News From CHEST Physician®

Original Research

Burden of Adult Community-Acquired, Health-care-Associated, Hospital-Acquired, and Ventilator-Associated Pneumonia: New York City, 2010 to 2014. By R. E. Corrado, et al.

Evidence-Based Medicine

Pharmacologic and Nonpharmacologic Treatment for Acute Cough Associated With the Common Cold: CHEST Expert Panel Report. By M. A. Malesker, et al, on behalf of the CHEST Expert Cough Panel.

Cough in Ambulatory Immunocompromised Adults: CHEST Expert Panel Report. By M. J. Rosen, et al, on behalf of the CHEST Expert Cough Panel.

Original Research

Burden of Adult Community-Acquired, Health-care-Associated, Hospital-Acquired, and Ventilator-Associated Pneumonia: New York City, 2010 to 2014. By R. E. Corrado, et al.

Evidence-Based Medicine

Pharmacologic and Nonpharmacologic Treatment for Acute Cough Associated With the Common Cold: CHEST Expert Panel Report. By M. A. Malesker, et al, on behalf of the CHEST Expert Cough Panel.

Cough in Ambulatory Immunocompromised Adults: CHEST Expert Panel Report. By M. J. Rosen, et al, on behalf of the CHEST Expert Cough Panel.

Original Research

Burden of Adult Community-Acquired, Health-care-Associated, Hospital-Acquired, and Ventilator-Associated Pneumonia: New York City, 2010 to 2014. By R. E. Corrado, et al.

Evidence-Based Medicine

Pharmacologic and Nonpharmacologic Treatment for Acute Cough Associated With the Common Cold: CHEST Expert Panel Report. By M. A. Malesker, et al, on behalf of the CHEST Expert Cough Panel.

Cough in Ambulatory Immunocompromised Adults: CHEST Expert Panel Report. By M. J. Rosen, et al, on behalf of the CHEST Expert Cough Panel.

Interventional Chest/Diagnostic Procedures

Cryobiopsy for ILD: Careful stewardship needed

Interest in transbronchial cryobiopsy has accelerated rapidly in recent years. This procedure is performed by advancing a cryoprobe into the peripheral lung via flexible bronchoscopy, where lung tissue freezes and adheres to the probe and is subsequently extracted as a cryobiopsy. The number of cryobiopsy-related publications has increased exponentially since it was described in 2009 (Babiak A, et al. Respiration. 2009;78[2]:203). This interest stems from reports of high diagnostic yields in patients with interstitial lung disease (ILD) while maintaining complication rates similar to that of conventional bronchoscopic biopsy.

Traditional bronchoscopic biopsies are notoriously insensitive; a specific diagnosis can be established in fewer than a third of cases (Sheth JS, et al. Chest. 2017;151[2]:389). As such, surgical lung biopsy continues to be recommended but is associated with significant mortality (2%) and morbidity (30%) in patients with ILD (Hutchinson JP, et al. ARJCCM. 2016;193[10]:1161). Cryobiopsy, which appears to rival surgical lung biopsy in terms of ability to contribute to a specific diagnosis, is, therefore, a highly promising alternative (Tomassetti S, et al. AJRCCM. 2016;193[7]:745).

As cryobiopsy is increasingly adopted around the world, however, troubling reports of serious complications have surfaced. Most notable is the recently reported experience of the initial 25 cases performed at the University of Pennsylvania, in which almost one in four patients suffered serious complications (DiBardino DM, et al. Ann Am Thorac Soc. 2017;14[6]:851). The authors pointed to lack of a predefined procedural protocol, as well as several choices relating to the specific technique used, including inconsistent use of fluoroscopy, lack of prophylactic bronchial blocker placement, and predominant use of laryngeal mask airways as potential contributing factors. Indeed, many variations of the basic cryobiopsy procedure have been described (Lentz RJ, et al. J Thoracic Dis. 2017;9[7]:2186), with no formal guidance or training available to inform advanced bronchoscopists interested in this procedure.

It is incumbent on the interventional pulmonology and ILD specialist communities to be responsible stewards of this promising procedure. Implementation of three parallel efforts to standardize and rigorously study this procedure should be considered as soon as possible: creation of expert consensus guidelines establishing best-practices for safe and effective biopsy technique; a training requirement before independent performance of the procedure; and creation of an international cryobiopsy registry to facilitate higher-quality research into optimal technique and outcomes. We owe this to our patients.

Robert J. Lentz, MD
NetWork Member

Fabien Maldonado, MD, FCCP
NetWork Member

Pediatric Chest Medicine

Chronic cough in children: New guidelines

A chronic cough is a common complaint among children whose parents seek medical evaluation. Chronic wet cough can indicate an underlying illness; therefore, an early diagnosis can lead to prevention of complications of the disease and improvement in quality of life.

CHEST is a leading resource in evidence and consensus-based guidelines on important topics affecting children. The most recent guidelines entitled Management of Children with Chronic Wet Cough and Protracted Bacterial Bronchitis (Chest. 2017;151(4):884-890) and Use of Management Pathways or Algorithms in Children with Chronic Cough (Chest. 2017;151(4):875-873) are updates from the 2006 CHEST guidelines on chronic cough in children.

The present updates utilized the CHEST methodological guidelines with chronic wet or productive cough and Grading of Recommendations Assessment, Development, and Evaluation framework and also performed a systematic review addressing key questions concerning the management of childhood disease for children 14 years and younger.

Guidance provided by the expert panel focused on recommendations to answer six key questions concerning the management of children 14 years and younger with a chronic wet cough unrelated to established chronic lung disease. The recommendations are:

1. Chronic cough is defined as the presence of a cough 4 weeks or longer in duration.

2. Assessment of the effect of the cough on the child and the family be undertaken as part of clinical consultation.

3. Evaluation of a chronic cough should be done with a systematic approach with pediatric-specific cough management protocols or algorithms.

4. Chest radiograph and, when age appropriate, spirometry with bronchodilator be undertaken as evaluation; tests for pertussis infection only to be performed if clinically suspected.

5. Chronic wet cough with no specific clinical features should receive antibiotics for 2 weeks targeted for common respiratory bacteria (Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis).

6. When cough persists despite 2 weeks of appropriate antibiotics, it is recommended to continue for an additional 2 weeks.

7. Additional tests (eg skin prick test, Mantoux, bronchoscopy, chest CT scan) should be individualized in accordance with the clinical setting and child’s clinical symptoms and signs.

The panel recognizes the need for prospective studies to assess current algorithms outcomes of children with chronic cough. Both articles can be found on the guidelines section of the CHEST site.

John Bishara, DO
Fellow-in-Training Member

Pulmonary Physiology, Function, and Rehabilitation

Functional imaging of the lung

Quantifying heterogeneity of ventilation and gas exchange in lung diseases remains a clinical challenge. Conventional pulmonary function test is insensitive to regional changes. The multiple inert gas elimination technique can quantify ventilation-perfusion distribution, but it requires invasive instrumentation (eg, pulmonary artery catheterization) and is not practical for clinical use. Computed tomography (CT) scans delineate spatial changes in lung structures but do not directly measure changes in ventilation and gas exchange. With its radiation, it is difficult to apply CT scanning repeatedly in patients. More recently, MR imaging techniques have been developed to directly “visualize” and quantify regional lung function (Kruger SJ, et al. J Magn Reson Imaging. 2016;43(2):295; Roos JE, et al. Magn Reson Imaging Clin N Am. 2015;23(2):217). These techniques employ inhalation of gases, such as oxygen, perfluorinated gases, and hyperpolarized ³He and ¹²⁹Xe. Hyperpolarized ³He has been studied the most; however, the dwindling supply of ³He gas and its rising cost have prevented its further development. ¹²⁹Xe has abundant supply and has emerged to be the inert gas of choice for MR imaging. Hyperpolarized ¹²⁹Xe can measure ventilation, like hyperpolarized ³He. In addition, Xe diffuses into alveolar barrier (interstitium and plasma) and red blood cells, where it exhibits distinct resonant frequency shifts that can be captured by MR. Therefore, in one test, information on pulmonary ventilation and gas transfer can be obtained. To date, the results from MR imaging studies have provided new insights into the pathophysiology of obstructive and restrictive lung diseases. With continuous development, MR imaging of the lung could become a clinically useful tool in the near future.

Yuh-Chin T. Huang, MD, MHS, FCCP

Steering Committee Member

Immune-mediated pneumonitis and PD-1 inhibition

Inhibitors of the programmed cell death 1 receptor (PD-1) have shown significant promise in the treatment of advanced stage malignancy. With the recent expansion of indications for use of these agents, the number of patients treated will continue to grow. Clinicians must be aware of their potential for serious adverse side effects, including dermatitis, colitis, and potentially life-threatening pneumonitis.

The development of pneumonitis secondary to PD-1 inhibitions is reported to occur in 2% to 5% of patients and can present at any time during therapy, with 1% of patients developing grade 3 or higher pneumonitis.^1,2 The most common symptoms are dyspnea and cough, though one-third of patients are asymptomatic at presentation.² Radiographic and pathologic features vary greatly and include organizing pneumonia, interstitial pneumonitis, hypersensitivity pneumonitis, or diffuse alveolar damage.³ While pneumonitis due to PD-1 inhibition is reportedly uncommon, the increasing number of patients expected to receive these medications will predictably result in increasing overall frequency of pneumonitis cases. In addition, the lack of large prospective randomized trials and reliance on radiographic rather than pathologic data in diagnosing immune-mediated pneumonitis gives one pause. Given the variability of presentation, lack of routine pathologic data, and increasing use of dual agents (eg, PD-1 and CTLA-4), chest physicians and medical oncologists should have a high index of suspicion yet practice equipoise in patients receiving immunotherapy who develop unexplained pulmonary symptoms or infiltrates. More research is needed to help improve the multidisciplinary diagnosis and treatment of this potentially serious complication.

David Maurice Chambers, MD
Fellow-in-Training Member

Jason Atticus Akulian, MD, MPH
Steering Committee Member

References

1. Nishino M, et al. Incidence of programmed cell death 1 inhibitor-related pneumonitis in patients with advanced cancer: a systematic review and meta-analysis. JAMA Oncology. 2016;2(12):1607.

2. Naidoo J, et al. Pneumonitis in patients treated with anti-programmed death-1/programmed death ligand 1 therapy. J Clin Oncol. 2017;35(7):709.

3. Nishino M, et al. PD-1 inhibitor-related pneumonitis in advanced cancer patients: radiographic patterns and clinical course. Clin Cancer Res. 2016;22(24):6051.

Pulmonary Vascular Disease

Pulmonary Arterial Hypertension Associated With SLE

While pulmonary arterial hypertension (PAH) commonly complicates scleroderma (SSc), it is a rare complication of other connective tissue diseases (CTD), such as systemic lupus erythematosus (SLE). In the few prospective studies that utilize right-sided heart catheterization (RHC), the estimated prevalence of PAH in SLE is about 4%. However, since the prevalence of SLE is 10 to 15 times greater than SSc in the United States, the true prevalence of SLE-PAH may be higher than previously thought, and, thus, clinically relevant. Despite this, little is known about SLE-PAH.

