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Detecting PH in IPF ‘more art than science’
LOS ANGELES – When it comes to the optimal management of pulmonary hypertension (PH) in patients with idiopathic pulmonary fibrosis (IPF), there are more questions than definitive answers, according to Brett E. Fenster, MD, FACC.
“Is PH in IPF a disease marker, an independent treatment target, or both?” he asked attendees at the annual meeting of the American College of Chest Physicians. “I think we have conflicting information about that.”
The prevalence of PH is estimated to be 10% in patients with mild to moderate IPF and tends to progress slowly. Common features of PH in IPF patients include shortness of breath, a greater degree of exertional desaturation, and an increased mortality rate.
Dr. Fenster described the ability to detect PH in IPF patients as “more art than science. A lot of different work has been done to look at different testing to get at the patients that may have PH that is a comorbid disease to their IPF. But a lot of times it comes down to assessing their level of dyspnea proportional to their level of disease. In those patients where we think there is something else going on besides their IPF, we’ll oftentimes get an echocardiogram and try to look at their right heart to see if they have features of PH. If it looks like they do, we will circle back and look at the amount of lung disease they have as characterized by their chest imaging, by their pulmonary function testing, and getting a blood gas. If this patient has findings of right heart enlargement, systolic dysfunction, et cetera, that clues us more into looking at PH and referring them to a center that has expertise in that version of PH.”
According to the most recent European Society of Cardiology/European Respiratory Society guidelines, the diagnosis of chronic obstructive pulmonary disease (COPD)/IPF/combined pulmonary fibrosis and emphysema (CPFE) without PH can be considered when the mean pulmonary artery pressure (mPAP) on right heart catheterization is less than 25 mm Hg. The diagnosis of COPD/IPF/CPFE with PH, based on these same guidelines, can be considered when the mPAP is 25 mm Hg or more. A patient may have COPD/IPF/CPFE with severe PH when his or her mPAP exceeds 35 mm Hg, or is 25 mm Hg or greater in the presence of a low cardiac output, the guidelines says (Eur Heart J. 2016;37:67-119). “That begins to separate out a group that may potentially benefit from targeted PH therapy,” Dr. Fenster said.
Current treatment approaches include long-term oxygen, diuretics, transplant, and pulmonary rehabilitation, but Dr. Fenster said there is sparse data on the optimal treatment approach. A study of sildenafil in IPF known as STEP-IPF failed to increase 6-minute walking test distance but improved diffusion capacity of carbon monoxide, quality of life, and arterial oxygenation (N Engl J Med. 2010;363:620-8). A study evaluating riociguat for idiopathic interstitial pneumonitis PH was discontinued early because of increased risk of death and adverse events. More recently, the drug ambrisentan was found to be ineffective at reducing the rate of IPF progression and was linked to an increase in disease progression events, including a decline in pulmonary function test values, hospitalization, and death, in the ARTEMIS-IPF trial (Ann Intern Med. 2013;158:641-9).
Randomized, placebo-controlled studies of bosentan in IPF give researchers pause for hope, Dr. Fenster said. BUILD-1 demonstrated a trend toward delayed time to death, delayed disease progression, improved quality of life, and no clear worsening of IPF (Am J Respir Crit Care Med. 2008;177[1]:75-81), while BUILD-3 showed a significant improvement in forced vital capacity (FVC) and carbon monoxide diffusing capacity (Am J Respir Crit Care Med. 2011;184[1]:92-9). A more recent trial evaluated IV treprostinil in 15 patients with interstitial lung disease and PH (Thorax 2014;69[2]:123-9). Eight of the patients had IPF. “After 12 weeks of treprostinil therapy, almost all of them experienced some degree of improvement in their walk distance,” said Dr. Fenster, who was not involved with the study. “Perhaps more importantly there were significant improvements in almost all parameters from their right heart catheterizations. So when we think about how to treat these patients, we have to weigh the risks and benefits of what we make potentially worse with our IPF therapy, such as worsening hypoxia, V/Q mismatch, disease progression, and volume overload. On the flip side, we might be improving right heart hemodynamics and RV function, which are prognostic in this disease. What’s the net balance of these things in terms of how it translates into functional capacity, quality of life, hospitalization, and mortality? We don’t know.”
According to Dr. Fenster, current data suggest that future IPF PH research should focus on prostanoid pathways and not on the estrogen-receptor and riociguat pathways to determine effective treatments. “We have numerous studies showing potential harm with IPF PH therapy, so we need to very much wade cautiously into this arena,” he said. “There is a potential role for PH therapy in IPF, but we will likely need to study patients with severe PH and IPF to show benefit. I think that’s where we’ll have the most success.”
Dr. Fenster reported having no relevant financial disclosures.
LOS ANGELES – When it comes to the optimal management of pulmonary hypertension (PH) in patients with idiopathic pulmonary fibrosis (IPF), there are more questions than definitive answers, according to Brett E. Fenster, MD, FACC.
“Is PH in IPF a disease marker, an independent treatment target, or both?” he asked attendees at the annual meeting of the American College of Chest Physicians. “I think we have conflicting information about that.”
The prevalence of PH is estimated to be 10% in patients with mild to moderate IPF and tends to progress slowly. Common features of PH in IPF patients include shortness of breath, a greater degree of exertional desaturation, and an increased mortality rate.
Dr. Fenster described the ability to detect PH in IPF patients as “more art than science. A lot of different work has been done to look at different testing to get at the patients that may have PH that is a comorbid disease to their IPF. But a lot of times it comes down to assessing their level of dyspnea proportional to their level of disease. In those patients where we think there is something else going on besides their IPF, we’ll oftentimes get an echocardiogram and try to look at their right heart to see if they have features of PH. If it looks like they do, we will circle back and look at the amount of lung disease they have as characterized by their chest imaging, by their pulmonary function testing, and getting a blood gas. If this patient has findings of right heart enlargement, systolic dysfunction, et cetera, that clues us more into looking at PH and referring them to a center that has expertise in that version of PH.”
According to the most recent European Society of Cardiology/European Respiratory Society guidelines, the diagnosis of chronic obstructive pulmonary disease (COPD)/IPF/combined pulmonary fibrosis and emphysema (CPFE) without PH can be considered when the mean pulmonary artery pressure (mPAP) on right heart catheterization is less than 25 mm Hg. The diagnosis of COPD/IPF/CPFE with PH, based on these same guidelines, can be considered when the mPAP is 25 mm Hg or more. A patient may have COPD/IPF/CPFE with severe PH when his or her mPAP exceeds 35 mm Hg, or is 25 mm Hg or greater in the presence of a low cardiac output, the guidelines says (Eur Heart J. 2016;37:67-119). “That begins to separate out a group that may potentially benefit from targeted PH therapy,” Dr. Fenster said.
Current treatment approaches include long-term oxygen, diuretics, transplant, and pulmonary rehabilitation, but Dr. Fenster said there is sparse data on the optimal treatment approach. A study of sildenafil in IPF known as STEP-IPF failed to increase 6-minute walking test distance but improved diffusion capacity of carbon monoxide, quality of life, and arterial oxygenation (N Engl J Med. 2010;363:620-8). A study evaluating riociguat for idiopathic interstitial pneumonitis PH was discontinued early because of increased risk of death and adverse events. More recently, the drug ambrisentan was found to be ineffective at reducing the rate of IPF progression and was linked to an increase in disease progression events, including a decline in pulmonary function test values, hospitalization, and death, in the ARTEMIS-IPF trial (Ann Intern Med. 2013;158:641-9).
Randomized, placebo-controlled studies of bosentan in IPF give researchers pause for hope, Dr. Fenster said. BUILD-1 demonstrated a trend toward delayed time to death, delayed disease progression, improved quality of life, and no clear worsening of IPF (Am J Respir Crit Care Med. 2008;177[1]:75-81), while BUILD-3 showed a significant improvement in forced vital capacity (FVC) and carbon monoxide diffusing capacity (Am J Respir Crit Care Med. 2011;184[1]:92-9). A more recent trial evaluated IV treprostinil in 15 patients with interstitial lung disease and PH (Thorax 2014;69[2]:123-9). Eight of the patients had IPF. “After 12 weeks of treprostinil therapy, almost all of them experienced some degree of improvement in their walk distance,” said Dr. Fenster, who was not involved with the study. “Perhaps more importantly there were significant improvements in almost all parameters from their right heart catheterizations. So when we think about how to treat these patients, we have to weigh the risks and benefits of what we make potentially worse with our IPF therapy, such as worsening hypoxia, V/Q mismatch, disease progression, and volume overload. On the flip side, we might be improving right heart hemodynamics and RV function, which are prognostic in this disease. What’s the net balance of these things in terms of how it translates into functional capacity, quality of life, hospitalization, and mortality? We don’t know.”
According to Dr. Fenster, current data suggest that future IPF PH research should focus on prostanoid pathways and not on the estrogen-receptor and riociguat pathways to determine effective treatments. “We have numerous studies showing potential harm with IPF PH therapy, so we need to very much wade cautiously into this arena,” he said. “There is a potential role for PH therapy in IPF, but we will likely need to study patients with severe PH and IPF to show benefit. I think that’s where we’ll have the most success.”
Dr. Fenster reported having no relevant financial disclosures.
LOS ANGELES – When it comes to the optimal management of pulmonary hypertension (PH) in patients with idiopathic pulmonary fibrosis (IPF), there are more questions than definitive answers, according to Brett E. Fenster, MD, FACC.
“Is PH in IPF a disease marker, an independent treatment target, or both?” he asked attendees at the annual meeting of the American College of Chest Physicians. “I think we have conflicting information about that.”
The prevalence of PH is estimated to be 10% in patients with mild to moderate IPF and tends to progress slowly. Common features of PH in IPF patients include shortness of breath, a greater degree of exertional desaturation, and an increased mortality rate.
Dr. Fenster described the ability to detect PH in IPF patients as “more art than science. A lot of different work has been done to look at different testing to get at the patients that may have PH that is a comorbid disease to their IPF. But a lot of times it comes down to assessing their level of dyspnea proportional to their level of disease. In those patients where we think there is something else going on besides their IPF, we’ll oftentimes get an echocardiogram and try to look at their right heart to see if they have features of PH. If it looks like they do, we will circle back and look at the amount of lung disease they have as characterized by their chest imaging, by their pulmonary function testing, and getting a blood gas. If this patient has findings of right heart enlargement, systolic dysfunction, et cetera, that clues us more into looking at PH and referring them to a center that has expertise in that version of PH.”
According to the most recent European Society of Cardiology/European Respiratory Society guidelines, the diagnosis of chronic obstructive pulmonary disease (COPD)/IPF/combined pulmonary fibrosis and emphysema (CPFE) without PH can be considered when the mean pulmonary artery pressure (mPAP) on right heart catheterization is less than 25 mm Hg. The diagnosis of COPD/IPF/CPFE with PH, based on these same guidelines, can be considered when the mPAP is 25 mm Hg or more. A patient may have COPD/IPF/CPFE with severe PH when his or her mPAP exceeds 35 mm Hg, or is 25 mm Hg or greater in the presence of a low cardiac output, the guidelines says (Eur Heart J. 2016;37:67-119). “That begins to separate out a group that may potentially benefit from targeted PH therapy,” Dr. Fenster said.
