Is expectant management a safe alternative to immediate delivery in patients with PPROM close to term?

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Preterm premature rupture of membranes (PPROM) refers to rupture of membranes prior to the onset of labor before 37 weeks’ gestation. It accounts for one-third of all preterm births.1 Pregnancy complications associated with PPROM include intrauterine infection (chorioamnionitis), preterm labor, and placental abruption. Should such complications develop, immediate delivery is indicated. When to recommend elective delivery in the absence of complications, however, remains controversial.

The American College of Obstetricians and Gynecologists (ACOG) currently recommends elective delivery at or after 34 weeks’ gestation,2 because the prevailing evidence suggests that the risk of pregnancy-related complications (especially ascending infection) exceeds the risks of iatrogenic prematurity at this gestational age. However, ACOG acknowledges that this recommendation is based on “limited and inconsistent scientific evidence.”2 To address deficiencies in the literature, investigators designed the PPROMT (preterm prelabor rupture of the membranes close to term) trial to study women with ruptured membranes before the onset of labor between 34 and 37 weeks’ gestation.

PPROMT study designMorris and colleagues present results of their multicenter, international, randomized controlled trial (RCT) of expectant management versus planned delivery in pregnancies complicated by PPROM at 34 0/7 through 36 6/7 weeks’ gestation carried out in 65 centers across 11 countries. A total of 1,839 women not requiring urgent delivery were randomly assigned to either immediate delivery (n = 924) or expectant management (n = 915).

No difference was noted in the primary outcome of neonatal sepsis between the immediate birth (n = 23 [2%]) and expectant management groups (n = 29 [3%]; relative risk [RR], 0.8; 95% confidence interval [CI], 0.5–1.3). This also was true in the subgroup of women who were colonized with group B streptococcus (RR, 0.9; 95% CI, 0.2–4.5).

There also was no difference in the secondary outcome measure, a composite metric including sepsis, ventilation for 24 or more hours, or death (73 [8%] in the immediate delivery group vs 61 [7%] in the expectant management group; RR, 1.2; 95% CI, 0.9–1.6). However, infants born to women randomly assigned to immediate delivery, versus expectant management, had a significantly higher rate of respiratory distress syndrome (RR, 1.6; 95% CI, 1.1–2.3) and mechanical ventilation (RR, 1.4; 95% CI, 1.0–1.8). In addition, the immediate-delivery infants had a longer median stay in the special care nursery/neonatal intensive care unit (4.0 days, interquartile range [IQR], 0.0–10.0 vs 2.0 days, IQR, 0.0–7.0) and total hospital stay (6.0 days, IQR, 3.0–10.0 vs 4.0 days, IQR, 3.0–8.0). As expected, women in the expectant management group had a significantly longer hospital stay than women in the immediate delivery group, because 75% (688/912) were managed as inpatients. Interestingly, women in the immediate delivery group had a higher cesarean delivery rate than those in the expectant management group (239 [26%] vs 169 [19%], respectively; RR, 1.4; 95% CI, 1.2–1.7), although no explanation was offered.

Strengths and limitationsMajor strengths of this study include the large sample size and superior study design. It is by far the largest RCT to address this question. Because this was a pragmatic RCT, certain practices (such as the choice of latency antibiotic regimen) varied across centers, although randomization would be expected to minimize the effect of such variables on study outcome.

A major limitation is that participant recruitment occurred over a period of more than 10 years, during which time antenatal and neonatal intensive care unit practices likely would have changed.

What this evidence means for practiceFew clinical studies have the potential to significantly change obstetric management. This report by Morris and colleagues is one such study. It was well designed, well executed, and powered to look at the most clinically relevant outcome, namely, neonatal sepsis. While these study results do call into question the current American College of Obstetricians and Gynecologists recommendations to electively deliver patients with PPROM at or after 34 weeks’ gestation, additional discussion is needed at the national level before these recommendations can be changed.
—Denis A. Vaughan, MBBCh, BAO, MRCPI, and Errol R. Norwitz, MD, PhD

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

References
  1. Goldenberg RL, Rouse DJ. Prevention of premature birth. N Engl J Med. 1998;339(5):313–320.
  2. American College of Obstetricians and Gynecologists Committee on Practice Bulletins–Obstetrics. ACOG Practice Bulletin No. 160: premature rupture of membranes. Obstet Gynecol. 2016;127(1):192–194.
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Dr. Vaughan is from the Department of Obstetrics and Gynecology, Tufts Medical Center, Boston, Massachusetts.

Dr. Norwitz is Professor of Obstetrics and Gynecology, Tufts University School of Medicine, and Chairman of the Department of Obstetrics and Gynecology, Tufts Medical Center. Dr. Norwitz serves on the OBG Management Board of Editors.

The authors report no financial relationships relevant to this article.

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Dr. Vaughan is from the Department of Obstetrics and Gynecology, Tufts Medical Center, Boston, Massachusetts.

Dr. Norwitz is Professor of Obstetrics and Gynecology, Tufts University School of Medicine, and Chairman of the Department of Obstetrics and Gynecology, Tufts Medical Center. Dr. Norwitz serves on the OBG Management Board of Editors.

