Get Help

Call the Lung Health Information Line

1-888-344-LUNG (5864)

Our certified respiratory
educators are ready to take your questions
(M-F 8:30am-4:30pm)

2014-2015

Research Funded (2014-2015)

Asthma →
Chronic Obstructive Pulmonary Disease (COPD) →
Cystic Fibrosis (CF) →
Idiopathic Pulmonary Fibrosis (IPF) →
Legionnaire’s Disease →
Lung Disease →
Lung Injury →
Lung Transplantation →
Mechanical Ventilation →
Sleep Apnea →
Tuberculosis (TB) →

 


Asthma

Diane Loughheed
Bronchodilating and Bronchoprotective Effects of Deep Inspirations in Asthma, Cough Variant Asthma and Chronic Cough with Normal Airway Sensitivity

Cough variant asthma is a term used when cough is the main or only symptom of asthma. This is generally a ‘mild’ form of asthma, which does not usually lead to life-threatening attacks. However, it often does not respond to typical asthma treatment. As a result, cough variant asthma can be incredibly disabling, disrupting sleep, leading to school and work absenteeism and reducing quality of life. Improved understanding of what causes cough in asthma and cough variant asthma and related conditions is a first step towards finding more effective treatments and reducing the morbidity of cough variant asthma.

The purpose of this research is to find out whether one of the fundamental differences between individuals with asthma and cough variant asthma compared to individuals who do not have either of these conditions but who cough during asthma challenge tests is whether or not a deep breath opens up their airways (bronchodilates) and protects against subsequent airway narrowing.

Back to top

Chronic Obstructive Pulmonary Disease (COPD)

Denis E. O’Donnell
Effects of Inspiratory Muscle Training on Exertional Dyspnea in Patients with COPD

Many patients with more severe COPD suffer sustained and intolerable breathlessness which is very difficult to manage. Among other factors, breathlessness in COPD is linked to overburdened and weakened muscles of breathing. In the past, efforts to increase inspiratory muscle strength by specific training [Inspiratory Muscle Training (IMT)] have not been uniformly successful in relieving breathlessness. IMT is therefore not routinely used. However, recent studies which have tested the effect of a newly improved training technique in carefully selected patients, have provided more promising results: IMT was well tolerated and was linked to improved performance of the breathing muscles, less breathlessness and increased exercise capacity. The underlying mechanisms by which IMT improves these important clinical outcomes are not yet known and this question is the main focus of the current proposal.

The overall objective is to better understand the role of breathing muscle weakness in causing breathlessness in COPD. Specifically, we plan to: 1) measure the effect of IMT on the strength and endurance of the breathing muscles in patients with COPD (with weak breathing muscles) during rest; and 2) measure the effect of change in breathing muscle performance on perceived breathlessness during physical activity.

Douglas Hoover
Individualized Function-Guided Radiotherapy to Improve Quality of Life in Patients with Chronic Obstructive Pulmonary Disease and Advanced Lung Cancer

Lung cancer is the leading cause of death for patients with mild COPD. Many of these patients with lung cancer and COPD require aggressive treatment of their cancers with chemotherapy and radiation therapy. Although some patients can be cured with this treatment, the treatment can damage the lungs, leading to reduced quality of life, permanent shortness of breath, oxygen dependence and sometimes death. We need a better method to treat COPD patients with radiation in order to reduce the risk of lung injury.

Currently, when radiation treatments are designed for lung cancer patients, we attempt to minimize the amount of radiation deposited within the lung tissue. In COPD patients not all parts of the lung are the same; some parts of the lung may have very good airflow while other areas may not (airflow into and out of the lungs is called ventilation). Standard imaging tests such as a chest x-ray or CT cannot distinguish between these areas of good and poor ventilation. Therefore, standard radiation planning does not account for which areas of the lung are functioning well.

We are one of only a few institutions in the world with a special type of MRI scan that can detect, probably better than any other test currently available, where the ventilation is actually occurring. If we can identify areas of good ventilation beforehand, we can reduce the radiation dose delivered to these areas during treatment. This should lead to better breathing after treatment and a better quality of life. The goal of this study is to test a new type of radiation planning that attempts to avoid as much of the functioning lung as possible when designing radiation treatments for COPD patients.

