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Low-dose steroids may not increase cardiovascular risk in rheumatoid arthritis
A daily prednisolone dose of 5 mg or higher is associated with increased risk for major adverse cardiovascular events (MACE) among patients with rheumatoid arthritis (RA), data suggest. Patients taking daily doses below this threshold did not appear to have an increased risk of MACE, compared with those not taking glucocorticoids (GCs).
Other studies of GCs and CV risk among RA patients have yielded conflicting results, especially for low-dose GCs. Findings from a 2020 study published in PLOS Medicine suggested that patients who had several immune-mediated inflammatory diseases – including RA – and who took less than a 5-mg prednisolone-equivalent dose daily had 74% higher risk for all-cause CVD, compared with nonusers. But results from a 2021 study published in Annals of the Rheumatic Diseases suggested that a daily prednisone dose of 4 mg or less did not increase cardiovascular events over a period of 6 months to 1 year.
These contradictory results were “primarily due to incomplete control of confounding variables, such as failure to adjust for C-reactive protein (CRP) levels,” Dr. Tam said. “Our study aimed to use a big data analytical approach to determine the effect of systemic GC dose and duration on the risk of major adverse cardiovascular events in patients with RA, while controlling for systemic inflammation, traditional CV risk factors, and other therapies.”
Is there a ‘safe’ dose for glucocorticoids?
To analyze this relationship, Dr. Lam and colleagues used the Hospital Authority Data Collaboration Laboratory, a citywide health care database. The investigators recruited patients with RA who had no history of MACE from 2006 to 2015 and followed them until the end of 2018. The primary outcome was the first occurrence of a MACE, defined as a composite of myocardial infarction (MI), unstable angina, ischemic or hemorrhagic cerebrovascular accident, transient ischemic attack, and CV death.
The study was published in Annals of the Rheumatic Diseases.
The analysis included 12,233 patients with RA and had over 105,826 person-years of follow-up. The average follow-up time was 8.7 years. During the study period, 860 patients had their first MACE. After controlling for confounding factors, a daily prednisolone dose of 5 mg or higher doubled the risk for MACE, compared with GC nonusers. MACE risk increased by 7% per month.
Long-term glucocorticoid use discouraged
Daily doses of less than 5 mg were not associated with higher MACE risk, but more research is necessary to understand whether these low doses are clinically efficacious, Dr. Tam said. “The study results suggest that a very-low-dose GC (less than 5 mg prednisolone daily) may be cardiovascular risk–neutral. However, further evaluation is needed to determine whether this dose is therapeutic. Other potential side effects, such as bone loss, increased infection risk, dyslipidemia, and hyperglycemia, should also be considered.”
Both the American College of Rheumatology and the European Alliance of Associations for Rheumatology acknowledge that short-term GCs may be necessary for some RA patients, but they emphasize using the smallest necessary dose for the shortest period possible because of the known toxicity of GCs.
“We recommend stopping GCs as soon as it is clinically feasible, in line with previous recommendations, until these issues are investigated further,” Dr. Tam added.
Dr. Bartels agreed that long-term use of GCs should be avoided if possible, even at lower doses, because although CV risk may be less of an issue, studies have shown an increased risk for infection even at GC doses of less than 5 mg a day.
How might risk increase with dose?
While the study showed a distinct difference in risk with doses of prednisolone higher and lower than 5 mg, more information on how risk increases with dose could be useful, said Beth Wallace, MD, an assistant professor in internal medicine at the University of Michigan, Ann Arbor, and a staff rheumatologist at the VA Ann Arbor Healthcare Center. She was also unaffiliated with the research. “If someone is on 5-10 mg ... how much better is that than being on 10-20 mg or being on 20-30 mg?” she asked. While these study findings are “very important,” she said, it would be useful to know the risk associated with 7.5 mg vs. a higher dose.
But even in this relatively healthy population in Hong Kong, “taking more than 5 mg of prednisolone doubles the risk of cardiovascular disease,” Dr. Wallace added. This is important for clinicians to know, especially if they are more cautious about prescribing steroids to older or sicker patients but are “using [the drugs] a little more indiscriminately in younger people and healthier people.”
The study did not receive outside funding. Dr. Tam and Dr. Bartels report no relevant financial relationships. Dr. Wallace has received a grant from the Department of Veterans Affairs Administration to study steroid tapering in RA.
A version of this article first appeared on Medscape.com.
A daily prednisolone dose of 5 mg or higher is associated with increased risk for major adverse cardiovascular events (MACE) among patients with rheumatoid arthritis (RA), data suggest. Patients taking daily doses below this threshold did not appear to have an increased risk of MACE, compared with those not taking glucocorticoids (GCs).
Other studies of GCs and CV risk among RA patients have yielded conflicting results, especially for low-dose GCs. Findings from a 2020 study published in PLOS Medicine suggested that patients who had several immune-mediated inflammatory diseases – including RA – and who took less than a 5-mg prednisolone-equivalent dose daily had 74% higher risk for all-cause CVD, compared with nonusers. But results from a 2021 study published in Annals of the Rheumatic Diseases suggested that a daily prednisone dose of 4 mg or less did not increase cardiovascular events over a period of 6 months to 1 year.
These contradictory results were “primarily due to incomplete control of confounding variables, such as failure to adjust for C-reactive protein (CRP) levels,” Dr. Tam said. “Our study aimed to use a big data analytical approach to determine the effect of systemic GC dose and duration on the risk of major adverse cardiovascular events in patients with RA, while controlling for systemic inflammation, traditional CV risk factors, and other therapies.”
Is there a ‘safe’ dose for glucocorticoids?
To analyze this relationship, Dr. Lam and colleagues used the Hospital Authority Data Collaboration Laboratory, a citywide health care database. The investigators recruited patients with RA who had no history of MACE from 2006 to 2015 and followed them until the end of 2018. The primary outcome was the first occurrence of a MACE, defined as a composite of myocardial infarction (MI), unstable angina, ischemic or hemorrhagic cerebrovascular accident, transient ischemic attack, and CV death.
The study was published in Annals of the Rheumatic Diseases.
The analysis included 12,233 patients with RA and had over 105,826 person-years of follow-up. The average follow-up time was 8.7 years. During the study period, 860 patients had their first MACE. After controlling for confounding factors, a daily prednisolone dose of 5 mg or higher doubled the risk for MACE, compared with GC nonusers. MACE risk increased by 7% per month.
Long-term glucocorticoid use discouraged
Daily doses of less than 5 mg were not associated with higher MACE risk, but more research is necessary to understand whether these low doses are clinically efficacious, Dr. Tam said. “The study results suggest that a very-low-dose GC (less than 5 mg prednisolone daily) may be cardiovascular risk–neutral. However, further evaluation is needed to determine whether this dose is therapeutic. Other potential side effects, such as bone loss, increased infection risk, dyslipidemia, and hyperglycemia, should also be considered.”
Both the American College of Rheumatology and the European Alliance of Associations for Rheumatology acknowledge that short-term GCs may be necessary for some RA patients, but they emphasize using the smallest necessary dose for the shortest period possible because of the known toxicity of GCs.
“We recommend stopping GCs as soon as it is clinically feasible, in line with previous recommendations, until these issues are investigated further,” Dr. Tam added.
Dr. Bartels agreed that long-term use of GCs should be avoided if possible, even at lower doses, because although CV risk may be less of an issue, studies have shown an increased risk for infection even at GC doses of less than 5 mg a day.
How might risk increase with dose?
While the study showed a distinct difference in risk with doses of prednisolone higher and lower than 5 mg, more information on how risk increases with dose could be useful, said Beth Wallace, MD, an assistant professor in internal medicine at the University of Michigan, Ann Arbor, and a staff rheumatologist at the VA Ann Arbor Healthcare Center. She was also unaffiliated with the research. “If someone is on 5-10 mg ... how much better is that than being on 10-20 mg or being on 20-30 mg?” she asked. While these study findings are “very important,” she said, it would be useful to know the risk associated with 7.5 mg vs. a higher dose.
But even in this relatively healthy population in Hong Kong, “taking more than 5 mg of prednisolone doubles the risk of cardiovascular disease,” Dr. Wallace added. This is important for clinicians to know, especially if they are more cautious about prescribing steroids to older or sicker patients but are “using [the drugs] a little more indiscriminately in younger people and healthier people.”
The study did not receive outside funding. Dr. Tam and Dr. Bartels report no relevant financial relationships. Dr. Wallace has received a grant from the Department of Veterans Affairs Administration to study steroid tapering in RA.
A version of this article first appeared on Medscape.com.
A daily prednisolone dose of 5 mg or higher is associated with increased risk for major adverse cardiovascular events (MACE) among patients with rheumatoid arthritis (RA), data suggest. Patients taking daily doses below this threshold did not appear to have an increased risk of MACE, compared with those not taking glucocorticoids (GCs).
Other studies of GCs and CV risk among RA patients have yielded conflicting results, especially for low-dose GCs. Findings from a 2020 study published in PLOS Medicine suggested that patients who had several immune-mediated inflammatory diseases – including RA – and who took less than a 5-mg prednisolone-equivalent dose daily had 74% higher risk for all-cause CVD, compared with nonusers. But results from a 2021 study published in Annals of the Rheumatic Diseases suggested that a daily prednisone dose of 4 mg or less did not increase cardiovascular events over a period of 6 months to 1 year.
These contradictory results were “primarily due to incomplete control of confounding variables, such as failure to adjust for C-reactive protein (CRP) levels,” Dr. Tam said. “Our study aimed to use a big data analytical approach to determine the effect of systemic GC dose and duration on the risk of major adverse cardiovascular events in patients with RA, while controlling for systemic inflammation, traditional CV risk factors, and other therapies.”
Is there a ‘safe’ dose for glucocorticoids?
To analyze this relationship, Dr. Lam and colleagues used the Hospital Authority Data Collaboration Laboratory, a citywide health care database. The investigators recruited patients with RA who had no history of MACE from 2006 to 2015 and followed them until the end of 2018. The primary outcome was the first occurrence of a MACE, defined as a composite of myocardial infarction (MI), unstable angina, ischemic or hemorrhagic cerebrovascular accident, transient ischemic attack, and CV death.
The study was published in Annals of the Rheumatic Diseases.
The analysis included 12,233 patients with RA and had over 105,826 person-years of follow-up. The average follow-up time was 8.7 years. During the study period, 860 patients had their first MACE. After controlling for confounding factors, a daily prednisolone dose of 5 mg or higher doubled the risk for MACE, compared with GC nonusers. MACE risk increased by 7% per month.
Long-term glucocorticoid use discouraged
Daily doses of less than 5 mg were not associated with higher MACE risk, but more research is necessary to understand whether these low doses are clinically efficacious, Dr. Tam said. “The study results suggest that a very-low-dose GC (less than 5 mg prednisolone daily) may be cardiovascular risk–neutral. However, further evaluation is needed to determine whether this dose is therapeutic. Other potential side effects, such as bone loss, increased infection risk, dyslipidemia, and hyperglycemia, should also be considered.”
Both the American College of Rheumatology and the European Alliance of Associations for Rheumatology acknowledge that short-term GCs may be necessary for some RA patients, but they emphasize using the smallest necessary dose for the shortest period possible because of the known toxicity of GCs.
“We recommend stopping GCs as soon as it is clinically feasible, in line with previous recommendations, until these issues are investigated further,” Dr. Tam added.
Dr. Bartels agreed that long-term use of GCs should be avoided if possible, even at lower doses, because although CV risk may be less of an issue, studies have shown an increased risk for infection even at GC doses of less than 5 mg a day.
How might risk increase with dose?
While the study showed a distinct difference in risk with doses of prednisolone higher and lower than 5 mg, more information on how risk increases with dose could be useful, said Beth Wallace, MD, an assistant professor in internal medicine at the University of Michigan, Ann Arbor, and a staff rheumatologist at the VA Ann Arbor Healthcare Center. She was also unaffiliated with the research. “If someone is on 5-10 mg ... how much better is that than being on 10-20 mg or being on 20-30 mg?” she asked. While these study findings are “very important,” she said, it would be useful to know the risk associated with 7.5 mg vs. a higher dose.
But even in this relatively healthy population in Hong Kong, “taking more than 5 mg of prednisolone doubles the risk of cardiovascular disease,” Dr. Wallace added. This is important for clinicians to know, especially if they are more cautious about prescribing steroids to older or sicker patients but are “using [the drugs] a little more indiscriminately in younger people and healthier people.”
The study did not receive outside funding. Dr. Tam and Dr. Bartels report no relevant financial relationships. Dr. Wallace has received a grant from the Department of Veterans Affairs Administration to study steroid tapering in RA.
A version of this article first appeared on Medscape.com.
FROM ANNALS OF THE RHEUMATIC DISEASES
Obesity cardiomyopathy tied to sudden cardiac death
a new case-control study suggests.
Researchers who analyzed hearts taken at autopsy from people who had died from sudden cardiac death found that a number of the hearts obtained from obese decedents were heavier than those from normal-weight decedents and that the hazard ratio of unexplained cardiomegaly in this cohort was 5.3, compared with normal-weight individuals.
“Even when we ruled out any conditions that could potentially cause enlargement of the heart, including hypertension, heart valve problems, diabetes, and other cardiovascular risk factors, the association with obesity cardiomyopathy, or OCM, and sudden cardiac death remained,” lead author Joseph Westaby, PhD, from the Cardiac Risk in the Young (CRY) Cardiovascular Pathology Laboratories at St George’s University of London, said in an interview.
The study was published online in JACC: Advances.
Intrigued by this finding, Dr. Westaby and associates sought to characterize the clinical and pathological features of OCM associated with sudden cardiac death by comparing this population to two control groups: sudden cardiac death patients who were either obese or of normal weight, and had morphologically normal hearts.
Their group is uniquely positioned to do such research, Dr. Westaby explained.
“Here at St George’s University of London, we have a specialized cardiovascular pathology service. ... All hearts obtained at autopsy from individuals who have died from sudden cardiac death, or who were suspected to have had a cardiovascular cause of death, anywhere in the U.K., are referred to the CRY Centre for further analysis,” he said.
Patients were divided into two groups according to body mass index: an obesity group (BMI > 30 kg/m2) and a normal-weight group (BMI, 18.5-24.9).
An increased heart weight above 550 g in men and 450 g in women in the absence of coronary artery disease, hypertension, diabetes, or valvular disease was classified as unexplained cardiomegaly, and individuals with obesity and cardiomegaly were defined as obesity cardiomyopathy.
Age- and sex-matched controls with obesity (n = 106) were selected based on a BMI greater than 30, with a morphologically normal heart weighing less than 550 g in men and than 450 g in women.
Age- and sex-matched normal weight controls (n = 106) were selected based on a BMI of 18.5-24.9 and a morphologically normal heart weighing less than 550 g in men and less than 450 g in women.
The researchers identified 53 OCM cases from a cohort of more than 4,500 sudden cardiac death cases that had BMI measurements. In normal-weight patients, there were 14 cases of unexplained cardiomegaly.
The mean age at death of individuals with OCM was 42 years (range, 30-54 years). Most of the deaths occurred in men (n = 34; 64%), who also died younger than women (40 ± 13 years vs. 45 ± 10 years; P = .036).
The average heart weight in OCM patients was 598 ± 93 g. Risk of sudden cardiac death increased when BMI reached 35.
Compared with matched controls, there were increases in right and left ventricular wall thickness (all P < .05) in OCM cases. Right ventricular epicardial fat was increased in OCM cases, compared with normal-weight controls only.
Left ventricular fibrosis was identified in seven (13%) OCM cases.
Role of genetics to be explored
“This study highlights the need for further investigation into these individuals because, at the moment, we can’t be sure that the only contributing factor to this is the obesity,” said Dr. Westaby.
In the works are plans to see if there may be an underlying genetic predisposition in obese individuals that may have contributed to the development of an enlarged heart. The group also plans to study the families of the deceased individuals to determine if they are at risk of developing cardiomegaly, he said.
“This paper makes an important contribution to the literature that raises many important questions for future research,” Timothy P. Fitzgibbons, MD, PhD, from the University of Massachusetts, Worcester, wrote in an accompanying editorial.
Being able to access so many autopsy samples gives the current study considerable heft, Dr. Fitzgibbons said in an interview.
“A lot has been made of the obesity paradox and the perhaps benign nature of obesity but this paper suggests the opposite, that it is a very serious problem and can, in fact, in and of itself, cause heart abnormalities that could cause sudden death,” he noted.
The fact that only 13% of OCM cases had fibrosis on histology suggests that fibrosis was not the main cause of sudden cardiac death, he said.
“Often we will do MRIs to look for areas of fibrosis within the heart because those areas make patients prone to re-entry arrhythmias, in particular, ventricular tachycardia. But the authors suggest that the enlarged myocytes may themselves be predisposing to arrhythmias, rather than fibrosis,” Dr. Fitzgibbons said.
The study was supported by Cardiac Risk in the Young. Dr. Westaby and Dr. Fitzgibbons have reported no relevant financial relationships.
A version of this article appeared on Medscape.com.
a new case-control study suggests.
Researchers who analyzed hearts taken at autopsy from people who had died from sudden cardiac death found that a number of the hearts obtained from obese decedents were heavier than those from normal-weight decedents and that the hazard ratio of unexplained cardiomegaly in this cohort was 5.3, compared with normal-weight individuals.
“Even when we ruled out any conditions that could potentially cause enlargement of the heart, including hypertension, heart valve problems, diabetes, and other cardiovascular risk factors, the association with obesity cardiomyopathy, or OCM, and sudden cardiac death remained,” lead author Joseph Westaby, PhD, from the Cardiac Risk in the Young (CRY) Cardiovascular Pathology Laboratories at St George’s University of London, said in an interview.
The study was published online in JACC: Advances.
Intrigued by this finding, Dr. Westaby and associates sought to characterize the clinical and pathological features of OCM associated with sudden cardiac death by comparing this population to two control groups: sudden cardiac death patients who were either obese or of normal weight, and had morphologically normal hearts.
Their group is uniquely positioned to do such research, Dr. Westaby explained.
“Here at St George’s University of London, we have a specialized cardiovascular pathology service. ... All hearts obtained at autopsy from individuals who have died from sudden cardiac death, or who were suspected to have had a cardiovascular cause of death, anywhere in the U.K., are referred to the CRY Centre for further analysis,” he said.
Patients were divided into two groups according to body mass index: an obesity group (BMI > 30 kg/m2) and a normal-weight group (BMI, 18.5-24.9).
An increased heart weight above 550 g in men and 450 g in women in the absence of coronary artery disease, hypertension, diabetes, or valvular disease was classified as unexplained cardiomegaly, and individuals with obesity and cardiomegaly were defined as obesity cardiomyopathy.
Age- and sex-matched controls with obesity (n = 106) were selected based on a BMI greater than 30, with a morphologically normal heart weighing less than 550 g in men and than 450 g in women.
Age- and sex-matched normal weight controls (n = 106) were selected based on a BMI of 18.5-24.9 and a morphologically normal heart weighing less than 550 g in men and less than 450 g in women.
The researchers identified 53 OCM cases from a cohort of more than 4,500 sudden cardiac death cases that had BMI measurements. In normal-weight patients, there were 14 cases of unexplained cardiomegaly.
The mean age at death of individuals with OCM was 42 years (range, 30-54 years). Most of the deaths occurred in men (n = 34; 64%), who also died younger than women (40 ± 13 years vs. 45 ± 10 years; P = .036).
The average heart weight in OCM patients was 598 ± 93 g. Risk of sudden cardiac death increased when BMI reached 35.
Compared with matched controls, there were increases in right and left ventricular wall thickness (all P < .05) in OCM cases. Right ventricular epicardial fat was increased in OCM cases, compared with normal-weight controls only.
Left ventricular fibrosis was identified in seven (13%) OCM cases.
Role of genetics to be explored
“This study highlights the need for further investigation into these individuals because, at the moment, we can’t be sure that the only contributing factor to this is the obesity,” said Dr. Westaby.
In the works are plans to see if there may be an underlying genetic predisposition in obese individuals that may have contributed to the development of an enlarged heart. The group also plans to study the families of the deceased individuals to determine if they are at risk of developing cardiomegaly, he said.
“This paper makes an important contribution to the literature that raises many important questions for future research,” Timothy P. Fitzgibbons, MD, PhD, from the University of Massachusetts, Worcester, wrote in an accompanying editorial.
Being able to access so many autopsy samples gives the current study considerable heft, Dr. Fitzgibbons said in an interview.
“A lot has been made of the obesity paradox and the perhaps benign nature of obesity but this paper suggests the opposite, that it is a very serious problem and can, in fact, in and of itself, cause heart abnormalities that could cause sudden death,” he noted.
The fact that only 13% of OCM cases had fibrosis on histology suggests that fibrosis was not the main cause of sudden cardiac death, he said.
“Often we will do MRIs to look for areas of fibrosis within the heart because those areas make patients prone to re-entry arrhythmias, in particular, ventricular tachycardia. But the authors suggest that the enlarged myocytes may themselves be predisposing to arrhythmias, rather than fibrosis,” Dr. Fitzgibbons said.
The study was supported by Cardiac Risk in the Young. Dr. Westaby and Dr. Fitzgibbons have reported no relevant financial relationships.
A version of this article appeared on Medscape.com.
a new case-control study suggests.
Researchers who analyzed hearts taken at autopsy from people who had died from sudden cardiac death found that a number of the hearts obtained from obese decedents were heavier than those from normal-weight decedents and that the hazard ratio of unexplained cardiomegaly in this cohort was 5.3, compared with normal-weight individuals.
“Even when we ruled out any conditions that could potentially cause enlargement of the heart, including hypertension, heart valve problems, diabetes, and other cardiovascular risk factors, the association with obesity cardiomyopathy, or OCM, and sudden cardiac death remained,” lead author Joseph Westaby, PhD, from the Cardiac Risk in the Young (CRY) Cardiovascular Pathology Laboratories at St George’s University of London, said in an interview.
The study was published online in JACC: Advances.
Intrigued by this finding, Dr. Westaby and associates sought to characterize the clinical and pathological features of OCM associated with sudden cardiac death by comparing this population to two control groups: sudden cardiac death patients who were either obese or of normal weight, and had morphologically normal hearts.
Their group is uniquely positioned to do such research, Dr. Westaby explained.
“Here at St George’s University of London, we have a specialized cardiovascular pathology service. ... All hearts obtained at autopsy from individuals who have died from sudden cardiac death, or who were suspected to have had a cardiovascular cause of death, anywhere in the U.K., are referred to the CRY Centre for further analysis,” he said.
Patients were divided into two groups according to body mass index: an obesity group (BMI > 30 kg/m2) and a normal-weight group (BMI, 18.5-24.9).
An increased heart weight above 550 g in men and 450 g in women in the absence of coronary artery disease, hypertension, diabetes, or valvular disease was classified as unexplained cardiomegaly, and individuals with obesity and cardiomegaly were defined as obesity cardiomyopathy.
Age- and sex-matched controls with obesity (n = 106) were selected based on a BMI greater than 30, with a morphologically normal heart weighing less than 550 g in men and than 450 g in women.
Age- and sex-matched normal weight controls (n = 106) were selected based on a BMI of 18.5-24.9 and a morphologically normal heart weighing less than 550 g in men and less than 450 g in women.
The researchers identified 53 OCM cases from a cohort of more than 4,500 sudden cardiac death cases that had BMI measurements. In normal-weight patients, there were 14 cases of unexplained cardiomegaly.
The mean age at death of individuals with OCM was 42 years (range, 30-54 years). Most of the deaths occurred in men (n = 34; 64%), who also died younger than women (40 ± 13 years vs. 45 ± 10 years; P = .036).
The average heart weight in OCM patients was 598 ± 93 g. Risk of sudden cardiac death increased when BMI reached 35.
Compared with matched controls, there were increases in right and left ventricular wall thickness (all P < .05) in OCM cases. Right ventricular epicardial fat was increased in OCM cases, compared with normal-weight controls only.
Left ventricular fibrosis was identified in seven (13%) OCM cases.
Role of genetics to be explored
“This study highlights the need for further investigation into these individuals because, at the moment, we can’t be sure that the only contributing factor to this is the obesity,” said Dr. Westaby.
In the works are plans to see if there may be an underlying genetic predisposition in obese individuals that may have contributed to the development of an enlarged heart. The group also plans to study the families of the deceased individuals to determine if they are at risk of developing cardiomegaly, he said.
“This paper makes an important contribution to the literature that raises many important questions for future research,” Timothy P. Fitzgibbons, MD, PhD, from the University of Massachusetts, Worcester, wrote in an accompanying editorial.
Being able to access so many autopsy samples gives the current study considerable heft, Dr. Fitzgibbons said in an interview.
“A lot has been made of the obesity paradox and the perhaps benign nature of obesity but this paper suggests the opposite, that it is a very serious problem and can, in fact, in and of itself, cause heart abnormalities that could cause sudden death,” he noted.
The fact that only 13% of OCM cases had fibrosis on histology suggests that fibrosis was not the main cause of sudden cardiac death, he said.
“Often we will do MRIs to look for areas of fibrosis within the heart because those areas make patients prone to re-entry arrhythmias, in particular, ventricular tachycardia. But the authors suggest that the enlarged myocytes may themselves be predisposing to arrhythmias, rather than fibrosis,” Dr. Fitzgibbons said.
The study was supported by Cardiac Risk in the Young. Dr. Westaby and Dr. Fitzgibbons have reported no relevant financial relationships.
A version of this article appeared on Medscape.com.
FROM JACC: ADVANCES
Heat waves plus air pollution tied to doubling of fatal MI
, a study from China suggests.
The researchers estimate that up to 3% of all deaths due to MI could be attributed to the combination of extreme temperatures and high levels of ambient fine particulate matter (PM2.5).
“Our findings provide evidence that reducing exposure to both extreme temperatures and fine particulate pollution may be useful to prevent premature deaths from heart attack,” senior author Yuewei Liu, MD, PhD, with Sun Yat-sen University in Guangzhou, China, said in a statement.
There is “long-standing evidence” of the harmful cardiovascular effects of air pollution, Jonathan Newman, MD, MPH, cardiologist at NYU Langone Heart in New York, who wasn’t involved in the study, said in an interview.
The added value of this study was finding an interaction between extreme hot temperatures and air pollution, “which is worrisome with global warming,” said Dr. Newman, assistant professor, department of medicine, the Leon H. Charney Division of Cardiology at NYU Langone Health.
The study was published online in Circulation.
Intensity and duration matter
The researchers analyzed data on 202,678 adults (mean age, 77.6 years; 52% male) who suffered fatal MI between 2015 and 2020 in Jiangsu province, a region with four distinct seasons and a wide range of temperatures and ambient PM2.5.
They evaluated the association of exposure to extreme temperature events, including both hot and cold spells, and PM2.5 with MI mortality, and their interactive effects.
Among the key findings:
- The risk of fatal MI was 18% higher during 2-day heat waves with heat indexes at or above the 90th percentile (ranging from 82.6° to 97.9° F) and 74% higher during 4-day heat waves with heat indexes at or above the 97.5th percentile (ranging from 94.8° to 109.4° F), compared with control days.
- The risk of fatal MI was 4% higher during 2-day cold snaps with temperatures at or below the 10th percentile (ranging from 33.3° to 40.5° F) and 12% higher during 3-day cold snaps with temperatures at or below the 2.5th percentile (ranging from 27.0° to 37.2° F).
- The risk of fatal MI was twice as high during 4-day heat waves that had PM2.5 above 37.5 mcg/m3. Days with high levels of PM2.5 during cold snaps did not have an equivalent increase in the risk of fatal MI.
- Up to 2.8% of MI deaths during the 5-year study period may be attributable to the combination of extreme temperature exposure and PM2.5 at levels exceeding World Health Organization air quality guidelines (37.5 mcg/m3).
- The risk of fatal MI was generally higher among women than men during heat waves and was higher among adults 80 years old and older than in younger adults during heat waves, cold snaps, or days with high levels of PM2.5.
The finding that adults over age 80 are particularly susceptible to the effects of heat and air pollution and the interaction of the two is “notable and particularly relevant given the aging of the population,” Dr. Newman told this news organization.
Mitigating both extreme temperature events and PM2.5 exposures “may bring health cobenefits in preventing premature deaths from MI,” the researchers write.
“To improve public health, it is important to take fine particulate pollution into consideration when providing extreme temperature warnings to the public,” Dr. Liu adds in the statement.
In an earlier study, Dr. Liu and colleagues showed that exposure to both large and small particulate matter, as well as nitrogen dioxide, was significantly associated with increased odds of death from MI.
This study was funded by China’s Ministry of Science and Technology. The authors and Dr. Newman have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, a study from China suggests.
The researchers estimate that up to 3% of all deaths due to MI could be attributed to the combination of extreme temperatures and high levels of ambient fine particulate matter (PM2.5).
“Our findings provide evidence that reducing exposure to both extreme temperatures and fine particulate pollution may be useful to prevent premature deaths from heart attack,” senior author Yuewei Liu, MD, PhD, with Sun Yat-sen University in Guangzhou, China, said in a statement.
There is “long-standing evidence” of the harmful cardiovascular effects of air pollution, Jonathan Newman, MD, MPH, cardiologist at NYU Langone Heart in New York, who wasn’t involved in the study, said in an interview.
The added value of this study was finding an interaction between extreme hot temperatures and air pollution, “which is worrisome with global warming,” said Dr. Newman, assistant professor, department of medicine, the Leon H. Charney Division of Cardiology at NYU Langone Health.
The study was published online in Circulation.
Intensity and duration matter
The researchers analyzed data on 202,678 adults (mean age, 77.6 years; 52% male) who suffered fatal MI between 2015 and 2020 in Jiangsu province, a region with four distinct seasons and a wide range of temperatures and ambient PM2.5.
They evaluated the association of exposure to extreme temperature events, including both hot and cold spells, and PM2.5 with MI mortality, and their interactive effects.
Among the key findings:
- The risk of fatal MI was 18% higher during 2-day heat waves with heat indexes at or above the 90th percentile (ranging from 82.6° to 97.9° F) and 74% higher during 4-day heat waves with heat indexes at or above the 97.5th percentile (ranging from 94.8° to 109.4° F), compared with control days.
- The risk of fatal MI was 4% higher during 2-day cold snaps with temperatures at or below the 10th percentile (ranging from 33.3° to 40.5° F) and 12% higher during 3-day cold snaps with temperatures at or below the 2.5th percentile (ranging from 27.0° to 37.2° F).
- The risk of fatal MI was twice as high during 4-day heat waves that had PM2.5 above 37.5 mcg/m3. Days with high levels of PM2.5 during cold snaps did not have an equivalent increase in the risk of fatal MI.
- Up to 2.8% of MI deaths during the 5-year study period may be attributable to the combination of extreme temperature exposure and PM2.5 at levels exceeding World Health Organization air quality guidelines (37.5 mcg/m3).
- The risk of fatal MI was generally higher among women than men during heat waves and was higher among adults 80 years old and older than in younger adults during heat waves, cold snaps, or days with high levels of PM2.5.
The finding that adults over age 80 are particularly susceptible to the effects of heat and air pollution and the interaction of the two is “notable and particularly relevant given the aging of the population,” Dr. Newman told this news organization.
Mitigating both extreme temperature events and PM2.5 exposures “may bring health cobenefits in preventing premature deaths from MI,” the researchers write.
“To improve public health, it is important to take fine particulate pollution into consideration when providing extreme temperature warnings to the public,” Dr. Liu adds in the statement.
In an earlier study, Dr. Liu and colleagues showed that exposure to both large and small particulate matter, as well as nitrogen dioxide, was significantly associated with increased odds of death from MI.
This study was funded by China’s Ministry of Science and Technology. The authors and Dr. Newman have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, a study from China suggests.
The researchers estimate that up to 3% of all deaths due to MI could be attributed to the combination of extreme temperatures and high levels of ambient fine particulate matter (PM2.5).
“Our findings provide evidence that reducing exposure to both extreme temperatures and fine particulate pollution may be useful to prevent premature deaths from heart attack,” senior author Yuewei Liu, MD, PhD, with Sun Yat-sen University in Guangzhou, China, said in a statement.
There is “long-standing evidence” of the harmful cardiovascular effects of air pollution, Jonathan Newman, MD, MPH, cardiologist at NYU Langone Heart in New York, who wasn’t involved in the study, said in an interview.
The added value of this study was finding an interaction between extreme hot temperatures and air pollution, “which is worrisome with global warming,” said Dr. Newman, assistant professor, department of medicine, the Leon H. Charney Division of Cardiology at NYU Langone Health.
The study was published online in Circulation.
Intensity and duration matter
The researchers analyzed data on 202,678 adults (mean age, 77.6 years; 52% male) who suffered fatal MI between 2015 and 2020 in Jiangsu province, a region with four distinct seasons and a wide range of temperatures and ambient PM2.5.
They evaluated the association of exposure to extreme temperature events, including both hot and cold spells, and PM2.5 with MI mortality, and their interactive effects.
Among the key findings:
- The risk of fatal MI was 18% higher during 2-day heat waves with heat indexes at or above the 90th percentile (ranging from 82.6° to 97.9° F) and 74% higher during 4-day heat waves with heat indexes at or above the 97.5th percentile (ranging from 94.8° to 109.4° F), compared with control days.
- The risk of fatal MI was 4% higher during 2-day cold snaps with temperatures at or below the 10th percentile (ranging from 33.3° to 40.5° F) and 12% higher during 3-day cold snaps with temperatures at or below the 2.5th percentile (ranging from 27.0° to 37.2° F).
- The risk of fatal MI was twice as high during 4-day heat waves that had PM2.5 above 37.5 mcg/m3. Days with high levels of PM2.5 during cold snaps did not have an equivalent increase in the risk of fatal MI.
- Up to 2.8% of MI deaths during the 5-year study period may be attributable to the combination of extreme temperature exposure and PM2.5 at levels exceeding World Health Organization air quality guidelines (37.5 mcg/m3).
- The risk of fatal MI was generally higher among women than men during heat waves and was higher among adults 80 years old and older than in younger adults during heat waves, cold snaps, or days with high levels of PM2.5.
The finding that adults over age 80 are particularly susceptible to the effects of heat and air pollution and the interaction of the two is “notable and particularly relevant given the aging of the population,” Dr. Newman told this news organization.
Mitigating both extreme temperature events and PM2.5 exposures “may bring health cobenefits in preventing premature deaths from MI,” the researchers write.
“To improve public health, it is important to take fine particulate pollution into consideration when providing extreme temperature warnings to the public,” Dr. Liu adds in the statement.
In an earlier study, Dr. Liu and colleagues showed that exposure to both large and small particulate matter, as well as nitrogen dioxide, was significantly associated with increased odds of death from MI.
This study was funded by China’s Ministry of Science and Technology. The authors and Dr. Newman have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM CIRCULATION
Class I recall of GE Healthcare TruSignal SpO2 sensors
The Food and Drug Administration has identified this as a class I recall, the most serious type. The company has not received any reports of patient injury or deaths as a result of these issues.*
The recall includes the TruSignal Adult Pediatric Sensor, TruSignal AllFit Sensor, TruSignal Sensitive Skin Sensor, TruSignal Wrap Sensor, TruSignal Ear Sensor, TruSignal Integrated Ear Sensor with GE Connector, TruSignal Integrated Ear Sensor With Datex Connector, TruSignal Integrated Ear Sensor With Datex Connector, and TruSignal Integrated Ear Sensor With Ohmeda Connector.
The sensors were distributed in the United States from Jan. 1, 2021, to March 4, 2023.
According to the recall notice, the malfunctioning sensors “may reduce the amount of energy sent to the heart during defibrillation without any notification to the care provider, which could prevent delivery of lifesaving therapy in a critical situation.
“This issue is most hazardous to hospitalized patients who may need defibrillation for cardiac arrest. Affected sensors may also unintentionally expose patients to electrical currents from other sources or may provide inaccurate measurements of SpO2, which can impact treatment decisions,” the notice warns.
In an urgent device correction letter sent to health care professionals in May, GE HealthCare recommends that health care professionals do the following:
- Use an alternate method for SpO2 monitoring, including TruSignal sensors not impacted or an alternate SpO2 device.
- If alternate methods are not available, use affected TruSignal SpO2 sensors as long as they have not been saturated with fluids.
- If defibrillation is necessary when affected TruSignal SpO2 sensors are being used, remove the affected TruSignal SpO2 sensor, defibrillate per hospital protocol, and reattach the affected TruSignal SpO2 sensor after defibrillation is no longer needed.
- For Adult/Pediatric SpO2 sensors, confirm that material does not cover the emitter or detector before using.
- Discard the sensor and use another sensor if any additional material is present.
- Make sure all potential users are made aware of this safety notification and the recommended actions, and retain this notice.
Customers are also asked to complete and return the acknowledgment form attached to the notice to Recall.39004@ge.com.
For questions or concerns about this recall, contact GE HealthCare Service at 1-800-437-1171 or a local service representative.
Health care professionals can report adverse reactions or quality problems they experience using these devices to the FDA’s MedWatch program.
A version of this article first appeared on Medscape.com.
*Correction, 8/3/23: An earlier version of this article mischaracterized the reports received by the company.
The Food and Drug Administration has identified this as a class I recall, the most serious type. The company has not received any reports of patient injury or deaths as a result of these issues.*
The recall includes the TruSignal Adult Pediatric Sensor, TruSignal AllFit Sensor, TruSignal Sensitive Skin Sensor, TruSignal Wrap Sensor, TruSignal Ear Sensor, TruSignal Integrated Ear Sensor with GE Connector, TruSignal Integrated Ear Sensor With Datex Connector, TruSignal Integrated Ear Sensor With Datex Connector, and TruSignal Integrated Ear Sensor With Ohmeda Connector.
The sensors were distributed in the United States from Jan. 1, 2021, to March 4, 2023.
According to the recall notice, the malfunctioning sensors “may reduce the amount of energy sent to the heart during defibrillation without any notification to the care provider, which could prevent delivery of lifesaving therapy in a critical situation.
“This issue is most hazardous to hospitalized patients who may need defibrillation for cardiac arrest. Affected sensors may also unintentionally expose patients to electrical currents from other sources or may provide inaccurate measurements of SpO2, which can impact treatment decisions,” the notice warns.
In an urgent device correction letter sent to health care professionals in May, GE HealthCare recommends that health care professionals do the following:
- Use an alternate method for SpO2 monitoring, including TruSignal sensors not impacted or an alternate SpO2 device.
- If alternate methods are not available, use affected TruSignal SpO2 sensors as long as they have not been saturated with fluids.
- If defibrillation is necessary when affected TruSignal SpO2 sensors are being used, remove the affected TruSignal SpO2 sensor, defibrillate per hospital protocol, and reattach the affected TruSignal SpO2 sensor after defibrillation is no longer needed.
- For Adult/Pediatric SpO2 sensors, confirm that material does not cover the emitter or detector before using.
- Discard the sensor and use another sensor if any additional material is present.
- Make sure all potential users are made aware of this safety notification and the recommended actions, and retain this notice.
Customers are also asked to complete and return the acknowledgment form attached to the notice to Recall.39004@ge.com.
For questions or concerns about this recall, contact GE HealthCare Service at 1-800-437-1171 or a local service representative.
Health care professionals can report adverse reactions or quality problems they experience using these devices to the FDA’s MedWatch program.
A version of this article first appeared on Medscape.com.
*Correction, 8/3/23: An earlier version of this article mischaracterized the reports received by the company.
The Food and Drug Administration has identified this as a class I recall, the most serious type. The company has not received any reports of patient injury or deaths as a result of these issues.*
The recall includes the TruSignal Adult Pediatric Sensor, TruSignal AllFit Sensor, TruSignal Sensitive Skin Sensor, TruSignal Wrap Sensor, TruSignal Ear Sensor, TruSignal Integrated Ear Sensor with GE Connector, TruSignal Integrated Ear Sensor With Datex Connector, TruSignal Integrated Ear Sensor With Datex Connector, and TruSignal Integrated Ear Sensor With Ohmeda Connector.
The sensors were distributed in the United States from Jan. 1, 2021, to March 4, 2023.
According to the recall notice, the malfunctioning sensors “may reduce the amount of energy sent to the heart during defibrillation without any notification to the care provider, which could prevent delivery of lifesaving therapy in a critical situation.
“This issue is most hazardous to hospitalized patients who may need defibrillation for cardiac arrest. Affected sensors may also unintentionally expose patients to electrical currents from other sources or may provide inaccurate measurements of SpO2, which can impact treatment decisions,” the notice warns.
In an urgent device correction letter sent to health care professionals in May, GE HealthCare recommends that health care professionals do the following:
- Use an alternate method for SpO2 monitoring, including TruSignal sensors not impacted or an alternate SpO2 device.
- If alternate methods are not available, use affected TruSignal SpO2 sensors as long as they have not been saturated with fluids.
- If defibrillation is necessary when affected TruSignal SpO2 sensors are being used, remove the affected TruSignal SpO2 sensor, defibrillate per hospital protocol, and reattach the affected TruSignal SpO2 sensor after defibrillation is no longer needed.
- For Adult/Pediatric SpO2 sensors, confirm that material does not cover the emitter or detector before using.
- Discard the sensor and use another sensor if any additional material is present.
- Make sure all potential users are made aware of this safety notification and the recommended actions, and retain this notice.
Customers are also asked to complete and return the acknowledgment form attached to the notice to Recall.39004@ge.com.
For questions or concerns about this recall, contact GE HealthCare Service at 1-800-437-1171 or a local service representative.
Health care professionals can report adverse reactions or quality problems they experience using these devices to the FDA’s MedWatch program.
A version of this article first appeared on Medscape.com.
*Correction, 8/3/23: An earlier version of this article mischaracterized the reports received by the company.
Mortality post perioperative CPR climbs with patient frailty
And the frailer that patients were going into surgery, according to their scores on an established frailty index, the greater their adjusted mortality risk at 30 days and the likelier they were to be discharged to a location other than their home.
The findings are based on more than 3,000 patients in an American College of Surgeons (ACS) quality improvement registry who underwent CPR at noncardiac surgery, about one-fourth of whom scored a least 40 on the revised Risk Analysis Index (RAI). The frailty index accounts for the patient’s comorbidities, cognition, functional and nutritional status, and other factors as predictors of postoperative mortality risk.
Such CPR for perioperative cardiac arrest “should not be considered futile just because a patient is frail, but neither should cardiac arrest be considered as ‘reversible’ in this population, as previously thought,” lead author Matthew B. Allen, MD, of Brigham and Women’s Hospital, Boston, said in an interview.
“We know that patients who are frail have higher risk of complications and mortality after surgery, and recent studies have demonstrated that frailty is associated with very poor outcomes following CPR in nonsurgical settings,” said Dr. Allen, an attending physician in the department of anesthesiology, perioperative, and pain medicine at his center.
Although cardiac arrest is typically regarded as being “more reversible” in the setting of surgery and anesthesia than elsewhere in the hospital, he observed, there’s very little data on whether that is indeed the case for frail patients.
The current analysis provides “a heretofore absent base of evidence to guide decision-making regarding CPR in patients with frailty who undergo surgery,” states the report, published in JAMA Network Open.
The 3,058 patients in the analysis, from the ACS National Surgical Quality Improvement database, received CPR for cardiac arrest during or soon after noncardiac surgery. Their mean age was 71 and 44% were women.
Their RAI scores ranged from 14 to 71 and averaged 37.7; one-fourth of the patients had scores of 40 or higher, the study’s threshold for identifying patients as “frail.”
Overall in the cohort, more cardiac arrests occurred during surgeries that entailed low-to-moderate physiologic stress (an Operative Stress Score of 1 to 3) than in the setting of emergency surgery: 67.9% vs. 39.1%, respectively.
During emergency surgeries, a greater proportion of frail than nonfrail patients experienced cardiac arrest, 42% and 38%, respectively. The same relationship was observed during low-to-moderate stress surgeries: 76.6% of frail patients and 64.8% of nonfrail patients. General anesthesia was used in about 93% of procedures for both frail and nonfrail patients, the report states.
The primary endpoint, 30-day mortality, was 58.6% overall, 67.4% in frail patients, and 55.6% for nonfrail patients. Frailty and mortality were positively associated, with an adjusted odds ratio (AOR) of 1.35 (95% confidence interval [CI], 1.11-1.65, P = .003) in multivariate analysis.
Of the cohort’s 1,164 patients who had been admitted from home and survived to discharge, 38.6% were discharged to a destination other than home; the corresponding rates for frail and nonfrail patients were 59.3% and 33.9%, respectively. Frailty and nonhome discharge were positively correlated with an AOR of 1.85 (95% CI, 1.31-2.62, P < .001).
“There is no such thing as a low-risk procedure in patients who are frail,” Dr. Allen said in an interview. “Frail patients should be medically optimized prior to undergoing surgery and anesthesia, and plans should be tailored to patients’ vulnerabilities to reduce the risk of complications and facilitate rapid recognition and treatment when they occur.”
Moreover, he said, management of clinical decompensation in the perioperative period should be a part of the shared decision-making process “to establish a plan aligned with the patients’ priorities whenever possible.”
The current study quantifies risk associated with frailty in the surgical setting, and “this quantification can help providers, patients, and insurers better grasp the growing frailty problem,” Balachundhar Subramaniam, MD, MPH, of Harvard Medical School, Boston, said in an interview.
Universal screening for frailty is “a must in all surgical patients” to help identify those who are high-risk and reduce their chances for perioperative adverse events, said Dr. Subramaniam, who was not involved in the study.
“Prehabilitation with education, nutrition, physical fitness, and psychological support offer the best chance of significantly reducing poor outcomes” in frail patients, he said, along with “continuous education” in the care of frail patients.
University of Colorado surgeon Joseph Cleveland, MD, not part of the current study, said that it “provides a framework for counseling patients” regarding their do-not-resuscitate status.
“We can counsel patients with frailty with this information,” he said, “that if their heart should stop or go into in irregular rhythm, their chances of surviving are not greater than 50% and they have a more than 50% chance of not being discharged home.”
Dr. Allen reported receiving a clinical translational starter grant from Brigham and Women’s Hospital Department of Anesthesiology; disclosures for the other authors are in the original article. Dr. Subramaniam disclosed research funding from Masimo and Merck and serving as an education consultant for Masimo. Dr. Cleveland reported no relevant financial relationships.
A version of this article appeared on Medscape.com.
And the frailer that patients were going into surgery, according to their scores on an established frailty index, the greater their adjusted mortality risk at 30 days and the likelier they were to be discharged to a location other than their home.
The findings are based on more than 3,000 patients in an American College of Surgeons (ACS) quality improvement registry who underwent CPR at noncardiac surgery, about one-fourth of whom scored a least 40 on the revised Risk Analysis Index (RAI). The frailty index accounts for the patient’s comorbidities, cognition, functional and nutritional status, and other factors as predictors of postoperative mortality risk.
Such CPR for perioperative cardiac arrest “should not be considered futile just because a patient is frail, but neither should cardiac arrest be considered as ‘reversible’ in this population, as previously thought,” lead author Matthew B. Allen, MD, of Brigham and Women’s Hospital, Boston, said in an interview.
“We know that patients who are frail have higher risk of complications and mortality after surgery, and recent studies have demonstrated that frailty is associated with very poor outcomes following CPR in nonsurgical settings,” said Dr. Allen, an attending physician in the department of anesthesiology, perioperative, and pain medicine at his center.
Although cardiac arrest is typically regarded as being “more reversible” in the setting of surgery and anesthesia than elsewhere in the hospital, he observed, there’s very little data on whether that is indeed the case for frail patients.
The current analysis provides “a heretofore absent base of evidence to guide decision-making regarding CPR in patients with frailty who undergo surgery,” states the report, published in JAMA Network Open.
The 3,058 patients in the analysis, from the ACS National Surgical Quality Improvement database, received CPR for cardiac arrest during or soon after noncardiac surgery. Their mean age was 71 and 44% were women.
Their RAI scores ranged from 14 to 71 and averaged 37.7; one-fourth of the patients had scores of 40 or higher, the study’s threshold for identifying patients as “frail.”
Overall in the cohort, more cardiac arrests occurred during surgeries that entailed low-to-moderate physiologic stress (an Operative Stress Score of 1 to 3) than in the setting of emergency surgery: 67.9% vs. 39.1%, respectively.
During emergency surgeries, a greater proportion of frail than nonfrail patients experienced cardiac arrest, 42% and 38%, respectively. The same relationship was observed during low-to-moderate stress surgeries: 76.6% of frail patients and 64.8% of nonfrail patients. General anesthesia was used in about 93% of procedures for both frail and nonfrail patients, the report states.
The primary endpoint, 30-day mortality, was 58.6% overall, 67.4% in frail patients, and 55.6% for nonfrail patients. Frailty and mortality were positively associated, with an adjusted odds ratio (AOR) of 1.35 (95% confidence interval [CI], 1.11-1.65, P = .003) in multivariate analysis.
Of the cohort’s 1,164 patients who had been admitted from home and survived to discharge, 38.6% were discharged to a destination other than home; the corresponding rates for frail and nonfrail patients were 59.3% and 33.9%, respectively. Frailty and nonhome discharge were positively correlated with an AOR of 1.85 (95% CI, 1.31-2.62, P < .001).
“There is no such thing as a low-risk procedure in patients who are frail,” Dr. Allen said in an interview. “Frail patients should be medically optimized prior to undergoing surgery and anesthesia, and plans should be tailored to patients’ vulnerabilities to reduce the risk of complications and facilitate rapid recognition and treatment when they occur.”
Moreover, he said, management of clinical decompensation in the perioperative period should be a part of the shared decision-making process “to establish a plan aligned with the patients’ priorities whenever possible.”
The current study quantifies risk associated with frailty in the surgical setting, and “this quantification can help providers, patients, and insurers better grasp the growing frailty problem,” Balachundhar Subramaniam, MD, MPH, of Harvard Medical School, Boston, said in an interview.
Universal screening for frailty is “a must in all surgical patients” to help identify those who are high-risk and reduce their chances for perioperative adverse events, said Dr. Subramaniam, who was not involved in the study.
“Prehabilitation with education, nutrition, physical fitness, and psychological support offer the best chance of significantly reducing poor outcomes” in frail patients, he said, along with “continuous education” in the care of frail patients.
University of Colorado surgeon Joseph Cleveland, MD, not part of the current study, said that it “provides a framework for counseling patients” regarding their do-not-resuscitate status.
“We can counsel patients with frailty with this information,” he said, “that if their heart should stop or go into in irregular rhythm, their chances of surviving are not greater than 50% and they have a more than 50% chance of not being discharged home.”
Dr. Allen reported receiving a clinical translational starter grant from Brigham and Women’s Hospital Department of Anesthesiology; disclosures for the other authors are in the original article. Dr. Subramaniam disclosed research funding from Masimo and Merck and serving as an education consultant for Masimo. Dr. Cleveland reported no relevant financial relationships.
A version of this article appeared on Medscape.com.
And the frailer that patients were going into surgery, according to their scores on an established frailty index, the greater their adjusted mortality risk at 30 days and the likelier they were to be discharged to a location other than their home.
The findings are based on more than 3,000 patients in an American College of Surgeons (ACS) quality improvement registry who underwent CPR at noncardiac surgery, about one-fourth of whom scored a least 40 on the revised Risk Analysis Index (RAI). The frailty index accounts for the patient’s comorbidities, cognition, functional and nutritional status, and other factors as predictors of postoperative mortality risk.
Such CPR for perioperative cardiac arrest “should not be considered futile just because a patient is frail, but neither should cardiac arrest be considered as ‘reversible’ in this population, as previously thought,” lead author Matthew B. Allen, MD, of Brigham and Women’s Hospital, Boston, said in an interview.
“We know that patients who are frail have higher risk of complications and mortality after surgery, and recent studies have demonstrated that frailty is associated with very poor outcomes following CPR in nonsurgical settings,” said Dr. Allen, an attending physician in the department of anesthesiology, perioperative, and pain medicine at his center.
Although cardiac arrest is typically regarded as being “more reversible” in the setting of surgery and anesthesia than elsewhere in the hospital, he observed, there’s very little data on whether that is indeed the case for frail patients.
The current analysis provides “a heretofore absent base of evidence to guide decision-making regarding CPR in patients with frailty who undergo surgery,” states the report, published in JAMA Network Open.
The 3,058 patients in the analysis, from the ACS National Surgical Quality Improvement database, received CPR for cardiac arrest during or soon after noncardiac surgery. Their mean age was 71 and 44% were women.
Their RAI scores ranged from 14 to 71 and averaged 37.7; one-fourth of the patients had scores of 40 or higher, the study’s threshold for identifying patients as “frail.”
Overall in the cohort, more cardiac arrests occurred during surgeries that entailed low-to-moderate physiologic stress (an Operative Stress Score of 1 to 3) than in the setting of emergency surgery: 67.9% vs. 39.1%, respectively.
During emergency surgeries, a greater proportion of frail than nonfrail patients experienced cardiac arrest, 42% and 38%, respectively. The same relationship was observed during low-to-moderate stress surgeries: 76.6% of frail patients and 64.8% of nonfrail patients. General anesthesia was used in about 93% of procedures for both frail and nonfrail patients, the report states.
The primary endpoint, 30-day mortality, was 58.6% overall, 67.4% in frail patients, and 55.6% for nonfrail patients. Frailty and mortality were positively associated, with an adjusted odds ratio (AOR) of 1.35 (95% confidence interval [CI], 1.11-1.65, P = .003) in multivariate analysis.
Of the cohort’s 1,164 patients who had been admitted from home and survived to discharge, 38.6% were discharged to a destination other than home; the corresponding rates for frail and nonfrail patients were 59.3% and 33.9%, respectively. Frailty and nonhome discharge were positively correlated with an AOR of 1.85 (95% CI, 1.31-2.62, P < .001).
“There is no such thing as a low-risk procedure in patients who are frail,” Dr. Allen said in an interview. “Frail patients should be medically optimized prior to undergoing surgery and anesthesia, and plans should be tailored to patients’ vulnerabilities to reduce the risk of complications and facilitate rapid recognition and treatment when they occur.”
Moreover, he said, management of clinical decompensation in the perioperative period should be a part of the shared decision-making process “to establish a plan aligned with the patients’ priorities whenever possible.”
The current study quantifies risk associated with frailty in the surgical setting, and “this quantification can help providers, patients, and insurers better grasp the growing frailty problem,” Balachundhar Subramaniam, MD, MPH, of Harvard Medical School, Boston, said in an interview.
Universal screening for frailty is “a must in all surgical patients” to help identify those who are high-risk and reduce their chances for perioperative adverse events, said Dr. Subramaniam, who was not involved in the study.
“Prehabilitation with education, nutrition, physical fitness, and psychological support offer the best chance of significantly reducing poor outcomes” in frail patients, he said, along with “continuous education” in the care of frail patients.
University of Colorado surgeon Joseph Cleveland, MD, not part of the current study, said that it “provides a framework for counseling patients” regarding their do-not-resuscitate status.
“We can counsel patients with frailty with this information,” he said, “that if their heart should stop or go into in irregular rhythm, their chances of surviving are not greater than 50% and they have a more than 50% chance of not being discharged home.”
Dr. Allen reported receiving a clinical translational starter grant from Brigham and Women’s Hospital Department of Anesthesiology; disclosures for the other authors are in the original article. Dr. Subramaniam disclosed research funding from Masimo and Merck and serving as an education consultant for Masimo. Dr. Cleveland reported no relevant financial relationships.
A version of this article appeared on Medscape.com.
FROM JAMA NETWORK OPEN
MD rushes in after lightning strikes four people at White House
It was one of those dog days of August where the humidity is palpable and the pressure is so hot and thick you can almost feel the ions in the air. At the time (2022), I was a White House fellow and senior adviser in the West Wing Office of Public Engagement and in the Office of the Vice President.
I was leaving the White House around 7:00 p.m. through the front gate on Lafayette Square. I had a dinner reservation with a friend, so I was in a rush. It was super overcast. Lo and behold, three steps after I closed the gate behind me, it started pouring. Rain came down so hard I had to take shelter.
There’s a stone building in front of the White House with archways, so I took cover underneath one of them, hoping that in a couple of minutes the rain would pass. Behind the archways are these thick, black, iron gates.
Just as I was about to make a run for it, I heard: BOOM!
It was like a bomb had gone off. In one moment, I saw the lightning bolt, heard the thunder, and felt the heat. It was all one rush of sensation. I couldn’t remember having been that scared in a long time.
I thought, “I definitely have to get out of here. In a couple of minutes there might be another strike, and I’m sitting next to iron gates!” I saw a little bit of a window in the downpour, so I started booking it. I knew there was a sheltered Secret Service area around the corner where they park their cars. A much safer place to be.
I was sprinting on the sidewalk and spotted a bunch of Secret Service agents on their bikes riding in the opposite direction, back toward the park. I knew they wouldn’t be out on bikes in this mess without a reason. As they reached me, one agent said, “Clear the sidewalk! We’re coming through with a bunch of equipment.”
I yelled, “What’s going on?”
“Four people were just struck by lightning,” he said as he zoomed past.
I thought: “Sh*t. I have to go back.”
It was like two different parts of my brain were active at the exact same time. My subcortical brain at the level of the amygdala was like: “You just ran from there, idiot. Why are you running back?” And another part of my brain was like: “This is who you are.”
The lightning had struck one of the largest trees in the park. Four bodies splayed out in one direction from the tree. They’d been taking shelter underneath it when they were hit and were blown off to one side. By the time I got there, two Secret Service agents were on the scene doing CPR. Some bystanders had started to run over.
I did a quick round of pulse checks to see everyone’s status, and all four were apneic and pulseless. I told the two Secret Service agents to keep doing compressions on the first person. Two bystanders also began compressions on another person, an older man.
More Secret Service agents arrived, and I said, “We need to do compressions on this other person right now.” One of the agents took a moment to question who I could be and why I was there. I said, “I’m a doctor. I know I’m not dressed like one, but I’m a physician.”
I told some agents to go find an AED, because these people needed to be shocked.
After they left, I was effectively trying to triage which of these four people would get the AED first. Initially, I spent more of my time on the young man, and we began to get some response from him. I then spent some time with the young woman.
It turned out there were AEDs in the pouches on the Secret Service bikes, but they were very small, dinky AEDs. We tried to apply the pads, but it was downpouring so much that the adhesive wouldn’t stick. I told one of the agents we needed a towel.
Through all this I was concerned we were going to be struck again. I mean, the metal statue of Lafayette was right there! They say lighting doesn’t strike in the same place twice, but who knows if that’s really true?
The towel arrived, and we were able to get the chests of the younger people dry enough for the AED pads. We applied two shocks first to the woman, then the young man. We got his pulse back quickly. The woman’s came back as well, but it felt much weaker.
EMS arrived shortly thereafter. We got all four patients on the transport, and they were transferred to the hospital.
The whole experience had taken 14 minutes.
At the time, I felt confident that the young man was going to survive. We’re taught that lightning bolt strikes are survivable if you can shock someone quickly. He also got pretty good CPR. But the next day I was watching the news and learned that he had passed away. So, of course I was thinking the worst about the others as well.
But a week and a half later, I learned that the young woman had been discharged from the ICU. She was the only one who made it. Her name is Amber, and we got connected through a reporter. About 2 weeks later, I invited her to the White House. I took her to the Oval Office. I met her mom and dad and husband, and we had dinner. We’ve been in touch ever since.
I remember the first time we talked on the phone, Amber said something along the lines of, “This sucks. Obviously, I was not planning for any of this to happen. But I also think there’s something good that could come from this.”
I was so surprised and happy to hear her say that. I had something similar happen to me when I was a teenager – caught in the wrong place at the wrong time. I tried to intervene in a gang fight in my neighborhood. I thought a kid was going to get killed, so I jumped in, imagining I could save the day. I didn’t. They broke a bunch of my bones and I was in the hospital for a bit.
I remember thinking then that my life was over. But after some time, I found a new perspective, which was: Maybe that life is over. But maybe this could be the beginning of a new one. And maybe those things that I’ve been afraid of doing, the dreams that I have, maybe now I’m actually free to go after them.
I told Amber, if there are things that you have been waiting to do, this could be the time. She wants to be an international human rights activist, and she is kicking butt in a graduate school program to begin on that pathway. It’s been really cool to watch her chase this dream with way more vigor than she had before.
I think we bonded because we’ve gone through – obviously not the same thing, but a similar moment of being confronted with your own mortality. Realizing that life can just shatter. And so, while we’re here, we might as well go for it with all the force of a person who knows this could all disappear in an instant.
It was an extremely humbling moment. It reaffirmed that my life is not about me. I have to use the time that I’ve got on behalf of other people as much as I can. What is my life about if not being useful?
Dr. Martin is an emergency medicine physician and faculty member at the MGH Center for Social Justice and Health Equity at Harvard Medical School, Boston.
A version of this article first appeared on Medscape.com.
It was one of those dog days of August where the humidity is palpable and the pressure is so hot and thick you can almost feel the ions in the air. At the time (2022), I was a White House fellow and senior adviser in the West Wing Office of Public Engagement and in the Office of the Vice President.
I was leaving the White House around 7:00 p.m. through the front gate on Lafayette Square. I had a dinner reservation with a friend, so I was in a rush. It was super overcast. Lo and behold, three steps after I closed the gate behind me, it started pouring. Rain came down so hard I had to take shelter.
There’s a stone building in front of the White House with archways, so I took cover underneath one of them, hoping that in a couple of minutes the rain would pass. Behind the archways are these thick, black, iron gates.
Just as I was about to make a run for it, I heard: BOOM!
It was like a bomb had gone off. In one moment, I saw the lightning bolt, heard the thunder, and felt the heat. It was all one rush of sensation. I couldn’t remember having been that scared in a long time.
I thought, “I definitely have to get out of here. In a couple of minutes there might be another strike, and I’m sitting next to iron gates!” I saw a little bit of a window in the downpour, so I started booking it. I knew there was a sheltered Secret Service area around the corner where they park their cars. A much safer place to be.
I was sprinting on the sidewalk and spotted a bunch of Secret Service agents on their bikes riding in the opposite direction, back toward the park. I knew they wouldn’t be out on bikes in this mess without a reason. As they reached me, one agent said, “Clear the sidewalk! We’re coming through with a bunch of equipment.”
I yelled, “What’s going on?”
“Four people were just struck by lightning,” he said as he zoomed past.
I thought: “Sh*t. I have to go back.”
It was like two different parts of my brain were active at the exact same time. My subcortical brain at the level of the amygdala was like: “You just ran from there, idiot. Why are you running back?” And another part of my brain was like: “This is who you are.”
The lightning had struck one of the largest trees in the park. Four bodies splayed out in one direction from the tree. They’d been taking shelter underneath it when they were hit and were blown off to one side. By the time I got there, two Secret Service agents were on the scene doing CPR. Some bystanders had started to run over.
I did a quick round of pulse checks to see everyone’s status, and all four were apneic and pulseless. I told the two Secret Service agents to keep doing compressions on the first person. Two bystanders also began compressions on another person, an older man.
More Secret Service agents arrived, and I said, “We need to do compressions on this other person right now.” One of the agents took a moment to question who I could be and why I was there. I said, “I’m a doctor. I know I’m not dressed like one, but I’m a physician.”
I told some agents to go find an AED, because these people needed to be shocked.
After they left, I was effectively trying to triage which of these four people would get the AED first. Initially, I spent more of my time on the young man, and we began to get some response from him. I then spent some time with the young woman.
It turned out there were AEDs in the pouches on the Secret Service bikes, but they were very small, dinky AEDs. We tried to apply the pads, but it was downpouring so much that the adhesive wouldn’t stick. I told one of the agents we needed a towel.
Through all this I was concerned we were going to be struck again. I mean, the metal statue of Lafayette was right there! They say lighting doesn’t strike in the same place twice, but who knows if that’s really true?
The towel arrived, and we were able to get the chests of the younger people dry enough for the AED pads. We applied two shocks first to the woman, then the young man. We got his pulse back quickly. The woman’s came back as well, but it felt much weaker.
EMS arrived shortly thereafter. We got all four patients on the transport, and they were transferred to the hospital.
The whole experience had taken 14 minutes.
At the time, I felt confident that the young man was going to survive. We’re taught that lightning bolt strikes are survivable if you can shock someone quickly. He also got pretty good CPR. But the next day I was watching the news and learned that he had passed away. So, of course I was thinking the worst about the others as well.
But a week and a half later, I learned that the young woman had been discharged from the ICU. She was the only one who made it. Her name is Amber, and we got connected through a reporter. About 2 weeks later, I invited her to the White House. I took her to the Oval Office. I met her mom and dad and husband, and we had dinner. We’ve been in touch ever since.
I remember the first time we talked on the phone, Amber said something along the lines of, “This sucks. Obviously, I was not planning for any of this to happen. But I also think there’s something good that could come from this.”
I was so surprised and happy to hear her say that. I had something similar happen to me when I was a teenager – caught in the wrong place at the wrong time. I tried to intervene in a gang fight in my neighborhood. I thought a kid was going to get killed, so I jumped in, imagining I could save the day. I didn’t. They broke a bunch of my bones and I was in the hospital for a bit.
I remember thinking then that my life was over. But after some time, I found a new perspective, which was: Maybe that life is over. But maybe this could be the beginning of a new one. And maybe those things that I’ve been afraid of doing, the dreams that I have, maybe now I’m actually free to go after them.
I told Amber, if there are things that you have been waiting to do, this could be the time. She wants to be an international human rights activist, and she is kicking butt in a graduate school program to begin on that pathway. It’s been really cool to watch her chase this dream with way more vigor than she had before.
I think we bonded because we’ve gone through – obviously not the same thing, but a similar moment of being confronted with your own mortality. Realizing that life can just shatter. And so, while we’re here, we might as well go for it with all the force of a person who knows this could all disappear in an instant.
It was an extremely humbling moment. It reaffirmed that my life is not about me. I have to use the time that I’ve got on behalf of other people as much as I can. What is my life about if not being useful?
Dr. Martin is an emergency medicine physician and faculty member at the MGH Center for Social Justice and Health Equity at Harvard Medical School, Boston.
A version of this article first appeared on Medscape.com.
It was one of those dog days of August where the humidity is palpable and the pressure is so hot and thick you can almost feel the ions in the air. At the time (2022), I was a White House fellow and senior adviser in the West Wing Office of Public Engagement and in the Office of the Vice President.
I was leaving the White House around 7:00 p.m. through the front gate on Lafayette Square. I had a dinner reservation with a friend, so I was in a rush. It was super overcast. Lo and behold, three steps after I closed the gate behind me, it started pouring. Rain came down so hard I had to take shelter.
There’s a stone building in front of the White House with archways, so I took cover underneath one of them, hoping that in a couple of minutes the rain would pass. Behind the archways are these thick, black, iron gates.
Just as I was about to make a run for it, I heard: BOOM!
It was like a bomb had gone off. In one moment, I saw the lightning bolt, heard the thunder, and felt the heat. It was all one rush of sensation. I couldn’t remember having been that scared in a long time.
I thought, “I definitely have to get out of here. In a couple of minutes there might be another strike, and I’m sitting next to iron gates!” I saw a little bit of a window in the downpour, so I started booking it. I knew there was a sheltered Secret Service area around the corner where they park their cars. A much safer place to be.
I was sprinting on the sidewalk and spotted a bunch of Secret Service agents on their bikes riding in the opposite direction, back toward the park. I knew they wouldn’t be out on bikes in this mess without a reason. As they reached me, one agent said, “Clear the sidewalk! We’re coming through with a bunch of equipment.”
I yelled, “What’s going on?”
“Four people were just struck by lightning,” he said as he zoomed past.
I thought: “Sh*t. I have to go back.”
It was like two different parts of my brain were active at the exact same time. My subcortical brain at the level of the amygdala was like: “You just ran from there, idiot. Why are you running back?” And another part of my brain was like: “This is who you are.”
The lightning had struck one of the largest trees in the park. Four bodies splayed out in one direction from the tree. They’d been taking shelter underneath it when they were hit and were blown off to one side. By the time I got there, two Secret Service agents were on the scene doing CPR. Some bystanders had started to run over.
I did a quick round of pulse checks to see everyone’s status, and all four were apneic and pulseless. I told the two Secret Service agents to keep doing compressions on the first person. Two bystanders also began compressions on another person, an older man.
More Secret Service agents arrived, and I said, “We need to do compressions on this other person right now.” One of the agents took a moment to question who I could be and why I was there. I said, “I’m a doctor. I know I’m not dressed like one, but I’m a physician.”
I told some agents to go find an AED, because these people needed to be shocked.
After they left, I was effectively trying to triage which of these four people would get the AED first. Initially, I spent more of my time on the young man, and we began to get some response from him. I then spent some time with the young woman.
It turned out there were AEDs in the pouches on the Secret Service bikes, but they were very small, dinky AEDs. We tried to apply the pads, but it was downpouring so much that the adhesive wouldn’t stick. I told one of the agents we needed a towel.
Through all this I was concerned we were going to be struck again. I mean, the metal statue of Lafayette was right there! They say lighting doesn’t strike in the same place twice, but who knows if that’s really true?
The towel arrived, and we were able to get the chests of the younger people dry enough for the AED pads. We applied two shocks first to the woman, then the young man. We got his pulse back quickly. The woman’s came back as well, but it felt much weaker.
EMS arrived shortly thereafter. We got all four patients on the transport, and they were transferred to the hospital.
The whole experience had taken 14 minutes.
At the time, I felt confident that the young man was going to survive. We’re taught that lightning bolt strikes are survivable if you can shock someone quickly. He also got pretty good CPR. But the next day I was watching the news and learned that he had passed away. So, of course I was thinking the worst about the others as well.
But a week and a half later, I learned that the young woman had been discharged from the ICU. She was the only one who made it. Her name is Amber, and we got connected through a reporter. About 2 weeks later, I invited her to the White House. I took her to the Oval Office. I met her mom and dad and husband, and we had dinner. We’ve been in touch ever since.
I remember the first time we talked on the phone, Amber said something along the lines of, “This sucks. Obviously, I was not planning for any of this to happen. But I also think there’s something good that could come from this.”
I was so surprised and happy to hear her say that. I had something similar happen to me when I was a teenager – caught in the wrong place at the wrong time. I tried to intervene in a gang fight in my neighborhood. I thought a kid was going to get killed, so I jumped in, imagining I could save the day. I didn’t. They broke a bunch of my bones and I was in the hospital for a bit.
I remember thinking then that my life was over. But after some time, I found a new perspective, which was: Maybe that life is over. But maybe this could be the beginning of a new one. And maybe those things that I’ve been afraid of doing, the dreams that I have, maybe now I’m actually free to go after them.
I told Amber, if there are things that you have been waiting to do, this could be the time. She wants to be an international human rights activist, and she is kicking butt in a graduate school program to begin on that pathway. It’s been really cool to watch her chase this dream with way more vigor than she had before.
I think we bonded because we’ve gone through – obviously not the same thing, but a similar moment of being confronted with your own mortality. Realizing that life can just shatter. And so, while we’re here, we might as well go for it with all the force of a person who knows this could all disappear in an instant.
It was an extremely humbling moment. It reaffirmed that my life is not about me. I have to use the time that I’ve got on behalf of other people as much as I can. What is my life about if not being useful?
Dr. Martin is an emergency medicine physician and faculty member at the MGH Center for Social Justice and Health Equity at Harvard Medical School, Boston.
A version of this article first appeared on Medscape.com.
AHA statement addresses equity in cardio-oncology care
A new scientific statement from the American Heart Association focuses on equity in cardio-oncology care and research.
A “growing body of evidence” suggests that women and people from underrepresented patient groups experience disproportionately higher cardiovascular effects from new and emerging anticancer therapies, the writing group, led by Daniel Addison, MD, with the Ohio State University, Columbus, pointed out.
For example, women appear to be at higher risk of immune checkpoint inhibitor–related toxicities, whereas Black patients with cancer face up to a threefold higher risk of cardiotoxicity with anticancer therapies.
With reduced screening and delayed preventive measures, Hispanic patients have more complex heart disease, cancer is diagnosed at later stages, and they receive more cardiotoxic regimens because of a lack of eligibility for novel treatments. Ultimately, this contributes to a higher incidence of treatment complications, cardiac dysfunction, and adverse patient outcomes for this patient group, they write.
Although no studies have specifically addressed cardio-oncology disparities in the LGBTQIA+ population, such disparities can be inferred from known cardiovascular disease and oncology disparities, the writing group noted.
These disparities are supported by “disparately high” risk of death after a cancer diagnosis among women and individuals from underrepresented groups, even after accounting for socioeconomic and behavioral patterns, they pointed out.
The scientific statement was published online in Circulation.
Evidence gaps and the path forward
“Despite advances in strategies to limit the risks of cardiovascular events among cancer survivors, relatively limited guidance is available to address the rapidly growing problem of disparate cardiotoxic risks among women and underrepresented patient populations,” the writing group said.
Decentralized and sporadic evaluations have led to a lack of consensus on the definitions, investigations, and potential optimal strategies to address disparate cardiotoxicity with contemporary cancer immunotherapy, as well as biologic and cytotoxic therapies, they noted.
They said caution is needed when interpreting clinical trial data about cardiotoxicity and in generalizing the results because people from diverse racial and ethnic groups have not been well represented in many trials.
The writing group outlined key evidence gaps and future research directions for addressing cardio-oncology disparities, as well as strategies to improve equity in cardio-oncology care and research.
These include the following:
- Identifying specific predictive factors of long-term cardiotoxic risk with targeted and immune-based cancer therapies in women and underrepresented populations.
- Investigating biological mechanisms that may underlie differences in cardiotoxicities between different patient groups.
- Developing personalized cardioprotection strategies that integrate biological, genetic, and social determinant markers.
- Intentionally diversifying clinical trials and identifying optimal strategies to improve representation in cancer clinical trials.
- Determining the role of technology, such as artificial intelligence, in improving cardiotoxicity disparities.
“Conscientiously leveraging technology and designing trials with outcomes related to these issues in practice (considering feasibility and cost) will critically accelerate the field of cardio-oncology in the 21st century. With tangible goals, we can improve health inequities in cardio-oncology,” the writing group said.
The research had no commercial funding. No conflicts of interest were reported.
A version of this article originally appeared on Medscape.com.
A new scientific statement from the American Heart Association focuses on equity in cardio-oncology care and research.
A “growing body of evidence” suggests that women and people from underrepresented patient groups experience disproportionately higher cardiovascular effects from new and emerging anticancer therapies, the writing group, led by Daniel Addison, MD, with the Ohio State University, Columbus, pointed out.
For example, women appear to be at higher risk of immune checkpoint inhibitor–related toxicities, whereas Black patients with cancer face up to a threefold higher risk of cardiotoxicity with anticancer therapies.
With reduced screening and delayed preventive measures, Hispanic patients have more complex heart disease, cancer is diagnosed at later stages, and they receive more cardiotoxic regimens because of a lack of eligibility for novel treatments. Ultimately, this contributes to a higher incidence of treatment complications, cardiac dysfunction, and adverse patient outcomes for this patient group, they write.
Although no studies have specifically addressed cardio-oncology disparities in the LGBTQIA+ population, such disparities can be inferred from known cardiovascular disease and oncology disparities, the writing group noted.
These disparities are supported by “disparately high” risk of death after a cancer diagnosis among women and individuals from underrepresented groups, even after accounting for socioeconomic and behavioral patterns, they pointed out.
The scientific statement was published online in Circulation.
Evidence gaps and the path forward
“Despite advances in strategies to limit the risks of cardiovascular events among cancer survivors, relatively limited guidance is available to address the rapidly growing problem of disparate cardiotoxic risks among women and underrepresented patient populations,” the writing group said.
Decentralized and sporadic evaluations have led to a lack of consensus on the definitions, investigations, and potential optimal strategies to address disparate cardiotoxicity with contemporary cancer immunotherapy, as well as biologic and cytotoxic therapies, they noted.
They said caution is needed when interpreting clinical trial data about cardiotoxicity and in generalizing the results because people from diverse racial and ethnic groups have not been well represented in many trials.
The writing group outlined key evidence gaps and future research directions for addressing cardio-oncology disparities, as well as strategies to improve equity in cardio-oncology care and research.
These include the following:
- Identifying specific predictive factors of long-term cardiotoxic risk with targeted and immune-based cancer therapies in women and underrepresented populations.
- Investigating biological mechanisms that may underlie differences in cardiotoxicities between different patient groups.
- Developing personalized cardioprotection strategies that integrate biological, genetic, and social determinant markers.
- Intentionally diversifying clinical trials and identifying optimal strategies to improve representation in cancer clinical trials.
- Determining the role of technology, such as artificial intelligence, in improving cardiotoxicity disparities.
“Conscientiously leveraging technology and designing trials with outcomes related to these issues in practice (considering feasibility and cost) will critically accelerate the field of cardio-oncology in the 21st century. With tangible goals, we can improve health inequities in cardio-oncology,” the writing group said.
The research had no commercial funding. No conflicts of interest were reported.
A version of this article originally appeared on Medscape.com.
A new scientific statement from the American Heart Association focuses on equity in cardio-oncology care and research.
A “growing body of evidence” suggests that women and people from underrepresented patient groups experience disproportionately higher cardiovascular effects from new and emerging anticancer therapies, the writing group, led by Daniel Addison, MD, with the Ohio State University, Columbus, pointed out.
For example, women appear to be at higher risk of immune checkpoint inhibitor–related toxicities, whereas Black patients with cancer face up to a threefold higher risk of cardiotoxicity with anticancer therapies.
With reduced screening and delayed preventive measures, Hispanic patients have more complex heart disease, cancer is diagnosed at later stages, and they receive more cardiotoxic regimens because of a lack of eligibility for novel treatments. Ultimately, this contributes to a higher incidence of treatment complications, cardiac dysfunction, and adverse patient outcomes for this patient group, they write.
Although no studies have specifically addressed cardio-oncology disparities in the LGBTQIA+ population, such disparities can be inferred from known cardiovascular disease and oncology disparities, the writing group noted.
These disparities are supported by “disparately high” risk of death after a cancer diagnosis among women and individuals from underrepresented groups, even after accounting for socioeconomic and behavioral patterns, they pointed out.
The scientific statement was published online in Circulation.
Evidence gaps and the path forward
“Despite advances in strategies to limit the risks of cardiovascular events among cancer survivors, relatively limited guidance is available to address the rapidly growing problem of disparate cardiotoxic risks among women and underrepresented patient populations,” the writing group said.
Decentralized and sporadic evaluations have led to a lack of consensus on the definitions, investigations, and potential optimal strategies to address disparate cardiotoxicity with contemporary cancer immunotherapy, as well as biologic and cytotoxic therapies, they noted.
They said caution is needed when interpreting clinical trial data about cardiotoxicity and in generalizing the results because people from diverse racial and ethnic groups have not been well represented in many trials.
The writing group outlined key evidence gaps and future research directions for addressing cardio-oncology disparities, as well as strategies to improve equity in cardio-oncology care and research.
These include the following:
- Identifying specific predictive factors of long-term cardiotoxic risk with targeted and immune-based cancer therapies in women and underrepresented populations.
- Investigating biological mechanisms that may underlie differences in cardiotoxicities between different patient groups.
- Developing personalized cardioprotection strategies that integrate biological, genetic, and social determinant markers.
- Intentionally diversifying clinical trials and identifying optimal strategies to improve representation in cancer clinical trials.
- Determining the role of technology, such as artificial intelligence, in improving cardiotoxicity disparities.
“Conscientiously leveraging technology and designing trials with outcomes related to these issues in practice (considering feasibility and cost) will critically accelerate the field of cardio-oncology in the 21st century. With tangible goals, we can improve health inequities in cardio-oncology,” the writing group said.
The research had no commercial funding. No conflicts of interest were reported.
A version of this article originally appeared on Medscape.com.
FROM CIRCULATION
Upping CO2 does not benefit OHCA patients: TAME
The Targeted Therapeutic Mild Hypercapnia After Resuscitated Cardiac Arrest (TAME) study showed that the intervention failed to improve neurologic or functional outcomes or quality of life at 6 months. However, the researchers also found that slightly elevated CO2 levels were not associated with worse outcomes.
“I think these results show that our hypothesis – that raising CO2 levels as applied in this trial may be beneficial for these patients – was not effective, even though previous work suggested that it would be,” co–lead investigator Alistair Nichol, MD, said in an interview.
“This was a rigorous trial; the intervention was well delivered, and the results are pretty clear. Unfortunately, we have proved a null hypothesis – that this approach doesn’t seem to work,” Dr. Nichol, who is professor of critical care medicine at University College Dublin, said.
“However, we did find that hypercapnia was safe. This is an important finding, as sometimes in very sick patients such as those who develop pneumonia, we have to drive the ventilator less hard to minimize injury to the lungs, and this can lead to higher CO2 levels,” he added. “Our results show that this practice should not be harmful, which is reassuring.”
The TAME study was presented at the Critical Care Reviews 2023 Meeting (CCR23) held in Belfast, Northern Ireland.
It was simultaneously published online in the New England Journal of Medicine.
The researchers explain that after the return of spontaneous circulation, brain hypoperfusion may contribute to cerebral hypoxia, exacerbate brain damage, and lead to poor neurologic outcomes. The partial pressure of arterial carbon dioxide (PaCO2) is the major physiologic regulator of cerebrovascular tone, and increasing CO2 levels increases cerebral blood flow.
Two previous observational studies showed that exposure to hypercapnia was associated with an increase in the likelihood of being discharged home and better neurologic outcomes at 12 months, compared with hypocapnia or normocapnia.
In addition, a physiologic study showed that deliberate increases in PaCO2 induced higher cerebral oxygen saturations, compared with normocapnia. A phase 2 randomized trial showed that hypercapnia significantly attenuated the release of neuron-specific enolase, a biomarker of brain injury, and also suggested better 6-month neurologic recovery with hypercapnia compared with normocapnia.
The current TAME trial was conducted to try to confirm these results in a larger, more definitive study.
For the trial, 1,700 adults with coma who had been resuscitated after out-of-hospital cardiac arrest were randomly assigned to receive either 24 hours of mild hypercapnia (target PaCO2, 50-55 mm Hg) or normocapnia (target PaCO2, 35-45 mm Hg).
The primary outcome – a favorable neurologic outcome, defined as a score of 5 or higher on the Glasgow Outcome Scale–Extended at 6 months – occurred in 43.5% in the mild hypercapnia group and in 44.6% in the normocapnia group (relative risk, 0.98; P = .76).
By 6 months, 48.2% of those in the mild hypercapnia group and 45.9% in the normocapnia group had died (relative risk with mild hypercapnia, 1.05; 95% confidence interval, 0.94-1.16). In the mild hypercapnia group, 53.4% had a poor functional outcome, defined as a Modified Rankin Scale score of 4-6, compared with 51.3% in the normocapnia group.
Health-related quality of life, as assessed by the EQ Visual Analogue Scale component of the EuroQol-5D-5L, was similar in the two groups.
In terms of safety, results showed that mild hypercapnia did not increase the incidence of prespecified adverse events.
The authors note that there is concern that mild hypercapnia may worsen cerebral edema and elevate intracranial pressure; however, elevated intracranial pressure is uncommon in the first 72 hours after the return of spontaneous circulation.
In the TAME trial, there was one case of cerebral edema in the hypercapnia group. “This is a very low rate and would be expected in a group this size, so this does not indicate a safety concern,” Dr. Nichol commented.
The researchers are planning further analyses of biological samples to look for possible prognostic markers.
“These out-of-hospital cardiac arrest patients are a very diverse group, and it may be possible that some patients could have benefited from hypercapnia while others may have been harmed,” Dr. Nichol noted.
“Raising CO2 levels does improve overall delivery of oxygen to the brain, but this might not have occurred in the right areas. It may be possible that some patients benefited, and analysis of biological samples will help us look more closely at this.”
He added that other ongoing trials are investigating hypercapnia in patients with traumatic brain injury.
“These patients are managed differently and often have probes in their brain to measure the response to CO2, so more of a precision medicine approach is possible,” he explained.
He also noted that the TAME study, which was conducted in conjunction with the TTM-2 study investigating hypothermia in out-of-hospital cardiac arrest patients, has established a network of ICU teams around the world, providing an infrastructure for further trials to be performed in this patient population in the future.
The TAME trial was funded by the National Health and Medical Research Council of Australia, the Health Research Board of Ireland, and the Health Research Council of New Zealand.
A version of this article originally appeared on Medscape.com.
The Targeted Therapeutic Mild Hypercapnia After Resuscitated Cardiac Arrest (TAME) study showed that the intervention failed to improve neurologic or functional outcomes or quality of life at 6 months. However, the researchers also found that slightly elevated CO2 levels were not associated with worse outcomes.
“I think these results show that our hypothesis – that raising CO2 levels as applied in this trial may be beneficial for these patients – was not effective, even though previous work suggested that it would be,” co–lead investigator Alistair Nichol, MD, said in an interview.
“This was a rigorous trial; the intervention was well delivered, and the results are pretty clear. Unfortunately, we have proved a null hypothesis – that this approach doesn’t seem to work,” Dr. Nichol, who is professor of critical care medicine at University College Dublin, said.
“However, we did find that hypercapnia was safe. This is an important finding, as sometimes in very sick patients such as those who develop pneumonia, we have to drive the ventilator less hard to minimize injury to the lungs, and this can lead to higher CO2 levels,” he added. “Our results show that this practice should not be harmful, which is reassuring.”
The TAME study was presented at the Critical Care Reviews 2023 Meeting (CCR23) held in Belfast, Northern Ireland.
It was simultaneously published online in the New England Journal of Medicine.
The researchers explain that after the return of spontaneous circulation, brain hypoperfusion may contribute to cerebral hypoxia, exacerbate brain damage, and lead to poor neurologic outcomes. The partial pressure of arterial carbon dioxide (PaCO2) is the major physiologic regulator of cerebrovascular tone, and increasing CO2 levels increases cerebral blood flow.
Two previous observational studies showed that exposure to hypercapnia was associated with an increase in the likelihood of being discharged home and better neurologic outcomes at 12 months, compared with hypocapnia or normocapnia.
In addition, a physiologic study showed that deliberate increases in PaCO2 induced higher cerebral oxygen saturations, compared with normocapnia. A phase 2 randomized trial showed that hypercapnia significantly attenuated the release of neuron-specific enolase, a biomarker of brain injury, and also suggested better 6-month neurologic recovery with hypercapnia compared with normocapnia.
The current TAME trial was conducted to try to confirm these results in a larger, more definitive study.
For the trial, 1,700 adults with coma who had been resuscitated after out-of-hospital cardiac arrest were randomly assigned to receive either 24 hours of mild hypercapnia (target PaCO2, 50-55 mm Hg) or normocapnia (target PaCO2, 35-45 mm Hg).
The primary outcome – a favorable neurologic outcome, defined as a score of 5 or higher on the Glasgow Outcome Scale–Extended at 6 months – occurred in 43.5% in the mild hypercapnia group and in 44.6% in the normocapnia group (relative risk, 0.98; P = .76).
By 6 months, 48.2% of those in the mild hypercapnia group and 45.9% in the normocapnia group had died (relative risk with mild hypercapnia, 1.05; 95% confidence interval, 0.94-1.16). In the mild hypercapnia group, 53.4% had a poor functional outcome, defined as a Modified Rankin Scale score of 4-6, compared with 51.3% in the normocapnia group.
Health-related quality of life, as assessed by the EQ Visual Analogue Scale component of the EuroQol-5D-5L, was similar in the two groups.
In terms of safety, results showed that mild hypercapnia did not increase the incidence of prespecified adverse events.
The authors note that there is concern that mild hypercapnia may worsen cerebral edema and elevate intracranial pressure; however, elevated intracranial pressure is uncommon in the first 72 hours after the return of spontaneous circulation.
In the TAME trial, there was one case of cerebral edema in the hypercapnia group. “This is a very low rate and would be expected in a group this size, so this does not indicate a safety concern,” Dr. Nichol commented.
The researchers are planning further analyses of biological samples to look for possible prognostic markers.
“These out-of-hospital cardiac arrest patients are a very diverse group, and it may be possible that some patients could have benefited from hypercapnia while others may have been harmed,” Dr. Nichol noted.
“Raising CO2 levels does improve overall delivery of oxygen to the brain, but this might not have occurred in the right areas. It may be possible that some patients benefited, and analysis of biological samples will help us look more closely at this.”
He added that other ongoing trials are investigating hypercapnia in patients with traumatic brain injury.
“These patients are managed differently and often have probes in their brain to measure the response to CO2, so more of a precision medicine approach is possible,” he explained.
He also noted that the TAME study, which was conducted in conjunction with the TTM-2 study investigating hypothermia in out-of-hospital cardiac arrest patients, has established a network of ICU teams around the world, providing an infrastructure for further trials to be performed in this patient population in the future.
The TAME trial was funded by the National Health and Medical Research Council of Australia, the Health Research Board of Ireland, and the Health Research Council of New Zealand.
A version of this article originally appeared on Medscape.com.
The Targeted Therapeutic Mild Hypercapnia After Resuscitated Cardiac Arrest (TAME) study showed that the intervention failed to improve neurologic or functional outcomes or quality of life at 6 months. However, the researchers also found that slightly elevated CO2 levels were not associated with worse outcomes.
“I think these results show that our hypothesis – that raising CO2 levels as applied in this trial may be beneficial for these patients – was not effective, even though previous work suggested that it would be,” co–lead investigator Alistair Nichol, MD, said in an interview.
“This was a rigorous trial; the intervention was well delivered, and the results are pretty clear. Unfortunately, we have proved a null hypothesis – that this approach doesn’t seem to work,” Dr. Nichol, who is professor of critical care medicine at University College Dublin, said.
“However, we did find that hypercapnia was safe. This is an important finding, as sometimes in very sick patients such as those who develop pneumonia, we have to drive the ventilator less hard to minimize injury to the lungs, and this can lead to higher CO2 levels,” he added. “Our results show that this practice should not be harmful, which is reassuring.”
The TAME study was presented at the Critical Care Reviews 2023 Meeting (CCR23) held in Belfast, Northern Ireland.
It was simultaneously published online in the New England Journal of Medicine.
The researchers explain that after the return of spontaneous circulation, brain hypoperfusion may contribute to cerebral hypoxia, exacerbate brain damage, and lead to poor neurologic outcomes. The partial pressure of arterial carbon dioxide (PaCO2) is the major physiologic regulator of cerebrovascular tone, and increasing CO2 levels increases cerebral blood flow.
Two previous observational studies showed that exposure to hypercapnia was associated with an increase in the likelihood of being discharged home and better neurologic outcomes at 12 months, compared with hypocapnia or normocapnia.
In addition, a physiologic study showed that deliberate increases in PaCO2 induced higher cerebral oxygen saturations, compared with normocapnia. A phase 2 randomized trial showed that hypercapnia significantly attenuated the release of neuron-specific enolase, a biomarker of brain injury, and also suggested better 6-month neurologic recovery with hypercapnia compared with normocapnia.
The current TAME trial was conducted to try to confirm these results in a larger, more definitive study.
For the trial, 1,700 adults with coma who had been resuscitated after out-of-hospital cardiac arrest were randomly assigned to receive either 24 hours of mild hypercapnia (target PaCO2, 50-55 mm Hg) or normocapnia (target PaCO2, 35-45 mm Hg).
The primary outcome – a favorable neurologic outcome, defined as a score of 5 or higher on the Glasgow Outcome Scale–Extended at 6 months – occurred in 43.5% in the mild hypercapnia group and in 44.6% in the normocapnia group (relative risk, 0.98; P = .76).
By 6 months, 48.2% of those in the mild hypercapnia group and 45.9% in the normocapnia group had died (relative risk with mild hypercapnia, 1.05; 95% confidence interval, 0.94-1.16). In the mild hypercapnia group, 53.4% had a poor functional outcome, defined as a Modified Rankin Scale score of 4-6, compared with 51.3% in the normocapnia group.
Health-related quality of life, as assessed by the EQ Visual Analogue Scale component of the EuroQol-5D-5L, was similar in the two groups.
In terms of safety, results showed that mild hypercapnia did not increase the incidence of prespecified adverse events.
The authors note that there is concern that mild hypercapnia may worsen cerebral edema and elevate intracranial pressure; however, elevated intracranial pressure is uncommon in the first 72 hours after the return of spontaneous circulation.
In the TAME trial, there was one case of cerebral edema in the hypercapnia group. “This is a very low rate and would be expected in a group this size, so this does not indicate a safety concern,” Dr. Nichol commented.
The researchers are planning further analyses of biological samples to look for possible prognostic markers.
“These out-of-hospital cardiac arrest patients are a very diverse group, and it may be possible that some patients could have benefited from hypercapnia while others may have been harmed,” Dr. Nichol noted.
“Raising CO2 levels does improve overall delivery of oxygen to the brain, but this might not have occurred in the right areas. It may be possible that some patients benefited, and analysis of biological samples will help us look more closely at this.”
He added that other ongoing trials are investigating hypercapnia in patients with traumatic brain injury.
“These patients are managed differently and often have probes in their brain to measure the response to CO2, so more of a precision medicine approach is possible,” he explained.
He also noted that the TAME study, which was conducted in conjunction with the TTM-2 study investigating hypothermia in out-of-hospital cardiac arrest patients, has established a network of ICU teams around the world, providing an infrastructure for further trials to be performed in this patient population in the future.
The TAME trial was funded by the National Health and Medical Research Council of Australia, the Health Research Board of Ireland, and the Health Research Council of New Zealand.
A version of this article originally appeared on Medscape.com.
FROM CCR23
Guide explains nonsurgical management of major hemorrhage
A new guide offers recommendations for the nonsurgical management of major hemorrhage, which is a challenging clinical problem.
Major hemorrhage is a significant cause of death and can occur in a myriad of clinical settings.
“In Ontario, we’ve been collecting quality metrics on major hemorrhages to try and make sure that a higher percentage of patients gets the best possible care when they are experiencing significant bleeding,” author Jeannie Callum, MD, professor and director of transfusion medicine at Kingston (Ont.) Health Sciences Centre and Queen’s University, also in Kingston, said in an interview. “There were some gaps, so this is our effort to get open, clear information out to the emergency doctors, intensive care unit doctors, the surgeons, and everyone else involved in managing major hemorrhage, to help close these gaps.”
The guide was published in the Canadian Medical Association Journal.
Fast care essential
The guide aims to provide answers, based on the latest research, to questions such as when to activate a massive hemorrhage protocol (MHP), which patients should receive tranexamic acid (TXA), which blood products should be transfused before laboratory results are available, how to monitor the effects of blood transfusion, and when fibrinogen concentrate or prothrombin complex concentrate should be given.
Not all recommendations will be followed, Dr. Callum said, especially in rural hospitals with limited resources. But the guide is adaptable, and rural hospitals can create protocols that are customized to their unique circumstances.
Care must be “perfect and fast” in the first hour of major injury, said Dr. Callum. “You need to get a proclotting drug in that first hour if you have a traumatic or postpartum bleed. You have to make sure your clotting factors never fail you throughout your resuscitation. You have to be fast with the transfusion. You have to monitor for the complications of the transfusion, electrolyte disturbances, and the patient’s temperature dropping. It’s a complicated situation that needs a multidisciplinary team.”
Bleeding affects everybody in medicine, from family doctors in smaller institutions who work in emergency departments to obstetricians and surgeons, she added.
“For people under the age of 45, trauma is the most common cause of death. When people die of trauma, they die of bleeding. So many people experience these extreme bleeds. We believe that some of them might be preventable with faster, more standardized, more aggressive care. That’s why we wrote this review,” said Dr. Callum.
Administer TXA quickly
The first recommendation is to ensure that every hospital has a massive hemorrhage protocol. Such a protocol is vital for the emergency department, operating room, and obstetric unit. “Making sure you’ve got a protocol that is updated every 3 years and adjusted to the local hospital context is essential,” said Dr. Callum.
Smaller hospitals will have to adjust their protocols according to the capabilities of their sites. “Some smaller hospitals do not have platelets in stock and get their platelets from another hospital, so you need to adjust your protocol to what you are able to do. Not every hospital can control bleeding in a trauma patient, so your protocol would be to stabilize and call a helicopter. Make sure all of this is detailed so that implementing it becomes automatic,” said Dr. Callum.
An MHP should be activated for patients with uncontrolled hemorrhage who meet the clinical criteria of the local hospital and are expected to need blood product support and red blood cells.
“Lots of people bleed, but not everybody is bleeding enough that they need a code transfusion,” said Dr. Callum. Most patients with gastrointestinal bleeds caused by NSAID use can be managed with uncrossed matched blood from the local blood bank. “But in patients who need the full code transfusion because they are going to need plasma, clotting factor replacement, and many other drugs, that is when the MHP should be activated. Don’t activate it when you don’t need it, because doing so activates the whole hospital and diverts care away from other patients.”
TXA should be administered as soon as possible after onset of hemorrhage in most patients, with the exception of gastrointestinal hemorrhage, where a benefit has not been shown.
TXA has been a major advance in treating massive bleeding, Dr. Callum said. “TXA was invented by a Japanese husband-and-wife research team. We know that it reduces the death rate in trauma and in postpartum hemorrhage, and it reduces the chance of major bleeding with major surgical procedures. We give it routinely in surgical procedures. If a patient gets TXA within 60 minutes of injury, it dramatically reduces the death rate. And it costs $10 per patient. It’s cheap, it’s easy, it has no side effects. It’s just amazing.”
Future research must address several unanswered questions, said Dr. Callum. These questions include whether prehospital transfusion improves patient outcomes, whether whole blood has a role in the early management of major hemorrhage, and what role factor concentrates play in patients with major bleeding.
‘Optimal recommendations’
Commenting on the document, Bourke Tillmann, MD, PhD, trauma team leader at Sunnybrook Health Sciences Centre and the Ross Tilley Burn Center in Toronto, said: “Overall, I think it is a good overview of MHPs as an approach to major hemorrhage.”
The review also is timely, since Ontario released its MHP guidelines in 2021, he added. “I would have liked to see more about the treatment aspects than just an overview of an MHP. But if you are the person overseeing the emergency department or running the blood bank, these protocols are incredibly useful and incredibly important.”
“This report is a nice and thoughtful overview of best practices in many areas, especially trauma, and makes recommendations that are optimal, although they are not necessarily practical in all centers,” Eric L. Legome, MD, professor and chair of emergency medicine at Mount Sinai West and Mount Sinai Morningside, New York, said in an interview.
“If you’re in a small rural hospital with one lab technician, trying to do all of these things, it will not be possible. These are optimal recommendations that people can use to the best of their ability, but they are not standard of care, because some places will not be able to provide this level of care,” he added. “This paper provides practical, reasonable advice that should be looked at as you are trying to implement transfusion policies and processes, with the understanding that it is not necessarily applicable or practical for very small hospitals in very rural centers that might not have access to these types of products and tools, but it’s a reasonable and nicely written paper.”
No outside funding for the guideline was reported. Dr. Callum has received research funding from Canadian Blood Services and Octapharma. She sits on the nominating committee with the Association for the Advancement of Blood & Biotherapies and on the data safety monitoring boards for the Tranexamic Acid for Subdural Hematoma trial and the Fibrinogen Replacement in Trauma trial. Dr. Tillmann and Dr. Legome reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
A new guide offers recommendations for the nonsurgical management of major hemorrhage, which is a challenging clinical problem.
Major hemorrhage is a significant cause of death and can occur in a myriad of clinical settings.
“In Ontario, we’ve been collecting quality metrics on major hemorrhages to try and make sure that a higher percentage of patients gets the best possible care when they are experiencing significant bleeding,” author Jeannie Callum, MD, professor and director of transfusion medicine at Kingston (Ont.) Health Sciences Centre and Queen’s University, also in Kingston, said in an interview. “There were some gaps, so this is our effort to get open, clear information out to the emergency doctors, intensive care unit doctors, the surgeons, and everyone else involved in managing major hemorrhage, to help close these gaps.”
The guide was published in the Canadian Medical Association Journal.
Fast care essential
The guide aims to provide answers, based on the latest research, to questions such as when to activate a massive hemorrhage protocol (MHP), which patients should receive tranexamic acid (TXA), which blood products should be transfused before laboratory results are available, how to monitor the effects of blood transfusion, and when fibrinogen concentrate or prothrombin complex concentrate should be given.
Not all recommendations will be followed, Dr. Callum said, especially in rural hospitals with limited resources. But the guide is adaptable, and rural hospitals can create protocols that are customized to their unique circumstances.
Care must be “perfect and fast” in the first hour of major injury, said Dr. Callum. “You need to get a proclotting drug in that first hour if you have a traumatic or postpartum bleed. You have to make sure your clotting factors never fail you throughout your resuscitation. You have to be fast with the transfusion. You have to monitor for the complications of the transfusion, electrolyte disturbances, and the patient’s temperature dropping. It’s a complicated situation that needs a multidisciplinary team.”
Bleeding affects everybody in medicine, from family doctors in smaller institutions who work in emergency departments to obstetricians and surgeons, she added.
“For people under the age of 45, trauma is the most common cause of death. When people die of trauma, they die of bleeding. So many people experience these extreme bleeds. We believe that some of them might be preventable with faster, more standardized, more aggressive care. That’s why we wrote this review,” said Dr. Callum.
Administer TXA quickly
The first recommendation is to ensure that every hospital has a massive hemorrhage protocol. Such a protocol is vital for the emergency department, operating room, and obstetric unit. “Making sure you’ve got a protocol that is updated every 3 years and adjusted to the local hospital context is essential,” said Dr. Callum.
Smaller hospitals will have to adjust their protocols according to the capabilities of their sites. “Some smaller hospitals do not have platelets in stock and get their platelets from another hospital, so you need to adjust your protocol to what you are able to do. Not every hospital can control bleeding in a trauma patient, so your protocol would be to stabilize and call a helicopter. Make sure all of this is detailed so that implementing it becomes automatic,” said Dr. Callum.
An MHP should be activated for patients with uncontrolled hemorrhage who meet the clinical criteria of the local hospital and are expected to need blood product support and red blood cells.
“Lots of people bleed, but not everybody is bleeding enough that they need a code transfusion,” said Dr. Callum. Most patients with gastrointestinal bleeds caused by NSAID use can be managed with uncrossed matched blood from the local blood bank. “But in patients who need the full code transfusion because they are going to need plasma, clotting factor replacement, and many other drugs, that is when the MHP should be activated. Don’t activate it when you don’t need it, because doing so activates the whole hospital and diverts care away from other patients.”
TXA should be administered as soon as possible after onset of hemorrhage in most patients, with the exception of gastrointestinal hemorrhage, where a benefit has not been shown.
TXA has been a major advance in treating massive bleeding, Dr. Callum said. “TXA was invented by a Japanese husband-and-wife research team. We know that it reduces the death rate in trauma and in postpartum hemorrhage, and it reduces the chance of major bleeding with major surgical procedures. We give it routinely in surgical procedures. If a patient gets TXA within 60 minutes of injury, it dramatically reduces the death rate. And it costs $10 per patient. It’s cheap, it’s easy, it has no side effects. It’s just amazing.”
Future research must address several unanswered questions, said Dr. Callum. These questions include whether prehospital transfusion improves patient outcomes, whether whole blood has a role in the early management of major hemorrhage, and what role factor concentrates play in patients with major bleeding.
‘Optimal recommendations’
Commenting on the document, Bourke Tillmann, MD, PhD, trauma team leader at Sunnybrook Health Sciences Centre and the Ross Tilley Burn Center in Toronto, said: “Overall, I think it is a good overview of MHPs as an approach to major hemorrhage.”
The review also is timely, since Ontario released its MHP guidelines in 2021, he added. “I would have liked to see more about the treatment aspects than just an overview of an MHP. But if you are the person overseeing the emergency department or running the blood bank, these protocols are incredibly useful and incredibly important.”
“This report is a nice and thoughtful overview of best practices in many areas, especially trauma, and makes recommendations that are optimal, although they are not necessarily practical in all centers,” Eric L. Legome, MD, professor and chair of emergency medicine at Mount Sinai West and Mount Sinai Morningside, New York, said in an interview.
“If you’re in a small rural hospital with one lab technician, trying to do all of these things, it will not be possible. These are optimal recommendations that people can use to the best of their ability, but they are not standard of care, because some places will not be able to provide this level of care,” he added. “This paper provides practical, reasonable advice that should be looked at as you are trying to implement transfusion policies and processes, with the understanding that it is not necessarily applicable or practical for very small hospitals in very rural centers that might not have access to these types of products and tools, but it’s a reasonable and nicely written paper.”
No outside funding for the guideline was reported. Dr. Callum has received research funding from Canadian Blood Services and Octapharma. She sits on the nominating committee with the Association for the Advancement of Blood & Biotherapies and on the data safety monitoring boards for the Tranexamic Acid for Subdural Hematoma trial and the Fibrinogen Replacement in Trauma trial. Dr. Tillmann and Dr. Legome reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
A new guide offers recommendations for the nonsurgical management of major hemorrhage, which is a challenging clinical problem.
Major hemorrhage is a significant cause of death and can occur in a myriad of clinical settings.
“In Ontario, we’ve been collecting quality metrics on major hemorrhages to try and make sure that a higher percentage of patients gets the best possible care when they are experiencing significant bleeding,” author Jeannie Callum, MD, professor and director of transfusion medicine at Kingston (Ont.) Health Sciences Centre and Queen’s University, also in Kingston, said in an interview. “There were some gaps, so this is our effort to get open, clear information out to the emergency doctors, intensive care unit doctors, the surgeons, and everyone else involved in managing major hemorrhage, to help close these gaps.”
The guide was published in the Canadian Medical Association Journal.
Fast care essential
The guide aims to provide answers, based on the latest research, to questions such as when to activate a massive hemorrhage protocol (MHP), which patients should receive tranexamic acid (TXA), which blood products should be transfused before laboratory results are available, how to monitor the effects of blood transfusion, and when fibrinogen concentrate or prothrombin complex concentrate should be given.
Not all recommendations will be followed, Dr. Callum said, especially in rural hospitals with limited resources. But the guide is adaptable, and rural hospitals can create protocols that are customized to their unique circumstances.
Care must be “perfect and fast” in the first hour of major injury, said Dr. Callum. “You need to get a proclotting drug in that first hour if you have a traumatic or postpartum bleed. You have to make sure your clotting factors never fail you throughout your resuscitation. You have to be fast with the transfusion. You have to monitor for the complications of the transfusion, electrolyte disturbances, and the patient’s temperature dropping. It’s a complicated situation that needs a multidisciplinary team.”
Bleeding affects everybody in medicine, from family doctors in smaller institutions who work in emergency departments to obstetricians and surgeons, she added.
“For people under the age of 45, trauma is the most common cause of death. When people die of trauma, they die of bleeding. So many people experience these extreme bleeds. We believe that some of them might be preventable with faster, more standardized, more aggressive care. That’s why we wrote this review,” said Dr. Callum.
Administer TXA quickly
The first recommendation is to ensure that every hospital has a massive hemorrhage protocol. Such a protocol is vital for the emergency department, operating room, and obstetric unit. “Making sure you’ve got a protocol that is updated every 3 years and adjusted to the local hospital context is essential,” said Dr. Callum.
Smaller hospitals will have to adjust their protocols according to the capabilities of their sites. “Some smaller hospitals do not have platelets in stock and get their platelets from another hospital, so you need to adjust your protocol to what you are able to do. Not every hospital can control bleeding in a trauma patient, so your protocol would be to stabilize and call a helicopter. Make sure all of this is detailed so that implementing it becomes automatic,” said Dr. Callum.
An MHP should be activated for patients with uncontrolled hemorrhage who meet the clinical criteria of the local hospital and are expected to need blood product support and red blood cells.
“Lots of people bleed, but not everybody is bleeding enough that they need a code transfusion,” said Dr. Callum. Most patients with gastrointestinal bleeds caused by NSAID use can be managed with uncrossed matched blood from the local blood bank. “But in patients who need the full code transfusion because they are going to need plasma, clotting factor replacement, and many other drugs, that is when the MHP should be activated. Don’t activate it when you don’t need it, because doing so activates the whole hospital and diverts care away from other patients.”
TXA should be administered as soon as possible after onset of hemorrhage in most patients, with the exception of gastrointestinal hemorrhage, where a benefit has not been shown.
TXA has been a major advance in treating massive bleeding, Dr. Callum said. “TXA was invented by a Japanese husband-and-wife research team. We know that it reduces the death rate in trauma and in postpartum hemorrhage, and it reduces the chance of major bleeding with major surgical procedures. We give it routinely in surgical procedures. If a patient gets TXA within 60 minutes of injury, it dramatically reduces the death rate. And it costs $10 per patient. It’s cheap, it’s easy, it has no side effects. It’s just amazing.”
Future research must address several unanswered questions, said Dr. Callum. These questions include whether prehospital transfusion improves patient outcomes, whether whole blood has a role in the early management of major hemorrhage, and what role factor concentrates play in patients with major bleeding.
‘Optimal recommendations’
Commenting on the document, Bourke Tillmann, MD, PhD, trauma team leader at Sunnybrook Health Sciences Centre and the Ross Tilley Burn Center in Toronto, said: “Overall, I think it is a good overview of MHPs as an approach to major hemorrhage.”
The review also is timely, since Ontario released its MHP guidelines in 2021, he added. “I would have liked to see more about the treatment aspects than just an overview of an MHP. But if you are the person overseeing the emergency department or running the blood bank, these protocols are incredibly useful and incredibly important.”
“This report is a nice and thoughtful overview of best practices in many areas, especially trauma, and makes recommendations that are optimal, although they are not necessarily practical in all centers,” Eric L. Legome, MD, professor and chair of emergency medicine at Mount Sinai West and Mount Sinai Morningside, New York, said in an interview.
“If you’re in a small rural hospital with one lab technician, trying to do all of these things, it will not be possible. These are optimal recommendations that people can use to the best of their ability, but they are not standard of care, because some places will not be able to provide this level of care,” he added. “This paper provides practical, reasonable advice that should be looked at as you are trying to implement transfusion policies and processes, with the understanding that it is not necessarily applicable or practical for very small hospitals in very rural centers that might not have access to these types of products and tools, but it’s a reasonable and nicely written paper.”
No outside funding for the guideline was reported. Dr. Callum has received research funding from Canadian Blood Services and Octapharma. She sits on the nominating committee with the Association for the Advancement of Blood & Biotherapies and on the data safety monitoring boards for the Tranexamic Acid for Subdural Hematoma trial and the Fibrinogen Replacement in Trauma trial. Dr. Tillmann and Dr. Legome reported no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
FROM THE CANADIAN MEDICAL ASSOCIATION JOURNAL
PTSD, anxiety linked to out-of-hospital cardiac arrest
Investigators compared more than 35,000 OHCA case patients with a similar number of matched control persons and found an almost 1.5 times higher hazard of long-term stress conditions among OHCA case patients, compared with control persons, with a similar hazard for anxiety. Posttraumatic stress disorder was associated with an almost twofold higher risk of OHCA.
The findings applied equally to men and women and were independent of the presence of cardiovascular disease (CVD).
“This study raises awareness of the higher risks of OHCA and early risk monitoring to prevent OHCA in patients with stress-related disorders and anxiety,” write Talip Eroglu, of the department of cardiology, Copenhagen University Hospital, and colleagues.
The study was published online in BMJ Open Heart.