A recent retrospective study from the French Pulmonary Hypertension Registry has added significantly to our understanding of this complication of SLE. Hachulla and colleagues studied 51 patients with RHC-proven SLE-PAH compared with 101 SLE control subjects without PAH. While the authors did not find any relevant differences in the demographics between groups, they did find a significantly higher prevalence of SSA and SSB antibodies in SLE-PAH. Interestingly, the presence of anti-U1 RNP antibody appeared to be less common in SLE-PAH patients; this lack of association is in contrast to prior studies in mixed CTD patients with anti-U1 RNP antibodies in which the prevalence of PAH can be as high as 60%. Further, none of the SLE-PAH patients demonstrated an acute response to vasodilator challenge during RHC, emphasizing that this maneuver does not need to be performed in SLE patients at risk of PAH. Trends toward improved survival in SLE-PAH patients treated with hydroxychloroquine are preliminary and hypothesis-generating but require confirmation in larger clinical studies.

Stephen Mathai, MD, FCCP
Chair

Leena Palwar, MD
Fellow-in-Training Member

References

Hachulla E, Jais X, Cinquetti G, et al. Pulmonary arterial hypertension associated with SLE: Results from the French pulmonary hypertension registry. Chest. 2017 Aug 26. pii: S0012-3692(17)31430-7. doi: 10.1016/j.chest.2017.08.014. [Epub ahead of print]

Chung L, Liu J, Parsons L, et al. Characterization of connective tissue disease-associated pulmonary arterial hypertension from REVEAL: identifying systemic sclerosis as a unique phenotype. Chest. 2010;138:1383-1394.

Shirai Y, Yasuoka H, Okano Y, Takeuchi T, Satoh T, Kuwana M. Clinical characteristics and survival of Japanese patients with connective tissue disease and pulmonary arterial hypertension: a singlecentre cohort. Rheumatology. 2012;51:1846-1854.

Hao YJ, Jiang X, Zhou W, et al. Connective tissue disease-associated pulmonary arterial hypertension in Chinese patients. Eur Respir J. 2014;44: 963-972.

Huang C, Li M, Liu Y, et al. Baseline characteristics and risk factors of pulmonary arterial hypertension in systemic lupus erythematosus patients. Medicine. 2016;95:e2761.

Pérez-Peñate GM, Rúa-Figueroa I, Juliá- Serdá G, et al. Pulmonary arterial hypertension in systemic lupus erythematosus: prevalence and predictors. J Rheumatol. 2016;43:323-329.

Alpert MA, Goldberg SH, Sindem BH, et al. Cardiovascular manifestations of mixed connective tissue disease in adults. Circulation. 1983;63:1182-1193.

Interventional Chest/Diagnostic Procedures

Cryobiopsy for ILD: Careful stewardship needed

Interest in transbronchial cryobiopsy has accelerated rapidly in recent years. This procedure is performed by advancing a cryoprobe into the peripheral lung via flexible bronchoscopy, where lung tissue freezes and adheres to the probe and is subsequently extracted as a cryobiopsy. The number of cryobiopsy-related publications has increased exponentially since it was described in 2009 (Babiak A, et al. Respiration. 2009;78[2]:203). This interest stems from reports of high diagnostic yields in patients with interstitial lung disease (ILD) while maintaining complication rates similar to that of conventional bronchoscopic biopsy.

Traditional bronchoscopic biopsies are notoriously insensitive; a specific diagnosis can be established in fewer than a third of cases (Sheth JS, et al. Chest. 2017;151[2]:389). As such, surgical lung biopsy continues to be recommended but is associated with significant mortality (2%) and morbidity (30%) in patients with ILD (Hutchinson JP, et al. ARJCCM. 2016;193[10]:1161). Cryobiopsy, which appears to rival surgical lung biopsy in terms of ability to contribute to a specific diagnosis, is, therefore, a highly promising alternative (Tomassetti S, et al. AJRCCM. 2016;193[7]:745).

As cryobiopsy is increasingly adopted around the world, however, troubling reports of serious complications have surfaced. Most notable is the recently reported experience of the initial 25 cases performed at the University of Pennsylvania, in which almost one in four patients suffered serious complications (DiBardino DM, et al. Ann Am Thorac Soc. 2017;14[6]:851). The authors pointed to lack of a predefined procedural protocol, as well as several choices relating to the specific technique used, including inconsistent use of fluoroscopy, lack of prophylactic bronchial blocker placement, and predominant use of laryngeal mask airways as potential contributing factors. Indeed, many variations of the basic cryobiopsy procedure have been described (Lentz RJ, et al. J Thoracic Dis. 2017;9[7]:2186), with no formal guidance or training available to inform advanced bronchoscopists interested in this procedure.

It is incumbent on the interventional pulmonology and ILD specialist communities to be responsible stewards of this promising procedure. Implementation of three parallel efforts to standardize and rigorously study this procedure should be considered as soon as possible: creation of expert consensus guidelines establishing best-practices for safe and effective biopsy technique; a training requirement before independent performance of the procedure; and creation of an international cryobiopsy registry to facilitate higher-quality research into optimal technique and outcomes. We owe this to our patients.

Robert J. Lentz, MD
NetWork Member

Fabien Maldonado, MD, FCCP
NetWork Member

Pediatric Chest Medicine

Chronic cough in children: New guidelines

A chronic cough is a common complaint among children whose parents seek medical evaluation. Chronic wet cough can indicate an underlying illness; therefore, an early diagnosis can lead to prevention of complications of the disease and improvement in quality of life.

CHEST is a leading resource in evidence and consensus-based guidelines on important topics affecting children. The most recent guidelines entitled Management of Children with Chronic Wet Cough and Protracted Bacterial Bronchitis (Chest. 2017;151(4):884-890) and Use of Management Pathways or Algorithms in Children with Chronic Cough (Chest. 2017;151(4):875-873) are updates from the 2006 CHEST guidelines on chronic cough in children.

The present updates utilized the CHEST methodological guidelines with chronic wet or productive cough and Grading of Recommendations Assessment, Development, and Evaluation framework and also performed a systematic review addressing key questions concerning the management of childhood disease for children 14 years and younger.

Guidance provided by the expert panel focused on recommendations to answer six key questions concerning the management of children 14 years and younger with a chronic wet cough unrelated to established chronic lung disease. The recommendations are:

1. Chronic cough is defined as the presence of a cough 4 weeks or longer in duration.

2. Assessment of the effect of the cough on the child and the family be undertaken as part of clinical consultation.

3. Evaluation of a chronic cough should be done with a systematic approach with pediatric-specific cough management protocols or algorithms.

4. Chest radiograph and, when age appropriate, spirometry with bronchodilator be undertaken as evaluation; tests for pertussis infection only to be performed if clinically suspected.

5. Chronic wet cough with no specific clinical features should receive antibiotics for 2 weeks targeted for common respiratory bacteria (Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis).

6. When cough persists despite 2 weeks of appropriate antibiotics, it is recommended to continue for an additional 2 weeks.

7. Additional tests (eg skin prick test, Mantoux, bronchoscopy, chest CT scan) should be individualized in accordance with the clinical setting and child’s clinical symptoms and signs.

The panel recognizes the need for prospective studies to assess current algorithms outcomes of children with chronic cough. Both articles can be found on the guidelines section of the CHEST site.

John Bishara, DO
Fellow-in-Training Member

Pulmonary Physiology, Function, and Rehabilitation

Functional imaging of the lung

Quantifying heterogeneity of ventilation and gas exchange in lung diseases remains a clinical challenge. Conventional pulmonary function test is insensitive to regional changes. The multiple inert gas elimination technique can quantify ventilation-perfusion distribution, but it requires invasive instrumentation (eg, pulmonary artery catheterization) and is not practical for clinical use. Computed tomography (CT) scans delineate spatial changes in lung structures but do not directly measure changes in ventilation and gas exchange. With its radiation, it is difficult to apply CT scanning repeatedly in patients. More recently, MR imaging techniques have been developed to directly “visualize” and quantify regional lung function (Kruger SJ, et al. J Magn Reson Imaging. 2016;43(2):295; Roos JE, et al. Magn Reson Imaging Clin N Am. 2015;23(2):217). These techniques employ inhalation of gases, such as oxygen, perfluorinated gases, and hyperpolarized ³He and ¹²⁹Xe. Hyperpolarized ³He has been studied the most; however, the dwindling supply of ³He gas and its rising cost have prevented its further development. ¹²⁹Xe has abundant supply and has emerged to be the inert gas of choice for MR imaging. Hyperpolarized ¹²⁹Xe can measure ventilation, like hyperpolarized ³He. In addition, Xe diffuses into alveolar barrier (interstitium and plasma) and red blood cells, where it exhibits distinct resonant frequency shifts that can be captured by MR. Therefore, in one test, information on pulmonary ventilation and gas transfer can be obtained. To date, the results from MR imaging studies have provided new insights into the pathophysiology of obstructive and restrictive lung diseases. With continuous development, MR imaging of the lung could become a clinically useful tool in the near future.

Yuh-Chin T. Huang, MD, MHS, FCCP

Steering Committee Member

Immune-mediated pneumonitis and PD-1 inhibition

Inhibitors of the programmed cell death 1 receptor (PD-1) have shown significant promise in the treatment of advanced stage malignancy. With the recent expansion of indications for use of these agents, the number of patients treated will continue to grow. Clinicians must be aware of their potential for serious adverse side effects, including dermatitis, colitis, and potentially life-threatening pneumonitis.

The development of pneumonitis secondary to PD-1 inhibitions is reported to occur in 2% to 5% of patients and can present at any time during therapy, with 1% of patients developing grade 3 or higher pneumonitis.^1,2 The most common symptoms are dyspnea and cough, though one-third of patients are asymptomatic at presentation.² Radiographic and pathologic features vary greatly and include organizing pneumonia, interstitial pneumonitis, hypersensitivity pneumonitis, or diffuse alveolar damage.³ While pneumonitis due to PD-1 inhibition is reportedly uncommon, the increasing number of patients expected to receive these medications will predictably result in increasing overall frequency of pneumonitis cases. In addition, the lack of large prospective randomized trials and reliance on radiographic rather than pathologic data in diagnosing immune-mediated pneumonitis gives one pause. Given the variability of presentation, lack of routine pathologic data, and increasing use of dual agents (eg, PD-1 and CTLA-4), chest physicians and medical oncologists should have a high index of suspicion yet practice equipoise in patients receiving immunotherapy who develop unexplained pulmonary symptoms or infiltrates. More research is needed to help improve the multidisciplinary diagnosis and treatment of this potentially serious complication.

David Maurice Chambers, MD
Fellow-in-Training Member

Jason Atticus Akulian, MD, MPH
Steering Committee Member

References

1. Nishino M, et al. Incidence of programmed cell death 1 inhibitor-related pneumonitis in patients with advanced cancer: a systematic review and meta-analysis. JAMA Oncology. 2016;2(12):1607.

2. Naidoo J, et al. Pneumonitis in patients treated with anti-programmed death-1/programmed death ligand 1 therapy. J Clin Oncol. 2017;35(7):709.