If successful, our novel technique will prevent radiation induced lung injury, improve quality of life and lead to improved survival for these patients with COPD, representing a significant step forward in the treatment of one of the most serious threats to lung health, and health in general, in Canada today.

Nicholas Vozoris
Epidemiology and Adverse Respiratory Outcomes Associated with Narcotic Drug Use among Older Adults with COPD

Chronic obstructive pulmonary disease (COPD), commonly caused by cigarette smoking, more frequently occurs in older adults. Narcotics are a commonly prescribed class of pain medications. Physiologic studies suggest that narcotics can potentially negatively affect the breathing of individuals with COPD, but studies evaluating for narcotic-related negative respiratory outcomes are lacking. We also do not understand to what extent and in what ways narcotics are used in the COPD population.

The purpose of this research is two-fold: 1) to describe the scope and pattern of narcotic use in the older adult COPD population; and, 2) to examine for potential negative respiratory outcomes associated with narcotic use among older adults with COPD.

This study is unique because it makes use of a very large population-based database of about 200,000 older Ontarians with COPD. It also fills a gap in knowledge that presently exists relating to the scope and pattern of narcotic drug use, as well as the potential negative respiratory outcomes associated with use of this medication class, among older adults with COPD.

The results of this research may facilitate more thoughtful and responsible prescription of narcotics by doctors, and as a result, possible negative narcotic-related respiratory outcomes may be lessened among older adults with COPD.

Back to top

Idiopathic Pulmonary Fibrosis (IPF)

Jonathan Draper
Modelling Pulmonary Fibrosis with Human Induced Pluripotent Stem Cells
Breathe New Life Award Recipient

Idiopathic pulmonary fibrosis is a disease that damages the lung in a way that prevents that patient from breathing normally and currently has no cure. This disease usually kills patients within three years of diagnosis. How idiopathic pulmonary fibrosis begins and then destroys normal structure of the lung is not understood, mostly because the early stages of the disease are not easily watched in the lungs of patients, and also because the disease is difficult to mimic when lung cells are grown in a dish in a laboratory.

Our objective is to create a system for studying idiopathic pulmonary fibrosis in a laboratory dish, providing a simple and easily accessible way to watch the start and continuation of the disease. We are using stem cells, which are cells that can be converted or differentiated into any cell type in the body by treating the stem cells step-by-step with different culture media. In addition, adult cells in the body like skin can be converted back to stem cells and then converted to any cell type.

By using stem cells to model IPF in a laboratory dish, we will have created a system that gives us the ability to understand aspects of IPF outside the body that may not be possible to study in the patients themselves. It may help us determine the causes of IPF and how genetic mutations make patients susceptible to fibrosis-causing agents. Since stem cells can be expanded in culture and maintained in an unspecialized state, this provides an infinite population of patient-specific cells for use in disease modelling. In addition, generating lung tissue in a dish from patient skin-derived stem cells provides an alternative to collecting lung biopsies.

A system that captures the characteristics of idiopathic pulmonary fibrosis in a laboratory dish would greatly help in understanding and preventing the start of this deadly disease. Such a system will later allow the finding and testing of new drugs and treatments that will stop the disease from killing patients. Importantly, the system that we have created could also be used to understand other forms of lung disease, including cystic fibrosis, emphysema or bronchitis.

Back to top

Lung Disease

Labiris, N. Renee
Identification of Drug Induced Interstitial Lung Disease using V/Q SPECT Imaging

More than 380 medications are known to be toxic to the lung. This adverse reaction in the lung could lead to permanent lung damage. It can occur during treatment or months after stopping the medication. There is no agreement on how to monitor the development of what is known as drug induced respiratory disease or DIRD, but the importance of early diagnosis is emphasized. Monitoring is typically don using a test of the lung’s ability to transfer gas from inhaled air to blood (DLco). When DLco is decreased, high resolution computed tomography (HRCT) is used to confirm the presence of DIRD. Frequent monitoring with HRCT may cause adverse effects related to radiation exposure and provides no information on the functional impact of the pathology or early pathological changes. Another test with similar sensitivity but less hazardous is needed to detect early disease so suspect medication can be stopped and treatment of the adverse lung reaction initiated.

Ventilation (V) and perfusion (Q) imaging has been used for decades to study the distribution of ventilation and blood flow for the diagnosis of pulmonary embolism. This technique can be applied to diseases such as COPD, asthma, pulmonary fibrosis to detect disease induced impairments in lung function. Although this imaging technique does involve radioactivity, the radiation dose is significantly less than a CT and below the annual background radiation dose for people living in North America.

