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Vaginal microbiome does not affect infant gut microbiome
The findings suggest that practices such as vaginal seeding are ineffective.
A longitudinal, prospective cohort study of more than 600 pregnant Canadian women and their newborns showed significant differences in an infant’s stool composition by delivery mode at 10 days post partum, but the differences could not be explained by the mother’s vaginal microbiome, and they effectively disappeared by 3 months.
The findings were surprising, Scott Dos Santos, a PhD candidate at the University of Saskatchewan in Saskatoon, told this news organization. “The bacteria living in the maternal vagina are the first microbes that vaginally delivered infants are exposed to. … so it sounds intuitive that different kinds of vaginal microbiomes could end up influencing the development of a baby’s gut microbiome in different ways. But the maternal vaginal microbiome didn’t seem to have any role in predicting what the infant stool microbiome looked like.”
Therefore, women should not be concerned about cesarean delivery having an adverse effect on their baby’s gut microbiome, said Mr. Dos Santos. Moreover, “vaginal seeding is not safe or advised. Professional bodies, including the Society of Obstetricians and Gynecologists of Canada and the American College of Obstetricians and Gynecologists, strongly advise against this practice.”
The study was published online in Frontiers in Cellular and Infection Microbiology.
Independent communities
The investigators analyzed vaginal and stool microbiome profiles from 442 mother-infant dyads. The mothers were healthy, low-risk women who delivered at term. They were recruited into the Maternal Microbiome LEGACY Project from three hospitals in British Columbia.
The mean age of the mothers at delivery was 34.6 years, which is typical of the study hospitals’ delivery populations. Participants identified themselves as White (54.7%), Asian (21.2%), South Asian (8.3%), and of other ethnicities.
A nurse, midwife, or clinician collected maternal vaginal swabs of the posterior fornix and lateral vaginal wall at first presentation to the labor and delivery area. Neonatal meconium, which was defined as the first stool specimen collected within 72 hours of birth, and two infant stool samples were collected at follow-up visits at 10 days and 3 months post partum.
A principal component analysis of infant stool microbiomes showed no significant clustering of microbiome profiles at 10 days or 3 months by maternal community state types (that is, microbial species).
Correspondence analyses also showed no coclustering of maternal and infant clusters at either time. In addition, there were no differences in the distribution of maternal vaginal microbiome clusters among infant stool microbiome clusters, regardless of delivery mode.
Vaginal microbiome clusters were distributed across infant stool clusters in proportion to their frequency in the overall maternal population, indicating that the two communities were independent of each other.
Intrapartum antibiotic administration was identified as a confounder of infant stool microbiome differences and was associated with lower abundances of Escherichia coli, Bacteroides vulgatus, Bifidobacterium longum, and Parabacteroides distasonis.
“Our findings demonstrate that maternal vaginal microbiome composition at delivery does not affect infant stool microbiome composition and development, suggesting that practices to amend infant stool microbiome composition focus on factors other than maternal vaginal microbes,” the authors conclude.
More evidence needed
Commenting on the study, Emily H. Adhikari, MD, assistant professor of obstetrics and gynecology at UT Southwestern Medical Center in Dallas, and medical director of perinatal infectious diseases for the Parkland Health and Hospital System, said, “These findings contribute significantly more data to an understudied area of research into factors that affect the infant gut microbiome from the earliest hours of life. Prior studies have been small and often conflicting, and the authors reference recent larger studies, which corroborate their findings.”
The data regarding whether delivery mode or antibiotic-associated differences in infant microbiomes persist remain controversial, said Dr. Adhikari. “More evidence is needed involving a more ethnically diverse sampling of patients.” In addition, prospectively evaluating vaginal seeding in a rigorously designed clinical trial setting is “imperative to understand any potential benefit and certainly to understand the potential harms of the practice. To date, this does not exist.”
The study was funded by a Canadian Institutes of Health Research grant. Mr. Dos Santos and Dr. Adhikari have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
The findings suggest that practices such as vaginal seeding are ineffective.
A longitudinal, prospective cohort study of more than 600 pregnant Canadian women and their newborns showed significant differences in an infant’s stool composition by delivery mode at 10 days post partum, but the differences could not be explained by the mother’s vaginal microbiome, and they effectively disappeared by 3 months.
The findings were surprising, Scott Dos Santos, a PhD candidate at the University of Saskatchewan in Saskatoon, told this news organization. “The bacteria living in the maternal vagina are the first microbes that vaginally delivered infants are exposed to. … so it sounds intuitive that different kinds of vaginal microbiomes could end up influencing the development of a baby’s gut microbiome in different ways. But the maternal vaginal microbiome didn’t seem to have any role in predicting what the infant stool microbiome looked like.”
Therefore, women should not be concerned about cesarean delivery having an adverse effect on their baby’s gut microbiome, said Mr. Dos Santos. Moreover, “vaginal seeding is not safe or advised. Professional bodies, including the Society of Obstetricians and Gynecologists of Canada and the American College of Obstetricians and Gynecologists, strongly advise against this practice.”
The study was published online in Frontiers in Cellular and Infection Microbiology.
Independent communities
The investigators analyzed vaginal and stool microbiome profiles from 442 mother-infant dyads. The mothers were healthy, low-risk women who delivered at term. They were recruited into the Maternal Microbiome LEGACY Project from three hospitals in British Columbia.
The mean age of the mothers at delivery was 34.6 years, which is typical of the study hospitals’ delivery populations. Participants identified themselves as White (54.7%), Asian (21.2%), South Asian (8.3%), and of other ethnicities.
A nurse, midwife, or clinician collected maternal vaginal swabs of the posterior fornix and lateral vaginal wall at first presentation to the labor and delivery area. Neonatal meconium, which was defined as the first stool specimen collected within 72 hours of birth, and two infant stool samples were collected at follow-up visits at 10 days and 3 months post partum.
A principal component analysis of infant stool microbiomes showed no significant clustering of microbiome profiles at 10 days or 3 months by maternal community state types (that is, microbial species).
Correspondence analyses also showed no coclustering of maternal and infant clusters at either time. In addition, there were no differences in the distribution of maternal vaginal microbiome clusters among infant stool microbiome clusters, regardless of delivery mode.
Vaginal microbiome clusters were distributed across infant stool clusters in proportion to their frequency in the overall maternal population, indicating that the two communities were independent of each other.
Intrapartum antibiotic administration was identified as a confounder of infant stool microbiome differences and was associated with lower abundances of Escherichia coli, Bacteroides vulgatus, Bifidobacterium longum, and Parabacteroides distasonis.
“Our findings demonstrate that maternal vaginal microbiome composition at delivery does not affect infant stool microbiome composition and development, suggesting that practices to amend infant stool microbiome composition focus on factors other than maternal vaginal microbes,” the authors conclude.
More evidence needed
Commenting on the study, Emily H. Adhikari, MD, assistant professor of obstetrics and gynecology at UT Southwestern Medical Center in Dallas, and medical director of perinatal infectious diseases for the Parkland Health and Hospital System, said, “These findings contribute significantly more data to an understudied area of research into factors that affect the infant gut microbiome from the earliest hours of life. Prior studies have been small and often conflicting, and the authors reference recent larger studies, which corroborate their findings.”
The data regarding whether delivery mode or antibiotic-associated differences in infant microbiomes persist remain controversial, said Dr. Adhikari. “More evidence is needed involving a more ethnically diverse sampling of patients.” In addition, prospectively evaluating vaginal seeding in a rigorously designed clinical trial setting is “imperative to understand any potential benefit and certainly to understand the potential harms of the practice. To date, this does not exist.”
The study was funded by a Canadian Institutes of Health Research grant. Mr. Dos Santos and Dr. Adhikari have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
The findings suggest that practices such as vaginal seeding are ineffective.
A longitudinal, prospective cohort study of more than 600 pregnant Canadian women and their newborns showed significant differences in an infant’s stool composition by delivery mode at 10 days post partum, but the differences could not be explained by the mother’s vaginal microbiome, and they effectively disappeared by 3 months.
The findings were surprising, Scott Dos Santos, a PhD candidate at the University of Saskatchewan in Saskatoon, told this news organization. “The bacteria living in the maternal vagina are the first microbes that vaginally delivered infants are exposed to. … so it sounds intuitive that different kinds of vaginal microbiomes could end up influencing the development of a baby’s gut microbiome in different ways. But the maternal vaginal microbiome didn’t seem to have any role in predicting what the infant stool microbiome looked like.”
Therefore, women should not be concerned about cesarean delivery having an adverse effect on their baby’s gut microbiome, said Mr. Dos Santos. Moreover, “vaginal seeding is not safe or advised. Professional bodies, including the Society of Obstetricians and Gynecologists of Canada and the American College of Obstetricians and Gynecologists, strongly advise against this practice.”
The study was published online in Frontiers in Cellular and Infection Microbiology.
Independent communities
The investigators analyzed vaginal and stool microbiome profiles from 442 mother-infant dyads. The mothers were healthy, low-risk women who delivered at term. They were recruited into the Maternal Microbiome LEGACY Project from three hospitals in British Columbia.
The mean age of the mothers at delivery was 34.6 years, which is typical of the study hospitals’ delivery populations. Participants identified themselves as White (54.7%), Asian (21.2%), South Asian (8.3%), and of other ethnicities.
A nurse, midwife, or clinician collected maternal vaginal swabs of the posterior fornix and lateral vaginal wall at first presentation to the labor and delivery area. Neonatal meconium, which was defined as the first stool specimen collected within 72 hours of birth, and two infant stool samples were collected at follow-up visits at 10 days and 3 months post partum.
A principal component analysis of infant stool microbiomes showed no significant clustering of microbiome profiles at 10 days or 3 months by maternal community state types (that is, microbial species).
Correspondence analyses also showed no coclustering of maternal and infant clusters at either time. In addition, there were no differences in the distribution of maternal vaginal microbiome clusters among infant stool microbiome clusters, regardless of delivery mode.
Vaginal microbiome clusters were distributed across infant stool clusters in proportion to their frequency in the overall maternal population, indicating that the two communities were independent of each other.
Intrapartum antibiotic administration was identified as a confounder of infant stool microbiome differences and was associated with lower abundances of Escherichia coli, Bacteroides vulgatus, Bifidobacterium longum, and Parabacteroides distasonis.
“Our findings demonstrate that maternal vaginal microbiome composition at delivery does not affect infant stool microbiome composition and development, suggesting that practices to amend infant stool microbiome composition focus on factors other than maternal vaginal microbes,” the authors conclude.
More evidence needed
Commenting on the study, Emily H. Adhikari, MD, assistant professor of obstetrics and gynecology at UT Southwestern Medical Center in Dallas, and medical director of perinatal infectious diseases for the Parkland Health and Hospital System, said, “These findings contribute significantly more data to an understudied area of research into factors that affect the infant gut microbiome from the earliest hours of life. Prior studies have been small and often conflicting, and the authors reference recent larger studies, which corroborate their findings.”
The data regarding whether delivery mode or antibiotic-associated differences in infant microbiomes persist remain controversial, said Dr. Adhikari. “More evidence is needed involving a more ethnically diverse sampling of patients.” In addition, prospectively evaluating vaginal seeding in a rigorously designed clinical trial setting is “imperative to understand any potential benefit and certainly to understand the potential harms of the practice. To date, this does not exist.”
The study was funded by a Canadian Institutes of Health Research grant. Mr. Dos Santos and Dr. Adhikari have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
FROM FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
Spherical heart may predict cardiomyopathy, AFib
A round heart, or left ventricle sphericity, predicted cardiomyopathy and atrial fibrillation (AFib) in a deep learning analysis of MRI images from close to 39,000 participants in the UK Biobank, a new study shows.
An increase of 1 standard deviation in the sphericity index (short axis length/long axis length) was associated with a 47% increased incidence of cardiomyopathy and a 20% increased incidence of AFib, independent of clinical factors and traditional MRI measures.
Furthermore, a genetic analysis suggested a shared architecture between sphericity and nonischemic cardiomyopathy, pointing to NICM as a possible causal factor for left ventricle sphericity among individuals with normal LV size and function.
“Physicians have known the heart gets rounder after heart attacks and as we get older,” David Ouyang, MD, a cardiologist in the Smidt Heart Institute at Cedars-Sinai Medical Center, Los Angeles, and a researcher in the division of artificial intelligence in medicine, said in an interview. “We wanted to see if this sphericity is prognostic of future disease even in healthy individuals.”
Although it is too early to recommend heart shape assessment in healthy asymptomatic people, he said, “physicians should be extra careful and think about treatments when they notice a patient’s heart is particularly round.”
The study was published online March 29 in the journal Med.
Sphericity index key
The investigators hypothesized that there is variation in LV sphericity within the spectrum of normal LV chamber size and systolic function, and that such variation might be a marker of cardiac risk with genetic influences.
To test this hypothesis, they used automated deep-learning segmentation of cardiac MRI data to estimate and analyze the sphericity index in a cohort of 38,897 individuals participating in the UK Biobank.
After adjustment for age at MRI and sex, an increased sphericity index was associated with an increased risk for cardiomyopathy (hazard ratio, 1.57), AFib (HR, 1.35), and heart failure (HR, 1.37).
No significant association was seen with cardiac arrest.
The team then stratified the cohort into quintiles and compared the top 20%, middle 60%, and bottom 20%. The relationship between the sphericity index and risk extended across the distribution; individuals with higher than median sphericity had increased disease incidence, and those with lower than median sphericity had decreased incidence.
Overall, a single standard deviation in the sphericity index was associated with increased risk of cardiomyopathy (HR, 1.47) and of AFib (HR, 1.20), independent of clinical factors and usual MRI measurements.
In a minimally adjusted model, the sphericity index was a predictor of incident cardiomyopathy, AFib, and heart failure.
Adjustment for clinical factors partially attenuated the heart failure association; additional adjustment for MRI measurements fully attenuated that association and partially attenuated the association with AFib.
However, in all adjusted models, the association with cardiomyopathy showed little attenuation.
Furthermore, the team identified four loci associated with sphericity at genomewide significance – PLN, ANGPT1, PDZRN3, and HLA DR/DQ – and Mendelian randomization supported NICM as a cause of LV sphericity.
Looking ahead
“While conventional imaging metrics have significant diagnostic and prognostic value, some of these measurements have been adopted out of convenience or tradition,” the authors noted. “By representing a specific multidimensional remodeling phenotype, sphericity has emerged as a distinct morphologic trait with features not adequately captured by conventional measurements.
“We expect that the search space of potential imaging measurements is vast, and we have only begun to scratch at the surface of disease associations.”
Indeed, Dr. Ouyang said his group is “trying to evaluate the sphericity in echocardiograms or heart ultrasounds, which are more common and cheaper than MRI.”
“The main caveat is translating the information directly to patient care,” Richard C. Becker, MD, director and physician-in-chief of the University of Cincinnati Heart, Lung, and Vascular Institute, said in an interview. “Near-term yield could include using the spherical calculation in routine MRI of the heart, and based on the findings, following patients more closely if there is an abnormal shape. Or performing an MRI and targeted gene testing if there is a family history of cardiomyopathy or [of] an abnormal shape of the heart.”
“Validation of the findings and large-scale evaluation of the genes identified, and how they interact with patient and environmental factors, will be very important,” he added.
Nevertheless, “the study was well done and may serve as a foundation for future research,” Dr. Becker said. “The investigators used several powerful tools, including MRI, genomics, and [artificial intelligence] to draw their conclusions. This is precisely the way that ‘big data’ should be used – in a complementary fashion.”
The study authors and Dr. Becker reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A round heart, or left ventricle sphericity, predicted cardiomyopathy and atrial fibrillation (AFib) in a deep learning analysis of MRI images from close to 39,000 participants in the UK Biobank, a new study shows.
An increase of 1 standard deviation in the sphericity index (short axis length/long axis length) was associated with a 47% increased incidence of cardiomyopathy and a 20% increased incidence of AFib, independent of clinical factors and traditional MRI measures.
Furthermore, a genetic analysis suggested a shared architecture between sphericity and nonischemic cardiomyopathy, pointing to NICM as a possible causal factor for left ventricle sphericity among individuals with normal LV size and function.
“Physicians have known the heart gets rounder after heart attacks and as we get older,” David Ouyang, MD, a cardiologist in the Smidt Heart Institute at Cedars-Sinai Medical Center, Los Angeles, and a researcher in the division of artificial intelligence in medicine, said in an interview. “We wanted to see if this sphericity is prognostic of future disease even in healthy individuals.”
Although it is too early to recommend heart shape assessment in healthy asymptomatic people, he said, “physicians should be extra careful and think about treatments when they notice a patient’s heart is particularly round.”
The study was published online March 29 in the journal Med.
Sphericity index key
The investigators hypothesized that there is variation in LV sphericity within the spectrum of normal LV chamber size and systolic function, and that such variation might be a marker of cardiac risk with genetic influences.
To test this hypothesis, they used automated deep-learning segmentation of cardiac MRI data to estimate and analyze the sphericity index in a cohort of 38,897 individuals participating in the UK Biobank.
After adjustment for age at MRI and sex, an increased sphericity index was associated with an increased risk for cardiomyopathy (hazard ratio, 1.57), AFib (HR, 1.35), and heart failure (HR, 1.37).
No significant association was seen with cardiac arrest.
The team then stratified the cohort into quintiles and compared the top 20%, middle 60%, and bottom 20%. The relationship between the sphericity index and risk extended across the distribution; individuals with higher than median sphericity had increased disease incidence, and those with lower than median sphericity had decreased incidence.
