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VIDEO: What are physicians’ top legal risks in 2016?
AUSTIN, TEX. – With ongoing changes in health delivery and ever-increasing government scrutiny over care, physicians face a number of pressing legal risks this year.
At an American Health Lawyers Association meeting, Birmingham, Ala., health law attorney William W. Horton shared the top legal dangers for doctors in 2016.
From False Claims Act investigations and whistle-blower claims to liability connected to value-based care, clinicians have a lot to consider, said Mr. Horton, who is chair of the American Bar Association Health Law Section.
In a video interview, Mr. Horton also discussed how to reduce liability and limit government inquiries.
On Twitter @legal_med
AUSTIN, TEX. – With ongoing changes in health delivery and ever-increasing government scrutiny over care, physicians face a number of pressing legal risks this year.
At an American Health Lawyers Association meeting, Birmingham, Ala., health law attorney William W. Horton shared the top legal dangers for doctors in 2016.
From False Claims Act investigations and whistle-blower claims to liability connected to value-based care, clinicians have a lot to consider, said Mr. Horton, who is chair of the American Bar Association Health Law Section.
In a video interview, Mr. Horton also discussed how to reduce liability and limit government inquiries.
On Twitter @legal_med
AUSTIN, TEX. – With ongoing changes in health delivery and ever-increasing government scrutiny over care, physicians face a number of pressing legal risks this year.
At an American Health Lawyers Association meeting, Birmingham, Ala., health law attorney William W. Horton shared the top legal dangers for doctors in 2016.
From False Claims Act investigations and whistle-blower claims to liability connected to value-based care, clinicians have a lot to consider, said Mr. Horton, who is chair of the American Bar Association Health Law Section.
In a video interview, Mr. Horton also discussed how to reduce liability and limit government inquiries.
On Twitter @legal_med
EXPERT ANALYSIS FROM THE PHYSICIANS AND HOSPITALS LAW INSTITUTE
Q.N.S.
In the early 1970’s, the three letters that a pediatric house officer hated to see on a slip returning from the lab were Q.N.S. Quality Not Sufficient meant that the minutes, which seemed like hours, you had invested torturing some poor sick child to obtain just a few cc’s of blood had been wasted. It also meant returning to the patient’s crib or bedside to explain to the child and her parents that the torture you had promised was over for the day was in fact not over.
Tourniquets were fished out of lapel buttonholes, and the search for a decent vein had to begin all over again. If the child was chubby or bloated with retained fluid, those veins were invisible. If the child had been ill for weeks – particularly if the patient had been on chemotherapy – all of the good veins had been blown or had clotted days ago.
Many of the patients were saintly and eerily cooperative despite your fumbling attempts at venipuncture, but most were not. Some parents were so supportive of your efforts that you wanted to hug them when the ordeal was over (and you did). A few parents amped up the tension at the bedside so much that you wanted to ask them to leave (but you didn’t). If a parent was understandably incapable of effectively restraining the child, you needed to find an experienced nurse to help. A few of the best nurses were so good that the house officer merely needed to hold the needle still, and the child was repositioned in just the right orientation so that the puncture occurred miraculously.
There were some last ditch efforts at phlebotomy that were so ghastly that you had to ask the parents to leave. I don’t know if the infamous internal jugular stick is still used, but it wasn’t pretty. And it was almost as frightening for the physician holding the needle as it was for the patient. Even in the big teaching hospitals, dedicated phlebotomists hadn’t been invented yet. A few nurses had earned reputations as good vein finders, but for the most part it was on-the-job training for the house officers.
It was not until 1973 that Dr. John Broviac’s central line catheters became available in some hospitals and 1979 until Dr. Robert Hickman’s version appeared. It took a few more years before techniques were perfected for safely drawing specimens from these lines that had been originally intended for infusion. But for me and my cohort of house officers and our unfortunate patients, it was years too late. I am sure that caring for hospitalized pediatric cancer patients today continues to be dominated by challenges. But for those of us tasked with drawing blood from patients without the benefit of central line catheters, it was gut wrenching.
Those battles for a few cc’s of blood left their scars. I have seldom ordered any blood test without asking myself whether there wasn’t a bloodless way of assessing the patient’s condition. Or couldn’t we just do the test on a drop or two of blood? Of course, as I as finishing my training, more tests were downsized so that they could be done “micro.” But as you know, getting enough blood from a heel stick or finger prick isn’t always as easy as it sounds. If the child is shocky or cold, a good blood flow is hard to obtain. Warming helps but squeezing doesn’t because tissue juices can dilute the sample, and the trauma of squeezing can contaminate the sample.
A study published in the American Journal of Clinical Pathology raises the question of how accurately even a single drop of blood reflects what is going on in the patient’s total blood pool (“Drop by drop variation in the cellular components of fingerprick blood: Implications for point-of-care diagnostic development” [Am J Clin Pathol. 2015 Dec;144(6):885-94]). Two bioengineers from Rice University discovered that six successive drops of blood from a single finger prick varied by a significant amount when analyzed for a variety of cellular components. For example, the drop-to-drop variability for hemoglobin was five times that of a sample collected by venipuncture.
You and I may dream of the day when just a drop will do it and we can put our needles away for good. Unfortunately, for now, the answer is that a single drop of blood is a Q.N.S.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.”
In the early 1970’s, the three letters that a pediatric house officer hated to see on a slip returning from the lab were Q.N.S. Quality Not Sufficient meant that the minutes, which seemed like hours, you had invested torturing some poor sick child to obtain just a few cc’s of blood had been wasted. It also meant returning to the patient’s crib or bedside to explain to the child and her parents that the torture you had promised was over for the day was in fact not over.
Tourniquets were fished out of lapel buttonholes, and the search for a decent vein had to begin all over again. If the child was chubby or bloated with retained fluid, those veins were invisible. If the child had been ill for weeks – particularly if the patient had been on chemotherapy – all of the good veins had been blown or had clotted days ago.
Many of the patients were saintly and eerily cooperative despite your fumbling attempts at venipuncture, but most were not. Some parents were so supportive of your efforts that you wanted to hug them when the ordeal was over (and you did). A few parents amped up the tension at the bedside so much that you wanted to ask them to leave (but you didn’t). If a parent was understandably incapable of effectively restraining the child, you needed to find an experienced nurse to help. A few of the best nurses were so good that the house officer merely needed to hold the needle still, and the child was repositioned in just the right orientation so that the puncture occurred miraculously.