3. Nishino M, et al. PD-1 inhibitor-related pneumonitis in advanced cancer patients: radiographic patterns and clinical course. Clin Cancer Res. 2016;22(24):6051.

Pulmonary Vascular Disease

Pulmonary Arterial Hypertension Associated With SLE

While pulmonary arterial hypertension (PAH) commonly complicates scleroderma (SSc), it is a rare complication of other connective tissue diseases (CTD), such as systemic lupus erythematosus (SLE). In the few prospective studies that utilize right-sided heart catheterization (RHC), the estimated prevalence of PAH in SLE is about 4%. However, since the prevalence of SLE is 10 to 15 times greater than SSc in the United States, the true prevalence of SLE-PAH may be higher than previously thought, and, thus, clinically relevant. Despite this, little is known about SLE-PAH.

A recent retrospective study from the French Pulmonary Hypertension Registry has added significantly to our understanding of this complication of SLE. Hachulla and colleagues studied 51 patients with RHC-proven SLE-PAH compared with 101 SLE control subjects without PAH. While the authors did not find any relevant differences in the demographics between groups, they did find a significantly higher prevalence of SSA and SSB antibodies in SLE-PAH. Interestingly, the presence of anti-U1 RNP antibody appeared to be less common in SLE-PAH patients; this lack of association is in contrast to prior studies in mixed CTD patients with anti-U1 RNP antibodies in which the prevalence of PAH can be as high as 60%. Further, none of the SLE-PAH patients demonstrated an acute response to vasodilator challenge during RHC, emphasizing that this maneuver does not need to be performed in SLE patients at risk of PAH. Trends toward improved survival in SLE-PAH patients treated with hydroxychloroquine are preliminary and hypothesis-generating but require confirmation in larger clinical studies.

Stephen Mathai, MD, FCCP
Chair

Leena Palwar, MD
Fellow-in-Training Member

References

Hachulla E, Jais X, Cinquetti G, et al. Pulmonary arterial hypertension associated with SLE: Results from the French pulmonary hypertension registry. Chest. 2017 Aug 26. pii: S0012-3692(17)31430-7. doi: 10.1016/j.chest.2017.08.014. [Epub ahead of print]

Chung L, Liu J, Parsons L, et al. Characterization of connective tissue disease-associated pulmonary arterial hypertension from REVEAL: identifying systemic sclerosis as a unique phenotype. Chest. 2010;138:1383-1394.

Shirai Y, Yasuoka H, Okano Y, Takeuchi T, Satoh T, Kuwana M. Clinical characteristics and survival of Japanese patients with connective tissue disease and pulmonary arterial hypertension: a singlecentre cohort. Rheumatology. 2012;51:1846-1854.

Hao YJ, Jiang X, Zhou W, et al. Connective tissue disease-associated pulmonary arterial hypertension in Chinese patients. Eur Respir J. 2014;44: 963-972.

Huang C, Li M, Liu Y, et al. Baseline characteristics and risk factors of pulmonary arterial hypertension in systemic lupus erythematosus patients. Medicine. 2016;95:e2761.

Pérez-Peñate GM, Rúa-Figueroa I, Juliá- Serdá G, et al. Pulmonary arterial hypertension in systemic lupus erythematosus: prevalence and predictors. J Rheumatol. 2016;43:323-329.

Alpert MA, Goldberg SH, Sindem BH, et al. Cardiovascular manifestations of mixed connective tissue disease in adults. Circulation. 1983;63:1182-1193.

Interventional Chest/Diagnostic Procedures

Cryobiopsy for ILD: Careful stewardship needed

Interest in transbronchial cryobiopsy has accelerated rapidly in recent years. This procedure is performed by advancing a cryoprobe into the peripheral lung via flexible bronchoscopy, where lung tissue freezes and adheres to the probe and is subsequently extracted as a cryobiopsy. The number of cryobiopsy-related publications has increased exponentially since it was described in 2009 (Babiak A, et al. Respiration. 2009;78[2]:203). This interest stems from reports of high diagnostic yields in patients with interstitial lung disease (ILD) while maintaining complication rates similar to that of conventional bronchoscopic biopsy.

Traditional bronchoscopic biopsies are notoriously insensitive; a specific diagnosis can be established in fewer than a third of cases (Sheth JS, et al. Chest. 2017;151[2]:389). As such, surgical lung biopsy continues to be recommended but is associated with significant mortality (2%) and morbidity (30%) in patients with ILD (Hutchinson JP, et al. ARJCCM. 2016;193[10]:1161). Cryobiopsy, which appears to rival surgical lung biopsy in terms of ability to contribute to a specific diagnosis, is, therefore, a highly promising alternative (Tomassetti S, et al. AJRCCM. 2016;193[7]:745).

As cryobiopsy is increasingly adopted around the world, however, troubling reports of serious complications have surfaced. Most notable is the recently reported experience of the initial 25 cases performed at the University of Pennsylvania, in which almost one in four patients suffered serious complications (DiBardino DM, et al. Ann Am Thorac Soc. 2017;14[6]:851). The authors pointed to lack of a predefined procedural protocol, as well as several choices relating to the specific technique used, including inconsistent use of fluoroscopy, lack of prophylactic bronchial blocker placement, and predominant use of laryngeal mask airways as potential contributing factors. Indeed, many variations of the basic cryobiopsy procedure have been described (Lentz RJ, et al. J Thoracic Dis. 2017;9[7]:2186), with no formal guidance or training available to inform advanced bronchoscopists interested in this procedure.

It is incumbent on the interventional pulmonology and ILD specialist communities to be responsible stewards of this promising procedure. Implementation of three parallel efforts to standardize and rigorously study this procedure should be considered as soon as possible: creation of expert consensus guidelines establishing best-practices for safe and effective biopsy technique; a training requirement before independent performance of the procedure; and creation of an international cryobiopsy registry to facilitate higher-quality research into optimal technique and outcomes. We owe this to our patients.

Robert J. Lentz, MD
NetWork Member

Fabien Maldonado, MD, FCCP
NetWork Member

Pediatric Chest Medicine

Chronic cough in children: New guidelines

A chronic cough is a common complaint among children whose parents seek medical evaluation. Chronic wet cough can indicate an underlying illness; therefore, an early diagnosis can lead to prevention of complications of the disease and improvement in quality of life.

CHEST is a leading resource in evidence and consensus-based guidelines on important topics affecting children. The most recent guidelines entitled Management of Children with Chronic Wet Cough and Protracted Bacterial Bronchitis (Chest. 2017;151(4):884-890) and Use of Management Pathways or Algorithms in Children with Chronic Cough (Chest. 2017;151(4):875-873) are updates from the 2006 CHEST guidelines on chronic cough in children.

The present updates utilized the CHEST methodological guidelines with chronic wet or productive cough and Grading of Recommendations Assessment, Development, and Evaluation framework and also performed a systematic review addressing key questions concerning the management of childhood disease for children 14 years and younger.

Guidance provided by the expert panel focused on recommendations to answer six key questions concerning the management of children 14 years and younger with a chronic wet cough unrelated to established chronic lung disease. The recommendations are:

1. Chronic cough is defined as the presence of a cough 4 weeks or longer in duration.

2. Assessment of the effect of the cough on the child and the family be undertaken as part of clinical consultation.

3. Evaluation of a chronic cough should be done with a systematic approach with pediatric-specific cough management protocols or algorithms.

4. Chest radiograph and, when age appropriate, spirometry with bronchodilator be undertaken as evaluation; tests for pertussis infection only to be performed if clinically suspected.

5. Chronic wet cough with no specific clinical features should receive antibiotics for 2 weeks targeted for common respiratory bacteria (Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis).

6. When cough persists despite 2 weeks of appropriate antibiotics, it is recommended to continue for an additional 2 weeks.

7. Additional tests (eg skin prick test, Mantoux, bronchoscopy, chest CT scan) should be individualized in accordance with the clinical setting and child’s clinical symptoms and signs.

The panel recognizes the need for prospective studies to assess current algorithms outcomes of children with chronic cough. Both articles can be found on the guidelines section of the CHEST site.

John Bishara, DO
Fellow-in-Training Member

Pulmonary Physiology, Function, and Rehabilitation

Functional imaging of the lung

Quantifying heterogeneity of ventilation and gas exchange in lung diseases remains a clinical challenge. Conventional pulmonary function test is insensitive to regional changes. The multiple inert gas elimination technique can quantify ventilation-perfusion distribution, but it requires invasive instrumentation (eg, pulmonary artery catheterization) and is not practical for clinical use. Computed tomography (CT) scans delineate spatial changes in lung structures but do not directly measure changes in ventilation and gas exchange. With its radiation, it is difficult to apply CT scanning repeatedly in patients. More recently, MR imaging techniques have been developed to directly “visualize” and quantify regional lung function (Kruger SJ, et al. J Magn Reson Imaging. 2016;43(2):295; Roos JE, et al. Magn Reson Imaging Clin N Am. 2015;23(2):217). These techniques employ inhalation of gases, such as oxygen, perfluorinated gases, and hyperpolarized ³He and ¹²⁹Xe. Hyperpolarized ³He has been studied the most; however, the dwindling supply of ³He gas and its rising cost have prevented its further development. ¹²⁹Xe has abundant supply and has emerged to be the inert gas of choice for MR imaging. Hyperpolarized ¹²⁹Xe can measure ventilation, like hyperpolarized ³He. In addition, Xe diffuses into alveolar barrier (interstitium and plasma) and red blood cells, where it exhibits distinct resonant frequency shifts that can be captured by MR. Therefore, in one test, information on pulmonary ventilation and gas transfer can be obtained. To date, the results from MR imaging studies have provided new insights into the pathophysiology of obstructive and restrictive lung diseases. With continuous development, MR imaging of the lung could become a clinically useful tool in the near future.

Yuh-Chin T. Huang, MD, MHS, FCCP

Steering Committee Member

Immune-mediated pneumonitis and PD-1 inhibition

Inhibitors of the programmed cell death 1 receptor (PD-1) have shown significant promise in the treatment of advanced stage malignancy. With the recent expansion of indications for use of these agents, the number of patients treated will continue to grow. Clinicians must be aware of their potential for serious adverse side effects, including dermatitis, colitis, and potentially life-threatening pneumonitis.

The development of pneumonitis secondary to PD-1 inhibitions is reported to occur in 2% to 5% of patients and can present at any time during therapy, with 1% of patients developing grade 3 or higher pneumonitis.^1,2 The most common symptoms are dyspnea and cough, though one-third of patients are asymptomatic at presentation.² Radiographic and pathologic features vary greatly and include organizing pneumonia, interstitial pneumonitis, hypersensitivity pneumonitis, or diffuse alveolar damage.³ While pneumonitis due to PD-1 inhibition is reportedly uncommon, the increasing number of patients expected to receive these medications will predictably result in increasing overall frequency of pneumonitis cases. In addition, the lack of large prospective randomized trials and reliance on radiographic rather than pathologic data in diagnosing immune-mediated pneumonitis gives one pause. Given the variability of presentation, lack of routine pathologic data, and increasing use of dual agents (eg, PD-1 and CTLA-4), chest physicians and medical oncologists should have a high index of suspicion yet practice equipoise in patients receiving immunotherapy who develop unexplained pulmonary symptoms or infiltrates. More research is needed to help improve the multidisciplinary diagnosis and treatment of this potentially serious complication.