Current treatment approaches include long-term oxygen, diuretics, transplant, and pulmonary rehabilitation, but Dr. Fenster said there is sparse data on the optimal treatment approach. A study of sildenafil in IPF known as STEP-IPF failed to increase 6-minute walking test distance but improved diffusion capacity of carbon monoxide, quality of life, and arterial oxygenation (N Engl J Med. 2010;363:620-8). A study evaluating riociguat for idiopathic interstitial pneumonitis PH was discontinued early because of increased risk of death and adverse events. More recently, the drug ambrisentan was found to be ineffective at reducing the rate of IPF progression and was linked to an increase in disease progression events, including a decline in pulmonary function test values, hospitalization, and death, in the ARTEMIS-IPF trial (Ann Intern Med. 2013;158:641-9).
Randomized, placebo-controlled studies of bosentan in IPF give researchers pause for hope, Dr. Fenster said. BUILD-1 demonstrated a trend toward delayed time to death, delayed disease progression, improved quality of life, and no clear worsening of IPF (Am J Respir Crit Care Med. 2008;177[1]:75-81), while BUILD-3 showed a significant improvement in forced vital capacity (FVC) and carbon monoxide diffusing capacity (Am J Respir Crit Care Med. 2011;184[1]:92-9). A more recent trial evaluated IV treprostinil in 15 patients with interstitial lung disease and PH (Thorax 2014;69[2]:123-9). Eight of the patients had IPF. “After 12 weeks of treprostinil therapy, almost all of them experienced some degree of improvement in their walk distance,” said Dr. Fenster, who was not involved with the study. “Perhaps more importantly there were significant improvements in almost all parameters from their right heart catheterizations. So when we think about how to treat these patients, we have to weigh the risks and benefits of what we make potentially worse with our IPF therapy, such as worsening hypoxia, V/Q mismatch, disease progression, and volume overload. On the flip side, we might be improving right heart hemodynamics and RV function, which are prognostic in this disease. What’s the net balance of these things in terms of how it translates into functional capacity, quality of life, hospitalization, and mortality? We don’t know.”
According to Dr. Fenster, current data suggest that future IPF PH research should focus on prostanoid pathways and not on the estrogen-receptor and riociguat pathways to determine effective treatments. “We have numerous studies showing potential harm with IPF PH therapy, so we need to very much wade cautiously into this arena,” he said. “There is a potential role for PH therapy in IPF, but we will likely need to study patients with severe PH and IPF to show benefit. I think that’s where we’ll have the most success.”
Dr. Fenster reported having no relevant financial disclosures.
Home oxygen upped survival in PAH with severely impaired DLCO
LOS ANGELES – Pulmonary arterial hypertension (PAH) patients with severely impaired diffusing capacity of the lung for carbon monoxide (DLCO) were much more likely to survive when they received home oxygen therapy, according to a disease registry analysis.
“We all know that supplemental oxygen is widely used with PAH,” said Harrison W. Farber, MD, director of the pulmonary hypertension center at Boston University. But there are practically no data showing that it is successful, and there are even fewer data for patients with PAH who have very low diffusion capacity, he added.
That knowledge gap prompted Dr. Farber and his colleagues to analyze data from the Registry to Evaluate Early and Long-Term PAH Disease Management (REVEAL), the largest disease registry in the world of patients with PAH.
“Patients in that group – the severe DLCO group – who got oxygen had poorer prognostic features but improved overall survival relative to those who didn’t,” Dr. Farber explained during a presentation at the annual meeting of the American College of Chest Physicians. “Based on this, it makes us think that home oxygen, supplemental oxygen treatment, is associated with improved survival in patients, especially those with severe DLCO and PAH.”
The 3,046 patients analyzed by Dr. Farber and his colleagues had World Health Organization Group 1 PAH with right heart catheterization hemodynamic criteria: a mean pulmonary artery pressure greater than 25 mm Hg, a pulmonary capillary wedge pressure less than or equal to 15 mm Hg, and a pulmonary vascular resistance of at least 3 Wood units (WU). Patients were at least 18 years of age and grouped by oxygen use, which was defined as any use at any time from study enrollment to the end of follow-up, and by DLCO group.
A total of 57% of the patients (1,734) received oxygen, and the remaining 43% of the patients (1,312) did not receive oxygen. Among the patients who received oxygen, 71% (1,227) received the therapy continuously, and 24% (408) received oxygen at night only.
The 424 patients with a DLCO of less than 40% were considered to have a severe DLCO impairment. The other two groups comprised 505 patients with a moderate DLCO impairment (at least 40%, but less than 60%) and 844 patients with a mild to normal DLCO (at least 60%). The DLCOs of 1,273 patients analyzed were unknown.
Among those patients with severe DLCO impairment, the risk of death was significantly lower in those who received oxygen, compared with those who did not receive oxygen (hazard ratio, 0.56; P = .0033). Oxygen use was associated with significant improvements in overall survival in both the newly diagnosed (HR, 0.47; P = .029) and previously diagnosed (HR, 0.59; P = .026) severe DLCO cohorts, Dr. Farber said.
Patients receiving oxygen were more likely to be treated with PAH-specific medications, regardless of their DLCO group.
Among the analysis’s limitations was that the lengths of time patients had been undergoing oxygen treatment were unknown. That prevented adjustments for duration of oxygen treatment, according to Dr. Farber.
Dr. Farber disclosed serving on the steering committees or advisory boards for Actelion, Bayer, Bellerophon, Gilead, and United Therapeutics. He has received research support from Actelion, Gilead, and United Therapeutics, and has been a speaker for Actelion, Bayer, and Gilead.
LOS ANGELES – Pulmonary arterial hypertension (PAH) patients with severely impaired diffusing capacity of the lung for carbon monoxide (DLCO) were much more likely to survive when they received home oxygen therapy, according to a disease registry analysis.
“We all know that supplemental oxygen is widely used with PAH,” said Harrison W. Farber, MD, director of the pulmonary hypertension center at Boston University. But there are practically no data showing that it is successful, and there are even fewer data for patients with PAH who have very low diffusion capacity, he added.
That knowledge gap prompted Dr. Farber and his colleagues to analyze data from the Registry to Evaluate Early and Long-Term PAH Disease Management (REVEAL), the largest disease registry in the world of patients with PAH.
“Patients in that group – the severe DLCO group – who got oxygen had poorer prognostic features but improved overall survival relative to those who didn’t,” Dr. Farber explained during a presentation at the annual meeting of the American College of Chest Physicians. “Based on this, it makes us think that home oxygen, supplemental oxygen treatment, is associated with improved survival in patients, especially those with severe DLCO and PAH.”
The 3,046 patients analyzed by Dr. Farber and his colleagues had World Health Organization Group 1 PAH with right heart catheterization hemodynamic criteria: a mean pulmonary artery pressure greater than 25 mm Hg, a pulmonary capillary wedge pressure less than or equal to 15 mm Hg, and a pulmonary vascular resistance of at least 3 Wood units (WU). Patients were at least 18 years of age and grouped by oxygen use, which was defined as any use at any time from study enrollment to the end of follow-up, and by DLCO group.
A total of 57% of the patients (1,734) received oxygen, and the remaining 43% of the patients (1,312) did not receive oxygen. Among the patients who received oxygen, 71% (1,227) received the therapy continuously, and 24% (408) received oxygen at night only.
The 424 patients with a DLCO of less than 40% were considered to have a severe DLCO impairment. The other two groups comprised 505 patients with a moderate DLCO impairment (at least 40%, but less than 60%) and 844 patients with a mild to normal DLCO (at least 60%). The DLCOs of 1,273 patients analyzed were unknown.
Among those patients with severe DLCO impairment, the risk of death was significantly lower in those who received oxygen, compared with those who did not receive oxygen (hazard ratio, 0.56; P = .0033). Oxygen use was associated with significant improvements in overall survival in both the newly diagnosed (HR, 0.47; P = .029) and previously diagnosed (HR, 0.59; P = .026) severe DLCO cohorts, Dr. Farber said.
Patients receiving oxygen were more likely to be treated with PAH-specific medications, regardless of their DLCO group.
Among the analysis’s limitations was that the lengths of time patients had been undergoing oxygen treatment were unknown. That prevented adjustments for duration of oxygen treatment, according to Dr. Farber.
Dr. Farber disclosed serving on the steering committees or advisory boards for Actelion, Bayer, Bellerophon, Gilead, and United Therapeutics. He has received research support from Actelion, Gilead, and United Therapeutics, and has been a speaker for Actelion, Bayer, and Gilead.
LOS ANGELES – Pulmonary arterial hypertension (PAH) patients with severely impaired diffusing capacity of the lung for carbon monoxide (DLCO) were much more likely to survive when they received home oxygen therapy, according to a disease registry analysis.
“We all know that supplemental oxygen is widely used with PAH,” said Harrison W. Farber, MD, director of the pulmonary hypertension center at Boston University. But there are practically no data showing that it is successful, and there are even fewer data for patients with PAH who have very low diffusion capacity, he added.
That knowledge gap prompted Dr. Farber and his colleagues to analyze data from the Registry to Evaluate Early and Long-Term PAH Disease Management (REVEAL), the largest disease registry in the world of patients with PAH.
“Patients in that group – the severe DLCO group – who got oxygen had poorer prognostic features but improved overall survival relative to those who didn’t,” Dr. Farber explained during a presentation at the annual meeting of the American College of Chest Physicians. “Based on this, it makes us think that home oxygen, supplemental oxygen treatment, is associated with improved survival in patients, especially those with severe DLCO and PAH.”
The 3,046 patients analyzed by Dr. Farber and his colleagues had World Health Organization Group 1 PAH with right heart catheterization hemodynamic criteria: a mean pulmonary artery pressure greater than 25 mm Hg, a pulmonary capillary wedge pressure less than or equal to 15 mm Hg, and a pulmonary vascular resistance of at least 3 Wood units (WU). Patients were at least 18 years of age and grouped by oxygen use, which was defined as any use at any time from study enrollment to the end of follow-up, and by DLCO group.
A total of 57% of the patients (1,734) received oxygen, and the remaining 43% of the patients (1,312) did not receive oxygen. Among the patients who received oxygen, 71% (1,227) received the therapy continuously, and 24% (408) received oxygen at night only.
The 424 patients with a DLCO of less than 40% were considered to have a severe DLCO impairment. The other two groups comprised 505 patients with a moderate DLCO impairment (at least 40%, but less than 60%) and 844 patients with a mild to normal DLCO (at least 60%). The DLCOs of 1,273 patients analyzed were unknown.
Among those patients with severe DLCO impairment, the risk of death was significantly lower in those who received oxygen, compared with those who did not receive oxygen (hazard ratio, 0.56; P = .0033). Oxygen use was associated with significant improvements in overall survival in both the newly diagnosed (HR, 0.47; P = .029) and previously diagnosed (HR, 0.59; P = .026) severe DLCO cohorts, Dr. Farber said.
Patients receiving oxygen were more likely to be treated with PAH-specific medications, regardless of their DLCO group.
Among the analysis’s limitations was that the lengths of time patients had been undergoing oxygen treatment were unknown. That prevented adjustments for duration of oxygen treatment, according to Dr. Farber.