There were some last ditch efforts at phlebotomy that were so ghastly that you had to ask the parents to leave. I don’t know if the infamous internal jugular stick is still used, but it wasn’t pretty. And it was almost as frightening for the physician holding the needle as it was for the patient. Even in the big teaching hospitals, dedicated phlebotomists hadn’t been invented yet. A few nurses had earned reputations as good vein finders, but for the most part it was on-the-job training for the house officers.
It was not until 1973 that Dr. John Broviac’s central line catheters became available in some hospitals and 1979 until Dr. Robert Hickman’s version appeared. It took a few more years before techniques were perfected for safely drawing specimens from these lines that had been originally intended for infusion. But for me and my cohort of house officers and our unfortunate patients, it was years too late. I am sure that caring for hospitalized pediatric cancer patients today continues to be dominated by challenges. But for those of us tasked with drawing blood from patients without the benefit of central line catheters, it was gut wrenching.
Those battles for a few cc’s of blood left their scars. I have seldom ordered any blood test without asking myself whether there wasn’t a bloodless way of assessing the patient’s condition. Or couldn’t we just do the test on a drop or two of blood? Of course, as I as finishing my training, more tests were downsized so that they could be done “micro.” But as you know, getting enough blood from a heel stick or finger prick isn’t always as easy as it sounds. If the child is shocky or cold, a good blood flow is hard to obtain. Warming helps but squeezing doesn’t because tissue juices can dilute the sample, and the trauma of squeezing can contaminate the sample.
A study published in the American Journal of Clinical Pathology raises the question of how accurately even a single drop of blood reflects what is going on in the patient’s total blood pool (“Drop by drop variation in the cellular components of fingerprick blood: Implications for point-of-care diagnostic development” [Am J Clin Pathol. 2015 Dec;144(6):885-94]). Two bioengineers from Rice University discovered that six successive drops of blood from a single finger prick varied by a significant amount when analyzed for a variety of cellular components. For example, the drop-to-drop variability for hemoglobin was five times that of a sample collected by venipuncture.
You and I may dream of the day when just a drop will do it and we can put our needles away for good. Unfortunately, for now, the answer is that a single drop of blood is a Q.N.S.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.”
In the early 1970’s, the three letters that a pediatric house officer hated to see on a slip returning from the lab were Q.N.S. Quality Not Sufficient meant that the minutes, which seemed like hours, you had invested torturing some poor sick child to obtain just a few cc’s of blood had been wasted. It also meant returning to the patient’s crib or bedside to explain to the child and her parents that the torture you had promised was over for the day was in fact not over.
Tourniquets were fished out of lapel buttonholes, and the search for a decent vein had to begin all over again. If the child was chubby or bloated with retained fluid, those veins were invisible. If the child had been ill for weeks – particularly if the patient had been on chemotherapy – all of the good veins had been blown or had clotted days ago.
Many of the patients were saintly and eerily cooperative despite your fumbling attempts at venipuncture, but most were not. Some parents were so supportive of your efforts that you wanted to hug them when the ordeal was over (and you did). A few parents amped up the tension at the bedside so much that you wanted to ask them to leave (but you didn’t). If a parent was understandably incapable of effectively restraining the child, you needed to find an experienced nurse to help. A few of the best nurses were so good that the house officer merely needed to hold the needle still, and the child was repositioned in just the right orientation so that the puncture occurred miraculously.
There were some last ditch efforts at phlebotomy that were so ghastly that you had to ask the parents to leave. I don’t know if the infamous internal jugular stick is still used, but it wasn’t pretty. And it was almost as frightening for the physician holding the needle as it was for the patient. Even in the big teaching hospitals, dedicated phlebotomists hadn’t been invented yet. A few nurses had earned reputations as good vein finders, but for the most part it was on-the-job training for the house officers.
It was not until 1973 that Dr. John Broviac’s central line catheters became available in some hospitals and 1979 until Dr. Robert Hickman’s version appeared. It took a few more years before techniques were perfected for safely drawing specimens from these lines that had been originally intended for infusion. But for me and my cohort of house officers and our unfortunate patients, it was years too late. I am sure that caring for hospitalized pediatric cancer patients today continues to be dominated by challenges. But for those of us tasked with drawing blood from patients without the benefit of central line catheters, it was gut wrenching.
Those battles for a few cc’s of blood left their scars. I have seldom ordered any blood test without asking myself whether there wasn’t a bloodless way of assessing the patient’s condition. Or couldn’t we just do the test on a drop or two of blood? Of course, as I as finishing my training, more tests were downsized so that they could be done “micro.” But as you know, getting enough blood from a heel stick or finger prick isn’t always as easy as it sounds. If the child is shocky or cold, a good blood flow is hard to obtain. Warming helps but squeezing doesn’t because tissue juices can dilute the sample, and the trauma of squeezing can contaminate the sample.
A study published in the American Journal of Clinical Pathology raises the question of how accurately even a single drop of blood reflects what is going on in the patient’s total blood pool (“Drop by drop variation in the cellular components of fingerprick blood: Implications for point-of-care diagnostic development” [Am J Clin Pathol. 2015 Dec;144(6):885-94]). Two bioengineers from Rice University discovered that six successive drops of blood from a single finger prick varied by a significant amount when analyzed for a variety of cellular components. For example, the drop-to-drop variability for hemoglobin was five times that of a sample collected by venipuncture.
You and I may dream of the day when just a drop will do it and we can put our needles away for good. Unfortunately, for now, the answer is that a single drop of blood is a Q.N.S.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics including “How to Say No to Your Toddler.”
AATS 96th Annual Meeting
May 14-18, 2016
Baltimore, MD
President & Annual Meeting Chair
Joseph S. Coselli
Annual Meeting Co-Chairs
Charles D. Fraser
David R. Jones
View Preliminary Program, Speakers, Presentations and Full Abstracts
The 96th Annual Meeting is a five-day program of state-of-the-art presentations by renowned experts. Attendees will enhance their knowledge and skills in a wide-range of subjects including general and specialized cardiac surgery, emerging technologies, congenital heart disease, critical care and aortic/endovascular surgery.