The objective of the proposed research is to investigate if V/Q imaging can detect changes in lung pathology similar to CT. We will be investigating if V/Q imaging can be used to detect early DIRD before irreversible damage occurs. By combining our novel automated regional 3D quantitative image analysis with V/Q imaging, impairments in lung function at a regional level can be objectively investigated. This will allow physicians and researchers to identify malfunctioning tissue areas at early stages of disease.

We believe that detecting early changes in lung pathology using V/Q imaging, a test readily available in all nuclear medicine departments, will lead to earlier and more precise diagnosis, prognosis and treatment of DIRD. This work will provide experimental evidence that V/Q imaging is as sensitive as CT using a substantially lower level of radiation and lower cost to the health-care system.

Back to top

Lung Injury

Sean E. Gill
Pulmonary Microvascular Endothelial Cell Dysfunction during Sepsis is Mediated by TIMP3

Lung injury often leads to acute respiratory distress syndrome (ARDS), which affects many Canadians every year and can be fatal. This lung injury can result from a widespread (throughout the body) infection called sepsis. One of the serious complications from ARDS is the leak of fluid and protein from the blood vessels into the airspaces within the lung, leading to fluid-filled lungs and difficulty breathing. There is currently no effective treatment for ARDS patients and as a result, death occurs in almost 40 per cent of patients.

Our research focuses on understanding how fluid and protein leak from the blood vessels into the airspaces of the lung. A group of enzymes, called metalloproteinases, and their inhibitors, called tissue inhibitors of metalloproteinases (TIMPs), are known to control this leak in other tissues following injury, but this has yet to be shown in the context of lung injury. We will examine how the metalloproteinases and TIMPs control the function of blood vessel cells within the lung during both health and infection.

Our studies will help us understand how fluid and protein leak from blood vessels into the airspaces of the lungs is controlled following sepsis/ARDS and may provide information regarding possible therapeutic targets. These therapeutic targets would potentially decrease death following ARDS/sepsis, which currently is the main outcome. Importantly, of the patients that do survive ARDS, many have ongoing difficulties such as shortness of breath and reduced quality of life. Therapeutic targets identified by our work would decrease the damage occurring in the lung as a result of ARDS, which would improve lung function leading to enhanced quality of life of patients following injury.

Back to top

Legionnaire’s Disease

Mauricio Terebiznik
Molecular Mediators of the Binding of Legionella Pneumophilia to Lung Epithelial Cells

Legionellosis or Legionnaire’s disease is a lung infection acquired by inhaling water droplets contaminated with the bacterium Legionella pneumophila. Legionellosis can be fatal in the elderly, in patients that are weakened by other conditions, or those who are not treated on time, or properly for the infection. However, the mortality associated with the infection can be drastically reduced with rapid diagnosis and efficient treatment. This emphasizes the need to develop diagnostic tools and to gain scientific knowledge on the mechanisms by which Legionella pneumophila causes diseases.

Our main objective is to investigate how Legionella pneumophila interacts with the cells in the lung to produce Legionnaire’s disease. To avoid being expelled from the body or removed by immune defences, disease causing bacteria must attach to exposed surfaces in the organism. This is a critical primary step in the infection process that leads to the disease. In collaboration with Dr. Cyril Guyard (Ontario Agency for Health Protection and Promotion), we discovered that Legionella pneumophila produces during the disease the protein known as Lcl and that this protein could be responsible for the binding the bacteria to the human lung. We propose to investigate how Lcl attaches to the lungs and its contribution to the disease. This research will allow us to identify new tools to more efficiently diagnose Legionella infections and treating legionellosis.

This major public health concern emphasizes the need to study Legionella’s interactions with the lung to develop new diagnostic tools and treatments in order to prevent and control Legionnaire’s disease, the main objective of this grant.

Mauricio Terebiznik
Molecular Mediators of the Binding of Legionella Pneumophilia to Lung Epithelial Cells

Legionellosis or Legionnaire’s disease is a lung infection acquired by inhaling water droplets contaminated with the bacterium Legionella pneumophila. Legionellosis can be fatal in the elderly, in patients that are weakened by other conditions, or those who are not treated on time, or properly for the infection. However, the mortality associated with the infection can be drastically reduced with rapid diagnosis and efficient treatment. This emphasizes the need to develop diagnostic tools and to gain scientific knowledge on the mechanisms by which Legionella pneumophila causes diseases.