Dr. Farber disclosed serving on the steering committees or advisory boards for Actelion, Bayer, Bellerophon, Gilead, and United Therapeutics. He has received research support from Actelion, Gilead, and United Therapeutics, and has been a speaker for Actelion, Bayer, and Gilead.
Key clinical point:
Major finding: PAH patients with severe DLCO impairment who received oxygen had a significantly higher probability of survival than those who didn’t receive oxygen (HR, 0.56; P = .0033).
Data source: An analysis of 3,046 patients in the U.S. multicenter, observational REVEAL disease registry.
Disclosures: Dr. Farber disclosed serving on the steering committees or advisory boards for Actelion, Bayer, Bellerophon, Gilead, and United Therapeutics. He has received research support from Actelion, Gilead, and United Therapeutics, and has been a speaker for Actelion, Bayer, and Gilead.
Delayed bleeding possible with EBUS-TBNA on antiplatelets
LOS ANGELES – There might be a slight increase in delayed bleeding when patients have endobronchial ultrasound with transbronchial needle aspiration within 5 days of taking oral antiplatelets, according to a review of 404 patients at Riverside Methodist Hospital in Columbus, Ohio.
This study is unusual in that it looked at the 48 hour mark. Previous studies have tended to focus on immediate bleeding events that require the procedure to be stopped; only some of that research has found an increased bleeding risk with antiplatelet therapy.
In the study at Riverside Methodist, none of the 20 patients on dual antiplatelet therapy – clopidogrel (Plavix) plus aspirin – bled during the procedure, but one (5%) had a hemoglobin drop of more than 2 g within 48 hours and another was readmitted to the hospital within 48 hours for procedure-related hemoptysis. Overall, the delayed bleeding event rate for patients using the dual antiplatelet therapy was 10%. Additionally, one of the 13 patients (7.7%) on clopidogrel alone experienced a greater than 2 g drop in hemoglobin.
Among the 270 patients not exposed to antiplatelets, the overall bleeding event rate was 2.6%, and the event rate for delayed bleeding was 1.1%. Four patients (1.5%) bled during the procedure, two (0.7%) had hemoglobin drops greater than 2 g within 48 hours, and one (0.4%) was readmitted for hemoptysis.
There were no bleeding events in the 101 patients who only took aspirin.
“There was a trend toward delayed bleeding events in patients” on clopidogrel or dual antiplatelets. “It’s worth considering a thoughtful pause in decision making. Maybe with the bleeding events we’re seeing, it would be worthwhile, if possible, to defer” endobronchial ultrasound with transbronchial needle aspiration “until after the antiplatelet therapy,” said Kevin Swiatek, DO, a medicine resident at Riverside.
Patients were excluded from the study if they had histories of bleeding or clotting disorders; low platelet counts; or if they were on anticoagulation. Subjects on antiplatelets were about 10 years older, on average, than those who were not (about 68 versus 59 years old), and more likely to have had a heart attack or stroke, and to be hypertensive.
There was no industry funding for the work, and the investigators had no disclosures.
LOS ANGELES – There might be a slight increase in delayed bleeding when patients have endobronchial ultrasound with transbronchial needle aspiration within 5 days of taking oral antiplatelets, according to a review of 404 patients at Riverside Methodist Hospital in Columbus, Ohio.
This study is unusual in that it looked at the 48 hour mark. Previous studies have tended to focus on immediate bleeding events that require the procedure to be stopped; only some of that research has found an increased bleeding risk with antiplatelet therapy.
In the study at Riverside Methodist, none of the 20 patients on dual antiplatelet therapy – clopidogrel (Plavix) plus aspirin – bled during the procedure, but one (5%) had a hemoglobin drop of more than 2 g within 48 hours and another was readmitted to the hospital within 48 hours for procedure-related hemoptysis. Overall, the delayed bleeding event rate for patients using the dual antiplatelet therapy was 10%. Additionally, one of the 13 patients (7.7%) on clopidogrel alone experienced a greater than 2 g drop in hemoglobin.
Among the 270 patients not exposed to antiplatelets, the overall bleeding event rate was 2.6%, and the event rate for delayed bleeding was 1.1%. Four patients (1.5%) bled during the procedure, two (0.7%) had hemoglobin drops greater than 2 g within 48 hours, and one (0.4%) was readmitted for hemoptysis.
There were no bleeding events in the 101 patients who only took aspirin.
“There was a trend toward delayed bleeding events in patients” on clopidogrel or dual antiplatelets. “It’s worth considering a thoughtful pause in decision making. Maybe with the bleeding events we’re seeing, it would be worthwhile, if possible, to defer” endobronchial ultrasound with transbronchial needle aspiration “until after the antiplatelet therapy,” said Kevin Swiatek, DO, a medicine resident at Riverside.
Patients were excluded from the study if they had histories of bleeding or clotting disorders; low platelet counts; or if they were on anticoagulation. Subjects on antiplatelets were about 10 years older, on average, than those who were not (about 68 versus 59 years old), and more likely to have had a heart attack or stroke, and to be hypertensive.
There was no industry funding for the work, and the investigators had no disclosures.
LOS ANGELES – There might be a slight increase in delayed bleeding when patients have endobronchial ultrasound with transbronchial needle aspiration within 5 days of taking oral antiplatelets, according to a review of 404 patients at Riverside Methodist Hospital in Columbus, Ohio.
This study is unusual in that it looked at the 48 hour mark. Previous studies have tended to focus on immediate bleeding events that require the procedure to be stopped; only some of that research has found an increased bleeding risk with antiplatelet therapy.
In the study at Riverside Methodist, none of the 20 patients on dual antiplatelet therapy – clopidogrel (Plavix) plus aspirin – bled during the procedure, but one (5%) had a hemoglobin drop of more than 2 g within 48 hours and another was readmitted to the hospital within 48 hours for procedure-related hemoptysis. Overall, the delayed bleeding event rate for patients using the dual antiplatelet therapy was 10%. Additionally, one of the 13 patients (7.7%) on clopidogrel alone experienced a greater than 2 g drop in hemoglobin.
Among the 270 patients not exposed to antiplatelets, the overall bleeding event rate was 2.6%, and the event rate for delayed bleeding was 1.1%. Four patients (1.5%) bled during the procedure, two (0.7%) had hemoglobin drops greater than 2 g within 48 hours, and one (0.4%) was readmitted for hemoptysis.
There were no bleeding events in the 101 patients who only took aspirin.
“There was a trend toward delayed bleeding events in patients” on clopidogrel or dual antiplatelets. “It’s worth considering a thoughtful pause in decision making. Maybe with the bleeding events we’re seeing, it would be worthwhile, if possible, to defer” endobronchial ultrasound with transbronchial needle aspiration “until after the antiplatelet therapy,” said Kevin Swiatek, DO, a medicine resident at Riverside.
Patients were excluded from the study if they had histories of bleeding or clotting disorders; low platelet counts; or if they were on anticoagulation. Subjects on antiplatelets were about 10 years older, on average, than those who were not (about 68 versus 59 years old), and more likely to have had a heart attack or stroke, and to be hypertensive.
There was no industry funding for the work, and the investigators had no disclosures.
AT CHEST 2016
Key clinical point:
Major finding: Ten percent of patients on dual antiplatelet therapy bled within 48 hours, versus 1.1% of those not on antiplatelet therapy.
Data source: Single-center review of 404 patients.
Disclosures: There was no industry funding for the work, and the investigators had no disclosures.
Indacaterol/glycopyrronium OK as preferred COPD treatment
AT CHEST 2016
LOS ANGELES – Indacaterol/glycopyrronium was superior to salmeterol/fluticasone at reducing the risk and rate of moderate to severe exacerbations in chronic obstructive pulmonary disease (COPD) patients with more than one or zero to one exacerbations in the previous year, results from an indirect comparison showed.
“Acute exacerbations of COPD are associated with accelerated decline in lung function and increased mortality,” Kenneth R. Chapman, MD, said at the annual meeting of the American College of Chest Physicians. “Current GOLD [Global Initiative for Chronic Obstructive Lung Disease] strategy recommends LABA/ICS [long-acting beta-agonist/inhaled corticosteroid] combination, and/or LAMA [long-acting muscarinic antagonist] as the first-line treatment, and LABA/LAMA as an alternative treatment for COPD patients at a high risk of exacerbations.”
In an effort to examine the reduction in moderate or severe exacerbations in COPD patients taking indacaterol/glycopyrronium (a combination of a LABA bronchodilator and a LAMA bronchodilator) or salmeterol/fluticasone (a LABA and inhaled glucocorticoid combination), researchers compared results from the FLAME and LANTERN trials. The FLAME study evaluated the rate and risk of exacerbations with indacaterol/glycopyrronium versus salmeterol/fluticasone in 3,362 moderate to very severe COPD patients with at least one exacerbation in the previous year (N Engl J Med. 2016;374[23]:2222-34).The LANTERN study compared the efficacy and safety of indacaterol/glycopyrronium versus salmeterol/fluticasone in 744 moderate to very severe COPD patients with 0-1 exacerbation in the previous year (Int J Chron Obstruct Pulmon Dis. 2015;10:1015-26).
Dr. Chapman, professor of medicine at the University of Toronto, reported that in the FLAME study, which was 52 weeks long, indacaterol/glycopyrronium significantly reduced the annualized rate of moderate or severe COPD exacerbations in patients who had one or more exacerbation in the previous year (a rate ratio of 0.83; P less than 0.001), which translated in to a clinically meaningful 17% reduction, compared with their counterparts taking salmeterol/fluticasone. In the LANTERN study, which was 26 weeks long, indacaterol/glycopyrronium also significantly reduced the annualized rate of patients who had 0-1 exacerbation in the previous year, compared with those taking salmeterol/fluticasone (RR, 0.69; P = .048).
In FLAME, indacaterol/glycopyrronium significantly delayed the time to first moderate or severe exacerbation, with a clinically meaningful 22% risk reduction, compared with salmeterol/fluticasone (hazard ratio, 0.78; P less than .001). Similar findings were observed in LANTERN; indacaterol/glycopyrronium significantly delayed the time to first moderate or severe exacerbation, with a clinically meaningful 35% risk reduction, compared with salmeterol/fluticasone (HR, 0.65; P less than .028).
“These results suggest that LABA/LAMA combinations such as indacaterol/glycopyrronium can be considered as a preferred treatment option in the management of COPD patients, irrespective of exacerbation history,” Dr. Chapman said.He went on to note that in FLAME, the incidence of pneumonia was 3.2% in the indacaterol/glycopyrronium group, compared with 4.8% in the salmeterol/fluticasone group P = .02). In LANTERN, the incidence of pneumonia was 0.8% in the indacaterol/glycopyrronium group, compared with 2.7% in the salmeterol/fluticasone group. Finally, in FLAME, the incidence of oral candidiasis was 1.2% in the indacaterol/glycopyrronium group, compared with 4.2% in the salmeterol/fluticasone group (P less than .001). In LANTERN, the respective values were 0% and 0.3%.
