

saturation


Another measure is called forced vital capacity, which is the volume of air a person can exhale after taking a deep breath. While all three patients have gradually improved on this measure, none have returned to the normal range of 80 percent of total lung capacity.

Mr. Muñoz’s forced vital capacity has increased to about 40 percent from 29 percent. Mr. Kennedy’s has increased to 59 percent from about 38 percent. Ms. Rodríguez’s has increased to 55 percent from 39 percent.

These numbers, and even the most detailed lung scans, tell only part of the story of infection and recovery. Mr. Muñoz’s girlfriend, Melissa Raymundo, said that early on, medical staff indicated that his chances of survival were low and discussed with her the possibility of letting him die. “Nobody thought he was going to make it,” she said.

Mr. Muñoz sits on a backyard swing with his portable oxygen tank. His two sons, wearing swim trunks, swing enthusiastically next to him.

“Breathing is still pretty hard,” Mr. Muñoz said. “But I’m home, I’m with my boys.”

Meridith Kohut for The New York Times

Mr. Muñoz missed months with his two young sons. He remembers saying good night to them in a call from the hospital just before being connected to ECMO. “I woke up three months later,” he said.

During those months, doctors kept him heavily sedated so he wouldn’t move and disrupt the lifesaving machine. It took months longer to wean him from the sedatives and for his lungs to become strong enough to breathe on their own.

Nearly two years after his infection, he cannot work and needs round-the-clock oxygen at home. He has developed pulmonary hypertension, a serious condition of high blood pressure in blood vessels leading from the heart to the lungs.

“Breathing is still pretty hard,” he said. “But I’m home, I’m with my boys.”

“Most important, you’re alive,” Ms. Raymundo said.

Mr. Kennedy walks over to his home oxygen machine while on a phone call, checking on the suitcase-size machine he is tethered to by a long green oxygen tube.

Tom Kennedy is tethered to a bulky oxygen machine with tubing that he calls “this leash that tugs at my nose.”

Meridith Kohut for The New York Times

Mr. Kennedy choked back tears as he recounted being in the hospital.

“I remember telling my wife to tell my children that I loved them,” he said. And he recalled being on the ventilator while his wife, Gayle, read aloud from one of his favorite books, “The Screwtape Letters.” While hospitalized, he experienced delirium, hallucinating that he had been kidnapped.

Mr. Kennedy and his wife, Gayle, pray together before dinner in their Houston home. Plates of salad and pasta sit on the table in front of them.

Mr. Kennedy prayed with his wife, Gayle, before dinner in their Houston home.

Meridith Kohut for The New York Times

He has gradually returned to his job as general counsel of USA DeBusk, which provides services for oil and chemical companies. He works from home because he is continually tethered to a bulky oxygen machine with tubing that he calls “this leash that tugs at my nose.”

He said, “I don’t like it one bit, but it’s a lot better than where I thought I was headed.” Over time, the amount of oxygen he needs has diminished and, with a portable tank, he can play golf.

“I get tired, I feel bad a lot, but that’s just my new normal,” Mr. Kennedy said. He feels grateful.

“Whatever is the final stage before you die, that’s where I was,” he said. “But now I’m just in the group that deals with people that have really bad lungs.”

Ms. Rodríguez blows bubbles with her young son during a backyard family party.

Ms. Rodríguez no longer needs supplemental oxygen, but she still becomes winded lifting heavy items or doing taxing activities like climbing stairs.

Meridith Kohut for The New York Times

Ms. Rodríguez didn’t meet her newborn daughter, Vianney, until she was removed from the ECMO machine, two and a half months after the baby was born.

She briefly returned to work as a receptionist at a plant nursery, but after getting laid off and trying another job, she and her husband, José, who has a chronic medical condition, decided, for health and financial reasons, to move in with his parents. Now she spends her days caring for her three young children.

“I don’t feel the same as how I used to,” she said. She becomes winded when lifting heavy items or doing vigorous activities. She has experienced back pain and takes anxiety medication.

Still, it’s “one of the most remarkable recoveries,” Dr. Sayah said. “I don’t mean to imply that she’s recovered normal lung function, but when the expectation was that this person would for sure die without a lung transplant, to go from death to living at home without supplemental oxygen is a huge sort of success.”

Today, with coronavirus vaccines, antiviral treatments and other developments, doctors say they encounter few patients who are so severely afflicted. But they worry about those who wrestle with Covid’s enduring effects.

“People think that it’s kind of a one-and-done thing, like you can get over it like a common cold,” Dr. Huang said. “We’re left with a population of people like this that are kind of in this limbo state.”

Sources

The 3-D lung visualizations were created from reconstructed computerized tomography (C.T.) scans that calculated tissue density. C.T. scans use X-rays to calculate the differences between blood, bones, internal organs and other soft tissue.

Each scan produced hundreds of slices of the lungs, at different angles, that The New York Times combined into volumetric models for rendering in 3-D software. Reconstructing the slices produced more than 700 million 3-D cells, called voxels, that were evaluated and programmatically filtered, based on density, to isolate the bones and lungs.

The Times reviewed the C.T. scans, the underlying data and the resulting 3-D visualizations with pulmonologists and with radiology and visualization experts:

  • Dr. Howard Huang, lung transplantation section chief at Houston Methodist J.C. Walter Jr. Transplant Center

  • Dr. John W. Nance, Jr., associate professor of clinical radiology at the Houston Methodist Academic Institute

  • Dr. David Sayah, clinical chief of the division of pulmonary & critical care medicine at U.C.L.A. Health

  • Dr. Ayodeji Adegunsoye, assistant professor of medicine at the University of Chicago

  • Dr. Kristin Schwab, pulmonologist at U.C.L.A. Health

  • Dr. William Moore, clinical director of radiology information technology at N.Y.U. Langone Health

  • Dr. Elliot Fishman, director of diagnostic imaging and body computed tomography in the department of radiology and radiological science at Johns Hopkins Medicine

  • Sebastian Krüger, conceptual engineer at Siemens

  • Alexander Brost, head of clinical innovation and concepts at Siemens

The healthy lung scan shown for comparison was of a 54-year-old midwestern woman and was performed at the Houston Methodist Outpatient Center.

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Best Lung Health Supplements: Herbal Support for Respiratory System




The lungs are paramount to overall health, facilitating oxygen and carbon dioxide exchange. The use of respiratory supplements and a healthy lifestyle can support the lungs and help ensure their function. The following article provides insights into some of the best lung health supplements, explaining how certain herbs can contribute to respiratory health. 

Herbs for Respiratory Health and Lung Support

Mullein

Mullein, scientifically known as Verbascum thapsus, has a long history of use in herbal medicine, particularly in treatments involving the respiratory system. It has been widely utilized due to its beneficial properties for lung health, acting as a potent respiratory supplement.

Mullein possesses attributes that may help alleviate the symptoms of the flu. While it should not replace medical treatment, its antiviral properties have been shown to combat flu-causing viruses in laboratory settings.

More importantly, Mullein shines when it comes to maintaining lung health. It demonstrates impressive expectorant properties, aiding in removing mucus from the lungs. This property relieves irritation in the airways and minimizes coughing, making it one of the best lung health supplements available.

Moreover, Mullein exhibits antibacterial and antiviral traits, making it effective against harmful germs such as Bacillus cereus, E. coli, and Influenza. By inhibiting these pathogens, Mullein offers a protective layer for lung health.

With its potent combination of expectorant, antiviral, and antibacterial properties, Mullein serves as a comprehensive herbal supplement for maintaining healthy lungs. However, as with all herbal supplements for healthy lungs, it's essential to consult a healthcare professional before incorporating Mullein into your health regimen.

Spearmint

Spearmint is a versatile herb known for its refreshing aroma and medicinal properties. As a breathing supplement, it can offer significant lung health benefits. According to a study featured on sweetishhill.com, spearmint oil reduced malondialdehyde (MDA), a marker for oxidative stress, in lung tissue, thereby suggesting its potential for managing lung inflammation. It also boosted the expression of the Nrf2 protein, which plays a crucial role in the body's antioxidant defense mechanism. Thus, spearmint can effectively manage conditions like Chronic Obstructive Pulmonary Disease (COPD) and other respiratory ailments by alleviating inflammation and oxidative stress.

Stinging Nettle

Stinging Nettle, scientifically known as Urtica dioica, is renowned for its extensive health benefits. The plant is packed with various vitamins, minerals, and polyphenols that support a healthy inflammatory response. Its young leaves, harvested in early spring, serve as a natural detoxifier, offering nourishment to the body. In Ayurvedic medicine, Stinging Nettle is considered a Rasayana - a rejuvenating herb - that can stimulate the Vata dosha while balancing the Pitta and Kapha doshas. Thus, its potent properties render it a significant part of respiratory supplements.

Ashwagandha

Ashwagandha, also known as "Indian Ginseng," is a potent adaptogen used for centuries in Ayurvedic medicine. This versatile herb is noted for its impressive lung-supporting properties. According to a report by peninsulaacupuncture.com, Ashwagandha protects the lungs from chemical-induced lung cancer by preventing free radical attacks. It also shields the lungs from pulmonary hypertension, a condition where high blood pressure affects the arteries in the lungs. 

Lobelia

Lobelia is a renowned herb that has been traditionally used for a variety of respiratory conditions. Lobelia's primary active compound, lobeline, may help relax the airways, stimulate breathing, and clear mucus from the lungs. These properties make it beneficial for managing symptoms of asthma, including wheezing, coughing, and chest tightness. It also holds the potential to relieve symptoms of pneumonia and bronchitis, both characterized by coughing and difficulty breathing. Although research is still ongoing, preliminary animal studies suggest that lobeline may also help combat lung injury by inhibiting the production of inflammatory proteins and preventing swelling.

Lomatium

Lomatium dissectum, commonly referred to as Lomatium is an herb that has shown notable potential in supporting respiratory health. It works as a potent antioxidant, fighting harmful free radicals, thereby assisting in maintaining healthy lung function. This herb is particularly adept at reducing irritation in the airways, offering a soothing effect. This makes it a valuable addition to supplements for lung support. Its antiviral, antibacterial, and antimicrobial properties add to its benefits, effectively warding off various infections. By potentially stimulating the immune system and enhancing the efficacy of white blood cells, Lomatium serves as a robust ally for lung health.

Conclusion

Proper lung health is vital for overall well-being, and nature offers us a wealth of herbal aids to support it. From the mucus-expelling properties of Mullein to the antioxidative powers of Lomatium, these herbs provide an array of benefits that bolster respiratory health. These best lung health supplements enhance respiratory function and contribute to general wellness. As you consider incorporating these supplements for lung support into your routine, it's essential to consult a healthcare professional to ensure they're suitable for your specific needs.



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There is no cure for pulmonary arterial hypertension (PAH). However, treatment can lead to reduced symptoms and improved quality of life.

PAH occurs when the pressure within the blood vessels linking the heart and the lungs is high. This high pressure can cause the narrowing of tiny arteries in the lungs, restricting blood flow and damaging the right-hand side of the heart.

Symptoms of PAH may include:

PAH increases the risk of right heart failure and death. It is extremely rare. According to the American Lung Association, approximately 500-1,000 people receive a diagnosis of PAH each year in the United States.

Continue reading to learn whether PAH is reversible, what treatment options exist, and the outlook for a person with PAH.

While there is no cure for PAH, treatment options may improve the quality of life and outcomes in people with the condition.

Developments in medical therapies have also shown evidence of potentially reversing PAH.

For example, a 2018 study investigating the effects of a drug on the HIF-2α gene found that the drug effectively reversed right heart failure and vascular remodeling in rodents with PAH. The HIF-2α gene promotes arterial wall thickening, which is a key step in the development of PAH. However, the drug does not cure PAH.

Vascular remodeling is a change to the structure of the cells and fibroblasts in the arteries.

However, PAH is often idiopathic, meaning it occurs spontaneously, without any underlying or known cause. Idiopathic PAH or PAH associated with underlying lung or connective tissue disease is more difficult to reverse or treat.

Treatment options for PAH aim to improve symptoms, increase exercise capacity and slow disease progression. The suitability of a treatment option will depend on a number of factors, including the severity of PAH.

Medication

A number of drugs exist to treat PAH. These include:

Oxygen therapy

Oxygen therapy involves administering oxygen to a person with low blood oxygen levels.

A 2021 study found that supplemental oxygen may have therapeutic benefits for people with PAH. This is because oxygen is a pulmonary vasodilator, meaning it expands the vessels of the lungs.

Lung transplantation

Lung transplantation involves the replacement of a diseased lung with a healthy lung from a donor. Transplantation may involve the replacement of a single lung or both lungs.

A small 2018 study found that lung transplantation provides good long-term and short-term survival for individuals with PAH.

Surgery

Some surgical options may provide better symptom control and exercise capability in people with PAH.

For example, atrial septostomy is a surgical procedure that involves creating a hole between the upper chambers of the heart. This allows the blood to flow from the right side of the heart to the left side, reducing pressure on the right side.

A small 2023 retrospective study involving 12 people with PAH and severe right heart failure found that this surgical option improved survival rates.

Pulmonary rehabilitation

Pulmonary rehabilitation is a program that typically involves breathing techniques, exercises, and education to help improve the physical and psychological health of individuals with respiratory conditions and diseases.

Pulmonary rehabilitation aims to improve physical function, reduce symptom impact, and improve quality of life.

A 2020 study found that treatment programs that incorporate exercise significantly improve exercise capacity and quality of life in individuals with PAH.

PAH can cause death if left untreated.

The mean survival rate for untreated idiopathic PAH is 2-3 years from the PAH diagnosis.

PAH is a condition that affects the pressure in the blood vessels between the heart and the lungs.

It might be possible to reverse PAH that has a known cause by treating the underlying condition.

Treatment options for PAH include medication, surgery, and oxygen therapy.

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Chronic thromboembolic pulmonary hypertension (CTEPH) is increased blood pressure in the arteries in the lungs due to long-term blood clots. It is possible to treat the condition with surgery.

The condition occurs due to a chronic or long-term blood clot in the lungs called a pulmonary embolism. The blood clot or embolism obstructs the blood flow in the lungs, which increases the pressure in the arteries in the lungs.

Read on to learn more about CTEPH. This article discusses symptoms, causes, treatment options, and more.

Researchers do not know exactly why some people with a blood clot develop CTEPH.

The condition most often follows pulmonary embolism. About 75% of people with CTEPH have had one or more blood clots in the lungs. This means that conditions that increase the risk of a pulmonary embolism also increase the risk of CTEPH.

CTEPH can also occur in people that do not have a known history of blood clots. A 2016 article reports that a small number of people with CTEPH do not have a history of pulmonary embolism.

Risk factors for developing CTEPH include:

  • long-term inflammatory conditions
  • having a spleen removed
  • family history of blood clots
  • thyroid replacement therapy
  • blood clotting conditions
  • cancer

Certain factors can also increase the chances of developing a pulmonary embolism, including:

In most cases, if there is an early diagnosis, it is possible to treat CTEPH with surgery.

Currently, the recommended treatment for CTEPH is pulmonary thromboendarterectomy (PTE). PTE is a surgical procedure that involves removing blood clots from the vessels in the lungs.

Not everyone with CTEPH is a candidate for surgery. More than 30% of people do not qualify for surgery.

If surgery is not an option, treatment can involve medical therapy to dilate the pulmonary arteries and balloon pulmonary angioplasty (BPA). BPA involves inflating a small balloon in the artery and temporarily inflating it.

Learn about recovering from a blood clot in the lungs.

Usually, the path to diagnosis of CTEPH involves a two-step process. The first part of the diagnostic process involves evaluating for pulmonary hypertension. The second step involves determining if blood clots cause elevated pulmonary pressure.

Possible diagnostic tests orders to confirm a diagnosis include:

  • Echocardiogram: An echocardiogram involves using sound waves to determine if the pressure on the right side of the heart is high.
  • Cardiac catheterization: This procedure allows doctors to measure the pressure in the pulmonary artery.
  • Ventilation-perfusion scan: This scan helps the doctor determine how efficiently air and blood move through the lungs.
  • Computed tomography pulmonary angiography: A CT pulmonary angiography creates images of the pulmonary arteries. These pictures help determine the extent and location of blood clots in the lungs.

CTEPH is a rare condition with an overall incidence of about 3–30 in every 30 million people in the general population.

It affects about 0.4–4.8% of all people with a pulmonary embolism.

Chronic thromboembolic pulmonary hypertension (CTEPH) refers to increased blood pressure in the arteries in the lungs. It often develops due to long-term blood clots in the lungs.

Symptoms may include trouble breathing, fatigue, and light-headedness. The preferred treatment involves surgery to remove the blood clots. Other treatments may be suitable if a person is unable to undergo surgery.

As early diagnosis can help improve the efficacy of surgery, it is best for a person with concerns about CTEPH to contact their doctor as early as possible.

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World renowned pulmonologists from the Mount Sinai Health System in New York City have prepared research for the American Thoracic Society (ATS) 2023 International Conference in Washington, D.C. from May 19–May 24. Please let me know if you would like to coordinate an interview involving their work. Also, our experts are available to comment on breaking news and other trending topics and studies.

Sessions and Symposiums
(All abstracts listed below are under embargo until the scheduled start time of the event):

Sunday, May 21
*Thematic Poster Session
A54: PEDIATRIC PULMONARY VASCULAR DISEASE
11:30 –1:15 p.m. ET  
Walter E. Washington Convention Center, Area F, Hall C (Lower Level)
P619 - Prevalence of Pulmonary Hypertension in Children With Severe Obstructive Sleep Apnea- a Single Center Study
Jason Bronstein, MD, Associate Professor of Pediatrics and Medicine (Pulmonary, Critical Care and Sleep Medicine) at the Icahn School of Medicine at Mount Sinai

*Thematic Poster Session
A62: B-A-C-T-E-R-I-A, FIND OUT WHAT IT MEANS TO ME
11:30 a.m. – 1:15 p.m. ET     
Walter E. Washington Convention Center, Area I, Hall C (Lower Level)
P904 - Assessing Bias in Treatment of Empyema
Lina Miyakawa, MD, Assistant Professor of Medicine (Pulmonary, Critical Care and Sleep Medicine) at the Icahn School of Medicine at Mount Sinai

*Mini Symposium
A99: CLINICAL TRIALS IN CHRONIC LUNG DISEASE

2:39 – 2:51 p.m. ET   
Marriott Marquis Washington, Independence Ballroom Salons A-D (Level M4)    
Associations of a Plant Centered Diet and Lung Function Decline Across Early to Mid-adulthood: The Cardia Lung Study
Elliot Eisenberg, MD, Assistant Professor of Medicine (Pulmonary, Critical Care and Sleep Medicine) at the Icahn School of Medicine at Mount Sinai; Sonali Bose, MD, MPH, Associate Professor of Medicine (Pulmonary, Critical Care and Sleep Medicine) and Pediatrics at the Icahn School of Medicine at Mount Sinai 

*Poster Discussion Session
A104: NOVEL INSIGHTS ON CANNABIS, TOBACCO, AND E-CIGARETTE USE
2:15 – 4:15 p.m. ET
Marriott Marquis Washington, Marquis Ballroom, Salons 1-2 (Level M2) 
102 - Respiratory Symptoms as a Predictor of Future Smoking Patterns: The Cardia Lung Study    
Sonali Bose, MD, MPH, Associate Professor of Medicine (Pulmonary, Critical Care and Sleep Medicine) and Pediatrics at the Icahn School of Medicine at Mount Sinai 

Monday, May 22
* Thematic Poster Session
B44: FRAILTY, NUTRITION, AND PROLONGED MECHANICAL VENTILATION
11:30 a.m. – 1:15 p.m. ET     
Walter E. Washington Convention Center, Area I, Hall C (Lower Level)
Clinical Outcomes of Tracheostomized Patients: COVID-19 Vs Non-COVID-19
Predictors of Length of Stay, Ventilator Wean, Decannulation, and Mortality in Tracheostomized Patients
Characteristics of Tracheostomized Patients: COVID-19 Vs Non-COVID-19
Complications of Tracheostomies in the COVID-19 Era
Jennifer Y. Fung, MD, Assistant Professor of Medicine (Pulmonary, Critical Care and Sleep Medicine) at the Icahn School of Medicine at Mount Sinai; Young Im Lee, MD, Associate Professor of Medicine (Pulmonary, Critical Care and Sleep Medicine) and Pediatrics at the Icahn School of Medicine at Mount Sinai 

* Thematic Poster Session
B51: ENVIRONMENTAL AND CLINICAL EPIDEMIOLOGY OF AIRWAY DISEASE, ASTHMA, AND COPD
11:30 a.m. – 1:15 p.m. ET     
Walter E. Washington Convention Center, Area H, Hall C (Lower Level)
P796 - Feasibility of Multi-dimensional Remote Monitoring of Indoor Air Quality and Asthma Control Among High-risk Urban Pregnant Women
Sonali Bose, MD, MPH, Associate Professor of Medicine (Pulmonary, Critical Care and Sleep Medicine) and Pediatrics at the Icahn School of Medicine at Mount Sinai; Najla Abdurrahman, MD, Pulmonary, Critical Care and Sleep Medicine Fellow at the Icahn School of Medicine at Mount Sinai