Don’t miss this year’s exciting program including:
Saturday Skills Courses featuring Combined Luncheon Speaker: Denton A. Cooley, followed by Hands-On Sessions
Sunday Postgraduate Symposia with Legends Luncheons featuring Joel D. Cooper and John L. Ochsner
New: Survival Guide for the Cardiothoracic Surgical Team course following by a Hands-On Session (Available to Residents, Fellows and Health Care Professionals Only)
Presidential Address: Competition: Perspiration to Inspiration “Aut viam inveniam aut faciam”, Joseph S. Coselli, Baylor College of Medicine
Basic Science Lecture: Stopping Incurable Cancers through Eliminating their Anti-Oxidative Defenses, James D. Watson, a Nobel Prize-winning biophysicist and researcher who is credited with co-discovering the double-helix structure of DNA.
Honored Guest Lecture: Brian Kelly, Notre Dame Head Football Coach and a veteran of 23 seasons as a collegiate head coach. Brian Kelly brings a championship tradition to his fifth year as the 29th head football coach at the University of Notre Dame.
Emerging Technologies & Techniques For: Adult Cardiac and General Thoracic
VAD/ECMO SessionMasters of Surgery: Video Sessions
AATS Learning Center: Featuring cutting-edge case videos of novel procedures and surgical techniques.
May 14-18, 2016
Baltimore, MD
President & Annual Meeting Chair
Joseph S. Coselli
Annual Meeting Co-Chairs
Charles D. Fraser
David R. Jones
View Preliminary Program, Speakers, Presentations and Full Abstracts
The 96th Annual Meeting is a five-day program of state-of-the-art presentations by renowned experts. Attendees will enhance their knowledge and skills in a wide-range of subjects including general and specialized cardiac surgery, emerging technologies, congenital heart disease, critical care and aortic/endovascular surgery.
Don’t miss this year’s exciting program including:
Saturday Skills Courses featuring Combined Luncheon Speaker: Denton A. Cooley, followed by Hands-On Sessions
Sunday Postgraduate Symposia with Legends Luncheons featuring Joel D. Cooper and John L. Ochsner
New: Survival Guide for the Cardiothoracic Surgical Team course following by a Hands-On Session (Available to Residents, Fellows and Health Care Professionals Only)
Presidential Address: Competition: Perspiration to Inspiration “Aut viam inveniam aut faciam”, Joseph S. Coselli, Baylor College of Medicine
Basic Science Lecture: Stopping Incurable Cancers through Eliminating their Anti-Oxidative Defenses, James D. Watson, a Nobel Prize-winning biophysicist and researcher who is credited with co-discovering the double-helix structure of DNA.
Honored Guest Lecture: Brian Kelly, Notre Dame Head Football Coach and a veteran of 23 seasons as a collegiate head coach. Brian Kelly brings a championship tradition to his fifth year as the 29th head football coach at the University of Notre Dame.
Emerging Technologies & Techniques For: Adult Cardiac and General Thoracic
VAD/ECMO SessionMasters of Surgery: Video Sessions
AATS Learning Center: Featuring cutting-edge case videos of novel procedures and surgical techniques.
May 14-18, 2016
Baltimore, MD
President & Annual Meeting Chair
Joseph S. Coselli
Annual Meeting Co-Chairs
Charles D. Fraser
David R. Jones
View Preliminary Program, Speakers, Presentations and Full Abstracts
The 96th Annual Meeting is a five-day program of state-of-the-art presentations by renowned experts. Attendees will enhance their knowledge and skills in a wide-range of subjects including general and specialized cardiac surgery, emerging technologies, congenital heart disease, critical care and aortic/endovascular surgery.
Don’t miss this year’s exciting program including:
Saturday Skills Courses featuring Combined Luncheon Speaker: Denton A. Cooley, followed by Hands-On Sessions
Sunday Postgraduate Symposia with Legends Luncheons featuring Joel D. Cooper and John L. Ochsner
New: Survival Guide for the Cardiothoracic Surgical Team course following by a Hands-On Session (Available to Residents, Fellows and Health Care Professionals Only)
Presidential Address: Competition: Perspiration to Inspiration “Aut viam inveniam aut faciam”, Joseph S. Coselli, Baylor College of Medicine
Basic Science Lecture: Stopping Incurable Cancers through Eliminating their Anti-Oxidative Defenses, James D. Watson, a Nobel Prize-winning biophysicist and researcher who is credited with co-discovering the double-helix structure of DNA.
Honored Guest Lecture: Brian Kelly, Notre Dame Head Football Coach and a veteran of 23 seasons as a collegiate head coach. Brian Kelly brings a championship tradition to his fifth year as the 29th head football coach at the University of Notre Dame.
Emerging Technologies & Techniques For: Adult Cardiac and General Thoracic
VAD/ECMO SessionMasters of Surgery: Video Sessions
AATS Learning Center: Featuring cutting-edge case videos of novel procedures and surgical techniques.
AATS Aortic Symposium
May 12–13, 2016
New York, NY
Course Directors
Joseph S. Coselli
Steven L. Lansman
The 2016 AATS Aortic Symposium is a two-day symposium focused on the pathophysiology, diagnosis and treatment of aortic aneurysms and dissections. The conference is designed for cardiovascular and thoracic surgeons, residents, perfusionists, ICU and OR nurses and others involved in aortic disease patient care. Faculty members include world leaders in the field who will share their experiences treating difficult aortic disease cases.
May 12–13, 2016
New York, NY
Course Directors
Joseph S. Coselli
Steven L. Lansman
The 2016 AATS Aortic Symposium is a two-day symposium focused on the pathophysiology, diagnosis and treatment of aortic aneurysms and dissections. The conference is designed for cardiovascular and thoracic surgeons, residents, perfusionists, ICU and OR nurses and others involved in aortic disease patient care. Faculty members include world leaders in the field who will share their experiences treating difficult aortic disease cases.
May 12–13, 2016
New York, NY
Course Directors
Joseph S. Coselli
Steven L. Lansman
The 2016 AATS Aortic Symposium is a two-day symposium focused on the pathophysiology, diagnosis and treatment of aortic aneurysms and dissections. The conference is designed for cardiovascular and thoracic surgeons, residents, perfusionists, ICU and OR nurses and others involved in aortic disease patient care. Faculty members include world leaders in the field who will share their experiences treating difficult aortic disease cases.
Take Advantage of AATS Annual Meeting Registration Packages
Health Care Professional Package: Includes Saturday Courses, Sunday Symposia and the 96th Annual Meeting (Monday-Wednesday). Register before March 25, 2016 for only $400 — a savings of $300.
