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Ambulatory BP monitoring shows hypertension prevalence 1 year after preeclampsia
as it misses forms of hypertension commonly experienced in that population, according to a study published Feb. 5 in Hypertension.
Researchers at Erasmus University, Rotterdam, the Netherlands, conducted a retrospective cohort study of 200 women who underwent 24-hour ambulatory BP monitoring and office BP measurement at a 1-year follow-up for delivery with severe preeclampsia. Measurements were taken between 9 months and 15 months after delivery.
“Current clinical guidelines on the prevention of [cardiovascular disease] and stroke after a hypertensive pregnancy disorder lack advice on [ambulatory BP monitoring] after delivery. We think that [ambulatory BP monitoring] should be offered to all women who experienced severe preeclampsia for more accurate BP assessment,” wrote Laura Benschop, MD, and her coauthors.
SOURCE: Benschop L et al. Hypertension. 2018 Feb;71:491-8.
as it misses forms of hypertension commonly experienced in that population, according to a study published Feb. 5 in Hypertension.
Researchers at Erasmus University, Rotterdam, the Netherlands, conducted a retrospective cohort study of 200 women who underwent 24-hour ambulatory BP monitoring and office BP measurement at a 1-year follow-up for delivery with severe preeclampsia. Measurements were taken between 9 months and 15 months after delivery.
“Current clinical guidelines on the prevention of [cardiovascular disease] and stroke after a hypertensive pregnancy disorder lack advice on [ambulatory BP monitoring] after delivery. We think that [ambulatory BP monitoring] should be offered to all women who experienced severe preeclampsia for more accurate BP assessment,” wrote Laura Benschop, MD, and her coauthors.
SOURCE: Benschop L et al. Hypertension. 2018 Feb;71:491-8.
as it misses forms of hypertension commonly experienced in that population, according to a study published Feb. 5 in Hypertension.
Researchers at Erasmus University, Rotterdam, the Netherlands, conducted a retrospective cohort study of 200 women who underwent 24-hour ambulatory BP monitoring and office BP measurement at a 1-year follow-up for delivery with severe preeclampsia. Measurements were taken between 9 months and 15 months after delivery.
“Current clinical guidelines on the prevention of [cardiovascular disease] and stroke after a hypertensive pregnancy disorder lack advice on [ambulatory BP monitoring] after delivery. We think that [ambulatory BP monitoring] should be offered to all women who experienced severe preeclampsia for more accurate BP assessment,” wrote Laura Benschop, MD, and her coauthors.
SOURCE: Benschop L et al. Hypertension. 2018 Feb;71:491-8.
FROM HYPERTENSION
On Diagnosing Sepsis
Two years ago, a panel appointed by the Society of Critical Care Medicine and the European Society of Intensive Care Medicine, referred to as a consensus conference, proposed a new definition for sepsis and new diagnostic criteria for sepsis and septic shock, known as Sepsis-3 (Singer M, et al. JAMA. 2016;315[8]:801). The panel proposed that sepsis be defined as life-threatening organ dysfunction due to a dysregulated host response to infection. Upon reflection, one could see that what we had called definitions of sepsis, severe sepsis, and septic shock for over 2 decades actually represented diagnostic criteria more than concise definitions. In that regard, a concise definition is a useful addition in the tool kit for training all health-care professionals to recognize sepsis and to treat it early and aggressively.
However, the diagnostic criteria leave something to be desired, in terms of both practicality and sensitivity for detecting patients whose infection has made them seriously ill. Those who participate in quality improvement efforts in their own hospitals will recognize that to promote change and to achieve a goal of better, higher quality care, it is important to remove obstacles in the system and to structure it so that doing the right thing is easier than not doing it. For sepsis, the first step in the process, recognizing that sepsis is present, has always been complex enough that it has been the bane of the enterprise. As many as two-thirds of patients with sepsis presenting to the ED with severe sepsis never receive that diagnosis while in the hospital. (Deis AS, et al. Chest. 2018;153[1]:39). As any sepsis core measure coordinator can attest, diagnostic criteria that are readily visible on retrospective examination are often unnoticed or misinterpreted in real time.
The crux of this issue is that the very entity of sepsis is not a definite thing but a not-quite-focused idea. Much is known of pathophysiologic features that seem to be important, but there is no one unifying pathologic condition. Contrast that with another critical illness, myocardial infarction. The very name states the unifying pathology. Our predecessors were able to work backward from an understanding that acute blockage of a small artery led to ischemia and infarction, in order to identify methods to detect it while it is happening—measuring enzymes and evaluating an ECG. For sepsis, we don’t even understand why patients are sick or why they die. There is a complex interaction of inflammation, microcirculatory thrombosis, mitochondrial dysfunction, immune suppression, but there is no one combination of those things that is yet understood in a way that lends itself to diagnostic testing. The best we can say is that the patient reacted to their infection in a way that was detrimental to their own body’s functioning. Rather than recognizing a few symptoms and sending a confirmatory test, with sepsis, we must tote up the signs and symptoms in the domains of recognizing infection and recognizing organ dysfunction, then determine whether they are present in sufficient amounts; it is an exercise that requires mental discipline.
If the diagnostic criteria we use, whether Sepsis-1, 2, or 3, are all gross descriptions of complex internal interactions that are not specific, then the syndrome that any of these criteria identifies is also not specific for anything particular. It falls to the medical community, as a whole, to determine exactly what it is that we desire a given syndrome to be indicative of. The Sepsis-3 authors decided that the appropriate syndrome should predict death or prolonged ICU stay. They used several large data sets to develop and validate infection-associated variables that would have good predictive ability for that outcome, and they compared what they found with sepsis by the Sepsis-1 definition, infection plus SIRS (Seymour C, et al. JAMA. 2016;315[8]:762). Infection + SIRS is a strawman in this comparison, because they tested its predictive ability for the outcome against that of the Sequential Organ Failure Assessment (SOFA) and the Logistic Organ Dysfunction Score (LODS). These two scoring systems were developed as severity of injury scales and validated as mortality predictors; the higher the score, the likelier mortality, whereas SIRS clearly contains no information about organ dysfunction. The comparator of interest for this outcome is actually severe sepsis, infection plus SIRS plus organ dysfunction.
Although the criteria the Sepsis-3 investigators used for defining patients with suspected infection were novel and reasonable, we lack additional important information about the patients they studied. They did not report the spectrum of treatments for sepsis in their cohort, whether early or late, adequate or inadequate, so it is impossible to determine whether the criteria address patients who are undertreated, patients who are treated late, patients who will die regardless of adequate therapy, or some combination. In other words, there is no way to tell whether patients who were recognized early in their course via Sepsis-1 criteria and treated aggressively and effectively may have avoided shock, ICU admission, and death. It is, of course, the business of physicians and nurses to help patients avoid exactly those things. Multiple studies have now demonstrated that SIRS criteria are more sensitive than SOFA-based screens, specifically qSOFA, for identifying infection with organ dysfunction, and that qSOFA is more specific for mortality (Serafim, et al. Chest. 2017; http://dx.doi.org/10.1016/j.chest.2017.12.015).
In contrast, the Sepsis-1 authors proposed infection plus SIRS as a sensitive screening tool that could warn of the possibility of an associated organ dysfunction (Sprung, et al. Crit Care Med. 2017;45[9]:1564). Previous to the Sepsis-1 conference, Bone and colleagues had defined the sepsis syndrome, which incorporated both SIRS and organ dysfunction (Bone, et al. Crit Care Med. 1989;17[5]:389). It was the collective insight of the Sepsis-1 participants to recognize that SIRS induced by infection could be a harbinger of organ failure. The Sepsis-3 authors believe that SIRS is a “normal and adaptive” part of infection and that it is “not useful” in the diagnosis of sepsis. That analysis neglects a couple of important things about SIRS. First, numerous studies demonstrate that infection with SIRS is associated with a mortality rate of 7% to 9%, which is by no means trivial (Rangel-Frausto MS, et al. JAMA. 1995;273[2]:117). Second, the components of SIRS have been recognized as representative of serious illness for millennia; the assertion that the Sepsis-1 definitions are not evidence-based is mistaken and discounts the collective experience of the medical profession.
Finally, SIRS is criticized on the basis of being nonspecific. “If I climb a flight of stairs, I get SIRS.” This is clearly a true statement. In fact, one could propose that the name could more accurately be Systemic Stress Response Syndrome, though “scissors” is certainly less catchy than “sirs” when one says it aloud. However, the critique neglects an important concept, encapsulated in Bayes’ Theorem. The value of any positive test result is largely dependent on the prevalence of the disease being tested for in the population being tested. It is unlikely that the prevalence of sepsis is very high among patients whose SIRS is induced by climbing a flight of stairs. On the other hand, tachycardia and tachypnea in a patient who is indulging in no activity while lying on a bed feeling miserable should prompt a search for both the infection that could be causing it and the organ dysfunction that could be associated with it. The specificity of SIRS derives from the population in which it is witnessed, and its sensitivity is to be respected.