*Mini Symposium
B99: ALL THAT WHEEZES: TRANSLATIONAL STUDIES IN ASTHMA
2:15 – 2:27 p.m. ET   
Walter E. Washington Convention Center, Room 143 A-C (Street Level)
Sex Differences in Asthma Control, Lung Function and Exacerbations: The Atlantis Study
Monica Kraft, MD, Professor of Medicine (Pulmonary, Critical Care and Sleep Medicine), and System Chair for the Department of Medicine at the Icahn School of Medicine at Mount Sinai                

Tuesday, May 23
*Mini Symposium
C17: IN THIS TOGETHER: CONFRONTING ENVIRONMENTAL HEALTH CHALLENGES AROUND THE WORLD
9:00 – 11:00 a.m. ET
Walter E. Washington Convention Center, Room 150 A-B (Street Level)
•  Several talks covering the topics of Environmental, Occupational and Population Health
Moderator: Alison Lee, MD, MS, Associate Professor of Global Health, Medicine (Pulmonary, Critical Care and Sleep Medicine) and Pediatrics at the Icahn School of Medicine at Mount Sinai

*Thematic Poster Session
C31 - BIOLOGICS WANT TO RULE THE (ASTHMA) WORLD
11:30 a.m. – 1:15 p.m. ET
Walter E. Washington Convention Center, Area F, Hall C (Lower Level)
P605 - Efficacy of Tezepelumab in Patients With Severe, Uncontrolled Asthma by Sex: Results From the Phase 3 Navigator Study
 Monica Kraft, MD, Professor of Medicine (Pulmonary, Critical Care and Sleep Medicine), and System Chair for the Department of Medicine at the Icahn School of Medicine at Mount Sinai     

*Thematic Poster Session
C74: DO NOT MISS: SLEEP DISORDERS IN VULNERABLE POPULATIONS
11:30 a.m. –1:15 p.m. ET
Walter E. Washington Convention Center, Area I, Hall C (Lower Level)   
•  P942 - Sleep Disorders and Chronic Rhinosinusitis in World Trade Center (WTC) Responders and a Sleep Clinic Population
Andrew W. Varga, MD, PhD, Associate Professor of Medicine (Pulmonary, Critical Care and Sleep Medicine) at the Icahn School of Medicine at Mount Sinai
•  P947- Dysfunctional Breathing Patterns in Post-Acute Sequelae of SARS-CoV-2 (PASC) Patients Can Be Identified Using Approximate Entropy      
Ankit Parekh, PhD, Assistant Professor of Medicine (Pulmonary, Critical Care and Sleep Medicine) at the Icahn School of Medicine at Mount Sinai

*Mini Symposium
C98 - RISKY BUSINESS: PREDICTING CONSEQUENCES OF OSA
2:15 – 4:15 p.m. ET
Marriott Marquis Washington, Independence Ballroom, Salons E-H (Level M4)
•  Several talks covering the topics of Sleep Medicine and Respiratory Neurobiology
Moderator: Vaishnavi Kundel, MD, MS, Assistant Professor of Medicine (Pulmonary, Critical Care and Sleep Medicine) at the Icahn School of Medicine at Mount Sinai
• ~ 3:03 – 3:15 p.m. ET: Combination of Ventilatory, Hypoxic, and Arousal Burden Predicts Short- and Long-term Consequences of OSA Better Than the Apnea-hypopnea Index
Andrew W. Varga, MD, PhD, Associate Professor of Medicine (Pulmonary, Critical Care and Sleep Medicine) at the Icahn School of Medicine at Mount Sinai   
• ~ 3:15 – 3:27 p.m. ET: Use of Machine Learning and Prediction Tools to Assess Cardiovascular Disease Risk in Obstructive Sleep Apnea
Neomi A. Shah, MD, Professor of Medicine (Pulmonary, Critical Care and Sleep Medicine) at the Icahn School of Medicine at Mount Sinai; Oren Cohen, MD, Pulmonary, Critical Care and Sleep Medicine Fellow at the Icahn School of Medicine at Mount Sinai

About the Mount Sinai Health System
The Mount Sinai Health System is New York City’s largest academic medical system, encompassing eight hospitals, a leading medical school, and a vast network of ambulatory practices throughout the greater New York region. Mount Sinai advances medicine and health through unrivaled education and translational research and discovery to deliver care that is the safest, highest-quality, most accessible and equitable, and the best value of any health system in the nation. The Health System includes approximately 7,300 primary and specialty care physicians; 13 joint-venture ambulatory surgery centers; more than 415 ambulatory practices throughout the five boroughs of New York City, Westchester, Long Island, and Florida; and more than 30 affiliated community health centers.

For more information, visit www.mountsinai.org or find Mount Sinai on Facebook, Twitter and YouTube.




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The cause is a destruction or thickening of the vessel walls, their narrowing or obstruction, either total or partial.

This condition causes a fatigue of the right ventricle, which – if neglected – can culminate in heart failure of varying severity, up to and including death.

What is pulmonary hypertension?

Before gaining a better understanding of what pulmonary hypertension is, it is appropriate to do a little review of the exchanges that the heart and lungs have.

In a normal condition, the blood starts from the right side of the heart and, through the pulmonary arteries, irrigates all the blood vessels of the lungs, until it reaches the capillaries.

It is in these small vessels that the exchange between carbon dioxide and oxygen occurs.

The pulmonary pressure is generally low, so the right side of the heart has less muscularity than the left side (which instead sends blood to all the other parts of the body), which needs more pressure.

Sometimes, however, it happens that due to structural changes in the blood vessels (narrowing, obstruction, parietal thickening) the pressure increases from an average of 14mmHg to 25mmHg.

Under these conditions, the right ventricle is subjected to an excessive load of pressure and volume and could reach contractile failure and thus decompensation.

Or, it could happen that the right ventricle thickens and swells excessively, developing the so-called pulmonary heart, resulting in right heart failure.

If neglected or not properly treated, pulmonary hypertension can even culminate in fatal heart failure.

What are the causes?

To identify the causes of pulmonary hypertension, a distinction must be made in the disease.

It is possible for it to occur in the absence of any particular trigger or previous illness: we speak in this case of primary or idiopathic pulmonary hypertension.

Women – twice as many as men – between 30 and 50 years of age are particularly affected. In this case, the cause is unknown, but as research progresses, some associations with genetic mutations are being identified.

Unfortunately, the mechanism by which these mutations cause pulmonary hypertension is still unknown.

In addition, it has become apparent that the intake of drugs and substances such as fenfluramine (a substance used in weight loss), amphetamines, cocaine and Selective Serotonin Reuptake Inhibitors (SSRIs) can be serious risk factors for developing the disease.

Pulmonary hypertension can also develop in association with other diseases, in this case we speak of acquired or secondary hypertension, which is much more common than the former.

But what are these driving diseases? Emphysema, pulmonary fibrosis, chronic obstructive pulmonary disease and other pulmonary diseases, as well as sleep apnoea, respiratory pathologies linked to sleep disorders.

Still remaining in the lung area, hypertension can be caused by embolisms in the area.

Heart defects or diseases of the left heart can also be a cause, as can autoimmune diseases of the connective tissue, such as scleroderma or lupus erythematosus.

Finally, there are other diseases that can become a trigger for pulmonary hypertension, such as sickle cell anaemia, chronic liver disease and HIV.

Symptoms of pulmonary hypertension

Generally, pulmonary hypertension is manifested by rather abnormal shortness of breath (or dyspnoea), which occurs even during very light physical activity.

Accompanying dyspnoea is an easy loss of energy, chronic fatigue, feeling light-headed, light-headedness under even mild exertion and fainting.

In the more advanced stages of the disease, symptoms worsen: one may have difficulty breathing even at rest, pain very similar to angina pectoris, caused by the suffering of the right heart, and fluid stagnation, resulting in oedema of the lower limbs.

The diagnosis

Obviously, it is not possible to make a self-diagnosis of pulmonary hypertension; if you realise that something is wrong with your health to such an extent that you suspect this pathology, it is always a good idea to consult your general practitioner first, who will direct you to the appropriate specialist.

The case of secondary pulmonary hypertension is different: generally with that type of pathology listed above, one is already being followed by a specialist who will know how to prescribe the right diagnostic tests to best formulate the diagnosis.

Let’s take a step-by-step look at what tests are usually prescribed for a correct diagnosis.

Chest X-ray, which highlights any dilation of the pulmonary arteries.

Transthoracic echocardiography. This provides an accurate view of the heart and any morphological changes in the right atrium and ventricle, which we have seen are a consequence of increased pulmonary pressure. In addition, if an echodoppler is performed, an indirect estimate of the maximum pressure in the pulmonary artery can also be obtained.

Spirometry to detect lung abnormalities. This involves blowing into a tube connected to a device that measures various breathing parameters.

Angio computed tomography of the chest, an X-ray test to observe the pulmonary arteries and detect the presence of occlusions

Pulmonary perfusory scintigraphy, an investigation that allows the blood circulation of the lungs to be photographed in order to observe obstructions or defects in blood supply.

All these tests are non-invasive and are preliminary to the introduction of a catheter into the heart, the only method for a definitive diagnosis.

The catheter will have to start in an arm or leg to reach the right heart and be able to directly measure certain parameters, such as atrium pressure, mean pulmonary pressure and cardiac output.

In addition, only with cardiac catheterisation is it possible to perform the pulmonary vaso-reactivity test: the pulmonary blood vessels are dilated using certain drugs in order to identify any problems in the vessels.

Other tests can also be administered to confirm the diagnosis of pulmonary hypertension, measure its severity and establish its cause:

Blood tests to rule out the presence of autoimmune diseases.

CT angiography to examine for blood clots in the lungs.

EGA, Haemogasanalysis to measure the amount of oxygen and carbon dioxide in the blood through an arterial sampling.

Cardiopulmonary stress test.

Is it possible to prevent pulmonary hypertension?

As far as primary pulmonary hypertension is concerned, it is difficult to think of prevention, other than to advise against taking the substances listed above that could promote the onset of the disease.

Nor is there any real prevention for secondary pulmonary hypertension, other than treating one’s medical condition as best one can to reduce the risk factors that could cause hypertension.

How is pulmonary hypertension treated?

Fortunately, research and medical innovations are progressing from year to year: until recently, the only possible solution to pulmonary hypertension was a lung transplant or, in the case of severe heart impairment, a heart and lung transplant.

Obviously, this was a solution that was only practised in the most severe cases because the risks and contraindications are so many.

Today, however, there are several treatments that do not definitively solve the problem but slow down the progression of the disease and definitely improve the quality of life.

It must be said, however, that in the most extreme cases of patients in whom the progression of hypertension is not stopped, the only solution still remains transplantation.

Obviously, treatment will be easier when there is an exactly identified cause.

Let us now look specifically at what treatments are used in most cases:

  • Administration of drugs that manage to vasodilate the pulmonary circulation: calcium antagonists, prostacyclins, anti-endothelin drugs and phosphodiesterase type 5 inhibitors (sildenafil and the like).
  • These substances are able to reduce blood pressure in the pulmonary arteries. This can decisively improve the quality of the patient’s everyday life, extend life expectancy and reduce the likelihood of an impending transplant. Generally, vasodilators are tested on the patient during carotid catheterisation, because they may be dangerous in some individuals.
  • Administration of oral anticoagulants, which can be combined with diuretics and other heart failure therapies in the event of circulatory decompensation. These drugs may also be prescribed to prevent symptomatic complications. In particular, diuretics are used to ensure that the right ventricle maintains a normal volume and to reduce swelling in the limbs; while anticoagulants, by preventing blood clotting, reduce the risk of pulmonary embolism.
  • If reduced blood oxygenation is noted in the patient, oxygen can be administered via nasal cannulae or oxygen masks. The consequence will be to reduce the blood pressure in the pulmonary arteries and relieve shortness of breath.

Obviously, the case of a secondary form of the disease will be different: therapy will mainly be based on treatments to cure the condition.

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PRESS RELEASE

Published May 22, 2023

New York: As per the market analysis at PMR, the medical gas market is valued at US$ 6.5 Billion in 2022 and is expected to reach US$ 13.0 billion by 2032, flourishing at an average CAGR of 7.2% through 2032.

Increasing chronic diseases, including chronic respiratory diseases like asthma and pulmonary hypertension, coupled with government initiatives, including demand for home healthcare and covid-19 has helped the medical gas market expand its roots in the new regional spaces.

As chronic diseases have brought traction to the medical gas through the increasing demands of cure for occupational lung diseases, pulmonary hypertension, chronic obstructive pulmonary and asthma. These diseases demand self-care units that include medical gas.

The medical gas market outlook explains the latest trends and puts forth the versatility of medical gases like helium, oxygen, carbon dioxide, nitrogen, and nitrogen oxide. These breathing issues caused by the severe conditions of covid-19 are also increasing the demand for medical gas.

New medical gas manufacturing units are being set up along with the growing demand for oxygen gas due to chronic diseases and severe stages of covid-19, enhancing and structuring the healthcare supplies globally.

The COVID-19, along with increasing awareness about self-care and health monitoring, has gained traction in the medical gas market. The market creates opportunities for new oxygen manufacturers, oxygen tank vendors, and oxygen transportation.

Get Sample Copy of this Report @ www.persistencemarketresearch.com/samples/33119

KEY TAKEAWAYS:

  • The medical gas market is divided by Gas Type, Equipment Outlook, Application and End- User, segmenting it into small segments that exceed the growth prospects for the medical gas market.
  • The leading segment in the gas type category is pure gases, growing with a CAGR of 7.0% between 2022 and 2032, while the segment was flourishing at a higher CAGR of 7.7% I the last forecast (2015-2021). Its growth is attributed to the effective use of pure gases in chronic diseases, pulmonary lung disorders and chest infections through covid-19.
  • The biggest segment in the application category is the hospital segment, growing at a slightly higher CAGR of 7.9%, the hospital segment now flourishes at a CAGR of 7.4%, increasing the medical gas market size.
  • The United States has the highest growth potential in the market as it thrives on a CAGR of 6.9% between 2022 and 2032, large number of covid-19 cases, severe patients coupled with geriatric generations are pushing the demand for the sales of medical gas.

COMPETITIVE LANDSCAPE:

Some of the medical gas market key players listed in the PMR study are Air Liquide, Praxair, Atla Copco, The Linde Group, and Airgas, Inc.

Recent Developments

  • Air Liquide has introduced its upgraded line of gas cylinders including oxygen, air, allenox, nitrous oxide and nitrogen. This gains traction and increases the medical gas market size.
  • Atla Copco has launched its breathing air solutions, surgical equipment along with new gas solutions, increasing the sales of medical gas globally.

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About us: –

Persistence Market Research is a U.S.-based full-service market intelligence firm specializing in syndicated research, custom research, and consulting services. Persistence Market Research boasts market research expertise across the Healthcare, Chemicals and Materials, Technology and Media, Energy and Mining, Food and Beverages, Semiconductors and Electronics, Consumer Goods, and Shipping and Transportation industries. The company draws from its multi-disciplinary capabilities and high-pedigree team of analysts to share data that precisely corresponds to clients’ business needs.

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Liquidia Corporation

Liquidia Corporation

MORRISVILLE, N.C., May 19, 2023 (GLOBE NEWSWIRE) -- Liquidia Corporation (NASDAQ: LQDA) (“Liquidia” or the “Company”) today announced the Company will present data related to the investigational use of YUTREPIA™ (treprostinil) inhalation powder at the 2023 American Thoracic Society (ATS) International Conference, taking place May 19-24, 2023, in Washington, D.C.

Thematic Poster Session: B64 - The Multiple Components of Pulmonary Rehabilitation
Date and time: Monday, May 22, 2023, 11:30 a.m. – 1:15 p.m. ET
Location: Area J, Hall C (Lower Level), Walter E. Washington Convention Center
Presenting Author: Charles Burger, M.D., from the Mayo Clinic, Jacksonville, Florida
Abstract: Exploratory Efficacy Analysis of INSPIRE Open Label Extension Study with Inhaled Treprostinil (Yutrepia™)

Following the presentation, the poster will be available on the Company’s website at liquidia.com/print-technology/publications/.

About YUTREPIA™(treprostinil) inhalation powder
YUTREPIA is an investigational, inhaled dry powder formulation of treprostinil delivered through a convenient, low-resistance, palm-sized device. On November 5, 2021, the FDA issued a tentative approval for YUTREPIA, which is indicated for the treatment of pulmonary arterial hypertension (PAH) to improve exercise ability in adult patients with New York Heart Association (NYHA) Functional Class II-III symptoms. The FDA has confirmed that YUTREPIA may add the indication to treat pulmonary hypertension with interstitial lung disease (PH-ILD) without additional clinical studies. YUTREPIA was designed using Liquidia’s PRINT® technology, which enables the development of drug particles that are precise and uniform in size, shape, and composition, and that are engineered for enhanced deposition in the lung following oral inhalation. Liquidia has completed INSPIRE, or Investigation of the Safety and Pharmacology of Dry Powder Inhalation of Treprostinil, an open-label, multi-center phase 3 clinical study of YUTREPIA in patients diagnosed with PAH who are naïve to inhaled treprostinil or who are transitioning from Tyvaso® (nebulized treprostinil). YUTREPIA was previously referred to as LIQ861 in investigational studies.

About Liquidia Corporation
Liquidia Corporation is a biopharmaceutical company focused on the development and commercialization of products in pulmonary hypertension and other applications of its PRINT® Technology. The company operates through its two wholly owned subsidiaries, Liquidia Technologies, Inc. and Liquidia PAH, LLC. Liquidia Technologies has developed YUTREPIA™ (treprostinil) inhalation powder for the treatment of pulmonary arterial hypertension (PAH). Liquidia PAH provides the commercialization for pharmaceutical products to treat pulmonary disease, such as generic Treprostinil Injection. For more information, please visit www.liquidia.com.

Contact Information for Media & Investors
Jason Adair
Senior Vice President, Corporate Development and Strategy
919.328.4400
[email protected]

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Dehydrated infant with fast breathing and sunken anterior fontanel | Image Credit: © kieferpix - © kieferpix - stock.adobe.com.

THE CASE

A 9-month-old girl presents to the emergency department (ED) from her primary care provider’s office for further evaluation of grunting and poor weight gain. She was seen in the office on the day of presentation for her well-child check when the nurse practitioner noticed that she was grunting, tachypneic, and appeared dehydrated with a sunken anterior fontanel.

Additional history reveals sweating and fatigue with feeds beginning around aged 2 months. Patient can breastfeed for maximum 5 to 10 minutes on 1 breast before fatiguing. She also eats some puréed food and baby snacks. Parents deny any episodes of cyanosis, with no blue discoloration ever noted centrally or peripherally. At aged 6 months, patient’s weight plateaued and she was referred to gastroenterology but has not been seen at time of presentation. She is otherwise described as developmentally appropriate and is up to date on her immunizations.

Examination and imaging studies

On physical exam her vitals are as follows: temperature, 98.6 °F (37.0 °C); heart rate, 130 beats/min; respiratory rate, 51 breaths/min; and blood pressure 91/67 mm Hg. Her weight is below the 1st percentile for her age (6.38 kg, 0.92%), as is her weight for length (6.38 kg/71.1 cm, 0.07%). Her respiratory exam is notable for tachypnea, occasional grunting, and both subcostal and supraclavicular retractions. Cardiac exam reveals tachycardia, S1/S2 with appreciable gallop, and a grade 3/6 systolic murmur heard throughout the precordium but loudest at the left sternal border. Peripheral pulses are slightly diminished. She has hepatomegaly with liver edge palpable 3 cm below right costal margin. Remainder of exam is unremarkable. Initial workup includes normal complete blood count and basic metabolic panel. Chest x-ray (CXR) obtained showing impressive cardiomegaly and bilateral vascular congestion. B-type natriuretic peptide (BNP) elevated to 2,709 pg/ml with a normal troponin-I of 0.023 ng/ml. Further testing ultimately revealed the diagnosis.

Differential diagnosis

For this patient’s respiratory symptoms and failure to gain weight appropriately, differential diagnosis includes cardiac (congenital heart defect, arrythmia, myocarditis, pulmonary hypertension), inborn error of metabolism, hyperthyroidism, hematologic (such as severe anemia), neoplasm, and pulmonary (such as cystic fibrosis and primary ciliary dyskinesia). Her lack of growth is suggestive of an underlying disease process. When coupled with her exam findings consistent with heart failure, the diagnosis of congenital heart disease becomes the most likely. Inborn error of metabolism is possible but less likely given normal basic metabolic panel. Myocarditis secondary to illness as cause of heart failure should be considered.

ACTUAL DIAGNOSIS

Because of the patient’s concerning CXR and elevated BNP, pediatric cardiology is consulted for suspected cardiac anomaly. An echocardiogram demonstrates a massively dilated left atrium and left ventricle with severe mitral regurgitation. The pulmonary artery is markedly dilated as well. The right coronary artery is dilated and visualized but the left coronary artery cannot be seen. As a result of these findings, the patient is transferred to a local children’s hospital with a cardiac intensive care unit. She is given a dose of furosemide prior to transfer given her degree of volume overload.