Overall, a single standard deviation in the sphericity index was associated with increased risk of cardiomyopathy (HR, 1.47) and of AFib (HR, 1.20), independent of clinical factors and usual MRI measurements.
In a minimally adjusted model, the sphericity index was a predictor of incident cardiomyopathy, AFib, and heart failure.
Adjustment for clinical factors partially attenuated the heart failure association; additional adjustment for MRI measurements fully attenuated that association and partially attenuated the association with AFib.
However, in all adjusted models, the association with cardiomyopathy showed little attenuation.
Furthermore, the team identified four loci associated with sphericity at genomewide significance – PLN, ANGPT1, PDZRN3, and HLA DR/DQ – and Mendelian randomization supported NICM as a cause of LV sphericity.
Looking ahead
“While conventional imaging metrics have significant diagnostic and prognostic value, some of these measurements have been adopted out of convenience or tradition,” the authors noted. “By representing a specific multidimensional remodeling phenotype, sphericity has emerged as a distinct morphologic trait with features not adequately captured by conventional measurements.
“We expect that the search space of potential imaging measurements is vast, and we have only begun to scratch at the surface of disease associations.”
Indeed, Dr. Ouyang said his group is “trying to evaluate the sphericity in echocardiograms or heart ultrasounds, which are more common and cheaper than MRI.”
“The main caveat is translating the information directly to patient care,” Richard C. Becker, MD, director and physician-in-chief of the University of Cincinnati Heart, Lung, and Vascular Institute, said in an interview. “Near-term yield could include using the spherical calculation in routine MRI of the heart, and based on the findings, following patients more closely if there is an abnormal shape. Or performing an MRI and targeted gene testing if there is a family history of cardiomyopathy or [of] an abnormal shape of the heart.”
“Validation of the findings and large-scale evaluation of the genes identified, and how they interact with patient and environmental factors, will be very important,” he added.
Nevertheless, “the study was well done and may serve as a foundation for future research,” Dr. Becker said. “The investigators used several powerful tools, including MRI, genomics, and [artificial intelligence] to draw their conclusions. This is precisely the way that ‘big data’ should be used – in a complementary fashion.”
The study authors and Dr. Becker reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
A round heart, or left ventricle sphericity, predicted cardiomyopathy and atrial fibrillation (AFib) in a deep learning analysis of MRI images from close to 39,000 participants in the UK Biobank, a new study shows.
An increase of 1 standard deviation in the sphericity index (short axis length/long axis length) was associated with a 47% increased incidence of cardiomyopathy and a 20% increased incidence of AFib, independent of clinical factors and traditional MRI measures.
Furthermore, a genetic analysis suggested a shared architecture between sphericity and nonischemic cardiomyopathy, pointing to NICM as a possible causal factor for left ventricle sphericity among individuals with normal LV size and function.
“Physicians have known the heart gets rounder after heart attacks and as we get older,” David Ouyang, MD, a cardiologist in the Smidt Heart Institute at Cedars-Sinai Medical Center, Los Angeles, and a researcher in the division of artificial intelligence in medicine, said in an interview. “We wanted to see if this sphericity is prognostic of future disease even in healthy individuals.”
Although it is too early to recommend heart shape assessment in healthy asymptomatic people, he said, “physicians should be extra careful and think about treatments when they notice a patient’s heart is particularly round.”
The study was published online March 29 in the journal Med.
Sphericity index key
The investigators hypothesized that there is variation in LV sphericity within the spectrum of normal LV chamber size and systolic function, and that such variation might be a marker of cardiac risk with genetic influences.
To test this hypothesis, they used automated deep-learning segmentation of cardiac MRI data to estimate and analyze the sphericity index in a cohort of 38,897 individuals participating in the UK Biobank.
After adjustment for age at MRI and sex, an increased sphericity index was associated with an increased risk for cardiomyopathy (hazard ratio, 1.57), AFib (HR, 1.35), and heart failure (HR, 1.37).
No significant association was seen with cardiac arrest.
The team then stratified the cohort into quintiles and compared the top 20%, middle 60%, and bottom 20%. The relationship between the sphericity index and risk extended across the distribution; individuals with higher than median sphericity had increased disease incidence, and those with lower than median sphericity had decreased incidence.
Overall, a single standard deviation in the sphericity index was associated with increased risk of cardiomyopathy (HR, 1.47) and of AFib (HR, 1.20), independent of clinical factors and usual MRI measurements.
In a minimally adjusted model, the sphericity index was a predictor of incident cardiomyopathy, AFib, and heart failure.
Adjustment for clinical factors partially attenuated the heart failure association; additional adjustment for MRI measurements fully attenuated that association and partially attenuated the association with AFib.
However, in all adjusted models, the association with cardiomyopathy showed little attenuation.
Furthermore, the team identified four loci associated with sphericity at genomewide significance – PLN, ANGPT1, PDZRN3, and HLA DR/DQ – and Mendelian randomization supported NICM as a cause of LV sphericity.
Looking ahead
“While conventional imaging metrics have significant diagnostic and prognostic value, some of these measurements have been adopted out of convenience or tradition,” the authors noted. “By representing a specific multidimensional remodeling phenotype, sphericity has emerged as a distinct morphologic trait with features not adequately captured by conventional measurements.
“We expect that the search space of potential imaging measurements is vast, and we have only begun to scratch at the surface of disease associations.”
Indeed, Dr. Ouyang said his group is “trying to evaluate the sphericity in echocardiograms or heart ultrasounds, which are more common and cheaper than MRI.”
“The main caveat is translating the information directly to patient care,” Richard C. Becker, MD, director and physician-in-chief of the University of Cincinnati Heart, Lung, and Vascular Institute, said in an interview. “Near-term yield could include using the spherical calculation in routine MRI of the heart, and based on the findings, following patients more closely if there is an abnormal shape. Or performing an MRI and targeted gene testing if there is a family history of cardiomyopathy or [of] an abnormal shape of the heart.”
“Validation of the findings and large-scale evaluation of the genes identified, and how they interact with patient and environmental factors, will be very important,” he added.
Nevertheless, “the study was well done and may serve as a foundation for future research,” Dr. Becker said. “The investigators used several powerful tools, including MRI, genomics, and [artificial intelligence] to draw their conclusions. This is precisely the way that ‘big data’ should be used – in a complementary fashion.”
The study authors and Dr. Becker reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM MED
Commotio cordis underrecognized, undertreated outside of sports
Sudden cardiac arrest (SCA) due to commotio cordis occurs more frequently in non–sport-related settings than is commonly thought, resulting in lower rates of resuscitation and increased mortality, especially among young women, a new review suggests.
The condition is rare, caused by an often fatal arrhythmia secondary to a blunt, nonpenetrating impact over the precordium, without direct structural damage to the heart itself. Common causes in nonsport settings include assault, motor vehicle accidents (MVAs), and daily activities such as occupational accidents.
“We found a stark difference in mortality outcomes between non–sport-related commotio cordis compared to sport-related events,” at 88% vs. 66%, Han S. Lim, MBBS, PhD, of the University of Melbourne, and Austin Health, Heidelberg, Australia, told this news organization. “Rates of cardiopulmonary resuscitation (CPR) (27% vs. 97%) and defibrillation (17% vs. 81%) were considerably lower in the non–sport-related events.”
“Although still being male-predominant, of concern, we saw a higher proportion of females in non–sport-related commotio cordis due to assault, MVAs, and other activities,” he noted. Such events may occur “in secluded domestic settings, may not be witnessed, or may occur as intentional harm, whereby the witness could also be the perpetrator, reducing the likelihood of prompt diagnosis, CPR, and defibrillation administration.”
The study was published online in JACC: Clinical Electrophysiology.
Young women affected
Dr. Lim and colleagues searched the literature through 2021 for all cases of commotio cordis. Three hundred and thirty-four cases from among 53 citations were included in the analysis; of those, 121 (36%) occurred in non–sport-related settings, including assault (76%), MVAs (7%), and daily activities (16%). “Daily activities” comprised activities that were expected in a person’s day-to-day routine such as falls, play fighting (in children), and occupational accidents.
Non–sport-related cases primarily involved nonprojectile etiologies (95%), including bodily contact (79%), such as impacts from fists, feet, and knees; impacts with handlebars or steering wheels; and solid stick-like weapons and flat surfaces.
Sport-related cases involved a significantly higher proportion of projectiles (94% vs. 5%) and occurred across a range of sports, mostly at the competitive level (66%).
Both sport-related and non–sport-related commotio cordis affected a similar younger demographic (mean age, 19; mostly males). No statistically significant differences between the two groups were seen with regard to previous cardiac history or family history of cardiac disease, or in arrhythmias on electrocardiogram, biomarkers, or imaging findings.
However, in non–sport-related events, the proportion of females affected was significantly higher (13% vs. 2%), as was mortality (88% vs. 66%). Rates were lower for CPR (27% vs. 97%) and defibrillation use (17% vs. 81%), and resuscitation was more commonly delayed beyond 3 minutes (80% vs. 5%).
The finding that more than a third of reported cases were non–sport-related “is higher than previously reported, and included data from 15 different countries,” the authors noted.
Study limitations included the use of data only from published studies, inclusion of a case series limited to fatal cases, small sample sizes, and lack of consistent reporting of demographic data, mechanisms, investigation results, management, and outcomes.
Increased awareness ‘essential’
Dr. Lim and colleagues concluded that increased awareness of non–sport-related commotio cordis is “essential” for early recognition, resuscitation, and mortality reduction.
Jim Cheung, MD, chair of the American College of Cardiology’s electrophysiology section, “completely agrees.” Greater awareness among the general population could reduce barriers to CPR and automated external defibrillator (AED) use, he said, which in turn, can lead to improved survival.
Furthermore, Dr. Cheung added, “This study underscores the importance of ensuring that non–cardiology-trained physicians such as emergency medicine physicians and trauma surgeons who might encounter patients with non–sports-related commotio cordis recognize the entity during the course of treatment.”
Because the review relied only on published cases, “it may not represent the true breadth of cases that are occurring in the real world,” he noted. “I suspect that cases that occur outside of sports-related activities, such as MVAs and assault, are more likely to be underreported and that the true proportion of non–sports-related commotio cordis may be significantly higher than 36%.” Increased reporting of cases as part of an international commotio cordis registry would help provide additional insights, he suggested.
“There is a common misperception that SCA only occurs among older patients and patients with known coronary artery disease or heart failure,” he said. “For us to move the needle on improving SCA survival, we will need to tackle the problem from multiple angles including increasing public awareness, training the public on CPR and AED use, and improving access to AEDs by addressing structural barriers.”
Dr. Cheung pointed to ongoing efforts by nonprofit, patient-driven organizations such as the SADS Foundation and Omar Carter Foundation, and professional societies such as the American College of Cardiology, the American Heart Association, and Heart Rhythm Society, to direct public awareness campaigns and legislative proposals to address this problem.
Similar efforts are underway among cardiac societies and SCA awareness groups in Australia, Dr. Lim said.
No funding or relevant financial relationships were disclosed.
A version of this article first appeared on Medscape.com.
Sudden cardiac arrest (SCA) due to commotio cordis occurs more frequently in non–sport-related settings than is commonly thought, resulting in lower rates of resuscitation and increased mortality, especially among young women, a new review suggests.
The condition is rare, caused by an often fatal arrhythmia secondary to a blunt, nonpenetrating impact over the precordium, without direct structural damage to the heart itself. Common causes in nonsport settings include assault, motor vehicle accidents (MVAs), and daily activities such as occupational accidents.
“We found a stark difference in mortality outcomes between non–sport-related commotio cordis compared to sport-related events,” at 88% vs. 66%, Han S. Lim, MBBS, PhD, of the University of Melbourne, and Austin Health, Heidelberg, Australia, told this news organization. “Rates of cardiopulmonary resuscitation (CPR) (27% vs. 97%) and defibrillation (17% vs. 81%) were considerably lower in the non–sport-related events.”
“Although still being male-predominant, of concern, we saw a higher proportion of females in non–sport-related commotio cordis due to assault, MVAs, and other activities,” he noted. Such events may occur “in secluded domestic settings, may not be witnessed, or may occur as intentional harm, whereby the witness could also be the perpetrator, reducing the likelihood of prompt diagnosis, CPR, and defibrillation administration.”
The study was published online in JACC: Clinical Electrophysiology.
Young women affected
Dr. Lim and colleagues searched the literature through 2021 for all cases of commotio cordis. Three hundred and thirty-four cases from among 53 citations were included in the analysis; of those, 121 (36%) occurred in non–sport-related settings, including assault (76%), MVAs (7%), and daily activities (16%). “Daily activities” comprised activities that were expected in a person’s day-to-day routine such as falls, play fighting (in children), and occupational accidents.
Non–sport-related cases primarily involved nonprojectile etiologies (95%), including bodily contact (79%), such as impacts from fists, feet, and knees; impacts with handlebars or steering wheels; and solid stick-like weapons and flat surfaces.
Sport-related cases involved a significantly higher proportion of projectiles (94% vs. 5%) and occurred across a range of sports, mostly at the competitive level (66%).
Both sport-related and non–sport-related commotio cordis affected a similar younger demographic (mean age, 19; mostly males). No statistically significant differences between the two groups were seen with regard to previous cardiac history or family history of cardiac disease, or in arrhythmias on electrocardiogram, biomarkers, or imaging findings.
However, in non–sport-related events, the proportion of females affected was significantly higher (13% vs. 2%), as was mortality (88% vs. 66%). Rates were lower for CPR (27% vs. 97%) and defibrillation use (17% vs. 81%), and resuscitation was more commonly delayed beyond 3 minutes (80% vs. 5%).
The finding that more than a third of reported cases were non–sport-related “is higher than previously reported, and included data from 15 different countries,” the authors noted.
Study limitations included the use of data only from published studies, inclusion of a case series limited to fatal cases, small sample sizes, and lack of consistent reporting of demographic data, mechanisms, investigation results, management, and outcomes.
Increased awareness ‘essential’
Dr. Lim and colleagues concluded that increased awareness of non–sport-related commotio cordis is “essential” for early recognition, resuscitation, and mortality reduction.
Jim Cheung, MD, chair of the American College of Cardiology’s electrophysiology section, “completely agrees.” Greater awareness among the general population could reduce barriers to CPR and automated external defibrillator (AED) use, he said, which in turn, can lead to improved survival.
Furthermore, Dr. Cheung added, “This study underscores the importance of ensuring that non–cardiology-trained physicians such as emergency medicine physicians and trauma surgeons who might encounter patients with non–sports-related commotio cordis recognize the entity during the course of treatment.”
Because the review relied only on published cases, “it may not represent the true breadth of cases that are occurring in the real world,” he noted. “I suspect that cases that occur outside of sports-related activities, such as MVAs and assault, are more likely to be underreported and that the true proportion of non–sports-related commotio cordis may be significantly higher than 36%.” Increased reporting of cases as part of an international commotio cordis registry would help provide additional insights, he suggested.
“There is a common misperception that SCA only occurs among older patients and patients with known coronary artery disease or heart failure,” he said. “For us to move the needle on improving SCA survival, we will need to tackle the problem from multiple angles including increasing public awareness, training the public on CPR and AED use, and improving access to AEDs by addressing structural barriers.”
Dr. Cheung pointed to ongoing efforts by nonprofit, patient-driven organizations such as the SADS Foundation and Omar Carter Foundation, and professional societies such as the American College of Cardiology, the American Heart Association, and Heart Rhythm Society, to direct public awareness campaigns and legislative proposals to address this problem.
Similar efforts are underway among cardiac societies and SCA awareness groups in Australia, Dr. Lim said.
No funding or relevant financial relationships were disclosed.
A version of this article first appeared on Medscape.com.
Sudden cardiac arrest (SCA) due to commotio cordis occurs more frequently in non–sport-related settings than is commonly thought, resulting in lower rates of resuscitation and increased mortality, especially among young women, a new review suggests.
The condition is rare, caused by an often fatal arrhythmia secondary to a blunt, nonpenetrating impact over the precordium, without direct structural damage to the heart itself. Common causes in nonsport settings include assault, motor vehicle accidents (MVAs), and daily activities such as occupational accidents.
“We found a stark difference in mortality outcomes between non–sport-related commotio cordis compared to sport-related events,” at 88% vs. 66%, Han S. Lim, MBBS, PhD, of the University of Melbourne, and Austin Health, Heidelberg, Australia, told this news organization. “Rates of cardiopulmonary resuscitation (CPR) (27% vs. 97%) and defibrillation (17% vs. 81%) were considerably lower in the non–sport-related events.”
“Although still being male-predominant, of concern, we saw a higher proportion of females in non–sport-related commotio cordis due to assault, MVAs, and other activities,” he noted. Such events may occur “in secluded domestic settings, may not be witnessed, or may occur as intentional harm, whereby the witness could also be the perpetrator, reducing the likelihood of prompt diagnosis, CPR, and defibrillation administration.”
The study was published online in JACC: Clinical Electrophysiology.
Young women affected
Dr. Lim and colleagues searched the literature through 2021 for all cases of commotio cordis. Three hundred and thirty-four cases from among 53 citations were included in the analysis; of those, 121 (36%) occurred in non–sport-related settings, including assault (76%), MVAs (7%), and daily activities (16%). “Daily activities” comprised activities that were expected in a person’s day-to-day routine such as falls, play fighting (in children), and occupational accidents.