Stress disorders and anxiety overrepresented
OHCA “predominantly arises from lethal cardiac arrhythmias ... that occur most frequently in the setting of coronary heart disease,” the authors write. However, increasing evidence suggests that rates of OHCA may also be increased in association with noncardiac diseases.
Individuals with stress-related disorders and anxiety are “overrepresented” among victims of cardiac arrest as well as those with multiple CVDs. But previous studies of OHCA have been limited by small numbers of cardiac arrests. In addition, those studies involved only data from selected populations or used in-hospital diagnosis to identify cardiac arrest, thereby potentially omitting OHCA patients who died prior to hospital admission.
The researchers therefore turned to data from Danish health registries that include a large, unselected cohort of patients with OHCA to investigate whether long-term stress conditions (that is, PTSD and adjustment disorder) or anxiety disorder were associated with OHCA.
They stratified the cohort according to sex, age, and CVD to identify which risk factor confers the highest risk of OHCA in patients with long-term stress conditions or anxiety, and they conducted sensitivity analyses of potential confounders, such as depression.
The design was a nested-case control model in which records at an individual patient level across registries were cross-linked to data from other national registries and were compared to matched control persons from the general population (35,195 OHCAs and 351,950 matched control persons; median IQR age, 72 [62-81] years; 66.82% men).
The prevalence of comorbidities and use of cardiovascular drugs were higher among OHCA case patients than among non-OHCA control persons.
Keep aware of stress and anxiety as risk factors
Among OHCA and non-OHCA participants, long-term stress conditions were diagnosed in 0.92% and 0.45%, respectively. Anxiety was diagnosed in 0.85% of OHCA case patients and in 0.37% of non-OHCA control persons.
These conditions were associated with a higher rate of OHCA after adjustment for common OHCA risk factors.
There were no significant differences in results when the researchers adjusted for the use of anxiolytics and antidepressants.
When they examined the prevalence of concomitant medication use or comorbidities, they found that depression was more frequent among patients with long-term stress and anxiety, compared with individuals with neither of those diagnoses. Additionally, patients with long-term stress and anxiety more often used anxiolytics, antidepressants, and QT-prolonging drugs.
Stratification of the analyses according to sex revealed that the OHCA rate was increased in both women and men with long-term stress and anxiety. There were no significant differences between the sexes. There were also no significant differences between the association among different age groups, nor between patients with and those without CVD, ischemic heart disease, or heart failure.
Previous research has shown associations of stress-related disorders or anxiety with cardiovascular outcomes, including myocardial infarction, heart failure, and cerebrovascular disease. These disorders might be “biological mediators in the causal pathway of OHCA” and contribute to the increased OHCA rate associated with stress-related disorders and anxiety, the authors suggest.
Nevertheless, they note, stress-related disorders and anxiety remained significantly associated with OHCA after controlling for these variables, “suggesting that it is unlikely that traditional risk factors of OHCA alone explain this relationship.”
They suggest several potential mechanisms. One is that the relationship is likely mediated by the activity of the sympathetic autonomic nervous system, which “leads to an increase in heart rate, release of neurotransmitters into the circulation, and local release of neurotransmitters in the heart.”
Each of these factors “may potentially influence cardiac electrophysiology and facilitate ventricular arrhythmias and OHCA.”
In addition to a biological mechanism, behavioral and psychosocial factors may also contribute to OHCA risk, since stress-related disorders and anxiety “often lead to unhealthy lifestyle, such as smoking and lower physical activity, which in turn may increase the risk of OHCA.” Given the absence of data on these features in the registries the investigators used, they were unable to account for them.
However, “it is unlikely that knowledge of these factors would have altered our conclusions considering that we have adjusted for all the relevant cardiovascular comorbidities.”
Similarly, other psychiatric disorders, such as depression, can contribute to OHCA risk, but they adjusted for depression in their multivariable analyses.
“Awareness of the higher risks of OHCA in patients with stress-related disorders and anxiety is important when treating these patients,” they conclude.
Detrimental to the heart, not just the psyche
Glenn Levine, MD, master clinician and professor of medicine, Baylor College of Medicine, Houston, called it an “important study in that it is a large, nationwide cohort study and thus provides important information to complement much smaller, focused studies.”
Like those other studies, “it finds that negative psychological health, specifically, long-term stress (as well as anxiety), is associated with a significantly increased risk of out-of-hospital cardiac arrest,” continued Dr. Levine, who is the chief of the cardiology section at Michael E. DeBakey VA Medical Center, Houston, and was not involved with the study.
Dr. Levine thinks the study “does a good job, as best one can for such a study, in trying to control for other factors, and zeroing in specifically on stress (and anxiety), trying to assess their independent contributions to the risk of developing cardiac arrest.”
The take-home message for clinicians and patients “is that negative psychological stress factors, such as stress and anxiety, are not only detrimental to one’s psychological health but likely increase one’s risk for adverse cardiac events, such as cardiac arrest,” he stated.
No specific funding for the study was disclosed. Mr. Eroglu has disclosed no relevant financial relationships. The other authors’ disclosures are listed in the original article. Dr. Levine reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Investigators compared more than 35,000 OHCA case patients with a similar number of matched control persons and found an almost 1.5 times higher hazard of long-term stress conditions among OHCA case patients, compared with control persons, with a similar hazard for anxiety. Posttraumatic stress disorder was associated with an almost twofold higher risk of OHCA.
The findings applied equally to men and women and were independent of the presence of cardiovascular disease (CVD).
“This study raises awareness of the higher risks of OHCA and early risk monitoring to prevent OHCA in patients with stress-related disorders and anxiety,” write Talip Eroglu, of the department of cardiology, Copenhagen University Hospital, and colleagues.
The study was published online in BMJ Open Heart.
Stress disorders and anxiety overrepresented
OHCA “predominantly arises from lethal cardiac arrhythmias ... that occur most frequently in the setting of coronary heart disease,” the authors write. However, increasing evidence suggests that rates of OHCA may also be increased in association with noncardiac diseases.
Individuals with stress-related disorders and anxiety are “overrepresented” among victims of cardiac arrest as well as those with multiple CVDs. But previous studies of OHCA have been limited by small numbers of cardiac arrests. In addition, those studies involved only data from selected populations or used in-hospital diagnosis to identify cardiac arrest, thereby potentially omitting OHCA patients who died prior to hospital admission.
The researchers therefore turned to data from Danish health registries that include a large, unselected cohort of patients with OHCA to investigate whether long-term stress conditions (that is, PTSD and adjustment disorder) or anxiety disorder were associated with OHCA.
They stratified the cohort according to sex, age, and CVD to identify which risk factor confers the highest risk of OHCA in patients with long-term stress conditions or anxiety, and they conducted sensitivity analyses of potential confounders, such as depression.
The design was a nested-case control model in which records at an individual patient level across registries were cross-linked to data from other national registries and were compared to matched control persons from the general population (35,195 OHCAs and 351,950 matched control persons; median IQR age, 72 [62-81] years; 66.82% men).
The prevalence of comorbidities and use of cardiovascular drugs were higher among OHCA case patients than among non-OHCA control persons.
Keep aware of stress and anxiety as risk factors
Among OHCA and non-OHCA participants, long-term stress conditions were diagnosed in 0.92% and 0.45%, respectively. Anxiety was diagnosed in 0.85% of OHCA case patients and in 0.37% of non-OHCA control persons.
These conditions were associated with a higher rate of OHCA after adjustment for common OHCA risk factors.
There were no significant differences in results when the researchers adjusted for the use of anxiolytics and antidepressants.
When they examined the prevalence of concomitant medication use or comorbidities, they found that depression was more frequent among patients with long-term stress and anxiety, compared with individuals with neither of those diagnoses. Additionally, patients with long-term stress and anxiety more often used anxiolytics, antidepressants, and QT-prolonging drugs.
Stratification of the analyses according to sex revealed that the OHCA rate was increased in both women and men with long-term stress and anxiety. There were no significant differences between the sexes. There were also no significant differences between the association among different age groups, nor between patients with and those without CVD, ischemic heart disease, or heart failure.
Previous research has shown associations of stress-related disorders or anxiety with cardiovascular outcomes, including myocardial infarction, heart failure, and cerebrovascular disease. These disorders might be “biological mediators in the causal pathway of OHCA” and contribute to the increased OHCA rate associated with stress-related disorders and anxiety, the authors suggest.
Nevertheless, they note, stress-related disorders and anxiety remained significantly associated with OHCA after controlling for these variables, “suggesting that it is unlikely that traditional risk factors of OHCA alone explain this relationship.”
They suggest several potential mechanisms. One is that the relationship is likely mediated by the activity of the sympathetic autonomic nervous system, which “leads to an increase in heart rate, release of neurotransmitters into the circulation, and local release of neurotransmitters in the heart.”
Each of these factors “may potentially influence cardiac electrophysiology and facilitate ventricular arrhythmias and OHCA.”
In addition to a biological mechanism, behavioral and psychosocial factors may also contribute to OHCA risk, since stress-related disorders and anxiety “often lead to unhealthy lifestyle, such as smoking and lower physical activity, which in turn may increase the risk of OHCA.” Given the absence of data on these features in the registries the investigators used, they were unable to account for them.
However, “it is unlikely that knowledge of these factors would have altered our conclusions considering that we have adjusted for all the relevant cardiovascular comorbidities.”
Similarly, other psychiatric disorders, such as depression, can contribute to OHCA risk, but they adjusted for depression in their multivariable analyses.
“Awareness of the higher risks of OHCA in patients with stress-related disorders and anxiety is important when treating these patients,” they conclude.
Detrimental to the heart, not just the psyche
Glenn Levine, MD, master clinician and professor of medicine, Baylor College of Medicine, Houston, called it an “important study in that it is a large, nationwide cohort study and thus provides important information to complement much smaller, focused studies.”
Like those other studies, “it finds that negative psychological health, specifically, long-term stress (as well as anxiety), is associated with a significantly increased risk of out-of-hospital cardiac arrest,” continued Dr. Levine, who is the chief of the cardiology section at Michael E. DeBakey VA Medical Center, Houston, and was not involved with the study.
Dr. Levine thinks the study “does a good job, as best one can for such a study, in trying to control for other factors, and zeroing in specifically on stress (and anxiety), trying to assess their independent contributions to the risk of developing cardiac arrest.”
The take-home message for clinicians and patients “is that negative psychological stress factors, such as stress and anxiety, are not only detrimental to one’s psychological health but likely increase one’s risk for adverse cardiac events, such as cardiac arrest,” he stated.
No specific funding for the study was disclosed. Mr. Eroglu has disclosed no relevant financial relationships. The other authors’ disclosures are listed in the original article. Dr. Levine reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Investigators compared more than 35,000 OHCA case patients with a similar number of matched control persons and found an almost 1.5 times higher hazard of long-term stress conditions among OHCA case patients, compared with control persons, with a similar hazard for anxiety. Posttraumatic stress disorder was associated with an almost twofold higher risk of OHCA.
The findings applied equally to men and women and were independent of the presence of cardiovascular disease (CVD).
“This study raises awareness of the higher risks of OHCA and early risk monitoring to prevent OHCA in patients with stress-related disorders and anxiety,” write Talip Eroglu, of the department of cardiology, Copenhagen University Hospital, and colleagues.
The study was published online in BMJ Open Heart.
Stress disorders and anxiety overrepresented
OHCA “predominantly arises from lethal cardiac arrhythmias ... that occur most frequently in the setting of coronary heart disease,” the authors write. However, increasing evidence suggests that rates of OHCA may also be increased in association with noncardiac diseases.
Individuals with stress-related disorders and anxiety are “overrepresented” among victims of cardiac arrest as well as those with multiple CVDs. But previous studies of OHCA have been limited by small numbers of cardiac arrests. In addition, those studies involved only data from selected populations or used in-hospital diagnosis to identify cardiac arrest, thereby potentially omitting OHCA patients who died prior to hospital admission.
The researchers therefore turned to data from Danish health registries that include a large, unselected cohort of patients with OHCA to investigate whether long-term stress conditions (that is, PTSD and adjustment disorder) or anxiety disorder were associated with OHCA.
They stratified the cohort according to sex, age, and CVD to identify which risk factor confers the highest risk of OHCA in patients with long-term stress conditions or anxiety, and they conducted sensitivity analyses of potential confounders, such as depression.
The design was a nested-case control model in which records at an individual patient level across registries were cross-linked to data from other national registries and were compared to matched control persons from the general population (35,195 OHCAs and 351,950 matched control persons; median IQR age, 72 [62-81] years; 66.82% men).
The prevalence of comorbidities and use of cardiovascular drugs were higher among OHCA case patients than among non-OHCA control persons.
Keep aware of stress and anxiety as risk factors
Among OHCA and non-OHCA participants, long-term stress conditions were diagnosed in 0.92% and 0.45%, respectively. Anxiety was diagnosed in 0.85% of OHCA case patients and in 0.37% of non-OHCA control persons.
These conditions were associated with a higher rate of OHCA after adjustment for common OHCA risk factors.
There were no significant differences in results when the researchers adjusted for the use of anxiolytics and antidepressants.
When they examined the prevalence of concomitant medication use or comorbidities, they found that depression was more frequent among patients with long-term stress and anxiety, compared with individuals with neither of those diagnoses. Additionally, patients with long-term stress and anxiety more often used anxiolytics, antidepressants, and QT-prolonging drugs.
Stratification of the analyses according to sex revealed that the OHCA rate was increased in both women and men with long-term stress and anxiety. There were no significant differences between the sexes. There were also no significant differences between the association among different age groups, nor between patients with and those without CVD, ischemic heart disease, or heart failure.
Previous research has shown associations of stress-related disorders or anxiety with cardiovascular outcomes, including myocardial infarction, heart failure, and cerebrovascular disease. These disorders might be “biological mediators in the causal pathway of OHCA” and contribute to the increased OHCA rate associated with stress-related disorders and anxiety, the authors suggest.
Nevertheless, they note, stress-related disorders and anxiety remained significantly associated with OHCA after controlling for these variables, “suggesting that it is unlikely that traditional risk factors of OHCA alone explain this relationship.”
They suggest several potential mechanisms. One is that the relationship is likely mediated by the activity of the sympathetic autonomic nervous system, which “leads to an increase in heart rate, release of neurotransmitters into the circulation, and local release of neurotransmitters in the heart.”
Each of these factors “may potentially influence cardiac electrophysiology and facilitate ventricular arrhythmias and OHCA.”
In addition to a biological mechanism, behavioral and psychosocial factors may also contribute to OHCA risk, since stress-related disorders and anxiety “often lead to unhealthy lifestyle, such as smoking and lower physical activity, which in turn may increase the risk of OHCA.” Given the absence of data on these features in the registries the investigators used, they were unable to account for them.
However, “it is unlikely that knowledge of these factors would have altered our conclusions considering that we have adjusted for all the relevant cardiovascular comorbidities.”
Similarly, other psychiatric disorders, such as depression, can contribute to OHCA risk, but they adjusted for depression in their multivariable analyses.
“Awareness of the higher risks of OHCA in patients with stress-related disorders and anxiety is important when treating these patients,” they conclude.
Detrimental to the heart, not just the psyche
Glenn Levine, MD, master clinician and professor of medicine, Baylor College of Medicine, Houston, called it an “important study in that it is a large, nationwide cohort study and thus provides important information to complement much smaller, focused studies.”
Like those other studies, “it finds that negative psychological health, specifically, long-term stress (as well as anxiety), is associated with a significantly increased risk of out-of-hospital cardiac arrest,” continued Dr. Levine, who is the chief of the cardiology section at Michael E. DeBakey VA Medical Center, Houston, and was not involved with the study.
Dr. Levine thinks the study “does a good job, as best one can for such a study, in trying to control for other factors, and zeroing in specifically on stress (and anxiety), trying to assess their independent contributions to the risk of developing cardiac arrest.”
The take-home message for clinicians and patients “is that negative psychological stress factors, such as stress and anxiety, are not only detrimental to one’s psychological health but likely increase one’s risk for adverse cardiac events, such as cardiac arrest,” he stated.
No specific funding for the study was disclosed. Mr. Eroglu has disclosed no relevant financial relationships. The other authors’ disclosures are listed in the original article. Dr. Levine reports no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM BMJ OPEN HEART