THE CONDITION

Anomalous origin of the left coronary artery from the pulmonary artery, or ALCAPA, is a rare condition and the prevalence has not been well described.1 Coronary artery anomalies have been estimated to occur in 0.2 to 1.2% of the general population based on imaging studies, however the majority have little clinical significance.2 In normal anatomic development, both the right and left coronary arteries originate from the aorta. However, in ALCAPA, the left coronary artery arises from the main pulmonary artery (or less commonly, from the right pulmonary artery) and then runs along the aorta before following the usual left coronary distribution. The blood flow in the coronary artery is dependent on the diastolic pressure which places ALCAPA patients at risk of left ventricular dysfunction and ischemia whenever the diastolic pressure in the pulmonary artery decreases.

Symptoms presenting in infancy typically include crying or sweating during feeds, rapid breathing, poor feeding, and signs of pain or distress that are often confused with colic. In instances of symptom development, there are no collaterals arising from the right coronary artery. As pulmonary vascular resistance decreases, coronary steal occurs from the myocardium and blood flows instead into the pulmonary artery. There is limited blood supply to the left ventricle and because of decreased myocardial perfusion, patients develop mitral insufficiency and congestive heart failure or dilated cardiomyopathy. In children older than 2 years, there is substantial collateral vessel formation and patients will often be asymptomatic with findings of a murmur on exam or cardiomegaly on chest radiography. However, even in the absence of symptoms, there is ischemic injury and eventually development of progressive left ventricular dilatation.3

Management

The mainstay of therapy for ALCAPA presenting as congestive heart failure is surgical correction to return a 2­–coronary-artery circulation. This often consists of reimplantation surgery in which the coronary artery is detached from the pulmonary artery and then sutured to the aorta in the correct location. Following surgery, most patients do well with a good quality of life. Medications, such as diuretics, are often needed initially but weaned off over weeks to months following surgery. Without surgical correction, the mortality rate is estimated to be close to 90% within the first year of life for those with infantile ALCAPA.4

PATIENT COURSE

The patient underwent surgical correction on hospital day 2. Following discharge from the hospital, she was followed by pediatric cardiology weekly and then spaced to 2-month interval visits. Parents report that patient is now 5 months post-op and doing very well. Her sweating has improved and she no longer has evidence of respiratory distress. She lost weight in the initial postoperative period but since then has slowly been gaining weight with fortified formula. She is active and playful and recently celebrated her first birthday.

DISCUSSION

Congenital heart disease impacts approximately 8 in 1000 live births with about one-third of these babies requiring intervention by catheterization or surgery within the first year of life. The critical congenital heart disease (CCHD) screen performed prior to discharge from the hospital of newborns in all 50 states has resulted in a 33% decrease in early infant death from critical congenital heart disease.5 However, the sensitivity of CCHD screening is estimated to be only 50% to 76% and there are multiple conditions that are not picked up by this screening.6,7 The pediatric health care provider must carefully watch for the develop of symptoms in their patients that would indicate the presence of congenital heart disease (Table).

In the case presented, the parents reported that the patient was sweaty and tired with feeds since aged 2 months, if not before. They describe that she would “snack” and could not feed for longer than 5 to 10 minutes at a time without getting tired and sweating profusely. Once the patient began crawling and became more active, parents reported profuse diaphoresis which they attributed to the warm climate and summer heat. It is important for the pediatrician to screen for these symptoms during routine well-child checks to ensure that patients with congenital heart disease who are not identified by routine newborn screening are later identified.

References:

1. Jinmei Z, Yunfei L, Yue W, Yongjun Q. Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) diagnosed in children and adolescents. J Cardiothorac Surg. 2020;15(1):90. doi:10.1186/s13019-020-01116-z

2. Angelini P. Novel imaging of coronary artery anomalies to assess their prevalence, the causes of clinical symptoms, and the risk of sudden cardiac death. Circ Cardiovasc Imaging. 2014;7(4):747-754. doi:10.1161/CIRCIMAGING.113.000278

3. Hauser M. Congenital anomalies of the coronary arteries. Heart. 2005;91(9):1240-1245. doi:10.1136/hrt.2004.057299

4. Dodge-Khatami A, Mavroudis C, Backer C. Anomalous origin of the left coronary artery from the pulmonary artery: collective review of surgical therapy. Ann Thorac Surg. 2002;74(3):946-955. doi:10.1016/s0003-4975(02)03633-0

5. Abouk R, Grosse SD, Ailes EC, Oster ME. Association of US state implementation of newborn screening policies for critical congenital heart disease with early infant cardiac deaths. JAMA. 2017;318(21): 2111-2118. doi:10.1001/jama/2017.17627

6. Ailes EC, Gilboa SM, Honein MA, Oster ME. Estimated number of infants detected and missed by critical congenital heart defect screening. Pediatrics. 2015;135(6):1000-1008. doi:10.1542/peds.2014-3662

7. Fisher JD, Bechtel RJ, et al. Clinical spectrum of previously undiagnosed pediatric cardiac disease. Am J Emerg Med. 2019;37(5): 933-936.doi:10.1016/j.ajem.2019.02.029

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Introduction

Chronic obstructive pulmonary disease (COPD), characterized by persistent respiratory symptoms and airflow limitation, is a debilitating respiratory disorder that has emerged as a major global health problem.1 COPD contributes to a significant economic and social burden worldwide and is responsible for more than 3 million deaths annually.2 In addition, COPD patients are at an increased risk of developing cardiovascular diseases, which are increasingly recognized as both an exacerbating factor and a complication associated with increased mortality.3 Previous research has established the link between cardiovascular disease and COPD, highlighting its clinical significance.3

Natriuretic peptides are hormones secreted by the brain, heart, and kidneys.4 Brain natriuretic peptide (BNP), produced mainly by ventricular myocytes, is released into circulation after pressure overload, volume expansion, and increased myocardial wall stress.4 A blood protease cleaves pre-proBNP to produce biologically active BNP and an amino-terminal pro-brain natriuretic peptide (NT-proBNP) of unknown function.5 BNP has sodium excretion, diuretic and vasodilatory effects.6 Previous studies have also shown that both are primarily used are primarily used for diagnosis, risk stratification and management in the diagnosis of heart failure.7 The half-life of BNP is 22 min and that of NT-proBNP is 70 min.8 NT-proBNP is relatively stable and potentially more accurate in diagnosing disease.8 Recent studies have shown that NT-proBNP levels are gaining attention in clinical practice in a wider range of disorders, including COPD, where variation in NT-proBNP levels may reflect different states of the disease.9

The study suggests that chronic hypoxia or concomitant pulmonary hypertension in COPD patients may cause increased pulmonary vascular pressure and right heart afterload, stimulating increased secretion of NT-proBNP, which is an indicator of poor patient prognosis.10,11 Ozdemirel et al observed higher NT-proBNP levels in outpatients with COPD compared to the healthy population.12 Liu et al and Boschetto et al examined patients in a respiratory clinic and found significantly higher NT-proBNP levels in COPD patients compared to healthy individuals.13,14 Gulen et al still observed a significant increase in NT-proBNP levels in COPD patients excluding cardiovascular compared to the healthy population.15 However, Urban et al did not find a significant increase in NT-proBNP levels in COPD patients who also excluded cardiovascular disease, and Wang et al did not observe a significant increase in NT-proBNP levels in COPD patients in their study.16,17 Therefore, the aim of this systematic review and meta-analysis was to assess the differences in NT-proBNP levels in different patient groups with COPD and to provide a basis for further research into the exact clinical value of NT-proBNP in COPD.

Materials and Methods

This systematic review and meta-analysis follows the PRISMA statements.18 The procedure is based on a protocol registered in the PROSPERO register of systematic reviews (#CRD 42022316536).

Search Strategy

4 databases including PubMed, Embase, Cochrane Library and Web of Science were searched for literatures published up to Mar 6, 2022. To define the population, “chronic obstructive pulmonary disease” was combined by the Boolean operator “AND” with terms that potentially evaluated Amino-terminal pro-brain natriuretic peptide levels, supplementation such as “NT-proBNP”, “N-terminal pro-BNP”, etc.

Study Selection

All relevant publications were assessed separately by two researchers (H.Y., T.L.), a third researcher (J.L.) re-assessed when there are different opinions about articles. In situations where there were differences in opinion among the reviewers, a third investigator (X.S.) facilitated a discussion to reach a consensus.

Eligibility Criteria

Studies were considered eligible if they met the following criteria:

  1. Patients with confirmed COPD or AECOPD (over 40 years of age).
  2. The studies included the results of NT-proBNP levels in patients with COPD or AECOPD, or NT-proBNP levels in COPD with cardiovascular disease.
  3. COPD or AECOPD was diagnosed based on the pulmonary function tests or the latest reference standard during the study, such as the GOLD criteria.
  4. No publication date, status, or language restrictions were applied. Clinical original articles were included, while secondary studies, conference abstracts, editorials, and animal studies were excluded.
  5. Full‐text publications.

Data Extraction and Quality Assessment

A pre-established data extraction form was created using standardization techniques by X.S., T.L., and H.Y. The data were then extracted independently by two reviewers (T.S., H.G.) with discrepancies reconciled through integration by a third reviewer (Z.F.) Furthermore, two authors (H.Y., T.L.), conducted individual quality assessments to ensure the accuracy and reliability of the data.

The quality of all studies was evaluated using the National Institutes of Health (NIH) dedicated tool, which is a standardized measure for assessing study quality. Each study was assessed individually, and an overall rating of poor, fair, or good was assigned based on the results of the assessment. This approach allows for a comprehensive and objective evaluation of the studies included in the analysis.19

Statistical Analysis

All data we extracted for pooling are continuous, and the heterogeneity between studies is diverse, hence standardized mean difference (SMD) was utilized. I2 test was utilized to quantify the heterogeneity among studies. We considered P-value≤0.05 and I2≥50% as high heterogeneity. In this case, we selected a random effect model to analyze data. Otherwise, a fixed effect model was chosen. Only when two tailed P values were smaller than 0.05 could it be deemed as statistically significant. R (version 4.2.1, meta package [version 5.5–0]) was used to perform all statistical analysis. We conducted sensitivity analysis to detect if the results were reliable and stable.

In this study, both subgroup analysis and sensitivity analysis were utilized to investigate the origin of heterogeneity. To evaluate the impact of individual studies on the combined results, a sensitivity analysis was conducted for each study group. Specifically, a single study was removed at a time, and the effect sizes of the remaining studies were evaluated to determine if they remained statistically significant. If the effect sizes did not change significantly, the stability of the results was confirmed and the findings were considered reliable. This approach allows researchers to identify potential sources of bias and ensure the robustness of their conclusions.

Results

Eligible Studies

This study conducted a systematic review and meta-analysis, retrieving a total of 3512 records from four electronic databases and additional sources. Following the removal of duplications, 1183 studies remained. The title and abstract screening process excluded 2328 articles. The full text of the remaining 91 studies was reviewed, resulting in 29 studies that met eligibility criteria. This analysis included 29 studies, which involved 8534 patients. (Figure 1).

Figure 1 Flowchart of information through the different phases of this systematic review and meta-analysis.

Abbreviation: BNP, brain natriuretic peptide.

Description of Included Studies

The majority of the studies utilized GOLD criteria for diagnosing COPD. Among the 29 studies included, there were eight case-control studies, eight prospective cohort studies, four retrospective cohort studies, and thirteen cross-sectional studies. A total of five studies were deemed to be of good quality while 18 were considered fair quality. Due to a limited number of studies (<10) per item, it was not possible to evaluate publication bias. The detailed characteristics of each study are presented in Table S1,12,14–17,20–43 while the findings are summarized in Table S2.

The Levels of NT-proBNP for COPD Patients versus Non-COPD Patients

9 studies were conducted to compare the levels of NT-proBNP between COPD and non-COPD patients. 7 of these studies utilized healthy subjects as a control group, while the remaining two used non-healthy subjects as a control group. Within each study, NT-proBNP levels were examined in both the COPD patient group and the non-COPD patient group. The forest plot presented that compared with the Non-COPD patients group, the NT-proBNP level of COPD patients was significantly increased (SMD [95CI%]=0.46 [0.22,0.70]; p=0.0002). (Figure 2). It suggests that elevated NT-proBNP levels are associated with a high risk of COPD.

Figure 2 Forest plot of NT-proBNP level between COPD patients and Non-COPD patients.

Abbreviations: NT-proBNP, amino-terminal pro-brain natriuretic peptide; COPD, chronic obstructive pulmonary disease; SMD, standardized mean difference; CI, Confidence Interval; SD, Standard Deviation.

Based on the high heterogeneity of the results (I2 = 66%; p<0.01), we performed a subgroup analysis. Compared with the healthy group, the NT-proBNP level was significantly increased in COPD patients (SMD [95CI%]=0.56 [0.25,0.87]; p=0.0004), and the heterogeneity was (I2= 61% p = 0.02)(Figure 3). As for the Non-COPD patients, the NT-proBNP level also increased (SMD [95CI%]=0.21 [0.11,0.31]; p<0.0001), and the heterogeneity was insubstantial (I2= 0%; p = 0.62) (Figure 3). Therefore, we suggest that heterogeneity may originate from different control groups of the population. We also performed a sensitivity analysis and found that the results were stable (Figure 4). Although there was heterogeneity in 9 studies, it had no significant effect on the results.

Figure 3 Forest plot of NT-proBNP level between COPD patients and Non-COPD patients subgroups.

Abbreviations: NT-proBNP, amino-terminal pro-brain natriuretic peptide; COPD, chronic obstructive pulmonary disease; SMD, standardized mean difference; CI, Confidence Interval; SD, Standard Deviation.

Figure 4 Sensitivity analysis plot of NT-proBNP level between COPD patients and Non-COPD patients.

Abbreviations: NT-proBNP, amino-terminal pro-brain natriuretic peptide; COPD, chronic obstructive pulmonary disease; SMD, standardized mean difference; CI, Confidence Interval; SD, Standard Deviation.

The Levels of NT-proBNP for Stable COPD Patients versus Healthy Control

The levels of NT-proBNP for stable COPD patients versus Healthy Control was reported in 6 studies. The forest plot showed that compared with the healthy control group, the NT-proBNP level of stable COPD patients was significantly increased (SMD [95CI%]=0.51 [0.13,0.89]; p=0.0092), and the heterogeneity was (I2= 68%; p<0.01) (Figure 5). It suggests that elevated NT-proBNP levels are associated with a high risk of stable COPD. Sensitivity analysis showed no significant effect of heterogeneity on the stability of the results. (Figure 6).

Figure 5 Forest plot of NT-proBNP level between stable COPD patients and healthy control.

Abbreviations: NT-proBNP, amino-terminal pro-brain natriuretic peptide; COPD, chronic obstructive pulmonary disease; SCOPD, stable chronic obstructive pulmonary disease; SMD, standardized mean difference; CI, Confidence Interval; SD, Standard Deviation.

Figure 6 Sensitivity analysis plot of NT-proBNP level between COPD patients and healthy control.

Abbreviations: NT-proBNP, amino-terminal pro-brain natriuretic peptide; COPD, chronic obstructive pulmonary disease; SCOPD, stable chronic obstructive pulmonary disease; SMD, standardized mean difference; CI, Confidence Interval; SD, Standard Deviation.

The Levels of NT-proBNP for AECOPD Patients versus SCOPD Patients

The levels of NT-proBNP in differentiating AECOPD from stable COPD was reported in 3 studies. Compared with the stable COPD group, the level of NT-proBNP Significant increase in AECOPD (SMD [95CI%]=1.18 [0.07,2.29]; p=0.037), and high heterogeneity was found (I2 = 95%; p<0.01) (Figure 7). It demonstrated that elevated NT-proBNP levels were associated with a high risk of AECOPD. Sensitivity analysis showed that the results were stable (Figure 8). The heterogeneity may originate from the studies of Patel et al and Jiang et al24,25 We found that the older age of the population studied by Patel et al and the differences in the test methods of the three studies may have contributed to the large heterogeneity.24

Figure 7 Forest plot of NT-proBNP level between stable COPD patients and AECOPD patients.

Abbreviations: NT-proBNP, amino-terminal pro-brain natriuretic peptide; COPD, chronic obstructive pulmonary disease; AECOPD, acute exacerbation of chronic obstructive pulmonary disease; SCOPD, stable chronic obstructive pulmonary disease; SMD, standardized mean difference; CI, Confidence Interval; SD, Standard Deviation.

Figure 8 Sensitivity analysis plot of NT-proBNP level between stable COPD patients and AECOPD patients.

Abbreviations: NT-proBNP, amino-terminal pro-brain natriuretic peptide; COPD, chronic obstructive pulmonary disease; AECOPD, acute exacerbation of chronic obstructive pulmonary disease; SCOPD, stable chronic obstructive pulmonary disease; SMD, standardized mean difference; CI, Confidence Interval; SD, Standard Deviation.

The Levels of NT-proBNP for Different Severities of COPD

6 studies reported the levels of NT-proBNP in relation to various severities of COPD. Pulmonary function was assessed using predicted forced expiratory volume in one second (FEV1%) values, with patients categorized into Non-severe group (predicted FEV1% ⩾ 50%) and Severe group (predicted FEV1% < 50%).Compared with the non-severe group, the level of NT-proBNP Significant increase in severe group (SMD [95CI%]=0.17 [0.05,0.29]; p=0.0058), and no heterogeneity was found (I2 = 0%; p=0.54) (Figure 9).

Figure 9 Forest plot of NT-proBNP level between Severe group and Non-severe group.

Abbreviations: NT-proBNP, amino-terminal pro-brain natriuretic peptide; COPD, chronic obstructive pulmonary disease; SMD, standardized mean difference; CI, Confidence Interval; SD, Standard Deviation.

The Levels of NT-proBNP for Different Risks of in-Hospital Mortality in Patients with AECOPD

In this section, 3 studies report NT-proBNP levels for different risks of in-hospital mortality in patients with AECOPD. Compared with the survivors group, the level of NT-proBNP significant increase in Non-survivors (SMD [95CI%]=1.67 [0.47,2.88]; p=0.0063), and high heterogeneity was found (I2 = 95%; p<0.0001) (Figure 10). Studies have shown that elevated NT-proBNP levels are associated with a high risk of death in hospitalized AECOPD patients. Sensitivity analysis showed that the results were stable (Figure 11). The observed heterogeneity in the results could potentially be attributed to the studies conducted by Spannella et al and Li et al32,33 Disparities in the timing, techniques, and specimens utilized in the three studies may be considered as the primary causative factors underlying the observed heterogeneity.

Figure 10 Forest plot of NT-proBNP level between Survivors and Non-survivors during hospitalisation.

Abbreviations: NT-proBNP, amino-terminal pro-brain natriuretic peptide; COPD, chronic obstructive pulmonary disease; SMD, standardized mean difference; CI, Confidence Interval; SD, Standard Deviation.

Figure 11 Sensitivity analysis plot of NT-proBNP level between Survivors and Non-survivors.

Abbreviations: NT-proBNP, amino-terminal pro-brain natriuretic peptide; COPD, chronic obstructive pulmonary disease; SMD, standardized mean difference; CI, Confidence Interval; SD, Standard Deviation.

The Levels of NT-proBNP in Patients with COPD versus Patients with Chronic Heart Failure

This section presents a comparative analysis of COPD and CHF, individually contrasted with COPD and CHF together. The discriminatory power of NT-proBNP in identifying the coexistence of COPD and CHF versus just COPD, was evaluated in 7 studies. For the COPD without CHF patients, NT-proBNP levels increased notably (SMD [95CI%]=1.49 [0.96,2.01]; p<0.0001), and the heterogeneity was remarkable (I2 = 89%; p<0.01) (Figure 12). The results demonstrated that further increase in NT-proBNP levels indicates high risk of COPD with CHF. Sensitivity analysis showed that the results were stable (Figure 13). In terms of the prediction value of NT-proBNP for CHF with COPD, 4 studies reported the value of NT-proBNP in distinguishing CHF with COPD from CHF without COPD. For the CHF without COPD patients, NT-proBNP levels increased notably (SMD [95CI%]=0.21 [−0.20,0.62]; p=0.3171) (Figure 14), and the heterogeneity was significant (I2 = 71%; p=0.01). The results suggest that elevated NT-proBNP levels in patients with CHF do not effectively indicate a high risk of COPD with CHF. Sensitivity analysis showed that the results were stable (Figure 15).

Figure 12 Forest plot of NT-proBNP level between COPD with CHF patients and COPD patients.

Abbreviations: NT-proBNP, amino-terminal pro-brain natriuretic peptide; COPD, chronic obstructive pulmonary disease; CHF, chronic heart failure; SMD, standardized mean difference; CI, Confidence Interval; SD, Standard Deviation.

Figure 13 Sensitivity analysis plot of NT-proBNP level between COPD with CHF patients and COPD patients.

Abbreviations: NT-proBNP, amino-terminal pro-brain natriuretic peptide; COPD, chronic obstructive pulmonary disease; CHF, chronic heart failure; SMD, standardized mean difference; CI, Confidence Interval; SD, Standard Deviation.

Figure 14 Forest plot of NT-proBNP level between CHF with COPD patients and CHF patients.

Abbreviations: NT-proBNP, amino-terminal pro-brain natriuretic peptide; CHF, chronic heart failure; COPD, chronic obstructive pulmonary disease; SMD, standardized mean difference; CI, Confidence Interval; SD, Standard Deviation.

Figure 15 Sensitivity analysis plot of NT-proBNP level between CHF with COPD patients and CHF patients.