Non–sport-related cases primarily involved nonprojectile etiologies (95%), including bodily contact (79%), such as impacts from fists, feet, and knees; impacts with handlebars or steering wheels; and solid stick-like weapons and flat surfaces.
Sport-related cases involved a significantly higher proportion of projectiles (94% vs. 5%) and occurred across a range of sports, mostly at the competitive level (66%).
Both sport-related and non–sport-related commotio cordis affected a similar younger demographic (mean age, 19; mostly males). No statistically significant differences between the two groups were seen with regard to previous cardiac history or family history of cardiac disease, or in arrhythmias on electrocardiogram, biomarkers, or imaging findings.
However, in non–sport-related events, the proportion of females affected was significantly higher (13% vs. 2%), as was mortality (88% vs. 66%). Rates were lower for CPR (27% vs. 97%) and defibrillation use (17% vs. 81%), and resuscitation was more commonly delayed beyond 3 minutes (80% vs. 5%).
The finding that more than a third of reported cases were non–sport-related “is higher than previously reported, and included data from 15 different countries,” the authors noted.
Study limitations included the use of data only from published studies, inclusion of a case series limited to fatal cases, small sample sizes, and lack of consistent reporting of demographic data, mechanisms, investigation results, management, and outcomes.
Increased awareness ‘essential’
Dr. Lim and colleagues concluded that increased awareness of non–sport-related commotio cordis is “essential” for early recognition, resuscitation, and mortality reduction.
Jim Cheung, MD, chair of the American College of Cardiology’s electrophysiology section, “completely agrees.” Greater awareness among the general population could reduce barriers to CPR and automated external defibrillator (AED) use, he said, which in turn, can lead to improved survival.
Furthermore, Dr. Cheung added, “This study underscores the importance of ensuring that non–cardiology-trained physicians such as emergency medicine physicians and trauma surgeons who might encounter patients with non–sports-related commotio cordis recognize the entity during the course of treatment.”
Because the review relied only on published cases, “it may not represent the true breadth of cases that are occurring in the real world,” he noted. “I suspect that cases that occur outside of sports-related activities, such as MVAs and assault, are more likely to be underreported and that the true proportion of non–sports-related commotio cordis may be significantly higher than 36%.” Increased reporting of cases as part of an international commotio cordis registry would help provide additional insights, he suggested.
“There is a common misperception that SCA only occurs among older patients and patients with known coronary artery disease or heart failure,” he said. “For us to move the needle on improving SCA survival, we will need to tackle the problem from multiple angles including increasing public awareness, training the public on CPR and AED use, and improving access to AEDs by addressing structural barriers.”
Dr. Cheung pointed to ongoing efforts by nonprofit, patient-driven organizations such as the SADS Foundation and Omar Carter Foundation, and professional societies such as the American College of Cardiology, the American Heart Association, and Heart Rhythm Society, to direct public awareness campaigns and legislative proposals to address this problem.
Similar efforts are underway among cardiac societies and SCA awareness groups in Australia, Dr. Lim said.
No funding or relevant financial relationships were disclosed.
A version of this article first appeared on Medscape.com.
FROM JACC: CLINICAL ELECTROPHYSIOLOGY
Even small changes in fitness tied to lower mortality risk
Even relatively small changes in cardiorespiratory fitness (CRF) are associated with “considerable” impact on clinical symptoms and mortality risk among individuals with and without cardiovascular disease, new observational data in United States veterans suggest.
“We had a few surprises,” Peter Kokkinos, PhD, Robert Wood Johnson Medical School, New Brunswick, N. J., and the VA Medical Center, Washington, told this news organization. “First, the mortality risk was greatly attenuated in those who were moderate- and high-fit at baseline, despite a decline in fitness over time. In fact, in those with no CVD, the risk was not significantly elevated even when CRF declined by at least one MET [metabolic equivalent of task] for the moderate-fit and two or more METs for the high-fit group.”
“Second,” he said, “Our findings suggest that the impact of CRF on human health is not ephemeral, but rather carries a certain protection over time. Third, the changes in CRF necessary to impact mortality risk are relatively small (> 1.0 METs). This has a substantial clinical and public health significance.”
The study was published online in the Journal of the American College of Cardiology.
CRF up, mortality risk down
Dr. Kokkinos and colleagues analyzed data from 93,060 U.S. veterans; of these, 95% were men (mean age, 61.4 years) and 5% were women (mean age, 57.1 years). Overall, 72% of participants were White; 19.8%, African American; 5.2%, Hispanic; 1.9%, Native American, Asian, or Hawaiian; and 1.2%, unknown.
Participants were assigned to age-specific fitness quartiles based on peak METs achieved on a baseline exercise treadmill test (ETT). Each CRF quartile was stratified based on CRF changes (increase, decrease, no change) on the final ETT, with at least two ETT assessments at least 1 year apart.
The mean follow-up was 5.8 years (663,522 person-years), during which 18,302 deaths (19.7%) occurred, for an average annual mortality rate of 27.6 events per 1,000 person-years.
CRF was unchanged in 25.1% of the cohort, increased in 29.3%, and decreased in 45.6%. The trend was similar for those with and without CVD.
Significant differences were seen in all variables across CRF categories. In general, body weight, body mass index, CVD risk factors, and overall disease burden were progressively more unfavorable for those in the lowest CRF categories.
Conversely, medication use was progressively higher among those in low CRF categories.
After adjustment, higher CRF was inversely related to mortality risk for the entire cohort, with and without CVD. Cumulative survival rates across CRF categories declined progressively with increased fitness.
For patients with CVD (hazard ratio, 1.11), other significant predictors of all-cause mortality for patients were age (HR, 1.07), body mass index (HR, 0.98), chronic kidney disease (HR, 1.85), smoking (HR, 1.57), type 2 diabetes (HR, 1.42), hypertension (HR, 1.39), and cancers (HR, 1.37).
Generally, changes in CRF of at least 1.0 MET were associated with inverse and proportionate changes in mortality risk, regardless of baseline CRF status. For example, they note, a CRF decline of > 2.0 METs was associated with a 74% increased mortality risk for low-fit individuals with CVD, and a 69% increase for those without CVD.
A second analysis was done after excluding patients whose CRF declined and who died within 2 years of their last ETT, to account for the possibility that higher mortality rates and CRF declines were consequences of underlying disease (reverse causality). The association between changes in CRF and mortality risk persisted and remained similar to that observed in the entire cohort.
The authors add, “It is noteworthy that CRF increased by at least 1 MET in approximately 29% of the participants in the current study and decreased in approximately 46% of participants. This finding underscores the need to promote physical activity to maintain or increase CRF levels in middle-aged and older individuals.”
“Our findings make a persuasive argument that CRF is a strong and independent determinant of all-cause mortality risk, independent of genetic factors,” Dr. Kokkinos said. “We know that CRF is determined to some degree by genetic factors. However, improvements in aerobic capacity or CRF over time are largely the outcomes of regular engagement in aerobic activities of adequate intensity and volume.”
“Conversely,” he said, “a decline in CRF is likely the result of sedentary behavior, the onset of a chronic condition, or aging.”
If genetics were the sole contributor to mortality risk, then changes in CRF would not influence mortality risk, he concluded.
CRF impact “woefully underestimated”
Barry A. Franklin, PhD, past chair of both the American Heart Association’s Council on Physical Activity and Metabolism and the National Advocacy Committee, said the study substantiates previous smaller studies and is a “seminal” work.
“CRF is woefully underestimated as an index of health outcomes and survival,” said Dr. Franklin, director of preventive cardiology and cardiac rehabilitation at Beaumont Health in Royal Oak, Mich. “Moderate to vigorous physical activity should be regularly promoted by the medical community.”
Dr. Franklin’s recent review, published in Mayo Clinic Proceedings, provides evidence for other exercise benefits that clinicians may not be aware of, he noted. These include:
- Each 1 MET increase in CRF is generally associated with approximately 16% reduction in mortality.
- At any given risk factor profile or coronary calcium score, unfit people have 2-3 times the mortality as their fit counterparts.
- Fitness is inversely related to annual health care costs (each 1 MET increase in CRF is associated with approximately 6% lower annual health care costs).
- Physically active people hospitalized with acute coronary syndromes have better short-term outcomes (likely because of a phenomenon called ‘exercise preconditioning’).
- Fit people who undergo elective or emergent surgical procedures have better outcomes.
- Regular physical activity is a common characteristic in population subsets who routinely live into their 90s and to 100+.
Dr. Franklin had this advice for clinicians seeking to promote CRF increases of 1 MET or more among patients: “Sedentary people who embark on a walking program, who over time increase their walking speed to 3 mph or faster, invariably show at least a 1 MET increase in CRF during subsequent peak or symptom-limited treadmill testing.”
“Another general rule is that if an exercise program decreases heart rate at a given or fixed workload by about 10 beats per minute [bpm], the same treadmill workload that initially was accomplished at a heart rate of 120 bpm is now being accomplished at a heart rate of 110 bpm,” likely resulting in about a 1 MET increase in fitness.
“Accordingly,” he added, “a 20-bpm decrease would suggest a 2 MET increase in fitness!”
In a related editorial, Leonard A. Kaminsky, Ball State University, Muncie, Ind. and colleagues, write, “We agree with and believe the conclusion, reached by Kokkinos et al., bears repeating. We (again) call on both clinicians and public health professionals to adopt CRF as a key health indicator.”
“This should be done by coupling routine assessments of CRF with continued advocacy for promoting physical activity as an essential healthy lifestyle behavior,” they write.
No funding or relevant financial relationships were disclosed.
A version of this article first appeared on Medscape.com.
Even relatively small changes in cardiorespiratory fitness (CRF) are associated with “considerable” impact on clinical symptoms and mortality risk among individuals with and without cardiovascular disease, new observational data in United States veterans suggest.
“We had a few surprises,” Peter Kokkinos, PhD, Robert Wood Johnson Medical School, New Brunswick, N. J., and the VA Medical Center, Washington, told this news organization. “First, the mortality risk was greatly attenuated in those who were moderate- and high-fit at baseline, despite a decline in fitness over time. In fact, in those with no CVD, the risk was not significantly elevated even when CRF declined by at least one MET [metabolic equivalent of task] for the moderate-fit and two or more METs for the high-fit group.”
“Second,” he said, “Our findings suggest that the impact of CRF on human health is not ephemeral, but rather carries a certain protection over time. Third, the changes in CRF necessary to impact mortality risk are relatively small (> 1.0 METs). This has a substantial clinical and public health significance.”
The study was published online in the Journal of the American College of Cardiology.
CRF up, mortality risk down
Dr. Kokkinos and colleagues analyzed data from 93,060 U.S. veterans; of these, 95% were men (mean age, 61.4 years) and 5% were women (mean age, 57.1 years). Overall, 72% of participants were White; 19.8%, African American; 5.2%, Hispanic; 1.9%, Native American, Asian, or Hawaiian; and 1.2%, unknown.
Participants were assigned to age-specific fitness quartiles based on peak METs achieved on a baseline exercise treadmill test (ETT). Each CRF quartile was stratified based on CRF changes (increase, decrease, no change) on the final ETT, with at least two ETT assessments at least 1 year apart.
The mean follow-up was 5.8 years (663,522 person-years), during which 18,302 deaths (19.7%) occurred, for an average annual mortality rate of 27.6 events per 1,000 person-years.
CRF was unchanged in 25.1% of the cohort, increased in 29.3%, and decreased in 45.6%. The trend was similar for those with and without CVD.
Significant differences were seen in all variables across CRF categories. In general, body weight, body mass index, CVD risk factors, and overall disease burden were progressively more unfavorable for those in the lowest CRF categories.
Conversely, medication use was progressively higher among those in low CRF categories.
After adjustment, higher CRF was inversely related to mortality risk for the entire cohort, with and without CVD. Cumulative survival rates across CRF categories declined progressively with increased fitness.
For patients with CVD (hazard ratio, 1.11), other significant predictors of all-cause mortality for patients were age (HR, 1.07), body mass index (HR, 0.98), chronic kidney disease (HR, 1.85), smoking (HR, 1.57), type 2 diabetes (HR, 1.42), hypertension (HR, 1.39), and cancers (HR, 1.37).
Generally, changes in CRF of at least 1.0 MET were associated with inverse and proportionate changes in mortality risk, regardless of baseline CRF status. For example, they note, a CRF decline of > 2.0 METs was associated with a 74% increased mortality risk for low-fit individuals with CVD, and a 69% increase for those without CVD.
A second analysis was done after excluding patients whose CRF declined and who died within 2 years of their last ETT, to account for the possibility that higher mortality rates and CRF declines were consequences of underlying disease (reverse causality). The association between changes in CRF and mortality risk persisted and remained similar to that observed in the entire cohort.
The authors add, “It is noteworthy that CRF increased by at least 1 MET in approximately 29% of the participants in the current study and decreased in approximately 46% of participants. This finding underscores the need to promote physical activity to maintain or increase CRF levels in middle-aged and older individuals.”
“Our findings make a persuasive argument that CRF is a strong and independent determinant of all-cause mortality risk, independent of genetic factors,” Dr. Kokkinos said. “We know that CRF is determined to some degree by genetic factors. However, improvements in aerobic capacity or CRF over time are largely the outcomes of regular engagement in aerobic activities of adequate intensity and volume.”
“Conversely,” he said, “a decline in CRF is likely the result of sedentary behavior, the onset of a chronic condition, or aging.”
If genetics were the sole contributor to mortality risk, then changes in CRF would not influence mortality risk, he concluded.
CRF impact “woefully underestimated”
Barry A. Franklin, PhD, past chair of both the American Heart Association’s Council on Physical Activity and Metabolism and the National Advocacy Committee, said the study substantiates previous smaller studies and is a “seminal” work.
“CRF is woefully underestimated as an index of health outcomes and survival,” said Dr. Franklin, director of preventive cardiology and cardiac rehabilitation at Beaumont Health in Royal Oak, Mich. “Moderate to vigorous physical activity should be regularly promoted by the medical community.”
Dr. Franklin’s recent review, published in Mayo Clinic Proceedings, provides evidence for other exercise benefits that clinicians may not be aware of, he noted. These include:
- Each 1 MET increase in CRF is generally associated with approximately 16% reduction in mortality.
- At any given risk factor profile or coronary calcium score, unfit people have 2-3 times the mortality as their fit counterparts.
- Fitness is inversely related to annual health care costs (each 1 MET increase in CRF is associated with approximately 6% lower annual health care costs).
- Physically active people hospitalized with acute coronary syndromes have better short-term outcomes (likely because of a phenomenon called ‘exercise preconditioning’).
- Fit people who undergo elective or emergent surgical procedures have better outcomes.
- Regular physical activity is a common characteristic in population subsets who routinely live into their 90s and to 100+.
Dr. Franklin had this advice for clinicians seeking to promote CRF increases of 1 MET or more among patients: “Sedentary people who embark on a walking program, who over time increase their walking speed to 3 mph or faster, invariably show at least a 1 MET increase in CRF during subsequent peak or symptom-limited treadmill testing.”
“Another general rule is that if an exercise program decreases heart rate at a given or fixed workload by about 10 beats per minute [bpm], the same treadmill workload that initially was accomplished at a heart rate of 120 bpm is now being accomplished at a heart rate of 110 bpm,” likely resulting in about a 1 MET increase in fitness.
“Accordingly,” he added, “a 20-bpm decrease would suggest a 2 MET increase in fitness!”
In a related editorial, Leonard A. Kaminsky, Ball State University, Muncie, Ind. and colleagues, write, “We agree with and believe the conclusion, reached by Kokkinos et al., bears repeating. We (again) call on both clinicians and public health professionals to adopt CRF as a key health indicator.”
“This should be done by coupling routine assessments of CRF with continued advocacy for promoting physical activity as an essential healthy lifestyle behavior,” they write.
No funding or relevant financial relationships were disclosed.
A version of this article first appeared on Medscape.com.
Even relatively small changes in cardiorespiratory fitness (CRF) are associated with “considerable” impact on clinical symptoms and mortality risk among individuals with and without cardiovascular disease, new observational data in United States veterans suggest.
“We had a few surprises,” Peter Kokkinos, PhD, Robert Wood Johnson Medical School, New Brunswick, N. J., and the VA Medical Center, Washington, told this news organization. “First, the mortality risk was greatly attenuated in those who were moderate- and high-fit at baseline, despite a decline in fitness over time. In fact, in those with no CVD, the risk was not significantly elevated even when CRF declined by at least one MET [metabolic equivalent of task] for the moderate-fit and two or more METs for the high-fit group.”
“Second,” he said, “Our findings suggest that the impact of CRF on human health is not ephemeral, but rather carries a certain protection over time. Third, the changes in CRF necessary to impact mortality risk are relatively small (> 1.0 METs). This has a substantial clinical and public health significance.”
The study was published online in the Journal of the American College of Cardiology.
CRF up, mortality risk down
Dr. Kokkinos and colleagues analyzed data from 93,060 U.S. veterans; of these, 95% were men (mean age, 61.4 years) and 5% were women (mean age, 57.1 years). Overall, 72% of participants were White; 19.8%, African American; 5.2%, Hispanic; 1.9%, Native American, Asian, or Hawaiian; and 1.2%, unknown.
Participants were assigned to age-specific fitness quartiles based on peak METs achieved on a baseline exercise treadmill test (ETT). Each CRF quartile was stratified based on CRF changes (increase, decrease, no change) on the final ETT, with at least two ETT assessments at least 1 year apart.