David Maurice Chambers, MD
Fellow-in-Training Member

Jason Atticus Akulian, MD, MPH
Steering Committee Member

References

1. Nishino M, et al. Incidence of programmed cell death 1 inhibitor-related pneumonitis in patients with advanced cancer: a systematic review and meta-analysis. JAMA Oncology. 2016;2(12):1607.

2. Naidoo J, et al. Pneumonitis in patients treated with anti-programmed death-1/programmed death ligand 1 therapy. J Clin Oncol. 2017;35(7):709.

3. Nishino M, et al. PD-1 inhibitor-related pneumonitis in advanced cancer patients: radiographic patterns and clinical course. Clin Cancer Res. 2016;22(24):6051.

Pulmonary Vascular Disease

Pulmonary Arterial Hypertension Associated With SLE

While pulmonary arterial hypertension (PAH) commonly complicates scleroderma (SSc), it is a rare complication of other connective tissue diseases (CTD), such as systemic lupus erythematosus (SLE). In the few prospective studies that utilize right-sided heart catheterization (RHC), the estimated prevalence of PAH in SLE is about 4%. However, since the prevalence of SLE is 10 to 15 times greater than SSc in the United States, the true prevalence of SLE-PAH may be higher than previously thought, and, thus, clinically relevant. Despite this, little is known about SLE-PAH.

A recent retrospective study from the French Pulmonary Hypertension Registry has added significantly to our understanding of this complication of SLE. Hachulla and colleagues studied 51 patients with RHC-proven SLE-PAH compared with 101 SLE control subjects without PAH. While the authors did not find any relevant differences in the demographics between groups, they did find a significantly higher prevalence of SSA and SSB antibodies in SLE-PAH. Interestingly, the presence of anti-U1 RNP antibody appeared to be less common in SLE-PAH patients; this lack of association is in contrast to prior studies in mixed CTD patients with anti-U1 RNP antibodies in which the prevalence of PAH can be as high as 60%. Further, none of the SLE-PAH patients demonstrated an acute response to vasodilator challenge during RHC, emphasizing that this maneuver does not need to be performed in SLE patients at risk of PAH. Trends toward improved survival in SLE-PAH patients treated with hydroxychloroquine are preliminary and hypothesis-generating but require confirmation in larger clinical studies.

Stephen Mathai, MD, FCCP
Chair

Leena Palwar, MD
Fellow-in-Training Member

References

Hachulla E, Jais X, Cinquetti G, et al. Pulmonary arterial hypertension associated with SLE: Results from the French pulmonary hypertension registry. Chest. 2017 Aug 26. pii: S0012-3692(17)31430-7. doi: 10.1016/j.chest.2017.08.014. [Epub ahead of print]

Chung L, Liu J, Parsons L, et al. Characterization of connective tissue disease-associated pulmonary arterial hypertension from REVEAL: identifying systemic sclerosis as a unique phenotype. Chest. 2010;138:1383-1394.

Shirai Y, Yasuoka H, Okano Y, Takeuchi T, Satoh T, Kuwana M. Clinical characteristics and survival of Japanese patients with connective tissue disease and pulmonary arterial hypertension: a singlecentre cohort. Rheumatology. 2012;51:1846-1854.

Hao YJ, Jiang X, Zhou W, et al. Connective tissue disease-associated pulmonary arterial hypertension in Chinese patients. Eur Respir J. 2014;44: 963-972.

Huang C, Li M, Liu Y, et al. Baseline characteristics and risk factors of pulmonary arterial hypertension in systemic lupus erythematosus patients. Medicine. 2016;95:e2761.

Pérez-Peñate GM, Rúa-Figueroa I, Juliá- Serdá G, et al. Pulmonary arterial hypertension in systemic lupus erythematosus: prevalence and predictors. J Rheumatol. 2016;43:323-329.

Alpert MA, Goldberg SH, Sindem BH, et al. Cardiovascular manifestations of mixed connective tissue disease in adults. Circulation. 1983;63:1182-1193.

CHEST 2017 offers several contests and opportunities to win great prizes! Are you ready to take home the prize?
 

CHEST Events App Game: Click Game

Rules of participation

Are you a VITweep?

Get active on Twitter, and share your latest highlights for #CHEST2017! Sitting in on an interesting session? Having a great time visiting the posters? Let us know! The most active tweeters for the day will receive a special prize!

Share your selfies!

See a selfie spot and take advantage of it! We know there’s more to your trip than lectures and keynote speakers, and we want to see it!

Throughout the convention center, you’ll find many designated areas to snap and share photos of yourself and colleagues! Be sure to find them all and share your images on Twitter or Instagram using our #CHEST2017 hashtag. We’ll choose our favorite photo of the day and reshare your pic­ture with our social media followers. Don’t miss your chance to be featured!
 

Don’t miss out on CHEST Bingo

Take advantage of one of the many opportunities in the Exhibit Hall during CHEST. Play CHEST Bingo daily, starting Monday, October 30, through Wednesday, November 1, for a chance to win a prize!

How to play:

Find your bingo card in the program guide that you will receive during registration. Get each bingo letter to spell out C-H-E-S-T as you visit each of the five sponsors’ booths. You will then have a chance to win a $75 gift certificate to the CHEST bookstore. There will be a winner drawn every night!

Win an iPad®!

This year, attendees will have the opportunity to win a refurbished iPad for playing one of our Simulation Center’s arcade style GAMEs (Games Augmenting Medical Education). Last year, we gave away 15 refurbished iPad 2s; this year, we hope to give away 30 refurbished iPad 2s!

iPads will be awarded for the following:

• One each day for the fastest time on Aspirated!
• One each day for whoever has played the most games and Virtual Patient Tours (VPTs).
• Several for playing the games Peer Pressure and Nodal Nemesis.

Please refer to the program schedule in the CHEST Events app for dates and times of the GAMEs and VPTs.

CHEST 2017 offers several contests and opportunities to win great prizes! Are you ready to take home the prize?
 

CHEST Events App Game: Click Game

Rules of participation

Are you a VITweep?

Get active on Twitter, and share your latest highlights for #CHEST2017! Sitting in on an interesting session? Having a great time visiting the posters? Let us know! The most active tweeters for the day will receive a special prize!

Share your selfies!

See a selfie spot and take advantage of it! We know there’s more to your trip than lectures and keynote speakers, and we want to see it!

Throughout the convention center, you’ll find many designated areas to snap and share photos of yourself and colleagues! Be sure to find them all and share your images on Twitter or Instagram using our #CHEST2017 hashtag. We’ll choose our favorite photo of the day and reshare your pic­ture with our social media followers. Don’t miss your chance to be featured!
 

Don’t miss out on CHEST Bingo

Take advantage of one of the many opportunities in the Exhibit Hall during CHEST. Play CHEST Bingo daily, starting Monday, October 30, through Wednesday, November 1, for a chance to win a prize!

How to play:

Find your bingo card in the program guide that you will receive during registration. Get each bingo letter to spell out C-H-E-S-T as you visit each of the five sponsors’ booths. You will then have a chance to win a $75 gift certificate to the CHEST bookstore. There will be a winner drawn every night!

Win an iPad®!

This year, attendees will have the opportunity to win a refurbished iPad for playing one of our Simulation Center’s arcade style GAMEs (Games Augmenting Medical Education). Last year, we gave away 15 refurbished iPad 2s; this year, we hope to give away 30 refurbished iPad 2s!

iPads will be awarded for the following:

• One each day for the fastest time on Aspirated!
• One each day for whoever has played the most games and Virtual Patient Tours (VPTs).
• Several for playing the games Peer Pressure and Nodal Nemesis.

Please refer to the program schedule in the CHEST Events app for dates and times of the GAMEs and VPTs.

CHEST 2017 offers several contests and opportunities to win great prizes! Are you ready to take home the prize?
 

CHEST Events App Game: Click Game

Rules of participation

Are you a VITweep?

Get active on Twitter, and share your latest highlights for #CHEST2017! Sitting in on an interesting session? Having a great time visiting the posters? Let us know! The most active tweeters for the day will receive a special prize!

Share your selfies!

See a selfie spot and take advantage of it! We know there’s more to your trip than lectures and keynote speakers, and we want to see it!

Throughout the convention center, you’ll find many designated areas to snap and share photos of yourself and colleagues! Be sure to find them all and share your images on Twitter or Instagram using our #CHEST2017 hashtag. We’ll choose our favorite photo of the day and reshare your pic­ture with our social media followers. Don’t miss your chance to be featured!
 

Don’t miss out on CHEST Bingo

Take advantage of one of the many opportunities in the Exhibit Hall during CHEST. Play CHEST Bingo daily, starting Monday, October 30, through Wednesday, November 1, for a chance to win a prize!

How to play:

Find your bingo card in the program guide that you will receive during registration. Get each bingo letter to spell out C-H-E-S-T as you visit each of the five sponsors’ booths. You will then have a chance to win a $75 gift certificate to the CHEST bookstore. There will be a winner drawn every night!

Win an iPad®!

This year, attendees will have the opportunity to win a refurbished iPad for playing one of our Simulation Center’s arcade style GAMEs (Games Augmenting Medical Education). Last year, we gave away 15 refurbished iPad 2s; this year, we hope to give away 30 refurbished iPad 2s!

iPads will be awarded for the following:

• One each day for the fastest time on Aspirated!
• One each day for whoever has played the most games and Virtual Patient Tours (VPTs).
• Several for playing the games Peer Pressure and Nodal Nemesis.

Please refer to the program schedule in the CHEST Events app for dates and times of the GAMEs and VPTs.

John Studdard, MD, FCCP, has been a member of the American College of Chest Physicians for 36 years, and, this November, he will be inaugurated as CHEST President. This will not be Dr. Studdard’s first time in a presidential role for CHEST, as he served as CHEST Foundation President in 2013 and 2014. Currently, Dr. Studdard serves as a pulmonologist at Jackson Pulmonary in Jackson, Mississippi. Being a physician and being as heavily involved with an organization as Dr. Studdard is takes a lot of prioritizing, hard work, and dedication. Get to know CHEST’s new President through this interview.

Born and raised in Mississippi, Dr. Studdard says there were four factors that inspired him to become a physician:

1. I have always loved people and working with them, and I always admired the respect that physicians received in my community.

What are some of the biggest challenges you have encountered throughout your career?

Private practice makes you gain more independence and autonomy; you have to become more agile, more efficient, and you have awfully big workloads. However, you give up the academic stimulation of being in an academic center. It is a tough discipline in the private practice of medicine to try to stay up to date. Whether going to the CHEST Annual Meeting, reading our journal CHEST, or looking at CHEST education online products, those of us in the clinical practice of pulmonary, critical care, and sleep medicine are more dependent than any group on what our clinical educators write and teach.
 

How do/did you balance work and your personal life?