Our main objective is to investigate how Legionella pneumophila interacts with the cells in the lung to produce Legionnaire’s disease. To avoid being expelled from the body or removed by immune defences, disease causing bacteria must attach to exposed surfaces in the organism. This is a critical primary step in the infection process that leads to the disease. In collaboration with Dr. Cyril Guyard (Ontario Agency for Health Protection and Promotion), we discovered that Legionella pneumophila produces during the disease the protein known as Lcl and that this protein could be responsible for the binding the bacteria to the human lung. We propose to investigate how Lcl attaches to the lungs and its contribution to the disease. This research will allow us to identify new tools to more efficiently diagnose Legionella infections and treating legionellosis.

This major public health concern emphasizes the need to study Legionella’s interactions with the lung to develop new diagnostic tools and treatments in order to prevent and control Legionnaire’s disease, the main objective of this grant.

Alexander Ensminger
Defining the Host – Pathogen Interface in TNF-Alpha Depleted Cells

Legionnaires’ disease is a severe, often fatal bacterial pneumonia whose incidence is on the rise. The elderly, smokers, and patients undergoing treatment with a specific type of anti-inflammatory medicine, Tumor Necrosis Factor (TNF) inhibitors, are at significantly greater risk for developing the disease. We hypothesize that these at-risk patient populations may be infected by a different composition of bacterial strains than in the population at large. This would have profound implications to Canadian health, because the diagnostic tests used to detect Legionnaires’ disease are tailored to find the kinds of L. pneumophila that make up the majority of disease in the general population as a whole.

If patients undergoing TNF inhibitory therapy are at greater risk for infections by non-standard strains, they may be particularly ill-served by the rapid diagnostic tests that are critical for early detection and treatment of the disease. In this proposal, we will develop a powerful high-throughput screening approach to determine whether TNF inhibition increases the ability of specific types of L. pneumophila bacteria to cause disease. We will determine whether these therapies may also represent potential risk factors for the development of Legionnaires’ disease.

To date, we have no knowledge about how anti-TNF therapy might differentially impact the ability of specific L. pneumophila strains to cause Legionnaires’ disease. By precisely understanding how specific risk factors influence the types of strains that are able to replicate in human cells, we can develop strategies tailored to specific groups of individuals in order to ensure the rapid diagnosis of infection and the early treatment of disease.

Back to top

Cystic Fibrosis (CF)

Valerie Waters
The Role of the Lung Microbiome in Pseudomonas Eradication in CF

Cystic fibrosis (CF) is the most common fatal genetic disorder in the Caucasian population and the primary cause of death is respiratory failure due to chronic lung infection. Pseudomonas aeruginosa is the most common germ (bacteria) infecting the lungs of CF patients and infection with this germ causes lung damage and earlier death in these individuals. When children with CF are first infected with P. aeruginosa, we try to get rid of it by giving inhaled antibiotics but in 10-40% of times, we fail and we don’t know why.

The objective of our project is to find out what are the specific characteristics of the patient, of the P. aeruginosa germ (bacteria) and of all the other germs in the lung (microbiome), that predict whether a child with CF will fail our attempts to get rid of this germ in their lungs. Our ultimate goal is to discover better ways to treat these young children so that they don’t suffer the damaging effects of P. aeruginosa in their lungs and so that they can live longer.
We will study 80 children with CF that have developed first time P. aeruginosa lung infection

Our project is unique because to our knowledge, we are the only research group that has established a CF Sputum Biobank and therefore has access to a large collection of lung samples from all children with CF collected over a long period of time. This allows us to get an accurate picture of how all these germs are changing and interacting over time in the lungs of these children.

Cory Yamashita
Antimicrobial Peptide Fortified Surfactant for the Treatment of Cystic Fibrosis

Cystic fibrosis (CF) is an inherited condition that leads to recurrent lung infections as a result of a defect in the cells that line the inner surface of the lung. Over the course of time, recurrent infections lead to a progressive decline in lung function that results in premature death or need for lung transplantation. In order to treat bacteria that are associated with these recurrent infections, antibiotics are used on a routine basis in order to kill or keep bacterial levels to a minimum. Unfortunately, the heavy use of antibiotics leads to a predictable problem where bacteria develop resistance to these medications and the ability to treat lung infections in this situation are limited. We know that once patients acquire antibiotic resistant bacteria that they experience a more rapid decline in lung function and a reduction in their overall survival.