Dr. Chapman reported having numerous financial disclosures, including receiving consulting fees and research grants from Novartis.
dbrunk@frontlinemedcom.com
AT CHEST 2016
LOS ANGELES – Indacaterol/glycopyrronium was superior to salmeterol/fluticasone at reducing the risk and rate of moderate to severe exacerbations in chronic obstructive pulmonary disease (COPD) patients with more than one or zero to one exacerbations in the previous year, results from an indirect comparison showed.
“Acute exacerbations of COPD are associated with accelerated decline in lung function and increased mortality,” Kenneth R. Chapman, MD, said at the annual meeting of the American College of Chest Physicians. “Current GOLD [Global Initiative for Chronic Obstructive Lung Disease] strategy recommends LABA/ICS [long-acting beta-agonist/inhaled corticosteroid] combination, and/or LAMA [long-acting muscarinic antagonist] as the first-line treatment, and LABA/LAMA as an alternative treatment for COPD patients at a high risk of exacerbations.”
In an effort to examine the reduction in moderate or severe exacerbations in COPD patients taking indacaterol/glycopyrronium (a combination of a LABA bronchodilator and a LAMA bronchodilator) or salmeterol/fluticasone (a LABA and inhaled glucocorticoid combination), researchers compared results from the FLAME and LANTERN trials. The FLAME study evaluated the rate and risk of exacerbations with indacaterol/glycopyrronium versus salmeterol/fluticasone in 3,362 moderate to very severe COPD patients with at least one exacerbation in the previous year (N Engl J Med. 2016;374[23]:2222-34).The LANTERN study compared the efficacy and safety of indacaterol/glycopyrronium versus salmeterol/fluticasone in 744 moderate to very severe COPD patients with 0-1 exacerbation in the previous year (Int J Chron Obstruct Pulmon Dis. 2015;10:1015-26).
Dr. Chapman, professor of medicine at the University of Toronto, reported that in the FLAME study, which was 52 weeks long, indacaterol/glycopyrronium significantly reduced the annualized rate of moderate or severe COPD exacerbations in patients who had one or more exacerbation in the previous year (a rate ratio of 0.83; P less than 0.001), which translated in to a clinically meaningful 17% reduction, compared with their counterparts taking salmeterol/fluticasone. In the LANTERN study, which was 26 weeks long, indacaterol/glycopyrronium also significantly reduced the annualized rate of patients who had 0-1 exacerbation in the previous year, compared with those taking salmeterol/fluticasone (RR, 0.69; P = .048).
In FLAME, indacaterol/glycopyrronium significantly delayed the time to first moderate or severe exacerbation, with a clinically meaningful 22% risk reduction, compared with salmeterol/fluticasone (hazard ratio, 0.78; P less than .001). Similar findings were observed in LANTERN; indacaterol/glycopyrronium significantly delayed the time to first moderate or severe exacerbation, with a clinically meaningful 35% risk reduction, compared with salmeterol/fluticasone (HR, 0.65; P less than .028).
“These results suggest that LABA/LAMA combinations such as indacaterol/glycopyrronium can be considered as a preferred treatment option in the management of COPD patients, irrespective of exacerbation history,” Dr. Chapman said.He went on to note that in FLAME, the incidence of pneumonia was 3.2% in the indacaterol/glycopyrronium group, compared with 4.8% in the salmeterol/fluticasone group P = .02). In LANTERN, the incidence of pneumonia was 0.8% in the indacaterol/glycopyrronium group, compared with 2.7% in the salmeterol/fluticasone group. Finally, in FLAME, the incidence of oral candidiasis was 1.2% in the indacaterol/glycopyrronium group, compared with 4.2% in the salmeterol/fluticasone group (P less than .001). In LANTERN, the respective values were 0% and 0.3%.
Dr. Chapman reported having numerous financial disclosures, including receiving consulting fees and research grants from Novartis.
dbrunk@frontlinemedcom.com
AT CHEST 2016
LOS ANGELES – Indacaterol/glycopyrronium was superior to salmeterol/fluticasone at reducing the risk and rate of moderate to severe exacerbations in chronic obstructive pulmonary disease (COPD) patients with more than one or zero to one exacerbations in the previous year, results from an indirect comparison showed.
“Acute exacerbations of COPD are associated with accelerated decline in lung function and increased mortality,” Kenneth R. Chapman, MD, said at the annual meeting of the American College of Chest Physicians. “Current GOLD [Global Initiative for Chronic Obstructive Lung Disease] strategy recommends LABA/ICS [long-acting beta-agonist/inhaled corticosteroid] combination, and/or LAMA [long-acting muscarinic antagonist] as the first-line treatment, and LABA/LAMA as an alternative treatment for COPD patients at a high risk of exacerbations.”
In an effort to examine the reduction in moderate or severe exacerbations in COPD patients taking indacaterol/glycopyrronium (a combination of a LABA bronchodilator and a LAMA bronchodilator) or salmeterol/fluticasone (a LABA and inhaled glucocorticoid combination), researchers compared results from the FLAME and LANTERN trials. The FLAME study evaluated the rate and risk of exacerbations with indacaterol/glycopyrronium versus salmeterol/fluticasone in 3,362 moderate to very severe COPD patients with at least one exacerbation in the previous year (N Engl J Med. 2016;374[23]:2222-34).The LANTERN study compared the efficacy and safety of indacaterol/glycopyrronium versus salmeterol/fluticasone in 744 moderate to very severe COPD patients with 0-1 exacerbation in the previous year (Int J Chron Obstruct Pulmon Dis. 2015;10:1015-26).
Dr. Chapman, professor of medicine at the University of Toronto, reported that in the FLAME study, which was 52 weeks long, indacaterol/glycopyrronium significantly reduced the annualized rate of moderate or severe COPD exacerbations in patients who had one or more exacerbation in the previous year (a rate ratio of 0.83; P less than 0.001), which translated in to a clinically meaningful 17% reduction, compared with their counterparts taking salmeterol/fluticasone. In the LANTERN study, which was 26 weeks long, indacaterol/glycopyrronium also significantly reduced the annualized rate of patients who had 0-1 exacerbation in the previous year, compared with those taking salmeterol/fluticasone (RR, 0.69; P = .048).
In FLAME, indacaterol/glycopyrronium significantly delayed the time to first moderate or severe exacerbation, with a clinically meaningful 22% risk reduction, compared with salmeterol/fluticasone (hazard ratio, 0.78; P less than .001). Similar findings were observed in LANTERN; indacaterol/glycopyrronium significantly delayed the time to first moderate or severe exacerbation, with a clinically meaningful 35% risk reduction, compared with salmeterol/fluticasone (HR, 0.65; P less than .028).
“These results suggest that LABA/LAMA combinations such as indacaterol/glycopyrronium can be considered as a preferred treatment option in the management of COPD patients, irrespective of exacerbation history,” Dr. Chapman said.He went on to note that in FLAME, the incidence of pneumonia was 3.2% in the indacaterol/glycopyrronium group, compared with 4.8% in the salmeterol/fluticasone group P = .02). In LANTERN, the incidence of pneumonia was 0.8% in the indacaterol/glycopyrronium group, compared with 2.7% in the salmeterol/fluticasone group. Finally, in FLAME, the incidence of oral candidiasis was 1.2% in the indacaterol/glycopyrronium group, compared with 4.2% in the salmeterol/fluticasone group (P less than .001). In LANTERN, the respective values were 0% and 0.3%.
Dr. Chapman reported having numerous financial disclosures, including receiving consulting fees and research grants from Novartis.
dbrunk@frontlinemedcom.com
Key clinical point:
Major finding: Indacaterol/glycopyrronium significantly reduced the annualized rate of moderate or severe COPD exacerbations in patients who had one or more exacerbation in the previous year (a rate ratio of 0.83; P less than 0.001), which translated into a clinically meaningful 17% reduction, compared with their counterparts taking salmeterol/fluticasone.
Data source: An indirect comparison of 3,362 patients in the FLAME study and 744 patients in the LANTERN study.
Disclosures: Dr. Chapman reported having numerous financial disclosures, including receiving consulting fees and research grants from Novartis.
Optimal MPE management requires early pulmonology referral
LOS ANGELES – About half of patients with symptomatic malignant pleural effusions at McGill University Health Centre in Montreal had unnecessary procedures and hospital admissions before definitive treatment with chemical pleurodesis or indwelling pleural catheters, according to researchers.
Instead of chest taps to relieve symptoms followed by referrals for definitive treatment, some patients got chest tubes – without pleurodesis – after presenting to the emergency department and being referred to radiology; they were then admitted to the hospital for a few days while the tubes were in place. In short, cancer patients were wasting what time they had left on medical care they didn’t need, and incurring unnecessary costs, said lead investigator Benjamin Shieh, MD, formerly at McGill but now an interventional pulmonology fellow at the University of Calgary. 
McGill is a tertiary care center able to perform both definitive procedures, so “we should be a center of excellence. I imagine there are similar situations” at other hospitals, especially those without the resources of McGill, Dr. Shieh said at the annual meeting of the American College of Chest Physicians.
McGill has taken several steps to address the problem, including early ED referral to the pulmonology service and discouraging radiology from placing chest tubes for malignant pleural effusions (MPE). “I think we can avoid a big proportion of hospitalizations for MPE, and certainly a proportion of repeat [ED] visits,” said senior author Anne Gonzalez, MD, an attending pulmonologist at McGill.
The investigators looked into the issue after noting that a lot of their MPE cases had been hospitalized with chest tubes. They reviewed 72 symptomatic MPE cases in 69 patients treated in 2014 and 2015. Management was ideal in 36 cases (50%), meaning that, prior to definitive treatment, patients had no more than two pleural taps for symptom relief, no more than one ED visit, no chest tubes without pleurodesis, and no hospitalizations. “We thought this would be reasonable to try to achieve for MPE,” since there’s no definition of ideal management, Dr. Shieh said.
Nonideal patients had a mean of 2.5 pleural procedures – almost twice the number in the ideal group – before definitive palliation, with no respiratory consult beforehand. Chest tubes were placed in 27 cases (38%) for an average of 3.7 days; 28 cases (39%) were hospitalized. Nonideal patients were far more likely to present first to the ED, and ED presentations were more likely to get chest tubes and be admitted. All the cases were eventually treated definitively, 68 with indwelling pleural catheters and 4 by thoracoscopic talc insufflation. Time from initial presentation to definitive palliation was about 1 month in both groups. The investigators didn’t consider rate of effusion recurrence, which might help explain why the ideal group wasn’t treated sooner; they might not have needed it. The higher number of ED visits in the nonideal group suggests that they may have had quicker recurrences, and should have been treated sooner, Dr. Gonzalez said.
The patients were 70 years old, on average, and about 60% were women. Lung and breast were the most common cancers.
There was no industry funding for the work, and the investigators had no disclosures.
LOS ANGELES – About half of patients with symptomatic malignant pleural effusions at McGill University Health Centre in Montreal had unnecessary procedures and hospital admissions before definitive treatment with chemical pleurodesis or indwelling pleural catheters, according to researchers.
Instead of chest taps to relieve symptoms followed by referrals for definitive treatment, some patients got chest tubes – without pleurodesis – after presenting to the emergency department and being referred to radiology; they were then admitted to the hospital for a few days while the tubes were in place. In short, cancer patients were wasting what time they had left on medical care they didn’t need, and incurring unnecessary costs, said lead investigator Benjamin Shieh, MD, formerly at McGill but now an interventional pulmonology fellow at the University of Calgary.