Abbreviations: NT-proBNP, amino-terminal pro-brain natriuretic peptide; CHF, chronic heart failure; COPD, chronic obstructive pulmonary disease; SMD, standardized mean difference; CI, Confidence Interval; SD, Standard Deviation.

The Levels of NT-proBNP for COPD Patients with Pulmonary Hypertension versus COPD Patients

The levels of NT-proBNP for COPD patients with pulmonary hypertension versus COPD patients was reported in 4 studies. For the COPD without pulmonary hypertension patients, NT-proBNP levels increased notably (SMD [95CI%]=0.82 [0.69,0.96]; p<0.0001). (Figure 16), and the heterogeneity was negligible (I2 = 0%; p=0.96). The results showed that further increase in NT-proBNP levels indicates high risk of COPD with PH.

Figure 16 Forest plot of NT-proBNP level between COPD with PH patients and COPD patients.

Abbreviations: NT-proBNP, amino-terminal pro-brain natriuretic peptide; COPD, chronic obstructive pulmonary disease; PH, pulmonary hypertension; SMD, standardized mean difference; CI, Confidence Interval; SD, Standard Deviation.

Discussion

This meta-analysis demonstrated significant differences in NT-proBNP levels between patient groups with COPD. NT-proBNP is a widely used biomarker in clinical heart failure that was found to be significantly higher in COPD patients following an acute exacerbation and remained significantly different in early non-severe and late severe disease states. Moreover, NT-proBNP levels were significantly higher in patients with COPD combined with PH and CHF compared to COPD patients alone, while patients with CHF combined with COPD did not show significant differences in NT-proBNP levels compared to CHF alone. The study also found significant differences in NT-proBNP levels between surviving and non-surviving patients during hospitalization for AECOPD.

The study found that patients with stable COPD had higher NT-proBNP levels compared to the healthy population, and different levels were detected in patients with varying severity of COPD. We conclude that cardiopulmonary interactions contribute to the elevated NT-proBNP levels. There are two potential hypotheses for the observed phenomenon. Firstly, despite the exclusion of cardiovascular disease in COPD patients during our study, there may still exist underlying and incipient stages of cardiovascular disease that have evaded detection by current diagnostic technologies.44 It has been shown that COPD is associated with alterations in the structure and mechanics of the pulmonary vascular bed.10,45 As the pathophysiology of COPD advances, it triggers a structural remodeling of the pulmonary circulation, culminating in Pulmonary Arterial Hypertension (PH) and consequent Chronic Pulmonary Heart Disease. This phenomenon culminates in an augmented load on the right ventricle, ultimately leading to functional failure.11 The ventricular wall experiences augmented traction, which triggers the release of NT-proBNP.12 Our hypothesis suggests that this could be a significant etiology of heightened levels of NT-proBNP.46 According to the study conducted by Hilde et al, patients with COPD exhibit mild dysfunction of the right ventricle, as evidenced by only a slight elevation in the mean pulmonary artery pressure. This suggests that COPD can have a negative impact on the cardiovascular system, specifically on the right heart, which is responsible for pumping blood into the lungs for oxygenation.44 It is postulated that COPD induces cardiovascular damage, resulting in an increase in the circulating levels of NT-proBNP.10 Second, hypoxia, which refers to a condition in which there is an inadequate supply of oxygen to the body tissues, has been identified as a potential contributor to the upregulation of NT-proBNP levels.47,48 Casals et al conducted a study that demonstrated the induction of B-type natriuretic peptide (BNP) release in cell lines derived from human cardiomyocytes under hypoxic conditions.49 A significant proportion of COPD patients have varying degrees of decreased oxygen saturation due to decreased spirometry.50 Our hypothesis proposes that the persistent deficiency of oxygen, known as chronic hypoxia, in patients who suffer from COPD triggers a response in the myocardium which results in the secretion of NT-proBNP. Recent research has suggested plausible hypotheses regarding the elevated NT-proBNP levels observed in patients with COPD. Specifically, it is postulated that these elevated levels may stem from the activity of various pro-inflammatory cytokines.29 Prior research has posited that pro-inflammatory cytokines, such as interleukin-1(IL-1β) and tumor necrosis factor-alpha (TNF-α), may serve as stimuli for the release of NT-proBNP from cardiac myocytes.51 Kenneth et al demonstrated that Brain Natriuretic Peptide (BNP) is upregulated as a result of the synergistic interplay between IL-1β, TNF-α and IL-6. This implies that the overproduction of BNP may be attributed to an inflammatory response mediated by these cytokines, which are well-known regulators of immune and metabolic processes.51 Airway inflammation refers to the activation of immune cells and release of pro-inflammatory mediators in the airways, which plays a crucial role in the pathogenesis and progression of COPD.2 Furthermore, this local inflammation can spread to other organs and tissues through systemic circulation, leading to systemic inflammation.2 Inflammatory cytokines, including IL-1β, TNF-α, and IL-6, have been demonstrated to be upregulated in COPD.13,52 Based on our analysis, we propose that NT-proBNP levels may reflect inflammation in patients and thus help identify COPD disease in the healthy population. The aforementioned variables can further deteriorate in tandem with the progression of chronic obstructive pulmonary disease (COPD).2 Thus, NT-proBNP exhibits different degrees of elevation at different severities of COPD.26 We believe that NT-proBNP might help to differentiate the severity of COPD disease.

Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are episodes of worsening symptoms that often lead to a poor prognosis for patients and need to be supplemented with relevant therapeutic measures.53 In the field of COPD, patients experiencing acute exacerbations and those who passed away during their hospitalization exhibited markedly increased concentrations of NT-proBNP. Regarding the former, it is hypothesized that an upregulation in pro-inflammatory cytokines and heightened cardiovascular load may give rise to the elevated levels of NT-proBNP. It is well known that acute exacerbations of COPD are usually caused by infections and present with acute dyspnea, hypoxemia and respiratory symptoms.53 During an acute exacerbation state, there is an upregulation of inflammatory mediators which can trigger the release of cytokines, leukotrienes, and other pro-inflammatory factors. These molecules can stimulate the production of natriuretic peptides such as NT-proBNP from cardiac cells. During a state of hypoxemia, the oxygen supply to tissues is insufficient, and this can lead to an increase in cardiac workload as the heart attempts to compensate for the lack of oxygen. This increased burden on the heart can trigger the release of NT-proBNP from cardiac cells. Similarly, dyspnea, or difficulty breathing, can also cause an elevation in NT-proBNP levels due to the additional stress it places on the cardiovascular system.54 The results imply that the assessment of NT-proBNP levels can serve as a valuable biomarker for identifying high-risk patients and facilitating clinical decision-making in the management of AECOPD.

The study investigated the hospital prognosis of patients with AECOPD and found that those who died exhibited significantly elevated levels of NT-proBNP compared to those who survived. This implies that a high NT-proBNP level is a robust predictor of unfavorable outcomes in AECOPD. The observed trend may suggest an association between the severity of pulmonary impairment and comorbid cardiovascular disease, which may have contributed to the increased NT-proBNP levels in non-survivors. Andrijevic et al conducted a study which determined that NT-proBNP is a valuable indicator of mortality risk in patients with AECOPD who have concurrent cardiovascular disease.31 In the study conducted by Spannella et al, it was found that elevated levels of NT-proBNP indicate a compromised cardiopulmonary foundation, and are associated with an escalated mortality risk in patients experiencing AECOPD.32 The inclusion criteria for our study did not involve complete exclusion of AECOPD co-occurring with cardiovascular disease, given the high prevalence of hospitalized AECOPD patients with cardiac insufficiency.31 Apart from the aforementioned etiologies, NT-proBNP may signify concomitant cardiopulmonary dysfunction.55 For patients who have been chronically depleted, this is more likely to lead to life-threatening conditions.56 Studies have demonstrated that NT-proBNP exhibits a significant correlation with both short- and long-term mortality among patients suffering from COPD.57 Chang et al conducted a study indicating that increased levels of NT-proBNP serve as a reliable prognostic marker for premature mortality amongst patients admitted to the hospital due to AECOPD.58 The lack of sensitivity and specificity data limits our ability to establish a definitive correlation between elevated NT-proBNP levels and in-hospital mortality risk in AECOPD. As such, we can only put forth conjectures that suggest a potential association between NT-proBNP levels and increased risk of mortality during hospitalization for AECOPD. Hence, focusing on high levels of NT-proBNP can assist clinicians in making decisions such as transfer to intensive care unit and discharge from the hospital.

COPD is a respiratory disorder characterized by chronic oxidative stress, systemic inflammation, hypoxemia, and respiratory distress. These factors can lead to the development of cardiovascular complications, such as pulmonary hypertension (PH) and chronic heart failure (CHF), particularly in the late stages of COPD.3 COPD with PH gradually progresses to right heart failure as pulmonary artery pressure increases and right heart afterload increases.10 Pulmonary hypertension (PH) is diagnosed through the gold standard method of right heart catheterization, which involves the insertion of a catheter into the pulmonary artery to measure pressures. However, this diagnostic technique is invasive and poses challenges for implementation in clinical settings due to its difficulty in performing and associated risks.11 Echocardiography, a diagnostic tool that employs ultrasound waves to produce images of the heart, has gained widespread acceptance in clinical practice as a non-invasive test.11 The current study proposes that in patients with COPD who have developed PH, augmented right ventricular afterload leads to heightened secretion of NT-proBNP.11 The study revealed that NT-proBNP exhibited notable variations in patients suffering from COPD with PH as compared to COPD patients without PH. NT-proBNP is emerging as a promising diagnostic tool and can be utilized to exclude the possibility of PH.59 In the context of comorbidities, COPD and decreased cardiac function can lead to a complex interplay between pulmonary and cardiovascular systems. While right heart insufficiency caused by PH is a common manifestation in patients with COPD, it is important to note that the presence of decreased cardiac function requires a comprehensive evaluation of left heart function as well. NT-proBNP is a commonly utilized biomarker in clinical settings. It plays a vital role in distinguishing between cardiogenic and pulmonary dyspnea. In this context, we aimed to investigate the expression of NT-proBNP in COPD patients with accompanying CHF.60 The study conducted a comparative analysis of COPD patients with comorbid CHF and compared them separately with COPD patients and CHF patients. The levels of NT-proBNP were assessed and it was observed that there was a statistically significant difference between COPD patients alone and those with COPD and CHF. However, when compared to the CHF group, the COPD and CHF group did not exhibit significantly elevated levels of NT-proBNP. This outcome is in opposition to the findings of Khaletskaya et al and Karoli et al, indicating a discrepancy or divergence in their respective research outcomes.35,61 This could be attributed to several factors, such as differences in sample size, methodology, or statistical analysis techniques employed by the researchers. It is essential to further investigate the reasons behind the conflicting results to better understand the underlying mechanisms and potential implications for future studies in the field. Our study suggests that COPD may promote the secretion of NT-proBNP primarily by increasing the cardiac burden. In contrast, in patients with congestive heart failure (CHF), cardiac insufficiency alone is sufficient to stimulate significant NT-proBNP secretion, which could partially mask the effect of COPD on NT-proBNP secretion. Nonetheless, we observed significantly higher levels of NT-proBNP in COPD patients with concomitant cardiac insufficiency, and these patients had a poor prognosis. Therefore, measuring NT-proBNP levels in COPD patients can aid in clinical screening and early intervention to improve the prognosis of patients with COPD and concurrent cardiovascular disease.

Limitation

The study has several limitations. Firstly, the included studies had small sample sizes, resulting in inaccurate pooled results. Secondly, certain factors that affect NT-proBNP such as renal disease and oxygen saturation level were not assessed in the original study. Thirdly, errors due to differences in NT-proBNP detection methods and instruments were difficult to avoid. Fourthly, publication bias could not be assessed as there were fewer than 10 studies in each section. Fifthly, the majority of studies included were cross-sectional, which failed to explore the correlation between NT-proBNP and COPD. Finally, the possibility of confounding by other diseases was present due to the inclusion of cardiovascular disease in all studies except for the COPD versus healthy controls study.

Conclusion

NT-proBNP, a biomarker commonly used in clinical practice to evaluate cardiovascular disease, demonstrates significant variations in different stages of COPD and during the progression of the disease. The fluctuations in NT-proBNP levels could be indicative of the severity of pulmonary hypoxia and inflammation and cardiovascular stress among COPD patients. Therefore, assessing NT-proBNP levels in COPD patients can aid in making informed clinical decisions. However, due to the limited quality and quantity of evidence available in the partial results, it is advisable to interpret them with caution.

Abbreviation

COPD, chronic obstructive pulmonary disease; BNP, brain natriuretic peptide; NT-proBNP, amino-terminal pro-brain natriuretic peptide; SCOPD, stable chronic obstructive pulmonary disease; AECOPD, acute exacerbations of chronic obstructive pulmonary disease; pg/mL, picograms per milliliter; FEV1, forced expiratory volume in the first second; FEV1%pred, the forced expiratory volume in the first second in percent predicted values; PRISMA, Preferred Reporting Items for Systematic Review and Meta-analyses; CI, confidence interval; SD, standard difference; SMD, standardized mean difference; CHF, chronic heart failure; PH, pulmonary hypertension; IL-1β, interleukin-1β; IL-6, interleukin-6; CRP, c-reactive protein; TNF-α, tumor necrosis factor-α.

Consent for Publication

All details of any images, videos, recordings, etc presented in this article can be published, and all authors agree with the article contents to be published. All authors are able to provide copies of signed consent forms to the journal editorial office if requested.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Funding

This work was supported by the Science and Technology Projects of Gansu Province (grant number 20YF8FA082). Funder had no role in the design of the study, the collection and analysis of the data, or the preparation of the manuscript.

Disclosure

All authors promise that there is no conflict of interests in this work.

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36. Karoli N, Borodkin A, Rebrov A. Features of the clinic and diagnosis of chronic heart failure in patients with chronic obstructive pulmonary disease. Kardiologiia. 2019;59:47–55.

37. Losip A, Pop D, Sitar-Taut A, et al. NT-proBNP and Uric acid levels correlate in patients with COPD and heart failure. Acta Med Mediterranea. 2018;34(1):189.

38. Kovacs G, Avian A, Bachmaier G, et al. Severe Pulmonary Hypertension in COPD: impact on Survival and Diagnostic Approach. Chest. 2022;162(1):202–212.

39. Zuo H, Xie X, Peng J, et al. Predictive Value of Novel Inflammation-Based Biomarkers for Pulmonary Hypertension in the Acute Exacerbation of Chronic Obstructive Pulmonary Disease. Anal Cell Pathol. 2019;2019:5189165.

40. Tian F, Song W, Wang L, et al. NT-pro BNP in AECOPD-PH: old biomarker, new insights-based on a large retrospective case-controlled study. Respir Res. 2021;22(1):321.

41. Marcun R, Stankovic I, Vidakovic R, et al. Prognostic implications of heart failure with preserved ejection fraction in patients with an exacerbation of chronic obstructive pulmonary disease. Intern Emerg Med. 2016;11(4):519–527.

42. Koliev V, Sarapulova I, Ryabova L. Diagnosis of chronic heart failure in patients with chronic obstructive pulmonary disease. Kazan Medical Journal. 2019;100:530–536.

43. Vyshnyvetskyy I, Kholopov L, Batashova-Halynska V. Clinical characteristics of the respiratory and cardiovascular systems in patients with combination of chronic obstructive pulmonary disease and heart failure. Zaporozhye Med J. 2017;1:65.

44. Hilde JM, Skjørten I, Grøtta OJ, et al. Right ventricular dysfunction and remodeling in chronic obstructive pulmonary disease without pulmonary hypertension. J Am Coll Cardiol. 2013;62(12):1103–1111.

45. Nasir SA, Singh S, Fotedar M, et al. Echocardiographic Evaluation of Right Ventricular Function and its Role in the Prognosis of Chronic Obstructive Pulmonary Disease. J Cardiovasc Echogr. 2020;30(3):125–130.

46. Buchan A, Bennett R, Coad A, et al. The role of cardiac biomarkers for predicting left ventricular dysfunction and cardiovascular mortality in acute exacerbations of COPD. Open Heart. 2015;2(1):e000052.

47. Hall C. NT-ProBNP: the mechanism behind the marker. J Card Fail. 2005;11(5 Suppl):S81–83.

48. Hopkins WE, Chen Z, Fukagawa NK, et al. Increased atrial and brain natriuretic peptides in adults with cyanotic congenital heart disease: enhanced understanding of the relationship between hypoxia and natriuretic peptide secretion. Circulation. 2004;109(23):2872–2877.

49. Casals G, Ros J, Sionis A, et al. Hypoxia induces B-type natriuretic peptide release in cell lines derived from human cardiomyocytes. Am J Physiol Heart Circ Physiol. 2009;297(2):H550–555.

50. Zysman M, Deslee G, Perez T, et al. Burden and Characteristics of Severe Chronic Hypoxemia in a Real-World Cohort of Subjects with COPD. Int J Chron Obstruct Pulmon Dis. 2021;16:1275–1284.

51. Ma KK, Ogawa T, de Bold AJ. Selective upregulation of cardiac brain natriuretic peptide at the transcriptional and translational levels by pro-inflammatory cytokines and by conditioned medium derived from mixed lymphocyte reactions via p38 MAP kinase. J Mol Cell Cardiol. 2004;36(4):505–513.

52. Shyam Prasad Shetty B, Chaya SK, Kumar VS, et al. Inflammatory Biomarkers Interleukin 1 Beta (IL-1β) and Tumour Necrosis Factor Alpha (TNF-α) Are Differentially Elevated in Tobacco Smoke Associated COPD and Biomass Smoke Associated COPD. Toxics. 2021;9(4):543.

53. Ko FW, Chan KP, Hui DS, et al. Acute exacerbation of COPD. Respirology. 2016;21(7):1152–1165.

54. Ritchie AI, Wedzicha JA. Definition, Causes, Pathogenesis, and Consequences of Chronic Obstructive Pulmonary Disease Exacerbations. Clin Chest Med. 2020;41(3):421–438.

55. Hillas G, Perlikos F, Tzanakis N. Acute exacerbation of COPD: is it the “stroke of the lungs”? Int J Chron Obstruct Pulmon Dis. 2016;11:1579–1586.

56. McDonald MN, Wouters EFM, Rutten E, et al. It’s more than low BMI: prevalence of cachexia and associated mortality in COPD. Respir Res. 2019;20(1):100.

57. Pavasini R, Tavazzi G, Biscaglia S, et al. Amino terminal pro brain natriuretic peptide predicts all-cause mortality in patients with chronic obstructive pulmonary disease: systematic review and meta-analysis. Chron Respir Dis. 2017;14(2):117–126.

58. Chang CL, Robinson SC, Mills GD, et al. Biochemical markers of cardiac dysfunction predict mortality in acute exacerbations of COPD. Thorax. 2011;66(9):764–768.

59. McCrory DC, Coeytaux RR, Schmit KM, et al. AHRQ Comparative Effectiveness Reviews. Pulmonary Arterial Hypertension: Screening, Management, and Treatment. Rockville (MD): Agency for Healthcare Research and Quality (US); 2013.

60. Cao Z, Jia Y, Zhu B. NT-proBNP as Diagnostic Biomarkers for Cardiac Dysfunction in Both Clinical and Forensic Medicine. Int J Mol Sci. 2019;20:548.

61. Karoli NA, Borodkin AV, Kosheleva NA, et al. Факторы риска развития неблагоприятных исходов у пациентов с хронической обструктивной болезнью легких и хронической сердечной недостаточностью[Prognostic markers for the development of adverse outcomes in patients with chronic obstructive pulmonary disease and chronic heart failure]. Kardiologiia. 2018;58(Suppl 9):39–47. Russian.

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Chronic lower respiratory disease, primarily chronic obstructive pulmonary disease (COPD), is the fourth leading cause of death in the United States.1,2 Almost 15.7 million Americans (6.4%) have been diagnosed with COPD.1 More than 50% of adults with low pulmonary function are undiagnosed and unaware that they have this disease. Once thought to be a disease predominantly affecting men, more women than men are currently living with (and dying from) COPD in the United States.1,3 Best practices for the diagnosis and management of COPD are evolving, as reflected in the 2023 Global Initiative for Chronic Obstructive Lung Disease (GOLD) Report.