The authors report no financial relationships relevant to this article.

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Preterm premature rupture of membranes (PPROM) refers to rupture of membranes prior to the onset of labor before 37 weeks’ gestation. It accounts for one-third of all preterm births.1 Pregnancy complications associated with PPROM include intrauterine infection (chorioamnionitis), preterm labor, and placental abruption. Should such complications develop, immediate delivery is indicated. When to recommend elective delivery in the absence of complications, however, remains controversial.

The American College of Obstetricians and Gynecologists (ACOG) currently recommends elective delivery at or after 34 weeks’ gestation,2 because the prevailing evidence suggests that the risk of pregnancy-related complications (especially ascending infection) exceeds the risks of iatrogenic prematurity at this gestational age. However, ACOG acknowledges that this recommendation is based on “limited and inconsistent scientific evidence.”2 To address deficiencies in the literature, investigators designed the PPROMT (preterm prelabor rupture of the membranes close to term) trial to study women with ruptured membranes before the onset of labor between 34 and 37 weeks’ gestation.

PPROMT study designMorris and colleagues present results of their multicenter, international, randomized controlled trial (RCT) of expectant management versus planned delivery in pregnancies complicated by PPROM at 34 0/7 through 36 6/7 weeks’ gestation carried out in 65 centers across 11 countries. A total of 1,839 women not requiring urgent delivery were randomly assigned to either immediate delivery (n = 924) or expectant management (n = 915).

No difference was noted in the primary outcome of neonatal sepsis between the immediate birth (n = 23 [2%]) and expectant management groups (n = 29 [3%]; relative risk [RR], 0.8; 95% confidence interval [CI], 0.5–1.3). This also was true in the subgroup of women who were colonized with group B streptococcus (RR, 0.9; 95% CI, 0.2–4.5).

There also was no difference in the secondary outcome measure, a composite metric including sepsis, ventilation for 24 or more hours, or death (73 [8%] in the immediate delivery group vs 61 [7%] in the expectant management group; RR, 1.2; 95% CI, 0.9–1.6). However, infants born to women randomly assigned to immediate delivery, versus expectant management, had a significantly higher rate of respiratory distress syndrome (RR, 1.6; 95% CI, 1.1–2.3) and mechanical ventilation (RR, 1.4; 95% CI, 1.0–1.8). In addition, the immediate-delivery infants had a longer median stay in the special care nursery/neonatal intensive care unit (4.0 days, interquartile range [IQR], 0.0–10.0 vs 2.0 days, IQR, 0.0–7.0) and total hospital stay (6.0 days, IQR, 3.0–10.0 vs 4.0 days, IQR, 3.0–8.0). As expected, women in the expectant management group had a significantly longer hospital stay than women in the immediate delivery group, because 75% (688/912) were managed as inpatients. Interestingly, women in the immediate delivery group had a higher cesarean delivery rate than those in the expectant management group (239 [26%] vs 169 [19%], respectively; RR, 1.4; 95% CI, 1.2–1.7), although no explanation was offered.

Strengths and limitationsMajor strengths of this study include the large sample size and superior study design. It is by far the largest RCT to address this question. Because this was a pragmatic RCT, certain practices (such as the choice of latency antibiotic regimen) varied across centers, although randomization would be expected to minimize the effect of such variables on study outcome.

A major limitation is that participant recruitment occurred over a period of more than 10 years, during which time antenatal and neonatal intensive care unit practices likely would have changed.

What this evidence means for practiceFew clinical studies have the potential to significantly change obstetric management. This report by Morris and colleagues is one such study. It was well designed, well executed, and powered to look at the most clinically relevant outcome, namely, neonatal sepsis. While these study results do call into question the current American College of Obstetricians and Gynecologists recommendations to electively deliver patients with PPROM at or after 34 weeks’ gestation, additional discussion is needed at the national level before these recommendations can be changed.
—Denis A. Vaughan, MBBCh, BAO, MRCPI, and Errol R. Norwitz, MD, PhD

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

Preterm premature rupture of membranes (PPROM) refers to rupture of membranes prior to the onset of labor before 37 weeks’ gestation. It accounts for one-third of all preterm births.1 Pregnancy complications associated with PPROM include intrauterine infection (chorioamnionitis), preterm labor, and placental abruption. Should such complications develop, immediate delivery is indicated. When to recommend elective delivery in the absence of complications, however, remains controversial.

The American College of Obstetricians and Gynecologists (ACOG) currently recommends elective delivery at or after 34 weeks’ gestation,2 because the prevailing evidence suggests that the risk of pregnancy-related complications (especially ascending infection) exceeds the risks of iatrogenic prematurity at this gestational age. However, ACOG acknowledges that this recommendation is based on “limited and inconsistent scientific evidence.”2 To address deficiencies in the literature, investigators designed the PPROMT (preterm prelabor rupture of the membranes close to term) trial to study women with ruptured membranes before the onset of labor between 34 and 37 weeks’ gestation.

PPROMT study designMorris and colleagues present results of their multicenter, international, randomized controlled trial (RCT) of expectant management versus planned delivery in pregnancies complicated by PPROM at 34 0/7 through 36 6/7 weeks’ gestation carried out in 65 centers across 11 countries. A total of 1,839 women not requiring urgent delivery were randomly assigned to either immediate delivery (n = 924) or expectant management (n = 915).

No difference was noted in the primary outcome of neonatal sepsis between the immediate birth (n = 23 [2%]) and expectant management groups (n = 29 [3%]; relative risk [RR], 0.8; 95% confidence interval [CI], 0.5–1.3). This also was true in the subgroup of women who were colonized with group B streptococcus (RR, 0.9; 95% CI, 0.2–4.5).

There also was no difference in the secondary outcome measure, a composite metric including sepsis, ventilation for 24 or more hours, or death (73 [8%] in the immediate delivery group vs 61 [7%] in the expectant management group; RR, 1.2; 95% CI, 0.9–1.6). However, infants born to women randomly assigned to immediate delivery, versus expectant management, had a significantly higher rate of respiratory distress syndrome (RR, 1.6; 95% CI, 1.1–2.3) and mechanical ventilation (RR, 1.4; 95% CI, 1.0–1.8). In addition, the immediate-delivery infants had a longer median stay in the special care nursery/neonatal intensive care unit (4.0 days, interquartile range [IQR], 0.0–10.0 vs 2.0 days, IQR, 0.0–7.0) and total hospital stay (6.0 days, IQR, 3.0–10.0 vs 4.0 days, IQR, 3.0–8.0). As expected, women in the expectant management group had a significantly longer hospital stay than women in the immediate delivery group, because 75% (688/912) were managed as inpatients. Interestingly, women in the immediate delivery group had a higher cesarean delivery rate than those in the expectant management group (239 [26%] vs 169 [19%], respectively; RR, 1.4; 95% CI, 1.2–1.7), although no explanation was offered.

Strengths and limitationsMajor strengths of this study include the large sample size and superior study design. It is by far the largest RCT to address this question. Because this was a pragmatic RCT, certain practices (such as the choice of latency antibiotic regimen) varied across centers, although randomization would be expected to minimize the effect of such variables on study outcome.

A major limitation is that participant recruitment occurred over a period of more than 10 years, during which time antenatal and neonatal intensive care unit practices likely would have changed.

What this evidence means for practiceFew clinical studies have the potential to significantly change obstetric management. This report by Morris and colleagues is one such study. It was well designed, well executed, and powered to look at the most clinically relevant outcome, namely, neonatal sepsis. While these study results do call into question the current American College of Obstetricians and Gynecologists recommendations to electively deliver patients with PPROM at or after 34 weeks’ gestation, additional discussion is needed at the national level before these recommendations can be changed.
—Denis A. Vaughan, MBBCh, BAO, MRCPI, and Errol R. Norwitz, MD, PhD

Share your thoughts! Send your Letter to the Editor to rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

References
  1. Goldenberg RL, Rouse DJ. Prevention of premature birth. N Engl J Med. 1998;339(5):313–320.
  2. American College of Obstetricians and Gynecologists Committee on Practice Bulletins–Obstetrics. ACOG Practice Bulletin No. 160: premature rupture of membranes. Obstet Gynecol. 2016;127(1):192–194.
References
  1. Goldenberg RL, Rouse DJ. Prevention of premature birth. N Engl J Med. 1998;339(5):313–320.
  2. American College of Obstetricians and Gynecologists Committee on Practice Bulletins–Obstetrics. ACOG Practice Bulletin No. 160: premature rupture of membranes. Obstet Gynecol. 2016;127(1):192–194.
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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.

agallegos@frontlinemedcom.com

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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.

agallegos@frontlinemedcom.com

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.

agallegos@frontlinemedcom.com

On Twitter @legal_med

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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.

Dr. William G. Wilkoff

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.”

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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.

Dr. William G. Wilkoff

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.

Dr. William G. Wilkoff

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.”

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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.

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May 14-18, 2016
Baltimore, MD

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Joseph S. Coselli

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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.

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May 12–13, 2016
New York, NY

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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.

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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.

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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.

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Take Advantage of AATS Annual Meeting Registration Packages

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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.

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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.

Learn More

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.

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AATS Week 2016 Registration & Housing Open!

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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

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May 14-18, 2016
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Register for AATS Week 2016 today & receive a $100 discount off the AATS Aortic Symposium registration fee

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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

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Webcast: Factors that contribute to overall contraceptive efficacy and risks

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ISC: Cryptogenic stroke linked to PSVT in absence of atrial fibrillation

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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. Hooman Kamel

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.

aotto@frontlinemedcom.com

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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. Hooman Kamel

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.

aotto@frontlinemedcom.com

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. Hooman Kamel

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.

aotto@frontlinemedcom.com

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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

Treating OSA a “worthy goal” for BP
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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.

©viola83181/iStockphoto.com

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.

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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).

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Body

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).

Body

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).

Title
Treating OSA a “worthy goal” for BP
Treating OSA a “worthy goal” for BP

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.

©viola83181/iStockphoto.com

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.

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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.

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FROM AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE

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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.