We are busy in practice, particularly when taking on volunteer opportunities, and that time comes out of something: time with family, hobbies, it has to come from somewhere. But it is not unique to those of us in medicine. My daughter is a 33-year-old mother to a 20-month-old beautiful granddaughter of ours and is pregnant with another child, and she and her husband both work full time. Our son and his wife also both work and must find ways to balance work/life issues. So work-life balance, particularly in today’s world, is more difficult than ever for everyone. I am blessed that my wife is the daughter of a general surgeon, and she understood a little bit about stressors in a physician’s life – sometimes she seems to understand more than others—she is a unique person. Work-life balance is all about priorities – our priority was our family. We spent a ton of time with our children, great vacations, rarely missed a program or ballgame (there were lots of them), and frequently that involved going to work early in the morning, coming home early in the evening, and going back to the hospital to finish up late at night. A lot of being a good parent is being lucky. We either did a lot of things right, or were lucky, or a combination of both, because I think our kids turned out pretty darn well.
 

What has been your favorite project throughout your involvement with CHEST?

Early in my days as a member of CHEST, a mentor of mine from training at the Mayo Clinic, Dr. Doug Gracey, gave me the opportunity to join the CHEST Government Relations Committee, which he chaired. After a few years, I was given the opportunity to serve as its Chair. We became heavily involved in the tobacco wars, as some people called them. Our Attorney General in Mississippi at the time, Mike Moore, and a plaintiff’s attorney in Mississippi, Dick Scruggs, whom I knew from some work I had done from the defense side of asbestos litigation, took a lead role in the Attorney General’s Master Settlement - a group of attorney generals suing the tobacco industry (basically, state’s Medicaid was suing the tobacco industry for reimbursement of funds). It was a completely different approach. The tobacco industry turned its nose up at it at first – they did not think it had a chance to fly, but it did. CHEST got involved early on, and then a big a group of people, including Tobacco Free Kids, the American Cancer Society, and many others in the public health space, got involved. CHEST represented the public health community during part of the negotiations that led to the Attorney General’s Master Settlement. We should be very proud of the role CHEST played in this critical public health effort. If I can look back at my time spent in CHEST leadership, and see it as fondly as I do when I look back at my time just being a part of our CHEST Foundation, I will feel incredibly fulfilled.
 

What made you want to be President of CHEST?

I believe it is always important to give back to the people who gave you something. CHEST has given me a ton over the last 36 years, so giving back to CHEST is easy.
 

What are you looking forward to as President of CHEST?

On a personal level, I am looking forward to what we are doing right now, meeting new people, and learning from young people.

Because of my background and upbringing, I have a passion for diversity and inclusion; I think we need to continue to talk about, learn about, care about, be open about, and be transparent about diversity of thought, inclusion, and care disparity. The word “diversity” means something different to every person, and, for that, we have to have respect.

As Dr. Studdard prepares to take on his new role in CHEST leadership this October, he is optimistic about what the future will bring and about the things that he will learn. He considers himself incredibly lucky to be in the position that he is in, and he values each relationship he has made during his involvement with CHEST. He is looking forward to all that is in store during his time as President. He left us with a quote from Wyatt Cooper:

“The only immortality we can be sure of is that part of ourselves we invest in others—the contribution we make to the totality of man, the knowledge we have shared, the truths we have found, the causes we have served, the lessons we have lived.”

John Studdard, MD, FCCP, has been a member of the American College of Chest Physicians for 36 years, and, this November, he will be inaugurated as CHEST President. This will not be Dr. Studdard’s first time in a presidential role for CHEST, as he served as CHEST Foundation President in 2013 and 2014. Currently, Dr. Studdard serves as a pulmonologist at Jackson Pulmonary in Jackson, Mississippi. Being a physician and being as heavily involved with an organization as Dr. Studdard is takes a lot of prioritizing, hard work, and dedication. Get to know CHEST’s new President through this interview.

Born and raised in Mississippi, Dr. Studdard says there were four factors that inspired him to become a physician:

1. I have always loved people and working with them, and I always admired the respect that physicians received in my community.

What are some of the biggest challenges you have encountered throughout your career?

Private practice makes you gain more independence and autonomy; you have to become more agile, more efficient, and you have awfully big workloads. However, you give up the academic stimulation of being in an academic center. It is a tough discipline in the private practice of medicine to try to stay up to date. Whether going to the CHEST Annual Meeting, reading our journal CHEST, or looking at CHEST education online products, those of us in the clinical practice of pulmonary, critical care, and sleep medicine are more dependent than any group on what our clinical educators write and teach.
 

How do/did you balance work and your personal life?

We are busy in practice, particularly when taking on volunteer opportunities, and that time comes out of something: time with family, hobbies, it has to come from somewhere. But it is not unique to those of us in medicine. My daughter is a 33-year-old mother to a 20-month-old beautiful granddaughter of ours and is pregnant with another child, and she and her husband both work full time. Our son and his wife also both work and must find ways to balance work/life issues. So work-life balance, particularly in today’s world, is more difficult than ever for everyone. I am blessed that my wife is the daughter of a general surgeon, and she understood a little bit about stressors in a physician’s life – sometimes she seems to understand more than others—she is a unique person. Work-life balance is all about priorities – our priority was our family. We spent a ton of time with our children, great vacations, rarely missed a program or ballgame (there were lots of them), and frequently that involved going to work early in the morning, coming home early in the evening, and going back to the hospital to finish up late at night. A lot of being a good parent is being lucky. We either did a lot of things right, or were lucky, or a combination of both, because I think our kids turned out pretty darn well.
 

What has been your favorite project throughout your involvement with CHEST?

Early in my days as a member of CHEST, a mentor of mine from training at the Mayo Clinic, Dr. Doug Gracey, gave me the opportunity to join the CHEST Government Relations Committee, which he chaired. After a few years, I was given the opportunity to serve as its Chair. We became heavily involved in the tobacco wars, as some people called them. Our Attorney General in Mississippi at the time, Mike Moore, and a plaintiff’s attorney in Mississippi, Dick Scruggs, whom I knew from some work I had done from the defense side of asbestos litigation, took a lead role in the Attorney General’s Master Settlement - a group of attorney generals suing the tobacco industry (basically, state’s Medicaid was suing the tobacco industry for reimbursement of funds). It was a completely different approach. The tobacco industry turned its nose up at it at first – they did not think it had a chance to fly, but it did. CHEST got involved early on, and then a big a group of people, including Tobacco Free Kids, the American Cancer Society, and many others in the public health space, got involved. CHEST represented the public health community during part of the negotiations that led to the Attorney General’s Master Settlement. We should be very proud of the role CHEST played in this critical public health effort. If I can look back at my time spent in CHEST leadership, and see it as fondly as I do when I look back at my time just being a part of our CHEST Foundation, I will feel incredibly fulfilled.
 

What made you want to be President of CHEST?

I believe it is always important to give back to the people who gave you something. CHEST has given me a ton over the last 36 years, so giving back to CHEST is easy.
 

What are you looking forward to as President of CHEST?

On a personal level, I am looking forward to what we are doing right now, meeting new people, and learning from young people.

Because of my background and upbringing, I have a passion for diversity and inclusion; I think we need to continue to talk about, learn about, care about, be open about, and be transparent about diversity of thought, inclusion, and care disparity. The word “diversity” means something different to every person, and, for that, we have to have respect.

As Dr. Studdard prepares to take on his new role in CHEST leadership this October, he is optimistic about what the future will bring and about the things that he will learn. He considers himself incredibly lucky to be in the position that he is in, and he values each relationship he has made during his involvement with CHEST. He is looking forward to all that is in store during his time as President. He left us with a quote from Wyatt Cooper:

“The only immortality we can be sure of is that part of ourselves we invest in others—the contribution we make to the totality of man, the knowledge we have shared, the truths we have found, the causes we have served, the lessons we have lived.”

John Studdard, MD, FCCP, has been a member of the American College of Chest Physicians for 36 years, and, this November, he will be inaugurated as CHEST President. This will not be Dr. Studdard’s first time in a presidential role for CHEST, as he served as CHEST Foundation President in 2013 and 2014. Currently, Dr. Studdard serves as a pulmonologist at Jackson Pulmonary in Jackson, Mississippi. Being a physician and being as heavily involved with an organization as Dr. Studdard is takes a lot of prioritizing, hard work, and dedication. Get to know CHEST’s new President through this interview.

Born and raised in Mississippi, Dr. Studdard says there were four factors that inspired him to become a physician:

1. I have always loved people and working with them, and I always admired the respect that physicians received in my community.

What are some of the biggest challenges you have encountered throughout your career?

Private practice makes you gain more independence and autonomy; you have to become more agile, more efficient, and you have awfully big workloads. However, you give up the academic stimulation of being in an academic center. It is a tough discipline in the private practice of medicine to try to stay up to date. Whether going to the CHEST Annual Meeting, reading our journal CHEST, or looking at CHEST education online products, those of us in the clinical practice of pulmonary, critical care, and sleep medicine are more dependent than any group on what our clinical educators write and teach.
 

How do/did you balance work and your personal life?

We are busy in practice, particularly when taking on volunteer opportunities, and that time comes out of something: time with family, hobbies, it has to come from somewhere. But it is not unique to those of us in medicine. My daughter is a 33-year-old mother to a 20-month-old beautiful granddaughter of ours and is pregnant with another child, and she and her husband both work full time. Our son and his wife also both work and must find ways to balance work/life issues. So work-life balance, particularly in today’s world, is more difficult than ever for everyone. I am blessed that my wife is the daughter of a general surgeon, and she understood a little bit about stressors in a physician’s life – sometimes she seems to understand more than others—she is a unique person. Work-life balance is all about priorities – our priority was our family. We spent a ton of time with our children, great vacations, rarely missed a program or ballgame (there were lots of them), and frequently that involved going to work early in the morning, coming home early in the evening, and going back to the hospital to finish up late at night. A lot of being a good parent is being lucky. We either did a lot of things right, or were lucky, or a combination of both, because I think our kids turned out pretty darn well.
 

What has been your favorite project throughout your involvement with CHEST?

Early in my days as a member of CHEST, a mentor of mine from training at the Mayo Clinic, Dr. Doug Gracey, gave me the opportunity to join the CHEST Government Relations Committee, which he chaired. After a few years, I was given the opportunity to serve as its Chair. We became heavily involved in the tobacco wars, as some people called them. Our Attorney General in Mississippi at the time, Mike Moore, and a plaintiff’s attorney in Mississippi, Dick Scruggs, whom I knew from some work I had done from the defense side of asbestos litigation, took a lead role in the Attorney General’s Master Settlement - a group of attorney generals suing the tobacco industry (basically, state’s Medicaid was suing the tobacco industry for reimbursement of funds). It was a completely different approach. The tobacco industry turned its nose up at it at first – they did not think it had a chance to fly, but it did. CHEST got involved early on, and then a big a group of people, including Tobacco Free Kids, the American Cancer Society, and many others in the public health space, got involved. CHEST represented the public health community during part of the negotiations that led to the Attorney General’s Master Settlement. We should be very proud of the role CHEST played in this critical public health effort. If I can look back at my time spent in CHEST leadership, and see it as fondly as I do when I look back at my time just being a part of our CHEST Foundation, I will feel incredibly fulfilled.
 