The mean follow-up was 5.8 years (663,522 person-years), during which 18,302 deaths (19.7%) occurred, for an average annual mortality rate of 27.6 events per 1,000 person-years.
CRF was unchanged in 25.1% of the cohort, increased in 29.3%, and decreased in 45.6%. The trend was similar for those with and without CVD.
Significant differences were seen in all variables across CRF categories. In general, body weight, body mass index, CVD risk factors, and overall disease burden were progressively more unfavorable for those in the lowest CRF categories.
Conversely, medication use was progressively higher among those in low CRF categories.
After adjustment, higher CRF was inversely related to mortality risk for the entire cohort, with and without CVD. Cumulative survival rates across CRF categories declined progressively with increased fitness.
For patients with CVD (hazard ratio, 1.11), other significant predictors of all-cause mortality for patients were age (HR, 1.07), body mass index (HR, 0.98), chronic kidney disease (HR, 1.85), smoking (HR, 1.57), type 2 diabetes (HR, 1.42), hypertension (HR, 1.39), and cancers (HR, 1.37).
Generally, changes in CRF of at least 1.0 MET were associated with inverse and proportionate changes in mortality risk, regardless of baseline CRF status. For example, they note, a CRF decline of > 2.0 METs was associated with a 74% increased mortality risk for low-fit individuals with CVD, and a 69% increase for those without CVD.
A second analysis was done after excluding patients whose CRF declined and who died within 2 years of their last ETT, to account for the possibility that higher mortality rates and CRF declines were consequences of underlying disease (reverse causality). The association between changes in CRF and mortality risk persisted and remained similar to that observed in the entire cohort.
The authors add, “It is noteworthy that CRF increased by at least 1 MET in approximately 29% of the participants in the current study and decreased in approximately 46% of participants. This finding underscores the need to promote physical activity to maintain or increase CRF levels in middle-aged and older individuals.”
“Our findings make a persuasive argument that CRF is a strong and independent determinant of all-cause mortality risk, independent of genetic factors,” Dr. Kokkinos said. “We know that CRF is determined to some degree by genetic factors. However, improvements in aerobic capacity or CRF over time are largely the outcomes of regular engagement in aerobic activities of adequate intensity and volume.”
“Conversely,” he said, “a decline in CRF is likely the result of sedentary behavior, the onset of a chronic condition, or aging.”
If genetics were the sole contributor to mortality risk, then changes in CRF would not influence mortality risk, he concluded.
CRF impact “woefully underestimated”
Barry A. Franklin, PhD, past chair of both the American Heart Association’s Council on Physical Activity and Metabolism and the National Advocacy Committee, said the study substantiates previous smaller studies and is a “seminal” work.
“CRF is woefully underestimated as an index of health outcomes and survival,” said Dr. Franklin, director of preventive cardiology and cardiac rehabilitation at Beaumont Health in Royal Oak, Mich. “Moderate to vigorous physical activity should be regularly promoted by the medical community.”
Dr. Franklin’s recent review, published in Mayo Clinic Proceedings, provides evidence for other exercise benefits that clinicians may not be aware of, he noted. These include:
- Each 1 MET increase in CRF is generally associated with approximately 16% reduction in mortality.
- At any given risk factor profile or coronary calcium score, unfit people have 2-3 times the mortality as their fit counterparts.
- Fitness is inversely related to annual health care costs (each 1 MET increase in CRF is associated with approximately 6% lower annual health care costs).
- Physically active people hospitalized with acute coronary syndromes have better short-term outcomes (likely because of a phenomenon called ‘exercise preconditioning’).
- Fit people who undergo elective or emergent surgical procedures have better outcomes.
- Regular physical activity is a common characteristic in population subsets who routinely live into their 90s and to 100+.
Dr. Franklin had this advice for clinicians seeking to promote CRF increases of 1 MET or more among patients: “Sedentary people who embark on a walking program, who over time increase their walking speed to 3 mph or faster, invariably show at least a 1 MET increase in CRF during subsequent peak or symptom-limited treadmill testing.”
“Another general rule is that if an exercise program decreases heart rate at a given or fixed workload by about 10 beats per minute [bpm], the same treadmill workload that initially was accomplished at a heart rate of 120 bpm is now being accomplished at a heart rate of 110 bpm,” likely resulting in about a 1 MET increase in fitness.
“Accordingly,” he added, “a 20-bpm decrease would suggest a 2 MET increase in fitness!”
In a related editorial, Leonard A. Kaminsky, Ball State University, Muncie, Ind. and colleagues, write, “We agree with and believe the conclusion, reached by Kokkinos et al., bears repeating. We (again) call on both clinicians and public health professionals to adopt CRF as a key health indicator.”
“This should be done by coupling routine assessments of CRF with continued advocacy for promoting physical activity as an essential healthy lifestyle behavior,” they write.
No funding or relevant financial relationships were disclosed.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Concussion burden tied to later hypertension in football players
a new study suggests.
Among more than 4,000 participants, 37% had hypertension at a median of 24 years post career and reported a median concussion symptom score (CSS) of 23 on a scale of 0 to 130.
“We have long seen an incompletely explained link between football participation and later-life cardiovascular disease,” Aaron L. Baggish, MD, of Massachusetts Hospital and Harvard Medical School, Boston, told this news organization.
“This study tested [whether] concussion burden during years of active play would be a determinant of later-life hypertension, the most common cause of cardiovascular disease, and indeed found this relationship to be a strong one.”
The study was published online in Circulation.
Link to cognitive decline?
Dr. Baggish and colleagues recruited former professional American-style football (ASF) players to participate in a survey administered by the Football Players Health Study at Harvard University.
Concussion burden was quantified with respect to the occurrence and severity of common concussion symptoms – e.g., headaches, nausea, dizziness, confusion, loss of consciousness (LOC), disorientation, and feeling unsteady on one’s feet – over years of active participation.
Prevalent hypertension was determined either by the participants’ previously receiving from a clinician a recommendation for medication for “high blood pressure” or by the participants’ taking such medication at the time of survey completion. Diabetes status was determined by the participants’ receiving a prior recommendation for or prescription for “diabetes or high blood sugar” medication.
Of 15,070 invited to participate in the study, 4,168 did so. The mean age of the participants was 51.8 years; 39.4% were Black; the mean body mass index was 31.3; and 33.9% were linemen. Participants played for a mean of 6.9 seasons and were surveyed at a median 24.1 years post ASF career completion. The median CSS was 23.
A total of 1,542 participants (37.3%) had hypertension, and 8.8% had diabetes.
After adjustment for established hypertension risk factors, including smoking, race, diabetes, age, and BMI, there was a graded association between CSS category and odds of later-life hypertension and between high CSS exposure and prevalent hypertension.
Results persisted when LOC, a single highly specific severe concussion symptom, was used in isolation as a surrogate for CSS, the investigators noted.
“These results suggest that repetitive early-life brain injury may have later-life implications for cardiovascular health,” they wrote. They also noted that hypertension has been shown to independently increase the risk of cognitive decline.
While premature cognitive decline among ASF players is generally attributed to chronic traumatic encephalopathy, “data from the current study raise the possibility that some element of cognitive decline among former ASF players may be attributable to hypertension,” which is potentially treatable.
“Future studies clarifying associations and causal pathways between brain injury, hypertension, and brain health are warranted,” they concluded.
Dr. Baggish added, “We hope that clinicians will now understand that head injury is an independent risk factor for high blood pressure and will screen vulnerable populations accordingly, as this may lead to better recognition of previously underdiagnosed hypertension with subsequent opportunities for intervention.”
Close monitoring
Commenting on the study, Jonathan Kim, MD, chair-elect of the American College of Cardiology’s Sports–Cardiology Section and chief of sports cardiology at Emory University in Atlanta, said, “They clearly show an independent association, which is not causality but is a new finding that requires more research. To me, it really emphasizes that cardiovascular risk is the most important health consequence that we should be worried about in retired NFL [National Football League] players.
“There are multifactorial reasons – not just repetitive head trauma – why this athletic population is at risk for the development of high blood pressure, even among college players,” he said.
Dr. Kim’s team has shown in studies conducted in collaboration with Dr. Baggish and others that collegiate football players who gain weight and develop increased systolic blood pressure are at risk of developing a “pathologic” cardiovascular phenotype.
Other research from this group showed links between nonsteroidal anti-inflammatory drug use among high school and collegiate ASF players and increased cardiovascular risk, as well as ASF-associated hypertension and ventricular-arterial coupling.
The suggestion that late-life hypertension could play a role in premature cognitive decline among ASF players “warrants further study,” Dr. Kim said, “because we do know that hypertension in the general population can be associated with cognitive decline. So that’s an important future direction.”
He concluded: “It’s a matter of focusing on cardiac prevention.” After their careers, players should be counseled on the importance of losing weight and adopting heart-healthy habits. In addition to some of the traditional concerns that might lead to closer follow-up of these patients, “having a lot of concussions in the history could potentially be another risk factor that should warrant close monitoring of blood pressure and, of course, treatment if necessary.”
The study was supported by Harvard Catalyst/the Harvard Clinical and Translational Science Center and the NFL Players Association. Dr. Baggish and several coauthors have received funding from the NFL Players Association.
A version of this article originally appeared on Medscape.com.
a new study suggests.
Among more than 4,000 participants, 37% had hypertension at a median of 24 years post career and reported a median concussion symptom score (CSS) of 23 on a scale of 0 to 130.
“We have long seen an incompletely explained link between football participation and later-life cardiovascular disease,” Aaron L. Baggish, MD, of Massachusetts Hospital and Harvard Medical School, Boston, told this news organization.
“This study tested [whether] concussion burden during years of active play would be a determinant of later-life hypertension, the most common cause of cardiovascular disease, and indeed found this relationship to be a strong one.”
The study was published online in Circulation.
Link to cognitive decline?
Dr. Baggish and colleagues recruited former professional American-style football (ASF) players to participate in a survey administered by the Football Players Health Study at Harvard University.
Concussion burden was quantified with respect to the occurrence and severity of common concussion symptoms – e.g., headaches, nausea, dizziness, confusion, loss of consciousness (LOC), disorientation, and feeling unsteady on one’s feet – over years of active participation.
Prevalent hypertension was determined either by the participants’ previously receiving from a clinician a recommendation for medication for “high blood pressure” or by the participants’ taking such medication at the time of survey completion. Diabetes status was determined by the participants’ receiving a prior recommendation for or prescription for “diabetes or high blood sugar” medication.
Of 15,070 invited to participate in the study, 4,168 did so. The mean age of the participants was 51.8 years; 39.4% were Black; the mean body mass index was 31.3; and 33.9% were linemen. Participants played for a mean of 6.9 seasons and were surveyed at a median 24.1 years post ASF career completion. The median CSS was 23.
A total of 1,542 participants (37.3%) had hypertension, and 8.8% had diabetes.
After adjustment for established hypertension risk factors, including smoking, race, diabetes, age, and BMI, there was a graded association between CSS category and odds of later-life hypertension and between high CSS exposure and prevalent hypertension.
Results persisted when LOC, a single highly specific severe concussion symptom, was used in isolation as a surrogate for CSS, the investigators noted.
“These results suggest that repetitive early-life brain injury may have later-life implications for cardiovascular health,” they wrote. They also noted that hypertension has been shown to independently increase the risk of cognitive decline.
While premature cognitive decline among ASF players is generally attributed to chronic traumatic encephalopathy, “data from the current study raise the possibility that some element of cognitive decline among former ASF players may be attributable to hypertension,” which is potentially treatable.
“Future studies clarifying associations and causal pathways between brain injury, hypertension, and brain health are warranted,” they concluded.
Dr. Baggish added, “We hope that clinicians will now understand that head injury is an independent risk factor for high blood pressure and will screen vulnerable populations accordingly, as this may lead to better recognition of previously underdiagnosed hypertension with subsequent opportunities for intervention.”
Close monitoring
Commenting on the study, Jonathan Kim, MD, chair-elect of the American College of Cardiology’s Sports–Cardiology Section and chief of sports cardiology at Emory University in Atlanta, said, “They clearly show an independent association, which is not causality but is a new finding that requires more research. To me, it really emphasizes that cardiovascular risk is the most important health consequence that we should be worried about in retired NFL [National Football League] players.
“There are multifactorial reasons – not just repetitive head trauma – why this athletic population is at risk for the development of high blood pressure, even among college players,” he said.
Dr. Kim’s team has shown in studies conducted in collaboration with Dr. Baggish and others that collegiate football players who gain weight and develop increased systolic blood pressure are at risk of developing a “pathologic” cardiovascular phenotype.
Other research from this group showed links between nonsteroidal anti-inflammatory drug use among high school and collegiate ASF players and increased cardiovascular risk, as well as ASF-associated hypertension and ventricular-arterial coupling.
The suggestion that late-life hypertension could play a role in premature cognitive decline among ASF players “warrants further study,” Dr. Kim said, “because we do know that hypertension in the general population can be associated with cognitive decline. So that’s an important future direction.”
He concluded: “It’s a matter of focusing on cardiac prevention.” After their careers, players should be counseled on the importance of losing weight and adopting heart-healthy habits. In addition to some of the traditional concerns that might lead to closer follow-up of these patients, “having a lot of concussions in the history could potentially be another risk factor that should warrant close monitoring of blood pressure and, of course, treatment if necessary.”
The study was supported by Harvard Catalyst/the Harvard Clinical and Translational Science Center and the NFL Players Association. Dr. Baggish and several coauthors have received funding from the NFL Players Association.
A version of this article originally appeared on Medscape.com.
a new study suggests.
Among more than 4,000 participants, 37% had hypertension at a median of 24 years post career and reported a median concussion symptom score (CSS) of 23 on a scale of 0 to 130.
“We have long seen an incompletely explained link between football participation and later-life cardiovascular disease,” Aaron L. Baggish, MD, of Massachusetts Hospital and Harvard Medical School, Boston, told this news organization.
“This study tested [whether] concussion burden during years of active play would be a determinant of later-life hypertension, the most common cause of cardiovascular disease, and indeed found this relationship to be a strong one.”
The study was published online in Circulation.
Link to cognitive decline?
Dr. Baggish and colleagues recruited former professional American-style football (ASF) players to participate in a survey administered by the Football Players Health Study at Harvard University.
Concussion burden was quantified with respect to the occurrence and severity of common concussion symptoms – e.g., headaches, nausea, dizziness, confusion, loss of consciousness (LOC), disorientation, and feeling unsteady on one’s feet – over years of active participation.
Prevalent hypertension was determined either by the participants’ previously receiving from a clinician a recommendation for medication for “high blood pressure” or by the participants’ taking such medication at the time of survey completion. Diabetes status was determined by the participants’ receiving a prior recommendation for or prescription for “diabetes or high blood sugar” medication.
Of 15,070 invited to participate in the study, 4,168 did so. The mean age of the participants was 51.8 years; 39.4% were Black; the mean body mass index was 31.3; and 33.9% were linemen. Participants played for a mean of 6.9 seasons and were surveyed at a median 24.1 years post ASF career completion. The median CSS was 23.
A total of 1,542 participants (37.3%) had hypertension, and 8.8% had diabetes.
After adjustment for established hypertension risk factors, including smoking, race, diabetes, age, and BMI, there was a graded association between CSS category and odds of later-life hypertension and between high CSS exposure and prevalent hypertension.
Results persisted when LOC, a single highly specific severe concussion symptom, was used in isolation as a surrogate for CSS, the investigators noted.
“These results suggest that repetitive early-life brain injury may have later-life implications for cardiovascular health,” they wrote. They also noted that hypertension has been shown to independently increase the risk of cognitive decline.
While premature cognitive decline among ASF players is generally attributed to chronic traumatic encephalopathy, “data from the current study raise the possibility that some element of cognitive decline among former ASF players may be attributable to hypertension,” which is potentially treatable.
“Future studies clarifying associations and causal pathways between brain injury, hypertension, and brain health are warranted,” they concluded.
Dr. Baggish added, “We hope that clinicians will now understand that head injury is an independent risk factor for high blood pressure and will screen vulnerable populations accordingly, as this may lead to better recognition of previously underdiagnosed hypertension with subsequent opportunities for intervention.”
Close monitoring
Commenting on the study, Jonathan Kim, MD, chair-elect of the American College of Cardiology’s Sports–Cardiology Section and chief of sports cardiology at Emory University in Atlanta, said, “They clearly show an independent association, which is not causality but is a new finding that requires more research. To me, it really emphasizes that cardiovascular risk is the most important health consequence that we should be worried about in retired NFL [National Football League] players.
“There are multifactorial reasons – not just repetitive head trauma – why this athletic population is at risk for the development of high blood pressure, even among college players,” he said.
Dr. Kim’s team has shown in studies conducted in collaboration with Dr. Baggish and others that collegiate football players who gain weight and develop increased systolic blood pressure are at risk of developing a “pathologic” cardiovascular phenotype.
Other research from this group showed links between nonsteroidal anti-inflammatory drug use among high school and collegiate ASF players and increased cardiovascular risk, as well as ASF-associated hypertension and ventricular-arterial coupling.
The suggestion that late-life hypertension could play a role in premature cognitive decline among ASF players “warrants further study,” Dr. Kim said, “because we do know that hypertension in the general population can be associated with cognitive decline. So that’s an important future direction.”