The objective of our proposal is to evaluate a new type of therapy for the treatment of CF. This new therapy takes advantage of two therapeutic compounds: antimicrobial peptides (AMP) and pulmonary surfactant. AMPs have been shown to have very potent antibacterial properties which, unlike current antibiotics, are not susceptible to the development of resistance by bacteria. Furthermore, pulmonary surfactant is a natural substance produced in human lungs which has physical properties which allow it to spread over the entire surface of the lung. We propose that combining AMP with pulmonary surfactant allows for an efficient therapeutic in which surfactant acts as carrier for an antimicrobial peptide to the CF lung.

The innovative feature of our study is the utilization of the spreading capability of a natural lung component (pulmonary surfactant) to deliver a novel therapeutic (AMP) to the site of infection.

The outcomes of the current project will have the potential to improve the quality of life for those living with CF, and also have wider reaching implications to bacterial lung infections associated with other disease processes.

Back to top

Tuberculosis (TB)

Zhou Xing
Mechanisms of Enhanced Protection Against Pulmonary Tuberculosis by Allergic Immunity

Lung tuberculosis (TB) remains a serious global health problem, particularly in many African, Asian and Eastern European countries. On the other hand, there is an increased incidence of allergic diseases in the lung in these regions. Up to now, little is understood about the impact of allergic conditions on tuberculous infection in the same host.

The main objective of our project is to understand whether having ongoing allergic condition in the lung may influence how the immune system reacts to subsequent exposure to the bacterium that causes TB, and if so, what are the mechanisms. Our project sets out to investigate a clinically relevant question that has hardly been addressed before.

Our preliminary data is surprising and goes against the current dogma. We expect that the new knowledge spawned from this project will establish a new paradigm that may help change our way of understanding the relationship of allergic immunity to anti-TB immunity.

As TB still remains a significant health issue in Canada, particularly in the First Nation communities and recent immigration populations, the new knowledge from our project will help identify the new molecular pathways that may be exploited for preventing or treating TB.

Back to top

Lung Transplantation

Lianne Singer
Frailty in Advanced Lung Disease

Over the years, lung transplant programs have been accepting older patients with more chronic health problems. It is possible that some of these patients are frail – in other words, their bodies are less able to withstand stress. We do not know how best to measure frailty in patients with lung disease, or what effect frailty has on their health-related quality of life. We also do not know if frail patients get as much benefit from transplantation as non-frail individuals, or how to help frail patients with lung disease have longer and better lives before and after lung transplantation.

Our objective is to study different ways of measuring frailty in patients on the lung transplant waiting list, and the impact of frailty on patients’ quality of life and other important health outcomes.

Frailty has not been directly studied in patients with severe lung disease. We will develop new tools to assess frailty in these patients, and gain a better understanding of the prevalence and impact of frailty in very sick patients awaiting lung transplantation.

The ability to measure and understand the impact of frailty in people with severe lung disease will lead to new treatment approaches to reduce the burden of frailty, and improve the quality of life of people with lung disease.

Marcelo Cypel
Measurement of Extravascular Lung Water to Predict Primary Graft Dysfunction and Outcomes Following Lung Transplant

A common complication following lung transplantation is injury to the new lungs as they receive the flow of blood from the recipient after a period of cold storage during transportation. This is known as primary graft dysfunction (PGD, poor functioning of the new lung). The treatment of PGD involves trying to protect the lung from further injury by careful use of the breathing machine, and by giving the minimal required amount of intravenous fluids to patients. In critically ill patients, however, it is often difficult to determine exactly how much fluid is needed.

A new monitor allows us to determine how much fluid has leaked into the damaged lungs. This in turn may help determine if patients can tolerate more fluid administration in situations where they are in shock versus having their blood pressure supported by additional medications.

This new technique has never been evaluated in lung transplant. If we see that there is a relationship between the information from this monitor and its ability to detect and predict PGD, this could help impact the care of lung transplant patients in the intensive care unit, particularly for guiding treatment of PGD, leading to better function and survival after transplant.