What made you want to be President of CHEST?

I believe it is always important to give back to the people who gave you something. CHEST has given me a ton over the last 36 years, so giving back to CHEST is easy.
 

What are you looking forward to as President of CHEST?

On a personal level, I am looking forward to what we are doing right now, meeting new people, and learning from young people.

Because of my background and upbringing, I have a passion for diversity and inclusion; I think we need to continue to talk about, learn about, care about, be open about, and be transparent about diversity of thought, inclusion, and care disparity. The word “diversity” means something different to every person, and, for that, we have to have respect.

As Dr. Studdard prepares to take on his new role in CHEST leadership this October, he is optimistic about what the future will bring and about the things that he will learn. He considers himself incredibly lucky to be in the position that he is in, and he values each relationship he has made during his involvement with CHEST. He is looking forward to all that is in store during his time as President. He left us with a quote from Wyatt Cooper:

“The only immortality we can be sure of is that part of ourselves we invest in others—the contribution we make to the totality of man, the knowledge we have shared, the truths we have found, the causes we have served, the lessons we have lived.”

Be sure to check out our ever-growing presence at CHEST 2017, showcasing the numerous ways we support CHEST members, patients, and the community. Have time for a break or interested in networking with leaders in CHEST medicine? Stop by one of our many open invitation activities listed below to learn more about how the CHEST Foundation can support you in your efforts to champion lung health through clinical research grants, community service, and patient education.
 

SATURDAY OCTOBER 28

2:00 PM – 4:00 PM (Open Invitation)

SUNDAY OCTOBER 29

9:00 AM - 5:00 PM
Donor Lounge
Convention Center, 803B



3:15 PM - 4:15 PM
Foundation Session: Severe Asthma Care at Its Best: Shared Decision Making
Convention Center, 716A



4:30 PM - 5:30 PM
Foundation Session: No Money, No Mission: Tips for Getting Your Grant Funded
Convention Center, 716B
 

MONDAY OCTOBER 30

9:00 AM - 5:00 PM

TUESDAY OCTOBER 31

9:00 AM - 5:00 PM
Donor Lounge
Convention Center, 803B
 

WEDNESDAY NOVEMBER 1

9:00 AM - 12:00 PM
Donor Lounge
Convention Center, 803B
 

ADD YOUR VOICE

and champion lung health at the Actelion Booth #1322. For every addition to the graffiti wall, Actelion will donate $25 to the CHEST Foundation.
 

Thank you for your support of the CHEST Foundation and our mission of championing lung health!

Be sure to check out our ever-growing presence at CHEST 2017, showcasing the numerous ways we support CHEST members, patients, and the community. Have time for a break or interested in networking with leaders in CHEST medicine? Stop by one of our many open invitation activities listed below to learn more about how the CHEST Foundation can support you in your efforts to champion lung health through clinical research grants, community service, and patient education.
 

SATURDAY OCTOBER 28

2:00 PM – 4:00 PM (Open Invitation)

SUNDAY OCTOBER 29

9:00 AM - 5:00 PM
Donor Lounge
Convention Center, 803B



3:15 PM - 4:15 PM
Foundation Session: Severe Asthma Care at Its Best: Shared Decision Making
Convention Center, 716A



4:30 PM - 5:30 PM
Foundation Session: No Money, No Mission: Tips for Getting Your Grant Funded
Convention Center, 716B
 

MONDAY OCTOBER 30

9:00 AM - 5:00 PM

TUESDAY OCTOBER 31

9:00 AM - 5:00 PM
Donor Lounge
Convention Center, 803B
 

WEDNESDAY NOVEMBER 1

9:00 AM - 12:00 PM
Donor Lounge
Convention Center, 803B
 

ADD YOUR VOICE

and champion lung health at the Actelion Booth #1322. For every addition to the graffiti wall, Actelion will donate $25 to the CHEST Foundation.
 

Thank you for your support of the CHEST Foundation and our mission of championing lung health!

Be sure to check out our ever-growing presence at CHEST 2017, showcasing the numerous ways we support CHEST members, patients, and the community. Have time for a break or interested in networking with leaders in CHEST medicine? Stop by one of our many open invitation activities listed below to learn more about how the CHEST Foundation can support you in your efforts to champion lung health through clinical research grants, community service, and patient education.
 

SATURDAY OCTOBER 28

2:00 PM – 4:00 PM (Open Invitation)

SUNDAY OCTOBER 29

9:00 AM - 5:00 PM
Donor Lounge
Convention Center, 803B



3:15 PM - 4:15 PM
Foundation Session: Severe Asthma Care at Its Best: Shared Decision Making
Convention Center, 716A



4:30 PM - 5:30 PM
Foundation Session: No Money, No Mission: Tips for Getting Your Grant Funded
Convention Center, 716B
 

MONDAY OCTOBER 30

9:00 AM - 5:00 PM

TUESDAY OCTOBER 31

9:00 AM - 5:00 PM
Donor Lounge
Convention Center, 803B
 

WEDNESDAY NOVEMBER 1

9:00 AM - 12:00 PM
Donor Lounge
Convention Center, 803B
 

ADD YOUR VOICE

and champion lung health at the Actelion Booth #1322. For every addition to the graffiti wall, Actelion will donate $25 to the CHEST Foundation.
 

Thank you for your support of the CHEST Foundation and our mission of championing lung health!

Blood transfusions are common in critically ill patients; two in five adults admitted to an ICU receive at least one transfusion during their hospitalization (Corwin HL, et al. Crit Care Med. 2004;32[1]:39). Recently, there has been growing concern about the potential dangers involved with prolonged blood storage. Several provocative observational and retrospective studies found that prolonged storage time (ie, the age of the blood being transfused) negatively affects clinical outcomes (Wang D, et al. Transfusion. 2012;52[6]:1184). But now, some newly published trials on blood transfusion practice, including one published in late September 2017 (Cooper DJ, et al. N Engl J Med. Published online, September 27, 2017) seem to debunk much of this literature. Was all of the concern about age of blood overblown?

The appeal of “fresh” blood is intuitive. As consumers, we’re conditioned that the fresher the better. Fresh food tastes best. Carbonated beverages go “flat” over time. The newest iPhone® device is superior to your old one. So, of course, it follows that fresh blood is also better for your health than older blood.
But, in order to have a viable transfusion service, blood has to be stored. Blood is a scarce resource, and blood banks need to keep an adequate supply on hand for expected clinical necessities, as well as for emergencies. Donors can’t be on standby, waiting in the hospital to provide immediate whole blood transfusion. Also, blood needs to be tested for infections and for potential interactions with the patient, and whole blood must be broken down into individual components for transfusion. All of this requires time and storage.

Vlad/Fotolia

Dr. Carroll is Professor of Pediatrics, University of Connecticut, Division of Critical Care, Connecticut Children’s Medical Center, Hartford, Connecticut.

Blood transfusions are common in critically ill patients; two in five adults admitted to an ICU receive at least one transfusion during their hospitalization (Corwin HL, et al. Crit Care Med. 2004;32[1]:39). Recently, there has been growing concern about the potential dangers involved with prolonged blood storage. Several provocative observational and retrospective studies found that prolonged storage time (ie, the age of the blood being transfused) negatively affects clinical outcomes (Wang D, et al. Transfusion. 2012;52[6]:1184). But now, some newly published trials on blood transfusion practice, including one published in late September 2017 (Cooper DJ, et al. N Engl J Med. Published online, September 27, 2017) seem to debunk much of this literature. Was all of the concern about age of blood overblown?

The appeal of “fresh” blood is intuitive. As consumers, we’re conditioned that the fresher the better. Fresh food tastes best. Carbonated beverages go “flat” over time. The newest iPhone® device is superior to your old one. So, of course, it follows that fresh blood is also better for your health than older blood.
But, in order to have a viable transfusion service, blood has to be stored. Blood is a scarce resource, and blood banks need to keep an adequate supply on hand for expected clinical necessities, as well as for emergencies. Donors can’t be on standby, waiting in the hospital to provide immediate whole blood transfusion. Also, blood needs to be tested for infections and for potential interactions with the patient, and whole blood must be broken down into individual components for transfusion. All of this requires time and storage.

Vlad/Fotolia

Dr. Carroll is Professor of Pediatrics, University of Connecticut, Division of Critical Care, Connecticut Children’s Medical Center, Hartford, Connecticut.

Blood transfusions are common in critically ill patients; two in five adults admitted to an ICU receive at least one transfusion during their hospitalization (Corwin HL, et al. Crit Care Med. 2004;32[1]:39). Recently, there has been growing concern about the potential dangers involved with prolonged blood storage. Several provocative observational and retrospective studies found that prolonged storage time (ie, the age of the blood being transfused) negatively affects clinical outcomes (Wang D, et al. Transfusion. 2012;52[6]:1184). But now, some newly published trials on blood transfusion practice, including one published in late September 2017 (Cooper DJ, et al. N Engl J Med. Published online, September 27, 2017) seem to debunk much of this literature. Was all of the concern about age of blood overblown?

The appeal of “fresh” blood is intuitive. As consumers, we’re conditioned that the fresher the better. Fresh food tastes best. Carbonated beverages go “flat” over time. The newest iPhone® device is superior to your old one. So, of course, it follows that fresh blood is also better for your health than older blood.
But, in order to have a viable transfusion service, blood has to be stored. Blood is a scarce resource, and blood banks need to keep an adequate supply on hand for expected clinical necessities, as well as for emergencies. Donors can’t be on standby, waiting in the hospital to provide immediate whole blood transfusion. Also, blood needs to be tested for infections and for potential interactions with the patient, and whole blood must be broken down into individual components for transfusion. All of this requires time and storage.

Vlad/Fotolia

Dr. Carroll is Professor of Pediatrics, University of Connecticut, Division of Critical Care, Connecticut Children’s Medical Center, Hartford, Connecticut.

A Multicenter, Randomized Trial of Ramped Position vs Sniffing Position During Endotracheal Intubation of Critically Ill Adults.

By Dr. M. W. Semler, et al.

Sleep Apnea and Hypertension: Are There Sex Differences? The Vitoria Sleep Cohort.

By Dr. I. Cano-Pumarega, et al.

A Multicenter, Randomized Trial of Ramped Position vs Sniffing Position During Endotracheal Intubation of Critically Ill Adults.

By Dr. M. W. Semler, et al.

Sleep Apnea and Hypertension: Are There Sex Differences? The Vitoria Sleep Cohort.

By Dr. I. Cano-Pumarega, et al.

A Multicenter, Randomized Trial of Ramped Position vs Sniffing Position During Endotracheal Intubation of Critically Ill Adults.

By Dr. M. W. Semler, et al.

Sleep Apnea and Hypertension: Are There Sex Differences? The Vitoria Sleep Cohort.

By Dr. I. Cano-Pumarega, et al.

There will be a number of changes to Current Procedural Terminology (CPT®) codes of interest to pulmonary/critical care providers in January 2018. A thorough understanding of these changes is important for appropriate coding and reimbursement for the services described by these codes.