He concluded: “It’s a matter of focusing on cardiac prevention.” After their careers, players should be counseled on the importance of losing weight and adopting heart-healthy habits. In addition to some of the traditional concerns that might lead to closer follow-up of these patients, “having a lot of concussions in the history could potentially be another risk factor that should warrant close monitoring of blood pressure and, of course, treatment if necessary.”
The study was supported by Harvard Catalyst/the Harvard Clinical and Translational Science Center and the NFL Players Association. Dr. Baggish and several coauthors have received funding from the NFL Players Association.
A version of this article originally appeared on Medscape.com.
FROM CIRCULATION
Cardiac issues twice as likely with COVID plus high troponin
Hospitalized COVID-19 patients with high troponin levels are twice as likely to have cardiac abnormalities than those with normal troponin, with or without COVID-19, a multicenter U.K. study suggests.
The causes were diverse, myocarditis prevalence was lower than previously reported, and myocardial scar emerged as an independent risk factor for adverse cardiovascular outcomes at 12 months.
“We know that multiorgan involvement in hospitalized patients with COVID-19 is common ... and may result in acute myocardial injury, detected by an increase in cardiac troponin concentrations,” John P. Greenwood, PhD, of the University of Leeds (England), told this news organization. “Elevated cardiac troponin is associated with a worse prognosis.”
“Multiple mechanisms of myocardial injury have been proposed and ... mitigation or prevention strategies likely depend on the underpinning mechanisms,” he said. “The sequelae of scar may predispose to late events.”
The study, published online in Circulation, also identified a new pattern of microinfarction on cardiac magnetic resonance (CMR) imaging, highlighting the pro-thrombotic nature of SARS-CoV-2, Dr. Greenwood said.
Injury patterns different
Three hundred and forty-two patients with COVID-19 and elevated troponin levels (COVID+/troponin+) across 25 centers were enrolled between June 2020 and March 2021 in COVID-HEART, deemed an “urgent public health study” in the United Kingdom. The aim was to characterize myocardial injury and its associations and sequelae in convalescent patients after hospitalization with COVID-19.
Enrollment took place during the Wuhan and Alpha waves of COVID-19: before vaccination and when dexamethasone and anticoagulant protocols were emerging. All participants underwent CMR at a median of 21 days after discharge.
Two prospective control groups also were recruited: 64 patients with COVID-19 and normal troponin levels (COVID+/troponin−) and 113 without COVID-19 or elevated troponin matched by age and cardiovascular comorbidities (COVID−/comorbidity+).
Overall, participants’ median age was 61 years and 69% were men. Common comorbidities included hypertension (47%), obesity (43%), and diabetes (25%).
The frequency of any heart abnormality – for example, left or right ventricular impairment, scar, or pericardial disease – was twice as great (61%) in COVID+/troponin+ cases, compared with controls (36% for COVID+/troponin− patients versus 31% for COVID−/comorbidity+ patients).
Specifically, more cases than controls had ventricular impairment (17.2% vs. 3.1% and 7.1%) or scar (42% vs. 7% and 23%).
The myocardial injury pattern differed between cases and controls, with cases more likely to have infarction (13% vs. 2% and 7%) or microinfarction (9% vs. 0% and 1%).
However, there was no between-group difference in nonischemic scar (13% vs. 5% and 14%).
The prevalence of probable recent myocarditis was 6.7% in cases, compared with 1.7% in controls without COVID-19 – “much lower” than in previous studies, Dr. Greenwood noted.
During follow-up, four COVID+/troponin+ patients (1.2%) died, and 34 (10%) experienced a subsequent major adverse cardiovascular event (MACE; 10.2%), which was similar to controls (6.1%).
Myocardial scar, but not previous COVID-19 infection or troponin level, was an independent predictor of MACE (odds ratio, 2.25).
“These findings suggest that macroangiopathic and microangiopathic thrombosis may be the key pathologic process for myocardial injury in COVID-19 survivors,” the authors conclude.
Dr. Greenwood added, “We are currently analyzing the 6-month follow-up CMR scans, the quality-of-life questionnaires, and the 6-minute walk tests. These will give us great understanding of how the heart repairs after acute myocardial injury associated with COVID-19. It will also allow us to assess the impact on patient quality of life and functional capacity.”
‘Tour de force’
James A. de Lemos, MD, co-chair of the American Heart Association’s COVID-19 CVD Registry Steering Committee and a professor of medicine at the University of Texas Southwestern Medical Center, Dallas, said, “This is a tour de force collaboration – obtaining this many MRIs across multiple centers in the pandemic is quite remarkable. The study highlights the multiple different processes that lead to cardiac injury in COVID patients, complements autopsy studies and prior smaller MRI studies, [and] also provides the best data on the rate of myocarditis to date among the subset of COVID patients with cardiac injury.”
Overall, he said, the findings “do support closer follow-up for patients who had COVID and elevated troponins. We need to see follow-up MRI results in this cohort, as well as longer term outcomes. We also need studies on newer, more benign variants that are likely to have lower rates of cardiac injury and even fewer MRI abnormalities.”
Matthias Stuber, PhD, and Aaron L. Baggish, MD, both of Lausanne University Hospital and University of Lausanne, Switzerland, noted in a related editorial, “We are also reminded that the clinical severity of COVID-19 is most often dictated by the presence of pre-existing comorbidity, with antecedent ischemic scar now added to the long list of bad actors. Although not the primary focus of the COVID-HEART study, the question of whether cardiac troponin levels should be checked routinely and universally during the index admission for COVID-19 remains unresolved,” they noted.
“In general, we are most effective as clinicians when we use tests to confirm or rule out the specific disease processes suspected by careful basic clinical assessment rather than in a shotgun manner among undifferentiated all-comers,” they conclude.
No commercial funding or relevant financial relationships were reported.
A version of this article originally appeared on Medscape.com.
Hospitalized COVID-19 patients with high troponin levels are twice as likely to have cardiac abnormalities than those with normal troponin, with or without COVID-19, a multicenter U.K. study suggests.
The causes were diverse, myocarditis prevalence was lower than previously reported, and myocardial scar emerged as an independent risk factor for adverse cardiovascular outcomes at 12 months.
“We know that multiorgan involvement in hospitalized patients with COVID-19 is common ... and may result in acute myocardial injury, detected by an increase in cardiac troponin concentrations,” John P. Greenwood, PhD, of the University of Leeds (England), told this news organization. “Elevated cardiac troponin is associated with a worse prognosis.”
“Multiple mechanisms of myocardial injury have been proposed and ... mitigation or prevention strategies likely depend on the underpinning mechanisms,” he said. “The sequelae of scar may predispose to late events.”
The study, published online in Circulation, also identified a new pattern of microinfarction on cardiac magnetic resonance (CMR) imaging, highlighting the pro-thrombotic nature of SARS-CoV-2, Dr. Greenwood said.
Injury patterns different
Three hundred and forty-two patients with COVID-19 and elevated troponin levels (COVID+/troponin+) across 25 centers were enrolled between June 2020 and March 2021 in COVID-HEART, deemed an “urgent public health study” in the United Kingdom. The aim was to characterize myocardial injury and its associations and sequelae in convalescent patients after hospitalization with COVID-19.
Enrollment took place during the Wuhan and Alpha waves of COVID-19: before vaccination and when dexamethasone and anticoagulant protocols were emerging. All participants underwent CMR at a median of 21 days after discharge.
Two prospective control groups also were recruited: 64 patients with COVID-19 and normal troponin levels (COVID+/troponin−) and 113 without COVID-19 or elevated troponin matched by age and cardiovascular comorbidities (COVID−/comorbidity+).
Overall, participants’ median age was 61 years and 69% were men. Common comorbidities included hypertension (47%), obesity (43%), and diabetes (25%).
The frequency of any heart abnormality – for example, left or right ventricular impairment, scar, or pericardial disease – was twice as great (61%) in COVID+/troponin+ cases, compared with controls (36% for COVID+/troponin− patients versus 31% for COVID−/comorbidity+ patients).
Specifically, more cases than controls had ventricular impairment (17.2% vs. 3.1% and 7.1%) or scar (42% vs. 7% and 23%).
The myocardial injury pattern differed between cases and controls, with cases more likely to have infarction (13% vs. 2% and 7%) or microinfarction (9% vs. 0% and 1%).
However, there was no between-group difference in nonischemic scar (13% vs. 5% and 14%).
The prevalence of probable recent myocarditis was 6.7% in cases, compared with 1.7% in controls without COVID-19 – “much lower” than in previous studies, Dr. Greenwood noted.
During follow-up, four COVID+/troponin+ patients (1.2%) died, and 34 (10%) experienced a subsequent major adverse cardiovascular event (MACE; 10.2%), which was similar to controls (6.1%).
Myocardial scar, but not previous COVID-19 infection or troponin level, was an independent predictor of MACE (odds ratio, 2.25).
“These findings suggest that macroangiopathic and microangiopathic thrombosis may be the key pathologic process for myocardial injury in COVID-19 survivors,” the authors conclude.
Dr. Greenwood added, “We are currently analyzing the 6-month follow-up CMR scans, the quality-of-life questionnaires, and the 6-minute walk tests. These will give us great understanding of how the heart repairs after acute myocardial injury associated with COVID-19. It will also allow us to assess the impact on patient quality of life and functional capacity.”
‘Tour de force’
James A. de Lemos, MD, co-chair of the American Heart Association’s COVID-19 CVD Registry Steering Committee and a professor of medicine at the University of Texas Southwestern Medical Center, Dallas, said, “This is a tour de force collaboration – obtaining this many MRIs across multiple centers in the pandemic is quite remarkable. The study highlights the multiple different processes that lead to cardiac injury in COVID patients, complements autopsy studies and prior smaller MRI studies, [and] also provides the best data on the rate of myocarditis to date among the subset of COVID patients with cardiac injury.”
Overall, he said, the findings “do support closer follow-up for patients who had COVID and elevated troponins. We need to see follow-up MRI results in this cohort, as well as longer term outcomes. We also need studies on newer, more benign variants that are likely to have lower rates of cardiac injury and even fewer MRI abnormalities.”
Matthias Stuber, PhD, and Aaron L. Baggish, MD, both of Lausanne University Hospital and University of Lausanne, Switzerland, noted in a related editorial, “We are also reminded that the clinical severity of COVID-19 is most often dictated by the presence of pre-existing comorbidity, with antecedent ischemic scar now added to the long list of bad actors. Although not the primary focus of the COVID-HEART study, the question of whether cardiac troponin levels should be checked routinely and universally during the index admission for COVID-19 remains unresolved,” they noted.
“In general, we are most effective as clinicians when we use tests to confirm or rule out the specific disease processes suspected by careful basic clinical assessment rather than in a shotgun manner among undifferentiated all-comers,” they conclude.
No commercial funding or relevant financial relationships were reported.
A version of this article originally appeared on Medscape.com.
Hospitalized COVID-19 patients with high troponin levels are twice as likely to have cardiac abnormalities than those with normal troponin, with or without COVID-19, a multicenter U.K. study suggests.
The causes were diverse, myocarditis prevalence was lower than previously reported, and myocardial scar emerged as an independent risk factor for adverse cardiovascular outcomes at 12 months.
“We know that multiorgan involvement in hospitalized patients with COVID-19 is common ... and may result in acute myocardial injury, detected by an increase in cardiac troponin concentrations,” John P. Greenwood, PhD, of the University of Leeds (England), told this news organization. “Elevated cardiac troponin is associated with a worse prognosis.”
“Multiple mechanisms of myocardial injury have been proposed and ... mitigation or prevention strategies likely depend on the underpinning mechanisms,” he said. “The sequelae of scar may predispose to late events.”
The study, published online in Circulation, also identified a new pattern of microinfarction on cardiac magnetic resonance (CMR) imaging, highlighting the pro-thrombotic nature of SARS-CoV-2, Dr. Greenwood said.
Injury patterns different
Three hundred and forty-two patients with COVID-19 and elevated troponin levels (COVID+/troponin+) across 25 centers were enrolled between June 2020 and March 2021 in COVID-HEART, deemed an “urgent public health study” in the United Kingdom. The aim was to characterize myocardial injury and its associations and sequelae in convalescent patients after hospitalization with COVID-19.
Enrollment took place during the Wuhan and Alpha waves of COVID-19: before vaccination and when dexamethasone and anticoagulant protocols were emerging. All participants underwent CMR at a median of 21 days after discharge.
Two prospective control groups also were recruited: 64 patients with COVID-19 and normal troponin levels (COVID+/troponin−) and 113 without COVID-19 or elevated troponin matched by age and cardiovascular comorbidities (COVID−/comorbidity+).
Overall, participants’ median age was 61 years and 69% were men. Common comorbidities included hypertension (47%), obesity (43%), and diabetes (25%).
The frequency of any heart abnormality – for example, left or right ventricular impairment, scar, or pericardial disease – was twice as great (61%) in COVID+/troponin+ cases, compared with controls (36% for COVID+/troponin− patients versus 31% for COVID−/comorbidity+ patients).
Specifically, more cases than controls had ventricular impairment (17.2% vs. 3.1% and 7.1%) or scar (42% vs. 7% and 23%).
The myocardial injury pattern differed between cases and controls, with cases more likely to have infarction (13% vs. 2% and 7%) or microinfarction (9% vs. 0% and 1%).
However, there was no between-group difference in nonischemic scar (13% vs. 5% and 14%).
The prevalence of probable recent myocarditis was 6.7% in cases, compared with 1.7% in controls without COVID-19 – “much lower” than in previous studies, Dr. Greenwood noted.
During follow-up, four COVID+/troponin+ patients (1.2%) died, and 34 (10%) experienced a subsequent major adverse cardiovascular event (MACE; 10.2%), which was similar to controls (6.1%).
Myocardial scar, but not previous COVID-19 infection or troponin level, was an independent predictor of MACE (odds ratio, 2.25).
“These findings suggest that macroangiopathic and microangiopathic thrombosis may be the key pathologic process for myocardial injury in COVID-19 survivors,” the authors conclude.
Dr. Greenwood added, “We are currently analyzing the 6-month follow-up CMR scans, the quality-of-life questionnaires, and the 6-minute walk tests. These will give us great understanding of how the heart repairs after acute myocardial injury associated with COVID-19. It will also allow us to assess the impact on patient quality of life and functional capacity.”
‘Tour de force’
James A. de Lemos, MD, co-chair of the American Heart Association’s COVID-19 CVD Registry Steering Committee and a professor of medicine at the University of Texas Southwestern Medical Center, Dallas, said, “This is a tour de force collaboration – obtaining this many MRIs across multiple centers in the pandemic is quite remarkable. The study highlights the multiple different processes that lead to cardiac injury in COVID patients, complements autopsy studies and prior smaller MRI studies, [and] also provides the best data on the rate of myocarditis to date among the subset of COVID patients with cardiac injury.”
Overall, he said, the findings “do support closer follow-up for patients who had COVID and elevated troponins. We need to see follow-up MRI results in this cohort, as well as longer term outcomes. We also need studies on newer, more benign variants that are likely to have lower rates of cardiac injury and even fewer MRI abnormalities.”
Matthias Stuber, PhD, and Aaron L. Baggish, MD, both of Lausanne University Hospital and University of Lausanne, Switzerland, noted in a related editorial, “We are also reminded that the clinical severity of COVID-19 is most often dictated by the presence of pre-existing comorbidity, with antecedent ischemic scar now added to the long list of bad actors. Although not the primary focus of the COVID-HEART study, the question of whether cardiac troponin levels should be checked routinely and universally during the index admission for COVID-19 remains unresolved,” they noted.
“In general, we are most effective as clinicians when we use tests to confirm or rule out the specific disease processes suspected by careful basic clinical assessment rather than in a shotgun manner among undifferentiated all-comers,” they conclude.
No commercial funding or relevant financial relationships were reported.
A version of this article originally appeared on Medscape.com.
Acute cardiac events common during COVID hospitalization
particularly among those with underlying heart disease, and are associated with more severe disease outcomes, a new study suggests.
“We expected to see acute cardiac events occurring among adults hospitalized with COVID-19 but were surprised by how frequently they occurred,” Rebecca C. Woodruff, PhD, MPH, of the U.S. Centers for Disease Control and Prevention, Atlanta, told this news organization.
Overall, she said, “about 1 in 10 adults experienced an acute cardiac event – including heart attacks and acute heart failure – while hospitalized with COVID-19, and this included people with no preexisting heart disease.”
However, she added, “about a quarter of those with underlying heart disease had an acute cardiac event. These patients tended to experience more severe disease outcomes relative to patients hospitalized with COVID-19 who did not experience an acute cardiac event.”
The findings might be relevant to hospitalizations for other viral diseases, “though we can’t say for sure,” she noted. “This study was modeled off a previous study conducted before the COVID-19 pandemic among adults hospitalized with influenza. About 11.7% of [those] adults experienced an acute cardiac event, which was a similar percentage as what we found among patients hospitalized with COVID-19.”
The study was published online in the Journal of the American College of Cardiology.
Underlying cardiac disease key
Dr. Woodruff and colleagues analyzed medical records on a probability sample of 8,460 adults hospitalized with SARS-CoV-2 infection identified from 99 U.S. counties in 14 U.S. states (about 10% of the United States population) from January to November 2021.
Among participants, 11.4% had an acute cardiac event during their hospitalization. The median age was 69 years; 56.5% were men; 48.7%, non-Hispanic White; 33.6%, non-Hispanic Black; 7.4%, Hispanic; and 7.1%, non-Hispanic Asian or Pacific Islander.