McGill is a tertiary care center able to perform both definitive procedures, so “we should be a center of excellence. I imagine there are similar situations” at other hospitals, especially those without the resources of McGill, Dr. Shieh said at the annual meeting of the American College of Chest Physicians.
McGill has taken several steps to address the problem, including early ED referral to the pulmonology service and discouraging radiology from placing chest tubes for malignant pleural effusions (MPE). “I think we can avoid a big proportion of hospitalizations for MPE, and certainly a proportion of repeat [ED] visits,” said senior author Anne Gonzalez, MD, an attending pulmonologist at McGill.
The investigators looked into the issue after noting that a lot of their MPE cases had been hospitalized with chest tubes. They reviewed 72 symptomatic MPE cases in 69 patients treated in 2014 and 2015. Management was ideal in 36 cases (50%), meaning that, prior to definitive treatment, patients had no more than two pleural taps for symptom relief, no more than one ED visit, no chest tubes without pleurodesis, and no hospitalizations. “We thought this would be reasonable to try to achieve for MPE,” since there’s no definition of ideal management, Dr. Shieh said.
Nonideal patients had a mean of 2.5 pleural procedures – almost twice the number in the ideal group – before definitive palliation, with no respiratory consult beforehand. Chest tubes were placed in 27 cases (38%) for an average of 3.7 days; 28 cases (39%) were hospitalized. Nonideal patients were far more likely to present first to the ED, and ED presentations were more likely to get chest tubes and be admitted. All the cases were eventually treated definitively, 68 with indwelling pleural catheters and 4 by thoracoscopic talc insufflation. Time from initial presentation to definitive palliation was about 1 month in both groups. The investigators didn’t consider rate of effusion recurrence, which might help explain why the ideal group wasn’t treated sooner; they might not have needed it. The higher number of ED visits in the nonideal group suggests that they may have had quicker recurrences, and should have been treated sooner, Dr. Gonzalez said.
The patients were 70 years old, on average, and about 60% were women. Lung and breast were the most common cancers.
There was no industry funding for the work, and the investigators had no disclosures.
LOS ANGELES – About half of patients with symptomatic malignant pleural effusions at McGill University Health Centre in Montreal had unnecessary procedures and hospital admissions before definitive treatment with chemical pleurodesis or indwelling pleural catheters, according to researchers.
Instead of chest taps to relieve symptoms followed by referrals for definitive treatment, some patients got chest tubes – without pleurodesis – after presenting to the emergency department and being referred to radiology; they were then admitted to the hospital for a few days while the tubes were in place. In short, cancer patients were wasting what time they had left on medical care they didn’t need, and incurring unnecessary costs, said lead investigator Benjamin Shieh, MD, formerly at McGill but now an interventional pulmonology fellow at the University of Calgary.
McGill is a tertiary care center able to perform both definitive procedures, so “we should be a center of excellence. I imagine there are similar situations” at other hospitals, especially those without the resources of McGill, Dr. Shieh said at the annual meeting of the American College of Chest Physicians.
McGill has taken several steps to address the problem, including early ED referral to the pulmonology service and discouraging radiology from placing chest tubes for malignant pleural effusions (MPE). “I think we can avoid a big proportion of hospitalizations for MPE, and certainly a proportion of repeat [ED] visits,” said senior author Anne Gonzalez, MD, an attending pulmonologist at McGill.
The investigators looked into the issue after noting that a lot of their MPE cases had been hospitalized with chest tubes. They reviewed 72 symptomatic MPE cases in 69 patients treated in 2014 and 2015. Management was ideal in 36 cases (50%), meaning that, prior to definitive treatment, patients had no more than two pleural taps for symptom relief, no more than one ED visit, no chest tubes without pleurodesis, and no hospitalizations. “We thought this would be reasonable to try to achieve for MPE,” since there’s no definition of ideal management, Dr. Shieh said.
Nonideal patients had a mean of 2.5 pleural procedures – almost twice the number in the ideal group – before definitive palliation, with no respiratory consult beforehand. Chest tubes were placed in 27 cases (38%) for an average of 3.7 days; 28 cases (39%) were hospitalized. Nonideal patients were far more likely to present first to the ED, and ED presentations were more likely to get chest tubes and be admitted. All the cases were eventually treated definitively, 68 with indwelling pleural catheters and 4 by thoracoscopic talc insufflation. Time from initial presentation to definitive palliation was about 1 month in both groups. The investigators didn’t consider rate of effusion recurrence, which might help explain why the ideal group wasn’t treated sooner; they might not have needed it. The higher number of ED visits in the nonideal group suggests that they may have had quicker recurrences, and should have been treated sooner, Dr. Gonzalez said.
The patients were 70 years old, on average, and about 60% were women. Lung and breast were the most common cancers.
There was no industry funding for the work, and the investigators had no disclosures.
AT CHEST 2016
Key clinical point:
Major finding: Those patients had a mean of 2.5 pleural procedures before definitive palliation, with no respiratory consult beforehand. Chest tubes were placed for an average of 3.7 days.
Data source: Review of 72 MPE cases in 69 patients.
Disclosures: There was no industry funding for the work, and the investigators had no disclosures.
Mitral valve disease often missed in pulmonary hypertension
LOS ANGELES – Dyspnea in pulmonary hypertension is caused by mitral valve disease until proven otherwise, according to Paul Forfia, MD, director of pulmonary hypertension, right heart failure, and pulmonary thromboendarterectomy at Temple University, Philadelphia.
Although mitral valve disease is a well-recognized cause of pulmonary hypertension, its significance is often underestimated in practice.
“Whether the valve is regurgitant or stenotic makes absolutely no difference. When you delay” repair or replacement, “the patient keeps getting sicker,” he said. In time, “everyone is standing around wringing their hands going, ‘Oh my god, what are we going to do? Are you serious? Fix the valve.’ We see this type of patient a couple times a month,” Dr. Forfia said at the American College of Chest Physicians annual meeting.
“I have seen lifesaving mitral valve surgery put off for many years in patients with pulmonary hypertension, when all they needed was to have their valve fixed,” he said.
Whatever the case, pulmonologists who want the valve fixed often end up playing patient ping pong with cardiologists who want the hypertension controlled beforehand, but “if I treat the pulmonary circulation first, all I am going to do is unmask the left heart failure. There will be no functional improvement whatsoever,” Dr. Forfia said.
Surgery is the best solution as long as patients are well enough to recover. “With pulmonary hypertension in the setting of severe mitral valve regurgitation or stenosis, whether the pulmonary hypertension is related to passive left heart congestion or associated with pulmonary arteriopathy, the only sensible option is to correct the underlying valvular abnormality,” he said. The surgery should be done at an institution capable of managing postop pulmonary arteriopathy, if present.
The ping pong solution is to send patients to an expert pulmonology center; the mitral valve problem will be spotted right away.
“There is no pulmonary pressure cutoff that should prohibit surgery” in patients able to recover. “There is no such thing as a pulmonary artery pressure too high to be explained by mitral valve disease. The pulmonary pressure can be as high as it wants to be. You will get nowhere by thinking the pressure is too high to address the valve,” Dr. Forfia said.
Often “you hear, ‘I’m afraid the person is going to die on the table.’ I always say ‘if the patient is not going to die on the table, they are going to die in their living room of progressive heart failure because you [didn’t] fix their valve. I have never had a patient with pulmonary hypertension not separate from cardiopulmonary bypass. It’s a myth,” he said.
When there’s a “question if the dyspnea is coming from the mitral valve, we routinely use exercise right heart catheterization to probe the situation. We have a recumbent bike in the cath lab. You’ll often provoke significant left heart congestion with a low workload. It’s very revealing to the significance of mitral valve disease,” he said.
Aortic valve disease is also missed in pulmonary hypertension. “It’s not [a] similar” problem; “it’s the same” problem, Dr. Forfia said.
Dr. Forfia is a consultant for Bayer, Actelion, and United Therapeutics.
LOS ANGELES – Dyspnea in pulmonary hypertension is caused by mitral valve disease until proven otherwise, according to Paul Forfia, MD, director of pulmonary hypertension, right heart failure, and pulmonary thromboendarterectomy at Temple University, Philadelphia.
Although mitral valve disease is a well-recognized cause of pulmonary hypertension, its significance is often underestimated in practice.
“Whether the valve is regurgitant or stenotic makes absolutely no difference. When you delay” repair or replacement, “the patient keeps getting sicker,” he said. In time, “everyone is standing around wringing their hands going, ‘Oh my god, what are we going to do? Are you serious? Fix the valve.’ We see this type of patient a couple times a month,” Dr. Forfia said at the American College of Chest Physicians annual meeting.
“I have seen lifesaving mitral valve surgery put off for many years in patients with pulmonary hypertension, when all they needed was to have their valve fixed,” he said.
Whatever the case, pulmonologists who want the valve fixed often end up playing patient ping pong with cardiologists who want the hypertension controlled beforehand, but “if I treat the pulmonary circulation first, all I am going to do is unmask the left heart failure. There will be no functional improvement whatsoever,” Dr. Forfia said.
Surgery is the best solution as long as patients are well enough to recover. “With pulmonary hypertension in the setting of severe mitral valve regurgitation or stenosis, whether the pulmonary hypertension is related to passive left heart congestion or associated with pulmonary arteriopathy, the only sensible option is to correct the underlying valvular abnormality,” he said. The surgery should be done at an institution capable of managing postop pulmonary arteriopathy, if present.
The ping pong solution is to send patients to an expert pulmonology center; the mitral valve problem will be spotted right away.
“There is no pulmonary pressure cutoff that should prohibit surgery” in patients able to recover. “There is no such thing as a pulmonary artery pressure too high to be explained by mitral valve disease. The pulmonary pressure can be as high as it wants to be. You will get nowhere by thinking the pressure is too high to address the valve,” Dr. Forfia said.
Often “you hear, ‘I’m afraid the person is going to die on the table.’ I always say ‘if the patient is not going to die on the table, they are going to die in their living room of progressive heart failure because you [didn’t] fix their valve. I have never had a patient with pulmonary hypertension not separate from cardiopulmonary bypass. It’s a myth,” he said.
When there’s a “question if the dyspnea is coming from the mitral valve, we routinely use exercise right heart catheterization to probe the situation. We have a recumbent bike in the cath lab. You’ll often provoke significant left heart congestion with a low workload. It’s very revealing to the significance of mitral valve disease,” he said.
Aortic valve disease is also missed in pulmonary hypertension. “It’s not [a] similar” problem; “it’s the same” problem, Dr. Forfia said.
Dr. Forfia is a consultant for Bayer, Actelion, and United Therapeutics.
LOS ANGELES – Dyspnea in pulmonary hypertension is caused by mitral valve disease until proven otherwise, according to Paul Forfia, MD, director of pulmonary hypertension, right heart failure, and pulmonary thromboendarterectomy at Temple University, Philadelphia.
Although mitral valve disease is a well-recognized cause of pulmonary hypertension, its significance is often underestimated in practice.