Resident/Fellow and Medical Student Package: Includes Saturday Courses, Sunday Symposia and the 96th Annual Meeting (Monday-Wednesday). Register before March 25, 2016 and attend for no charge. After that date, the fee is $300 — a savings of $300.
Saturday Courses and Sunday Symposia Registration: Register for a Saturday course and/or a Sunday symposium and have access to all other courses/symposia taking place that same day. Note: Registration for the Saturday courses and/or Sunday symposium is separate from the Annual Meeting fee.
Health Care Professional Package: Includes Saturday Courses, Sunday Symposia and the 96th Annual Meeting (Monday-Wednesday). Register before March 25, 2016 for only $400 — a savings of $300.
Resident/Fellow and Medical Student Package: Includes Saturday Courses, Sunday Symposia and the 96th Annual Meeting (Monday-Wednesday). Register before March 25, 2016 and attend for no charge. After that date, the fee is $300 — a savings of $300.
Saturday Courses and Sunday Symposia Registration: Register for a Saturday course and/or a Sunday symposium and have access to all other courses/symposia taking place that same day. Note: Registration for the Saturday courses and/or Sunday symposium is separate from the Annual Meeting fee.
Health Care Professional Package: Includes Saturday Courses, Sunday Symposia and the 96th Annual Meeting (Monday-Wednesday). Register before March 25, 2016 for only $400 — a savings of $300.
Resident/Fellow and Medical Student Package: Includes Saturday Courses, Sunday Symposia and the 96th Annual Meeting (Monday-Wednesday). Register before March 25, 2016 and attend for no charge. After that date, the fee is $300 — a savings of $300.
Saturday Courses and Sunday Symposia Registration: Register for a Saturday course and/or a Sunday symposium and have access to all other courses/symposia taking place that same day. Note: Registration for the Saturday courses and/or Sunday symposium is separate from the Annual Meeting fee.
AATS Week 2016 Registration & Housing Open!
AATS Week 2016 includes Two Terrific Events
Aortic Symposium
May 12–13, 2016
New York, NY
96th Annual Meeting
May 14-18, 2016
Baltimore, MD
Register for AATS Week 2016 today & receive a $100 discount off the AATS Aortic Symposium registration fee
AATS Week 2016 includes Two Terrific Events
Aortic Symposium
May 12–13, 2016
New York, NY
96th Annual Meeting
May 14-18, 2016
Baltimore, MD
Register for AATS Week 2016 today & receive a $100 discount off the AATS Aortic Symposium registration fee
AATS Week 2016 includes Two Terrific Events
Aortic Symposium
May 12–13, 2016
New York, NY
96th Annual Meeting
May 14-18, 2016
Baltimore, MD
Register for AATS Week 2016 today & receive a $100 discount off the AATS Aortic Symposium registration fee
Webcast: Factors that contribute to overall contraceptive efficacy and risks
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
Access Dr. Burkman's Webcasts on contraception:
- Obesity and contraceptive efficacy and risks
- How to use the CDC's online tools to manage complex cases in contraception
Helpful resource for your practice:
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
Access Dr. Burkman's Webcasts on contraception:
- Obesity and contraceptive efficacy and risks
- How to use the CDC's online tools to manage complex cases in contraception
Helpful resource for your practice:
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
Access Dr. Burkman's Webcasts on contraception:
- Obesity and contraceptive efficacy and risks
- How to use the CDC's online tools to manage complex cases in contraception
Helpful resource for your practice:
ISC: Cryptogenic stroke linked to PSVT in absence of atrial fibrillation
LOS ANGELES – Paroxysmal supraventricular tachycardia is associated with subsequent ischemic stroke in patients without documented atrial fibrillation, according to a claims analysis of 42,152 Medicare enrollees at least 66 years old.
Atrial fibrillation accounts for perhaps 30% of cryptogenic strokes, “so clearly there’s something more to the story than just atrial fibrillation in” the other 70%, said investigator Dr. Hooman Kamel, a neurologist at Weill Cornell Medical College, New York. “Most cryptogenic strokes seem like they are embolic. The question is what are the undiscovered sources of embolism?”
Dr. Kamel and his colleagues focused on paroxysmal supraventricular tachycardia (PSVT) even though it’s generally considered benign. But “PSVT is increasingly recognized as a marker for underlying atrial dysfunction, especially in older patients. In some cases, the abnormal atrial substrate could cause thromboembolism even before atrial fibrillation [AF] appears,” he said at the International Stroke Conference.
To ensure regular heart rhythm monitoring, the study was limited to patients with implanted pacemakers or defibrillators. Patients with AF or stroke before or at the time of device implantation were excluded.
After a median of 1.8 years of follow-up, 2,245 patients (5.3%) were diagnosed with PSVT, and 1,007 (2.4%) had an ischemic stroke. The incidence of stroke without PSVT diagnosis was 0.95% per year, but 2.17% per year with a preceding PSVT diagnosis (P less than .001). Adjusting for age, gender, income, hypertension, diabetes, heart failure, and other potential confounders, the team found that a diagnosis of PSVT was associated with a doubling of ischemic stroke risk (HR, 2.0; 95% CI, 1.3-3.0), and an almost quadrupling of the risk for embolic stroke (HR, 3.6; 95% CI, 1.1-11.8).
“A lot more work needs to be done to nail this down, but potentially we are broadening the pool of atrial markers for stroke risk. These results build on recent findings that disturbances of atrial rhythm and function other than AF may” lead to stroke, Dr. Kamel said.
It’s way too soon to consider atrial ablation for PSVT to reduce stroke risk, he said, but his team is interrogating its administrative data for clues of its utility. “The idea of ablation for stroke is really interesting. I think ablation should help reduce the risk of stroke. It’s a really important question, and we don’t know the answer yet. There’s a lot more to be learned, [but] there does seem to be a definite progression from PSVT to AF,” Dr. Kamel said.
The National Institutes of Health funded the work. Dr. Kamel is a speaker for Genentech.
LOS ANGELES – Paroxysmal supraventricular tachycardia is associated with subsequent ischemic stroke in patients without documented atrial fibrillation, according to a claims analysis of 42,152 Medicare enrollees at least 66 years old.
Atrial fibrillation accounts for perhaps 30% of cryptogenic strokes, “so clearly there’s something more to the story than just atrial fibrillation in” the other 70%, said investigator Dr. Hooman Kamel, a neurologist at Weill Cornell Medical College, New York. “Most cryptogenic strokes seem like they are embolic. The question is what are the undiscovered sources of embolism?”