There are two changes in the CPT codes for bronchoscopy involving 31645 and 31646. CPT code 31645 describes a therapeutic bronchoscopy, eg, removal of viscous, copious or tenacious secretions from the airway. It had previously included wording that suggested it was used for abscess drainage, and this has been removed. If a therapeutic bronchoscopy procedure is repeated during the same hospital stay, then CPT code 31646 should be utilized. If a therapeutic bronchoscopy procedure is performed in the non-hospital setting and later repeated, then CPT code 31645 would be used for both procedures.

CPT code 94620 Pulmonary stress testing; simple (eg, 6-minute walk test, prolonged exercise test for bronchospasm with pre- and post-spirometry and oximetry) has been deleted and replaced by two new codes. CPT code 94617 Exercise test for bronchospasm, including pre- and postspirometry, electrocardiographic recording(s), and pulse oximetry describes the procedure used to assess for exercise-induced bronchospasm. CPT code 94618 Pulmonary stress testing (eg, 6-minute walk test), including measurement of heart rate, oximetry, and oxygen titration, when performed, describes the typical simple pulmonary stress test. After January 1, 2018, if CPT code 94620 is used, the claim will be denied. CPT code 94621 Cardiopulmonary exercise testing, including measurements of minute ventilation, CO₂ production, O₂ uptake, and electrocardiographic recordings has been reworded to better describe the procedure of cardiopulmonary exercise testing. Additionally, there are numerous parentheticals appended that list the CPT codes that may not be used in conjunction with 94617, 94618, and 94621. Please refer to the 2018 CPT manual for further information on these exclusions.

There will be a number of changes to Current Procedural Terminology (CPT®) codes of interest to pulmonary/critical care providers in January 2018. A thorough understanding of these changes is important for appropriate coding and reimbursement for the services described by these codes.

There are two changes in the CPT codes for bronchoscopy involving 31645 and 31646. CPT code 31645 describes a therapeutic bronchoscopy, eg, removal of viscous, copious or tenacious secretions from the airway. It had previously included wording that suggested it was used for abscess drainage, and this has been removed. If a therapeutic bronchoscopy procedure is repeated during the same hospital stay, then CPT code 31646 should be utilized. If a therapeutic bronchoscopy procedure is performed in the non-hospital setting and later repeated, then CPT code 31645 would be used for both procedures.

CPT code 94620 Pulmonary stress testing; simple (eg, 6-minute walk test, prolonged exercise test for bronchospasm with pre- and post-spirometry and oximetry) has been deleted and replaced by two new codes. CPT code 94617 Exercise test for bronchospasm, including pre- and postspirometry, electrocardiographic recording(s), and pulse oximetry describes the procedure used to assess for exercise-induced bronchospasm. CPT code 94618 Pulmonary stress testing (eg, 6-minute walk test), including measurement of heart rate, oximetry, and oxygen titration, when performed, describes the typical simple pulmonary stress test. After January 1, 2018, if CPT code 94620 is used, the claim will be denied. CPT code 94621 Cardiopulmonary exercise testing, including measurements of minute ventilation, CO₂ production, O₂ uptake, and electrocardiographic recordings has been reworded to better describe the procedure of cardiopulmonary exercise testing. Additionally, there are numerous parentheticals appended that list the CPT codes that may not be used in conjunction with 94617, 94618, and 94621. Please refer to the 2018 CPT manual for further information on these exclusions.

There will be a number of changes to Current Procedural Terminology (CPT®) codes of interest to pulmonary/critical care providers in January 2018. A thorough understanding of these changes is important for appropriate coding and reimbursement for the services described by these codes.

There are two changes in the CPT codes for bronchoscopy involving 31645 and 31646. CPT code 31645 describes a therapeutic bronchoscopy, eg, removal of viscous, copious or tenacious secretions from the airway. It had previously included wording that suggested it was used for abscess drainage, and this has been removed. If a therapeutic bronchoscopy procedure is repeated during the same hospital stay, then CPT code 31646 should be utilized. If a therapeutic bronchoscopy procedure is performed in the non-hospital setting and later repeated, then CPT code 31645 would be used for both procedures.

CPT code 94620 Pulmonary stress testing; simple (eg, 6-minute walk test, prolonged exercise test for bronchospasm with pre- and post-spirometry and oximetry) has been deleted and replaced by two new codes. CPT code 94617 Exercise test for bronchospasm, including pre- and postspirometry, electrocardiographic recording(s), and pulse oximetry describes the procedure used to assess for exercise-induced bronchospasm. CPT code 94618 Pulmonary stress testing (eg, 6-minute walk test), including measurement of heart rate, oximetry, and oxygen titration, when performed, describes the typical simple pulmonary stress test. After January 1, 2018, if CPT code 94620 is used, the claim will be denied. CPT code 94621 Cardiopulmonary exercise testing, including measurements of minute ventilation, CO₂ production, O₂ uptake, and electrocardiographic recordings has been reworded to better describe the procedure of cardiopulmonary exercise testing. Additionally, there are numerous parentheticals appended that list the CPT codes that may not be used in conjunction with 94617, 94618, and 94621. Please refer to the 2018 CPT manual for further information on these exclusions.

The definition of mild obstructive sleep apnea (OSA) has varied over the years depending upon several factors, but based upon all definitions, it is highly prevalent. Depending upon presence of symptoms and gender, the prevalence may be as high 28% in men and 26% in women. (Young et al. N Engl J Med. 1993;328:1230).

Typically, a combination of symptoms and frequency of respiratory events is required to make the diagnosis. Based upon the International Classification of Sleep Disorders-3rd edition (ICSD-3), the threshold apnea hypopnea index (AHI) for diagnosis depends upon the presence or absence of symptoms. If an individual has no symptoms, an AHI of 15 events per hour or more is required to make a diagnosis of OSA. However, there are several concerns about whether or not an individual may be “symptomatic.” This is most relevant when driving privileges may be at risk, such as with a commercial drivers’ licensing.

The presence of other comorbid disease can be used as criteria, including hypertension, mood disorder, cognitive dysfunction, coronary artery disease, stroke, congestive heart failure, atrial fibrillation, and type 2 diabetes mellitus. If no signs, symptoms, or comorbid diseases are present, then an AHI greater than 15 events per hour or more is required to make the diagnosis of OSA (Chowdrui et al. Am J Respir Crit Care Med. 2016;193:e37).

There is still debate regarding the association of mild OSA and cardiovascular disease and whether treatment may prevent or reduce cardiovascular outcomes. The four main clinical outcomes typically reported are hypertension, cardiovascular events, cardiovascular and all-cause mortality, and arrhythmias.

A large clinical cohort of patients referred for sleep studies showed no association of mild OSA with different composite outcomes. Kendzerska and colleagues evaluated a composite outcome (myocardial infarction, stroke, CHF, revascularization procedures, or death from any cause) during a median follow-up of 68 months. No association of mild OSA with the composite cardiovascular endpoint was identified compared with those without OSA (Kendzerska et al. PLoS Med. 2014;11[2]:e1001599). Only one population-based study (MrOS Sleep Study) looked at the association between mild OSA and nocturnal arrhythmias in elderly men. The study did not find an increased risk for atrial fibrillation or complex ventricular ectopy in patients with mild OSA vs no OSA (Mehra et al. Arch Intern Med. 2009; 169:1147).

Several cohort studies have reported mild OSA is not associated with increased cardiovascular mortality. In the 18-year follow-up of the Wisconsin Cohort Study, it was found that mild OSA was not associated with cardiovascular mortality (HR, 1.8; 95% CI, 0.7–4.9). All-cause mortality was also not significantly increased in the mild OSA group compared with the no-OSA group in the Wisconsin cohort after 8 years of follow-up (adjusted HR, 1.6; 95% CI, 0.8–2.8). In summary, compared with subjects without OSA, available evidence from population-based longitudinal studies indicates that mild OSA is not associated with increased cardiovascular or all-cause mortality.

Does treatment of mild OSA vs no treatment change cardiovascular or mortality outcomes? This is still debated with no definitive answer. There have been several studies that have examined different therapies for OSA to reduce cardiovascular events. Typical events include coronary artery disease, hypertension, heart failure, stroke, arrhythmias, and cardiovascular disease-related mortality. However, most studies have examined cohorts with moderate to severe OSA with limited evaluation in the mild OSA category.

An observational study evaluated the effects of CPAP specifically in patients with mild OSA. There was no significant difference in the risk of developing hypertension among those patients ineligible for CPAP therapy, active on therapy, or those who declined therapy (Marin et al. JAMA. 2012; 307:2169). In contrast, a retrospective longitudinal cohort with normal blood pressure at baseline (mild OSA without preexisting cardiovascular disease, diabetes, or hyperlipidemia) did show decrease in mean arterial blood pressure of 2 mm Hg in the treatment group (Jaimchariyatam et al. Sleep Med. 2010;11:837). The MOSAIC trial was a multicenter randomized trial that evaluated the effects of CPAP on cardiac function in minimally symptomatic patients with OSA. The use of CPAP reduced the oxygen desaturation index (ODI) and Epworth Sleepiness Scale values. However, 6 months of therapy did not change functional or structural parameters measured by echocardiogram or cardiac magnetic resonance scanning in patients with mild to moderate OSA (Craig et al. J Clin Sleep Med. 2015;11[9]:967). A single retrospective study reported the effects of CPAP in patients with mild OSA and all-cause mortality. The study compared treatment with patients using CPAP more than 4 hours vs a combined group of nonadherent and those who refused therapy (Hudgel et al. J Clin Sleep Med. 2012;8:9). There was no significant difference in all-cause mortality in the two groups. However, this study did not analyze the impact of therapy on cardiovascular-specific mortality.

To date, there have been no studies that have evaluated the impact of treatment of mild OSA on cardiovascular events, arrhythmias, or stroke. In addition, there have been no randomized studies assessing treatment of mild OSA on fatal and nonfatal cardiovascular events. There is inadequate evidence regarding the effect of mild OSA on elevated blood pressure, neurologic cognition, quality of life, and cardiovascular consequences. Future research is needed to investigate the impact of mild OSA on these outcomes.

In summary, mild OSA is a very prevalent disease but the association with hypertension remains unclear and the literature to date suggests no association with other cardiovascular outcomes. In addition, no clear prevention of cardiovascular outcomes with treatment has been proven in the setting of mild OSA.

Dr. Duthuluru is Assistant Professor, Dr. Nazir is Assistant Professor, and Dr. Stevens is Associate Professor at the University of Kansas Medical Center.

The definition of mild obstructive sleep apnea (OSA) has varied over the years depending upon several factors, but based upon all definitions, it is highly prevalent. Depending upon presence of symptoms and gender, the prevalence may be as high 28% in men and 26% in women. (Young et al. N Engl J Med. 1993;328:1230).

Typically, a combination of symptoms and frequency of respiratory events is required to make the diagnosis. Based upon the International Classification of Sleep Disorders-3rd edition (ICSD-3), the threshold apnea hypopnea index (AHI) for diagnosis depends upon the presence or absence of symptoms. If an individual has no symptoms, an AHI of 15 events per hour or more is required to make a diagnosis of OSA. However, there are several concerns about whether or not an individual may be “symptomatic.” This is most relevant when driving privileges may be at risk, such as with a commercial drivers’ licensing.