“Whether the valve is regurgitant or stenotic makes absolutely no difference. When you delay” repair or replacement, “the patient keeps getting sicker,” he said. In time, “everyone is standing around wringing their hands going, ‘Oh my god, what are we going to do? Are you serious? Fix the valve.’ We see this type of patient a couple times a month,” Dr. Forfia said at the American College of Chest Physicians annual meeting.
“I have seen lifesaving mitral valve surgery put off for many years in patients with pulmonary hypertension, when all they needed was to have their valve fixed,” he said.
Whatever the case, pulmonologists who want the valve fixed often end up playing patient ping pong with cardiologists who want the hypertension controlled beforehand, but “if I treat the pulmonary circulation first, all I am going to do is unmask the left heart failure. There will be no functional improvement whatsoever,” Dr. Forfia said.
Surgery is the best solution as long as patients are well enough to recover. “With pulmonary hypertension in the setting of severe mitral valve regurgitation or stenosis, whether the pulmonary hypertension is related to passive left heart congestion or associated with pulmonary arteriopathy, the only sensible option is to correct the underlying valvular abnormality,” he said. The surgery should be done at an institution capable of managing postop pulmonary arteriopathy, if present.
The ping pong solution is to send patients to an expert pulmonology center; the mitral valve problem will be spotted right away.
“There is no pulmonary pressure cutoff that should prohibit surgery” in patients able to recover. “There is no such thing as a pulmonary artery pressure too high to be explained by mitral valve disease. The pulmonary pressure can be as high as it wants to be. You will get nowhere by thinking the pressure is too high to address the valve,” Dr. Forfia said.
Often “you hear, ‘I’m afraid the person is going to die on the table.’ I always say ‘if the patient is not going to die on the table, they are going to die in their living room of progressive heart failure because you [didn’t] fix their valve. I have never had a patient with pulmonary hypertension not separate from cardiopulmonary bypass. It’s a myth,” he said.
When there’s a “question if the dyspnea is coming from the mitral valve, we routinely use exercise right heart catheterization to probe the situation. We have a recumbent bike in the cath lab. You’ll often provoke significant left heart congestion with a low workload. It’s very revealing to the significance of mitral valve disease,” he said.
Aortic valve disease is also missed in pulmonary hypertension. “It’s not [a] similar” problem; “it’s the same” problem, Dr. Forfia said.
Dr. Forfia is a consultant for Bayer, Actelion, and United Therapeutics.
EXPERT ANALYSIS FROM CHEST 2016
Blood assay rapidly identifies lung cancer mutations
LOS ANGELES – A newer blood test (GeneStrat from Biodesix) identified genetic mutations in lung tumors in about 24 hours, allowing for an early start of mutation-specific chemotherapy, in an investigation from Gundersen Health System in La Crosse, Wis.
Interventional pulmonologists drew blood samples when they performed biopsies on 84 patients with highly suspicious lung nodules and submitted both blood and tissue for mutation analysis. The blood was analyzed by Biodesix, the maker of GeneStrat, a commercially available digital droplet polymerase change reaction assay launched in 2015. The company sent the results back in an average of 24.1 hours, and all within 72 hours. The mutation results from tissue analysis took 2-3 weeks.
Fifteen patients (18%) had actionable epidermal growth factor receptor, anaplastic lymphoma kinase, or K-Ras protein gene mutations, and were candidates for targeted therapy. Compared with tissue testing, the blood assay had a sensitivity of 88% and a specificity of 99%. The tissue testing picked up two mutations missed by blood testing. One of the two mutations is rare and was not included in the blood assay. Meanwhile, the assay caught a mutation missed on tissue analysis.
She and her colleagues are now routinely using GeneStrat to guide initial lung cancer therapy. “The turnaround time is fantastic. It allows us to have [the mutation status] when oncologists meet with patients for the very first time,” she said.
It “definitely” makes a difference. “If you have an actionable mutation and there’s a targeted chemotherapy” – such as erlotinib (Tarceva) for epidermal growth factor receptor mutation patients – it can be started right out of the gate. “Time to treatment is very important,” not just psychologically for patients but also for them to have the best chance against the tumor. The sooner “we can start a targeted therapy,” the better outcomes are likely to be, Dr. Mattingley said.
When mutation status is delayed, patients might be started “on the wrong therapy upfront, and it’s really hard to back up and start over again,” she said.
“Once we give patients a diagnosis of lung cancer, the next thing they should hear right away is how we are going to attack it. We felt strongly [that there was a] need to look at this to see if we could truly expedite the time from diagnosis to treatment. We believe our patients should have no sleepless nights,” Dr. Mattingley said.
There’s also usually not much tissue left after genetic work-up to send into a clinical trial. Using blood to identify mutations “may allow us to conserve our tissue block for future trials, but still get the genetic information we need to start treatment plans for our patients,” she said.
There was no company funding for the work, but Dr. Mattingley is a speaker for GeneStrat’s maker, Biodesix.
The results of this study are very promising. The high concordance between liquid biopsies and tissue biopsies as well as the short turn-around time for the results of the liquid biopsies makes a big difference in terms of getting patients started on appropriate therapy sooner rather than later. We need additional studies to find out if liquid biopsies will be good for detection of other molecular alterations such as ROS-1 and EGFR acquired mutation T790M.
The results of this study are very promising. The high concordance between liquid biopsies and tissue biopsies as well as the short turn-around time for the results of the liquid biopsies makes a big difference in terms of getting patients started on appropriate therapy sooner rather than later. We need additional studies to find out if liquid biopsies will be good for detection of other molecular alterations such as ROS-1 and EGFR acquired mutation T790M.
The results of this study are very promising. The high concordance between liquid biopsies and tissue biopsies as well as the short turn-around time for the results of the liquid biopsies makes a big difference in terms of getting patients started on appropriate therapy sooner rather than later. We need additional studies to find out if liquid biopsies will be good for detection of other molecular alterations such as ROS-1 and EGFR acquired mutation T790M.
LOS ANGELES – A newer blood test (GeneStrat from Biodesix) identified genetic mutations in lung tumors in about 24 hours, allowing for an early start of mutation-specific chemotherapy, in an investigation from Gundersen Health System in La Crosse, Wis.
Interventional pulmonologists drew blood samples when they performed biopsies on 84 patients with highly suspicious lung nodules and submitted both blood and tissue for mutation analysis. The blood was analyzed by Biodesix, the maker of GeneStrat, a commercially available digital droplet polymerase change reaction assay launched in 2015. The company sent the results back in an average of 24.1 hours, and all within 72 hours. The mutation results from tissue analysis took 2-3 weeks.
Fifteen patients (18%) had actionable epidermal growth factor receptor, anaplastic lymphoma kinase, or K-Ras protein gene mutations, and were candidates for targeted therapy. Compared with tissue testing, the blood assay had a sensitivity of 88% and a specificity of 99%. The tissue testing picked up two mutations missed by blood testing. One of the two mutations is rare and was not included in the blood assay. Meanwhile, the assay caught a mutation missed on tissue analysis.
She and her colleagues are now routinely using GeneStrat to guide initial lung cancer therapy. “The turnaround time is fantastic. It allows us to have [the mutation status] when oncologists meet with patients for the very first time,” she said.
It “definitely” makes a difference. “If you have an actionable mutation and there’s a targeted chemotherapy” – such as erlotinib (Tarceva) for epidermal growth factor receptor mutation patients – it can be started right out of the gate. “Time to treatment is very important,” not just psychologically for patients but also for them to have the best chance against the tumor. The sooner “we can start a targeted therapy,” the better outcomes are likely to be, Dr. Mattingley said.
When mutation status is delayed, patients might be started “on the wrong therapy upfront, and it’s really hard to back up and start over again,” she said.
“Once we give patients a diagnosis of lung cancer, the next thing they should hear right away is how we are going to attack it. We felt strongly [that there was a] need to look at this to see if we could truly expedite the time from diagnosis to treatment. We believe our patients should have no sleepless nights,” Dr. Mattingley said.
There’s also usually not much tissue left after genetic work-up to send into a clinical trial. Using blood to identify mutations “may allow us to conserve our tissue block for future trials, but still get the genetic information we need to start treatment plans for our patients,” she said.
There was no company funding for the work, but Dr. Mattingley is a speaker for GeneStrat’s maker, Biodesix.
LOS ANGELES – A newer blood test (GeneStrat from Biodesix) identified genetic mutations in lung tumors in about 24 hours, allowing for an early start of mutation-specific chemotherapy, in an investigation from Gundersen Health System in La Crosse, Wis.
Interventional pulmonologists drew blood samples when they performed biopsies on 84 patients with highly suspicious lung nodules and submitted both blood and tissue for mutation analysis. The blood was analyzed by Biodesix, the maker of GeneStrat, a commercially available digital droplet polymerase change reaction assay launched in 2015. The company sent the results back in an average of 24.1 hours, and all within 72 hours. The mutation results from tissue analysis took 2-3 weeks.
Fifteen patients (18%) had actionable epidermal growth factor receptor, anaplastic lymphoma kinase, or K-Ras protein gene mutations, and were candidates for targeted therapy. Compared with tissue testing, the blood assay had a sensitivity of 88% and a specificity of 99%. The tissue testing picked up two mutations missed by blood testing. One of the two mutations is rare and was not included in the blood assay. Meanwhile, the assay caught a mutation missed on tissue analysis.
She and her colleagues are now routinely using GeneStrat to guide initial lung cancer therapy. “The turnaround time is fantastic. It allows us to have [the mutation status] when oncologists meet with patients for the very first time,” she said.
It “definitely” makes a difference. “If you have an actionable mutation and there’s a targeted chemotherapy” – such as erlotinib (Tarceva) for epidermal growth factor receptor mutation patients – it can be started right out of the gate. “Time to treatment is very important,” not just psychologically for patients but also for them to have the best chance against the tumor. The sooner “we can start a targeted therapy,” the better outcomes are likely to be, Dr. Mattingley said.
When mutation status is delayed, patients might be started “on the wrong therapy upfront, and it’s really hard to back up and start over again,” she said.
“Once we give patients a diagnosis of lung cancer, the next thing they should hear right away is how we are going to attack it. We felt strongly [that there was a] need to look at this to see if we could truly expedite the time from diagnosis to treatment. We believe our patients should have no sleepless nights,” Dr. Mattingley said.
There’s also usually not much tissue left after genetic work-up to send into a clinical trial. Using blood to identify mutations “may allow us to conserve our tissue block for future trials, but still get the genetic information we need to start treatment plans for our patients,” she said.
There was no company funding for the work, but Dr. Mattingley is a speaker for GeneStrat’s maker, Biodesix.
AT CHEST 2016
Key clinical point:
Major finding: Compared with tissue testing, the blood assay had a sensitivity of 88% and a specificity of 99%.
Data source: Eighty-four patients with highly suspicious lung nodules.
Disclosures: There was no company funding for the work, but the presenter is a paid speaker for GeneStrat’s maker, Biodesix.
Prognostic scores helpful in subset of COPD patients
LOS ANGELES – The Sequential Organ Failure Assessment (SOFA) score and the Glasgow Coma Scale (GCS) are simple, accurate tools for risk stratification of hospitalized patients with acute exacerbation of COPD, results from a single-center study showed.
“Acute exacerbations of chronic obstructive pulmonary disease often require hospitalization, may necessitate mechanical ventilation, and can be fatal,” Mohamed Metwally, MD, FCCP, said in an interview in advance of the annual meeting of the American College of Chest Physicians. “There are currently no validated disease-specific scores that measure the severity of acute exacerbation. Prognostic tools are needed to assess acute exacerbations of chronic obstructive pulmonary disease.”
For the 2-year study, Dr. Metwally and his associates prospectively evaluated 250 critically ill ICU AECOPD patients, mean age 65 years, at Assiut University Hospital between December 2012 and December 2014. The primary outcome was in-hospital mortality while the secondary endpoint was need for intubation and mechanical ventilation. The researchers excluded patients who died less than 24 hours after admission, those with underlying COPD who were admitted with another primary diagnosis such as an accident or a stroke, or for elective hospitalizations such as elective surgery or diagnostic procedures.
Dr. Metwally and his associates collected sociodemographic data, vital signs, and other clinical variables, and collected scores from five tools used to measure mortality prediction: the Acute Physiology and Chronic Health Evaluation (APACHE II), the SOFA score, the Early Warning Score (EWS), the GCS, and the Charlson Comorbidity Index (CCI). To assess performance of the scores, they used area under the receiver operating characteristic curve (AUC) analysis and the Hosmer-Lemeshow goodness-of-fit test for logistic regression.
Of the 250 patients, 43 (17%) died during their hospital stay and 54% required mechanical ventilation. All recorded scores were significantly higher in nonsurvivors, compared with survivors, and the risk of clinical deterioration increased with increasing scores. The discriminatory power of each score varied as measured by AUC analysis. The AUC of APACHE II, SOFA, EWS, GCS, and CCI were 0.79, 0.81, 0.76, 0.69, and 0.68, respectively “and all these models had good calibration in mortality prediction,” Dr. Metwally said. The SOFA score was the best in predicting mortality (its predicted mortality was 16%, compared with the actual mortality of 17%), while the APACHE II score overestimated mortality by at least twofold (46% vs. 17%). In addition, the EWS outperformed the GCS in predicting mortality. “This may be due to EWS containing all vital signs plus level of consciousness,” he said in an interview.
The GCS was found to be the most useful in predicting need for mechanical ventilation, with an AUC of 0.81. The AUCs of APACHE II, SOFA, EWS, and CCI were 0.79, 0.80, 0.73, and 0.61, respectively. All of the scores had good calibration in mortality prediction, Dr. Metwally said, with the exception of SOFA.
As for the APACHE II, Dr. Metwally said that instrument “can be used as a tool to predict both mortality and intubation in a specific group of patients, but with low discriminatory power.” He acknowledged certain limitations of the study, including the fact that it was limited to patients with AECOPD. “Future studies should include any critically ill respiratory patients,” he said.
He reported having no financial disclosures.
LOS ANGELES – The Sequential Organ Failure Assessment (SOFA) score and the Glasgow Coma Scale (GCS) are simple, accurate tools for risk stratification of hospitalized patients with acute exacerbation of COPD, results from a single-center study showed.
“Acute exacerbations of chronic obstructive pulmonary disease often require hospitalization, may necessitate mechanical ventilation, and can be fatal,” Mohamed Metwally, MD, FCCP, said in an interview in advance of the annual meeting of the American College of Chest Physicians. “There are currently no validated disease-specific scores that measure the severity of acute exacerbation. Prognostic tools are needed to assess acute exacerbations of chronic obstructive pulmonary disease.”
For the 2-year study, Dr. Metwally and his associates prospectively evaluated 250 critically ill ICU AECOPD patients, mean age 65 years, at Assiut University Hospital between December 2012 and December 2014. The primary outcome was in-hospital mortality while the secondary endpoint was need for intubation and mechanical ventilation. The researchers excluded patients who died less than 24 hours after admission, those with underlying COPD who were admitted with another primary diagnosis such as an accident or a stroke, or for elective hospitalizations such as elective surgery or diagnostic procedures.
Dr. Metwally and his associates collected sociodemographic data, vital signs, and other clinical variables, and collected scores from five tools used to measure mortality prediction: the Acute Physiology and Chronic Health Evaluation (APACHE II), the SOFA score, the Early Warning Score (EWS), the GCS, and the Charlson Comorbidity Index (CCI). To assess performance of the scores, they used area under the receiver operating characteristic curve (AUC) analysis and the Hosmer-Lemeshow goodness-of-fit test for logistic regression.
Of the 250 patients, 43 (17%) died during their hospital stay and 54% required mechanical ventilation. All recorded scores were significantly higher in nonsurvivors, compared with survivors, and the risk of clinical deterioration increased with increasing scores. The discriminatory power of each score varied as measured by AUC analysis. The AUC of APACHE II, SOFA, EWS, GCS, and CCI were 0.79, 0.81, 0.76, 0.69, and 0.68, respectively “and all these models had good calibration in mortality prediction,” Dr. Metwally said. The SOFA score was the best in predicting mortality (its predicted mortality was 16%, compared with the actual mortality of 17%), while the APACHE II score overestimated mortality by at least twofold (46% vs. 17%). In addition, the EWS outperformed the GCS in predicting mortality. “This may be due to EWS containing all vital signs plus level of consciousness,” he said in an interview.
The GCS was found to be the most useful in predicting need for mechanical ventilation, with an AUC of 0.81. The AUCs of APACHE II, SOFA, EWS, and CCI were 0.79, 0.80, 0.73, and 0.61, respectively. All of the scores had good calibration in mortality prediction, Dr. Metwally said, with the exception of SOFA.
As for the APACHE II, Dr. Metwally said that instrument “can be used as a tool to predict both mortality and intubation in a specific group of patients, but with low discriminatory power.” He acknowledged certain limitations of the study, including the fact that it was limited to patients with AECOPD. “Future studies should include any critically ill respiratory patients,” he said.
He reported having no financial disclosures.
LOS ANGELES – The Sequential Organ Failure Assessment (SOFA) score and the Glasgow Coma Scale (GCS) are simple, accurate tools for risk stratification of hospitalized patients with acute exacerbation of COPD, results from a single-center study showed.
“Acute exacerbations of chronic obstructive pulmonary disease often require hospitalization, may necessitate mechanical ventilation, and can be fatal,” Mohamed Metwally, MD, FCCP, said in an interview in advance of the annual meeting of the American College of Chest Physicians. “There are currently no validated disease-specific scores that measure the severity of acute exacerbation. Prognostic tools are needed to assess acute exacerbations of chronic obstructive pulmonary disease.”
For the 2-year study, Dr. Metwally and his associates prospectively evaluated 250 critically ill ICU AECOPD patients, mean age 65 years, at Assiut University Hospital between December 2012 and December 2014. The primary outcome was in-hospital mortality while the secondary endpoint was need for intubation and mechanical ventilation. The researchers excluded patients who died less than 24 hours after admission, those with underlying COPD who were admitted with another primary diagnosis such as an accident or a stroke, or for elective hospitalizations such as elective surgery or diagnostic procedures.
Dr. Metwally and his associates collected sociodemographic data, vital signs, and other clinical variables, and collected scores from five tools used to measure mortality prediction: the Acute Physiology and Chronic Health Evaluation (APACHE II), the SOFA score, the Early Warning Score (EWS), the GCS, and the Charlson Comorbidity Index (CCI). To assess performance of the scores, they used area under the receiver operating characteristic curve (AUC) analysis and the Hosmer-Lemeshow goodness-of-fit test for logistic regression.
Of the 250 patients, 43 (17%) died during their hospital stay and 54% required mechanical ventilation. All recorded scores were significantly higher in nonsurvivors, compared with survivors, and the risk of clinical deterioration increased with increasing scores. The discriminatory power of each score varied as measured by AUC analysis. The AUC of APACHE II, SOFA, EWS, GCS, and CCI were 0.79, 0.81, 0.76, 0.69, and 0.68, respectively “and all these models had good calibration in mortality prediction,” Dr. Metwally said. The SOFA score was the best in predicting mortality (its predicted mortality was 16%, compared with the actual mortality of 17%), while the APACHE II score overestimated mortality by at least twofold (46% vs. 17%). In addition, the EWS outperformed the GCS in predicting mortality. “This may be due to EWS containing all vital signs plus level of consciousness,” he said in an interview.
The GCS was found to be the most useful in predicting need for mechanical ventilation, with an AUC of 0.81. The AUCs of APACHE II, SOFA, EWS, and CCI were 0.79, 0.80, 0.73, and 0.61, respectively. All of the scores had good calibration in mortality prediction, Dr. Metwally said, with the exception of SOFA.
As for the APACHE II, Dr. Metwally said that instrument “can be used as a tool to predict both mortality and intubation in a specific group of patients, but with low discriminatory power.” He acknowledged certain limitations of the study, including the fact that it was limited to patients with AECOPD. “Future studies should include any critically ill respiratory patients,” he said.
He reported having no financial disclosures.
AT CHEST 2016
Key clinical point:
Major finding: The Sequential Organ Failure Assessment score was the best in predicting mortality of patients with acute exacerbation of COPD (its predicted mortality was 16%, compared with the actual mortality of 17%).
Data source: A prospective evaluation of 250 critically ill ICU patients hospitalized with acute exacerbation of COPD.
Disclosures: Dr. Metwally reported having no financial disclosures.
Comorbidities common in COPD patients
LOS ANGELES – Comorbidities are common in patients with chronic obstructive pulmonary disease, especially cardiovascular disease, diabetes, anemia, and osteoporosis, results from a single-center analysis showed.
“These affect the course and outcome of COPD, so identification and treatment of these comorbidities is very important,” Hamdy Mohammadien, MD, said in an interview in advance of the annual meeting of the American College of Chest Physicians.
In an effort to estimate the presence of comorbidities in patients with COPD and to assess the relationship of comorbid diseases with age, sex, C-reactive protein, and COPD severity, Dr. Mohammadien and his associates at Sohag (Egypt) University, retrospectively evaluated 400 COPD patients who were at least 40 years of age. Those who presented with bronchial asthma or other lung diseases were excluded from the analysis. The mean age of patients was 62 years, 69% were male, and 36% were current smokers. Their mean FEV1/FVC ratio (forced expiratory volume in 1 second/forced vital capacity) was 48%, and 57% had two or more exacerbations in the previous year.
Dr. Mohammadien reported that all patients had at least one comorbidity. The most common comorbidities were cardiovascular diseases (85%), diabetes (35%), dyslipidemia (23%), osteopenia (11%), anemia (10%), muscle wasting (9%), pneumonia (7%), osteoporosis (6%), GERD (2%), and lung cancer (2%). He also noted that the association between cardiovascular events, dyslipidemia, diabetes, osteoporosis, muscle wasting, and anemia was highly significant in COPD patients aged 60 years and older, in men, and in patients with stage III and IV COPD. In addition, a significant relationship was observed between a positive CRP level and each comorbidity, with the exception of gastroesophageal reflux disease and lung cancer. The three comorbidities with the greatest significance were ischemic heart disease (P = .0001), dyslipidemia (P = .0001), and pneumonia (P = .0003). Finally, frequent exacerbators were significantly more likely to have two or more comorbidities (odds ratio 2; P = .04) and to have more hospitalizations in the past year (P less than .01).