Dr. Kamel and his colleagues focused on paroxysmal supraventricular tachycardia (PSVT) even though it’s generally considered benign. But “PSVT is increasingly recognized as a marker for underlying atrial dysfunction, especially in older patients. In some cases, the abnormal atrial substrate could cause thromboembolism even before atrial fibrillation [AF] appears,” he said at the International Stroke Conference.
To ensure regular heart rhythm monitoring, the study was limited to patients with implanted pacemakers or defibrillators. Patients with AF or stroke before or at the time of device implantation were excluded.
After a median of 1.8 years of follow-up, 2,245 patients (5.3%) were diagnosed with PSVT, and 1,007 (2.4%) had an ischemic stroke. The incidence of stroke without PSVT diagnosis was 0.95% per year, but 2.17% per year with a preceding PSVT diagnosis (P less than .001). Adjusting for age, gender, income, hypertension, diabetes, heart failure, and other potential confounders, the team found that a diagnosis of PSVT was associated with a doubling of ischemic stroke risk (HR, 2.0; 95% CI, 1.3-3.0), and an almost quadrupling of the risk for embolic stroke (HR, 3.6; 95% CI, 1.1-11.8).
“A lot more work needs to be done to nail this down, but potentially we are broadening the pool of atrial markers for stroke risk. These results build on recent findings that disturbances of atrial rhythm and function other than AF may” lead to stroke, Dr. Kamel said.
It’s way too soon to consider atrial ablation for PSVT to reduce stroke risk, he said, but his team is interrogating its administrative data for clues of its utility. “The idea of ablation for stroke is really interesting. I think ablation should help reduce the risk of stroke. It’s a really important question, and we don’t know the answer yet. There’s a lot more to be learned, [but] there does seem to be a definite progression from PSVT to AF,” Dr. Kamel said.
The National Institutes of Health funded the work. Dr. Kamel is a speaker for Genentech.
LOS ANGELES – Paroxysmal supraventricular tachycardia is associated with subsequent ischemic stroke in patients without documented atrial fibrillation, according to a claims analysis of 42,152 Medicare enrollees at least 66 years old.
Atrial fibrillation accounts for perhaps 30% of cryptogenic strokes, “so clearly there’s something more to the story than just atrial fibrillation in” the other 70%, said investigator Dr. Hooman Kamel, a neurologist at Weill Cornell Medical College, New York. “Most cryptogenic strokes seem like they are embolic. The question is what are the undiscovered sources of embolism?”
Dr. Kamel and his colleagues focused on paroxysmal supraventricular tachycardia (PSVT) even though it’s generally considered benign. But “PSVT is increasingly recognized as a marker for underlying atrial dysfunction, especially in older patients. In some cases, the abnormal atrial substrate could cause thromboembolism even before atrial fibrillation [AF] appears,” he said at the International Stroke Conference.
To ensure regular heart rhythm monitoring, the study was limited to patients with implanted pacemakers or defibrillators. Patients with AF or stroke before or at the time of device implantation were excluded.
After a median of 1.8 years of follow-up, 2,245 patients (5.3%) were diagnosed with PSVT, and 1,007 (2.4%) had an ischemic stroke. The incidence of stroke without PSVT diagnosis was 0.95% per year, but 2.17% per year with a preceding PSVT diagnosis (P less than .001). Adjusting for age, gender, income, hypertension, diabetes, heart failure, and other potential confounders, the team found that a diagnosis of PSVT was associated with a doubling of ischemic stroke risk (HR, 2.0; 95% CI, 1.3-3.0), and an almost quadrupling of the risk for embolic stroke (HR, 3.6; 95% CI, 1.1-11.8).
“A lot more work needs to be done to nail this down, but potentially we are broadening the pool of atrial markers for stroke risk. These results build on recent findings that disturbances of atrial rhythm and function other than AF may” lead to stroke, Dr. Kamel said.
It’s way too soon to consider atrial ablation for PSVT to reduce stroke risk, he said, but his team is interrogating its administrative data for clues of its utility. “The idea of ablation for stroke is really interesting. I think ablation should help reduce the risk of stroke. It’s a really important question, and we don’t know the answer yet. There’s a lot more to be learned, [but] there does seem to be a definite progression from PSVT to AF,” Dr. Kamel said.
The National Institutes of Health funded the work. Dr. Kamel is a speaker for Genentech.
AT THE INTERNATIONAL STROKE CONFERENCE
Key clinical point: Paroxysmal supraventricular tachycardia could be an atrial marker for increased stroke risk when atrial fibrillation is not present, but additional research needs to confirm the finding.
Major finding: The incidence of stroke without PSVT diagnosis was 0.95% per year, but 2.17% per year with a preceding PSVT diagnosis (P less than .001).
Data source: Retrospective cohort of 42,152 Medicare enrollees.
Disclosures: The National Institutes of Health funded the work. The presenter is a speaker for Genentech.
In newly diagnosed hypertension with OSA, adding CPAP augmented the benefits of losartan
In patients with new-onset hypertension and obstructive sleep apnea, continuous positive airway pressure (CPAP) therapy plus antihypertensive treatment with losartan led to reductions in systolic blood pressure beyond those achieved with losartan alone, a two-phase study found.
“Adding CPAP treatment to losartan may reduce blood pressure in a clinically relevant way if the patients are compliant with the device,” said Dr. Erik Thunström of the Sahlgrenska Academy at the University of Gothenburg, Sweden, and his associates.
In their open-label study, 89 men and women with new-onset untreated hypertension – 54 of whom were found to have obstructive sleep apnea (OSA) through a home sleep study and 35 of whom were determined to not have OSA – were treated for 6 weeks with losartan, 50 mg daily. Ambulatory 24-hour blood pressure monitoring was performed before and after treatment.
The patients with OSA were then randomized to receive 6 weeks of nightly add-on CPAP therapy or to continue losartan alone. Ambulatory 24-hour blood pressure monitoring was performed again.
Losartan alone reduced blood pressure in patients with hypertension and concomitant OSA, but the effect was smaller than that seen in patients without OSA. Statistically significant differences were seen in the mean net reduction in morning systolic blood pressure and morning mean arterial pressure. Overall, losartan appeared to be less effective at night and during the early morning hours in patients with OSA, the researchers reported.