As indicated, the prevalence was higher among those with underlying cardiac disease (23.4%), compared with those without (6.2%).
Acute ischemic heart disease (5.5%) and acute heart failure (5.4%) were the most prevalent events; 0.3% of participants had acute myocarditis or pericarditis.
Risk factors varied, depending on underlying cardiac disease status. Those who experienced one or more acute cardiac events had a greater risk for intensive care unit admission (adjusted risk ratio,1.9) and in-hospital death (aRR, 1.7) versus those who did not.
In multivariable analyses, the risk of experiencing acute heart failure was significantly greater among men (aRR, 1.5) and among those with a history of congestive heart failure (aRR, 13.5), atrial fibrillation (aRR, 1.6) or hypertension (aRR,1.3).
Among patients who experienced one or more acute cardiac events, 39.2% required an intensive care unit stay for a median of 5 days. Approximately 22.4% required invasive mechanical ventilation or extracorporeal membrane oxygenation, and 21.1% died while hospitalized.
“Persons at greater risk for experiencing acute cardiac events during COVID-19–associated hospitalizations might benefit from more intensive clinical evaluation and monitoring during hospitalization,” the authors conclude.
The team currently is taking a closer look at acute myocarditis among patients hospitalized with COVID-19, Dr. Woodruff said. Preliminary results were presented at the 2022 annual scientific sessions of the American Heart Association and a paper is forthcoming.
Contemporary data needed
James A. de Lemos, MD, co-chair of the American Heart Association’s COVID-19 CVD Registry Steering Committee and professor of medicine at the University of Texas Southwestern Medical Center, Dallas, said the findings mirror his team’s clinical experience in 2020 and 2021 and echo what was seen in the AHA COVID registry: that is, a 0.3% rate of myocarditis.
“The major caveat is that [the findings] may not be generalizable to contemporary COVID infection, both due to changing viral variants and higher levels of immunity in the population,” he said.
“Rates of COVID hospitalization are markedly lower with the current dominant variants, and we would expect the cardiac risk to be lower as well. I would like to see more contemporary data with current variants, particularly focused on higher risk patients with cardiovascular disease,” Dr. de Lemos added.
In a related editorial, George A. Mensa, MD, of the National Heart, Lung, and Blood Institute in Bethesda, Md., and colleagues suggest that the broader impact of the COVID-19 pandemic on human health remains “incompletely examined.”
“The impact of COVID-19 on cardiovascular mortality, in particular, appears to have varied widely, with no large increases seen in a number of the most developed countries but marked increases in hypertensive heart disease mortality seen in the United States in 2021,” they conclude. “The potential contribution of COVID-19 to these deaths, either directly or indirectly, remains to be determined.”
No commercial funding or relevant financial relationships were reported.
A version of this article first appeared on Medscape.com.
particularly among those with underlying heart disease, and are associated with more severe disease outcomes, a new study suggests.
“We expected to see acute cardiac events occurring among adults hospitalized with COVID-19 but were surprised by how frequently they occurred,” Rebecca C. Woodruff, PhD, MPH, of the U.S. Centers for Disease Control and Prevention, Atlanta, told this news organization.
Overall, she said, “about 1 in 10 adults experienced an acute cardiac event – including heart attacks and acute heart failure – while hospitalized with COVID-19, and this included people with no preexisting heart disease.”
However, she added, “about a quarter of those with underlying heart disease had an acute cardiac event. These patients tended to experience more severe disease outcomes relative to patients hospitalized with COVID-19 who did not experience an acute cardiac event.”
The findings might be relevant to hospitalizations for other viral diseases, “though we can’t say for sure,” she noted. “This study was modeled off a previous study conducted before the COVID-19 pandemic among adults hospitalized with influenza. About 11.7% of [those] adults experienced an acute cardiac event, which was a similar percentage as what we found among patients hospitalized with COVID-19.”
The study was published online in the Journal of the American College of Cardiology.
Underlying cardiac disease key
Dr. Woodruff and colleagues analyzed medical records on a probability sample of 8,460 adults hospitalized with SARS-CoV-2 infection identified from 99 U.S. counties in 14 U.S. states (about 10% of the United States population) from January to November 2021.
Among participants, 11.4% had an acute cardiac event during their hospitalization. The median age was 69 years; 56.5% were men; 48.7%, non-Hispanic White; 33.6%, non-Hispanic Black; 7.4%, Hispanic; and 7.1%, non-Hispanic Asian or Pacific Islander.
As indicated, the prevalence was higher among those with underlying cardiac disease (23.4%), compared with those without (6.2%).
Acute ischemic heart disease (5.5%) and acute heart failure (5.4%) were the most prevalent events; 0.3% of participants had acute myocarditis or pericarditis.
Risk factors varied, depending on underlying cardiac disease status. Those who experienced one or more acute cardiac events had a greater risk for intensive care unit admission (adjusted risk ratio,1.9) and in-hospital death (aRR, 1.7) versus those who did not.
In multivariable analyses, the risk of experiencing acute heart failure was significantly greater among men (aRR, 1.5) and among those with a history of congestive heart failure (aRR, 13.5), atrial fibrillation (aRR, 1.6) or hypertension (aRR,1.3).
Among patients who experienced one or more acute cardiac events, 39.2% required an intensive care unit stay for a median of 5 days. Approximately 22.4% required invasive mechanical ventilation or extracorporeal membrane oxygenation, and 21.1% died while hospitalized.
“Persons at greater risk for experiencing acute cardiac events during COVID-19–associated hospitalizations might benefit from more intensive clinical evaluation and monitoring during hospitalization,” the authors conclude.
The team currently is taking a closer look at acute myocarditis among patients hospitalized with COVID-19, Dr. Woodruff said. Preliminary results were presented at the 2022 annual scientific sessions of the American Heart Association and a paper is forthcoming.
Contemporary data needed
James A. de Lemos, MD, co-chair of the American Heart Association’s COVID-19 CVD Registry Steering Committee and professor of medicine at the University of Texas Southwestern Medical Center, Dallas, said the findings mirror his team’s clinical experience in 2020 and 2021 and echo what was seen in the AHA COVID registry: that is, a 0.3% rate of myocarditis.
“The major caveat is that [the findings] may not be generalizable to contemporary COVID infection, both due to changing viral variants and higher levels of immunity in the population,” he said.
“Rates of COVID hospitalization are markedly lower with the current dominant variants, and we would expect the cardiac risk to be lower as well. I would like to see more contemporary data with current variants, particularly focused on higher risk patients with cardiovascular disease,” Dr. de Lemos added.
In a related editorial, George A. Mensa, MD, of the National Heart, Lung, and Blood Institute in Bethesda, Md., and colleagues suggest that the broader impact of the COVID-19 pandemic on human health remains “incompletely examined.”
“The impact of COVID-19 on cardiovascular mortality, in particular, appears to have varied widely, with no large increases seen in a number of the most developed countries but marked increases in hypertensive heart disease mortality seen in the United States in 2021,” they conclude. “The potential contribution of COVID-19 to these deaths, either directly or indirectly, remains to be determined.”
No commercial funding or relevant financial relationships were reported.
A version of this article first appeared on Medscape.com.
particularly among those with underlying heart disease, and are associated with more severe disease outcomes, a new study suggests.
“We expected to see acute cardiac events occurring among adults hospitalized with COVID-19 but were surprised by how frequently they occurred,” Rebecca C. Woodruff, PhD, MPH, of the U.S. Centers for Disease Control and Prevention, Atlanta, told this news organization.
Overall, she said, “about 1 in 10 adults experienced an acute cardiac event – including heart attacks and acute heart failure – while hospitalized with COVID-19, and this included people with no preexisting heart disease.”
However, she added, “about a quarter of those with underlying heart disease had an acute cardiac event. These patients tended to experience more severe disease outcomes relative to patients hospitalized with COVID-19 who did not experience an acute cardiac event.”
The findings might be relevant to hospitalizations for other viral diseases, “though we can’t say for sure,” she noted. “This study was modeled off a previous study conducted before the COVID-19 pandemic among adults hospitalized with influenza. About 11.7% of [those] adults experienced an acute cardiac event, which was a similar percentage as what we found among patients hospitalized with COVID-19.”
The study was published online in the Journal of the American College of Cardiology.
Underlying cardiac disease key
Dr. Woodruff and colleagues analyzed medical records on a probability sample of 8,460 adults hospitalized with SARS-CoV-2 infection identified from 99 U.S. counties in 14 U.S. states (about 10% of the United States population) from January to November 2021.
Among participants, 11.4% had an acute cardiac event during their hospitalization. The median age was 69 years; 56.5% were men; 48.7%, non-Hispanic White; 33.6%, non-Hispanic Black; 7.4%, Hispanic; and 7.1%, non-Hispanic Asian or Pacific Islander.
As indicated, the prevalence was higher among those with underlying cardiac disease (23.4%), compared with those without (6.2%).
Acute ischemic heart disease (5.5%) and acute heart failure (5.4%) were the most prevalent events; 0.3% of participants had acute myocarditis or pericarditis.
Risk factors varied, depending on underlying cardiac disease status. Those who experienced one or more acute cardiac events had a greater risk for intensive care unit admission (adjusted risk ratio,1.9) and in-hospital death (aRR, 1.7) versus those who did not.
In multivariable analyses, the risk of experiencing acute heart failure was significantly greater among men (aRR, 1.5) and among those with a history of congestive heart failure (aRR, 13.5), atrial fibrillation (aRR, 1.6) or hypertension (aRR,1.3).
Among patients who experienced one or more acute cardiac events, 39.2% required an intensive care unit stay for a median of 5 days. Approximately 22.4% required invasive mechanical ventilation or extracorporeal membrane oxygenation, and 21.1% died while hospitalized.
“Persons at greater risk for experiencing acute cardiac events during COVID-19–associated hospitalizations might benefit from more intensive clinical evaluation and monitoring during hospitalization,” the authors conclude.
The team currently is taking a closer look at acute myocarditis among patients hospitalized with COVID-19, Dr. Woodruff said. Preliminary results were presented at the 2022 annual scientific sessions of the American Heart Association and a paper is forthcoming.
Contemporary data needed
James A. de Lemos, MD, co-chair of the American Heart Association’s COVID-19 CVD Registry Steering Committee and professor of medicine at the University of Texas Southwestern Medical Center, Dallas, said the findings mirror his team’s clinical experience in 2020 and 2021 and echo what was seen in the AHA COVID registry: that is, a 0.3% rate of myocarditis.
“The major caveat is that [the findings] may not be generalizable to contemporary COVID infection, both due to changing viral variants and higher levels of immunity in the population,” he said.
“Rates of COVID hospitalization are markedly lower with the current dominant variants, and we would expect the cardiac risk to be lower as well. I would like to see more contemporary data with current variants, particularly focused on higher risk patients with cardiovascular disease,” Dr. de Lemos added.
In a related editorial, George A. Mensa, MD, of the National Heart, Lung, and Blood Institute in Bethesda, Md., and colleagues suggest that the broader impact of the COVID-19 pandemic on human health remains “incompletely examined.”
“The impact of COVID-19 on cardiovascular mortality, in particular, appears to have varied widely, with no large increases seen in a number of the most developed countries but marked increases in hypertensive heart disease mortality seen in the United States in 2021,” they conclude. “The potential contribution of COVID-19 to these deaths, either directly or indirectly, remains to be determined.”
No commercial funding or relevant financial relationships were reported.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Little evidence to support lasers for ‘vaginal rejuvenation’
Laser devices licensed in Canada to treat genitourinary syndrome of menopause (GSM) are often marketed for vaginal rejuvenation with claims that they will tighten the vagina and improve sexual function, despite lack of evidence, a new commentary reveals.
Vaginal lasers heat the vaginal epithelium and cause thermal necrosis. This intervention induces collagen remodeling and synthesis, neovascularization, and elastin formation and may result in improved vaginal elasticity and restoration of premenopausal epithelial function, according to coauthors Blayne Welk, MD, MSc, an associate professor of urologic surgery at Western University, London, Ont., and Erin Kelly, MD, a lecturer in obstetrics and gynecology at the University of Alberta, Edmonton.
Their patients’ questions and experiences with the laser devices prompted the commentary, they told this news organization.
“A large part of my practice involves addressing GSM and urinary incontinence,” said Dr. Kelly. “Many women present to the clinic having heard of vaginal laser procedures, having had vaginal laser procedures, or having been told they need vaginal laser procedures. My impression has been that these procedures are being marketed to women … without rigorous study.”
“Many women are reluctant to have mesh slings for stress incontinence due to some of the potential risks,” and they are looking for less invasive options, said Dr. Welk. Over the past few years, he has had increasing questions from patients about the use of lasers to improve this condition.
The commentary was published online in the Canadian Medical Association Journal.
Transparency needed
The first vaginal energy device was licensed by Health Canada in 2015 to treat GSM. That meant the device was deemed to have met basic safety, effectiveness, and quality criteria. But no controlled studies are required for regulatory approval of such devices, and after licensing, some providers rebranded the device indication from GSM to vaginal rejuvenation, said Dr. Kelly and Dr. Welk.
Vaginal laser therapies are offered throughout Canada, with at least one provider of vaginal rejuvenation procedures in the 10 most populous cities. Under the current system, the number of patients who pay for these procedures and the amount that they pay cannot be tracked. Nor can the number of vaginal laser systems active in Canada be tracked. Patients can refer themselves for the service, and providers’ publicly quoted costs (on websites, for example) are thousands of dollars for treatment.
The rebranding for vaginal rejuvenation “represents a difference between the licensing of a medical device by Health Canada and the way that these devices are used and marketed,” according to the commentary. “A procedure with limited high-quality evidence supporting its efficacy and a potential financial conflict of interest for providers may not be serving the best interests of people in Canada, even if the risk of adverse events is low.”
Updates to Canada’s medical devices action plan, including mandatory reporting of serious incidents and the ability to compel manufacturers to provide information on safety and effectiveness, “represent important progress,” according to Dr. Kelly and Dr. Welk. However, problems persist, including lack of a requirement for peer-reviewed, controlled studies.
Furthermore, women who undergo laser treatment for GSM, urinary incontinence, or vaginal rejuvenation may not receive a proper medical evaluation and standard treatments, the authors noted.
“I would like to see more transparency and public-facing information available on approved medical devices,” said Dr. Welk. “Health Canada has an online database of approved devices, but no information around the evidence submitted during the approval process is available, nor are the indications for the various devices.”
In addition, he said, many devices in the registry are listed by a serial number rather than the name that would be familiar to the public, “making it hard to match up information.”
Dr. Kelly added the “encouraging” news that the Canadian Society for Pelvic Medicine is working with Health Canada to “improve knowledge translation when it comes to transparency regarding medical devices.”
Medicine before marketing
“The commentary provides an accurate and evidence-based assessment of the use of vaginal laser treatments,” Jason Abbott, B Med (Hons), PhD, professor of gynecology at the University of New South Wales, Sydney, told this news organization. “The marketing of this device is a case of putting the cart before the horse. It is essential that strong, scientific, and reproducible studies be available on efficacy and safety before there is a direct-to-consumer marketing approach.”
Clinicians should advise patients when the treatment effect is likely to be minimal or risky, especially when there is a financial incentive to the clinician, he said. “Governments, regulators, and medical societies have a duty of care to the public to make sure that the medicine comes before the marketing. Otherwise, we are no better than snake oil sellers.
“Given the size of studies to date, the improvement in symptoms following treatment may be less than a few percent,” he noted. “That may be acceptable to some women. We don’t know.”
Dr. Abbott’s team is conducting research to define what women would want as a minimal level of improvement, the maximum cost, and the maximum risk from the laser procedure.
“In cancer … the benefit of a new treatment may only be a few percent for survival,” he said. “That may be completely acceptable for some or even many patients. What we cannot do, however, is extrapolate those same expectations to a treatment for a benign condition where quality of life is compromised.”
Echoing Dr. Kelly and Dr. Welk, Dr. Abbott said, “It is important that there be transparency in the clinical communication. Patients should be told that the best scientific studies that are judged based on their quality show there is no benefit to laser treatment for GSM or urinary incontinence.”
Although the medical risks may be low, he added, “financial risk also needs to be discussed. Patients should be encouraged to participate in clinical trials where there is no cost to them to gain the information first, before wholesale uptake of the treatment. … Should patients still wish to undergo the procedure once the risks and an honest account of the evidence is given to them, that of course is their choice.” Dr. Kelly, Dr. Welk, and Dr. Abbott had no commercial funding or relevant financial relationships to report.
A version of this article first appeared on Medscape.com.
Laser devices licensed in Canada to treat genitourinary syndrome of menopause (GSM) are often marketed for vaginal rejuvenation with claims that they will tighten the vagina and improve sexual function, despite lack of evidence, a new commentary reveals.
Vaginal lasers heat the vaginal epithelium and cause thermal necrosis. This intervention induces collagen remodeling and synthesis, neovascularization, and elastin formation and may result in improved vaginal elasticity and restoration of premenopausal epithelial function, according to coauthors Blayne Welk, MD, MSc, an associate professor of urologic surgery at Western University, London, Ont., and Erin Kelly, MD, a lecturer in obstetrics and gynecology at the University of Alberta, Edmonton.
Their patients’ questions and experiences with the laser devices prompted the commentary, they told this news organization.