To quote a friend, the remarkable CEO of a small Kansas hospital, “If a patient with an infection feels bad enough that they climb up on that gurney and place themselves at our mercy, we owe it to them to prove why they don’t have sepsis, rather than why they do.”
Editor’s Comment
The progress made in the last several years emphasizes the importance of early identification and aggressive treatment of sepsis. The Third International Consensus Definitions (Sepsis-3) have sparked great controversy in the sepsis community, because they delay the recognition of sepsis until organ damage occurs. In this Critical Care Commentary, Dr. Steven Q. Simpson asserts with solid arguments that the use of a screening tool with higher specificity for mortality, at the expense of sensitivity, is not a step in the right direction. Moving away from criteria that have been widely adopted in clinical trials and quality improvement initiatives throughout the world can be a setback in the battle to improve sepsis outcomes. Until prospectively validated criteria that allow earlier identification of sepsis are developed, there is no compelling reason for change.
Angel Coz, MD, FCCP
Section Editor
Dr. Simpson is Professor, Interim Director; Division of Pulmonary and Critical Care Medicine, University of Kansas, Kansas City, Kansas.
Two years ago, a panel appointed by the Society of Critical Care Medicine and the European Society of Intensive Care Medicine, referred to as a consensus conference, proposed a new definition for sepsis and new diagnostic criteria for sepsis and septic shock, known as Sepsis-3 (Singer M, et al. JAMA. 2016;315[8]:801). The panel proposed that sepsis be defined as life-threatening organ dysfunction due to a dysregulated host response to infection. Upon reflection, one could see that what we had called definitions of sepsis, severe sepsis, and septic shock for over 2 decades actually represented diagnostic criteria more than concise definitions. In that regard, a concise definition is a useful addition in the tool kit for training all health-care professionals to recognize sepsis and to treat it early and aggressively.
However, the diagnostic criteria leave something to be desired, in terms of both practicality and sensitivity for detecting patients whose infection has made them seriously ill. Those who participate in quality improvement efforts in their own hospitals will recognize that to promote change and to achieve a goal of better, higher quality care, it is important to remove obstacles in the system and to structure it so that doing the right thing is easier than not doing it. For sepsis, the first step in the process, recognizing that sepsis is present, has always been complex enough that it has been the bane of the enterprise. As many as two-thirds of patients with sepsis presenting to the ED with severe sepsis never receive that diagnosis while in the hospital. (Deis AS, et al. Chest. 2018;153[1]:39). As any sepsis core measure coordinator can attest, diagnostic criteria that are readily visible on retrospective examination are often unnoticed or misinterpreted in real time.
The crux of this issue is that the very entity of sepsis is not a definite thing but a not-quite-focused idea. Much is known of pathophysiologic features that seem to be important, but there is no one unifying pathologic condition. Contrast that with another critical illness, myocardial infarction. The very name states the unifying pathology. Our predecessors were able to work backward from an understanding that acute blockage of a small artery led to ischemia and infarction, in order to identify methods to detect it while it is happening—measuring enzymes and evaluating an ECG. For sepsis, we don’t even understand why patients are sick or why they die. There is a complex interaction of inflammation, microcirculatory thrombosis, mitochondrial dysfunction, immune suppression, but there is no one combination of those things that is yet understood in a way that lends itself to diagnostic testing. The best we can say is that the patient reacted to their infection in a way that was detrimental to their own body’s functioning. Rather than recognizing a few symptoms and sending a confirmatory test, with sepsis, we must tote up the signs and symptoms in the domains of recognizing infection and recognizing organ dysfunction, then determine whether they are present in sufficient amounts; it is an exercise that requires mental discipline.
If the diagnostic criteria we use, whether Sepsis-1, 2, or 3, are all gross descriptions of complex internal interactions that are not specific, then the syndrome that any of these criteria identifies is also not specific for anything particular. It falls to the medical community, as a whole, to determine exactly what it is that we desire a given syndrome to be indicative of. The Sepsis-3 authors decided that the appropriate syndrome should predict death or prolonged ICU stay. They used several large data sets to develop and validate infection-associated variables that would have good predictive ability for that outcome, and they compared what they found with sepsis by the Sepsis-1 definition, infection plus SIRS (Seymour C, et al. JAMA. 2016;315[8]:762). Infection + SIRS is a strawman in this comparison, because they tested its predictive ability for the outcome against that of the Sequential Organ Failure Assessment (SOFA) and the Logistic Organ Dysfunction Score (LODS). These two scoring systems were developed as severity of injury scales and validated as mortality predictors; the higher the score, the likelier mortality, whereas SIRS clearly contains no information about organ dysfunction. The comparator of interest for this outcome is actually severe sepsis, infection plus SIRS plus organ dysfunction.
Although the criteria the Sepsis-3 investigators used for defining patients with suspected infection were novel and reasonable, we lack additional important information about the patients they studied. They did not report the spectrum of treatments for sepsis in their cohort, whether early or late, adequate or inadequate, so it is impossible to determine whether the criteria address patients who are undertreated, patients who are treated late, patients who will die regardless of adequate therapy, or some combination. In other words, there is no way to tell whether patients who were recognized early in their course via Sepsis-1 criteria and treated aggressively and effectively may have avoided shock, ICU admission, and death. It is, of course, the business of physicians and nurses to help patients avoid exactly those things. Multiple studies have now demonstrated that SIRS criteria are more sensitive than SOFA-based screens, specifically qSOFA, for identifying infection with organ dysfunction, and that qSOFA is more specific for mortality (Serafim, et al. Chest. 2017; http://dx.doi.org/10.1016/j.chest.2017.12.015).
In contrast, the Sepsis-1 authors proposed infection plus SIRS as a sensitive screening tool that could warn of the possibility of an associated organ dysfunction (Sprung, et al. Crit Care Med. 2017;45[9]:1564). Previous to the Sepsis-1 conference, Bone and colleagues had defined the sepsis syndrome, which incorporated both SIRS and organ dysfunction (Bone, et al. Crit Care Med. 1989;17[5]:389). It was the collective insight of the Sepsis-1 participants to recognize that SIRS induced by infection could be a harbinger of organ failure. The Sepsis-3 authors believe that SIRS is a “normal and adaptive” part of infection and that it is “not useful” in the diagnosis of sepsis. That analysis neglects a couple of important things about SIRS. First, numerous studies demonstrate that infection with SIRS is associated with a mortality rate of 7% to 9%, which is by no means trivial (Rangel-Frausto MS, et al. JAMA. 1995;273[2]:117). Second, the components of SIRS have been recognized as representative of serious illness for millennia; the assertion that the Sepsis-1 definitions are not evidence-based is mistaken and discounts the collective experience of the medical profession.
Finally, SIRS is criticized on the basis of being nonspecific. “If I climb a flight of stairs, I get SIRS.” This is clearly a true statement. In fact, one could propose that the name could more accurately be Systemic Stress Response Syndrome, though “scissors” is certainly less catchy than “sirs” when one says it aloud. However, the critique neglects an important concept, encapsulated in Bayes’ Theorem. The value of any positive test result is largely dependent on the prevalence of the disease being tested for in the population being tested. It is unlikely that the prevalence of sepsis is very high among patients whose SIRS is induced by climbing a flight of stairs. On the other hand, tachycardia and tachypnea in a patient who is indulging in no activity while lying on a bed feeling miserable should prompt a search for both the infection that could be causing it and the organ dysfunction that could be associated with it. The specificity of SIRS derives from the population in which it is witnessed, and its sensitivity is to be respected.
To quote a friend, the remarkable CEO of a small Kansas hospital, “If a patient with an infection feels bad enough that they climb up on that gurney and place themselves at our mercy, we owe it to them to prove why they don’t have sepsis, rather than why they do.”
Editor’s Comment
The progress made in the last several years emphasizes the importance of early identification and aggressive treatment of sepsis. The Third International Consensus Definitions (Sepsis-3) have sparked great controversy in the sepsis community, because they delay the recognition of sepsis until organ damage occurs. In this Critical Care Commentary, Dr. Steven Q. Simpson asserts with solid arguments that the use of a screening tool with higher specificity for mortality, at the expense of sensitivity, is not a step in the right direction. Moving away from criteria that have been widely adopted in clinical trials and quality improvement initiatives throughout the world can be a setback in the battle to improve sepsis outcomes. Until prospectively validated criteria that allow earlier identification of sepsis are developed, there is no compelling reason for change.
Angel Coz, MD, FCCP
Section Editor
Dr. Simpson is Professor, Interim Director; Division of Pulmonary and Critical Care Medicine, University of Kansas, Kansas City, Kansas.
Two years ago, a panel appointed by the Society of Critical Care Medicine and the European Society of Intensive Care Medicine, referred to as a consensus conference, proposed a new definition for sepsis and new diagnostic criteria for sepsis and septic shock, known as Sepsis-3 (Singer M, et al. JAMA. 2016;315[8]:801). The panel proposed that sepsis be defined as life-threatening organ dysfunction due to a dysregulated host response to infection. Upon reflection, one could see that what we had called definitions of sepsis, severe sepsis, and septic shock for over 2 decades actually represented diagnostic criteria more than concise definitions. In that regard, a concise definition is a useful addition in the tool kit for training all health-care professionals to recognize sepsis and to treat it early and aggressively.
However, the diagnostic criteria leave something to be desired, in terms of both practicality and sensitivity for detecting patients whose infection has made them seriously ill. Those who participate in quality improvement efforts in their own hospitals will recognize that to promote change and to achieve a goal of better, higher quality care, it is important to remove obstacles in the system and to structure it so that doing the right thing is easier than not doing it. For sepsis, the first step in the process, recognizing that sepsis is present, has always been complex enough that it has been the bane of the enterprise. As many as two-thirds of patients with sepsis presenting to the ED with severe sepsis never receive that diagnosis while in the hospital. (Deis AS, et al. Chest. 2018;153[1]:39). As any sepsis core measure coordinator can attest, diagnostic criteria that are readily visible on retrospective examination are often unnoticed or misinterpreted in real time.
The crux of this issue is that the very entity of sepsis is not a definite thing but a not-quite-focused idea. Much is known of pathophysiologic features that seem to be important, but there is no one unifying pathologic condition. Contrast that with another critical illness, myocardial infarction. The very name states the unifying pathology. Our predecessors were able to work backward from an understanding that acute blockage of a small artery led to ischemia and infarction, in order to identify methods to detect it while it is happening—measuring enzymes and evaluating an ECG. For sepsis, we don’t even understand why patients are sick or why they die. There is a complex interaction of inflammation, microcirculatory thrombosis, mitochondrial dysfunction, immune suppression, but there is no one combination of those things that is yet understood in a way that lends itself to diagnostic testing. The best we can say is that the patient reacted to their infection in a way that was detrimental to their own body’s functioning. Rather than recognizing a few symptoms and sending a confirmatory test, with sepsis, we must tote up the signs and symptoms in the domains of recognizing infection and recognizing organ dysfunction, then determine whether they are present in sufficient amounts; it is an exercise that requires mental discipline.
If the diagnostic criteria we use, whether Sepsis-1, 2, or 3, are all gross descriptions of complex internal interactions that are not specific, then the syndrome that any of these criteria identifies is also not specific for anything particular. It falls to the medical community, as a whole, to determine exactly what it is that we desire a given syndrome to be indicative of. The Sepsis-3 authors decided that the appropriate syndrome should predict death or prolonged ICU stay. They used several large data sets to develop and validate infection-associated variables that would have good predictive ability for that outcome, and they compared what they found with sepsis by the Sepsis-1 definition, infection plus SIRS (Seymour C, et al. JAMA. 2016;315[8]:762). Infection + SIRS is a strawman in this comparison, because they tested its predictive ability for the outcome against that of the Sequential Organ Failure Assessment (SOFA) and the Logistic Organ Dysfunction Score (LODS). These two scoring systems were developed as severity of injury scales and validated as mortality predictors; the higher the score, the likelier mortality, whereas SIRS clearly contains no information about organ dysfunction. The comparator of interest for this outcome is actually severe sepsis, infection plus SIRS plus organ dysfunction.
Although the criteria the Sepsis-3 investigators used for defining patients with suspected infection were novel and reasonable, we lack additional important information about the patients they studied. They did not report the spectrum of treatments for sepsis in their cohort, whether early or late, adequate or inadequate, so it is impossible to determine whether the criteria address patients who are undertreated, patients who are treated late, patients who will die regardless of adequate therapy, or some combination. In other words, there is no way to tell whether patients who were recognized early in their course via Sepsis-1 criteria and treated aggressively and effectively may have avoided shock, ICU admission, and death. It is, of course, the business of physicians and nurses to help patients avoid exactly those things. Multiple studies have now demonstrated that SIRS criteria are more sensitive than SOFA-based screens, specifically qSOFA, for identifying infection with organ dysfunction, and that qSOFA is more specific for mortality (Serafim, et al. Chest. 2017; http://dx.doi.org/10.1016/j.chest.2017.12.015).
In contrast, the Sepsis-1 authors proposed infection plus SIRS as a sensitive screening tool that could warn of the possibility of an associated organ dysfunction (Sprung, et al. Crit Care Med. 2017;45[9]:1564). Previous to the Sepsis-1 conference, Bone and colleagues had defined the sepsis syndrome, which incorporated both SIRS and organ dysfunction (Bone, et al. Crit Care Med. 1989;17[5]:389). It was the collective insight of the Sepsis-1 participants to recognize that SIRS induced by infection could be a harbinger of organ failure. The Sepsis-3 authors believe that SIRS is a “normal and adaptive” part of infection and that it is “not useful” in the diagnosis of sepsis. That analysis neglects a couple of important things about SIRS. First, numerous studies demonstrate that infection with SIRS is associated with a mortality rate of 7% to 9%, which is by no means trivial (Rangel-Frausto MS, et al. JAMA. 1995;273[2]:117). Second, the components of SIRS have been recognized as representative of serious illness for millennia; the assertion that the Sepsis-1 definitions are not evidence-based is mistaken and discounts the collective experience of the medical profession.
Finally, SIRS is criticized on the basis of being nonspecific. “If I climb a flight of stairs, I get SIRS.” This is clearly a true statement. In fact, one could propose that the name could more accurately be Systemic Stress Response Syndrome, though “scissors” is certainly less catchy than “sirs” when one says it aloud. However, the critique neglects an important concept, encapsulated in Bayes’ Theorem. The value of any positive test result is largely dependent on the prevalence of the disease being tested for in the population being tested. It is unlikely that the prevalence of sepsis is very high among patients whose SIRS is induced by climbing a flight of stairs. On the other hand, tachycardia and tachypnea in a patient who is indulging in no activity while lying on a bed feeling miserable should prompt a search for both the infection that could be causing it and the organ dysfunction that could be associated with it. The specificity of SIRS derives from the population in which it is witnessed, and its sensitivity is to be respected.
To quote a friend, the remarkable CEO of a small Kansas hospital, “If a patient with an infection feels bad enough that they climb up on that gurney and place themselves at our mercy, we owe it to them to prove why they don’t have sepsis, rather than why they do.”
Editor’s Comment
The progress made in the last several years emphasizes the importance of early identification and aggressive treatment of sepsis. The Third International Consensus Definitions (Sepsis-3) have sparked great controversy in the sepsis community, because they delay the recognition of sepsis until organ damage occurs. In this Critical Care Commentary, Dr. Steven Q. Simpson asserts with solid arguments that the use of a screening tool with higher specificity for mortality, at the expense of sensitivity, is not a step in the right direction. Moving away from criteria that have been widely adopted in clinical trials and quality improvement initiatives throughout the world can be a setback in the battle to improve sepsis outcomes. Until prospectively validated criteria that allow earlier identification of sepsis are developed, there is no compelling reason for change.
Angel Coz, MD, FCCP
Section Editor
Dr. Simpson is Professor, Interim Director; Division of Pulmonary and Critical Care Medicine, University of Kansas, Kansas City, Kansas.
Shop the CHEST Store
Have you shopped at the CHEST Store lately? We’ve recently updated our merchandise to include several new items perfect for staff gifts or for yourself. Along with our old standbys, including lab coats and scrubs, we now feature CHEST-branded scarves, knit caps (perfect for winter), and insulated hot and cold drink mugs. And don’t forget, most items are customizable for a small, additional fee. For the more education-inclined, the store also features the best in CHEST print, including CHEST SEEKTM volumes, Coding for Chest Medicine, patient education guides, and much more.
Products can be ordered online, and most items are sold on-site at our live learning and board review courses and at the CHEST Annual Meeting. If you can’t purchase in person, visit the store at chestnet.org/store to stock up.
Have you shopped at the CHEST Store lately? We’ve recently updated our merchandise to include several new items perfect for staff gifts or for yourself. Along with our old standbys, including lab coats and scrubs, we now feature CHEST-branded scarves, knit caps (perfect for winter), and insulated hot and cold drink mugs. And don’t forget, most items are customizable for a small, additional fee. For the more education-inclined, the store also features the best in CHEST print, including CHEST SEEKTM volumes, Coding for Chest Medicine, patient education guides, and much more.
Products can be ordered online, and most items are sold on-site at our live learning and board review courses and at the CHEST Annual Meeting. If you can’t purchase in person, visit the store at chestnet.org/store to stock up.
Have you shopped at the CHEST Store lately? We’ve recently updated our merchandise to include several new items perfect for staff gifts or for yourself. Along with our old standbys, including lab coats and scrubs, we now feature CHEST-branded scarves, knit caps (perfect for winter), and insulated hot and cold drink mugs. And don’t forget, most items are customizable for a small, additional fee. For the more education-inclined, the store also features the best in CHEST print, including CHEST SEEKTM volumes, Coding for Chest Medicine, patient education guides, and much more.
Products can be ordered online, and most items are sold on-site at our live learning and board review courses and at the CHEST Annual Meeting. If you can’t purchase in person, visit the store at chestnet.org/store to stock up.
In Memoriam
CHEST has been informed of the following members’ deaths.
We extend our sincere condolences.
Nagesh V Salian, MD, FCCP (2016)
Ted A Calinog, MD, FCCP (2017)
Azam Ansari, MD (2017)
Arthur E. Schmidt, MD, FCCP (2017)
CHEST has been informed of the following members’ deaths.
We extend our sincere condolences.
Nagesh V Salian, MD, FCCP (2016)
Ted A Calinog, MD, FCCP (2017)
Azam Ansari, MD (2017)
Arthur E. Schmidt, MD, FCCP (2017)
CHEST has been informed of the following members’ deaths.
We extend our sincere condolences.
Nagesh V Salian, MD, FCCP (2016)
Ted A Calinog, MD, FCCP (2017)
Azam Ansari, MD (2017)
Arthur E. Schmidt, MD, FCCP (2017)
This Month in the Journal CHEST® Editor’s Picks
Giants In Chest Medicine Professor Nan-shan Zhong, MD.
By Wei-jie Guan.
Original Research
Long-term Use of Inhaled Corticosteroids in COPD and the Risk of Fracture. By Dr. A. V. Gonzalez, et al.
Cardiac Troponin Values in Patients With Acute Coronary Syndrome and Sleep Apnea: A Pilot Study. By Dr. A. Sánchez-de-la-Torre, et al.
CA-125 in Disease Progression and Treatment of Lymphangioleiomyomatosis. By Dr. C. G. Glasgow, et al.
Evidence-Based Medicine
Cough Due to TB and Other Chronic Infections: CHEST Guideline and Expert Panel Report. By Dr. S. K. Field, et al, on behalf of the CHEST Expert Cough Panel.
Giants In Chest Medicine Professor Nan-shan Zhong, MD.
By Wei-jie Guan.
Original Research
Long-term Use of Inhaled Corticosteroids in COPD and the Risk of Fracture. By Dr. A. V. Gonzalez, et al.
Cardiac Troponin Values in Patients With Acute Coronary Syndrome and Sleep Apnea: A Pilot Study. By Dr. A. Sánchez-de-la-Torre, et al.
CA-125 in Disease Progression and Treatment of Lymphangioleiomyomatosis. By Dr. C. G. Glasgow, et al.
Evidence-Based Medicine
Cough Due to TB and Other Chronic Infections: CHEST Guideline and Expert Panel Report. By Dr. S. K. Field, et al, on behalf of the CHEST Expert Cough Panel.
Giants In Chest Medicine Professor Nan-shan Zhong, MD.
By Wei-jie Guan.
Original Research
Long-term Use of Inhaled Corticosteroids in COPD and the Risk of Fracture. By Dr. A. V. Gonzalez, et al.
Cardiac Troponin Values in Patients With Acute Coronary Syndrome and Sleep Apnea: A Pilot Study. By Dr. A. Sánchez-de-la-Torre, et al.
CA-125 in Disease Progression and Treatment of Lymphangioleiomyomatosis. By Dr. C. G. Glasgow, et al.
Evidence-Based Medicine
Cough Due to TB and Other Chronic Infections: CHEST Guideline and Expert Panel Report. By Dr. S. K. Field, et al, on behalf of the CHEST Expert Cough Panel.
VIDEO: Painless PDT and other AK tricks
KAUAI, HAWAII – Imiquimod on the lip can be extremely painful, but it works wonders for actinic cheilitis, sometimes with only a few treatments.
Also, and how long patients stay under the lamp, advised Theodore Rosen, MD, professor of dermatology at Baylor College of Medicine, Houston.
These are just a few of the tips Dr. Rosen shared in a presentation about AKs at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.
In a video interview after his talk, he went into detail about the use of imiquimod for actinic cheilitis – AKs of the lip – and painless PDT, as well as how to discuss AKs with patients – and a quick, clever way to help distinguish AKs from squamous cell carcinoma.
Dr. Rosen is an adviser to Aclaris, Cipher, Pfizer, and Valeant.
SDEF/Global Academy for Medical Education and this news organization are owned by the same parent company.
KAUAI, HAWAII – Imiquimod on the lip can be extremely painful, but it works wonders for actinic cheilitis, sometimes with only a few treatments.
Also, and how long patients stay under the lamp, advised Theodore Rosen, MD, professor of dermatology at Baylor College of Medicine, Houston.
These are just a few of the tips Dr. Rosen shared in a presentation about AKs at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.
In a video interview after his talk, he went into detail about the use of imiquimod for actinic cheilitis – AKs of the lip – and painless PDT, as well as how to discuss AKs with patients – and a quick, clever way to help distinguish AKs from squamous cell carcinoma.
Dr. Rosen is an adviser to Aclaris, Cipher, Pfizer, and Valeant.
SDEF/Global Academy for Medical Education and this news organization are owned by the same parent company.
KAUAI, HAWAII – Imiquimod on the lip can be extremely painful, but it works wonders for actinic cheilitis, sometimes with only a few treatments.
Also, and how long patients stay under the lamp, advised Theodore Rosen, MD, professor of dermatology at Baylor College of Medicine, Houston.
These are just a few of the tips Dr. Rosen shared in a presentation about AKs at the Hawaii Dermatology Seminar provided by Global Academy for Medical Education/Skin Disease Education Foundation.
In a video interview after his talk, he went into detail about the use of imiquimod for actinic cheilitis – AKs of the lip – and painless PDT, as well as how to discuss AKs with patients – and a quick, clever way to help distinguish AKs from squamous cell carcinoma.
Dr. Rosen is an adviser to Aclaris, Cipher, Pfizer, and Valeant.
SDEF/Global Academy for Medical Education and this news organization are owned by the same parent company.
REPORTING FROM SDEF HAWAII DERMATOLOGY SEMINAR
Sequence of regorafenib, cetuximab matters in later-line CRC therapy
SAN FRANCISCO – The order in which targeted therapies are given to patients with previously treated metastatic colorectal cancer can have a marked impact on overall survival, according to results of the REVERCE trial reported at the 2018 GI Cancers Symposium.
Investigators led by Kohei Shitara, MD, National Cancer Center Hospital East, Kashiwa, Japan, enrolled in the multicenter, phase 2, randomized trial 101 patients with mainly KRAS wild-type metastatic colorectal cancer who had previously received fluoropyrimidine, oxaliplatin, and irinotecan, but not any therapy targeting epidermal growth factor receptor (EGFR).
Main results at a median follow-up of 29.0 months showed that median overall survival was almost 6 months longer when regorafenib was given first as compared with when cetuximab was given first, a difference translating to a 39% reduction in risk of death with the former sequence.
“These results suggest that overall survival was longer with regorafenib as the first treatment followed by cetuximab than that of the current standard sequence,” Dr. Shitara said. “Efficacy was observed in almost all subgroups.”
Progression-free survival on the first treatment did not differ significantly by agent, but on the second treatment, it was almost 3.5 months longer with cetuximab. “This might contribute to the overall survival difference,” he proposed.
The specific biologic mechanisms driving the differing efficacy of the two sequences are still unclear, but one possibility is that regorafenib downregulates MAP kinase and certain other signaling molecules, sensitizing cells to subsequent anti-EGFR therapy, Dr. Shitara said. “Biomarker analyses are still ongoing. We hope that further biomarker analysis will clarify the reason for the survival difference.”
The data did not reveal any unexpected safety signals. Although quality of life scores were lower with regorafenib during each treatment period, scores for all time on treatment were similar for the two sequences.
Clinical implications
“The amount of difference in overall survival [between sequences] was pretty striking. These were patients in second line and third line,” commented session chair Michael J. Hall, MD, of Fox Chase Cancer Center, Philadelphia.
“This trial adds excitement to the idea that there is still a lot of work to be done in sequencing of therapies and also our understanding of how induction of molecular events by one therapy, for instance, the cetuximab leading to RAS mutations, then affects how the downstream therapies work,” Dr. Hall maintained. “So maybe we need to think more intelligently about that.”
Study details
The REVERCE investigators planned to enroll 180 patients in the trial but stopped after 101 patients because of slow accrual. Most of those studied had previously received bevacizumab.
About 70% of patients in the regorafenib-first group needed a dose reduction at some point, compared with about 30% in the cetuximab-first group, a difference likely related to the longer duration of treatment for the former, Dr. Shitara speculated.
Median overall survival was 17.4 months when regorafenib was given first and 11.6 months when cetuximab was give first (hazard ratio, 0.61; P = .029), according to data reported at the symposium, which was sponsored by the American Gastroenterological Association, the American Society for Clinical Oncology, the American Society for Radiation Oncology, and the Society of Surgical Oncology.
In subgroup analyses, the regorafenib-first strategy yielded significantly better overall survival among patients with left-sided tumors (HR, 0.51; P = .011), but not among those with right-sided tumors (HR, 0.88).
The regorafenib-first strategy had similar benefit when restricted to patients with RAS/RAF wild-type tumors (18.2 vs. 12.7 months; HR, 0.60; P = .036).
Analysis of blood samples collected after the first agent indicated that 26% of patients had emergence of a RAS mutation after receiving cetuximab. However, these patients did not appear to have worse overall survival, according to Dr. Shitara.
Progression-free survival on the first agent was 2.4 months in the regorafenib-first group and 4.2 months in the cetuximab-first group, a nonsignificant difference. In contrast, for the second treatment, it was 5.2 months in the regorafenib-first group and just 1.8 months in the cetuximab-first group (HR, 0.29; P less than .0001).
Dr. Shitara disclosed that he receives honoraria from Abbvie, Novartis, Ono Pharmaceutical, and Yakult; has a consulting or advisory role with Astellas Pharma, Bristol-Myers Squibb, Lilly, Pfizer, and Takeda; and that his institution receives research funding from Chugai Pharma, Daiichi Sankyo, Dainippon Sumitomo Pharma, Lilly, MSD, Taiho Pharmaceutical, and Yakult. The trial was funded by Bayer Yahin.
SOURCE: Shitara et al. GI Cancers Symposium Abstract 557
SAN FRANCISCO – The order in which targeted therapies are given to patients with previously treated metastatic colorectal cancer can have a marked impact on overall survival, according to results of the REVERCE trial reported at the 2018 GI Cancers Symposium.
Investigators led by Kohei Shitara, MD, National Cancer Center Hospital East, Kashiwa, Japan, enrolled in the multicenter, phase 2, randomized trial 101 patients with mainly KRAS wild-type metastatic colorectal cancer who had previously received fluoropyrimidine, oxaliplatin, and irinotecan, but not any therapy targeting epidermal growth factor receptor (EGFR).
Main results at a median follow-up of 29.0 months showed that median overall survival was almost 6 months longer when regorafenib was given first as compared with when cetuximab was given first, a difference translating to a 39% reduction in risk of death with the former sequence.
“These results suggest that overall survival was longer with regorafenib as the first treatment followed by cetuximab than that of the current standard sequence,” Dr. Shitara said. “Efficacy was observed in almost all subgroups.”
Progression-free survival on the first treatment did not differ significantly by agent, but on the second treatment, it was almost 3.5 months longer with cetuximab. “This might contribute to the overall survival difference,” he proposed.
The specific biologic mechanisms driving the differing efficacy of the two sequences are still unclear, but one possibility is that regorafenib downregulates MAP kinase and certain other signaling molecules, sensitizing cells to subsequent anti-EGFR therapy, Dr. Shitara said. “Biomarker analyses are still ongoing. We hope that further biomarker analysis will clarify the reason for the survival difference.”
The data did not reveal any unexpected safety signals. Although quality of life scores were lower with regorafenib during each treatment period, scores for all time on treatment were similar for the two sequences.
Clinical implications
“The amount of difference in overall survival [between sequences] was pretty striking. These were patients in second line and third line,” commented session chair Michael J. Hall, MD, of Fox Chase Cancer Center, Philadelphia.
“This trial adds excitement to the idea that there is still a lot of work to be done in sequencing of therapies and also our understanding of how induction of molecular events by one therapy, for instance, the cetuximab leading to RAS mutations, then affects how the downstream therapies work,” Dr. Hall maintained. “So maybe we need to think more intelligently about that.”
Study details
The REVERCE investigators planned to enroll 180 patients in the trial but stopped after 101 patients because of slow accrual. Most of those studied had previously received bevacizumab.
About 70% of patients in the regorafenib-first group needed a dose reduction at some point, compared with about 30% in the cetuximab-first group, a difference likely related to the longer duration of treatment for the former, Dr. Shitara speculated.
Median overall survival was 17.4 months when regorafenib was given first and 11.6 months when cetuximab was give first (hazard ratio, 0.61; P = .029), according to data reported at the symposium, which was sponsored by the American Gastroenterological Association, the American Society for Clinical Oncology, the American Society for Radiation Oncology, and the Society of Surgical Oncology.
In subgroup analyses, the regorafenib-first strategy yielded significantly better overall survival among patients with left-sided tumors (HR, 0.51; P = .011), but not among those with right-sided tumors (HR, 0.88).
The regorafenib-first strategy had similar benefit when restricted to patients with RAS/RAF wild-type tumors (18.2 vs. 12.7 months; HR, 0.60; P = .036).
Analysis of blood samples collected after the first agent indicated that 26% of patients had emergence of a RAS mutation after receiving cetuximab. However, these patients did not appear to have worse overall survival, according to Dr. Shitara.
Progression-free survival on the first agent was 2.4 months in the regorafenib-first group and 4.2 months in the cetuximab-first group, a nonsignificant difference. In contrast, for the second treatment, it was 5.2 months in the regorafenib-first group and just 1.8 months in the cetuximab-first group (HR, 0.29; P less than .0001).
Dr. Shitara disclosed that he receives honoraria from Abbvie, Novartis, Ono Pharmaceutical, and Yakult; has a consulting or advisory role with Astellas Pharma, Bristol-Myers Squibb, Lilly, Pfizer, and Takeda; and that his institution receives research funding from Chugai Pharma, Daiichi Sankyo, Dainippon Sumitomo Pharma, Lilly, MSD, Taiho Pharmaceutical, and Yakult. The trial was funded by Bayer Yahin.
SOURCE: Shitara et al. GI Cancers Symposium Abstract 557
SAN FRANCISCO – The order in which targeted therapies are given to patients with previously treated metastatic colorectal cancer can have a marked impact on overall survival, according to results of the REVERCE trial reported at the 2018 GI Cancers Symposium.
Investigators led by Kohei Shitara, MD, National Cancer Center Hospital East, Kashiwa, Japan, enrolled in the multicenter, phase 2, randomized trial 101 patients with mainly KRAS wild-type metastatic colorectal cancer who had previously received fluoropyrimidine, oxaliplatin, and irinotecan, but not any therapy targeting epidermal growth factor receptor (EGFR).
Main results at a median follow-up of 29.0 months showed that median overall survival was almost 6 months longer when regorafenib was given first as compared with when cetuximab was given first, a difference translating to a 39% reduction in risk of death with the former sequence.
“These results suggest that overall survival was longer with regorafenib as the first treatment followed by cetuximab than that of the current standard sequence,” Dr. Shitara said. “Efficacy was observed in almost all subgroups.”
Progression-free survival on the first treatment did not differ significantly by agent, but on the second treatment, it was almost 3.5 months longer with cetuximab. “This might contribute to the overall survival difference,” he proposed.
The specific biologic mechanisms driving the differing efficacy of the two sequences are still unclear, but one possibility is that regorafenib downregulates MAP kinase and certain other signaling molecules, sensitizing cells to subsequent anti-EGFR therapy, Dr. Shitara said. “Biomarker analyses are still ongoing. We hope that further biomarker analysis will clarify the reason for the survival difference.”
The data did not reveal any unexpected safety signals. Although quality of life scores were lower with regorafenib during each treatment period, scores for all time on treatment were similar for the two sequences.
Clinical implications
“The amount of difference in overall survival [between sequences] was pretty striking. These were patients in second line and third line,” commented session chair Michael J. Hall, MD, of Fox Chase Cancer Center, Philadelphia.
“This trial adds excitement to the idea that there is still a lot of work to be done in sequencing of therapies and also our understanding of how induction of molecular events by one therapy, for instance, the cetuximab leading to RAS mutations, then affects how the downstream therapies work,” Dr. Hall maintained. “So maybe we need to think more intelligently about that.”
Study details
The REVERCE investigators planned to enroll 180 patients in the trial but stopped after 101 patients because of slow accrual. Most of those studied had previously received bevacizumab.
About 70% of patients in the regorafenib-first group needed a dose reduction at some point, compared with about 30% in the cetuximab-first group, a difference likely related to the longer duration of treatment for the former, Dr. Shitara speculated.
Median overall survival was 17.4 months when regorafenib was given first and 11.6 months when cetuximab was give first (hazard ratio, 0.61; P = .029), according to data reported at the symposium, which was sponsored by the American Gastroenterological Association, the American Society for Clinical Oncology, the American Society for Radiation Oncology, and the Society of Surgical Oncology.
In subgroup analyses, the regorafenib-first strategy yielded significantly better overall survival among patients with left-sided tumors (HR, 0.51; P = .011), but not among those with right-sided tumors (HR, 0.88).
The regorafenib-first strategy had similar benefit when restricted to patients with RAS/RAF wild-type tumors (18.2 vs. 12.7 months; HR, 0.60; P = .036).
Analysis of blood samples collected after the first agent indicated that 26% of patients had emergence of a RAS mutation after receiving cetuximab. However, these patients did not appear to have worse overall survival, according to Dr. Shitara.
Progression-free survival on the first agent was 2.4 months in the regorafenib-first group and 4.2 months in the cetuximab-first group, a nonsignificant difference. In contrast, for the second treatment, it was 5.2 months in the regorafenib-first group and just 1.8 months in the cetuximab-first group (HR, 0.29; P less than .0001).
Dr. Shitara disclosed that he receives honoraria from Abbvie, Novartis, Ono Pharmaceutical, and Yakult; has a consulting or advisory role with Astellas Pharma, Bristol-Myers Squibb, Lilly, Pfizer, and Takeda; and that his institution receives research funding from Chugai Pharma, Daiichi Sankyo, Dainippon Sumitomo Pharma, Lilly, MSD, Taiho Pharmaceutical, and Yakult. The trial was funded by Bayer Yahin.
SOURCE: Shitara et al. GI Cancers Symposium Abstract 557
REPORTING FROM THE 2018 GI CANCERS SYMPOSIUM
Key clinical point:
Major finding: Median overall survival was 17.4 months when regorafenib was given first and 11.6 months when cetuximab was given first (HR, 0.61; P = .029).
Data source: A multicenter, randomized, phase 2 trial of regorafenib followed by cetuximab, versus the reverse sequence, among 101 patients with metastatic colorectal cancer previously treated with fluoropyrimidine, oxaliplatin, and irinotecan (REVERCE trial).
Disclosures: Dr. Shitara disclosed that he receives honoraria from Abbvie, Novartis, Ono Pharmaceutical, and Yakult; has a consulting or advisory role with Astellas Pharma, Bristol-Myers Squibb, Lilly, Pfizer, and Takeda; and that his institution receives research funding from Chugai Pharma, Daiichi Sankyo, Dainippon Sumitomo Pharma, Lilly, MSD, Taiho Pharmaceutical, and Yakult. The trial was funded by Bayer Yahin.
Source: Shitara et al. GI Cancers Symposium Abstract 557
Advocating for reality
Our first daughter was born during my last year in medical school, and our second was born as I was finishing my second year in residency. Seeing those two little darlings grow and develop was a critical supplement to my pediatric training. And, watching my wife initially struggle and then succeed with breastfeeding provided a very personal experience and education about lactation that my interactions in the hospital and outpatient clinics didn’t offer.
We considered ourselves lucky because my wife wasn’t facing the additional challenge of returning to an out-of-the-home job. However, our good fortune did not confer immunity against the anxiety, insecurity, discomfort, and sleep deprivation–induced frustrations of breastfeeding. Watching my wife navigate the choppy waters of lactation certainly influenced my approach to counseling new mothers over my subsequent 4 decades of practice. I think I was a more sympathetic and realistic adviser based on my first-hand observations.
In a different survey of American Academy of Pediatrics fellows, more of the 832 pediatricians responding reported having had a personal experience with breastfeeding in 2014 than of the 620 responding in 1995 (68% vs. 42%). However, it is interesting that fewer of the respondents in 2014 felt that any mother can succeed at breastfeeding (predicted value = 70% in 1995, PV = 56% in 2014; P less than .05), and fewer in 2014 believed that the advantages of breastfeeding outweighed the difficulties than among those surveyed in 1995 (PV = 70% in 1995, PV = 50% in 2014; P less than .05) (Pediatrics. 2017 Oct;140[4]. pii: e20171229). These results suggest that, as more pediatricians gained personal experience with breastfeeding, more may have realized that the American Academy of Pediatrics recommendations for breastfeeding are unrealistic and may contribute to the negative experiences of some women, including pediatric trainees.
An implied assumption in the AAP News article is that a pediatrician who has had a negative breastfeeding experience is less likely to be a strong advocate for breastfeeding. I would argue that a pediatrician who has witnessed or personally experienced difficulties is more likely to be a sympathetic and realistic advocate of breastfeeding.
We must walk that fine line between actively advocating for lactation-friendly hospitals and work environments and supporting mothers who, due to circumstances beyond their control, can’t meet the expectations we have created for them.
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.”
Our first daughter was born during my last year in medical school, and our second was born as I was finishing my second year in residency. Seeing those two little darlings grow and develop was a critical supplement to my pediatric training. And, watching my wife initially struggle and then succeed with breastfeeding provided a very personal experience and education about lactation that my interactions in the hospital and outpatient clinics didn’t offer.
We considered ourselves lucky because my wife wasn’t facing the additional challenge of returning to an out-of-the-home job. However, our good fortune did not confer immunity against the anxiety, insecurity, discomfort, and sleep deprivation–induced frustrations of breastfeeding. Watching my wife navigate the choppy waters of lactation certainly influenced my approach to counseling new mothers over my subsequent 4 decades of practice. I think I was a more sympathetic and realistic adviser based on my first-hand observations.
In a different survey of American Academy of Pediatrics fellows, more of the 832 pediatricians responding reported having had a personal experience with breastfeeding in 2014 than of the 620 responding in 1995 (68% vs. 42%). However, it is interesting that fewer of the respondents in 2014 felt that any mother can succeed at breastfeeding (predicted value = 70% in 1995, PV = 56% in 2014; P less than .05), and fewer in 2014 believed that the advantages of breastfeeding outweighed the difficulties than among those surveyed in 1995 (PV = 70% in 1995, PV = 50% in 2014; P less than .05) (Pediatrics. 2017 Oct;140[4]. pii: e20171229). These results suggest that, as more pediatricians gained personal experience with breastfeeding, more may have realized that the American Academy of Pediatrics recommendations for breastfeeding are unrealistic and may contribute to the negative experiences of some women, including pediatric trainees.
An implied assumption in the AAP News article is that a pediatrician who has had a negative breastfeeding experience is less likely to be a strong advocate for breastfeeding. I would argue that a pediatrician who has witnessed or personally experienced difficulties is more likely to be a sympathetic and realistic advocate of breastfeeding.
We must walk that fine line between actively advocating for lactation-friendly hospitals and work environments and supporting mothers who, due to circumstances beyond their control, can’t meet the expectations we have created for them.
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.”
Our first daughter was born during my last year in medical school, and our second was born as I was finishing my second year in residency. Seeing those two little darlings grow and develop was a critical supplement to my pediatric training. And, watching my wife initially struggle and then succeed with breastfeeding provided a very personal experience and education about lactation that my interactions in the hospital and outpatient clinics didn’t offer.
We considered ourselves lucky because my wife wasn’t facing the additional challenge of returning to an out-of-the-home job. However, our good fortune did not confer immunity against the anxiety, insecurity, discomfort, and sleep deprivation–induced frustrations of breastfeeding. Watching my wife navigate the choppy waters of lactation certainly influenced my approach to counseling new mothers over my subsequent 4 decades of practice. I think I was a more sympathetic and realistic adviser based on my first-hand observations.
In a different survey of American Academy of Pediatrics fellows, more of the 832 pediatricians responding reported having had a personal experience with breastfeeding in 2014 than of the 620 responding in 1995 (68% vs. 42%). However, it is interesting that fewer of the respondents in 2014 felt that any mother can succeed at breastfeeding (predicted value = 70% in 1995, PV = 56% in 2014; P less than .05), and fewer in 2014 believed that the advantages of breastfeeding outweighed the difficulties than among those surveyed in 1995 (PV = 70% in 1995, PV = 50% in 2014; P less than .05) (Pediatrics. 2017 Oct;140[4]. pii: e20171229). These results suggest that, as more pediatricians gained personal experience with breastfeeding, more may have realized that the American Academy of Pediatrics recommendations for breastfeeding are unrealistic and may contribute to the negative experiences of some women, including pediatric trainees.
An implied assumption in the AAP News article is that a pediatrician who has had a negative breastfeeding experience is less likely to be a strong advocate for breastfeeding. I would argue that a pediatrician who has witnessed or personally experienced difficulties is more likely to be a sympathetic and realistic advocate of breastfeeding.
We must walk that fine line between actively advocating for lactation-friendly hospitals and work environments and supporting mothers who, due to circumstances beyond their control, can’t meet the expectations we have created for them.
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.”
STEMI success stagnating
SNOWMASS, COLO. – , Ajay J. Kirtane, MD, declared at the Annual Cardiovascular Conference at Snowmass.
“We have to recognize the fact that our success has somewhat plateaued. We’ve made great strides in shortening door-to-balloon times, but further reductions in [that measure] are not translating into further reductions in adverse outcomes,” observed Dr. Kirtane of Columbia University, New York.
He and others have identified a number of reasons why ST-elevation myocardial infarction (STEMI) mortality has flattened. One is the continued protracted lag time from symptom onset to arrival at the emergency department. Progress here will require effective public education programs.
“By the time patients are getting to the cath lab, we’re sort of running out of time to salvage the myocardium,” Dr. Kirtane said. “We need to get people to the lab really, really quickly and recognize that symptom onset is still an area in need of improvement.”
The greatest limitation of primary percutaneous coronary intervention (PCI) for treatment of STEMI, however, is poor recovery of left ventricular function. As STEMI mortality has fallen over the years, rates of heart failure caused by suboptimal salvage of myocardium have climbed. Only about two-thirds of patients undergoing primary PCI obtain successful reperfusion; that’s in part due to distal embolization, a problem that hasn’t yet been solved.
One hope for improved reperfusion success that has been dashed is aspiration thrombectomy. It was an attractive concept, but optical coherence imaging has shown that after aspiration, there is still a good deal of thrombus remaining in the vessel. And large randomized trials failed to show a reduction in ischemic events. Thus, the current American College of Cardiology/American Heart Association STEMI guidelines give routine aspiration thrombectomy before primary PCI a class III rating, meaning don’t do it (J Am Coll Cardiol. 2013 Jan. doi: 10.1016/j.jacc.2012.11.019).
What about nonculprit lesions?
A hot topic in STEMI management is what to do about residual disease in nonculprit vessels after primary PCI.
“Some people have drawn upon trials like COURAGE to inform their decision making, saying ‘Now the patient is stabilized, we’ve treated the STEMI, so we could now treat the patient like a COURAGE patient [with optimal medical therapy alone].’ I would caution against extrapolating the results of COURAGE and other stable ischemic heart disease paradigms to these types of patients. They’ve already presented with a very high risk feature – STEMI – and in addition, in the COURAGE trial there were only 118 patients that had acute coronary syndrome of less than 2 weeks’ duration out of more than 2,000 subjects,” Dr. Kirtane said.
“Intravascular ultrasound studies show that nonculprit plaques in stable angina are very different from those in STEMI: They’re typically fibrotic and stable, while even the nonculprit plaques in STEMI or non-STEMI ACS are much more inflamed and vulnerable,” he added.
He predicted clarity regarding best management in this area will come from the ongoing COMPLETE trial, a multinational study of nearly 4,000 patients randomized to staged nonculprit lesion PCI versus medical therapy plus culprit lesion-only revascularization. The study is due to be completed late in 2018.
Improving pharmacotherapy
Rates of hospital discharge on guideline-directed optimal medical therapy after primary PCI have risen steadily in recent years. However, studies indicate a significant minority of patients drop from dual-antiplatelet therapy to aspirin alone within a month after leaving the hospital.
Also, it’s essential to effectively inhibit both platelets and thrombus in the catheterization lab. But is that happening consistently? There is now evidence of delayed absorption of the potent oral antiplatelet agents in STEMI patients. Moreover, that delay is exacerbated by having morphine or fentanyl on board.
“It’s been shown that even with ticagrelor and prasugrel, in STEMI patients at 2 hours, you still don’t have sufficient inhibition of platelet aggregation, whereas if I gave one of those drugs to any of us here in the audience now we’d have full effect within an hour or 2 max. That’s one of the reasons why there’s a rationale for using an intravenous agent such as cangrelor [Kengreal], a nonthienopyridine direct P2Y12 inhibitor,” Dr. Kirtane said.
Transradial access for primary PCI
Dr. Kirtane argued in a recent editorial that widespread adoption of transradial PCI for STEMI will provide the next major advance in STEMI systems of care resulting in improved clinical outcomes (JAMA Cardiol. 2017 Oct 1;2[10]:1057-8).
This is a controversial issue, he acknowledged. “There are interventional cardiologists who say, ‘No way.’ ” But studies indicate that transradial PCI for STEMI reduces mortality by 16%-48% compared with transfemoral access, without a significant cost in terms of door-to-balloon time. For now, transfemoral access PCI remains the most common strategy for STEMI patients in the United States, although the use of transradial primary PCI is growing.
Dr. Kirtane reported receiving research grants from more than half a dozen medical device companies.
SNOWMASS, COLO. – , Ajay J. Kirtane, MD, declared at the Annual Cardiovascular Conference at Snowmass.
“We have to recognize the fact that our success has somewhat plateaued. We’ve made great strides in shortening door-to-balloon times, but further reductions in [that measure] are not translating into further reductions in adverse outcomes,” observed Dr. Kirtane of Columbia University, New York.
He and others have identified a number of reasons why ST-elevation myocardial infarction (STEMI) mortality has flattened. One is the continued protracted lag time from symptom onset to arrival at the emergency department. Progress here will require effective public education programs.
“By the time patients are getting to the cath lab, we’re sort of running out of time to salvage the myocardium,” Dr. Kirtane said. “We need to get people to the lab really, really quickly and recognize that symptom onset is still an area in need of improvement.”
The greatest limitation of primary percutaneous coronary intervention (PCI) for treatment of STEMI, however, is poor recovery of left ventricular function. As STEMI mortality has fallen over the years, rates of heart failure caused by suboptimal salvage of myocardium have climbed. Only about two-thirds of patients undergoing primary PCI obtain successful reperfusion; that’s in part due to distal embolization, a problem that hasn’t yet been solved.
One hope for improved reperfusion success that has been dashed is aspiration thrombectomy. It was an attractive concept, but optical coherence imaging has shown that after aspiration, there is still a good deal of thrombus remaining in the vessel. And large randomized trials failed to show a reduction in ischemic events. Thus, the current American College of Cardiology/American Heart Association STEMI guidelines give routine aspiration thrombectomy before primary PCI a class III rating, meaning don’t do it (J Am Coll Cardiol. 2013 Jan. doi: 10.1016/j.jacc.2012.11.019).
What about nonculprit lesions?
A hot topic in STEMI management is what to do about residual disease in nonculprit vessels after primary PCI.
“Some people have drawn upon trials like COURAGE to inform their decision making, saying ‘Now the patient is stabilized, we’ve treated the STEMI, so we could now treat the patient like a COURAGE patient [with optimal medical therapy alone].’ I would caution against extrapolating the results of COURAGE and other stable ischemic heart disease paradigms to these types of patients. They’ve already presented with a very high risk feature – STEMI – and in addition, in the COURAGE trial there were only 118 patients that had acute coronary syndrome of less than 2 weeks’ duration out of more than 2,000 subjects,” Dr. Kirtane said.
“Intravascular ultrasound studies show that nonculprit plaques in stable angina are very different from those in STEMI: They’re typically fibrotic and stable, while even the nonculprit plaques in STEMI or non-STEMI ACS are much more inflamed and vulnerable,” he added.
He predicted clarity regarding best management in this area will come from the ongoing COMPLETE trial, a multinational study of nearly 4,000 patients randomized to staged nonculprit lesion PCI versus medical therapy plus culprit lesion-only revascularization. The study is due to be completed late in 2018.
Improving pharmacotherapy
Rates of hospital discharge on guideline-directed optimal medical therapy after primary PCI have risen steadily in recent years. However, studies indicate a significant minority of patients drop from dual-antiplatelet therapy to aspirin alone within a month after leaving the hospital.
Also, it’s essential to effectively inhibit both platelets and thrombus in the catheterization lab. But is that happening consistently? There is now evidence of delayed absorption of the potent oral antiplatelet agents in STEMI patients. Moreover, that delay is exacerbated by having morphine or fentanyl on board.
“It’s been shown that even with ticagrelor and prasugrel, in STEMI patients at 2 hours, you still don’t have sufficient inhibition of platelet aggregation, whereas if I gave one of those drugs to any of us here in the audience now we’d have full effect within an hour or 2 max. That’s one of the reasons why there’s a rationale for using an intravenous agent such as cangrelor [Kengreal], a nonthienopyridine direct P2Y12 inhibitor,” Dr. Kirtane said.
Transradial access for primary PCI
Dr. Kirtane argued in a recent editorial that widespread adoption of transradial PCI for STEMI will provide the next major advance in STEMI systems of care resulting in improved clinical outcomes (JAMA Cardiol. 2017 Oct 1;2[10]:1057-8).
This is a controversial issue, he acknowledged. “There are interventional cardiologists who say, ‘No way.’ ” But studies indicate that transradial PCI for STEMI reduces mortality by 16%-48% compared with transfemoral access, without a significant cost in terms of door-to-balloon time. For now, transfemoral access PCI remains the most common strategy for STEMI patients in the United States, although the use of transradial primary PCI is growing.
Dr. Kirtane reported receiving research grants from more than half a dozen medical device companies.
SNOWMASS, COLO. – , Ajay J. Kirtane, MD, declared at the Annual Cardiovascular Conference at Snowmass.
“We have to recognize the fact that our success has somewhat plateaued. We’ve made great strides in shortening door-to-balloon times, but further reductions in [that measure] are not translating into further reductions in adverse outcomes,” observed Dr. Kirtane of Columbia University, New York.
He and others have identified a number of reasons why ST-elevation myocardial infarction (STEMI) mortality has flattened. One is the continued protracted lag time from symptom onset to arrival at the emergency department. Progress here will require effective public education programs.
“By the time patients are getting to the cath lab, we’re sort of running out of time to salvage the myocardium,” Dr. Kirtane said. “We need to get people to the lab really, really quickly and recognize that symptom onset is still an area in need of improvement.”
The greatest limitation of primary percutaneous coronary intervention (PCI) for treatment of STEMI, however, is poor recovery of left ventricular function. As STEMI mortality has fallen over the years, rates of heart failure caused by suboptimal salvage of myocardium have climbed. Only about two-thirds of patients undergoing primary PCI obtain successful reperfusion; that’s in part due to distal embolization, a problem that hasn’t yet been solved.
One hope for improved reperfusion success that has been dashed is aspiration thrombectomy. It was an attractive concept, but optical coherence imaging has shown that after aspiration, there is still a good deal of thrombus remaining in the vessel. And large randomized trials failed to show a reduction in ischemic events. Thus, the current American College of Cardiology/American Heart Association STEMI guidelines give routine aspiration thrombectomy before primary PCI a class III rating, meaning don’t do it (J Am Coll Cardiol. 2013 Jan. doi: 10.1016/j.jacc.2012.11.019).
What about nonculprit lesions?
A hot topic in STEMI management is what to do about residual disease in nonculprit vessels after primary PCI.
“Some people have drawn upon trials like COURAGE to inform their decision making, saying ‘Now the patient is stabilized, we’ve treated the STEMI, so we could now treat the patient like a COURAGE patient [with optimal medical therapy alone].’ I would caution against extrapolating the results of COURAGE and other stable ischemic heart disease paradigms to these types of patients. They’ve already presented with a very high risk feature – STEMI – and in addition, in the COURAGE trial there were only 118 patients that had acute coronary syndrome of less than 2 weeks’ duration out of more than 2,000 subjects,” Dr. Kirtane said.
“Intravascular ultrasound studies show that nonculprit plaques in stable angina are very different from those in STEMI: They’re typically fibrotic and stable, while even the nonculprit plaques in STEMI or non-STEMI ACS are much more inflamed and vulnerable,” he added.
He predicted clarity regarding best management in this area will come from the ongoing COMPLETE trial, a multinational study of nearly 4,000 patients randomized to staged nonculprit lesion PCI versus medical therapy plus culprit lesion-only revascularization. The study is due to be completed late in 2018.
Improving pharmacotherapy
Rates of hospital discharge on guideline-directed optimal medical therapy after primary PCI have risen steadily in recent years. However, studies indicate a significant minority of patients drop from dual-antiplatelet therapy to aspirin alone within a month after leaving the hospital.
Also, it’s essential to effectively inhibit both platelets and thrombus in the catheterization lab. But is that happening consistently? There is now evidence of delayed absorption of the potent oral antiplatelet agents in STEMI patients. Moreover, that delay is exacerbated by having morphine or fentanyl on board.
“It’s been shown that even with ticagrelor and prasugrel, in STEMI patients at 2 hours, you still don’t have sufficient inhibition of platelet aggregation, whereas if I gave one of those drugs to any of us here in the audience now we’d have full effect within an hour or 2 max. That’s one of the reasons why there’s a rationale for using an intravenous agent such as cangrelor [Kengreal], a nonthienopyridine direct P2Y12 inhibitor,” Dr. Kirtane said.
Transradial access for primary PCI
Dr. Kirtane argued in a recent editorial that widespread adoption of transradial PCI for STEMI will provide the next major advance in STEMI systems of care resulting in improved clinical outcomes (JAMA Cardiol. 2017 Oct 1;2[10]:1057-8).
This is a controversial issue, he acknowledged. “There are interventional cardiologists who say, ‘No way.’ ” But studies indicate that transradial PCI for STEMI reduces mortality by 16%-48% compared with transfemoral access, without a significant cost in terms of door-to-balloon time. For now, transfemoral access PCI remains the most common strategy for STEMI patients in the United States, although the use of transradial primary PCI is growing.
Dr. Kirtane reported receiving research grants from more than half a dozen medical device companies.
EXPERT ANALYSIS FROM THE CARDIOVASCULAR CONFERENCE AT SNOWMASS
… What comes naturally
When we were invited to a family gathering to celebrate a 60th birthday, we expected to hear an abundance of news about grandchildren. They are natural, and seldom controversial, topics of discussion. If there is a child still waiting in utero and destined to be the first grandchild on one or both sides of the family, the impending adventure in parenthood will dominate the conversation.
To our great surprise, despite the presence of one very pregnant young woman, who in 6 weeks would be giving birth to the first grandchild in my nephew’s family, my wife and I can recall only one brief dialogue in which I was asked about how one might go about selecting a pediatrician.
I’m not sure why the blessed event to come was being ignored, but I found the oversight unusual and refreshing. It is possible that there had been so much hype about the pregnancy on her side of the family that the couple relished its absence from the birthday party’s topics for discussion.
In the spirit of full disclosure, I must add that, as a result of my frequent claims of ignorance when asked about medically related topics, I am often referred to by the extended family as “Dr. I-Don’t-Know.” It may be that my presence influenced the conversation, but regardless of the reason, I was impressed with the ease at which this couple was approaching the birth of their first child.
I am sure they harbor some anxieties, and I am sure they have listened to some horror stories from their peers about sleep and breastfeeding problems. They are bright people who acknowledge that they are going to encounter some bumps along the road of parenthood. However, they seem to be immune to the epidemic of anxiety that for decades has been sweeping over cohorts of North Americans entering their family-building years.
The young couple my wife and I encountered are just as clueless about what parenthood has in store as their anxiety-driven peers are. The difference is that they are enjoying their pregnancy in blissful ignorance buffered by their refreshing confidence that, however they do it, they will be doing it naturally.
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.”
When we were invited to a family gathering to celebrate a 60th birthday, we expected to hear an abundance of news about grandchildren. They are natural, and seldom controversial, topics of discussion. If there is a child still waiting in utero and destined to be the first grandchild on one or both sides of the family, the impending adventure in parenthood will dominate the conversation.
To our great surprise, despite the presence of one very pregnant young woman, who in 6 weeks would be giving birth to the first grandchild in my nephew’s family, my wife and I can recall only one brief dialogue in which I was asked about how one might go about selecting a pediatrician.
I’m not sure why the blessed event to come was being ignored, but I found the oversight unusual and refreshing. It is possible that there had been so much hype about the pregnancy on her side of the family that the couple relished its absence from the birthday party’s topics for discussion.
In the spirit of full disclosure, I must add that, as a result of my frequent claims of ignorance when asked about medically related topics, I am often referred to by the extended family as “Dr. I-Don’t-Know.” It may be that my presence influenced the conversation, but regardless of the reason, I was impressed with the ease at which this couple was approaching the birth of their first child.
I am sure they harbor some anxieties, and I am sure they have listened to some horror stories from their peers about sleep and breastfeeding problems. They are bright people who acknowledge that they are going to encounter some bumps along the road of parenthood. However, they seem to be immune to the epidemic of anxiety that for decades has been sweeping over cohorts of North Americans entering their family-building years.
The young couple my wife and I encountered are just as clueless about what parenthood has in store as their anxiety-driven peers are. The difference is that they are enjoying their pregnancy in blissful ignorance buffered by their refreshing confidence that, however they do it, they will be doing it naturally.
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.”
When we were invited to a family gathering to celebrate a 60th birthday, we expected to hear an abundance of news about grandchildren. They are natural, and seldom controversial, topics of discussion. If there is a child still waiting in utero and destined to be the first grandchild on one or both sides of the family, the impending adventure in parenthood will dominate the conversation.
To our great surprise, despite the presence of one very pregnant young woman, who in 6 weeks would be giving birth to the first grandchild in my nephew’s family, my wife and I can recall only one brief dialogue in which I was asked about how one might go about selecting a pediatrician.
I’m not sure why the blessed event to come was being ignored, but I found the oversight unusual and refreshing. It is possible that there had been so much hype about the pregnancy on her side of the family that the couple relished its absence from the birthday party’s topics for discussion.
In the spirit of full disclosure, I must add that, as a result of my frequent claims of ignorance when asked about medically related topics, I am often referred to by the extended family as “Dr. I-Don’t-Know.” It may be that my presence influenced the conversation, but regardless of the reason, I was impressed with the ease at which this couple was approaching the birth of their first child.
I am sure they harbor some anxieties, and I am sure they have listened to some horror stories from their peers about sleep and breastfeeding problems. They are bright people who acknowledge that they are going to encounter some bumps along the road of parenthood. However, they seem to be immune to the epidemic of anxiety that for decades has been sweeping over cohorts of North Americans entering their family-building years.
The young couple my wife and I encountered are just as clueless about what parenthood has in store as their anxiety-driven peers are. The difference is that they are enjoying their pregnancy in blissful ignorance buffered by their refreshing confidence that, however they do it, they will be doing it naturally.
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.”