After 6 weeks of losartan alone, a blood pressure less than 130/80 mm Hg was achieved by 12.5% of the patients with OSA and by 29% of the patients without OSA.
After 6 weeks of add-on CPAP therapy, 25% of patients with OSA achieved blood pressures less than 130/80 mm Hg. The differences in blood pressures for the OSA patients receiving CPAP plus losartan and those receiving losartan alone were 4.4 mm Hg for 24-hour systolic blood pressure, 1.9 mm Hg for diastolic, and 2.5 mm Hg for mean arterial pressure.
The most “robust” blood pressure changes were seen in the patients who used CPAP therapy for more than 4 hours every night, reducing the mean 24-hour systolic blood pressure by 6.5 mm Hg, the diastolic pressure by 3.8 mm Hg, and the mean arterial blood pressure by 4.6 mm Hg, the researchers reported (Am J Respir Crit Care Med. 2016 Feb.;193:310-20). “Adding CPAP to treatment with losartan reduced the mean 24-hour systolic blood pressure by 6.5 mm Hg in the subgroup of patients with OSA who were adherent with CPAP,” they wrote.
Patients included in the study all had a body mass index of 35 kg/m2; those with OSA had slightly higher BMIs that did not differ significantly from those without OSA.
That CPAP seems to have additive blood pressure–lowering effect when used concomitantly with losartan “favors the idea that it contributes to a further down-regulation of RAAS [renin-angiotensin-aldosterone system] activity in new-onset hypertension and OSA,” the authors wrote.
RAAS activity is often changed in hypertension, and in animal studies it has been shown to be up-regulated by intermittent hypoxia. Angiotensin II receptor antagonists are thus viewed as a good choice in the treatment of patients with OSA and new-onset hypertension, they wrote.
Treating OSA may make hypertension easier to address pharmacologically. The effect of CPAP on blood pressure is relatively small when all patients are considered but is more substantial and clinically important for those who use CPAP for more than 4 hours per night.
Can treatment of OSA effectively reduce blood pressure in an otherwise asymptomatic hypertensive patient with OSA? I believe the study would suggest that the answer remains “maybe.”
Most of the patients in the study would require a higher dose of losartan or an additional antihypertensive drug, even while using CPAP, to get to target blood pressures. Getting patients to use CPAP is a difficult task, as is adherence with any long-term pharmacologic management.
All in all, however, CPAP could contribute to blood pressure control while also improving quality of life and possibly reducing the risk for cardiovascular disease.
Dr. David P. White is with Harvard Medical School in Boston. His comments are excerpted from an accompanying editorial (Am J Respir Crit Care Med. 2016 Feb;193:238-9).
Treating OSA may make hypertension easier to address pharmacologically. The effect of CPAP on blood pressure is relatively small when all patients are considered but is more substantial and clinically important for those who use CPAP for more than 4 hours per night.
Can treatment of OSA effectively reduce blood pressure in an otherwise asymptomatic hypertensive patient with OSA? I believe the study would suggest that the answer remains “maybe.”
Most of the patients in the study would require a higher dose of losartan or an additional antihypertensive drug, even while using CPAP, to get to target blood pressures. Getting patients to use CPAP is a difficult task, as is adherence with any long-term pharmacologic management.
All in all, however, CPAP could contribute to blood pressure control while also improving quality of life and possibly reducing the risk for cardiovascular disease.
Dr. David P. White is with Harvard Medical School in Boston. His comments are excerpted from an accompanying editorial (Am J Respir Crit Care Med. 2016 Feb;193:238-9).
Treating OSA may make hypertension easier to address pharmacologically. The effect of CPAP on blood pressure is relatively small when all patients are considered but is more substantial and clinically important for those who use CPAP for more than 4 hours per night.
Can treatment of OSA effectively reduce blood pressure in an otherwise asymptomatic hypertensive patient with OSA? I believe the study would suggest that the answer remains “maybe.”
Most of the patients in the study would require a higher dose of losartan or an additional antihypertensive drug, even while using CPAP, to get to target blood pressures. Getting patients to use CPAP is a difficult task, as is adherence with any long-term pharmacologic management.
All in all, however, CPAP could contribute to blood pressure control while also improving quality of life and possibly reducing the risk for cardiovascular disease.
Dr. David P. White is with Harvard Medical School in Boston. His comments are excerpted from an accompanying editorial (Am J Respir Crit Care Med. 2016 Feb;193:238-9).
In patients with new-onset hypertension and obstructive sleep apnea, continuous positive airway pressure (CPAP) therapy plus antihypertensive treatment with losartan led to reductions in systolic blood pressure beyond those achieved with losartan alone, a two-phase study found.
“Adding CPAP treatment to losartan may reduce blood pressure in a clinically relevant way if the patients are compliant with the device,” said Dr. Erik Thunström of the Sahlgrenska Academy at the University of Gothenburg, Sweden, and his associates.
In their open-label study, 89 men and women with new-onset untreated hypertension – 54 of whom were found to have obstructive sleep apnea (OSA) through a home sleep study and 35 of whom were determined to not have OSA – were treated for 6 weeks with losartan, 50 mg daily. Ambulatory 24-hour blood pressure monitoring was performed before and after treatment.
The patients with OSA were then randomized to receive 6 weeks of nightly add-on CPAP therapy or to continue losartan alone. Ambulatory 24-hour blood pressure monitoring was performed again.
Losartan alone reduced blood pressure in patients with hypertension and concomitant OSA, but the effect was smaller than that seen in patients without OSA. Statistically significant differences were seen in the mean net reduction in morning systolic blood pressure and morning mean arterial pressure. Overall, losartan appeared to be less effective at night and during the early morning hours in patients with OSA, the researchers reported.
After 6 weeks of losartan alone, a blood pressure less than 130/80 mm Hg was achieved by 12.5% of the patients with OSA and by 29% of the patients without OSA.
After 6 weeks of add-on CPAP therapy, 25% of patients with OSA achieved blood pressures less than 130/80 mm Hg. The differences in blood pressures for the OSA patients receiving CPAP plus losartan and those receiving losartan alone were 4.4 mm Hg for 24-hour systolic blood pressure, 1.9 mm Hg for diastolic, and 2.5 mm Hg for mean arterial pressure.