“Comorbidities are common in patients with COPD, and have a significant impact on health status and prognosis, thus justifying the need for a comprehensive and integrating therapeutic approach,” Dr. Mohammadien said at the meeting. “In the management of COPD all these conditions need to be carefully evaluated and treated.”
He acknowledged certain limitations of the study, including its relatively small sample size and the fact that bone density was measured by sonar and not by dual-energy x-ray absorptiometry. Dr. Mohammadien reported having no financial disclosures.
LOS ANGELES – Comorbidities are common in patients with chronic obstructive pulmonary disease, especially cardiovascular disease, diabetes, anemia, and osteoporosis, results from a single-center analysis showed.
“These affect the course and outcome of COPD, so identification and treatment of these comorbidities is very important,” Hamdy Mohammadien, MD, said in an interview in advance of the annual meeting of the American College of Chest Physicians.
In an effort to estimate the presence of comorbidities in patients with COPD and to assess the relationship of comorbid diseases with age, sex, C-reactive protein, and COPD severity, Dr. Mohammadien and his associates at Sohag (Egypt) University, retrospectively evaluated 400 COPD patients who were at least 40 years of age. Those who presented with bronchial asthma or other lung diseases were excluded from the analysis. The mean age of patients was 62 years, 69% were male, and 36% were current smokers. Their mean FEV1/FVC ratio (forced expiratory volume in 1 second/forced vital capacity) was 48%, and 57% had two or more exacerbations in the previous year.
Dr. Mohammadien reported that all patients had at least one comorbidity. The most common comorbidities were cardiovascular diseases (85%), diabetes (35%), dyslipidemia (23%), osteopenia (11%), anemia (10%), muscle wasting (9%), pneumonia (7%), osteoporosis (6%), GERD (2%), and lung cancer (2%). He also noted that the association between cardiovascular events, dyslipidemia, diabetes, osteoporosis, muscle wasting, and anemia was highly significant in COPD patients aged 60 years and older, in men, and in patients with stage III and IV COPD. In addition, a significant relationship was observed between a positive CRP level and each comorbidity, with the exception of gastroesophageal reflux disease and lung cancer. The three comorbidities with the greatest significance were ischemic heart disease (P = .0001), dyslipidemia (P = .0001), and pneumonia (P = .0003). Finally, frequent exacerbators were significantly more likely to have two or more comorbidities (odds ratio 2; P = .04) and to have more hospitalizations in the past year (P less than .01).
“Comorbidities are common in patients with COPD, and have a significant impact on health status and prognosis, thus justifying the need for a comprehensive and integrating therapeutic approach,” Dr. Mohammadien said at the meeting. “In the management of COPD all these conditions need to be carefully evaluated and treated.”
He acknowledged certain limitations of the study, including its relatively small sample size and the fact that bone density was measured by sonar and not by dual-energy x-ray absorptiometry. Dr. Mohammadien reported having no financial disclosures.
LOS ANGELES – Comorbidities are common in patients with chronic obstructive pulmonary disease, especially cardiovascular disease, diabetes, anemia, and osteoporosis, results from a single-center analysis showed.
“These affect the course and outcome of COPD, so identification and treatment of these comorbidities is very important,” Hamdy Mohammadien, MD, said in an interview in advance of the annual meeting of the American College of Chest Physicians.
In an effort to estimate the presence of comorbidities in patients with COPD and to assess the relationship of comorbid diseases with age, sex, C-reactive protein, and COPD severity, Dr. Mohammadien and his associates at Sohag (Egypt) University, retrospectively evaluated 400 COPD patients who were at least 40 years of age. Those who presented with bronchial asthma or other lung diseases were excluded from the analysis. The mean age of patients was 62 years, 69% were male, and 36% were current smokers. Their mean FEV1/FVC ratio (forced expiratory volume in 1 second/forced vital capacity) was 48%, and 57% had two or more exacerbations in the previous year.
Dr. Mohammadien reported that all patients had at least one comorbidity. The most common comorbidities were cardiovascular diseases (85%), diabetes (35%), dyslipidemia (23%), osteopenia (11%), anemia (10%), muscle wasting (9%), pneumonia (7%), osteoporosis (6%), GERD (2%), and lung cancer (2%). He also noted that the association between cardiovascular events, dyslipidemia, diabetes, osteoporosis, muscle wasting, and anemia was highly significant in COPD patients aged 60 years and older, in men, and in patients with stage III and IV COPD. In addition, a significant relationship was observed between a positive CRP level and each comorbidity, with the exception of gastroesophageal reflux disease and lung cancer. The three comorbidities with the greatest significance were ischemic heart disease (P = .0001), dyslipidemia (P = .0001), and pneumonia (P = .0003). Finally, frequent exacerbators were significantly more likely to have two or more comorbidities (odds ratio 2; P = .04) and to have more hospitalizations in the past year (P less than .01).
“Comorbidities are common in patients with COPD, and have a significant impact on health status and prognosis, thus justifying the need for a comprehensive and integrating therapeutic approach,” Dr. Mohammadien said at the meeting. “In the management of COPD all these conditions need to be carefully evaluated and treated.”
He acknowledged certain limitations of the study, including its relatively small sample size and the fact that bone density was measured by sonar and not by dual-energy x-ray absorptiometry. Dr. Mohammadien reported having no financial disclosures.
AT CHEST 2016
Key clinical point:
Major finding: The three most common comorbidities in COPD patients were cardiovascular diseases (85%), diabetes (35%), and dyslipidemia (23%).
Data source: A retrospective study of 400 patients with COPD.
Disclosures: Dr. Mohammadien reported having no financial disclosures.
Two factors associated with vocal cord dysfunction in study
LOS ANGELES – Female sex and the absence of wheezing were the only factors significantly associated with vocal cord dysfunction in patients with high pretest probability of disease, a retrospective analysis showed.
The findings differ from those of the Pittsburgh Vocal Cord Index, which identified symptoms of throat tightness, dysphonia, absence of wheezing, and the presence of odors as key features predictive of vocal cord dysfunction (VCD). “This proves the point that VCD is an elusive diagnosis,” lead study author Phalgoon Shah, MD, said, in an interview, at the annual meeting of the American College of Chest Physicians.
The researchers found that a history of depression or anxiety, throat tightness, dysphonia, odor symptom trigger, lack of response to bronchodilator or truncation, and flattening of the inspiratory volume curve did not predict VCD.
The patients were active duty military personnel and veterans who were referred to the pulmonary function lab at Tripler Army Medical Center, Honolulu, for suspected VCD between 2010 and 2014. The researchers identified patients by laryngoscopy procedure code and collected numerous variables, including demographic information, past medical history, pulmonary function test data, and clinical variables such as ED visits for dyspnea.
Dr. Shah of the division of pulmonary and critical care at Tripler said that direct laryngoscopic visualization is used to diagnose VCD in military personnel because the diagnosis is grounds for dismissal, but in other practice settings, the technique is not readily available, even though it is considered the gold standard. “You might still have a very high clinical suspicion of VCD in spite of a negative laryngoscopy, and you send these patients to speech therapy and they get better,” he said. “By logic, you can assume that these patients had VCD, you just didn’t catch it right in the lab. For the first time, we are saying that exercise laryngoscopy is not the gold standard.”
He emphasized that more research is required to develop a validated scoring system to predict a diagnosis of VCD and to distinguish it from asthma. He reported having no financial disclosures.
LOS ANGELES – Female sex and the absence of wheezing were the only factors significantly associated with vocal cord dysfunction in patients with high pretest probability of disease, a retrospective analysis showed.
The findings differ from those of the Pittsburgh Vocal Cord Index, which identified symptoms of throat tightness, dysphonia, absence of wheezing, and the presence of odors as key features predictive of vocal cord dysfunction (VCD). “This proves the point that VCD is an elusive diagnosis,” lead study author Phalgoon Shah, MD, said, in an interview, at the annual meeting of the American College of Chest Physicians.
The researchers found that a history of depression or anxiety, throat tightness, dysphonia, odor symptom trigger, lack of response to bronchodilator or truncation, and flattening of the inspiratory volume curve did not predict VCD.
The patients were active duty military personnel and veterans who were referred to the pulmonary function lab at Tripler Army Medical Center, Honolulu, for suspected VCD between 2010 and 2014. The researchers identified patients by laryngoscopy procedure code and collected numerous variables, including demographic information, past medical history, pulmonary function test data, and clinical variables such as ED visits for dyspnea.
Dr. Shah of the division of pulmonary and critical care at Tripler said that direct laryngoscopic visualization is used to diagnose VCD in military personnel because the diagnosis is grounds for dismissal, but in other practice settings, the technique is not readily available, even though it is considered the gold standard. “You might still have a very high clinical suspicion of VCD in spite of a negative laryngoscopy, and you send these patients to speech therapy and they get better,” he said. “By logic, you can assume that these patients had VCD, you just didn’t catch it right in the lab. For the first time, we are saying that exercise laryngoscopy is not the gold standard.”
He emphasized that more research is required to develop a validated scoring system to predict a diagnosis of VCD and to distinguish it from asthma. He reported having no financial disclosures.
LOS ANGELES – Female sex and the absence of wheezing were the only factors significantly associated with vocal cord dysfunction in patients with high pretest probability of disease, a retrospective analysis showed.
The findings differ from those of the Pittsburgh Vocal Cord Index, which identified symptoms of throat tightness, dysphonia, absence of wheezing, and the presence of odors as key features predictive of vocal cord dysfunction (VCD). “This proves the point that VCD is an elusive diagnosis,” lead study author Phalgoon Shah, MD, said, in an interview, at the annual meeting of the American College of Chest Physicians.
The researchers found that a history of depression or anxiety, throat tightness, dysphonia, odor symptom trigger, lack of response to bronchodilator or truncation, and flattening of the inspiratory volume curve did not predict VCD.
The patients were active duty military personnel and veterans who were referred to the pulmonary function lab at Tripler Army Medical Center, Honolulu, for suspected VCD between 2010 and 2014. The researchers identified patients by laryngoscopy procedure code and collected numerous variables, including demographic information, past medical history, pulmonary function test data, and clinical variables such as ED visits for dyspnea.
Dr. Shah of the division of pulmonary and critical care at Tripler said that direct laryngoscopic visualization is used to diagnose VCD in military personnel because the diagnosis is grounds for dismissal, but in other practice settings, the technique is not readily available, even though it is considered the gold standard. “You might still have a very high clinical suspicion of VCD in spite of a negative laryngoscopy, and you send these patients to speech therapy and they get better,” he said. “By logic, you can assume that these patients had VCD, you just didn’t catch it right in the lab. For the first time, we are saying that exercise laryngoscopy is not the gold standard.”
He emphasized that more research is required to develop a validated scoring system to predict a diagnosis of VCD and to distinguish it from asthma. He reported having no financial disclosures.
AT CHEST 2016
Key clinical point:
Major finding: The only variables significantly associated with VCD were female sex (P = .006) and the absence of wheezing (P = .037).
Data source: A retrospective analysis of 244 patients referred to a pulmonary function lab for suspected VCD.
Disclosures: Dr. Shah reported having no financial disclosures.