Back to top

Mechanical Ventilation

Karen Burns
Liberation from Mechanical Ventilation and Screening Frequency Trial: The Release Trial Background

Weaning is the process where the work of breathing is transferred from a breathing Screening protocols and tests of patient’s ability to breathe spontaneously to identify patients who may be ready to breathe on their own. Once daily screening is the current standard of care for recognizing weaning candidates in adult intensive care units (ICUs). In Canada, weaning is a collaborative effort involving respiratory therapists (RTs) and critical care physicians with screening largely performed by RTs. With RTs available in our national ICUs 24 hours a day/7 days per week, a significant opportunity exists to screen patients more frequently, conduct more frequent tests of patient’s ability to breathe spontaneously, and reduce the time spent on ventilators and in the ICU.

We plan to conduct a pilot randomized trial comparing ‘once daily’ screening to ‘at least twice daily’ screening to identify critically ill patients who are ready to breathe on their own
.
We will evaluate whether more frequent screening will result in earlier identification of weaning candidates, more frequent conduct of tests of spontaneous breathing, and reduce the time spent on breathing machines and in the ICU. More frequent screening is a simple and cost effective strategy that could change clinical practice, improve the care delivered to critically ill adults, and ultimately, improve their outcomes.

Niall Ferguson
Physiological Mechanisms of Weaning Failure in Mechanically Ventilated Patients

When patients become so sick that they cannot breathe on their own (“lung failure”), a breathing machine (“ventilator”) is used to help them breathe. It is often hard for doctors to know why these patients cannot breathe without the ventilator. One important reason is that the breathing muscles become very weak while patients are on a ventilator. It is unknown why the breathing muscles become weak and how this affects patients’ long-term recovery. Our study has three goals:

  • To help doctors decide why patients cannot breathe without help from the ventilator.
  • To understand why some patients develop weak breathing muscles while they are on the ventilator.
  • To learn whether weak breathing muscles make long-term recovery from lung-term more difficult.

This is the first study to specifically assess the impact of breathing muscle weakness on the long-term recovery of patients after they leave the intensive care unit. Patients with lung failure who require ventilator support for a long period of time often have severe difficulty recovering from their illness. Many are permanently disabled and some of them die within one year of leaving the intensive care unit.

Our study will help doctors diagnose the reasons why patients cannot breathe without assistance from the ventilator. Accurate diagnosis can guide treatment to help patients resume breathing without the ventilator and improve their long-term recovery.

Back to top

Sleep Apnea

Clodagh M. Ryan
Fluid Shifts in Pulmonary Hypertension With and Without Sleep-Disordered Breathing

Pulmonary hypertension increases the blood pressure in the pulmonary arteries or veins causing right heart failure and eventually death. Although, there are medical treatments available for pulmonary hypertension, death occurs in 11 per cent of patients at 2 years. Studies have shown that in those with pulmonary hypertension there is a high frequency of sleep-disordered breathing.

Sleep-disordered breathing is an umbrella term that includes obstructive sleep apnea, central sleep apnea and sleep related hypoventilation. These disorders occur when sleeping at night and result in interrupted or shallow breathing that causes sporadic reductions in oxygen levels. Sleep-disordered breathing also can cause strain and pressure on the right heart. However, it is not clear whether or not the sleep disordered breathing occurs as a result of the pulmonary hypertension or if it is a separate unrelated disease process.

It has been shown that when we lie down at night, fluid moves out of the legs and towards the head in people with sleep apnea and left heart failure. In pulmonary hypertension, there is excess fluid due to heart failure. We suggest that this excess fluid may be the cause of sleep disordered breathing in pulmonary hypertension patients and that treatment of the pulmonary hypertension by reducing fluid will improve the sleep-disordered breathing.

The objective of this study is to study the shift of fluid overnight in people with newly diagnosed pulmonary hypertension with and without sleep-disordered breathing. We will also see if the treatment of pulmonary hypertension has treated the sleep apnea by reducing the amount of fluid moving from the legs overnight.

Our research will study two lung diseases (pulmonary hypertension and sleep apnea) and by studying the role of fluid shifts it may change our approach to and treatment of patients with pulmonary hypertension and sleep apnea. It may also improve our understanding of the factors that cause sleep apnea in pulmonary hypertension, possibly altering the way we treat those individuals.

Back to top