The most “robust” blood pressure changes were seen in the patients who used CPAP therapy for more than 4 hours every night, reducing the mean 24-hour systolic blood pressure by 6.5 mm Hg, the diastolic pressure by 3.8 mm Hg, and the mean arterial blood pressure by 4.6 mm Hg, the researchers reported (Am J Respir Crit Care Med. 2016 Feb.;193:310-20). “Adding CPAP to treatment with losartan reduced the mean 24-hour systolic blood pressure by 6.5 mm Hg in the subgroup of patients with OSA who were adherent with CPAP,” they wrote.
Patients included in the study all had a body mass index of 35 kg/m2; those with OSA had slightly higher BMIs that did not differ significantly from those without OSA.
That CPAP seems to have additive blood pressure–lowering effect when used concomitantly with losartan “favors the idea that it contributes to a further down-regulation of RAAS [renin-angiotensin-aldosterone system] activity in new-onset hypertension and OSA,” the authors wrote.
RAAS activity is often changed in hypertension, and in animal studies it has been shown to be up-regulated by intermittent hypoxia. Angiotensin II receptor antagonists are thus viewed as a good choice in the treatment of patients with OSA and new-onset hypertension, they wrote.
In patients with new-onset hypertension and obstructive sleep apnea, continuous positive airway pressure (CPAP) therapy plus antihypertensive treatment with losartan led to reductions in systolic blood pressure beyond those achieved with losartan alone, a two-phase study found.
“Adding CPAP treatment to losartan may reduce blood pressure in a clinically relevant way if the patients are compliant with the device,” said Dr. Erik Thunström of the Sahlgrenska Academy at the University of Gothenburg, Sweden, and his associates.
In their open-label study, 89 men and women with new-onset untreated hypertension – 54 of whom were found to have obstructive sleep apnea (OSA) through a home sleep study and 35 of whom were determined to not have OSA – were treated for 6 weeks with losartan, 50 mg daily. Ambulatory 24-hour blood pressure monitoring was performed before and after treatment.
The patients with OSA were then randomized to receive 6 weeks of nightly add-on CPAP therapy or to continue losartan alone. Ambulatory 24-hour blood pressure monitoring was performed again.
Losartan alone reduced blood pressure in patients with hypertension and concomitant OSA, but the effect was smaller than that seen in patients without OSA. Statistically significant differences were seen in the mean net reduction in morning systolic blood pressure and morning mean arterial pressure. Overall, losartan appeared to be less effective at night and during the early morning hours in patients with OSA, the researchers reported.
After 6 weeks of losartan alone, a blood pressure less than 130/80 mm Hg was achieved by 12.5% of the patients with OSA and by 29% of the patients without OSA.
After 6 weeks of add-on CPAP therapy, 25% of patients with OSA achieved blood pressures less than 130/80 mm Hg. The differences in blood pressures for the OSA patients receiving CPAP plus losartan and those receiving losartan alone were 4.4 mm Hg for 24-hour systolic blood pressure, 1.9 mm Hg for diastolic, and 2.5 mm Hg for mean arterial pressure.
The most “robust” blood pressure changes were seen in the patients who used CPAP therapy for more than 4 hours every night, reducing the mean 24-hour systolic blood pressure by 6.5 mm Hg, the diastolic pressure by 3.8 mm Hg, and the mean arterial blood pressure by 4.6 mm Hg, the researchers reported (Am J Respir Crit Care Med. 2016 Feb.;193:310-20). “Adding CPAP to treatment with losartan reduced the mean 24-hour systolic blood pressure by 6.5 mm Hg in the subgroup of patients with OSA who were adherent with CPAP,” they wrote.
Patients included in the study all had a body mass index of 35 kg/m2; those with OSA had slightly higher BMIs that did not differ significantly from those without OSA.
That CPAP seems to have additive blood pressure–lowering effect when used concomitantly with losartan “favors the idea that it contributes to a further down-regulation of RAAS [renin-angiotensin-aldosterone system] activity in new-onset hypertension and OSA,” the authors wrote.
RAAS activity is often changed in hypertension, and in animal studies it has been shown to be up-regulated by intermittent hypoxia. Angiotensin II receptor antagonists are thus viewed as a good choice in the treatment of patients with OSA and new-onset hypertension, they wrote.
FROM AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
Key clinical point: In patients with new-onset hypertension and obstructive sleep apnea, adding continuous positive airway pressure may reduce blood pressure levels further than achieved with losartan alone.
Major finding: In adherent patients, CPAP reduced the mean 24-hour systolic blood pressure by an additional 6.5 mm Hg as compared to the levels seen in patients on losartan alone.
Data source: A study of 89 men and women with new-onset untreated hypertension who were treated with losartan for 6 weeks and tested for OSA. In a second 6-week study, patients found to have OSA were randomized to receive CPAP or no CPAP.
Disclosures: The researchers had no relevant financial disclosures.
Sleep apnea found in 57% of veterans with PTSD
Obstructive sleep apnea syndrome (OSAS) was diagnosed in more than half of 200 active duty service members with combat-related post-traumatic stress disorder (PTSD) who were studied at Walter Reed Army Medical Center in Washington.
Compared with age-matched peers with just one of these disorders, the service members with PTSD and OSAS had poorer somnolence and sleep-related quality of life and were less adherent and responsive to positive airway pressure therapy.
The findings “highlight the need for a high index of suspicion and a comprehensive approach to identifying and treating sleep-disordered breathing in these patients,” Dr. Christopher J. Lettieri of the Uniformed Services University in Bethesda, Md., and his associates wrote (Chest. 2016 Feb;149[2]:483-90). “Given the prevalence of OSAS in patients with PTSD and its adverse impact on symptoms and adherence, early identification may improve outcomes.”
In the observational cohort study, 200 consecutive active duty service members who were diagnosed with PTSD as part of post-deployment screening underwent sleep evaluations regardless of whether there was clinical suspicion of sleep-disordered breathing. More than half – about 57% – were diagnosed with OSAS. Almost 60% of the study group had mild traumatic brain injury, which has been connected in prior research to obstructive sleep apnea, and many had comorbid insomnia. Those who were diagnosed with OSAS were older and had higher BMIs than those not found to have OSAS.
All 200 patients were compared with 50 consecutive age-matched control patients who had OSAS but had not been deployed and did not have PTSD, as well as with 50 age-matched service members without prior deployment or either of the two disorders. All of the patients diagnosed with OSAS were prescribed positive airway pressure (PAP) therapy and evaluated after a month.