The GOLD Science Committee updated the definition of COPD to reflect the heterogeneous nature of this condition, stating that COPD is characterized by chronic respiratory symptoms (dyspnea, cough, sputum production, exacerbations) caused by abnormalities of the airways (bronchitis, bronchiolitis) and/or alveoli (emphysema) that result in persistent, often progressive, airflow obstruction.4 The 2023 GOLD report also updated risk factors and revised treatment guidelines.4

Etiology and Risk Factors

Chronic obstructive pulmonary disease is caused by a combination of genetic predisposition, inflammatory changes in the airways, immune reactivity, and environmental factors.4 Although tobacco smoking is a leading cause of COPD globally, the 2023 GOLD Report also emphasizes the role of inhalation of smoke from biomass fuel or ambient particulate matter from household and outdoor air pollution in the risk for COPD.4 Exposure to indoor smoke from biomass fuels is estimated to account for 35% of COPD cases globally.5 Occupational exposures are also associated with COPD. A study based on the Third National Health and Nutrition Examination Survey (NHANES III) reported that occupational exposure was attributable to COPD in 31.1% of nonsmokers, reflecting an increased prevalence of COPD among nonsmokers in certain industries and occupations.6 For example, different occupational dust and fumes, industrial and agricultural, have been associated with COPD and respiratory symptoms.4


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Alpha-1 antitrypsin deficiency (AATD) is also a rare genetic disorder that causes COPD.4 Alpha-1 antitrypsin (AAT) is a serine protease inhibitor that protects lung tissue from proteolytic damage by inhibiting elastase, an enzyme secreted by white blood cells. The disorder is caused by a single genetic variant and clinical manifestations include panacinar emphysema, airway hyperresponsiveness, and bronchiectasis.7

Clinical Manifestations

Chronic obstructive pulmonary disease causes a range of symptoms that lead to a daily burden and limitations of daily activity in the affected individual. The most common symptoms are dyspnea, cough, and sputum production.4 Patients also experience wheezing, fatigue, chest tightness, and chest congestion.4 Many persons report breathlessness that varies daily, weekly, or seasonally. Of the patients who report seasonal variability in their COPD symptoms, 56% report their symptom burden is greatest during the winter months.8 Winter is associated with an increased risk of COPD exacerbations and it is thought that the cold, damp environment prevailing during the winter months as well as increased exposure to respiratory viral infections at that time of year may partly explain this seasonal association.9

Physical findings that are associated with COPD include cyanosis, enlarged chest diameter, prolonged exhalation phase in breathing, and breathlessness with exertion. Cyanosis may be observed particularly in the lips and mucous membranes in persons with severe COPD and hypoxia. A large amount of retained air in the chest can create a barrel shape. Patients tend to have orthopnea; difficulty breathing in the supine position. Sitting forward or tripoding eases breathing. When auscultating the chest, diminished breath sounds, prolonged exhalation, and wheezing are found. Patients with cor pulmonale can have bilateral crackles and signs of right ventricular failure such as jugular venous distension and ankle edema.10

Diagnosis of COPD

Although COPD may be suspected based on findings from the history and physical examination, the diagnosis must be confirmed by spirometry to detect airflow obstruction and its severity, according to the GOLD 2023 Report.4 Spirometry measures 2 key factors: forced expiratory volume in 1 second (FEV1) and expiratory forced vital capacity (FVC). Chronic obstructive pulmonary disease is diagnosed when the postbronchodilator FEV1/FVC ratio is less than 0.7. Accurate assessment of the patient’s maximal effort is important, and testing should be repeated at least 3 times to get the best results.

The GOLD 2023 Report also recommends a comprehensive assessment of the patient with COPD based on spirometry postbronchodilator. The recommended bronchodilator is 400 mcg of a short-acting β-agonists (SABA), 160 mcg of a short-acting muscarinic antagonist (SAMA), or the 2 agents combined. The FEV1 should be measured 10 to 15 minutes after administration of the SABA or 30 to 45 minutes after the SAMA or combination is administered. Appropriate reference values should be used based on age, height, sex, and race.4

Patient Questionnaires Added to Assessment

In addition to spirometry, the patient’s self-assessment of their condition is considered an important factor in the management of COPD. The modified Medical Research Council (mMRC) dyspnea scale was the first questionnaire developed to measure breathlessness, which is a key symptom in many patients with COPD, although often unrecognized. The mMRC includes a question about the level of activity that causes breathlessness for the patient on a 0 to 4 scale. Zero indicates that the patient only experiences breathlessness with strenuous exercise, whereas a 4 indicates that the patient experiences too much breathlessness to leave the house or when dressing and undressing.4

COPD impacts patients in more ways beyond dyspnea. For this reason, multidimensional questionnaires are recommended. The most comprehensive disease-specific health status questionnaires such as the Chronic Respiratory Questionnaire (CRQ) and St. George’s Respiratory Questionnaire (SGRQ) are important research tools (but are too complex to use in routine practice). Shorter comprehensive measures, such as the COPD Assessment Test (CAT) and The COPD Control Questionnaire (CCQ) have been developed and are suitable for use in the clinic. The CAT tool is a Likert scale that asks questions about level of activity, episodes of cough, chest tightness, sleeping ability, with scores from 0 to 40.4

The GOLD 2023 diagnostic guidelines recommend use of the mMRC and CAT tools in the assessment of the patient.4

Other Laboratory Tests

Other tests that are useful in the clinical diagnosis of COPD include arterial blood gas test, which can reveal chronic hypercapnia and may prompt evaluation for oxygen therapy in select patients. A 6-minute walk test should be ordered in patients with progressively worsening dyspnea or lung function to assess for hypoxia on exertion and determine the need for long-term oxygen therapy. Eosinophil count on a complete blood count with differential can help guide the decision to initiate or discontinue inhaled corticosteroids (ICSs). Patients with high eosinophil counts (>300 cells/µL) respond to ICSs added to the regimen. Obtaining a chest computed tomography (CT) scan is important to rule out pulmonary embolism and assess for the presence of other coexisting pulmonary abnormalities including bronchiectasis, interstitial lung disease, and lung mass.4

Once the diagnosis is established, the FEV1 is used to define the severity of lung function impairment. The GOLD Report classifies the severity of airflow obstruction in COPD as4:

  • Mild: FEV1 ≥80% of predicted (GOLD Grade: 1)
  • Moderate: FEV1 of 50% to 79% of predicted (GOLD Grade: 2)
  • Severe: FEV1 of 30% to 49% of predicted (GOLD Grade: 3)
  • Very severe: FEV1 <30% predicted (Gold Grade: 4)

2023 GOLD Report COPD Treatment Guidelines

The goals of COPD treatment are to manage symptoms and prevent exacerbations. Classes of pharmacologic agents used to treat COPD are shown in the Table. Because most COPD pharmacotherapies are inhalers, patients need instruction on the proper inhaler technique. The choice of inhaler device needs to be individualized based on access as well as the patient’s ability and preference. Demonstration of the inhaler technique is critical and should be assessed at each visit. Studies show that improper inhaler technique is common and responsible for inadequate treatment.4

Table. Common Medications Used to Treat COPD

Class Drug (brand name)
SABAs Albuterol/salbutamol
Levalbuterol
LABAs Formoterol
Indacaterol
Olodaterol
Salmeterol
SAMAs Ipratropium bromide
Oxitropium bromide
LAMAs Aclidinium bromide
Tiotropium Umeclidinium
Combination: SABA + anticholinergic agents Fenoterol/ipratropium 
Albuterol/ipratropium
Combination: LABA + LAMA Formoterol/aclidinium
Indacaterol/glycopyrronium
Vilanterol/umeclidinium
Glycopyrrolate/formoterol Olodaterol/tiotropium
Combination: LABA + ICS Formoterol/budesonide 
Formoterol/mometasone 
Salmeterol/fluticasone
Methylxanthines Theophylline
Phosphodiesterase-4 inhibitor Roflumilast
ICS, inhaled corticosteroid; LABAs, long-acting β2-agonists; LAMAs, long-acting muscarinic antagonists; SABAs, short-acting β2-agonists; SAMAs, short-acting muscarinic antagonists

In general, long-acting agents are preferred for initial treatment of COPD except in patients with occasional dyspnea in whom short-acting agents may be used. Short-acting agents can also be used for immediate symptom relief during acute exacerbations in patients taking long-acting bronchodilators as maintenance therapy.

The 2023 GOLD Report updated its recommended treatment strategy to an ABE plan based on the control of the patient’s disorder, exacerbation frequency, scores on the mMRC and CAT assessment tools, and eosinophil count (Figure)4:

  • Group A: bronchodilator is recommended
  • Group B: long-acting muscarinic antagonist (LAMA) plus long-acting β2-agonist (LABA) is recommended and may be available in a single combination canister
  • Group E: LAMA plus LABA is recommended and may be available in a single combination canister. If the patient has a high eosinophil count >300 cells/µL, an ICS should be added to the regimen.
Figure. 2023 GOLD Report tool for assessing COPD exacerbations and initiating pharmacologic treatment. Adapted from: Global Initiative for Chronic Obstructive Lung Disease.4

Other Treatments for COPD Exacerbations

Between 30% and 50% of COPD exacerbations have a bacterial cause (Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, and Chlamydia pneumoniae).10 The majority of patients can be managed with antibiotics and stepped-up bronchodilator and corticosteroid therapies; however, some patients may require hospitalization.

The GOLD Report recommends antibiotics in patients with COPD exacerbations who meet one of the following criteria:

  • Have all 3 cardinal symptoms of exacerbation: dyspnea, increased sputum volume, and increased sputum purulence.
  • Have increased sputum purulence plus one other cardinal symptom (dyspnea or increased sputum volume)
  • Require mechanical ventilation (invasive or noninvasive)

The selection of the antibiotic agent should be based on local bacterial flora and the recommended duration for outpatient treatment of COPD exacerbations is 5 days or less.4 The recommended initial empirical treatment is an aminopenicillin with clavulanic acid, macrolide, tetracycline, or quinolone. Azithromycin or other macrolides should be avoided in patients with a prolonged corrected QT interval on electrocardiography and cardiac arrhythmias. Care should be taken to monitor patients for the development of bacterial resistance in sputum and for impaired hearing.

The role of antitussive agents in the treatment of COPD is inconclusive and the Gold Report does not recommend vasodilators for pulmonary hypertension in this population.4 Low doses of oral or parenteral long-acting opiates may ease dyspnea in patients with severe COPD, according to the report.4

In patients with FEV1 less than 50% and chronic bronchitis, clinicians may consider adding the selective phosphodiesterase-4 inhibitor roflumilast or a macrolide to the treatment regimen.4

Pulmonary rehabilitation is recommended after a COPD exacerbation and should be considered an important component of integrated patient management in combination with pharmacologic therapies.11 Findings from a Cochrane review of 65 randomized controlled trials involving 3822 patients show that pulmonary rehabilitation can relieve dyspnea and fatigue, improve emotional function, and enhance the sense of control that patients have over their condition.11

Supplemental Oxygen Therapy

All patients with COPD should be evaluated for hypoxemia at rest. In patients with oxygen saturation that is lower than 88% or partial pressure of arterial oxygen (PaO2) less than 55 mm Hg while the patient is breathing ambient air at sea level on 2 occasions over a 3-week period, supplemental oxygen is indicated. 4

In patients whose oxygen saturation is less than 90%, arterial blood gases should be measured while the patients are breathing room air. In those with hypoxemia without hypercapnia, low-flow oxygen is indicated to achieve a PaO2 value of 60 to 65 mm Hg (oxygen saturation, 91 to 94%).12 Oxygen supplementation should be titrated to maintain the patient at an SaO2 of 90% or more.12

Patients should also be considered for oxygen therapy if they have persistent hypercapnia with a pH of less than 7.35 but more than 7.15.14,15  

Indications for Hospitalization

Patients that have worsening resting dyspnea, decreased oxygen saturation, high respiratory rate, drowsiness, or confusion may need hospitalization. The primary care provider should look for signs of low oxygenation such as cyanosis and the effort of the patient to breathe. Assess if accessory muscles are being used and if wheezing has increased. If the patient has comorbidities, worsening peripheral edema can indicate heart failure. If an exacerbation is not responding to treatment or if there is inadequate home support, the patient commonly needs hospitalization.4

Lifestyle Changes and Vaccinations

Basic lifestyle modifications include smoking cessation, reducing exposure to pollutants and infection, regular physical activity, healthy diet, and preventive vaccinations. Treatment to assist the patient cease smoking includes varenicline, sustained-release bupropion, nortriptyline, nicotine gum, nicotine inhaler, nicotine nasal spray, and nicotine patches, and are recommended in the absence of contraindications.16 

Given that COPD exacerbations are often triggered by viral infection, COVID-19, influenza, and pneumococcal (PCV13 and PPSV23) vaccinations are recommended to decrease the risk of infection.4 The Centers for Disease Control and Prevention (CDC) recommends 1 dose of the 20 valent pneumococcal conjugate vaccine (PCV20) or 1 dose of 15 valent pneumococcal conjugate vaccine (PCV15) followed by 23 valent pneumococcal polysaccharide vaccine (PPSV23) in persons with COPD.17 The CDC also recommends Tdap vaccination for adults not vaccinated in adolescence as well as shingles vaccination for those 50 years and older.18

Conclusion

Primary care clinicians are often the primary health care provider for patients with COPD. All clinicians should consult the GOLD 2023 Report for up-to-date recommendations on the diagnosis and management of COPD patients.

Theresa Capriotti, DO, MSN, CRNP, RN, is a clinical professor at Villanova University M. Louise Fitzpatrick College of Nursing in Villanova, Pennsylvania. Rose Tomy and Mia Morales are BSN Honor Students at Villanova University M. Louise Fitzpatrick College of Nursing.

References

  1. National Center for Chronic Disease Prevention and Health Promotion, Division of Population Health. Basics about COPD. Centers for Disease Control and Prevention: June 9, 2021. Accessed April 28, 2023. www.cdc.gov/copd/basics-about.html
  2. Xu J, Murphy SL, Kockanek KD, Arias E. Mortality in the United States, 2018. NCHS Data Brief. 2020;(355):1-8.
  3. Aryal S, Diaz-Guzman E, Mannino DM. Influence of sex on chronic obstructive pulmonary disease risk and treatment outcomes. Int J Chron Obstruct Pulmon Dis. 2014;9:1145-1154. doi:10.2147/COPD.S54476
  4. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease, 2023 Report. Global Initiative for Chronic Obstructive Lung Disease.
  5. Safiri S, Carson-Chahhoud K, Noori M, et al. Burden of chronic obstructive pulmonary disease and its attributable risk factors in 204 countries and territories, 1990-2019: results from the Global Burden of Disease Study 2019. BMJ. 2022;378:e069679. doi:10.1136/bmj-2021-069679
  6. Hnizdo E, Sullivan PA, Bang KM, Wagner G. Association between chronic obstructive pulmonary disease and employment by industry and occupation in the US population: a study of data from the Third National Health and Nutrition Examination Survey. Am J Epidemiol. 2002;156(8):738-46. doi:10.1093/aje/kwf105
  7. Strange C. Alpha-1 antitrypsin deficiency associated COPD. Clin Chest Med. 2020;41(3):339-345. doi:10.1016/j.ccm.2020.05.003
  8. Kessler R, Partridge MR, Miravitlles M, et al. Symptom variability in patients with severe COPD: a pan-European cross-sectional study. Eur Respir J. 2011;37(2):264-72. doi:10.1183/09031936.00051110
  9. Donaldson GC, Wedzicha JA. The causes and consequences of seasonal variation in COPD exacerbations. Int J Chron Obstruct Pulmon Dis. 2014 6;9:1101-10. doi:10.2147/COPD.S54475
  10. Sheikh K, Coxson HO, Parraga G. This is what COPD looks like. Respirology. 2016;21(2):224-36. doi:10.1111/resp.12611
  11. Celli BR, Wedzicha JA. Update on clinical aspects of chronic obstructive pulmonary disease. N Engl J Med. 2019;381(13):1257-1266. doi:10.1056/NEJMra1900500
  12. Lacasse Y, Casaburi R, Sliwinski P, Chaouat A, Fletcher E, Haidl P, Maltais F. Home oxygen for moderate hypoxaemia in chronic obstructive pulmonary disease: a systematic review and meta-analysis. Lancet Respir Med. 2022;10(11):1029-1037. doi:10.1016/S2213-2600(22)00179-5
  13. McCarthy B, Casey D, Devane D, Murphy K, Murphy E, Lacasse Y. Pulmonary rehabilitation for chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2015;2015(2):CD003793. doi:10.1002/14651858.CD003793.pub3
  14. Wedzicha JA, Calverley PMA, Albert RK, et al. Prevention of COPD exacerbations: a European Respiratory Society/American Thoracic Society guideline. Eur Respir J. 2017;50(3):1602265. doi:10.1183/13993003.02265-2016
  15. Rochwerg B, Brochard L, Elliott MW, et al. Official ERS/ATS clinical practice guidelines: noninvasive ventilation for acute respiratory failure. Eur Respir J. 2017;50(2):1602426. doi:10.1183/13993003.02426-2016
  16. Cahill K, Stevens S, Perera R, Lancaster T. Pharmacological interventions for smoking cessation: an overview and network meta-analysis. Cochrane Database Syst Rev. 2013;2013(5):CD009329. doi:10.1002/14651858.CD009329.pub2
  17. Centers for Disease Control and Prevention. Pneumococcal vaccine recommendations. Updated February 13, 2023. Accessed May 2, 2023. www.cdc.gov/vaccines/vpd/pneumo/hcp/recommendations.html
  18. Havers FP, Moro PL, Hunter P, Hariri S, Bernstein H. Use of tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccines: updated recommendations of the Advisory Committee on Immunization Practices — United States, 2019. MMWR Morb Mortal Wkly Rep. 2020;69:77-83. doi:dx.doi.org/10.15585/mmwr.mm6903a5external icon

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Top Key Players:

AstraZeneca, Boehringer, GSK, Merck, Roche, Novartis, Abbott, Actavis, Afferent Pharmaceuticals, Alere, Almirall, Amgen, AptarGroup, Astellas, Aurobindo, Axis-Shield, Baxter, Bayer, Biogen, Biotest, Bristol-Myers Squibb, Chiesi Farmaceutici, Cipla, Cytos, Dainippon Sumitomo, Dr. Reddy’s Laboratories.

Breathing Disorders & Treatment Market by Type

Asthma, COPD, Allergic rhinitis, Pulmonary hypertension, Cystic fibrosis

Breathing Disorders & Treatment Market by Application:

Hospital, Clinics

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» North America (U.S., Canada, Mexico)

» Europe (Germany, U.K., France, Italy, Russia, Spain, Rest of Europe)

» Asia-Pacific (China, India, Japan, Singapore, Australia, New Zealand, Rest of APAC)

» South America (Brazil, Argentina, Rest of SA)

» Middle East & Africa (Turkey, Saudi Arabia, Iran, UAE, Africa, Rest of MEA)

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Explore the comprehensive report that offers an exclusive and in-depth analysis of the niche sector. With detailed tables, figures, and charts, you can access vital statistics, trends, and competitive landscape information that is crucial for making informed decisions

The “South America Pulse Oximeters Market” has recently been analyzed in a market research report, which segments it based on Regions, Country, Company, and other Segments. Key Players are currently dominating the global market and have implemented various strategies to increase their market share and strengthen their position in the industry. This report can serve as a valuable resource for stakeholders and other participants in the global South America Pulse Oximeters market to gain a competitive advantage for their business needs.

Customer-centric

1. Does this report consider the impact of COVID-19 and the Russia-Ukraine war on the South America Pulse Oximeters market?

Certainly. The report has taken into account the impact of both COVID-19 and the Russia-Ukraine war on the South America Pulse Oximeters market. These events have had a significant effect on global supply chains and the pricing of raw materials, and we have addressed their influence in detail throughout the report, particularly in dedicated chapters on the South America Pulse Oximeters industry.

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A pulse oximeter is a piece of equipment that uses light emissions at a specific wavelength to measure blood oxygen saturation levels. These devices are especially needed during and after sedation-related surgical procedures, as well as for health conditions like COPD (Chronic Obstructive Pulmonary Disease), anemia, lung cancer, asthma, and pneumonia, among others. which have an impact on breathing.

Insights into the Market During the Forecast Period (from 2023 to 28), the South America Pulse Oximeters Market is anticipated to expand at a CAGR of approximately 6%. The rising incidence of cardiovascular diseases like rheumatic heart disease, congenital heart disease, coronary heart disease, and cerebrovascular disease across the region, primarily as a result of sedentary lifestyles and poor eating habits, would drive most of the market expansion.

Due to the rising number of deaths caused by cardiovascular diseases, pulse oximeters, which are utilized actively in these medical conditions for the continuous monitoring of blood oxygen levels, are in high demand.

The market in South America benefited from the introduction of Covid-19. There was a significant demand for such products to measure hypoxic conditions in patients as the number of Covid cases skyrocketed. Brazil had the most Covid-19 cases in the entire region, which led to the highest sales.

The market is also being bolstered by the rising number of elderly people and respiratory conditions like asthma and pulmonary hypertension, both of which are on the rise. The ever-increasing number of patient care centers across South America to monitor patients’ health conditions is accelerating the industry as a result of the rising health concerns associated with the aging population.

The emergence of wearable pulse oximeters to track real-time blood oxygen concentration, particularly during strenuous physical activities, is encouraging industry expansion. Key Trend in the Market Accelerating Adoption of Wearable Pulse Oximeters As a result of the frequent depletion of blood oxygen levels caused by vigorous physical activity, constant monitoring is required.

As a result, athletes and young people are in high demand for these products as people become more health conscious. Numerous businesses, including Xiaomi, Huawei, are introducing novel medical devices in countries like Brazil, Argentina, etc., in order to meet the rising demands of consumers and encourage market expansion.

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Type-Based Market Segmentation:

Compact
Fingertip
Handheld
Wearable
Tabletop

Of both, compact sort procured a huge portion of the South America Heartbeat Oximeters Market during 2018-22, inferable from their moderateness and simple convenientce. Patients with asthma are the primary customers for these oximeters because they frequently experience hypoxic conditions that necessitate ongoing monitoring. The prevalence of asthma in Brazil is estimated to be around 20 million people in 2022, according to the Brazilian Society of Pneumology and Tisiology. This, in turn, has sped up the use of asthma products due to their ease of use.