The presence of other comorbid disease can be used as criteria, including hypertension, mood disorder, cognitive dysfunction, coronary artery disease, stroke, congestive heart failure, atrial fibrillation, and type 2 diabetes mellitus. If no signs, symptoms, or comorbid diseases are present, then an AHI greater than 15 events per hour or more is required to make the diagnosis of OSA (Chowdrui et al. Am J Respir Crit Care Med. 2016;193:e37).

There is still debate regarding the association of mild OSA and cardiovascular disease and whether treatment may prevent or reduce cardiovascular outcomes. The four main clinical outcomes typically reported are hypertension, cardiovascular events, cardiovascular and all-cause mortality, and arrhythmias.

A large clinical cohort of patients referred for sleep studies showed no association of mild OSA with different composite outcomes. Kendzerska and colleagues evaluated a composite outcome (myocardial infarction, stroke, CHF, revascularization procedures, or death from any cause) during a median follow-up of 68 months. No association of mild OSA with the composite cardiovascular endpoint was identified compared with those without OSA (Kendzerska et al. PLoS Med. 2014;11[2]:e1001599). Only one population-based study (MrOS Sleep Study) looked at the association between mild OSA and nocturnal arrhythmias in elderly men. The study did not find an increased risk for atrial fibrillation or complex ventricular ectopy in patients with mild OSA vs no OSA (Mehra et al. Arch Intern Med. 2009; 169:1147).

Several cohort studies have reported mild OSA is not associated with increased cardiovascular mortality. In the 18-year follow-up of the Wisconsin Cohort Study, it was found that mild OSA was not associated with cardiovascular mortality (HR, 1.8; 95% CI, 0.7–4.9). All-cause mortality was also not significantly increased in the mild OSA group compared with the no-OSA group in the Wisconsin cohort after 8 years of follow-up (adjusted HR, 1.6; 95% CI, 0.8–2.8). In summary, compared with subjects without OSA, available evidence from population-based longitudinal studies indicates that mild OSA is not associated with increased cardiovascular or all-cause mortality.

Does treatment of mild OSA vs no treatment change cardiovascular or mortality outcomes? This is still debated with no definitive answer. There have been several studies that have examined different therapies for OSA to reduce cardiovascular events. Typical events include coronary artery disease, hypertension, heart failure, stroke, arrhythmias, and cardiovascular disease-related mortality. However, most studies have examined cohorts with moderate to severe OSA with limited evaluation in the mild OSA category.

An observational study evaluated the effects of CPAP specifically in patients with mild OSA. There was no significant difference in the risk of developing hypertension among those patients ineligible for CPAP therapy, active on therapy, or those who declined therapy (Marin et al. JAMA. 2012; 307:2169). In contrast, a retrospective longitudinal cohort with normal blood pressure at baseline (mild OSA without preexisting cardiovascular disease, diabetes, or hyperlipidemia) did show decrease in mean arterial blood pressure of 2 mm Hg in the treatment group (Jaimchariyatam et al. Sleep Med. 2010;11:837). The MOSAIC trial was a multicenter randomized trial that evaluated the effects of CPAP on cardiac function in minimally symptomatic patients with OSA. The use of CPAP reduced the oxygen desaturation index (ODI) and Epworth Sleepiness Scale values. However, 6 months of therapy did not change functional or structural parameters measured by echocardiogram or cardiac magnetic resonance scanning in patients with mild to moderate OSA (Craig et al. J Clin Sleep Med. 2015;11[9]:967). A single retrospective study reported the effects of CPAP in patients with mild OSA and all-cause mortality. The study compared treatment with patients using CPAP more than 4 hours vs a combined group of nonadherent and those who refused therapy (Hudgel et al. J Clin Sleep Med. 2012;8:9). There was no significant difference in all-cause mortality in the two groups. However, this study did not analyze the impact of therapy on cardiovascular-specific mortality.

To date, there have been no studies that have evaluated the impact of treatment of mild OSA on cardiovascular events, arrhythmias, or stroke. In addition, there have been no randomized studies assessing treatment of mild OSA on fatal and nonfatal cardiovascular events. There is inadequate evidence regarding the effect of mild OSA on elevated blood pressure, neurologic cognition, quality of life, and cardiovascular consequences. Future research is needed to investigate the impact of mild OSA on these outcomes.

In summary, mild OSA is a very prevalent disease but the association with hypertension remains unclear and the literature to date suggests no association with other cardiovascular outcomes. In addition, no clear prevention of cardiovascular outcomes with treatment has been proven in the setting of mild OSA.

Dr. Duthuluru is Assistant Professor, Dr. Nazir is Assistant Professor, and Dr. Stevens is Associate Professor at the University of Kansas Medical Center.

The definition of mild obstructive sleep apnea (OSA) has varied over the years depending upon several factors, but based upon all definitions, it is highly prevalent. Depending upon presence of symptoms and gender, the prevalence may be as high 28% in men and 26% in women. (Young et al. N Engl J Med. 1993;328:1230).

Typically, a combination of symptoms and frequency of respiratory events is required to make the diagnosis. Based upon the International Classification of Sleep Disorders-3rd edition (ICSD-3), the threshold apnea hypopnea index (AHI) for diagnosis depends upon the presence or absence of symptoms. If an individual has no symptoms, an AHI of 15 events per hour or more is required to make a diagnosis of OSA. However, there are several concerns about whether or not an individual may be “symptomatic.” This is most relevant when driving privileges may be at risk, such as with a commercial drivers’ licensing.

The presence of other comorbid disease can be used as criteria, including hypertension, mood disorder, cognitive dysfunction, coronary artery disease, stroke, congestive heart failure, atrial fibrillation, and type 2 diabetes mellitus. If no signs, symptoms, or comorbid diseases are present, then an AHI greater than 15 events per hour or more is required to make the diagnosis of OSA (Chowdrui et al. Am J Respir Crit Care Med. 2016;193:e37).

There is still debate regarding the association of mild OSA and cardiovascular disease and whether treatment may prevent or reduce cardiovascular outcomes. The four main clinical outcomes typically reported are hypertension, cardiovascular events, cardiovascular and all-cause mortality, and arrhythmias.

A large clinical cohort of patients referred for sleep studies showed no association of mild OSA with different composite outcomes. Kendzerska and colleagues evaluated a composite outcome (myocardial infarction, stroke, CHF, revascularization procedures, or death from any cause) during a median follow-up of 68 months. No association of mild OSA with the composite cardiovascular endpoint was identified compared with those without OSA (Kendzerska et al. PLoS Med. 2014;11[2]:e1001599). Only one population-based study (MrOS Sleep Study) looked at the association between mild OSA and nocturnal arrhythmias in elderly men. The study did not find an increased risk for atrial fibrillation or complex ventricular ectopy in patients with mild OSA vs no OSA (Mehra et al. Arch Intern Med. 2009; 169:1147).

Several cohort studies have reported mild OSA is not associated with increased cardiovascular mortality. In the 18-year follow-up of the Wisconsin Cohort Study, it was found that mild OSA was not associated with cardiovascular mortality (HR, 1.8; 95% CI, 0.7–4.9). All-cause mortality was also not significantly increased in the mild OSA group compared with the no-OSA group in the Wisconsin cohort after 8 years of follow-up (adjusted HR, 1.6; 95% CI, 0.8–2.8). In summary, compared with subjects without OSA, available evidence from population-based longitudinal studies indicates that mild OSA is not associated with increased cardiovascular or all-cause mortality.

Does treatment of mild OSA vs no treatment change cardiovascular or mortality outcomes? This is still debated with no definitive answer. There have been several studies that have examined different therapies for OSA to reduce cardiovascular events. Typical events include coronary artery disease, hypertension, heart failure, stroke, arrhythmias, and cardiovascular disease-related mortality. However, most studies have examined cohorts with moderate to severe OSA with limited evaluation in the mild OSA category.

An observational study evaluated the effects of CPAP specifically in patients with mild OSA. There was no significant difference in the risk of developing hypertension among those patients ineligible for CPAP therapy, active on therapy, or those who declined therapy (Marin et al. JAMA. 2012; 307:2169). In contrast, a retrospective longitudinal cohort with normal blood pressure at baseline (mild OSA without preexisting cardiovascular disease, diabetes, or hyperlipidemia) did show decrease in mean arterial blood pressure of 2 mm Hg in the treatment group (Jaimchariyatam et al. Sleep Med. 2010;11:837). The MOSAIC trial was a multicenter randomized trial that evaluated the effects of CPAP on cardiac function in minimally symptomatic patients with OSA. The use of CPAP reduced the oxygen desaturation index (ODI) and Epworth Sleepiness Scale values. However, 6 months of therapy did not change functional or structural parameters measured by echocardiogram or cardiac magnetic resonance scanning in patients with mild to moderate OSA (Craig et al. J Clin Sleep Med. 2015;11[9]:967). A single retrospective study reported the effects of CPAP in patients with mild OSA and all-cause mortality. The study compared treatment with patients using CPAP more than 4 hours vs a combined group of nonadherent and those who refused therapy (Hudgel et al. J Clin Sleep Med. 2012;8:9). There was no significant difference in all-cause mortality in the two groups. However, this study did not analyze the impact of therapy on cardiovascular-specific mortality.

To date, there have been no studies that have evaluated the impact of treatment of mild OSA on cardiovascular events, arrhythmias, or stroke. In addition, there have been no randomized studies assessing treatment of mild OSA on fatal and nonfatal cardiovascular events. There is inadequate evidence regarding the effect of mild OSA on elevated blood pressure, neurologic cognition, quality of life, and cardiovascular consequences. Future research is needed to investigate the impact of mild OSA on these outcomes.

In summary, mild OSA is a very prevalent disease but the association with hypertension remains unclear and the literature to date suggests no association with other cardiovascular outcomes. In addition, no clear prevention of cardiovascular outcomes with treatment has been proven in the setting of mild OSA.

Dr. Duthuluru is Assistant Professor, Dr. Nazir is Assistant Professor, and Dr. Stevens is Associate Professor at the University of Kansas Medical Center.

The CHEST Foundation is proud to announce the winners of the first round of the 2017 NetWorks Challenge! Our first place winner, Home-Based Mechanical Ventilation and Neuromuscular Disease NetWork, and our second place finisher, Women’s Health NetWork, both receive session time at CHEST 2017 on a topic of their choice and two travel grants to help their NetWork members attend CHEST 2017.

The CHEST Foundation is proud to announce the winners of the first round of the 2017 NetWorks Challenge! Our first place winner, Home-Based Mechanical Ventilation and Neuromuscular Disease NetWork, and our second place finisher, Women’s Health NetWork, both receive session time at CHEST 2017 on a topic of their choice and two travel grants to help their NetWork members attend CHEST 2017.

The CHEST Foundation is proud to announce the winners of the first round of the 2017 NetWorks Challenge! Our first place winner, Home-Based Mechanical Ventilation and Neuromuscular Disease NetWork, and our second place finisher, Women’s Health NetWork, both receive session time at CHEST 2017 on a topic of their choice and two travel grants to help their NetWork members attend CHEST 2017.