Sleep quality was poor in the majority of patients with PTSD, and OSAS and PTSD were both independently associated with increased daytime sleepiness and lower quality-of-life index scores. However, patients with both conditions fared significantly worse, particularly with respect to quality of life as measured by the Functional Outcomes of Sleep Questionnaire (FOSQ).
FOSQ scores were abnormal at baseline in 60% of those with PTSD and OSAS, 43% with PTSD alone, 24% with OSAS alone, and 7% of those with neither condition.
Service members with both conditions also were less likely to adhere to therapy; 30% regularly used continuous PAP therapy, compared with 55% of those who had OSAS alone.
And while continuous PAP therapy improved daytime sleepiness and quality of life in patients with both PTSD and OSAS, the degree of improvement was less than that experienced by those with OSAS alone. PTSD “represents an independent barrier to the effective treatment of OSAS and should prompt multipronged and individualized care,” they wrote.
The researchers reported having no financial disclosures.
Obstructive sleep apnea syndrome (OSAS) was diagnosed in more than half of 200 active duty service members with combat-related post-traumatic stress disorder (PTSD) who were studied at Walter Reed Army Medical Center in Washington.
Compared with age-matched peers with just one of these disorders, the service members with PTSD and OSAS had poorer somnolence and sleep-related quality of life and were less adherent and responsive to positive airway pressure therapy.
The findings “highlight the need for a high index of suspicion and a comprehensive approach to identifying and treating sleep-disordered breathing in these patients,” Dr. Christopher J. Lettieri of the Uniformed Services University in Bethesda, Md., and his associates wrote (Chest. 2016 Feb;149[2]:483-90). “Given the prevalence of OSAS in patients with PTSD and its adverse impact on symptoms and adherence, early identification may improve outcomes.”
In the observational cohort study, 200 consecutive active duty service members who were diagnosed with PTSD as part of post-deployment screening underwent sleep evaluations regardless of whether there was clinical suspicion of sleep-disordered breathing. More than half – about 57% – were diagnosed with OSAS. Almost 60% of the study group had mild traumatic brain injury, which has been connected in prior research to obstructive sleep apnea, and many had comorbid insomnia. Those who were diagnosed with OSAS were older and had higher BMIs than those not found to have OSAS.
All 200 patients were compared with 50 consecutive age-matched control patients who had OSAS but had not been deployed and did not have PTSD, as well as with 50 age-matched service members without prior deployment or either of the two disorders. All of the patients diagnosed with OSAS were prescribed positive airway pressure (PAP) therapy and evaluated after a month.
Sleep quality was poor in the majority of patients with PTSD, and OSAS and PTSD were both independently associated with increased daytime sleepiness and lower quality-of-life index scores. However, patients with both conditions fared significantly worse, particularly with respect to quality of life as measured by the Functional Outcomes of Sleep Questionnaire (FOSQ).
FOSQ scores were abnormal at baseline in 60% of those with PTSD and OSAS, 43% with PTSD alone, 24% with OSAS alone, and 7% of those with neither condition.
Service members with both conditions also were less likely to adhere to therapy; 30% regularly used continuous PAP therapy, compared with 55% of those who had OSAS alone.
And while continuous PAP therapy improved daytime sleepiness and quality of life in patients with both PTSD and OSAS, the degree of improvement was less than that experienced by those with OSAS alone. PTSD “represents an independent barrier to the effective treatment of OSAS and should prompt multipronged and individualized care,” they wrote.
The researchers reported having no financial disclosures.
Obstructive sleep apnea syndrome (OSAS) was diagnosed in more than half of 200 active duty service members with combat-related post-traumatic stress disorder (PTSD) who were studied at Walter Reed Army Medical Center in Washington.
Compared with age-matched peers with just one of these disorders, the service members with PTSD and OSAS had poorer somnolence and sleep-related quality of life and were less adherent and responsive to positive airway pressure therapy.
The findings “highlight the need for a high index of suspicion and a comprehensive approach to identifying and treating sleep-disordered breathing in these patients,” Dr. Christopher J. Lettieri of the Uniformed Services University in Bethesda, Md., and his associates wrote (Chest. 2016 Feb;149[2]:483-90). “Given the prevalence of OSAS in patients with PTSD and its adverse impact on symptoms and adherence, early identification may improve outcomes.”
In the observational cohort study, 200 consecutive active duty service members who were diagnosed with PTSD as part of post-deployment screening underwent sleep evaluations regardless of whether there was clinical suspicion of sleep-disordered breathing. More than half – about 57% – were diagnosed with OSAS. Almost 60% of the study group had mild traumatic brain injury, which has been connected in prior research to obstructive sleep apnea, and many had comorbid insomnia. Those who were diagnosed with OSAS were older and had higher BMIs than those not found to have OSAS.
All 200 patients were compared with 50 consecutive age-matched control patients who had OSAS but had not been deployed and did not have PTSD, as well as with 50 age-matched service members without prior deployment or either of the two disorders. All of the patients diagnosed with OSAS were prescribed positive airway pressure (PAP) therapy and evaluated after a month.
Sleep quality was poor in the majority of patients with PTSD, and OSAS and PTSD were both independently associated with increased daytime sleepiness and lower quality-of-life index scores. However, patients with both conditions fared significantly worse, particularly with respect to quality of life as measured by the Functional Outcomes of Sleep Questionnaire (FOSQ).
FOSQ scores were abnormal at baseline in 60% of those with PTSD and OSAS, 43% with PTSD alone, 24% with OSAS alone, and 7% of those with neither condition.
Service members with both conditions also were less likely to adhere to therapy; 30% regularly used continuous PAP therapy, compared with 55% of those who had OSAS alone.
And while continuous PAP therapy improved daytime sleepiness and quality of life in patients with both PTSD and OSAS, the degree of improvement was less than that experienced by those with OSAS alone. PTSD “represents an independent barrier to the effective treatment of OSAS and should prompt multipronged and individualized care,” they wrote.
The researchers reported having no financial disclosures.
FROM CHEST
Key clinical point: Obstructive sleep apnea is prevalent in service members with PTSD.
Major finding: More than 57% of active duty service members with combat-related PTSD were diagnosed with OSAS.
Data source: A case-controlled observational cohort study conducted at an academic military medical center and involving 200 consecutive patients with PTSD.
Disclosures: Dr. Lettieri and his colleagues did not report any conflicts of interest.