Tabletop type, on the other hand, dominates the market. It is due to their increasing demand in intensive care units (ICUs), where measuring blood oxygen levels is the most important step in surgery or treatment, particularly for patients who are anesthetized and unconscious. As a result, the increasing demand for tabletop oximeters in hospitals is being exacerbated by the region’s rising number of plastic surgeries and myocardial bypass surgeries.

Considering End Users:

Hospitals Homecare Ambulatory Surgical Centers From 2018 to 22 due to the rising incidence of respiratory disorders in Brazil and Argentina and various government initiatives to increase the number of hospitals in the region to address these rising cases, hospitals held a significant share of this market.

Additionally, due to their small size, ease of use, and wireless nature, these devices are expected to see significant adoption in homecare settings in the coming years. In addition, the demand for such oximeters in the homecare market would significantly rise in tandem with the rising number of patients in the region who suffer from lung or heart conditions and frequently experience shortness of breath.

In addition, the governments of Brazil and Argentina are actively focusing on expanding the number of ambulatory surgical centers throughout the country because these facilities are useful for a variety of surgical procedures like cataract operations, knee arthroscopy, varicose vein surgery, and other similar procedures.

Ambulatory surgical centers make it easier to perform outpatient surgeries with fewer resources, at lower costs, with shorter wait times, and to the satisfaction of patients. Given the increasing number of patients who require immediate medical attention, they prove to be quite effective. As a result, the number of ambulatory surgical centers with the highest adoption rates is expected to skyrocket throughout the region over the coming years.

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Local Scene

Topographically, the South America Heartbeat Oximeters Market grows across:

Brazil
Argentina
Chile

Of all nations, Brazil is expected to overwhelm the market in South America. It is due to the rising number of cases of chronic respiratory conditions across the nation. Over the course of the past few years, Brazil has witnessed a significant number of viral diseases, which in turn has led to severe respiratory infections. For instance, according to Instituto Butantan, the Darwin variant of the influenza virus (H3N2) caused a viral outbreak in Brazil at the end of 2021. As a result, there has been an increase in demand for these medical condition monitoring devices.

In contrast, Argentina is expected to hold a significant share of the market in the coming years due to the rising number of pneumonia cases in the country. Heart diseases and chronic respiratory conditions are the leading causes of death in Argentina, according to the Ministry of Health. As a result, the country has seen an increase in the use of medical devices like pulse oximeters and an ever-increasing need to deal with the rising incidence of these diseases.

Trends in the Market:

The need for such medical devices has been steadily rising in South America over the past few years, primarily as a result of the rising prevalence of respiratory diseases in children. Key Driver Rising Prevalence of Respiratory Diseases in Children The most recognizable respiratory illness distinguished among kids is the RSV (Respiratory Syncytial Infection) in Sao Paulo, Brazil, which prompts respiratory pressure and affects the requirement for beat oximeters in clinics to follow the patients’ circumstances.

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The adults who have come into contact with respiratory syncytial viruses only experience mild illness, whereas the majority of children in this situation require medical attention. As a result, as the disease affects more children and more of them need to be admitted to a hospital, it becomes increasingly important to keep an eye on their oxygen levels all the time, which accelerates market growth in the region.

In addition, the demand for pulse oximeters has been rising as a result of the rising incidence of acute respiratory infections (ARI) in children, which are brought on by a variety of lifestyle factors. These infections serve as early indicators of a child’s need for medical attention.

Possible Limitation:

Increased Access to Pulse Oximeters Not Approved by the FDA Concerns about the dependability of homecare devices are limiting their use in South America. Consumers are concerned about the accuracy and safety of OTC pulse oximeters because most are not FDA-approved and can be purchased without a doctor’s prescription. Since ailments connected with respiratory and cardio messes are serious, patients require confirmation in regards to the items they use. As a result, customers’ doubts about the effectiveness of OTC pulse oximeters will impede market expansion in South America over the coming years.

Learning experience:

Increasing Demand for Smart Pulse Oximeters The Pulse Oximeter Market in South America has benefited from the development of cutting-edge, smart pulse oximeters that can be connected to smartphones and enable remote monitoring of blood oxygen levels. Biosensors in smart variants measure heart rate and blood oxygen concentration and store the results in connected mobile apps. These oximeters can be used remotely to continuously monitor blood oxygen levels, especially during physical activities, and most of them fall into the wearable category. As a result, the market is expected to grow between 2023 and 2028 due to the increasing availability of these devices that incorporate cutting-edge technologies.

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Table of Content:

  • Report Overview
  • Global Growth Trends
  • Competition Landscape by Key Players
  • Data Segments
  • North America Market Analysis
  • Europe Market Analysis
  • Asia-Pacific Market Analysis
  • Latin America Market Analysis
  • Middle East & Africa Market Analysis
  • Key Players Profiles Market Analysis
  • Analysts Viewpoints/Conclusions
  • Appendix

Key Questions Answered in The Report:

  • What are the strengths and weaknesses of the key vendors?
  • Who are the Leading key gamers and what are their Key Business plans in the close to future?
  • What will be the market increase price and measurement in the coming year?
  • What are the principal key elements riding the market?
  • What are the key market tendencies impacting the increase of the world Market?
  • Which are Trending elements influencing the market shares of the pinnacle areas throughout the globe?
  • What is the have an effect on of The Russia-Ukraine Crisis on the modern industry?
  • Who are the key gamers and what are their strategies in the international Market?
  • What are the market opportunities and threats confronted by using the carriers in the world Market?
  • What industrial trends, drivers, and challenges are manipulating its growth?
  • What are the key consequences of the 5 forces evaluation of the world industry?

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Introduction

Chronic obstructive pulmonary disease (COPD) is a destructive disease characterised by chronic airflow limitation that cannot be completely reversed and is usually progressive. It is a main cause of morbidity and mortality worldwide and its prevalence is increasing.1–3 Patients with COPD need invasive mechanical ventilation when they progress to respiratory failure.4,5 In routine clinical practice, sedatives, analgesics and muscle relaxants are used to facilitate direct laryngoscopy intubation. However, this technique may lead to severe haemodynamic instability and lung injury caused by subsequent mechanical ventilation.6–8 Compared with oral approach, awake nasotracheal intubation was usually easier with a higher success rate.9–11 Hawkyard et al12 showed that awake fibreoptic nasal intubation reduced the pressor response to endotracheal intubation in normotensive adults. Moreover, Putensen et al13 reported that the results suggested that spontaneous breathing during ventilator support did not have to be suppressed even in patients with severe pulmonary dysfunction. Xia et al14 showed that preserving spontaneous breathing could not only improve ventilatory function but also attenuate selected markers of ventilator-induced lung injury in mechanically ventilated healthy lung. Nasotracheal intubation guided by a fibreoptic bronchoscope (FB) is the most commonly used method with more advantages.11,15 However, most patients with COPD are older and often have cardio-cerebrovascular and/or other basic diseases. Even with gentle operation and perfect surface anaesthesia, intubation still causes a strong response, in addition to a high incidence of myocardial ischaemia, cardio-cerebrovascular accidents and other complications. Furthermore, intubation can even endanger the patient’s life.16–19

Traditionally, surface anaesthesia, sedatives and analgesics are used to establish intubation conditions, but a lower dose can cause a strong stress response and an excessive dose can result in respiratory depression or other risks of intubation. Therefore, how to improve patient safety is a clinical problem that needs to be solved urgently.20–22 Previous studies have shown that sufficient airway anaesthesia is essential to suppress gag, swallow and cough reflexes prior to awake endotracheal intubation, and with the development of ultrasound visualisation technology, ultrasound-guided internal branch of the superior laryngeal nerve block (UGISLNB) has many benefits for awake nasotracheal intubation guided by an FB.15,23–27 However, the clinical application of UGISLNB in patients with COPD who develop severe respiratory failure and require fibreoptic nasotracheal intubation has not been studied. Hence, the purpose of this randomised controlled clinical trial is to assess the time for intubation, adverse events, comfort score and stress response to UGISLNB in patients with severe COPD undergoing awake fibreoptic nasotracheal intubation; to verify its safety and efficacy; and to provide a clinical reference.

Patients and Methods

Study Design

This study was a randomised, double-blind, controlled, single-centre clinical trial. The study was approved by the Ethics Committee of The Second Hospital of Shandong University (No. KYLL-2020LW-057). The trial was registered at the Chinese Clinical Trial Registry (ChiCTR2000040185) prior to patient enrolment. The study was conducted in accordance with the Declaration of Helsinki, and written informed consent was obtained from all participants (and, if necessary, their guardians). A CONSORT checklist was used for patient enrolment and allocation (Figure 1).

Figure 1 Flow diagram of the study.

Participants

Participants were eligible for awake fibreoptic nasotracheal intubation if patients with COPD whose condition could not be relieved through a non-invasive ventilator (NIPPV) or who could not tolerate NIPPV and required invasive mechanical ventilation, according to Guidelines for COPD, from 1 December 2020 to 31 July 2021. The inclusion criteria were as follows: aged 35–85 years; American Society of Anaesthesiologists (ASA) score III–IV; and a signed informed consent form. The exclusion criteria were as follows: patients who refused to give consent; uncooperative patients; severe hypertension or heart disease (eg BP≥160 mmHg and/or ≥110 mmHg and HR≥100 bpm, New York Heart Association [NYHA] Class ≥ II, ischaemic heart disease, atrial fibrillation); severe hepatorenal insufficiency (HILD grade <10 and creatinine ≥500μmol/L); nasopharyngeal diseases or lower respiratory tract hypersensitivity diseases; laryngeal oedema, acute/chronic pharyngitis or acute airway inflammation (eg acute tracheobronchitis); asthma attack; abnormal coagulation; contraindications for nasotracheal intubation; contraindications for regional block (eg bleeding diathesis, local infection and local anaesthetic toxicity); recent use of sedatives, analgesics, β-blockers or β-agonists (within 2 weeks); allergy or contraindication to the drugs used in this study; anatomic abnormalities in the head, neck, face, nose, mouth or airway; pregnant or lactating women; body mass index (BMI) >30 kg/m2; fasting time <6h; difficult airway evaluated before operation; change in the intubation method; serious complications or other accidents; any reason not to cooperate with research and/or any factor influenced the results or the researchers thought that should be excluded (eg the patient’s respiratory or circulatory system deteriorated and they required immediate emergency treatment).

Interventions

The patients were randomly divided into two groups in a blinded fashion (a sealed opaque envelope) by the administrator who did not take part in the treatment: the UGISLNB group (group S, n=30) and the control group (group C, n=30).

All patients were administered intravenous (iv) raceanisodamine 0.3 mg for inhibition of gland secretion, iv fentanyl 0.5 μg/kg for analgesia, iv dexamethasone 0.2 mg/kg for oedema prophylaxis and iv ondansetron 8 mg to prevent vomiting before the operation. They also received education (eg on the awake fibreoptic intubation procedure) to relieve their anxiety. Electrocardiogram (ECG), mean arterial pressure (MAP), HR, saturation of peripheral oxygen (SPO2) and end-tidal carbon dioxide (ETCO2) monitoring were applied throughout the procedure. Furthermore, patients received high-flow oxygen inhalation via a nasal cannula (if necessary, moving to the non-intubated nostril). Both groups received dexmedetomidine (DEX) at a loading dose of 0.5–1 μg/kg over 15 min followed by a continuous infusion of 0.25 μg/kg/h. The surface of the FB and the endotracheal tube were coated with liquid paraffin oil. The more unobstructed side nasal cavity was chosen, and then 1% ephedrine was applied to contract the nasal mucosa and 3 mL of 2% lidocaine mucilage was smeared over the nasal cavity and the posterior nostril to reduce damage. Then, the hard palate, soft palate, tongue, root of the tongue, posterior pharyngeal wall, epiglottis and glottic cleft mucosa were sprayed with a total of 5 mL of 1% tetracaine. Besides, the cricothyroid membrane was injected with 3 mL of 2% lidocaine to anaesthetise the tracheal surface. Finally, UGISLNB was performed. The patients were placed in supine position, with the neck extended, and a high-frequency (11 MHz) linear ultrasound probe (Vivid S70N, GE Healthcare) was used. Using an aseptic technique, the transducer was placed over submandibular area with parasagittal orientation. The greater horn of hyoid bone and thyroid cartilage were identified as hyperechoic structures on ultrasonography. The thyrohyoid muscle and the thyrohyoid membrane were between the two structures. The superior laryngeal nerve (SLN) area was defined as bounded by the hyoid bone cephalad, the thyroid cartilage caudally, the thyrohyoid muscle anteriorly and the thyrohyoid membrane and the pre-epiglottic space posteriorly.28 Using an out-of-plane approach, 2 mL of 2% lidocaine in group S or normal saline in group C was injected using a 24G needle between the horn of the hyoid bone and the thyroid cartilage just above the thyrohyoid membrane, followed by local compression and observation for 5 min. Attention was paid to needle withdrawal after drug injection. The procedure was then performed on the opposite side (Figure 2).

Figure 2 The view of ultrasound-guided superior laryngeal nerve block. Hyoid bone, 1; thyroid cartilage, 2; thyrohyoid muscle, 3; thyrohyoid membrane, 4; superior laryngeal nerve, 5; the arrow denotes the puncture path of the needle.

Approximately 5 min after blockade, the tracheal tube (the size 6.5–7.0 mm diameter in men, 7.0–6.5 mm diameter in women by sex and nostril size) was gently advanced into the pharyngeal cavity through the prepared nasal cavity. The FB was inserted through the endotracheal tube gradually until the glottis could be seen. When the glottis was open, the FB was placed close to the tracheal carina, and then the tracheal tube was slowly inserted into the appropriate position. Finally, the FB was pulled out. The success of the tracheal intubation was confirmed by the ETCO2 waveform. If MAP was more than or less than 30% of baseline values, thenurapidil 12.5 mg or norepinephrine 50 μg, respectively, was injected intravenously. If tachycardia (HR>100bpm) or bradycardia (HR<60bpm) occurred, then esmolol 20 mg or atropine 0.5 mg, respectively, was injected intravenously and repeated, if needed. Patients were instructed to take a deep breath, and while holding their breath, there should be respiratory depression or a sharp fall in SPO2 in a short time. If the results were not satisfactory, they were switched to high-flow oxygen through the face mask immediately. The procedure was stopped if the patient had a severe cough or strong body movements. If necessary, sedatives, analgesics and muscle relaxants were added to complete this operation; in these cases, the patient was withdrawn from the study. If the patient’s anatomical structure was abnormal or unclear, the block could not be performed, which was considered as UGISLNB failure and discontinued intervention. If there were any signs of local anaesthetic systemic toxicity (eg oral numbness, dizziness or light-headedness, drowsiness or disorientation, visual or auditory disturbances, muscle twitching, seizures, loss of consciousness, hypertension, tachycardia, bradycardia, cardiac arrhythmias, asystole) were observed, the patient was withdrawn from the study. All treatment decisions were made by an experienced anaesthesiologist and pulmonary physician. Both consultant anaesthetists were present during all procedures. One was responsible for performing local anaesthesia and the awake nasal fibreoptic intubation, and the other administered the study drugs. A doctor collected anaesthetic data and perioperative records, and neither researchers nor patients knew of group assignments during the study.

Data Collection

The primary outcomes were the time for intubation (from the beginning of FB insertion through the nostril to successful endotracheal tube placement), adverse reactions, including nausea and vomiting (the nausea and vomiting occurred during and after intubation), cough, body movement (serious body reaction affecting the procedure), hypertension (BP>160/110mmHg), hypotension (BP<90/60mmHg), tachycardia (100>bpm) and bradycardia (HR<60 bpm) and the comfort score (1 = excellent, indicating a calm patient; 2 = good, indicating a comfortable patient; 3 = moderate, there is a need to pacify the patient; 4 = poor, indicating an uncomfortable patient; 5 = agitated patient).29 The secondary outcomes were hemodynamic changes (MAP and HR) and serum norepinephrine (NE) and adrenaline (AD) concentrations immediately before intubation (T0), immediately after intubation to laryngopharynx (T1); and immediately (T2), 5 min (T3) and 10 min (T4) after intubation. Peripheral venous blood samples (8 mL) were collected in EDTA anticoagulation test tube. They were centrifuged at 3000 rpm for 10 min at 4°C (centrifugal radius of 10 cm). The plasma was collected and stored at-80°C until analysis. The plasma AD and NE concentrations were determined by high-performance liquid chromatography (HPLC) (Agilent 1260 HPLC system, Agilent Technologies) with the electrochemical method.

Sample Size Calculation

The sample size was estimated using PASS 11.0 (NCSS-PASS 11, USA). According to the results of a preparatory experiment, the time for intubation, representing a major endpoint after intubation, was 83.7±13.5 in group S and 101.1±16.2 in group C, and the comfort score, representing another major endpoint after intubation, was 3.3±0.9 in group S and 4.1±0.5 in group C. The sample size was estimated separately based on the time for intubation and comfort score using a two-sample t-test with a significance level of 5% and β power of 0.10. The size of each group was estimated to be 16 cases based on the time for intubation and 18 cases based on the comfort score. We chose the maximum sample size (18), considering a 20% dropout rate, and then the sample size was N1=N2=18÷0.8=23 cases, 49 patients (25 cases in group S and 24 cases in group C) would be sufficient in this trial.

Statistical Analysis

The continuous variables were assessed for normality using the normal quantile–quantile plot, which showed that they obeyed a normal distribution. The AD and NE concentrations, HR and MAP were analysed by analysis of variance (ANOVA) for intra-group comparisons and one-way ANOVA for inter-group comparisons. The time for intubation and the comfort score were compared using independent sample t-tests. The incidence of postoperative adverse events was compared by Fisher’s exact test. Patient characteristics were analysed by independent sample t-test or Fisher’s exact test. P<0.05 was considered statistically significant. Data are expressed as mean ± standard deviation (SD) or the number (proportion) as appropriate. All the analyses were carried out with SPSS 23.0 version (IBM Corp., Armonk, NY, USA).

Results

A total of 79 patients were enrolled in the study. Twenty-three patients were excluded because they met the exclusion criteria (n=18) or did not provide consent (n=5). One patient developed heart failure and three patients had severe cough and thus had to be changed to method of intubation in group C. In addition, in group S one case was positive for fentanyl before the block and two cases had an unclear anatomical structure and the block could not be completed. These patients were excluded. UGSLNB and intubation of the other patients were completed on the first attempt. Finally, 56 patients were included in the study.

The patient characteristics at baseline were well balanced between the groups (Table 1). Compared with group C, the time for intubation, the incidence of adverse reactions and the comfort score in group S were significantly lower (P<0.01) (Figure 3 and Table 2). Compared with T0, MAP, HR, NE and AD were significantly higher at each time point (T1–T4) in group C (P<0.05), but they were not significantly higher in group S (P>0.05). MAP, HR, NE and AD in group S at each time point (T1–T4) were significantly lower than those in group C (P<0.05). There was no significant difference in MAP, HR, NE and AD between the groups at T0 (baseline) (P>0.05) (Figures 4 and 5).

Table 1 Patient and Procedure Characteristics in the Two Groups

Table 2 Time for Intubation, Comfort Score and Incidence of Adverse Reactions in the Two Groups

Figure 3 Comparison of the time for intubation (A), the incidence of adverse reactions (B) and the comfort score (C). (A and C) The data are expressed as the mean ± standard deviation compared with group C. The data were compared with an independent sample t-test; *P<0.01. (B) The data are expressed as the percentage, compared with group C. Data were compared with Fisher’s exact test; *P<0.01. Group S received ultrasound-guided superior laryngeal nerve block; group C was the control group.

Figure 4 Comparison of the mean arterial pressure (MAP) (A) and heart rate (HR) (B) between the groups immediately before intubation (T0); immediately after intubation to the laryngopharynx (T1); and immediately (T2), 5 min (T3) and 10 min (T4) after intubation (25 patients in group S and 24 patients in group (C). The data are expressed as mean ± standard deviation. #Based on analysis of variance (ANOVA), compared with T0, MAP and HR in group C was significantly higher at T1, T2, T3 and T4 (P<0.05). *Based on one-way ANOVA, MAP and HR in group S was significantly lower than in group C at T1, T2, T3 and T4 (P<0.05), whereas they were not significantly higher in group S(P>0.05). Based on one-way ANOVA, there was no significant difference in MAP and HR between groups at T0 (baseline) (P>0.05). Group S received ultrasound-guided superior laryngeal nerve block; group C was the control group.

Figure 5 Comparison of the norepinephrine (NE) (A) and Adrenaline (AD) (B) concentrations between the groups immediately before intubation (T0); immediately after intubation to the laryngopharynx (T1); and immediately (T2), 5 min (T3) and 10 min (T4) after intubation (25 patients in group S and 24 patients in group (C). The data are expressed as mean ± standard deviation. #Based on analysis of variance(ANOVA) compared with T0, NE and AD in group C was significantly higher at T1, T2, T3 and T4 (P<0.05), but not significantly higher in group S (P>0.05). *Based on one-way ANOVA, NE and AD in group S was significantly lower than in group C at T1, T2, T3 and T4 (P<0.05). Based on one-way ANOVA, there was no significant difference in NE and AD between groups at T0 (baseline) (P>0.05). Group S received ultrasound-guided superior laryngeal nerve block; group C was the control group.

Discussion

In this study, we have shown that the successful application of UGISLNB could effectively shorten the time for intubation, reduce incidence of adverse reactions, improve the comfort score, maintain considerable haemodynamic stability and inhibit the stress response of patients with severe COPD undergoing awake fibreoptic nasotracheal intubation.

It is well known that the keys to successful intubation are to provide adequate anaesthesia to ensure patient comfort as well as adequate sedation, to control secretions and to minimise adverse reactions. Only when the above factors are met can the time for intubation be controlled and kept to a minimum. In the present study, compared with group C, the time for intubation; the incidence of adverse reactions and the comfort score were lower in group S (P<0.01). There are several possible reasons: the block effect was so exact that the stress response was reduced, or the haemodynamic fluctuation was small and the adverse reaction was greatly decreased, resulting in active cooperation from the patients. As a result, there was an increase in the comfort score and a marked reduction in the intubation time. Besides, relaxation of laryngeal muscles and reducing vocal cord movement are also the key to awake intubation; these changes allow the catheter to pass through the airway more smoothly, and thus the time for intubation is shorter. The findings are similar to those reported by Gupta et al.25 In that study, comfort was better in the nerve block group compared with the nebulisation group, which was deduced from the patient assessment of procedure recall. Uday et al26 also showed that the quality of airway anaesthesia was better in UGISLNB group, including a shorter intubation duration and better patient tolerance. Studies have shown that combination of SLN block with topical airway anaesthesia produces better patient comfort.30 Zhou et al31 reported that UGISLNB can reduce the coughing score and decrease the incidence of hypoxemia, without increasing adverse events. Moreover, hypotension and bradycardia have also been associated with excessive manipulation of the larynx causing vasovagal reaction.32 These phenomena did not occur in our trial, possibly due to good effects of UGISLNB.

Endotracheal intubation is related to elevated BP, HR and catecholamines due to intense sympathetic discharge caused by stimulation of the upper respiratory tract. Although the transient stress response has little effect on young patients, haemodynamic changes may be fatal to more vulnerable patients. Therefore, it is important in older adult patients to avoid a significant stress response during tracheal intubation.18,33,34 In general, when the patient is awake, the glottic reflex is active, meaning that the intubation success rate is lower. The endotracheal tube stimulates the throat, glottis and tracheal mucosa, which may cause a strong stress response. Then, sympathetic-adrenal medulla system is activated, resulting in high BP and increased HR.35,36

Previous studies have shown that endotracheal intubation can induce a stress response and excite the sympathetic nervous system. In addition, the catecholamine concentration in the body increases sharply within a few seconds, and consequently the change in the plasma catecholamine concentration is the main indicator of stress response.37 Nasotracheal intubation involves the maxillary branch of the trigeminal nerve, the glossopharyngeal nerve, the tonsil nerve, the SLN and the recurrent laryngeal nerve. The SLN is divided into the inner branch and the external branch. The external branch contains motor fibres, which travel downward with the superior thyroid artery and innervate the cricothyroid muscle. The inner branch is the sensory portion of the nerve;it passes through the thyrohyoid membrane to the laryngeal cavity, and distributes to the pharynx, epiglottis, tongue base and the laryngeal mucosa above glottis rimae.38 Therefore, SLN block should theoretically provide effective inhibition of the stress response caused by stimulation of the laryngeal mucosa, maintain haemodynamic stability and make the throat muscles relax. Moreover, UGISLNB has other advantages, including decreasing perioperative cough, sore-throat and hoarseness of voice.39

In group C, MAP, HR, AD and NE were significantly higher at each time point (T1–T4) compared with T0 (P<0.05), whereas they were not obviously higher in group S (P>0.05). In group S, MAP, HR, AD and NE at T1–T4 were significantly lower than in group C (P<0.05). Although it has been suggested that awake fibreoptic nasotracheal intubation could cause a stress response, UGSLNB can effectively inhibit the stress response from perioperative intubation and maintain hemodynamic stability. This mechanism may be related to blocking the internal branch of the SLN. It could block the sensation of mucosa above the tongue base, epiglottis and glottis fissure, which partly inhibits the laryngopharyngeal reflex and relaxes the vocal cords. Opening the glottis reduces its stimulation by the FB, and to some extent helps reduce the airway and cardiovascular responses. Patients could be more cooperative with the operation because they would have less discomfort, and thus poor breathing and carbon dioxide accumulation could be reduced and vital signs could be stabilised. Some studies have reported that combination of SLN block with topical airway anaesthesia produced better haemodynamic stability.30 Uday et al26 found that high quality of airway anaesthesia might provide better haemodynamic stability in UGSLNB group. In a randomized controlled trial, Li et al27 demonstrated that UGSLNB blunted the haemodynamic response to a greater extent than the use of traditional local anaesthetics. Although there have been few clinical trials, our results are basically similar to previous studies. Ma et al40 reported that the hemodynamic parameters and respiration remained stable in awake fibreoptic orotracheal intubation under SLN block. In a prospective randomized clinical study, Ambi et al26 showed that HR and MAP were significantly more stable in the ultrasound group. Sawka et al41 reported that five patients who underwent UGSLNB tolerated subsequent awake fibreoptic intubation with either minimal or no sedation, which indicated no evidence of incomplete anaesthesia in the distribution of SLN. Although the experimental methods were different, these results are basically consistent with our study.

Although NIPPV is preferred over invasive ventilation as the initial mode of ventilation to treat respiratory failure in patients with acute COPD exacerbation, invasive mechanical ventilation should be the first choice when NIPPV fails or when other conditions (eg any haemodynamic instability, inability to improve dyspnoea, need to protect the airways or manage copious tracheal secretions, intolerance of mask ventilation, etc.) occur. However, our findings have put forward a new idea for effective treatment of such critically ill patients when they need endotracheal intubation.

To sum up, we presumed the possible mechanism of UGISLNB was as follows: UGISLNB successfully blocked the sensation of the mucosa above the tongue base, epiglottis and glottis fissure, the stress response was suppressed, and the laryngopharyngeal reflex was partially inhibited, as well as the vocal cords opened. As a result, the intubation could be implemented smoothly, and the intubation time was significantly shortened, which also inhibited stress response and maintained hemodynamic stability. Additionally, the incidences of adverse reactions were markedly decreased and the comfort score was significantly increased.

Limitations

This study has certain limitations. First, the sample size is small, and the findings should be confirmed with a larger sample size. Second, we used a single concentration and a single dose of local anaesthetic; additional investigations are required concerning the optimal concentration and dose of local anaesthetics. Third, some patients with difficult airways were excluded, but these patients are encountered in clinical practice. Difficult airway grades lead to different intubation times, which have a certain impact on the haemodynamic stability and comfort of patients. Furthermore, some patients with delirium or consciousness disturbance and serious respiratory distress were excluded from this study because of difficulties in performing stable ultrasound examinations. Fourth, other factors (eg blood, secretion, emesis, etc.) may obscure the fibreoptic view, which was not considered. Fifth, some demographic data and clinical data, such as the severity of COPD, lung function and underlying diseases, could not be considered, which might have influenced the results. Sixth, the deficiency of this study was that MAP, HR, NE and AD were not be recorded or monitored at UGSLNB, and the safety of UGSLNB at UGSLNB will be studied in the future. Finally, the effect of this method on the prognosis of the patients was not observed. In the future, we will continue to accumulate cases in the clinic and continue to assess its safety and applicability.

Conclusions

UGISLNB can effectively shorten the intubation time, reduce the incidence of adverse reactions, improve the comfort score, maintain haemodynamic stability and inhibit the stress response in patients with severe COPD undergoing awake fibreoptic nasotracheal intubation. Hence, this approach is worth popularising and applying in clinical practice.

Abbreviations

COPD, chronic obstructive pulmonary disease; ASA, American Society of Anaesthesiologists; UGSLNB, ultrasound-guided superior laryngeal nerve block; UGISLNB, ultrasound-guided the internal branch of the superior laryngeal nerve block; SLN, superior laryngeal nerve; FB, fibreoptic bronchoscope; ECG, electrocardiogram; MAP, mean arterial pressure; BP, blood pressure; HR, heart rate; SPO2, saturation of peripheral oxygen; DEX, dexmedetomidine; RR, respiration rate; ETCO2, end-tidal carbon dioxide; AD, adrenaline; NE, norepinephrine; PONV, postoperative nausea and vomiting; PaO2, partial pressure of arterial oxygen; FiO2, fraction of inspiration O2; PaCO2, partial pressure of arterial carbon dioxide; NIPPV, non-invasive positive pressure ventilation; SD, Standard deviation; ANOVA, analysis of variance.

Data Sharing Statement

The data used to support the findings of this study are available from the corresponding author upon request in 10 months.

Ethical Statement

The authors declare that all patients gave written informed consent before initiation of the study protocol and were conducted in accordance with the Declaration of Helsinki. The study was approved by the Ethics Committee of The Second Hospital of Shandong University (No. KYLL-2020LW-057).

Acknowledgments

We would like to thank the participants who enrolled in this study, and the study team for essential contributions. Additionally, we thank Professor Liyuan Liu for her help in statistics.

Author Contributions

All authors made substantial contributions to conception and design, acquisition of data or analysis and interpretation of data; took part in drafting the article or revising it critically for important intellectual content; agreed to submit to the current journal; gave final approval of the version to be published; and agree to be accountable for all aspects of the work.

Funding

Clinical research fund of Shandong Medical Association (No:YXH2022ZX02028).

Disclosure

The authors report no conflicts of interest in this work.

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The annual prevalence and incidence rates of idiopathic pulmonary fibrosis (IPF) increased drastically in Korea from 2011 to 2019, with higher rates occurring in men compared with women, researchers reported in BMC Pulmonary Medicine.

The retrospective cohort study investigated changes in the prevalence and incidence of IPF over time in Korea, as well as comorbidities and treatments commonly associated with IPF, using nationwide health claims data between 2011 and 2019 from the database of the Korean Health Insurance Review and Assessment (HIRA). Eligible participants made at least 1 claim per year for IPF.

The patients were compared by age (<70 vs ≥70 years), sex, Charlson comorbidity index (CCI; 0-3 vs ≥4), and pirfenidone use (>3 months [pirfenidone user group] and <3 months or not treated with pirfenidone [pirfenidone nonuser group]).

The annual prevalence rate for IPF increased from 7.50 to 23.20 per 100,000 persons, and the annual incidence rate increased from 3.56 to 7.91 per 100,000 person-years from 2011 to 2019 in the Korean population. The IPF prevalence and incidence rates were more than twice as high in men as in women since 2011. For example, in 2019, the incidence rate per 100,000 person-years in men was 11.81 vs 4.02 in women.

Many patients with IPF had respiratory and nonrespiratory comorbidities, although the prevalence was dependent on sex, age, and use of pirfenidone.

Comorbidity prevalence was assessed in 21,111 patients with IPF according to age and sex. In all subgroups, chronic obstructive pulmonary disease (COPD) was the most common respiratory comorbidity (37.34%), followed by lung cancer (3.34%). The most common nonrespiratory comorbidities were gastro-esophageal reflux disease (GERD, 70.83%), dyslipidemia (62.93%), and hypertension (59.04%).

COPD and lung cancer occurred more frequently in men vs women (COPD: 40.58% vs 29.32%; lung cancer; 4.11% vs 1.45%) and pulmonary hypertension was more prevalent in women vs men (2.43% vs 1.11%). The rates of diabetes mellitus and ischemic heart disease were increased in men, and those of GERD, anxiety, depression, and congestive heart failure were more common in women. COPD occurred in a higher proportion of patients aged 70 years and older than in those aged less than 70 years (39.39% vs 34.20%).

All nonrespiratory comorbidities except GERD occurred more frequently in patients aged 70 years and older compared with those aged less than 70 years. CCI was greater in men compared with women and higher in patients aged 70 years and older vs those aged less than 70 years.

A greater percentage of men and patients aged 70 years and older were found among the patients using pirfenidone vs among patients not using the drug. The proportion of patients with lung cancer was also greater among patients who received pirfenidone, and the proportion of pulmonary embolism and pulmonary hypertension was higher among untreated patients.

Patients with high CCI used more medical resources associated with admission within 90 days, and the low burden group used more resources associated with outpatient clinics. At 90 and 365 days, the total medical costs were higher in patients with high CCI vs low CCI.

Among several limitations, IPF was defined according to the 10th revision of the International Statistical Classification of Diseases and Related Health Problems code at the time of diagnosis, and a limited number of baseline characteristics were assessed. In addition, the only antifibrotic agent included in the study was pirfenidone.

“Many patients with IPF had respiratory and nonrespiratory comorbidities, although the prevalence was dependent on sex, age, and use of pirfenidone,” stated the researchers. “The prevalence of these comorbidities was higher 3 years after than at the time of IPF diagnosis and affected the use of pirfenidone and medical resources.”

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Grants support bioelectronic vagus nerve stimulation, five-year observational study of nighttime blood pressure

MANHASSET, N.Y.--(BUSINESS WIRE)--
The National Institutes of Health (NIH) has awarded Northwell Health’s Cohen Children’s Medical Center and The Feinstein Institutes for Medical Research, the homes of pediatric research at Northwell, two grants totaling $4.73 million to study nephrotic syndrome – a kidney disorder that causes the body to pass too much protein into the urine – specifically in children. Investigators will kickstart two different research studies, with the funding over the course of five years.

This press release features multimedia. View the full release here: www.businesswire.com/news/home/20230405005701/en/

Christine Sethna, MD, was awarded two different grants to study how vagus nerve stimulation could help children with kidney disease. (Credit: Feinstein Institutes)

Christine Sethna, MD, was awarded two different grants to study how vagus nerve stimulation could help children with kidney disease. (Credit: Feinstein Institutes)

Nephrotic syndrome is usually caused by damage to the clusters of small blood vessels in the kidneys that filter waste and excess water from the blood. This condition often causes swelling, particularly in the feet and ankles, and increases the risk of other health problems, including kidney failure.

Led by Christine B. Sethna, MD, division director of pediatric nephrology at Cohen Children's Medical Center and associate professor at the Donald and Barbara Zucker School of Medicine at Hofstra/Northwell and the Feinstein Institute, the $1.03 million grant was awarded last year and will be used to fund a new clinical trial for children with nephrotic syndrome using vagus nerve stimulation. Children with nephrotic syndrome are exposed to prolonged courses of steroids and other immunosuppressant medications which could have adverse effects. This research plans to study the mechanism of action by stimulating the vagus nerve – which can be activated non-invasively on the ear – to have immunomodulatory effects mediated by the inflammatory reflex and spleen.

The vagus nerve is often referred to as the body’s superhighway – it connects the brain with all major organs and controls functions like heart rate, breathing and gastrointestinal function. When the nerve is stimulated, it can reduce inflammation, which is a trigger for many diseases and helps reset the body’s immune system.

“This funding will allow us to study, and ultimately help, children living with nephrotic syndrome and better understand how the condition can best be treated without negative side effects that steroids and medications could potentially leave,” said Dr. Sethna, principal investigator on the studies. “These advancements can further the evidence that drugs are not always necessary to alleviate a problem, especially in young children.”

The second grant of $3.7 million was awarded last month and will be used to initiate the kNIGHT study, which will focus on nocturnal hypertension in children with nephrotic syndrome. The observational study will examine the nighttime blood pressure and cardiovascular outcomes in children with nephrotic syndrome at 22 different centers. This data will inform future research and trials around this common trait of high nighttime blood pressure.

“Dr. Sethna is conducting valuable research to better understand nephrotic syndrome in children,” said Charles Schleien, MD, MBA, the Philip Lanzkowsky MD Chair and Professor of Pediatrics and Anesthesiology and senior vice president of pediatric services at Northwell Health. “With the support of these two grants, one day children may have new treatment options to help manage their disease and improve their overall quality of life.”

The Feinstein Institutes is the global scientific home of bioelectronic medicine, which combines molecular medicine, neuroscience and biomedical engineering. At the Feinstein Institutes, medical researchers use modern technology to develop new device-based therapies to treat disease and injury.

“Children with nephrotic syndrome suffer from the symptoms of the illness and from the side effects of steroids used in treatment,” said Kevin J. Tracey, MD, president and CEO of the Feinstein Institutes, and Karches Family Distinguished Chair in Medical Research. “Dr. Sethna’s research into vagus nerve stimulation to reverse the inflammation is an important step towards finding alternate therapies.”

Built on years of research in molecular mechanisms of disease and the link between the nervous and immune systems, Feinstein Institutes researchers discover neural targets that can be activated or inhibited with neuromodulation devices, like vagus nerve implants, to control the body’s immune response and inflammation. If inflammation is successfully controlled, diseases – such as arthritis, pulmonary hypertension, Crohn's disease, inflammatory bowel diseases, diabetes, cancer and autoimmune diseases – can be treated more effectively.

Beyond inflammation, using novel brain-computer interfaces, our researchers developed techniques to bypass injuries of the nervous system so that people living with paralysis can regain sensation and use their limbs. By producing bioelectronic medicine knowledge, disease and injury could one day be treated with our own nerves without costly and potentially harmful pharmaceuticals.

About Northwell Health

Northwell Health is New York State’s largest health care provider and private employer, with 21 hospitals, about 900 outpatient facilities and more than 12,000 affiliated physicians. We care for over two million people annually in the New York metro area and beyond, thanks to philanthropic support from our communities. Our 83,000 employees – 18,900 nurses and 4,900 employed doctors, including members of Northwell Health Physician Partners – are working to change health care for the better. We’re making breakthroughs in medicine at the Feinstein Institutes for Medical Research. We're training the next generation of medical professionals at the visionary Donald and Barbara Zucker School of Medicine at Hofstra/Northwell and the Hofstra Northwell School of Nursing and Physician Assistant Studies. For information on our more than 100 medical specialties, visit northwell.edu/ and follow us @NorthwellHealth on Facebook, Twitter, Instagram and LinkedIn.

About the Feinstein Institutes

The Feinstein Institutes for Medical Research is the research arm of Northwell Health, the largest health care provider and private employer in New York State. Home to 50 research labs, 2,500 clinical research studies and 5,000 researchers and staff, the Feinstein Institutes raises the standard of medical innovation through its five institutes of behavioral science, bioelectronic medicine, cancer, health innovations and outcomes, and molecular medicine. We make breakthroughs in genetics, oncology, brain research, mental health, autoimmunity, and are the global scientific leader in bioelectronic medicine – a new field of science that has the potential to revolutionize medicine. For more information about how we produce knowledge to cure disease, visit feinstein.northwell.edu.

Julianne Mosher Allen

516-880-4824

[email protected]

Source: Northwell Health



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DelveInsight Business Research LLP

DelveInsight Business Research LLP

The breath analyzers market is expanding due to several factors, including the strict implementation of road safety laws around the world and the increasing adoption of breath analyzers in a variety of medical applications. Furthermore, rising alcohol and other drug consumption around the world, as well as a surge in the breath analyzers market for efficient and accurate detection devices, will drive the demand for breath analyzers.

New York, USA, March 30, 2023 (GLOBE NEWSWIRE) -- The Global Breath Analyzers Market to Upsurge at a Significant CAGR of ~12% by 2027 | DelveInsight

The breath analyzers market is expanding due to several factors, including the strict implementation of road safety laws around the world and the increasing adoption of breath analyzers in a variety of medical applications. Furthermore, rising alcohol and other drug consumption around the world, as well as a surge in the breath analyzers market for efficient and accurate detection devices, will drive the demand for breath analyzers.

DelveInsight’s Breath Analyzers Market Insights report provides the current and forecast market analysis, individual leading breath analyzers companies’ market shares, challenges, breath analyzers market drivers, barriers, and trends, and key breath analyzers companies in the market.

Key Takeaways from the Breath Analyzers Market Report

  • As per DelveInsight estimates, North America is anticipated to dominate the global breath analyzers market during the forecast period.

  • Notable breath analyzers companies such as Drägerwerk AG & Co. KGaA, Lifeloc Technologies, Inc., Quest products Inc., Intoximeters, Alcohol Countermeasure Systems Corp., AK GlobalTech Corp., Bedfont® Scientific Ltd., Tanita., Lion Laboratories, Shenzhen Ztsense Hi-Tech Co., Ltd, PAS Systems International, Inc., Alcolizer Pty Ltd., Honeywell International Inc., BACtrack., Advanced Safety Devices, AlcoPro., Smart Start LLC, Andatech., C4 Development Ltd., Intelligent Fingerprinting Limited, and several others are currently operating in the breath analyzers market.

  • In January 2023, Opteev Technologies announced that its ViraWarn breath analyzer, which detects respiratory viruses, will make its debut at CES 2023.

  • In November 2022, Opteev Technologies, Inc. announced the development of ViraWarn, a low-cost breath analyzer that detects COVID-19, Influenza, and RSV in less than 60 seconds. The multiple-use, rechargeable device has been submitted to the FDA for approval as a new simple, and convenient way to self-test for COVID-19 and other respiratory illnesses.

  • In August 2022, Imspex Diagnostics secured the CE Mark for BreathSpec, an instrument that detects COVID-19 using breath testing and analysis.

  • In April 2022, the Food and Drug Administration issued an emergency use authorization Thursday for InspectIR Systems’ “Covid-19 breathalyzer,” the first government-approved device capable of detecting coronavirus infections in patients’ breath.

To read more about the latest highlights related to the breath analyzers market, get a snapshot of the key highlights entailed in the Global Breath Analyzers Market Report

Breath Analyzers Overview

The breath analyzer is a portable medical device that detects the presence of alcohol or drugs in the blood via the exhaled breath. The analyzer works by passing exhaled breath through a sulfuric acid and potassium dichromate solution. The solution changes color proportionately to the amount of alcohol in the air sample, depicting the blood alcohol content. It can also provide quick and accurate results, which are used to diagnose tuberculosis, asthma, and other respiratory diseases.

Breath Analyzers Market Insights

North America dominated the global breath analyzers market in 2021 and will continue to do so through the forecast period of 2022–2027. Factors such as rising alcohol and other drug consumption in the region and stricter enforcement of road safety laws in response to an increase in the number of road accidents and drug abuse deaths, for breath analyzers will drive demand for breath analyzers in the North American breath analyzers market. In addition, an increase in product launches are also expected to boost the growth of the breath analyzers market in the North American region. For instance, in November 2022, Opteev Technologies, Inc. announced the development of ViraWarn, a low-cost breath analyzer that detects COVID-19, Influenza, and RSV in less than 60 seconds. The multiple-use, rechargeable device has been submitted to the FDA for approval as a new simple, and convenient way to self-test for COVID-19 and other respiratory illnesses.

To know more about why North America is leading the market growth in the breath analyzers market, get a snapshot of the Breath Analyzers Market Outlook

Breath Analyzers Market Dynamics

The increasing consumption of alcohol, and other drugs worldwide is a major driver for breath analyzers market growth. Furthermore, the rising prevalence of many respiratory disorders, such as asthma, COPD, COVID-19, and others, will drive up demand for breath analyzers, as these devices are also used to diagnose the aforementioned disorders. However, device accuracy concerns and the device’s susceptibility to external factors, such as temperature and others, can stymie the global breath analyzers market growth.

Additionally, the COVID-19 pandemic moderately impacted the breath analyzers market growth during the first few months due to lockdown impositions, border closures, and other factors causing disruption in the asthma spacers market’s manufacturing, supply, import, export, and other related activities. However, the breath analyzers market began to recover in the latter half of the pandemic due to the resumption of activities across industries, including the healthcare sector. Additionally, the breath analyzers market saw an increase in product demand as the number of cases of COVID-19 infection increased. The breath analyzers were used as a diagnostic tool for the COVID-19 infection, which increased their demand. Thus, the aforementioned factors increased demand for breath analyzers during the pandemic and are expected to do so again in the forecast period of 2022–2027.

Get a sneak peek at the breath analyzers market dynamics @ Breath Analyzers Market Dynamics Analysis

Report Metrics

Details

Coverage

Global

Study Period

2019–2027

Base Year

2021

Breath Analyzers Market CAGR

~12%

Projected Breath Analyzers Market Size by 2027

USD 1.25 Billion

Key Breath Analyzers Companies

Drägerwerk AG & Co. KGaA, Lifeloc Technologies, Inc., Quest products Inc., Intoximeters, Alcohol Countermeasure Systems Corp., AK GlobalTech Corp., Bedfont® Scientific Ltd., Tanita., Lion Laboratories, Shenzhen Ztsense Hi-Tech Co., Ltd, PAS Systems International, Inc., Alcolizer Pty Ltd., Honeywell International Inc., BACtrack., Advanced Safety Devices, AlcoPro., Smart Start LLC, Andatech., C4 Development Ltd., Intelligent Fingerprinting Limited, among others

Breath Analyzers Market Assessment

  • Breath Analyzers Market Segmentation

    • Market Segmentation By  Type: Device And Consumables (Mouth Piece, Cables and Adapters, and Others)

    • Market Segmentation By  Technology: Fuel Cell Technology, Semiconductor Sensor, Infrared (IR) Spectroscopy, and Others

    • Market Segmentation By Application: Alcohol Detection, Drug Abuse Detection, and Others

    • Market Segmentation By End User: Law Enforcement Agencies, Hospitals, and Medical Applications

    • Market Segmentation By Geography: North America, Europe, Asia-Pacific, and Rest of World

  • Porter’s Five Forces Analysis, Product Profiles, Case Studies, KOL’s Views, Analyst’s View

Which MedTech key players in the breath analyzers market are set to emerge as the trendsetter explore @ Breath Analyzers Companies 

Table of Contents 

1

Report Introduction

2

Executive summary

3

Regulatory and Patent Analysis

4

Key Factors Analysis

5

Porter’s Five Forces Analysis

6

COVID-19 Impact Analysis on Breath Analyzers Market

7

Breath Analyzers Market Layout

8

Global Company Share Analysis – Key 3-5 Companies

9

Breath Analyzers Market Company and Product Profiles

10

Project Approach

11

About DelveInsight

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A study finds that exercise therapy is safe and can help improve recovery and quality of life for people with heart failure. Niedring/Drentwett/Getty Images
  • Researchers investigated whether supervised exercise therapy could benefit those with heart failure.
  • They found that supervised exercise therapy improves exercise capacity and quality of life among patients.
  • They noted future research is needed to ensure long-term adherence to exercise programs.

Heart failure occurs when the heart can no longer pump blood and oxygen around the body. The condition represents around 8.5% of heart disease deaths in the United States.

Heart failure with preserved ejection fraction (HFpEF) causes around half of heart failure cases in the U.S. It happens when the heart’s left ventricle stiffens, increasing pressure inside the heart.

Studies show that exercise improves physical and cardiac function in patients with HFpEF and may lead to better outcomes than medication.

Understanding more about how exercise could benefit those with heart failure could help physicians improve treatment plans for the condition.

Recently, researchers reviewed recent studies investigating the impact of supervised exercise therapy on those with chronic, stable HFpEF.

They found that supervised exercise therapy improves exercise capacity and quality of life among patients with heart HFpEF.

“Currently in the United States, 1 in 2 Americans has diabetes or prediabetes and 3 in 4 are overweight or obese,” said Dr. Melody H. Hermel, a cardiologist at United Medical Doctors in La Jolla, CA, not involved in the study, in an interview with Medical News Today.

“To truly combat the comorbid conditions patients face, we need to combine traditional medication and procedures with nutrition, exercise, stress management, and preventative care to best address patients’ underlying risk factors and truly get at the heart of the matter,” Dr. Hermel added.

Dr. Vandana Sachdev, a senior research clinician and the director of the Echocardiography Laboratory in the Division of Intramural Research at the National Heart, Lung, and Blood Institute (NHLBI), first author of the study, said in a press release:

“Future work is needed to improve referral of appropriate patients to supervised exercise programs, and better strategies to improve long-term adherence to exercise training is needed. Hybrid programs combining supervised and home-based training may also be beneficial. Further, implementation efforts will need to include coverage by Medicare and other insurers.”

The study was published in Circulation.

For the study, the researchers analyzed results from 11 randomized controlled trials investigating supervised exercise therapy on HFpEF outcomes.

The studies included over 700 participants, mostly aged between 60 and 70 years old. Participants engaged in various activities, including walking, Greek dancing, and high intensity training three times per week for 1-8 months.

Supervised exercise training also improved quality of life scores on the 21-point Minnesota Living with Heart Failure questionnaire by 4-9 points.

“Exercising helps improve the heart’s pumping ability, decreases blood vessel stiffness and improves the function and energy capacity of skeletal muscle,” said Dr. Sachdev.

“Exercise capacity is an independent, clinically meaningful patient outcome, and research has indicated that guided exercise therapy is actually more effective at improving quality of life for people who have HFpEF than most medications,” she added.

“Supervised exercise allows people to have their blood pressure, heart rate, breathing capacity observed when they are recovering from an illness or a procedure and there is uncertainty about their basic skills in exercise, ability to perform exercise or their ability to increase the intensity of exercise or to perform some types of exercise correctly,” Dr. Charlie Porter, Cardio-oncologist at The University of Kansas Health System, not involved in the study, told MNT.

“The benefits of exercise cannot be duplicated by medication or procedures. Regular exercise of 2.5 hours weekly or that equivalent increases life expectancy, reduces the incidence of heart disease complications, and has been linked to reduced risk for some cancers, such as colon. Improved sense of well-being or quality of life is consistently demonstrated in studies of sustained safe exercise,” he added.

“Increasing evidence indicates that resistance exercise is helpful in some neurologic disorders. Early signals suggest that resistance exercise may improve decline in cognitive function over time. There is no other intervention that can provide this array of established and probable benefits. There are no other interventions that can offer this array of established or probable benefits,” he noted.

“There are so many benefits to supervised exercise for many people, but there may be particular benefits for people who also have diabetes, are overweight or depressed,” Dr. Martha Abshire Saylor, Ph.D., assistant professor at the Johns Hopkins School of Nursing, not involved in the study, told MNT.

“Starting a supervised exercise program may have social support benefits, including encouragement and accountability for participation, but also will help with physiologic benefits like reducing inflammation and lipid levels,” Dr. Saylor added.

Dr. Saylor cautioned, however, that supervision is key as vigorous physical activity can trigger acute cardiovascular events in those who are unfit, inactive, or with coronary artery disease.

Dr. Hermel added:

“Supervised exercise programs such as cardiac rehab have demonstrated significant benefit for patients with recent heart attack or another acute coronary syndrome, chronic stable angina, congestive heart failure, pulmonary hypertension, after stent placement, coronary artery bypass surgery, heart valve surgery or cardiac transplant.”

MNT also spoke to Dr. Yu-Ming Ni, a cardiologist of Non-Invasive Cardiology at MemorialCare Heart and Vascular Institute at Orange Coast Medical Center in Fountain Valley, CA, who was not involved in the study. Dr. Ni noted that the “biggest obstacle to successful use of supervised exercise programs is adherence to exercise sessions.”

“Unlike in clinical trials, patients in real life are less likely to come to exercise sessions, and are not always committed to staying for the entire hour of exercise. Thus, patients who stand to gain the most from supervised exercise programs are those who are motivated to attend,” he said.

When asked about limitations to the findings, Dr. Mirza Baig, a cardiologist with Memorial Hermann in Houston, Texas, not involved in the study, noted that the different studies included in the analyses had different selection criteria and endpoints.

Dr. Robert Segal, board certified cardiologist and founder of Manhattan Cardiology, Medical Offices of Manhattan, and co-founder of LabFinder, not involved in the study, also told MNT:

“Women, low socioeconomic status, minority racial and ethnic groups were small percentages of the demographic that were studied. Most of the studies don’t specify which type of heart failure (HFpEF vs Heart Failure With Reduced Ejection Fraction [HFrEF]) they are analyzing. The studies are short-term studies, a year or less. There were also issues with adherence to the exercise programs.”

Dr. Adedapo Iluyomade, a preventive cardiologist at Baptist Health Miami Cardiac & Vascular Institute, also not involved in the study, told MNT:

“There are several evidence gaps that need to be addressed, including the optimal exercise modalities, strategies to increase long-term adherence, and the use of exercise therapy for patients recently hospitalized with acute, decompensated heart failure.”

“Further research is needed to determine the potential effects of exercise-based therapies on hospitalization, death, cardiovascular events, and healthcare expenditures, as well as in the prevention of HFpEF in patients with multiple risk factors,” Dr. Illuyomade noted.

“This statement makes it clear that it is time for Medicare and Health plans to support the provision of supervised exercise programs to patients with HFpEF. The body of knowledge cited in this report indicates that further delays in expanding access to this important component of care is unwarranted,” noted Dr. Porter.

Dr. Ni added:

“Physicians should recommend supervised exercise programs to patients with heart failure with preserved fractions who are willing to attend regularly. If not qualified by insurance, physicians should recommend home exercise for patients with heart failure, as there are certainly enough benefits from exercise to justify routinely recommending it.

Patients with heart failure should take advantage of exercise programs covered by insurance to improve exercise capacity and quality of life.”

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Rheumatoid Arthritis is more than just a joint disease. Effective treatments are available and therefore, early diagnosis is important to limit or prevent permanent damage.

Rheumatoid Arthritis Affects Lungs: Check Symptoms, Treatment And Prevention
Rheumatoid Arthritis Affects Lungs: Check Symptoms, Treatment And Prevention

Rheumatoid arthritis (RA) is a common inflammatory disease of the joints. It affects multiple joints, mainly small joints of the hands and wrists but also larger ones. It causes painful joints with stiffness that is typically more in the morning and progresses with time causing joint deformities and, ultimately, a crippling state. Effective treatments are available and therefore, early diagnosis and regular treatment with monitoring of disease activity are important to limit or prevent permanent damage.

Can Rheumatoid Arthritis cause lung disease?

RA is more than just a joint disease. The inflammatory process also affects several other parts of the body. The most frequently affected are the lungs, besides skin, eyes, digestive system, heart, and blood vessels. The lung conditions that occur in patients with RA are of several types. More than 25 per cent of patients with RA will eventually develop lung conditions and diseases in their lifetime. If all patients with RA are screened for lung disease, even when there are no lung symptoms, more than half are found to have evidence of lung involvement.

Lung disease is next only to cardiac disease and cancer as the cause of death in patients with RA. Lung disease due to RA is a major contributor to a poorer quality of life besides mortality. Most often, lung disease follows joint involvement but rarely, RA may start as a lung disease and joint manifestations may follow later.

What are the different lung diseases caused by Rheumatoid Arthritis?

The most common lung disease caused by rheumatoid arthritis is a shrinkage of the lungs, called Interstitial Lung Disease (ILD). Other lung conditions and diseases that can occur in RA include pulmonary nodules (one or more rounded masses of tissue, of various sizes, confusing the possibility of lung cancer), pleural effusion (protein-rich fluid in the sac around the lungs), pleural thickening, bronchiectasis (dilatation of lung airways causing pooling of secretions and lung infections), bronchiolitis (narrowing of airways deep in the lung), pulmonary hypertension (high blood pressure in lung arteries) and increased tendency for lung infections like pneumonia. The drugs that are used to treat RA in general suppress immunity increasing the risk of lung infections.

What is an Interstitial Lung Disease?

ILDs are a group of conditions with diverse causations having in common a reduction in lung size due to fibrosis that usually worsens with time. RA is one of the more common causes of an ILD. There are several types of ILD patterns and treatment, prognosis and natural history differ according to the ILD pattern.

A patient with ILD develops breathlessness on exertion, initially on running or walking fast, especially up an incline. It progresses with time and, ultimately, even activities of daily living such as dressing, taking a bath, or even taking food cause breathlessness. The oxygen levels in the blood decrease, in the early stages of exertion, and later, even at rest. These patients require home oxygen to keep their oxygen in the normal range. Dry cough is the other major symptom. Patients with ILD sometimes get sudden flare-ups, called acute exacerbations, that acutely worsen respiratory failure and carry a high risk of mortality.

Males, smokers, those with a long history of joint disease, more active joint disease, and older age are more prone to develop ILD but many patients of RA with none of these risk factors can also develop ILD.

How is an ILD diagnosed and treated?

ILD is diagnosed by features on chest examination, breathing tests called spirometry and diffusion capacity, and imaging including a plain chest radiograph and a high-resolution computed tomogram (HRCT) of the chest that provides the clue to the pattern of ILD. In a case where the diagnosis of RA is already established by clinical features and characteristic blood tests, a lung biopsy is not required. Some of these tests are required from time to time after treatment is started to evaluate for a response as well as the progress of the disease.

Treatment of ILD due to RA has variable effectiveness and may produce relief in symptoms.

This is in addition to drugs that are being given for other symptoms of RA including joint disease. While effective treatments are now available for RA according to the severity and extent of the disease, treatment of lung diseases like ILD is more difficult. The drugs that work for the joints do not seem to work for the lungs in general. Drugs like corticosteroids that suppress immunologically mediated immune damage have a variable response. For those who have increased lung fibrosis, a newer class of drugs called antifibrotics may help in slowing down the increasing shrinkage. The fibrosis is not reversible.

What are the treatments for other lung diseases due to Rheumatoid Arthritis?

Management of a large pleural effusion would require drainage with a chest tube or a video-assisted thoracoscopy which is a minimal-access surgery. Treatment of lung infections requires appropriate antibiotics. Narrowing of lung airways requires inhaled medicines.

Apart from drugs, breathing exercises, and nutritional supplementation as required are given as part of what is called pulmonary rehabilitation. This reduces breathlessness and improves exercise tolerance. Patients who are unable to maintain normal blood oxygen, which can easily be measured by pulse oximeter and blood gas analysis, require oxygen therapy round the clock. This can be given using oxygen concentrators. Portable machines are also available.

The last resort for extensively scarred lungs is lung transplantation, a highly specialized and expensive surgery, now increasingly available in different cities in India.

How can patients with Rheumatoid Arthritis detect that they have a lung problem?

Once you are diagnosed to have RA, an assessment for the presence of lung disease is advisable as early lung disease may not produce any symptoms. Subsequently, any occurrence of prolonged cough, expectoration, and, most importantly, breathlessness with reduced exercise tolerance calls for an evaluation of a possible lung complication. Early diagnosis holds the best promise for a good response.

(Inputs IANS)




Published Date: March 22, 2023 3:09 PM IST



Updated Date: March 22, 2023 3:11 PM IST





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The vascular smooth muscle cells that normally give blood vessel walls strength and flexibility proliferate and become destructive in pulmonary hypertension, a typically rapidly progressing condition that makes it hard to get blood inside our lungs and oxygen to our bodies.

Now scientists have found that inhibiting a gene essential to making DNA so the cells can take on this uncharacteristic growth, can significantly reduce the destructive cell proliferation and disease progression, they report in the European Heart Journal.

The findings point toward a treatment target for a condition that can inexplicably affect females ages 30 to 60 and that currently does not have great treatment options."


Yuqing Huo, MD, PhD, Director of the Vascular Inflammation Program in the Vascular Biology Center at the Medical College of Georgia

Pulmonary hypertension is basically high blood pressure in the lungs that can make breathing difficult and damage or destroy the right side of a heart which has to pump against the abnormally high pressures. It's characterized by remodeling of the pulmonary arteries that feed oxygen-depleted blood to the lungs where it can take up oxygen and lose carbon dioxide, a byproduct of oxygen use. But there is much to be learned about why and how the cells manage the unusual growth and where therapy might best intervene.

The Vascular Biology Center team led by Huo reported late in 2022 in the journal Circulation that the vascular smooth muscle cells that encase blood vessels of the heart have the same adverse reaction when fat and cholesterol start getting deposited on their lining. The resulting abnormal proliferation and growth of vascular smooth muscle cells in this scenario worsens heart disease by prompting a thickening of the muscular wall of the blood vessels further narrowing the passageway for blood out to the body, where fat and cholesterol have already taken a stand.

Essential to cell growth, including this unhealthy proliferation, is more DNA, RNA and the proteins they produce. Key to that is purine, one of two chemical compounds in the body used to make the building blocks DNA and RNA. Key to purine production, is the gene ATIC, and in this case, more of it.

The new studies found that, as with the unhealthy proliferation in coronary arteries, when the scientists deleted ATIC from either the vascular smooth muscle cells or body wide, it reduced the development and progression of pulmonary hypertension in their mouse model of the breath-taking condition. It even mitigated a very severe form of the condition.

"If we block this process, the blood vessel wall will stay relatively normal and the blood will still pass through," Hou says.

When the scientists looked in mouse models as well as human pulmonary arteries and lung tissue, they found a similar scenario: Genes essential to production of purine are increased and so is actual purine production, and expression of the ATIC gene.

When they first looked at human genetic data, they had clues that is what they might find: They saw proliferation as well as increased expression of genes that indicated the cells were making purine from scratch, so called de novo purine synthesis, rather than from recycling, which is the body's other option. That's the same high energy purine producing process they found vascular smooth muscle cells on coronary arteries were using.

Huo and his colleagues note that when vascular smooth muscle cells begin to proliferate and become resistant to death, they start resembling cancer cells. What the scientists have now found underlines the similarities between metabolic shifts that occur in both the early development of pulmonary hypertension and cancer, Huo and his colleagues write. In fact, making purine from scratch also is increased in many cancer cells, which may make ATIC a logical treatment target there as well, Huo and his colleagues write. For example, one way the drug methotrexate, used to slow the growth of cancer cells, is thought to work is by inhibiting ATIC. Also, newer ATIC inhibitors for cancer are under study.

Huo also notes that more specific inhibitors are needed to treat pulmonary hypertension and that the same inhibitors likely would also work in the coronary arteries.

The lungs are extremely vascular and pulmonary arteries branch like a tree in the lungs until they eventually become smaller vessels called arterioles and eventually even smaller, single-layer blood vessels called capillaries, which surround the millions of air sacs in the lungs. The capillaries are where carbon dioxide escapes from the blood and where oxygen from the air we breathe moves in. Huo notes capillaries don't have the typical layer of smooth muscle cells only the endothelial cells that normally just line blood vessels.

Right heart failure is a leading cause of death in people with pulmonary hypertension and is even tougher to treat than left heart failure, which can result from more common problems like coronary artery disease, heart attack and high blood pressure, Huo says.

Postdoctoral Fellow Qian Ma, PhD, is first author on the new paper. The research was supported by the American Heart Association and the National Institutes of Health.

Source:

Journal reference:

Ma, Q., et al. (2023) Purine synthesis suppression reduces the development and progression of pulmonary hypertension in rodent models. European Heart Journal. doi.org/10.1093/eurheartj/ehad044.

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