“A large part of my practice involves addressing GSM and urinary incontinence,” said Dr. Kelly. “Many women present to the clinic having heard of vaginal laser procedures, having had vaginal laser procedures, or having been told they need vaginal laser procedures. My impression has been that these procedures are being marketed to women … without rigorous study.”
“Many women are reluctant to have mesh slings for stress incontinence due to some of the potential risks,” and they are looking for less invasive options, said Dr. Welk. Over the past few years, he has had increasing questions from patients about the use of lasers to improve this condition.
The commentary was published online in the Canadian Medical Association Journal.
Transparency needed
The first vaginal energy device was licensed by Health Canada in 2015 to treat GSM. That meant the device was deemed to have met basic safety, effectiveness, and quality criteria. But no controlled studies are required for regulatory approval of such devices, and after licensing, some providers rebranded the device indication from GSM to vaginal rejuvenation, said Dr. Kelly and Dr. Welk.
Vaginal laser therapies are offered throughout Canada, with at least one provider of vaginal rejuvenation procedures in the 10 most populous cities. Under the current system, the number of patients who pay for these procedures and the amount that they pay cannot be tracked. Nor can the number of vaginal laser systems active in Canada be tracked. Patients can refer themselves for the service, and providers’ publicly quoted costs (on websites, for example) are thousands of dollars for treatment.
The rebranding for vaginal rejuvenation “represents a difference between the licensing of a medical device by Health Canada and the way that these devices are used and marketed,” according to the commentary. “A procedure with limited high-quality evidence supporting its efficacy and a potential financial conflict of interest for providers may not be serving the best interests of people in Canada, even if the risk of adverse events is low.”
Updates to Canada’s medical devices action plan, including mandatory reporting of serious incidents and the ability to compel manufacturers to provide information on safety and effectiveness, “represent important progress,” according to Dr. Kelly and Dr. Welk. However, problems persist, including lack of a requirement for peer-reviewed, controlled studies.
Furthermore, women who undergo laser treatment for GSM, urinary incontinence, or vaginal rejuvenation may not receive a proper medical evaluation and standard treatments, the authors noted.
“I would like to see more transparency and public-facing information available on approved medical devices,” said Dr. Welk. “Health Canada has an online database of approved devices, but no information around the evidence submitted during the approval process is available, nor are the indications for the various devices.”
In addition, he said, many devices in the registry are listed by a serial number rather than the name that would be familiar to the public, “making it hard to match up information.”
Dr. Kelly added the “encouraging” news that the Canadian Society for Pelvic Medicine is working with Health Canada to “improve knowledge translation when it comes to transparency regarding medical devices.”
Medicine before marketing
“The commentary provides an accurate and evidence-based assessment of the use of vaginal laser treatments,” Jason Abbott, B Med (Hons), PhD, professor of gynecology at the University of New South Wales, Sydney, told this news organization. “The marketing of this device is a case of putting the cart before the horse. It is essential that strong, scientific, and reproducible studies be available on efficacy and safety before there is a direct-to-consumer marketing approach.”
Clinicians should advise patients when the treatment effect is likely to be minimal or risky, especially when there is a financial incentive to the clinician, he said. “Governments, regulators, and medical societies have a duty of care to the public to make sure that the medicine comes before the marketing. Otherwise, we are no better than snake oil sellers.
“Given the size of studies to date, the improvement in symptoms following treatment may be less than a few percent,” he noted. “That may be acceptable to some women. We don’t know.”
Dr. Abbott’s team is conducting research to define what women would want as a minimal level of improvement, the maximum cost, and the maximum risk from the laser procedure.
“In cancer … the benefit of a new treatment may only be a few percent for survival,” he said. “That may be completely acceptable for some or even many patients. What we cannot do, however, is extrapolate those same expectations to a treatment for a benign condition where quality of life is compromised.”
Echoing Dr. Kelly and Dr. Welk, Dr. Abbott said, “It is important that there be transparency in the clinical communication. Patients should be told that the best scientific studies that are judged based on their quality show there is no benefit to laser treatment for GSM or urinary incontinence.”
Although the medical risks may be low, he added, “financial risk also needs to be discussed. Patients should be encouraged to participate in clinical trials where there is no cost to them to gain the information first, before wholesale uptake of the treatment. … Should patients still wish to undergo the procedure once the risks and an honest account of the evidence is given to them, that of course is their choice.” Dr. Kelly, Dr. Welk, and Dr. Abbott had no commercial funding or relevant financial relationships to report.
A version of this article first appeared on Medscape.com.
Laser devices licensed in Canada to treat genitourinary syndrome of menopause (GSM) are often marketed for vaginal rejuvenation with claims that they will tighten the vagina and improve sexual function, despite lack of evidence, a new commentary reveals.
Vaginal lasers heat the vaginal epithelium and cause thermal necrosis. This intervention induces collagen remodeling and synthesis, neovascularization, and elastin formation and may result in improved vaginal elasticity and restoration of premenopausal epithelial function, according to coauthors Blayne Welk, MD, MSc, an associate professor of urologic surgery at Western University, London, Ont., and Erin Kelly, MD, a lecturer in obstetrics and gynecology at the University of Alberta, Edmonton.
Their patients’ questions and experiences with the laser devices prompted the commentary, they told this news organization.
“A large part of my practice involves addressing GSM and urinary incontinence,” said Dr. Kelly. “Many women present to the clinic having heard of vaginal laser procedures, having had vaginal laser procedures, or having been told they need vaginal laser procedures. My impression has been that these procedures are being marketed to women … without rigorous study.”
“Many women are reluctant to have mesh slings for stress incontinence due to some of the potential risks,” and they are looking for less invasive options, said Dr. Welk. Over the past few years, he has had increasing questions from patients about the use of lasers to improve this condition.
The commentary was published online in the Canadian Medical Association Journal.
Transparency needed
The first vaginal energy device was licensed by Health Canada in 2015 to treat GSM. That meant the device was deemed to have met basic safety, effectiveness, and quality criteria. But no controlled studies are required for regulatory approval of such devices, and after licensing, some providers rebranded the device indication from GSM to vaginal rejuvenation, said Dr. Kelly and Dr. Welk.
Vaginal laser therapies are offered throughout Canada, with at least one provider of vaginal rejuvenation procedures in the 10 most populous cities. Under the current system, the number of patients who pay for these procedures and the amount that they pay cannot be tracked. Nor can the number of vaginal laser systems active in Canada be tracked. Patients can refer themselves for the service, and providers’ publicly quoted costs (on websites, for example) are thousands of dollars for treatment.
The rebranding for vaginal rejuvenation “represents a difference between the licensing of a medical device by Health Canada and the way that these devices are used and marketed,” according to the commentary. “A procedure with limited high-quality evidence supporting its efficacy and a potential financial conflict of interest for providers may not be serving the best interests of people in Canada, even if the risk of adverse events is low.”
Updates to Canada’s medical devices action plan, including mandatory reporting of serious incidents and the ability to compel manufacturers to provide information on safety and effectiveness, “represent important progress,” according to Dr. Kelly and Dr. Welk. However, problems persist, including lack of a requirement for peer-reviewed, controlled studies.
Furthermore, women who undergo laser treatment for GSM, urinary incontinence, or vaginal rejuvenation may not receive a proper medical evaluation and standard treatments, the authors noted.
“I would like to see more transparency and public-facing information available on approved medical devices,” said Dr. Welk. “Health Canada has an online database of approved devices, but no information around the evidence submitted during the approval process is available, nor are the indications for the various devices.”
In addition, he said, many devices in the registry are listed by a serial number rather than the name that would be familiar to the public, “making it hard to match up information.”
Dr. Kelly added the “encouraging” news that the Canadian Society for Pelvic Medicine is working with Health Canada to “improve knowledge translation when it comes to transparency regarding medical devices.”
Medicine before marketing
“The commentary provides an accurate and evidence-based assessment of the use of vaginal laser treatments,” Jason Abbott, B Med (Hons), PhD, professor of gynecology at the University of New South Wales, Sydney, told this news organization. “The marketing of this device is a case of putting the cart before the horse. It is essential that strong, scientific, and reproducible studies be available on efficacy and safety before there is a direct-to-consumer marketing approach.”
Clinicians should advise patients when the treatment effect is likely to be minimal or risky, especially when there is a financial incentive to the clinician, he said. “Governments, regulators, and medical societies have a duty of care to the public to make sure that the medicine comes before the marketing. Otherwise, we are no better than snake oil sellers.
“Given the size of studies to date, the improvement in symptoms following treatment may be less than a few percent,” he noted. “That may be acceptable to some women. We don’t know.”
Dr. Abbott’s team is conducting research to define what women would want as a minimal level of improvement, the maximum cost, and the maximum risk from the laser procedure.
“In cancer … the benefit of a new treatment may only be a few percent for survival,” he said. “That may be completely acceptable for some or even many patients. What we cannot do, however, is extrapolate those same expectations to a treatment for a benign condition where quality of life is compromised.”
Echoing Dr. Kelly and Dr. Welk, Dr. Abbott said, “It is important that there be transparency in the clinical communication. Patients should be told that the best scientific studies that are judged based on their quality show there is no benefit to laser treatment for GSM or urinary incontinence.”
Although the medical risks may be low, he added, “financial risk also needs to be discussed. Patients should be encouraged to participate in clinical trials where there is no cost to them to gain the information first, before wholesale uptake of the treatment. … Should patients still wish to undergo the procedure once the risks and an honest account of the evidence is given to them, that of course is their choice.” Dr. Kelly, Dr. Welk, and Dr. Abbott had no commercial funding or relevant financial relationships to report.
A version of this article first appeared on Medscape.com.
Similar brain atrophy in obesity and Alzheimer’s disease
Comparisons of MRI scans for more than 1,000 participants indicate correlations between the two conditions, especially in areas of gray matter thinning, suggesting that managing excess weight might slow cognitive decline and lower the risk for AD, according to the researchers.
However, brain maps of obesity did not correlate with maps of amyloid or tau protein accumulation.
“The fact that obesity-related brain atrophy did not correlate with the distribution of amyloid and tau proteins in AD was not what we expected,” study author Filip Morys, PhD, a postdoctoral researcher at McGill University, Montreal, said in an interview. “But it might just show that the specific mechanisms underpinning obesity- and Alzheimer’s disease–related neurodegeneration are different. This remains to be confirmed.”
The study was published in the Journal of Alzheimer’s Disease.
Cortical Thinning
The current study was prompted by the team’s earlier study, which showed that obesity-related neurodegeneration patterns were visually similar to those of AD, said Dr. Morys. “It was known previously that obesity is a risk factor for AD, but we wanted to directly compare brain atrophy patterns in both, which is what we did in this new study.”
The researchers analyzed data from a pooled sample of more than 1,300 participants. From the ADNI database, the researchers selected participants with AD and age- and sex-matched cognitively healthy controls. From the UK Biobank, the researchers drew a sample of lean, overweight, and obese participants without neurologic disease.
To determine how the weight status of patients with AD affects the correspondence between AD and obesity maps, they categorized participants with AD and healthy controls from the ADNI database into lean, overweight, and obese subgroups.
Then, to investigate mechanisms that might drive the similarities between obesity-related brain atrophy and AD-related amyloid-beta accumulation, they looked for overlapping areas in PET brain maps between patients with these outcomes.
The investigations showed that obesity maps were highly correlated with AD maps, but not with amyloid-beta or tau protein maps. The researchers also found significant correlations between obesity and the lean individuals with AD.
Brain regions with the highest similarities between obesity and AD were located mainly in the left temporal and bilateral prefrontal cortices.
“Our research confirms that obesity-related gray matter atrophy resembles that of AD,” the authors concluded. “Excess weight management could lead to improved health outcomes, slow down cognitive decline in aging, and lower the risk for AD.”
Upcoming research “will focus on investigating how weight loss can affect the risk for AD, other dementias, and cognitive decline in general,” said Dr. Morys. “At this point, our study suggests that obesity prevention, weight loss, but also decreasing other metabolic risk factors related to obesity, such as type-2 diabetes or hypertension, might reduce the risk for AD and have beneficial effects on cognition.”
Lifestyle habits
Commenting on the findings, Claire Sexton, DPhil, vice president of scientific programs and outreach at the Alzheimer’s Association, cautioned that a single cross-sectional study isn’t conclusive. “Previous studies have illustrated that the relationship between obesity and dementia is complex. Growing evidence indicates that people can reduce their risk of cognitive decline by adopting key lifestyle habits, like regular exercise, a heart-healthy diet and staying socially and cognitively engaged.”
The Alzheimer’s Association is leading a 2-year clinical trial, U.S. Pointer, to study how targeting these risk factors in combination may reduce risk for cognitive decline in older adults.
The work was supported by a Foundation Scheme award from the Canadian Institutes of Health Research. Dr. Morys received a postdoctoral fellowship from Fonds de Recherche du Quebec – Santé. Data collection and sharing were funded by the Alzheimer’s Disease Neuroimaging Initiative, the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and multiple pharmaceutical companies and other private sector organizations. Dr. Morys and Dr. Sexton reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Comparisons of MRI scans for more than 1,000 participants indicate correlations between the two conditions, especially in areas of gray matter thinning, suggesting that managing excess weight might slow cognitive decline and lower the risk for AD, according to the researchers.
However, brain maps of obesity did not correlate with maps of amyloid or tau protein accumulation.
“The fact that obesity-related brain atrophy did not correlate with the distribution of amyloid and tau proteins in AD was not what we expected,” study author Filip Morys, PhD, a postdoctoral researcher at McGill University, Montreal, said in an interview. “But it might just show that the specific mechanisms underpinning obesity- and Alzheimer’s disease–related neurodegeneration are different. This remains to be confirmed.”
The study was published in the Journal of Alzheimer’s Disease.
Cortical Thinning
The current study was prompted by the team’s earlier study, which showed that obesity-related neurodegeneration patterns were visually similar to those of AD, said Dr. Morys. “It was known previously that obesity is a risk factor for AD, but we wanted to directly compare brain atrophy patterns in both, which is what we did in this new study.”
The researchers analyzed data from a pooled sample of more than 1,300 participants. From the ADNI database, the researchers selected participants with AD and age- and sex-matched cognitively healthy controls. From the UK Biobank, the researchers drew a sample of lean, overweight, and obese participants without neurologic disease.
To determine how the weight status of patients with AD affects the correspondence between AD and obesity maps, they categorized participants with AD and healthy controls from the ADNI database into lean, overweight, and obese subgroups.
Then, to investigate mechanisms that might drive the similarities between obesity-related brain atrophy and AD-related amyloid-beta accumulation, they looked for overlapping areas in PET brain maps between patients with these outcomes.
The investigations showed that obesity maps were highly correlated with AD maps, but not with amyloid-beta or tau protein maps. The researchers also found significant correlations between obesity and the lean individuals with AD.
Brain regions with the highest similarities between obesity and AD were located mainly in the left temporal and bilateral prefrontal cortices.
“Our research confirms that obesity-related gray matter atrophy resembles that of AD,” the authors concluded. “Excess weight management could lead to improved health outcomes, slow down cognitive decline in aging, and lower the risk for AD.”
Upcoming research “will focus on investigating how weight loss can affect the risk for AD, other dementias, and cognitive decline in general,” said Dr. Morys. “At this point, our study suggests that obesity prevention, weight loss, but also decreasing other metabolic risk factors related to obesity, such as type-2 diabetes or hypertension, might reduce the risk for AD and have beneficial effects on cognition.”
Lifestyle habits
Commenting on the findings, Claire Sexton, DPhil, vice president of scientific programs and outreach at the Alzheimer’s Association, cautioned that a single cross-sectional study isn’t conclusive. “Previous studies have illustrated that the relationship between obesity and dementia is complex. Growing evidence indicates that people can reduce their risk of cognitive decline by adopting key lifestyle habits, like regular exercise, a heart-healthy diet and staying socially and cognitively engaged.”
The Alzheimer’s Association is leading a 2-year clinical trial, U.S. Pointer, to study how targeting these risk factors in combination may reduce risk for cognitive decline in older adults.
The work was supported by a Foundation Scheme award from the Canadian Institutes of Health Research. Dr. Morys received a postdoctoral fellowship from Fonds de Recherche du Quebec – Santé. Data collection and sharing were funded by the Alzheimer’s Disease Neuroimaging Initiative, the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and multiple pharmaceutical companies and other private sector organizations. Dr. Morys and Dr. Sexton reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Comparisons of MRI scans for more than 1,000 participants indicate correlations between the two conditions, especially in areas of gray matter thinning, suggesting that managing excess weight might slow cognitive decline and lower the risk for AD, according to the researchers.
However, brain maps of obesity did not correlate with maps of amyloid or tau protein accumulation.
“The fact that obesity-related brain atrophy did not correlate with the distribution of amyloid and tau proteins in AD was not what we expected,” study author Filip Morys, PhD, a postdoctoral researcher at McGill University, Montreal, said in an interview. “But it might just show that the specific mechanisms underpinning obesity- and Alzheimer’s disease–related neurodegeneration are different. This remains to be confirmed.”
The study was published in the Journal of Alzheimer’s Disease.
Cortical Thinning
The current study was prompted by the team’s earlier study, which showed that obesity-related neurodegeneration patterns were visually similar to those of AD, said Dr. Morys. “It was known previously that obesity is a risk factor for AD, but we wanted to directly compare brain atrophy patterns in both, which is what we did in this new study.”
