Cardiology News

New research results reinforce the benefits of quitting smoking.
 

Not only does it stop further damage to the lungs, it appears that it also allows new, healthy cells to actively replenish the lining of the airways. This shift in the proportion of healthy cells to damaged cells could reduce the risk for lung cancer, say researchers.

The findings were published online in Nature (2020 Jan 29. doi: 10.1038/s41586-020-1961-1).

The team performed whole-genome sequencing on healthy airway cells collected (during a bronchoscopy for clinical indications) from current smokers and ex-smokers, as well as from adult never-smokers and children.

The investigators found, as expected, that the cells from current and ex-smokers had a far higher mutational burden than those of never-smokers and children, including an increased number of “driver” mutations, which increase the potential of cells to become cancerous.

However, they also found that in ex-smokers – but not in current smokers – up to 40% of the cells were near normal, with far less genetic damage and a low risk of developing cancer.

“People who have smoked heavily for 30, 40 or more years often say to me that it’s too late to stop smoking – the damage is already done,” commented senior author Peter J. Campbell, PhD, Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, England.

“What is so exciting about our study is that it shows that it’s never too late to quit. Some of the people in our study had smoked more than 15,000 packs of cigarettes over their life, but within a few years of quitting, many of the cells lining their airways showed no evidence of damage from tobacco,” he said. The comments appear in a press release issued by Cancer Research UK, which partly funded the study.

This study has “broadened our understanding of the effects of tobacco smoke on normal epithelial cells in the human lung,” Gerd P. Pfeifer, PhD, at the Center for Epigenetics, Van Andel Institute, Grand Rapids, Michigan, writes in an accompanying comment.

“It has shed light on how the protective effect of smoking cessation plays out at the molecular level in human lung tissue and raises many interesting questions worthy of future investigation,” he added.
 

‘Important public health message’

Joint senior author Sam M. Janes, PhD, Lungs for Living Research Center, UCL Respiratory, University College London, added that the study has “an important public health message.

“Stopping smoking at any age does not just slow the accumulation of further damage but could reawaken cells unharmed by past lifestyle choices,” he said.

“Further research into this process could help to understand how these cells protect against cancer and could potentially lead to new avenues of research into anticancer therapeutics,” Dr. James added.

In an interview, Dr. Campbell said that the team would next like to try “to find where this reservoir of normal cells hides out while the patient is smoking. We have some ideas from mouse models and we think, by adapting the methods we used in this study, we will be able to test that hypothesis directly.”

He continued: “If we can find this stem cell niche, then we can study the biology of the cells living in there and what makes them expand when a patient stops smoking.

“Once we understand that biology, we can think about therapies to target that population of cells in beneficial ways.”

Dr. Campbell concluded that they are “a long way away yet, but the toolkit exists for getting there.”
 

Tobacco and mutagenesis

In their article, the team notes that the model explaining how tobacco exposure causes lung cancer centers on the notion that the 60-plus carcinogens in cigarette smoke directly cause mutagenesis, which combines with the indirect effects of inflammation, immune suppression, and infection to lead to cancer.

However, this does not explain why individuals who stop smoking in middle age or earlier “avoid most of the risk of tobacco-associated lung cancer.”

They questioned the relationship between tobacco and mutagenesis. For two people who smoke the same number of cigarettes over their lifetime, the observation that the person with longer duration of cessation has a lower risk for lung cancer is difficult to explain if carcinogenesis is induced exclusively by an increase in the mutational burden, they noted.

To investigate further, the team set out to examine the “landscape” of somatic mutations in normal bronchial epithelium. They recruited 16 individuals: three children, four never-smokers, six ex-smokers, and three current smokers.

All the participants underwent bronchoscopy for clinical indications. Samples of airway epithelium were obtained from biopsies or brushings of main or secondary bronchi.

The researchers performed whole-genome sequencing of 632 colonies derived from single bronchial epithelial cells. In addition, cells from squamous cell carcinoma or carcinoma in situ from three of the patients were sequenced.
 

Cells show different mutational burdens

The results showed there was “considerable heterogeneity” in mutational burden both between patients and in individual patients.

Moreover, single-base substitutions increased significantly with age, at an estimated rate of 22 per cell per year (P = 10^–8). In addition, previous and current smoking substantially increased the substitution burden by an estimated 2,330 per cell in ex-smokers and 5,300 per cell in current smokers.

The team was surprised to find that smoking also increased the variability of the mutational burden from cell to cell, “even within the same individual.”

They calculated that, even between cells from a small biopsy sample of normal airway, the standard deviation in mutational burden was 2,350 per cell in ex-smokers and 2,100 per cell in current smokers, but only 140 per cell in children and 290 per cell in adult never-smokers (P less than 10^–16 for within-subject heterogeneity).

Between individuals, the mean substitution burden was 1,200 per cell in ex-smokers, 1,260 per cell in current smokers, and 90 per cell for nonsmokers (P = 10^–8 for heterogeneity).

Driver mutations were also more common in individuals who had a history of smoking. In those persons, they were seen in at least 25% of cells vs. 4%-14% of cells from adult never-smokers and none of the cells from children.

It was calculated that current smokers had a 2.1-fold increase in the number of driver mutations per cell in comparison with never-smokers (P = .04).

In addition, the number of driver mutations per cell increased 1.5-fold with every decade of life (P = .004) and twofold for every 5,000 extra somatic mutations per cell (P = .0003).

However, the team also found that some patients among the ex-smokers and current smokers had cells with a near-normal mutational burden, similar to that seen for never-smokers of the equivalent age.

Although these cells were rare in current smokers, their relative frequency was, the team reports, an average fourfold higher in ex-smokers and accounted for between 20% and 40% of all cells studied.

Further analysis showed that these near-normal cells had less damage from tobacco-specific mutational processes than other cells and that they had longer telomeres.

“Two points remain unclear: how these cells have avoided the high rates of mutations that are exhibited by neighbouring cells, and why this particular population of cells expands after smoking cessation,” the team writes.

They argue that the presence of longer telomeres suggests they are “recent descendants of quiescent stem cells,” which have been found in mice but “remain elusive” in human lungs.

“The apparent expansion of the near-normal cells could represent the expected physiology of a two-compartment model in which relatively short-lived proliferative progenitors are slowly replenished from a pool of quiescent stem cells, but the progenitors are more exposed to tobacco carcinogens,” they suggest.

“Only in ex-smokers would the difference in mutagenic environment be sufficient to distinguish newly produced progenitors from long-term occupants of the bronchial epithelial surface,” they add.

However, in his commentary, Dr. Pfeifer highlights that a “potential caveat” of the study is the small number of individuals (n = 16) from whom cells were taken.

In addition, Dr. Pfeifer notes that the “lack of knowledge” about the suggested “long-lived stem cells and information about the longevity of the different cell types in the human lung make it difficult to explain what occurred in the ex-smokers’ cells with few mutations.”

The study was supported by a Cancer Research UK Grand Challenge Award and the Wellcome Trust. Dr. Campbell and Dr. Janes are Wellcome Trust senior clinical fellows. The authors have disclosed no relevant financial relationships.
 

This article first appeared on Medscape.com.

New research results reinforce the benefits of quitting smoking.
 

Not only does it stop further damage to the lungs, it appears that it also allows new, healthy cells to actively replenish the lining of the airways. This shift in the proportion of healthy cells to damaged cells could reduce the risk for lung cancer, say researchers.

The findings were published online in Nature (2020 Jan 29. doi: 10.1038/s41586-020-1961-1).

The team performed whole-genome sequencing on healthy airway cells collected (during a bronchoscopy for clinical indications) from current smokers and ex-smokers, as well as from adult never-smokers and children.

The investigators found, as expected, that the cells from current and ex-smokers had a far higher mutational burden than those of never-smokers and children, including an increased number of “driver” mutations, which increase the potential of cells to become cancerous.

However, they also found that in ex-smokers – but not in current smokers – up to 40% of the cells were near normal, with far less genetic damage and a low risk of developing cancer.

“People who have smoked heavily for 30, 40 or more years often say to me that it’s too late to stop smoking – the damage is already done,” commented senior author Peter J. Campbell, PhD, Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, England.

“What is so exciting about our study is that it shows that it’s never too late to quit. Some of the people in our study had smoked more than 15,000 packs of cigarettes over their life, but within a few years of quitting, many of the cells lining their airways showed no evidence of damage from tobacco,” he said. The comments appear in a press release issued by Cancer Research UK, which partly funded the study.

This study has “broadened our understanding of the effects of tobacco smoke on normal epithelial cells in the human lung,” Gerd P. Pfeifer, PhD, at the Center for Epigenetics, Van Andel Institute, Grand Rapids, Michigan, writes in an accompanying comment.

“It has shed light on how the protective effect of smoking cessation plays out at the molecular level in human lung tissue and raises many interesting questions worthy of future investigation,” he added.
 

‘Important public health message’

Joint senior author Sam M. Janes, PhD, Lungs for Living Research Center, UCL Respiratory, University College London, added that the study has “an important public health message.

“Stopping smoking at any age does not just slow the accumulation of further damage but could reawaken cells unharmed by past lifestyle choices,” he said.

“Further research into this process could help to understand how these cells protect against cancer and could potentially lead to new avenues of research into anticancer therapeutics,” Dr. James added.

In an interview, Dr. Campbell said that the team would next like to try “to find where this reservoir of normal cells hides out while the patient is smoking. We have some ideas from mouse models and we think, by adapting the methods we used in this study, we will be able to test that hypothesis directly.”

He continued: “If we can find this stem cell niche, then we can study the biology of the cells living in there and what makes them expand when a patient stops smoking.

“Once we understand that biology, we can think about therapies to target that population of cells in beneficial ways.”

Dr. Campbell concluded that they are “a long way away yet, but the toolkit exists for getting there.”
 

Tobacco and mutagenesis

In their article, the team notes that the model explaining how tobacco exposure causes lung cancer centers on the notion that the 60-plus carcinogens in cigarette smoke directly cause mutagenesis, which combines with the indirect effects of inflammation, immune suppression, and infection to lead to cancer.

However, this does not explain why individuals who stop smoking in middle age or earlier “avoid most of the risk of tobacco-associated lung cancer.”

They questioned the relationship between tobacco and mutagenesis. For two people who smoke the same number of cigarettes over their lifetime, the observation that the person with longer duration of cessation has a lower risk for lung cancer is difficult to explain if carcinogenesis is induced exclusively by an increase in the mutational burden, they noted.

To investigate further, the team set out to examine the “landscape” of somatic mutations in normal bronchial epithelium. They recruited 16 individuals: three children, four never-smokers, six ex-smokers, and three current smokers.

All the participants underwent bronchoscopy for clinical indications. Samples of airway epithelium were obtained from biopsies or brushings of main or secondary bronchi.

The researchers performed whole-genome sequencing of 632 colonies derived from single bronchial epithelial cells. In addition, cells from squamous cell carcinoma or carcinoma in situ from three of the patients were sequenced.
 

Cells show different mutational burdens

The results showed there was “considerable heterogeneity” in mutational burden both between patients and in individual patients.

Moreover, single-base substitutions increased significantly with age, at an estimated rate of 22 per cell per year (P = 10^–8). In addition, previous and current smoking substantially increased the substitution burden by an estimated 2,330 per cell in ex-smokers and 5,300 per cell in current smokers.

The team was surprised to find that smoking also increased the variability of the mutational burden from cell to cell, “even within the same individual.”

They calculated that, even between cells from a small biopsy sample of normal airway, the standard deviation in mutational burden was 2,350 per cell in ex-smokers and 2,100 per cell in current smokers, but only 140 per cell in children and 290 per cell in adult never-smokers (P less than 10^–16 for within-subject heterogeneity).

Between individuals, the mean substitution burden was 1,200 per cell in ex-smokers, 1,260 per cell in current smokers, and 90 per cell for nonsmokers (P = 10^–8 for heterogeneity).

Driver mutations were also more common in individuals who had a history of smoking. In those persons, they were seen in at least 25% of cells vs. 4%-14% of cells from adult never-smokers and none of the cells from children.

It was calculated that current smokers had a 2.1-fold increase in the number of driver mutations per cell in comparison with never-smokers (P = .04).

In addition, the number of driver mutations per cell increased 1.5-fold with every decade of life (P = .004) and twofold for every 5,000 extra somatic mutations per cell (P = .0003).

However, the team also found that some patients among the ex-smokers and current smokers had cells with a near-normal mutational burden, similar to that seen for never-smokers of the equivalent age.

Although these cells were rare in current smokers, their relative frequency was, the team reports, an average fourfold higher in ex-smokers and accounted for between 20% and 40% of all cells studied.

Further analysis showed that these near-normal cells had less damage from tobacco-specific mutational processes than other cells and that they had longer telomeres.

“Two points remain unclear: how these cells have avoided the high rates of mutations that are exhibited by neighbouring cells, and why this particular population of cells expands after smoking cessation,” the team writes.

They argue that the presence of longer telomeres suggests they are “recent descendants of quiescent stem cells,” which have been found in mice but “remain elusive” in human lungs.

“The apparent expansion of the near-normal cells could represent the expected physiology of a two-compartment model in which relatively short-lived proliferative progenitors are slowly replenished from a pool of quiescent stem cells, but the progenitors are more exposed to tobacco carcinogens,” they suggest.

“Only in ex-smokers would the difference in mutagenic environment be sufficient to distinguish newly produced progenitors from long-term occupants of the bronchial epithelial surface,” they add.

However, in his commentary, Dr. Pfeifer highlights that a “potential caveat” of the study is the small number of individuals (n = 16) from whom cells were taken.

In addition, Dr. Pfeifer notes that the “lack of knowledge” about the suggested “long-lived stem cells and information about the longevity of the different cell types in the human lung make it difficult to explain what occurred in the ex-smokers’ cells with few mutations.”

The study was supported by a Cancer Research UK Grand Challenge Award and the Wellcome Trust. Dr. Campbell and Dr. Janes are Wellcome Trust senior clinical fellows. The authors have disclosed no relevant financial relationships.
 

This article first appeared on Medscape.com.

New research results reinforce the benefits of quitting smoking.
 

Not only does it stop further damage to the lungs, it appears that it also allows new, healthy cells to actively replenish the lining of the airways. This shift in the proportion of healthy cells to damaged cells could reduce the risk for lung cancer, say researchers.

The findings were published online in Nature (2020 Jan 29. doi: 10.1038/s41586-020-1961-1).

The team performed whole-genome sequencing on healthy airway cells collected (during a bronchoscopy for clinical indications) from current smokers and ex-smokers, as well as from adult never-smokers and children.

The investigators found, as expected, that the cells from current and ex-smokers had a far higher mutational burden than those of never-smokers and children, including an increased number of “driver” mutations, which increase the potential of cells to become cancerous.

However, they also found that in ex-smokers – but not in current smokers – up to 40% of the cells were near normal, with far less genetic damage and a low risk of developing cancer.

“People who have smoked heavily for 30, 40 or more years often say to me that it’s too late to stop smoking – the damage is already done,” commented senior author Peter J. Campbell, PhD, Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, England.

“What is so exciting about our study is that it shows that it’s never too late to quit. Some of the people in our study had smoked more than 15,000 packs of cigarettes over their life, but within a few years of quitting, many of the cells lining their airways showed no evidence of damage from tobacco,” he said. The comments appear in a press release issued by Cancer Research UK, which partly funded the study.

This study has “broadened our understanding of the effects of tobacco smoke on normal epithelial cells in the human lung,” Gerd P. Pfeifer, PhD, at the Center for Epigenetics, Van Andel Institute, Grand Rapids, Michigan, writes in an accompanying comment.

“It has shed light on how the protective effect of smoking cessation plays out at the molecular level in human lung tissue and raises many interesting questions worthy of future investigation,” he added.
 

‘Important public health message’

Joint senior author Sam M. Janes, PhD, Lungs for Living Research Center, UCL Respiratory, University College London, added that the study has “an important public health message.

“Stopping smoking at any age does not just slow the accumulation of further damage but could reawaken cells unharmed by past lifestyle choices,” he said.

“Further research into this process could help to understand how these cells protect against cancer and could potentially lead to new avenues of research into anticancer therapeutics,” Dr. James added.

In an interview, Dr. Campbell said that the team would next like to try “to find where this reservoir of normal cells hides out while the patient is smoking. We have some ideas from mouse models and we think, by adapting the methods we used in this study, we will be able to test that hypothesis directly.”

He continued: “If we can find this stem cell niche, then we can study the biology of the cells living in there and what makes them expand when a patient stops smoking.

“Once we understand that biology, we can think about therapies to target that population of cells in beneficial ways.”

Dr. Campbell concluded that they are “a long way away yet, but the toolkit exists for getting there.”
 

Tobacco and mutagenesis

In their article, the team notes that the model explaining how tobacco exposure causes lung cancer centers on the notion that the 60-plus carcinogens in cigarette smoke directly cause mutagenesis, which combines with the indirect effects of inflammation, immune suppression, and infection to lead to cancer.

However, this does not explain why individuals who stop smoking in middle age or earlier “avoid most of the risk of tobacco-associated lung cancer.”

They questioned the relationship between tobacco and mutagenesis. For two people who smoke the same number of cigarettes over their lifetime, the observation that the person with longer duration of cessation has a lower risk for lung cancer is difficult to explain if carcinogenesis is induced exclusively by an increase in the mutational burden, they noted.

To investigate further, the team set out to examine the “landscape” of somatic mutations in normal bronchial epithelium. They recruited 16 individuals: three children, four never-smokers, six ex-smokers, and three current smokers.

All the participants underwent bronchoscopy for clinical indications. Samples of airway epithelium were obtained from biopsies or brushings of main or secondary bronchi.

The researchers performed whole-genome sequencing of 632 colonies derived from single bronchial epithelial cells. In addition, cells from squamous cell carcinoma or carcinoma in situ from three of the patients were sequenced.
 

Cells show different mutational burdens

The results showed there was “considerable heterogeneity” in mutational burden both between patients and in individual patients.

Moreover, single-base substitutions increased significantly with age, at an estimated rate of 22 per cell per year (P = 10^–8). In addition, previous and current smoking substantially increased the substitution burden by an estimated 2,330 per cell in ex-smokers and 5,300 per cell in current smokers.

The team was surprised to find that smoking also increased the variability of the mutational burden from cell to cell, “even within the same individual.”

They calculated that, even between cells from a small biopsy sample of normal airway, the standard deviation in mutational burden was 2,350 per cell in ex-smokers and 2,100 per cell in current smokers, but only 140 per cell in children and 290 per cell in adult never-smokers (P less than 10^–16 for within-subject heterogeneity).

Between individuals, the mean substitution burden was 1,200 per cell in ex-smokers, 1,260 per cell in current smokers, and 90 per cell for nonsmokers (P = 10^–8 for heterogeneity).

Driver mutations were also more common in individuals who had a history of smoking. In those persons, they were seen in at least 25% of cells vs. 4%-14% of cells from adult never-smokers and none of the cells from children.

It was calculated that current smokers had a 2.1-fold increase in the number of driver mutations per cell in comparison with never-smokers (P = .04).

In addition, the number of driver mutations per cell increased 1.5-fold with every decade of life (P = .004) and twofold for every 5,000 extra somatic mutations per cell (P = .0003).

However, the team also found that some patients among the ex-smokers and current smokers had cells with a near-normal mutational burden, similar to that seen for never-smokers of the equivalent age.

Although these cells were rare in current smokers, their relative frequency was, the team reports, an average fourfold higher in ex-smokers and accounted for between 20% and 40% of all cells studied.

Further analysis showed that these near-normal cells had less damage from tobacco-specific mutational processes than other cells and that they had longer telomeres.

“Two points remain unclear: how these cells have avoided the high rates of mutations that are exhibited by neighbouring cells, and why this particular population of cells expands after smoking cessation,” the team writes.

They argue that the presence of longer telomeres suggests they are “recent descendants of quiescent stem cells,” which have been found in mice but “remain elusive” in human lungs.

“The apparent expansion of the near-normal cells could represent the expected physiology of a two-compartment model in which relatively short-lived proliferative progenitors are slowly replenished from a pool of quiescent stem cells, but the progenitors are more exposed to tobacco carcinogens,” they suggest.

“Only in ex-smokers would the difference in mutagenic environment be sufficient to distinguish newly produced progenitors from long-term occupants of the bronchial epithelial surface,” they add.

However, in his commentary, Dr. Pfeifer highlights that a “potential caveat” of the study is the small number of individuals (n = 16) from whom cells were taken.

In addition, Dr. Pfeifer notes that the “lack of knowledge” about the suggested “long-lived stem cells and information about the longevity of the different cell types in the human lung make it difficult to explain what occurred in the ex-smokers’ cells with few mutations.”

The study was supported by a Cancer Research UK Grand Challenge Award and the Wellcome Trust. Dr. Campbell and Dr. Janes are Wellcome Trust senior clinical fellows. The authors have disclosed no relevant financial relationships.
 

This article first appeared on Medscape.com.

Among Medicare beneficiaries admitted to the hospital between 2008 and 2016, there was an increase in postdischarge 30-day mortality for patients with heart failure, but not for those with acute myocardial infarction or pneumonia.

The finding comes from an effort to evaluate the use of services soon after discharge for conditions targeted in the U.S. Hospital Readmissions Reduction Program (HRRP), and patients’ outcomes.

“The announcement and implementation of the HRRP were associated with a reduction in readmissions within 30 days of discharge for heart failure, acute myocardial infarction, and pneumonia, as shown by a decrease in the overall national rate of readmissions,” first author Rohan Khera, MD, and colleagues wrote in a study published online Jan. 15, 2020, in the British Medical Journal (doi:10.1136/bmj.l6831).

“Concerns existed that pressures to reduce readmissions had led to the evolution of care patterns that may have adverse consequences through reducing access to care in appropriate settings. Therefore, determining whether patients who are seen in acute care settings, but not admitted to hospital, experience an increased risk of mortality is essential.”

Dr. Khera, a cardiologist at the University of Texas Southwestern Medical Center, Dallas, and colleagues limited the analysis to Medicare claims data from patients who were admitted to the hospital with heart failure, acute myocardial infarction (MI), or pneumonia between 2008 and 2016. Key outcomes of interest were: (1) postdischarge 30-day mortality; and (2) acute care utilization in inpatient units, observation units, and the ED during the postdischarge period.

During the study period there were 3,772,924 hospital admissions for heart failure, 1,570,113 for acute MI, and 3,131,162 for pneumonia. The greatest number of readmissions within 30 days of discharge was for heart failure patients (22.5%), followed by acute MI (17.5%), and pneumonia (17.2%).

The overall rates of observation stays were 1.7% for heart failure, 2.6% for acute MI, and 1.4% for pneumonia, while the overall rates of emergency department visits were 6.4% for heart failure, 6.8% for acute MI, and 6.3% for pneumonia. Cumulatively, about one-third of all admissions – 30.7% for heart failure, 26.9% for acute MI, and 24.8% for pneumonia – received postdischarge care in any acute care setting.

Dr. Khera and colleagues found that overall postdischarge 30-day mortality was 8.7% for heart failure, 7.3% for acute MI, and 8.4% for pneumonia. At the same time, postdischarge 30-day mortality was higher in patients with readmissions (13.2% for heart failure, 12.7% for acute MI, and 15.3% for pneumonia), compared with those who had observation stays (4.5% for heart failure, 2.7% for acute MI, and 4.6% for pneumonia), emergency department visits (9.7% for heart failure, 8.8% for acute MI, and 7.8% for pneumonia), or no postdischarge acute care (7.2% for heart failure, 6.0% for acute MI, and 6.9% for pneumonia). Risk adjusted mortality increased annually by 0.05% only for heart failure, while it decreased by 0.06% for acute MI, and did not significantly change for pneumonia.

“The study strongly suggests that the HRRP did not lead to harm through inappropriate triage of patients at high risk to observation units and the emergency department, and therefore provides evidence against calls to curtail the program owing to this theoretical concern (see JAMA 2018;320:2539-41),” the researchers concluded.

They acknowledged certain limitations of the study, including the fact that they were “unable to identify patterns of acute care during the index hospital admission that would be associated with a higher rate of postdischarge acute care in observation units and emergency departments and whether these visits represented avenues for planned postdischarge follow-up care. Moreover, the proportion of these care encounters that were preventable remains poorly understood.”

Dr. Khera disclosed that he is supported by the National Center for Advancing Translational Sciences of the National Institutes of Health. His coauthors reported having numerous disclosures.

[email protected]

SOURCE: Khera et al. BMJ 2020;368:l6831.

Among Medicare beneficiaries admitted to the hospital between 2008 and 2016, there was an increase in postdischarge 30-day mortality for patients with heart failure, but not for those with acute myocardial infarction or pneumonia.

The finding comes from an effort to evaluate the use of services soon after discharge for conditions targeted in the U.S. Hospital Readmissions Reduction Program (HRRP), and patients’ outcomes.

“The announcement and implementation of the HRRP were associated with a reduction in readmissions within 30 days of discharge for heart failure, acute myocardial infarction, and pneumonia, as shown by a decrease in the overall national rate of readmissions,” first author Rohan Khera, MD, and colleagues wrote in a study published online Jan. 15, 2020, in the British Medical Journal (doi:10.1136/bmj.l6831).

“Concerns existed that pressures to reduce readmissions had led to the evolution of care patterns that may have adverse consequences through reducing access to care in appropriate settings. Therefore, determining whether patients who are seen in acute care settings, but not admitted to hospital, experience an increased risk of mortality is essential.”

Dr. Khera, a cardiologist at the University of Texas Southwestern Medical Center, Dallas, and colleagues limited the analysis to Medicare claims data from patients who were admitted to the hospital with heart failure, acute myocardial infarction (MI), or pneumonia between 2008 and 2016. Key outcomes of interest were: (1) postdischarge 30-day mortality; and (2) acute care utilization in inpatient units, observation units, and the ED during the postdischarge period.

During the study period there were 3,772,924 hospital admissions for heart failure, 1,570,113 for acute MI, and 3,131,162 for pneumonia. The greatest number of readmissions within 30 days of discharge was for heart failure patients (22.5%), followed by acute MI (17.5%), and pneumonia (17.2%).

The overall rates of observation stays were 1.7% for heart failure, 2.6% for acute MI, and 1.4% for pneumonia, while the overall rates of emergency department visits were 6.4% for heart failure, 6.8% for acute MI, and 6.3% for pneumonia. Cumulatively, about one-third of all admissions – 30.7% for heart failure, 26.9% for acute MI, and 24.8% for pneumonia – received postdischarge care in any acute care setting.

Dr. Khera and colleagues found that overall postdischarge 30-day mortality was 8.7% for heart failure, 7.3% for acute MI, and 8.4% for pneumonia. At the same time, postdischarge 30-day mortality was higher in patients with readmissions (13.2% for heart failure, 12.7% for acute MI, and 15.3% for pneumonia), compared with those who had observation stays (4.5% for heart failure, 2.7% for acute MI, and 4.6% for pneumonia), emergency department visits (9.7% for heart failure, 8.8% for acute MI, and 7.8% for pneumonia), or no postdischarge acute care (7.2% for heart failure, 6.0% for acute MI, and 6.9% for pneumonia). Risk adjusted mortality increased annually by 0.05% only for heart failure, while it decreased by 0.06% for acute MI, and did not significantly change for pneumonia.

“The study strongly suggests that the HRRP did not lead to harm through inappropriate triage of patients at high risk to observation units and the emergency department, and therefore provides evidence against calls to curtail the program owing to this theoretical concern (see JAMA 2018;320:2539-41),” the researchers concluded.

They acknowledged certain limitations of the study, including the fact that they were “unable to identify patterns of acute care during the index hospital admission that would be associated with a higher rate of postdischarge acute care in observation units and emergency departments and whether these visits represented avenues for planned postdischarge follow-up care. Moreover, the proportion of these care encounters that were preventable remains poorly understood.”

Dr. Khera disclosed that he is supported by the National Center for Advancing Translational Sciences of the National Institutes of Health. His coauthors reported having numerous disclosures.

[email protected]

SOURCE: Khera et al. BMJ 2020;368:l6831.

Among Medicare beneficiaries admitted to the hospital between 2008 and 2016, there was an increase in postdischarge 30-day mortality for patients with heart failure, but not for those with acute myocardial infarction or pneumonia.

The finding comes from an effort to evaluate the use of services soon after discharge for conditions targeted in the U.S. Hospital Readmissions Reduction Program (HRRP), and patients’ outcomes.

“The announcement and implementation of the HRRP were associated with a reduction in readmissions within 30 days of discharge for heart failure, acute myocardial infarction, and pneumonia, as shown by a decrease in the overall national rate of readmissions,” first author Rohan Khera, MD, and colleagues wrote in a study published online Jan. 15, 2020, in the British Medical Journal (doi:10.1136/bmj.l6831).

“Concerns existed that pressures to reduce readmissions had led to the evolution of care patterns that may have adverse consequences through reducing access to care in appropriate settings. Therefore, determining whether patients who are seen in acute care settings, but not admitted to hospital, experience an increased risk of mortality is essential.”

Dr. Khera, a cardiologist at the University of Texas Southwestern Medical Center, Dallas, and colleagues limited the analysis to Medicare claims data from patients who were admitted to the hospital with heart failure, acute myocardial infarction (MI), or pneumonia between 2008 and 2016. Key outcomes of interest were: (1) postdischarge 30-day mortality; and (2) acute care utilization in inpatient units, observation units, and the ED during the postdischarge period.

During the study period there were 3,772,924 hospital admissions for heart failure, 1,570,113 for acute MI, and 3,131,162 for pneumonia. The greatest number of readmissions within 30 days of discharge was for heart failure patients (22.5%), followed by acute MI (17.5%), and pneumonia (17.2%).

The overall rates of observation stays were 1.7% for heart failure, 2.6% for acute MI, and 1.4% for pneumonia, while the overall rates of emergency department visits were 6.4% for heart failure, 6.8% for acute MI, and 6.3% for pneumonia. Cumulatively, about one-third of all admissions – 30.7% for heart failure, 26.9% for acute MI, and 24.8% for pneumonia – received postdischarge care in any acute care setting.

Dr. Khera and colleagues found that overall postdischarge 30-day mortality was 8.7% for heart failure, 7.3% for acute MI, and 8.4% for pneumonia. At the same time, postdischarge 30-day mortality was higher in patients with readmissions (13.2% for heart failure, 12.7% for acute MI, and 15.3% for pneumonia), compared with those who had observation stays (4.5% for heart failure, 2.7% for acute MI, and 4.6% for pneumonia), emergency department visits (9.7% for heart failure, 8.8% for acute MI, and 7.8% for pneumonia), or no postdischarge acute care (7.2% for heart failure, 6.0% for acute MI, and 6.9% for pneumonia). Risk adjusted mortality increased annually by 0.05% only for heart failure, while it decreased by 0.06% for acute MI, and did not significantly change for pneumonia.

“The study strongly suggests that the HRRP did not lead to harm through inappropriate triage of patients at high risk to observation units and the emergency department, and therefore provides evidence against calls to curtail the program owing to this theoretical concern (see JAMA 2018;320:2539-41),” the researchers concluded.

They acknowledged certain limitations of the study, including the fact that they were “unable to identify patterns of acute care during the index hospital admission that would be associated with a higher rate of postdischarge acute care in observation units and emergency departments and whether these visits represented avenues for planned postdischarge follow-up care. Moreover, the proportion of these care encounters that were preventable remains poorly understood.”

Dr. Khera disclosed that he is supported by the National Center for Advancing Translational Sciences of the National Institutes of Health. His coauthors reported having numerous disclosures.

[email protected]

SOURCE: Khera et al. BMJ 2020;368:l6831.

Metabolic syndrome is common among patients with schizophrenia, and those with metabolic syndrome are at significantly higher risk for cardiovascular disease, according to Shadi Naderyan Fe’li of the department of biostatistics and epidemiology at Shahid Sadoughi University of Medical Sciences in Yazd, Iran, and associates.

The cross-sectional study, performed on 100 patients with schizophrenia (83 men, 17 women), was published in the Medical Journal of the Islamic Republic of Iran. The overall prevalence of metabolic syndrome was 27% (men, 21.7%; women, 52.9%); the most common component of metabolic disorder was low HDL cholesterol in males and abdominal adiposity in females.

Based on Framingham Risk Scores, 76% of study participants had a low risk of cardiovascular disease, 16% had intermediate risk, and 8% had high risk. However, patients were almost twice as likely to have intermediate or high risk of cardiovascular disease if they also had metabolic syndrome (P = .042).

“Considering the findings of this study as well as other recent reports, psychiatrists and health care staff should be informed about the potential metabolic side effects of antipsychotics and unhealthy lifestyles among these patients. Furthermore, regular monitoring of metabolic risk factors is suggested. In addition, medical and behavioral interventions should be conducted for patients with [metabolic syndrome],” the investigators concluded.

The investigators reported that they had no conflicts of interest.

[email protected]

SOURCE: Fe’li SN et al. Med J Islam Repub Iran. 2019 Sep 16. doi: 10.34171/mjiri.33.97.

Metabolic syndrome is common among patients with schizophrenia, and those with metabolic syndrome are at significantly higher risk for cardiovascular disease, according to Shadi Naderyan Fe’li of the department of biostatistics and epidemiology at Shahid Sadoughi University of Medical Sciences in Yazd, Iran, and associates.

The cross-sectional study, performed on 100 patients with schizophrenia (83 men, 17 women), was published in the Medical Journal of the Islamic Republic of Iran. The overall prevalence of metabolic syndrome was 27% (men, 21.7%; women, 52.9%); the most common component of metabolic disorder was low HDL cholesterol in males and abdominal adiposity in females.

Based on Framingham Risk Scores, 76% of study participants had a low risk of cardiovascular disease, 16% had intermediate risk, and 8% had high risk. However, patients were almost twice as likely to have intermediate or high risk of cardiovascular disease if they also had metabolic syndrome (P = .042).

“Considering the findings of this study as well as other recent reports, psychiatrists and health care staff should be informed about the potential metabolic side effects of antipsychotics and unhealthy lifestyles among these patients. Furthermore, regular monitoring of metabolic risk factors is suggested. In addition, medical and behavioral interventions should be conducted for patients with [metabolic syndrome],” the investigators concluded.

The investigators reported that they had no conflicts of interest.

[email protected]

SOURCE: Fe’li SN et al. Med J Islam Repub Iran. 2019 Sep 16. doi: 10.34171/mjiri.33.97.

Metabolic syndrome is common among patients with schizophrenia, and those with metabolic syndrome are at significantly higher risk for cardiovascular disease, according to Shadi Naderyan Fe’li of the department of biostatistics and epidemiology at Shahid Sadoughi University of Medical Sciences in Yazd, Iran, and associates.

The cross-sectional study, performed on 100 patients with schizophrenia (83 men, 17 women), was published in the Medical Journal of the Islamic Republic of Iran. The overall prevalence of metabolic syndrome was 27% (men, 21.7%; women, 52.9%); the most common component of metabolic disorder was low HDL cholesterol in males and abdominal adiposity in females.

Based on Framingham Risk Scores, 76% of study participants had a low risk of cardiovascular disease, 16% had intermediate risk, and 8% had high risk. However, patients were almost twice as likely to have intermediate or high risk of cardiovascular disease if they also had metabolic syndrome (P = .042).

“Considering the findings of this study as well as other recent reports, psychiatrists and health care staff should be informed about the potential metabolic side effects of antipsychotics and unhealthy lifestyles among these patients. Furthermore, regular monitoring of metabolic risk factors is suggested. In addition, medical and behavioral interventions should be conducted for patients with [metabolic syndrome],” the investigators concluded.

The investigators reported that they had no conflicts of interest.

[email protected]

SOURCE: Fe’li SN et al. Med J Islam Repub Iran. 2019 Sep 16. doi: 10.34171/mjiri.33.97.

A new study has found that patients with atrial fibrillation (AF) who take oral anticoagulants and then suffer from lower GI bleeding have a much higher risk of being diagnosed with colorectal cancer.

“Our data indicate that lower GI bleeding in these patients should not be dismissed as a mere consequence of anticoagulation treatment,” wrote Peter Vibe Rasmussen, MD, of the University of Copenhagen in Denmark and his coauthors, adding that “timely examination could potentially provide early detection of malignant colorectal lesions.” The study was published in the European Heart Journal.

To determine whether being treated with oral anticoagulants (OACs) and subsequently undergoing GI bleeding indicates colorectal cancer, the researchers examined data from 125,418 Danish AF patients gathered from a nationwide registry. Their median age was 73 years old, and 58% (n = 73,271) were males.

Over a 3-year follow-up period, 2,576 cases of lower GI bleeding were identified; 140 of those cases led to a diagnosis of colorectal cancer within a year. The absolute 1-year risk of colorectal cancer after bleeding was 8.1% (95% confidence interval, 6.1-10.6%) in patients aged 76-80 and 3.7% (95% CI, 2.2-6.2%) in patients 65 years old or younger.

All age groups had a higher risk of colorectal cancer after bleeding, compared with patients without bleeding. Patients 65 or younger had a risk ratio of 24.2 (95% CI, 14.5-40.4) while patients over 85 had a risk ratio of 12.3 (95% CI, 7.9-19.0).

The authors acknowledged their study’s limitations, including a lack of information regarding certain risk factors, such as alcohol consumption, dietary habits, and obesity. In addition, they noted that the absolute risk of colorectal cancer in patients without bleeding is likely underdiagnosed, as “patients without GI bleeding are less likely to undergo diagnostic procedures.”

Two of the authors are employees at Bristol-Myers Squibb and Pfizer, respectively. Six additional authors reported receiving grants, speaker honoraria and consulting fees from various pharmaceutical companies. The remaining authors reported no conflicts of interest.

SOURCE: Rasmussen PV et al. Eur Heart J. 2020 Feb 7. doi: 10.1093/eurheartj/ehz964.

A new study has found that patients with atrial fibrillation (AF) who take oral anticoagulants and then suffer from lower GI bleeding have a much higher risk of being diagnosed with colorectal cancer.

“Our data indicate that lower GI bleeding in these patients should not be dismissed as a mere consequence of anticoagulation treatment,” wrote Peter Vibe Rasmussen, MD, of the University of Copenhagen in Denmark and his coauthors, adding that “timely examination could potentially provide early detection of malignant colorectal lesions.” The study was published in the European Heart Journal.

To determine whether being treated with oral anticoagulants (OACs) and subsequently undergoing GI bleeding indicates colorectal cancer, the researchers examined data from 125,418 Danish AF patients gathered from a nationwide registry. Their median age was 73 years old, and 58% (n = 73,271) were males.

Over a 3-year follow-up period, 2,576 cases of lower GI bleeding were identified; 140 of those cases led to a diagnosis of colorectal cancer within a year. The absolute 1-year risk of colorectal cancer after bleeding was 8.1% (95% confidence interval, 6.1-10.6%) in patients aged 76-80 and 3.7% (95% CI, 2.2-6.2%) in patients 65 years old or younger.

All age groups had a higher risk of colorectal cancer after bleeding, compared with patients without bleeding. Patients 65 or younger had a risk ratio of 24.2 (95% CI, 14.5-40.4) while patients over 85 had a risk ratio of 12.3 (95% CI, 7.9-19.0).

The authors acknowledged their study’s limitations, including a lack of information regarding certain risk factors, such as alcohol consumption, dietary habits, and obesity. In addition, they noted that the absolute risk of colorectal cancer in patients without bleeding is likely underdiagnosed, as “patients without GI bleeding are less likely to undergo diagnostic procedures.”

Two of the authors are employees at Bristol-Myers Squibb and Pfizer, respectively. Six additional authors reported receiving grants, speaker honoraria and consulting fees from various pharmaceutical companies. The remaining authors reported no conflicts of interest.

SOURCE: Rasmussen PV et al. Eur Heart J. 2020 Feb 7. doi: 10.1093/eurheartj/ehz964.

A new study has found that patients with atrial fibrillation (AF) who take oral anticoagulants and then suffer from lower GI bleeding have a much higher risk of being diagnosed with colorectal cancer.

“Our data indicate that lower GI bleeding in these patients should not be dismissed as a mere consequence of anticoagulation treatment,” wrote Peter Vibe Rasmussen, MD, of the University of Copenhagen in Denmark and his coauthors, adding that “timely examination could potentially provide early detection of malignant colorectal lesions.” The study was published in the European Heart Journal.

To determine whether being treated with oral anticoagulants (OACs) and subsequently undergoing GI bleeding indicates colorectal cancer, the researchers examined data from 125,418 Danish AF patients gathered from a nationwide registry. Their median age was 73 years old, and 58% (n = 73,271) were males.

Over a 3-year follow-up period, 2,576 cases of lower GI bleeding were identified; 140 of those cases led to a diagnosis of colorectal cancer within a year. The absolute 1-year risk of colorectal cancer after bleeding was 8.1% (95% confidence interval, 6.1-10.6%) in patients aged 76-80 and 3.7% (95% CI, 2.2-6.2%) in patients 65 years old or younger.

All age groups had a higher risk of colorectal cancer after bleeding, compared with patients without bleeding. Patients 65 or younger had a risk ratio of 24.2 (95% CI, 14.5-40.4) while patients over 85 had a risk ratio of 12.3 (95% CI, 7.9-19.0).

The authors acknowledged their study’s limitations, including a lack of information regarding certain risk factors, such as alcohol consumption, dietary habits, and obesity. In addition, they noted that the absolute risk of colorectal cancer in patients without bleeding is likely underdiagnosed, as “patients without GI bleeding are less likely to undergo diagnostic procedures.”

Two of the authors are employees at Bristol-Myers Squibb and Pfizer, respectively. Six additional authors reported receiving grants, speaker honoraria and consulting fees from various pharmaceutical companies. The remaining authors reported no conflicts of interest.

SOURCE: Rasmussen PV et al. Eur Heart J. 2020 Feb 7. doi: 10.1093/eurheartj/ehz964.

GRAPEVINE, TEX. – Blood pressure categories created by the American College of Cardiology (ACC) and American Heart Association (AHA) in 2017 identify patients with increased risk of preeclampsia, preterm birth, and perinatal death when applied to the first 20 weeks of pregnancy, according to a retrospective study presented at the meeting sponsored by the Society for Maternal-Fetal Medicine.

The absolute risk increases are small, and it is unknown whether treating these patients differently would be beneficial, said study author Martha Tesfalul, MD, maternal-fetal medicine clinical fellow at University of California, San Francisco. Nevertheless, the associations suggest that patients with hypertension during the first 20 weeks may benefit from additional monitoring and counseling, Dr. Tesfalul said.

Cutoffs with unclear implications

The ACC/AHA in November 2017 reclassified blood pressure in nonpregnant adults, but “implications of these categories in pregnancy are still unclear,” Dr. Tesfalul and colleagues said. Under the guidelines, normal blood pressure is systolic blood pressure less than 120 mm Hg and diastolic blood pressure less than 80 mm Hg. Elevated blood pressure is defined as systolic blood pressure between 120 and 129 mm Hg and diastolic blood pressure less than 80 mm Hg. Stage 1 hypertension is systolic blood pressure between 130 and 139 mm Hg or diastolic blood pressure between 80 and 89 mm Hg. And stage 2 hypertension is systolic blood pressure of at least 140 mm Hg or diastolic blood pressure of at least 90 mm Hg.

For the present analysis, the researchers retrospectively compared obstetric and perinatal outcomes for approximately 6,000 pregnancies at an academic center for which they had at least one blood pressure measurement prior to 20 weeks. The highest measurement was used to identify women with normal blood pressure, elevated blood pressure, or stage 1 hypertension according to the 2017 thresholds.

The researchers included singleton pregnancies with delivery between January 2014 and October 2017. They excluded patients with a prior diagnosis of chronic hypertension, autoimmune or chronic renal disease, or fetal anomalies. They examined rates of gestational hypertension, preeclampsia, preterm birth, neonatal intensive care admission, and perinatal death.

Adjusted relative risks

Dr. Tesfalul and colleagues identified about 3,500 pregnancies with normal blood pressure, more than 1,300 pregnancies with elevated blood pressure, and nearly 1,100 pregnancies with stage 1 hypertension.

After adjusting for relevant covariates – maternal age, nulliparity, race, body mass index, in vitro fertilization, tobacco use, pregestational diabetes, and aspirin use – elevated blood pressure and stage 1 hypertension were associated with a higher risk of preeclampsia and severe preeclampsia, relative to normal blood pressure. The proportion of patients with preeclampsia was 5.7% in the normal blood pressure group, 11.7% in the elevated blood pressure group (adjusted relative risk, 1.8), and 15% in the stage 1 hypertension group (adjusted RR, 2.1). The proportion with preeclampsia with severe features was 3.1% in the normal blood pressure group, 5.7% in the elevated blood pressure group (adjusted RR, 1.6), and 6.8% in the stage 1 hypertension group (adjusted RR, 1.8).

In addition, stage 1 hypertension, compared with normal blood pressure, was associated with increased odds of preterm birth at less than 37 weeks (7.9% vs. 5.1%; adjusted RR, 1.4) and perinatal death (0.7% vs. 0.4%; adjusted RR, 2.8).

“Patients with elevated blood pressure and stage 1 hypertension prior to 20 weeks are at increased risk of adverse outcomes,” the authors concluded. “Further research [is] needed to determine optimal care of patients with elevated blood pressure and stage 1 hypertension in pregnancy.”

Dr. Tesfalul receives support from the Foundation for SMFM.

[email protected]

SOURCE: Tesfalul M et al. Am J Obstet Gynecol. 2020 Jan;222(1):S92-3, Abstract 119.

GRAPEVINE, TEX. – Blood pressure categories created by the American College of Cardiology (ACC) and American Heart Association (AHA) in 2017 identify patients with increased risk of preeclampsia, preterm birth, and perinatal death when applied to the first 20 weeks of pregnancy, according to a retrospective study presented at the meeting sponsored by the Society for Maternal-Fetal Medicine.

The absolute risk increases are small, and it is unknown whether treating these patients differently would be beneficial, said study author Martha Tesfalul, MD, maternal-fetal medicine clinical fellow at University of California, San Francisco. Nevertheless, the associations suggest that patients with hypertension during the first 20 weeks may benefit from additional monitoring and counseling, Dr. Tesfalul said.

Cutoffs with unclear implications

The ACC/AHA in November 2017 reclassified blood pressure in nonpregnant adults, but “implications of these categories in pregnancy are still unclear,” Dr. Tesfalul and colleagues said. Under the guidelines, normal blood pressure is systolic blood pressure less than 120 mm Hg and diastolic blood pressure less than 80 mm Hg. Elevated blood pressure is defined as systolic blood pressure between 120 and 129 mm Hg and diastolic blood pressure less than 80 mm Hg. Stage 1 hypertension is systolic blood pressure between 130 and 139 mm Hg or diastolic blood pressure between 80 and 89 mm Hg. And stage 2 hypertension is systolic blood pressure of at least 140 mm Hg or diastolic blood pressure of at least 90 mm Hg.

For the present analysis, the researchers retrospectively compared obstetric and perinatal outcomes for approximately 6,000 pregnancies at an academic center for which they had at least one blood pressure measurement prior to 20 weeks. The highest measurement was used to identify women with normal blood pressure, elevated blood pressure, or stage 1 hypertension according to the 2017 thresholds.

The researchers included singleton pregnancies with delivery between January 2014 and October 2017. They excluded patients with a prior diagnosis of chronic hypertension, autoimmune or chronic renal disease, or fetal anomalies. They examined rates of gestational hypertension, preeclampsia, preterm birth, neonatal intensive care admission, and perinatal death.

Adjusted relative risks

Dr. Tesfalul and colleagues identified about 3,500 pregnancies with normal blood pressure, more than 1,300 pregnancies with elevated blood pressure, and nearly 1,100 pregnancies with stage 1 hypertension.

After adjusting for relevant covariates – maternal age, nulliparity, race, body mass index, in vitro fertilization, tobacco use, pregestational diabetes, and aspirin use – elevated blood pressure and stage 1 hypertension were associated with a higher risk of preeclampsia and severe preeclampsia, relative to normal blood pressure. The proportion of patients with preeclampsia was 5.7% in the normal blood pressure group, 11.7% in the elevated blood pressure group (adjusted relative risk, 1.8), and 15% in the stage 1 hypertension group (adjusted RR, 2.1). The proportion with preeclampsia with severe features was 3.1% in the normal blood pressure group, 5.7% in the elevated blood pressure group (adjusted RR, 1.6), and 6.8% in the stage 1 hypertension group (adjusted RR, 1.8).

In addition, stage 1 hypertension, compared with normal blood pressure, was associated with increased odds of preterm birth at less than 37 weeks (7.9% vs. 5.1%; adjusted RR, 1.4) and perinatal death (0.7% vs. 0.4%; adjusted RR, 2.8).

“Patients with elevated blood pressure and stage 1 hypertension prior to 20 weeks are at increased risk of adverse outcomes,” the authors concluded. “Further research [is] needed to determine optimal care of patients with elevated blood pressure and stage 1 hypertension in pregnancy.”

Dr. Tesfalul receives support from the Foundation for SMFM.

[email protected]

SOURCE: Tesfalul M et al. Am J Obstet Gynecol. 2020 Jan;222(1):S92-3, Abstract 119.

GRAPEVINE, TEX. – Blood pressure categories created by the American College of Cardiology (ACC) and American Heart Association (AHA) in 2017 identify patients with increased risk of preeclampsia, preterm birth, and perinatal death when applied to the first 20 weeks of pregnancy, according to a retrospective study presented at the meeting sponsored by the Society for Maternal-Fetal Medicine.

The absolute risk increases are small, and it is unknown whether treating these patients differently would be beneficial, said study author Martha Tesfalul, MD, maternal-fetal medicine clinical fellow at University of California, San Francisco. Nevertheless, the associations suggest that patients with hypertension during the first 20 weeks may benefit from additional monitoring and counseling, Dr. Tesfalul said.

Cutoffs with unclear implications

The ACC/AHA in November 2017 reclassified blood pressure in nonpregnant adults, but “implications of these categories in pregnancy are still unclear,” Dr. Tesfalul and colleagues said. Under the guidelines, normal blood pressure is systolic blood pressure less than 120 mm Hg and diastolic blood pressure less than 80 mm Hg. Elevated blood pressure is defined as systolic blood pressure between 120 and 129 mm Hg and diastolic blood pressure less than 80 mm Hg. Stage 1 hypertension is systolic blood pressure between 130 and 139 mm Hg or diastolic blood pressure between 80 and 89 mm Hg. And stage 2 hypertension is systolic blood pressure of at least 140 mm Hg or diastolic blood pressure of at least 90 mm Hg.

For the present analysis, the researchers retrospectively compared obstetric and perinatal outcomes for approximately 6,000 pregnancies at an academic center for which they had at least one blood pressure measurement prior to 20 weeks. The highest measurement was used to identify women with normal blood pressure, elevated blood pressure, or stage 1 hypertension according to the 2017 thresholds.

The researchers included singleton pregnancies with delivery between January 2014 and October 2017. They excluded patients with a prior diagnosis of chronic hypertension, autoimmune or chronic renal disease, or fetal anomalies. They examined rates of gestational hypertension, preeclampsia, preterm birth, neonatal intensive care admission, and perinatal death.

Adjusted relative risks

Dr. Tesfalul and colleagues identified about 3,500 pregnancies with normal blood pressure, more than 1,300 pregnancies with elevated blood pressure, and nearly 1,100 pregnancies with stage 1 hypertension.

After adjusting for relevant covariates – maternal age, nulliparity, race, body mass index, in vitro fertilization, tobacco use, pregestational diabetes, and aspirin use – elevated blood pressure and stage 1 hypertension were associated with a higher risk of preeclampsia and severe preeclampsia, relative to normal blood pressure. The proportion of patients with preeclampsia was 5.7% in the normal blood pressure group, 11.7% in the elevated blood pressure group (adjusted relative risk, 1.8), and 15% in the stage 1 hypertension group (adjusted RR, 2.1). The proportion with preeclampsia with severe features was 3.1% in the normal blood pressure group, 5.7% in the elevated blood pressure group (adjusted RR, 1.6), and 6.8% in the stage 1 hypertension group (adjusted RR, 1.8).

In addition, stage 1 hypertension, compared with normal blood pressure, was associated with increased odds of preterm birth at less than 37 weeks (7.9% vs. 5.1%; adjusted RR, 1.4) and perinatal death (0.7% vs. 0.4%; adjusted RR, 2.8).

“Patients with elevated blood pressure and stage 1 hypertension prior to 20 weeks are at increased risk of adverse outcomes,” the authors concluded. “Further research [is] needed to determine optimal care of patients with elevated blood pressure and stage 1 hypertension in pregnancy.”

Dr. Tesfalul receives support from the Foundation for SMFM.

[email protected]

SOURCE: Tesfalul M et al. Am J Obstet Gynecol. 2020 Jan;222(1):S92-3, Abstract 119.

SNOWMASS, COLO. – Myths and misconceptions abound regarding the merits of universal incorporation of the resting 12-lead ECG into preparticipation cardiovascular screening of young athletes, Aaron L. Baggish, MD, declared at the annual Cardiovascular Conference at Snowmass sponsored by the American College of Cardiology.

Bruce Jancin/MDedge News

Dr. Baggish, director of the Cardiovascular Performance Program at Massachusetts General Hospital and a cardiologist at Harvard Medical School, Boston, set out to pop the balloons of a handful of these widely floating myths. These are commonly held fictions: In an electronic poll at the outset of his talk, only one in five members of his large audience recognized all of the following boldface statements as false.

“Preparticipation cardiovascular screening (PPCVS) has been shown to reduce the incidence of sudden cardiac death (SCD) among young competitive athletes.”

FALSE. Not for PPCVS by history and physical examination alone, or with the addition of a screening 12-lead ECG. In Italy, where a cluster of high-profile sudden cardiac deaths led to passage of a 1982 national law mandating 12-lead ECG screening as part of the PPCVS, investigators presented studies purporting to demonstrate a subsequent reduction in the risk of SCD. But those studies were subsequently shown to be fraught with problems. And a high-quality study capable of convincingly demonstrating such a benefit would need to be prohibitively large and expensive. “Don’t hold your breath waiting for that to happen anytime soon,” advised Dr. Baggish, who is medical director for the Boston Marathon, as well as team cardiologist for Harvard University Athletics, the New England Patriots, the Boston Bruins, USRowing, and U.S. Soccer.

“Hypertrophic cardiomyopathy is the leading cause of sudden death among young competitive athletes.”

FALSE. A study of the National Collegiate Athletic Association (NCAA) comprehensive database, with 4.2 million athlete-years of follow-up, showed that the most common cause of SCD was autopsy-negative sudden unexplained death (SUD), accounting for 25% of cases. Hypertrophic cardiomyopathy was deemed the cause of 8% of the SCDs (Circulation. 2015 Jul 7;132[1]:10-9).

“The same thing has been shown in studies done in the United Kingdom and in Australia: The vast majority of people who drop dead at a young age have a totally normal-looking heart. Over the next 10 years, I suspect that one of the most important areas that we’ll be looking into will be this SUD area, perhaps using molecular autopsy to make some headway there,” according to the cardiologist.

SCD is rare. In the NCAA study, the incidence was 1 in 53,703 athlete-years. In sobering contrast, accidents, suicide, and homicide accounted for 50% of all deaths in the collegiate athletes.

“When you think about what’s important in terms of educating young people to be safe, the history and physical exam and 12-lead ECG are nowhere near as important as talking with them about minimizing accident risk and staying away from guns,” Dr. Baggish commented.

“Contemporary ECG interpretation criteria designed specifically for use in young athletes have eliminated the problem of false-positive testing.”

FALSE. The story of adding ECG screening to the PPCVS is one of dramatically improved sensitivity over history and physical exam alone, but always at the cost of reduced specificity. In the Harvard Athlete Initiative Study, Dr. Baggish and coworkers reported that adding the 12-lead ECG resulted in a 17% false-positive rate (Ann Intern Med. 2010 Mar 2;152[5]:269-75). Similar findings were reported in independent studies at two other large universities.

“An ECG false-positive rate of 16%-20%? That’s big trouble. Remember, the conditions we’re looking for are uncommon, with a prevalence of maybe 1 in 500 at most. So if you’re flagging one-fifth or one-sixth of your athletes, the ECG is really not an appropriate tool for screening,” he commented.

Recognition of this limitation has led to development of refined, improved ECG criteria: most notably, the 2012 Seattle criteria, with an associated false-positive rate of 4%-8%, followed by the 2017 International Consensus Criteria (J Am Coll Cardiol. 2017 Feb 28;69[8]:1057-75), with a false-positive rate of 1%-2%. That’s a great improvement. Still, when Dr. Baggish, a marathoner himself, thinks about the roughly 32,000 Boston Marathon runners at the starting line each year, that false-positive rate would translate into 320-640 of those individuals being needlessly subjected to the not-insignificant time and expense of further testing, along with considerable anxiety for the runners and their families, and perhaps even inappropriate disqualification.

“Current ACC/AHA guidelines recommend against the use of the 12-lead ECG during the PPCVS.”

FALSE. Dr. Baggish was a coauthor of the current guidelines, which he described as “an open-door invitation to local decisions, with some important caveats” (Circulation. 2015 Dec 1;132[22]:e267-72).

The guidelines state that the minimum requirement and legal standard for PPCVS of young competitive athletes is a focused history and physical examination, such as the American College of Cardiology/American Heart Association 14-point screen, which consists of 10 elements addressing personal and family history and 4 focused on the physical examination, or the American Academy of Pediatrics Preparticipation Physical Evaluation. Further, while mandatory universal inclusion of the 12-lead ECG is not recommended – it’s rated Class III, meaning don’t do it – the guidelines state that screening programs are at liberty to choose the 12-lead ECG as an additional tool, “provided that close physician involvement and sufficient quality control can be achieved. If undertaken, such initiatives should recognize the known and anticipated limitations of the 12-lead ECG as a population screening test, including the expected frequency of false-positive and false-negative test results, as well as the cost required to support these initiatives over time.”

Dr. Baggish considers the ACC/AHA guidelines to be one of the two most important developments in the field of SCD during sports in recent years. The other is the NCAA-sponsored multidisciplinary Interassociation Consensus Statement on Cardiovascular Care of College Student-Athletes, which he also coauthored (J Am Coll Cardiol. 2016 Jun 28;67[25]:2981-95).

The report lays out the case for a much broader than traditional view of the PPCVS, with “goals that extend beyond detection of occult high-risk pathology.”

“The NCAA has done something very interesting,” Dr. Baggish explained. “It has said that, if we’re going to be screening, we should be thinking about screening with a much broader rationale. It’s not just about finding the needle-in-a-haystack hypertrophic cardiomyopathy or anomalous coronary arteries, it’s about engaging student-athletes at an early point in their collegiate career and trying to improve their health overall – and not just while they’re in college, but over their lifespan.”

He reported having no financial conflicts regarding his presentation.

[email protected]

SNOWMASS, COLO. – Myths and misconceptions abound regarding the merits of universal incorporation of the resting 12-lead ECG into preparticipation cardiovascular screening of young athletes, Aaron L. Baggish, MD, declared at the annual Cardiovascular Conference at Snowmass sponsored by the American College of Cardiology.

Bruce Jancin/MDedge News

Dr. Baggish, director of the Cardiovascular Performance Program at Massachusetts General Hospital and a cardiologist at Harvard Medical School, Boston, set out to pop the balloons of a handful of these widely floating myths. These are commonly held fictions: In an electronic poll at the outset of his talk, only one in five members of his large audience recognized all of the following boldface statements as false.

“Preparticipation cardiovascular screening (PPCVS) has been shown to reduce the incidence of sudden cardiac death (SCD) among young competitive athletes.”

FALSE. Not for PPCVS by history and physical examination alone, or with the addition of a screening 12-lead ECG. In Italy, where a cluster of high-profile sudden cardiac deaths led to passage of a 1982 national law mandating 12-lead ECG screening as part of the PPCVS, investigators presented studies purporting to demonstrate a subsequent reduction in the risk of SCD. But those studies were subsequently shown to be fraught with problems. And a high-quality study capable of convincingly demonstrating such a benefit would need to be prohibitively large and expensive. “Don’t hold your breath waiting for that to happen anytime soon,” advised Dr. Baggish, who is medical director for the Boston Marathon, as well as team cardiologist for Harvard University Athletics, the New England Patriots, the Boston Bruins, USRowing, and U.S. Soccer.

“Hypertrophic cardiomyopathy is the leading cause of sudden death among young competitive athletes.”

FALSE. A study of the National Collegiate Athletic Association (NCAA) comprehensive database, with 4.2 million athlete-years of follow-up, showed that the most common cause of SCD was autopsy-negative sudden unexplained death (SUD), accounting for 25% of cases. Hypertrophic cardiomyopathy was deemed the cause of 8% of the SCDs (Circulation. 2015 Jul 7;132[1]:10-9).

“The same thing has been shown in studies done in the United Kingdom and in Australia: The vast majority of people who drop dead at a young age have a totally normal-looking heart. Over the next 10 years, I suspect that one of the most important areas that we’ll be looking into will be this SUD area, perhaps using molecular autopsy to make some headway there,” according to the cardiologist.

SCD is rare. In the NCAA study, the incidence was 1 in 53,703 athlete-years. In sobering contrast, accidents, suicide, and homicide accounted for 50% of all deaths in the collegiate athletes.

“When you think about what’s important in terms of educating young people to be safe, the history and physical exam and 12-lead ECG are nowhere near as important as talking with them about minimizing accident risk and staying away from guns,” Dr. Baggish commented.

“Contemporary ECG interpretation criteria designed specifically for use in young athletes have eliminated the problem of false-positive testing.”

FALSE. The story of adding ECG screening to the PPCVS is one of dramatically improved sensitivity over history and physical exam alone, but always at the cost of reduced specificity. In the Harvard Athlete Initiative Study, Dr. Baggish and coworkers reported that adding the 12-lead ECG resulted in a 17% false-positive rate (Ann Intern Med. 2010 Mar 2;152[5]:269-75). Similar findings were reported in independent studies at two other large universities.

“An ECG false-positive rate of 16%-20%? That’s big trouble. Remember, the conditions we’re looking for are uncommon, with a prevalence of maybe 1 in 500 at most. So if you’re flagging one-fifth or one-sixth of your athletes, the ECG is really not an appropriate tool for screening,” he commented.

Recognition of this limitation has led to development of refined, improved ECG criteria: most notably, the 2012 Seattle criteria, with an associated false-positive rate of 4%-8%, followed by the 2017 International Consensus Criteria (J Am Coll Cardiol. 2017 Feb 28;69[8]:1057-75), with a false-positive rate of 1%-2%. That’s a great improvement. Still, when Dr. Baggish, a marathoner himself, thinks about the roughly 32,000 Boston Marathon runners at the starting line each year, that false-positive rate would translate into 320-640 of those individuals being needlessly subjected to the not-insignificant time and expense of further testing, along with considerable anxiety for the runners and their families, and perhaps even inappropriate disqualification.

“Current ACC/AHA guidelines recommend against the use of the 12-lead ECG during the PPCVS.”

FALSE. Dr. Baggish was a coauthor of the current guidelines, which he described as “an open-door invitation to local decisions, with some important caveats” (Circulation. 2015 Dec 1;132[22]:e267-72).

The guidelines state that the minimum requirement and legal standard for PPCVS of young competitive athletes is a focused history and physical examination, such as the American College of Cardiology/American Heart Association 14-point screen, which consists of 10 elements addressing personal and family history and 4 focused on the physical examination, or the American Academy of Pediatrics Preparticipation Physical Evaluation. Further, while mandatory universal inclusion of the 12-lead ECG is not recommended – it’s rated Class III, meaning don’t do it – the guidelines state that screening programs are at liberty to choose the 12-lead ECG as an additional tool, “provided that close physician involvement and sufficient quality control can be achieved. If undertaken, such initiatives should recognize the known and anticipated limitations of the 12-lead ECG as a population screening test, including the expected frequency of false-positive and false-negative test results, as well as the cost required to support these initiatives over time.”

Dr. Baggish considers the ACC/AHA guidelines to be one of the two most important developments in the field of SCD during sports in recent years. The other is the NCAA-sponsored multidisciplinary Interassociation Consensus Statement on Cardiovascular Care of College Student-Athletes, which he also coauthored (J Am Coll Cardiol. 2016 Jun 28;67[25]:2981-95).

The report lays out the case for a much broader than traditional view of the PPCVS, with “goals that extend beyond detection of occult high-risk pathology.”

“The NCAA has done something very interesting,” Dr. Baggish explained. “It has said that, if we’re going to be screening, we should be thinking about screening with a much broader rationale. It’s not just about finding the needle-in-a-haystack hypertrophic cardiomyopathy or anomalous coronary arteries, it’s about engaging student-athletes at an early point in their collegiate career and trying to improve their health overall – and not just while they’re in college, but over their lifespan.”

He reported having no financial conflicts regarding his presentation.

[email protected]

SNOWMASS, COLO. – Myths and misconceptions abound regarding the merits of universal incorporation of the resting 12-lead ECG into preparticipation cardiovascular screening of young athletes, Aaron L. Baggish, MD, declared at the annual Cardiovascular Conference at Snowmass sponsored by the American College of Cardiology.

Bruce Jancin/MDedge News

Dr. Baggish, director of the Cardiovascular Performance Program at Massachusetts General Hospital and a cardiologist at Harvard Medical School, Boston, set out to pop the balloons of a handful of these widely floating myths. These are commonly held fictions: In an electronic poll at the outset of his talk, only one in five members of his large audience recognized all of the following boldface statements as false.

“Preparticipation cardiovascular screening (PPCVS) has been shown to reduce the incidence of sudden cardiac death (SCD) among young competitive athletes.”

FALSE. Not for PPCVS by history and physical examination alone, or with the addition of a screening 12-lead ECG. In Italy, where a cluster of high-profile sudden cardiac deaths led to passage of a 1982 national law mandating 12-lead ECG screening as part of the PPCVS, investigators presented studies purporting to demonstrate a subsequent reduction in the risk of SCD. But those studies were subsequently shown to be fraught with problems. And a high-quality study capable of convincingly demonstrating such a benefit would need to be prohibitively large and expensive. “Don’t hold your breath waiting for that to happen anytime soon,” advised Dr. Baggish, who is medical director for the Boston Marathon, as well as team cardiologist for Harvard University Athletics, the New England Patriots, the Boston Bruins, USRowing, and U.S. Soccer.

“Hypertrophic cardiomyopathy is the leading cause of sudden death among young competitive athletes.”

FALSE. A study of the National Collegiate Athletic Association (NCAA) comprehensive database, with 4.2 million athlete-years of follow-up, showed that the most common cause of SCD was autopsy-negative sudden unexplained death (SUD), accounting for 25% of cases. Hypertrophic cardiomyopathy was deemed the cause of 8% of the SCDs (Circulation. 2015 Jul 7;132[1]:10-9).

“The same thing has been shown in studies done in the United Kingdom and in Australia: The vast majority of people who drop dead at a young age have a totally normal-looking heart. Over the next 10 years, I suspect that one of the most important areas that we’ll be looking into will be this SUD area, perhaps using molecular autopsy to make some headway there,” according to the cardiologist.

SCD is rare. In the NCAA study, the incidence was 1 in 53,703 athlete-years. In sobering contrast, accidents, suicide, and homicide accounted for 50% of all deaths in the collegiate athletes.

“When you think about what’s important in terms of educating young people to be safe, the history and physical exam and 12-lead ECG are nowhere near as important as talking with them about minimizing accident risk and staying away from guns,” Dr. Baggish commented.

“Contemporary ECG interpretation criteria designed specifically for use in young athletes have eliminated the problem of false-positive testing.”

FALSE. The story of adding ECG screening to the PPCVS is one of dramatically improved sensitivity over history and physical exam alone, but always at the cost of reduced specificity. In the Harvard Athlete Initiative Study, Dr. Baggish and coworkers reported that adding the 12-lead ECG resulted in a 17% false-positive rate (Ann Intern Med. 2010 Mar 2;152[5]:269-75). Similar findings were reported in independent studies at two other large universities.

“An ECG false-positive rate of 16%-20%? That’s big trouble. Remember, the conditions we’re looking for are uncommon, with a prevalence of maybe 1 in 500 at most. So if you’re flagging one-fifth or one-sixth of your athletes, the ECG is really not an appropriate tool for screening,” he commented.

Recognition of this limitation has led to development of refined, improved ECG criteria: most notably, the 2012 Seattle criteria, with an associated false-positive rate of 4%-8%, followed by the 2017 International Consensus Criteria (J Am Coll Cardiol. 2017 Feb 28;69[8]:1057-75), with a false-positive rate of 1%-2%. That’s a great improvement. Still, when Dr. Baggish, a marathoner himself, thinks about the roughly 32,000 Boston Marathon runners at the starting line each year, that false-positive rate would translate into 320-640 of those individuals being needlessly subjected to the not-insignificant time and expense of further testing, along with considerable anxiety for the runners and their families, and perhaps even inappropriate disqualification.

“Current ACC/AHA guidelines recommend against the use of the 12-lead ECG during the PPCVS.”

FALSE. Dr. Baggish was a coauthor of the current guidelines, which he described as “an open-door invitation to local decisions, with some important caveats” (Circulation. 2015 Dec 1;132[22]:e267-72).

The guidelines state that the minimum requirement and legal standard for PPCVS of young competitive athletes is a focused history and physical examination, such as the American College of Cardiology/American Heart Association 14-point screen, which consists of 10 elements addressing personal and family history and 4 focused on the physical examination, or the American Academy of Pediatrics Preparticipation Physical Evaluation. Further, while mandatory universal inclusion of the 12-lead ECG is not recommended – it’s rated Class III, meaning don’t do it – the guidelines state that screening programs are at liberty to choose the 12-lead ECG as an additional tool, “provided that close physician involvement and sufficient quality control can be achieved. If undertaken, such initiatives should recognize the known and anticipated limitations of the 12-lead ECG as a population screening test, including the expected frequency of false-positive and false-negative test results, as well as the cost required to support these initiatives over time.”

Dr. Baggish considers the ACC/AHA guidelines to be one of the two most important developments in the field of SCD during sports in recent years. The other is the NCAA-sponsored multidisciplinary Interassociation Consensus Statement on Cardiovascular Care of College Student-Athletes, which he also coauthored (J Am Coll Cardiol. 2016 Jun 28;67[25]:2981-95).

The report lays out the case for a much broader than traditional view of the PPCVS, with “goals that extend beyond detection of occult high-risk pathology.”

“The NCAA has done something very interesting,” Dr. Baggish explained. “It has said that, if we’re going to be screening, we should be thinking about screening with a much broader rationale. It’s not just about finding the needle-in-a-haystack hypertrophic cardiomyopathy or anomalous coronary arteries, it’s about engaging student-athletes at an early point in their collegiate career and trying to improve their health overall – and not just while they’re in college, but over their lifespan.”

He reported having no financial conflicts regarding his presentation.

[email protected]

The Centers for Medicare & Medicaid Services’ latest maneuver to combat rising drug prices is the proposed addition of a second specialty drug tier for the Medicare Part D prescription drug benefit.

The proposal is part of a broader proposed update to Medicare Parts C and D for contract years 2021 and 2022.

Gurzzza/Thinkstock

The Centers for Medicare & Medicaid Services’ latest maneuver to combat rising drug prices is the proposed addition of a second specialty drug tier for the Medicare Part D prescription drug benefit.

The proposal is part of a broader proposed update to Medicare Parts C and D for contract years 2021 and 2022.

Gurzzza/Thinkstock

The Centers for Medicare & Medicaid Services’ latest maneuver to combat rising drug prices is the proposed addition of a second specialty drug tier for the Medicare Part D prescription drug benefit.

The proposal is part of a broader proposed update to Medicare Parts C and D for contract years 2021 and 2022.

Gurzzza/Thinkstock

The time has come for good men and women to unite and rise up against a common foe. For too long nurses and doctors have labored under the tyranny of a dictator who claimed to help them provide high-quality care for their patients while at the same time cutting their paperwork to nil. But like most autocrats he failed to engage his subjects in a meaningful dialogue as each new version of his promised improvements rolled off the drawing board. When the caregivers were slow to adopt these new nonsystems he offered them financial incentives and issued threats to their survival. Although they were warned that there might be uncomfortable adjustment periods, the caregivers were promised that the steep learning curves would level out and their professional lives would again be valued and productive.

Of course, the dictator is not a single person but a motley and disorganized conglomerate of user- and patient-unfriendly electronic health record nonsystems. Ask almost any nurse or physician for her feelings about computer-based medical record systems, and you will hear tales of long hours, disengagement, and frustration. Caregivers are unhappy at all levels, and patients have grown tired of their nurses and physicians spending most of their time looking at computer screens.

You certainly have heard this all before. But you are hearing it in hospital hallways and grocery store checkout lines as a low rumble of discontent emerging from separate individuals, not as a well-articulated and widely distributed voice of physicians as a group. To some extent this relative silence is because there is no such group, at least not in same mold as a labor union. The term “labor union” may make you uncomfortable. But given the current climate in medicine, unionizing may be the best and only way to effect change.

But organizing to effect change in the workplace isn’t part of the physician genome. In the 1960s, a group of house officers in Boston engaged in a heal-in to successfully improve their salaries and working conditions. But over the ensuing half century physicians have remained tragically silent in the face of a changing workplace landscape in which they have gone from being independent owner operators in control of their destinies to becoming employees feeling powerless to improve their working conditions. This perceived impotence has escalated in the face of the challenge posed by the introduction of dysfunctional EHRs.

Ironically, a solution is at almost every physician’s elbow. In a recent New York Times opinion piece Theresa Brown and Stephen Bergman acknowledge that physicians don’t seem prepared to mount a meaningful response to the challenge to the failed promise of EHRs (“Doctors, Nurses and the Paperwork Crisis That Could Unite Them,” Dec. 31, 2019). They point out that, over the last half century, physicians have remained isolated on the sidelines, finding just enough voice to grumble. Nurses have in a variety of situations organized to effect change in their working conditions – in some cases by forming labor unions.

The authors of this op-ed piece, a physician and a nurse, make a strong argument that the time has come for nurses and doctors shake off the shackles of their stereotypic roles and join in creating a loud, forceful, and effective voice to demand a working environment in which the computer functions as an asset and no longer as the terrible burden it has become. Neither group has the power to do it alone, but together they may be able to turn the tide. For physicians it will probably mean venturing several steps outside of their comfort zone. But working shoulder to shoulder with nurses may provide the courage to speak out.

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.” Email him at [email protected].

The time has come for good men and women to unite and rise up against a common foe. For too long nurses and doctors have labored under the tyranny of a dictator who claimed to help them provide high-quality care for their patients while at the same time cutting their paperwork to nil. But like most autocrats he failed to engage his subjects in a meaningful dialogue as each new version of his promised improvements rolled off the drawing board. When the caregivers were slow to adopt these new nonsystems he offered them financial incentives and issued threats to their survival. Although they were warned that there might be uncomfortable adjustment periods, the caregivers were promised that the steep learning curves would level out and their professional lives would again be valued and productive.

Of course, the dictator is not a single person but a motley and disorganized conglomerate of user- and patient-unfriendly electronic health record nonsystems. Ask almost any nurse or physician for her feelings about computer-based medical record systems, and you will hear tales of long hours, disengagement, and frustration. Caregivers are unhappy at all levels, and patients have grown tired of their nurses and physicians spending most of their time looking at computer screens.

You certainly have heard this all before. But you are hearing it in hospital hallways and grocery store checkout lines as a low rumble of discontent emerging from separate individuals, not as a well-articulated and widely distributed voice of physicians as a group. To some extent this relative silence is because there is no such group, at least not in same mold as a labor union. The term “labor union” may make you uncomfortable. But given the current climate in medicine, unionizing may be the best and only way to effect change.

But organizing to effect change in the workplace isn’t part of the physician genome. In the 1960s, a group of house officers in Boston engaged in a heal-in to successfully improve their salaries and working conditions. But over the ensuing half century physicians have remained tragically silent in the face of a changing workplace landscape in which they have gone from being independent owner operators in control of their destinies to becoming employees feeling powerless to improve their working conditions. This perceived impotence has escalated in the face of the challenge posed by the introduction of dysfunctional EHRs.

Ironically, a solution is at almost every physician’s elbow. In a recent New York Times opinion piece Theresa Brown and Stephen Bergman acknowledge that physicians don’t seem prepared to mount a meaningful response to the challenge to the failed promise of EHRs (“Doctors, Nurses and the Paperwork Crisis That Could Unite Them,” Dec. 31, 2019). They point out that, over the last half century, physicians have remained isolated on the sidelines, finding just enough voice to grumble. Nurses have in a variety of situations organized to effect change in their working conditions – in some cases by forming labor unions.

The authors of this op-ed piece, a physician and a nurse, make a strong argument that the time has come for nurses and doctors shake off the shackles of their stereotypic roles and join in creating a loud, forceful, and effective voice to demand a working environment in which the computer functions as an asset and no longer as the terrible burden it has become. Neither group has the power to do it alone, but together they may be able to turn the tide. For physicians it will probably mean venturing several steps outside of their comfort zone. But working shoulder to shoulder with nurses may provide the courage to speak out.

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.” Email him at [email protected].

The time has come for good men and women to unite and rise up against a common foe. For too long nurses and doctors have labored under the tyranny of a dictator who claimed to help them provide high-quality care for their patients while at the same time cutting their paperwork to nil. But like most autocrats he failed to engage his subjects in a meaningful dialogue as each new version of his promised improvements rolled off the drawing board. When the caregivers were slow to adopt these new nonsystems he offered them financial incentives and issued threats to their survival. Although they were warned that there might be uncomfortable adjustment periods, the caregivers were promised that the steep learning curves would level out and their professional lives would again be valued and productive.

Of course, the dictator is not a single person but a motley and disorganized conglomerate of user- and patient-unfriendly electronic health record nonsystems. Ask almost any nurse or physician for her feelings about computer-based medical record systems, and you will hear tales of long hours, disengagement, and frustration. Caregivers are unhappy at all levels, and patients have grown tired of their nurses and physicians spending most of their time looking at computer screens.

You certainly have heard this all before. But you are hearing it in hospital hallways and grocery store checkout lines as a low rumble of discontent emerging from separate individuals, not as a well-articulated and widely distributed voice of physicians as a group. To some extent this relative silence is because there is no such group, at least not in same mold as a labor union. The term “labor union” may make you uncomfortable. But given the current climate in medicine, unionizing may be the best and only way to effect change.

But organizing to effect change in the workplace isn’t part of the physician genome. In the 1960s, a group of house officers in Boston engaged in a heal-in to successfully improve their salaries and working conditions. But over the ensuing half century physicians have remained tragically silent in the face of a changing workplace landscape in which they have gone from being independent owner operators in control of their destinies to becoming employees feeling powerless to improve their working conditions. This perceived impotence has escalated in the face of the challenge posed by the introduction of dysfunctional EHRs.

Ironically, a solution is at almost every physician’s elbow. In a recent New York Times opinion piece Theresa Brown and Stephen Bergman acknowledge that physicians don’t seem prepared to mount a meaningful response to the challenge to the failed promise of EHRs (“Doctors, Nurses and the Paperwork Crisis That Could Unite Them,” Dec. 31, 2019). They point out that, over the last half century, physicians have remained isolated on the sidelines, finding just enough voice to grumble. Nurses have in a variety of situations organized to effect change in their working conditions – in some cases by forming labor unions.

The authors of this op-ed piece, a physician and a nurse, make a strong argument that the time has come for nurses and doctors shake off the shackles of their stereotypic roles and join in creating a loud, forceful, and effective voice to demand a working environment in which the computer functions as an asset and no longer as the terrible burden it has become. Neither group has the power to do it alone, but together they may be able to turn the tide. For physicians it will probably mean venturing several steps outside of their comfort zone. But working shoulder to shoulder with nurses may provide the courage to speak out.

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.” Email him at [email protected].

SNOWMASS, COLO. – Targeted temperature management maintained at 32-36 degrees Celsius is now a strong class I recommendation for all comatose patients who experience return of spontaneous circulation after out-of-hospital cardiac arrest, including those with nonshockable rhythms, Erin A. Bohula, MD, PhD, said at the annual Cardiovascular Conference at Snowmass sponsored by the American College of Cardiology.

Bruce Jancin/MDedge News

“Our practice is that there are no absolute contraindications to targeted temperature management at the Brigham. Everybody gets cooled,” said Dr. Bohula, a cardiologist and critical care specialist at Brigham and Women’s Hospital and Harvard Medical School, Boston.

The current ACC/AHA guidelines declare: “There are essentially no patients for whom temperature control somewhere in the range between 32 degrees C [89.6 F) and 36 degrees C [96.8 F] is contraindicated.” The writing committee cited “recent clinical trial data enrolling patients with all rhythms, the rarity of adverse effects in trials, the high neurologic morbidity and mortality without any specific interventions, and the preponderance of data suggesting that temperature is an important variable for neurologic recovery” (Circulation. 2015 Nov 3;132[18 Suppl 2]:S465-82).

“That’s a pretty strong statement,” Dr. Bohula observed.

The current guidelines, which date back to 2015, give a class I, level of evidence B recommendation for targeted temperature management (TTM) in patients who are comatose with return of spontaneous circulation (ROSC) after out-of-hospital cardiac arrest involving ventricular fibrillation or pulseless ventricular fibrillation. The bedside definition of comatose is lack of meaningful response to verbal commands to squeeze hands, blink, or move toes.

The current recommendation for TTM in patients resuscitated from out-of-hospital cardiac arrest with a nonshockable rhythm is class I, level of evidence C, meaning it’s based on expert consensus. However, that recommendation is now out of date and due for a level-of-evidence upgrade in light of the recent results of the French HYPERION trial, an open-label randomized trial of 584 patients resuscitated from cardiac arrest with a nonshockable rhythm. Although 90-day mortality was similarly high in the TTM and targeted normothermia groups, the rate of favorable neurologic outcome as assessed by a Cerebral Performance Category scale score of 1 or 2 was 10.2% in the TTM group, significantly better than the 5.7% rate in controls (N Engl J Med. 2019 Dec 12;381[24]:2327-37).

The 2010, ACC/AHA guidelines recommended a TTM range of 32-34 degrees C, but on the basis of subsequent persuasive randomized trial data, that range was broadened to 32-36 degrees C in the 2015 guidelines, with a class IB recommendation. Maintenance of TTM for at least 24 hours has a IIa, level of evidence C recommendation in the current guidelines.

The guidelines emphasize that specific features may favor selection of one temperature for TTM over another. For example, patients with seizures or cerebral edema might be better off with TTM at a lower temperature, while a higher temperature may be best for those with bleeding or severe bradycardia. At Brigham and Women’s Hospital, the default temperature is 33 degrees C. However, TTM with a goal of 36 degrees C is seriously considered in patients with recent head trauma, major surgery within the past 2 weeks, refractory hypotension, severe sepsis, pregnancy, or high bleeding risk. Rewarming is done at a rate of 0.25 degrees C per hour, with sedation maintained until the patient has been returned to 98.6 degrees F, according to Dr. Bohula.

Based on several negative studies of TTM using rapid infusion of chilled fluids in the ambulance en route to the hospital, the guidelines rate that practice class IIIA, meaning don’t do it. Avoidance of a systolic blood pressure below 90 mm Hg and a mean arterial pressure of less than 65 mm Hg gets a class IIb level of evidence C recommendation to lessen the risk of cerebral hypoxia.
 

TTM a major breakthrough

Prior to the introduction of TTM, comatose patients with ROSC after out-of-hospital cardiac arrest had a dreadful prognosis, with survival rates of 1%-10% in registry studies. In contrast, the survival rate in the landmark TTM clinical trials was 50%-60%. And while that’s a dramatic improvement, ROSC after cardiac arrest remains a high-mortality condition. Dr. Bohula was first author of a report by the Critical Care Cardiology Trials Network, composed of 16 tertiary cardiac intensive care units in the United States and Canada. Cardiac arrest was the primary indication for 8.7% of 3,049 consecutive admissions, and its 38% mortality rate was the highest of all cardiac critical care indications (JAMA Cardiol. 2019 Jul 24;4[9]:928-35).

TTM was developed in response to a recognition that two-thirds of deaths in patients who make it to the hospital after out-of-hospital cardiac arrest are neurologic – the result of brain anoxia – rather than being due to the myocardial ischemia that may have initially brought them to medical attention.

“Time is brain cells, the same way we think of time as cardiac muscle,” Dr. Bohula observed.

The main idea behind therapeutic hypothermia is that it lowers the cerebral metabolic rate of oxygen to reduce the consequences of ongoing anoxia. The brain doesn’t require as much perfusion when cooled.

TTM has other beneficial neurologic effects as well: It reduces cerebral blood volume via autoregulation, decreases intracranial pressure, and blunts the inflammatory response involved in the postcardiac arrest syndrome. In addition, TTM has anticonvulsant properties, an important effect because seizures and/or myoclonus occur in up to 15% of adults who achieve ROSC after cardiac arrest – and in even more of those who are comatose after doing so. And seizures increase the brain’s metabolic rate threefold, resulting in more cerebral ischemic injury, she explained.

Seizure activity can be difficult to distinguish from shivering in a patient on TTM. For this reason Dr. Bohula recommends putting patients on continuous EEG monitoring from the time of admission, as is the routine practice at the Brigham.

She reported serving as a consultant to Daiichi Sankyo, Servier, Lexicon, Kowa, Merck, Novartis, Novo Nordisk, and the National Institutes of Health. In addition, she generates institutional research grants provided by a half-dozen pharmaceutical companies.

[email protected]

SNOWMASS, COLO. – Targeted temperature management maintained at 32-36 degrees Celsius is now a strong class I recommendation for all comatose patients who experience return of spontaneous circulation after out-of-hospital cardiac arrest, including those with nonshockable rhythms, Erin A. Bohula, MD, PhD, said at the annual Cardiovascular Conference at Snowmass sponsored by the American College of Cardiology.

Bruce Jancin/MDedge News

“Our practice is that there are no absolute contraindications to targeted temperature management at the Brigham. Everybody gets cooled,” said Dr. Bohula, a cardiologist and critical care specialist at Brigham and Women’s Hospital and Harvard Medical School, Boston.

The current ACC/AHA guidelines declare: “There are essentially no patients for whom temperature control somewhere in the range between 32 degrees C [89.6 F) and 36 degrees C [96.8 F] is contraindicated.” The writing committee cited “recent clinical trial data enrolling patients with all rhythms, the rarity of adverse effects in trials, the high neurologic morbidity and mortality without any specific interventions, and the preponderance of data suggesting that temperature is an important variable for neurologic recovery” (Circulation. 2015 Nov 3;132[18 Suppl 2]:S465-82).

“That’s a pretty strong statement,” Dr. Bohula observed.

The current guidelines, which date back to 2015, give a class I, level of evidence B recommendation for targeted temperature management (TTM) in patients who are comatose with return of spontaneous circulation (ROSC) after out-of-hospital cardiac arrest involving ventricular fibrillation or pulseless ventricular fibrillation. The bedside definition of comatose is lack of meaningful response to verbal commands to squeeze hands, blink, or move toes.

The current recommendation for TTM in patients resuscitated from out-of-hospital cardiac arrest with a nonshockable rhythm is class I, level of evidence C, meaning it’s based on expert consensus. However, that recommendation is now out of date and due for a level-of-evidence upgrade in light of the recent results of the French HYPERION trial, an open-label randomized trial of 584 patients resuscitated from cardiac arrest with a nonshockable rhythm. Although 90-day mortality was similarly high in the TTM and targeted normothermia groups, the rate of favorable neurologic outcome as assessed by a Cerebral Performance Category scale score of 1 or 2 was 10.2% in the TTM group, significantly better than the 5.7% rate in controls (N Engl J Med. 2019 Dec 12;381[24]:2327-37).

The 2010, ACC/AHA guidelines recommended a TTM range of 32-34 degrees C, but on the basis of subsequent persuasive randomized trial data, that range was broadened to 32-36 degrees C in the 2015 guidelines, with a class IB recommendation. Maintenance of TTM for at least 24 hours has a IIa, level of evidence C recommendation in the current guidelines.

The guidelines emphasize that specific features may favor selection of one temperature for TTM over another. For example, patients with seizures or cerebral edema might be better off with TTM at a lower temperature, while a higher temperature may be best for those with bleeding or severe bradycardia. At Brigham and Women’s Hospital, the default temperature is 33 degrees C. However, TTM with a goal of 36 degrees C is seriously considered in patients with recent head trauma, major surgery within the past 2 weeks, refractory hypotension, severe sepsis, pregnancy, or high bleeding risk. Rewarming is done at a rate of 0.25 degrees C per hour, with sedation maintained until the patient has been returned to 98.6 degrees F, according to Dr. Bohula.

Based on several negative studies of TTM using rapid infusion of chilled fluids in the ambulance en route to the hospital, the guidelines rate that practice class IIIA, meaning don’t do it. Avoidance of a systolic blood pressure below 90 mm Hg and a mean arterial pressure of less than 65 mm Hg gets a class IIb level of evidence C recommendation to lessen the risk of cerebral hypoxia.
 

TTM a major breakthrough

Prior to the introduction of TTM, comatose patients with ROSC after out-of-hospital cardiac arrest had a dreadful prognosis, with survival rates of 1%-10% in registry studies. In contrast, the survival rate in the landmark TTM clinical trials was 50%-60%. And while that’s a dramatic improvement, ROSC after cardiac arrest remains a high-mortality condition. Dr. Bohula was first author of a report by the Critical Care Cardiology Trials Network, composed of 16 tertiary cardiac intensive care units in the United States and Canada. Cardiac arrest was the primary indication for 8.7% of 3,049 consecutive admissions, and its 38% mortality rate was the highest of all cardiac critical care indications (JAMA Cardiol. 2019 Jul 24;4[9]:928-35).

TTM was developed in response to a recognition that two-thirds of deaths in patients who make it to the hospital after out-of-hospital cardiac arrest are neurologic – the result of brain anoxia – rather than being due to the myocardial ischemia that may have initially brought them to medical attention.

“Time is brain cells, the same way we think of time as cardiac muscle,” Dr. Bohula observed.

The main idea behind therapeutic hypothermia is that it lowers the cerebral metabolic rate of oxygen to reduce the consequences of ongoing anoxia. The brain doesn’t require as much perfusion when cooled.

TTM has other beneficial neurologic effects as well: It reduces cerebral blood volume via autoregulation, decreases intracranial pressure, and blunts the inflammatory response involved in the postcardiac arrest syndrome. In addition, TTM has anticonvulsant properties, an important effect because seizures and/or myoclonus occur in up to 15% of adults who achieve ROSC after cardiac arrest – and in even more of those who are comatose after doing so. And seizures increase the brain’s metabolic rate threefold, resulting in more cerebral ischemic injury, she explained.

Seizure activity can be difficult to distinguish from shivering in a patient on TTM. For this reason Dr. Bohula recommends putting patients on continuous EEG monitoring from the time of admission, as is the routine practice at the Brigham.

She reported serving as a consultant to Daiichi Sankyo, Servier, Lexicon, Kowa, Merck, Novartis, Novo Nordisk, and the National Institutes of Health. In addition, she generates institutional research grants provided by a half-dozen pharmaceutical companies.

[email protected]

SNOWMASS, COLO. – Targeted temperature management maintained at 32-36 degrees Celsius is now a strong class I recommendation for all comatose patients who experience return of spontaneous circulation after out-of-hospital cardiac arrest, including those with nonshockable rhythms, Erin A. Bohula, MD, PhD, said at the annual Cardiovascular Conference at Snowmass sponsored by the American College of Cardiology.

Bruce Jancin/MDedge News

“Our practice is that there are no absolute contraindications to targeted temperature management at the Brigham. Everybody gets cooled,” said Dr. Bohula, a cardiologist and critical care specialist at Brigham and Women’s Hospital and Harvard Medical School, Boston.

The current ACC/AHA guidelines declare: “There are essentially no patients for whom temperature control somewhere in the range between 32 degrees C [89.6 F) and 36 degrees C [96.8 F] is contraindicated.” The writing committee cited “recent clinical trial data enrolling patients with all rhythms, the rarity of adverse effects in trials, the high neurologic morbidity and mortality without any specific interventions, and the preponderance of data suggesting that temperature is an important variable for neurologic recovery” (Circulation. 2015 Nov 3;132[18 Suppl 2]:S465-82).

“That’s a pretty strong statement,” Dr. Bohula observed.

The current guidelines, which date back to 2015, give a class I, level of evidence B recommendation for targeted temperature management (TTM) in patients who are comatose with return of spontaneous circulation (ROSC) after out-of-hospital cardiac arrest involving ventricular fibrillation or pulseless ventricular fibrillation. The bedside definition of comatose is lack of meaningful response to verbal commands to squeeze hands, blink, or move toes.

The current recommendation for TTM in patients resuscitated from out-of-hospital cardiac arrest with a nonshockable rhythm is class I, level of evidence C, meaning it’s based on expert consensus. However, that recommendation is now out of date and due for a level-of-evidence upgrade in light of the recent results of the French HYPERION trial, an open-label randomized trial of 584 patients resuscitated from cardiac arrest with a nonshockable rhythm. Although 90-day mortality was similarly high in the TTM and targeted normothermia groups, the rate of favorable neurologic outcome as assessed by a Cerebral Performance Category scale score of 1 or 2 was 10.2% in the TTM group, significantly better than the 5.7% rate in controls (N Engl J Med. 2019 Dec 12;381[24]:2327-37).

The 2010, ACC/AHA guidelines recommended a TTM range of 32-34 degrees C, but on the basis of subsequent persuasive randomized trial data, that range was broadened to 32-36 degrees C in the 2015 guidelines, with a class IB recommendation. Maintenance of TTM for at least 24 hours has a IIa, level of evidence C recommendation in the current guidelines.

The guidelines emphasize that specific features may favor selection of one temperature for TTM over another. For example, patients with seizures or cerebral edema might be better off with TTM at a lower temperature, while a higher temperature may be best for those with bleeding or severe bradycardia. At Brigham and Women’s Hospital, the default temperature is 33 degrees C. However, TTM with a goal of 36 degrees C is seriously considered in patients with recent head trauma, major surgery within the past 2 weeks, refractory hypotension, severe sepsis, pregnancy, or high bleeding risk. Rewarming is done at a rate of 0.25 degrees C per hour, with sedation maintained until the patient has been returned to 98.6 degrees F, according to Dr. Bohula.

Based on several negative studies of TTM using rapid infusion of chilled fluids in the ambulance en route to the hospital, the guidelines rate that practice class IIIA, meaning don’t do it. Avoidance of a systolic blood pressure below 90 mm Hg and a mean arterial pressure of less than 65 mm Hg gets a class IIb level of evidence C recommendation to lessen the risk of cerebral hypoxia.
 

TTM a major breakthrough

Prior to the introduction of TTM, comatose patients with ROSC after out-of-hospital cardiac arrest had a dreadful prognosis, with survival rates of 1%-10% in registry studies. In contrast, the survival rate in the landmark TTM clinical trials was 50%-60%. And while that’s a dramatic improvement, ROSC after cardiac arrest remains a high-mortality condition. Dr. Bohula was first author of a report by the Critical Care Cardiology Trials Network, composed of 16 tertiary cardiac intensive care units in the United States and Canada. Cardiac arrest was the primary indication for 8.7% of 3,049 consecutive admissions, and its 38% mortality rate was the highest of all cardiac critical care indications (JAMA Cardiol. 2019 Jul 24;4[9]:928-35).

TTM was developed in response to a recognition that two-thirds of deaths in patients who make it to the hospital after out-of-hospital cardiac arrest are neurologic – the result of brain anoxia – rather than being due to the myocardial ischemia that may have initially brought them to medical attention.

“Time is brain cells, the same way we think of time as cardiac muscle,” Dr. Bohula observed.

The main idea behind therapeutic hypothermia is that it lowers the cerebral metabolic rate of oxygen to reduce the consequences of ongoing anoxia. The brain doesn’t require as much perfusion when cooled.

TTM has other beneficial neurologic effects as well: It reduces cerebral blood volume via autoregulation, decreases intracranial pressure, and blunts the inflammatory response involved in the postcardiac arrest syndrome. In addition, TTM has anticonvulsant properties, an important effect because seizures and/or myoclonus occur in up to 15% of adults who achieve ROSC after cardiac arrest – and in even more of those who are comatose after doing so. And seizures increase the brain’s metabolic rate threefold, resulting in more cerebral ischemic injury, she explained.

Seizure activity can be difficult to distinguish from shivering in a patient on TTM. For this reason Dr. Bohula recommends putting patients on continuous EEG monitoring from the time of admission, as is the routine practice at the Brigham.

She reported serving as a consultant to Daiichi Sankyo, Servier, Lexicon, Kowa, Merck, Novartis, Novo Nordisk, and the National Institutes of Health. In addition, she generates institutional research grants provided by a half-dozen pharmaceutical companies.

[email protected]

The Food and Drug Administration has issued a public health alert warning consumers to avoid the use of dietary supplements that contain cesium chloride or any other cesium salt because of significant safety risks.

Cesium salts are sometimes advertised as an alternative treatment for cancer, the FDA said in the announcement, but these salts have never proved to be safe or effective at treating cancer or any other disease. Clinical case reports and nonclinical trials have shown that cesium salts are associated with a variety of adverse events, including cardiac arrhythmias, hypokalemia, seizures, syncope, and death.

The FDA warned health care providers that cesium salts presented a significant safety risk in compounding drugs in July 2018.

Health care providers should not recommend dietary supplements containing cesium salts to their patients, the FDA said, and if a patient experiences an adverse event while taking a supplement containing cesium salt, the event should be reported to the agency.

While there are few dietary supplements on the market that contain cesium salt, consumers should be aware of the risks and avoid these products. The FDA noted that “if claims sound too good to be true, they probably are.”

[email protected]

The Food and Drug Administration has issued a public health alert warning consumers to avoid the use of dietary supplements that contain cesium chloride or any other cesium salt because of significant safety risks.

Cesium salts are sometimes advertised as an alternative treatment for cancer, the FDA said in the announcement, but these salts have never proved to be safe or effective at treating cancer or any other disease. Clinical case reports and nonclinical trials have shown that cesium salts are associated with a variety of adverse events, including cardiac arrhythmias, hypokalemia, seizures, syncope, and death.

The FDA warned health care providers that cesium salts presented a significant safety risk in compounding drugs in July 2018.

Health care providers should not recommend dietary supplements containing cesium salts to their patients, the FDA said, and if a patient experiences an adverse event while taking a supplement containing cesium salt, the event should be reported to the agency.

While there are few dietary supplements on the market that contain cesium salt, consumers should be aware of the risks and avoid these products. The FDA noted that “if claims sound too good to be true, they probably are.”

[email protected]

The Food and Drug Administration has issued a public health alert warning consumers to avoid the use of dietary supplements that contain cesium chloride or any other cesium salt because of significant safety risks.

Cesium salts are sometimes advertised as an alternative treatment for cancer, the FDA said in the announcement, but these salts have never proved to be safe or effective at treating cancer or any other disease. Clinical case reports and nonclinical trials have shown that cesium salts are associated with a variety of adverse events, including cardiac arrhythmias, hypokalemia, seizures, syncope, and death.

The FDA warned health care providers that cesium salts presented a significant safety risk in compounding drugs in July 2018.

Health care providers should not recommend dietary supplements containing cesium salts to their patients, the FDA said, and if a patient experiences an adverse event while taking a supplement containing cesium salt, the event should be reported to the agency.

While there are few dietary supplements on the market that contain cesium salt, consumers should be aware of the risks and avoid these products. The FDA noted that “if claims sound too good to be true, they probably are.”

[email protected]