The researchers analyzed data from a pooled sample of more than 1,300 participants. From the ADNI database, the researchers selected participants with AD and age- and sex-matched cognitively healthy controls. From the UK Biobank, the researchers drew a sample of lean, overweight, and obese participants without neurologic disease.
To determine how the weight status of patients with AD affects the correspondence between AD and obesity maps, they categorized participants with AD and healthy controls from the ADNI database into lean, overweight, and obese subgroups.
Then, to investigate mechanisms that might drive the similarities between obesity-related brain atrophy and AD-related amyloid-beta accumulation, they looked for overlapping areas in PET brain maps between patients with these outcomes.
The investigations showed that obesity maps were highly correlated with AD maps, but not with amyloid-beta or tau protein maps. The researchers also found significant correlations between obesity and the lean individuals with AD.
Brain regions with the highest similarities between obesity and AD were located mainly in the left temporal and bilateral prefrontal cortices.
“Our research confirms that obesity-related gray matter atrophy resembles that of AD,” the authors concluded. “Excess weight management could lead to improved health outcomes, slow down cognitive decline in aging, and lower the risk for AD.”
Upcoming research “will focus on investigating how weight loss can affect the risk for AD, other dementias, and cognitive decline in general,” said Dr. Morys. “At this point, our study suggests that obesity prevention, weight loss, but also decreasing other metabolic risk factors related to obesity, such as type-2 diabetes or hypertension, might reduce the risk for AD and have beneficial effects on cognition.”
Lifestyle habits
Commenting on the findings, Claire Sexton, DPhil, vice president of scientific programs and outreach at the Alzheimer’s Association, cautioned that a single cross-sectional study isn’t conclusive. “Previous studies have illustrated that the relationship between obesity and dementia is complex. Growing evidence indicates that people can reduce their risk of cognitive decline by adopting key lifestyle habits, like regular exercise, a heart-healthy diet and staying socially and cognitively engaged.”
The Alzheimer’s Association is leading a 2-year clinical trial, U.S. Pointer, to study how targeting these risk factors in combination may reduce risk for cognitive decline in older adults.
The work was supported by a Foundation Scheme award from the Canadian Institutes of Health Research. Dr. Morys received a postdoctoral fellowship from Fonds de Recherche du Quebec – Santé. Data collection and sharing were funded by the Alzheimer’s Disease Neuroimaging Initiative, the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and multiple pharmaceutical companies and other private sector organizations. Dr. Morys and Dr. Sexton reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF ALZHEIMER’S DISEASE
Long QT syndrome overdiagnosis persists
Five factors underlie the ongoing overdiagnosis and misdiagnosis of long QT syndrome (LQTS), including temporary QT prolongation following vasovagal syncope, a “pseudo”-positive genetic test result, family history of sudden cardiac death, transient QT prolongation, and misinterpretation of the QTc interval, a new study suggests.
Awareness of these characteristics, which led to a diagnostic reversal in 290 of 1,841 (16%) patients, could reduce the burden of overdiagnosis on the health care system and on patients and families, senior author Michael J. Ackerman, MD, PhD, of Mayo Clinic, Rochester, Minn., and colleagues conclude.
“The findings are a disturbing and disappointing sequel to the paper we published about LQTS overdiagnosis back in 2007, which showed that 2 out of every 5 patients who came to Mayo Clinic for a second opinion left without the diagnosis,” Dr. Ackerman told this news organization.
To date, Dr. Ackerman has reversed the diagnosis for 350 patients, he said.
The consequences of an LQTS diagnosis are “profound,” he noted, including years of unnecessary drug therapy, implantation of a cardioverter defibrillator, disqualification from competitive sports, and emotional stress to the individual and family.
By pointing out the five biggest mistakes his team has seen, he said, “we hope to equip the diagnostician with the means to challenge and assess the veracity of a LQTS diagnosis.”
The study was published online in the Journal of the American College of Cardiology.
Time to do better
Dr. Ackerman and colleagues analyzed electronic medical records on 290 of 1,841 (16%) patients who presented with an outside diagnosis of LQTS but subsequently were dismissed as having normal findings. The mean age of these patients at their first Mayo Clinic evaluation was 22, 60% were female, and the mean QTc interval was 427 ±25 milliseconds.
Overall, 38% of misdiagnoses were the result of misinterpretation of clinical factors; 29%, to diagnostic test misinterpretations; 17%, to an apparently positive genetic test in the context of a weak or absent phenotype; and 16%, to a family history of false LQTS or of sudden cardiac or sudden unexplained death.
More specifically, the most common cause of an LQTS misdiagnosis was QT prolongation following vasovagal syncope, which was misinterpreted as LQTS-attributed syncope.
The second most common cause was an apparently positive genetic test for an LQTS gene that turned out to be a benign or likely benign variant.
The third most common cause was an LQTS diagnosis based solely on a family history of sudden unexplained death (26 patients), QT prolongation (11 patients), or sudden cardiac arrest (9 patients).
The fourth most common cause was an isolated event of QT prolongation (44 patients). The transient QT prolongation was observed under myriad conditions unrelated to LQTS. Yet, 31 patients received a diagnosis based solely on the event.
The fifth most common cause was inclusion of the U-wave in the calculation of the QTc interval (40 patients), leading to an inaccurate interpretation of the electrocardiogram.
Dr. Ackerman noted that these LQTS diagnoses were given by heart-rhythm specialists, and most patients self-referred for a second opinion because a family member questioned the diagnosis after doing their own research.
“It’s time that we step up to the plate and do better,” Dr. Ackerman said. The team’s evaluation of the impact of the misdiagnosis on the patients’ lifestyle and quality of life showed that 45% had been restricted from competitive sports (and subsequently resumed sports activity with no adverse events); 80% had been started on beta-blockers (the drugs were discontinued in 84% as a result of the Mayo Clinic evaluation, whereas 16% opted to continue); and 10 of 22 patients (45%) who received an implanted cardioverter device underwent an extraction of the device without complications.
The authors conclude: “Although missing a patient who truly has LQTS can lead to a tragic outcome, the implications of overdiagnosed LQTS are not trivial and are potentially tragic as well.”
‘Tricky diagnosis’
LQTS specialist Peter Aziz, MD, director of pediatric electrophysiology at the Cleveland Clinic, agreed with these findings.
“Most of us ‘channelopathists’ who see LQTS for a living have a good grasp of the disease, but it can be elusive for others,” he said in an interview. “This is a tricky diagnosis. There are ends of the spectrum where people for sure don’t have it and people for sure do. Most clinicians are able to identify that.”
However, he added, “A lot of patients fall into that gray area where it may not be clear at first, even to an expert. But the expert knows how to do a comprehensive evaluation, examining episodes and symptoms and understanding whether they are relevant to LQTS or completely red herrings, and feeling confident about how they calculate the acute interval on an electrocardiogram.”
“All of these may seem mundane, but without the experience, clinicians are vulnerable to miscalculations,” he said. “That’s why our bias, as channelopathists, is that every patient who has a suspected diagnosis or is being treated for LQTS really should see an expert.”
Similarly, Arthur A.M. Wilde, MD, PhD, of the University of Amsterdam, and Peter J. Schwartz, MD, of IRCCS Istituto Auxologico Italiano, Milan, write in a related editorial that it “has to be kept in mind that both diagnostic scores and risk scores are dynamic and can be modified by time and by appropriate therapy.
“Therefore, to make hasty diagnosis of a disease that requires life-long treatment is inappropriate, especially when this is done without the support of adequate, specific experience.”
No commercial funding or relevant financial relationships were reported.
A version of this article first appeared on Medscape.com.
Five factors underlie the ongoing overdiagnosis and misdiagnosis of long QT syndrome (LQTS), including temporary QT prolongation following vasovagal syncope, a “pseudo”-positive genetic test result, family history of sudden cardiac death, transient QT prolongation, and misinterpretation of the QTc interval, a new study suggests.
Awareness of these characteristics, which led to a diagnostic reversal in 290 of 1,841 (16%) patients, could reduce the burden of overdiagnosis on the health care system and on patients and families, senior author Michael J. Ackerman, MD, PhD, of Mayo Clinic, Rochester, Minn., and colleagues conclude.
“The findings are a disturbing and disappointing sequel to the paper we published about LQTS overdiagnosis back in 2007, which showed that 2 out of every 5 patients who came to Mayo Clinic for a second opinion left without the diagnosis,” Dr. Ackerman told this news organization.
To date, Dr. Ackerman has reversed the diagnosis for 350 patients, he said.
The consequences of an LQTS diagnosis are “profound,” he noted, including years of unnecessary drug therapy, implantation of a cardioverter defibrillator, disqualification from competitive sports, and emotional stress to the individual and family.
By pointing out the five biggest mistakes his team has seen, he said, “we hope to equip the diagnostician with the means to challenge and assess the veracity of a LQTS diagnosis.”
The study was published online in the Journal of the American College of Cardiology.
Time to do better
Dr. Ackerman and colleagues analyzed electronic medical records on 290 of 1,841 (16%) patients who presented with an outside diagnosis of LQTS but subsequently were dismissed as having normal findings. The mean age of these patients at their first Mayo Clinic evaluation was 22, 60% were female, and the mean QTc interval was 427 ±25 milliseconds.
Overall, 38% of misdiagnoses were the result of misinterpretation of clinical factors; 29%, to diagnostic test misinterpretations; 17%, to an apparently positive genetic test in the context of a weak or absent phenotype; and 16%, to a family history of false LQTS or of sudden cardiac or sudden unexplained death.
More specifically, the most common cause of an LQTS misdiagnosis was QT prolongation following vasovagal syncope, which was misinterpreted as LQTS-attributed syncope.
The second most common cause was an apparently positive genetic test for an LQTS gene that turned out to be a benign or likely benign variant.
The third most common cause was an LQTS diagnosis based solely on a family history of sudden unexplained death (26 patients), QT prolongation (11 patients), or sudden cardiac arrest (9 patients).
The fourth most common cause was an isolated event of QT prolongation (44 patients). The transient QT prolongation was observed under myriad conditions unrelated to LQTS. Yet, 31 patients received a diagnosis based solely on the event.
The fifth most common cause was inclusion of the U-wave in the calculation of the QTc interval (40 patients), leading to an inaccurate interpretation of the electrocardiogram.
Dr. Ackerman noted that these LQTS diagnoses were given by heart-rhythm specialists, and most patients self-referred for a second opinion because a family member questioned the diagnosis after doing their own research.
“It’s time that we step up to the plate and do better,” Dr. Ackerman said. The team’s evaluation of the impact of the misdiagnosis on the patients’ lifestyle and quality of life showed that 45% had been restricted from competitive sports (and subsequently resumed sports activity with no adverse events); 80% had been started on beta-blockers (the drugs were discontinued in 84% as a result of the Mayo Clinic evaluation, whereas 16% opted to continue); and 10 of 22 patients (45%) who received an implanted cardioverter device underwent an extraction of the device without complications.
The authors conclude: “Although missing a patient who truly has LQTS can lead to a tragic outcome, the implications of overdiagnosed LQTS are not trivial and are potentially tragic as well.”
‘Tricky diagnosis’
LQTS specialist Peter Aziz, MD, director of pediatric electrophysiology at the Cleveland Clinic, agreed with these findings.
“Most of us ‘channelopathists’ who see LQTS for a living have a good grasp of the disease, but it can be elusive for others,” he said in an interview. “This is a tricky diagnosis. There are ends of the spectrum where people for sure don’t have it and people for sure do. Most clinicians are able to identify that.”
However, he added, “A lot of patients fall into that gray area where it may not be clear at first, even to an expert. But the expert knows how to do a comprehensive evaluation, examining episodes and symptoms and understanding whether they are relevant to LQTS or completely red herrings, and feeling confident about how they calculate the acute interval on an electrocardiogram.”
“All of these may seem mundane, but without the experience, clinicians are vulnerable to miscalculations,” he said. “That’s why our bias, as channelopathists, is that every patient who has a suspected diagnosis or is being treated for LQTS really should see an expert.”
Similarly, Arthur A.M. Wilde, MD, PhD, of the University of Amsterdam, and Peter J. Schwartz, MD, of IRCCS Istituto Auxologico Italiano, Milan, write in a related editorial that it “has to be kept in mind that both diagnostic scores and risk scores are dynamic and can be modified by time and by appropriate therapy.
“Therefore, to make hasty diagnosis of a disease that requires life-long treatment is inappropriate, especially when this is done without the support of adequate, specific experience.”
No commercial funding or relevant financial relationships were reported.
A version of this article first appeared on Medscape.com.
Five factors underlie the ongoing overdiagnosis and misdiagnosis of long QT syndrome (LQTS), including temporary QT prolongation following vasovagal syncope, a “pseudo”-positive genetic test result, family history of sudden cardiac death, transient QT prolongation, and misinterpretation of the QTc interval, a new study suggests.
Awareness of these characteristics, which led to a diagnostic reversal in 290 of 1,841 (16%) patients, could reduce the burden of overdiagnosis on the health care system and on patients and families, senior author Michael J. Ackerman, MD, PhD, of Mayo Clinic, Rochester, Minn., and colleagues conclude.
“The findings are a disturbing and disappointing sequel to the paper we published about LQTS overdiagnosis back in 2007, which showed that 2 out of every 5 patients who came to Mayo Clinic for a second opinion left without the diagnosis,” Dr. Ackerman told this news organization.
To date, Dr. Ackerman has reversed the diagnosis for 350 patients, he said.
The consequences of an LQTS diagnosis are “profound,” he noted, including years of unnecessary drug therapy, implantation of a cardioverter defibrillator, disqualification from competitive sports, and emotional stress to the individual and family.
By pointing out the five biggest mistakes his team has seen, he said, “we hope to equip the diagnostician with the means to challenge and assess the veracity of a LQTS diagnosis.”
The study was published online in the Journal of the American College of Cardiology.
Time to do better
Dr. Ackerman and colleagues analyzed electronic medical records on 290 of 1,841 (16%) patients who presented with an outside diagnosis of LQTS but subsequently were dismissed as having normal findings. The mean age of these patients at their first Mayo Clinic evaluation was 22, 60% were female, and the mean QTc interval was 427 ±25 milliseconds.
Overall, 38% of misdiagnoses were the result of misinterpretation of clinical factors; 29%, to diagnostic test misinterpretations; 17%, to an apparently positive genetic test in the context of a weak or absent phenotype; and 16%, to a family history of false LQTS or of sudden cardiac or sudden unexplained death.
More specifically, the most common cause of an LQTS misdiagnosis was QT prolongation following vasovagal syncope, which was misinterpreted as LQTS-attributed syncope.
The second most common cause was an apparently positive genetic test for an LQTS gene that turned out to be a benign or likely benign variant.
The third most common cause was an LQTS diagnosis based solely on a family history of sudden unexplained death (26 patients), QT prolongation (11 patients), or sudden cardiac arrest (9 patients).
The fourth most common cause was an isolated event of QT prolongation (44 patients). The transient QT prolongation was observed under myriad conditions unrelated to LQTS. Yet, 31 patients received a diagnosis based solely on the event.
The fifth most common cause was inclusion of the U-wave in the calculation of the QTc interval (40 patients), leading to an inaccurate interpretation of the electrocardiogram.
Dr. Ackerman noted that these LQTS diagnoses were given by heart-rhythm specialists, and most patients self-referred for a second opinion because a family member questioned the diagnosis after doing their own research.
“It’s time that we step up to the plate and do better,” Dr. Ackerman said. The team’s evaluation of the impact of the misdiagnosis on the patients’ lifestyle and quality of life showed that 45% had been restricted from competitive sports (and subsequently resumed sports activity with no adverse events); 80% had been started on beta-blockers (the drugs were discontinued in 84% as a result of the Mayo Clinic evaluation, whereas 16% opted to continue); and 10 of 22 patients (45%) who received an implanted cardioverter device underwent an extraction of the device without complications.
The authors conclude: “Although missing a patient who truly has LQTS can lead to a tragic outcome, the implications of overdiagnosed LQTS are not trivial and are potentially tragic as well.”
‘Tricky diagnosis’
LQTS specialist Peter Aziz, MD, director of pediatric electrophysiology at the Cleveland Clinic, agreed with these findings.
“Most of us ‘channelopathists’ who see LQTS for a living have a good grasp of the disease, but it can be elusive for others,” he said in an interview. “This is a tricky diagnosis. There are ends of the spectrum where people for sure don’t have it and people for sure do. Most clinicians are able to identify that.”
However, he added, “A lot of patients fall into that gray area where it may not be clear at first, even to an expert. But the expert knows how to do a comprehensive evaluation, examining episodes and symptoms and understanding whether they are relevant to LQTS or completely red herrings, and feeling confident about how they calculate the acute interval on an electrocardiogram.”
“All of these may seem mundane, but without the experience, clinicians are vulnerable to miscalculations,” he said. “That’s why our bias, as channelopathists, is that every patient who has a suspected diagnosis or is being treated for LQTS really should see an expert.”
Similarly, Arthur A.M. Wilde, MD, PhD, of the University of Amsterdam, and Peter J. Schwartz, MD, of IRCCS Istituto Auxologico Italiano, Milan, write in a related editorial that it “has to be kept in mind that both diagnostic scores and risk scores are dynamic and can be modified by time and by appropriate therapy.
“Therefore, to make hasty diagnosis of a disease that requires life-long treatment is inappropriate, especially when this is done without the support of adequate, specific experience.”
No commercial funding or relevant financial relationships were reported.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY