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Elite soccer players have big hearts and that’s okay
Elite American soccer players have, on average, larger, thicker, and heavier hearts than the general population, according to a new study that provides clinicians with normative echocardiogram and electrocardiogram (ECG) cutoffs to use when assessing the heart health of competitive athletes.
To provide these age- and sex-specific reference values, a team from Massachusetts General Hospital, Boston, led by Timothy W. Churchill, MD, and Aaron L. Baggish, MD, analyzed data from 122 female and 116 male soccer players from the American national teams preparing for World Cup play and undergoing FIFA-mandated preparticipation screening.
The athletes frequently exceeded normal echocardiographic ranges for left ventricular (LV) mass, volume, and wall thickness – structural cardiac parameters responsive to exercise-induced remodeling – but with none showing pathologic findings that might indicate the need to restrict their participation in the sport.
Almost one-third (30%) of female athletes and 41% of male athletes exceeded the American Society of Echocardiography’s upper limit of normal for LV wall thickness, with a measure greater than 12 mm seen in 12% of men and 1% of women.
The majority (51% of females and 59% of males) exceeded normal ranges for body surface area–indexed LV mass, with 77% and 68%, respectively, having LV volumes above the normal range.
Dr. Baggish stressed in an interview, however, that these data tell a story about healthy hearts, not at-risk hearts.
“These are the healthiest, highest-performing elite soccer players that we have in the United States, and this is really a look at how adaptive the heart can be, how much it can grow and change in size, shape, structure, and function in response to sport,” said Dr. Baggish.
The mean age of screened athletes was 20 years (range, 15-40 years). The majority of the female players were White (71%), whereas the male players were more evenly divided between Black (34%), Hispanic (33%), and White (32%).
Screening was performed at U.S. Soccer training sites by experienced clinicians affiliated with the Massachusetts General Hospital cardiovascular performance program.
Interestingly, the study debunks the idea that women, on average, have smaller chamber sizes. “When we did body-size correction, the men and women actually looked pretty similar with respect to their ability to adapt to strenuous exercise,” noted Dr. Baggish.
They did see, however, that women were more likely than men to have abnormal ECG findings. Male athletes showed a higher prevalence of “normal” training-related ECG findings, whereas female athletes were more likely to have abnormal ECG patterns (11.5% vs. 0.0% in the male cohort), most often pathologic T-wave inversions (TWI) confined to the anterior precordial lead distribution.
“This is important because ECGs are the most common screening tool used and we wanted to alert people to the fact that these women who showed some abnormalities on ECG went on to have a total healthy-looking echo, so a false-positive ECG is something to consider,” said Dr. Baggish.
This excess in anterior TWIs has been seen in previous studies and is thought to be benign, although the mechanism remains unclear. Four of the nine female athletes with abnormal ECG findings on initial evaluation had normalized on repeat testing 2-4 years later. Serial data were available in only a subset of athletes.
Clarity needed after COVID
The data, published recently in JAMA Cardiology, are particularly valuable these days given concern over the effects of COVID-19 on the heart and return-to-play recommendations.
“Athletes who have had COVID are being sent for echocardiograms before they can return to play to check for COVID-induced heart disease – which is real – but what we’re seeing is that there’s confusion out there in terms of what is a COVID-related abnormality and what is a normal, adapted athletic heart,” said Dr. Baggish.
“In this paper, we provide a dataset of normal values – generated before COVID was on anyone’s radar – to let cardiologists know what’s ‘big good’ and not ‘big bad.’ ”
More sport-specific data needed
“Although these numbers are still small, this dataset is an important step forward in our understanding of athletic adaptations,” said Matthew Martinez, MD, in an interview. “Many factors impact physiologic athletic changes, and the study aids in our understanding of gender- and sport-specific changes in athletes.”
Dr. Martinez, who is the director of sports cardiology at Atlantic Health–Morristown (N.J.) Medical Center and the Gagnon Cardiovascular Institute, also in Morristown, and the chair of Sports and Exercise Cardiology Section Leadership Council for the American College of Cardiology, noted the relatively young mean age of screened athletes.
“The data represent collegiate-age athletes with some older groups mixed in, but it does not represent older established elite athlete changes,” he said.
Mean age was 21 years in the female players but only 18 years in the males because the men’s senior national team failed to qualify for the World Cup during the study period and was therefore not screened. The authors acknowledged the “dearth of older men in the cohort.”
There is, overall, little age-, sport-, and sex-specific normative data for differentiating training-related cardiovascular adaptations from potentially pathologic phenotypes, wrote the authors.
It exists for men playing in the National Football League and for both sexes participating in the National Basketball Association, but most other studies have mixed the sports and focused mainly on men. That said, Dr. Baggish does not consider these data to be applicable to all elite athletes.
“Soccer is kind of in a league of its own with respect to the mixed amount of explosive or resistant and aerobic work that these athletes have to do, and also it’s the most popular sport in the world, so we really wanted to focus on them,” said Dr. Baggish.
Although the findings are perhaps applicable to athletes from other team sports characterized by explosive spurts of high-intensity activity – like hockey, lacrosse, and field hockey – he would not suggest they be applied to, say, long-distance runners, cyclists, or other sports that require a similar type of aerobic output.
Dr. Baggish reported no relevant conflict of interest. Dr. Martinez is league cardiologist for Major League Soccer.
A version of this article first appeared on Medscape.com.
Elite American soccer players have, on average, larger, thicker, and heavier hearts than the general population, according to a new study that provides clinicians with normative echocardiogram and electrocardiogram (ECG) cutoffs to use when assessing the heart health of competitive athletes.
To provide these age- and sex-specific reference values, a team from Massachusetts General Hospital, Boston, led by Timothy W. Churchill, MD, and Aaron L. Baggish, MD, analyzed data from 122 female and 116 male soccer players from the American national teams preparing for World Cup play and undergoing FIFA-mandated preparticipation screening.
The athletes frequently exceeded normal echocardiographic ranges for left ventricular (LV) mass, volume, and wall thickness – structural cardiac parameters responsive to exercise-induced remodeling – but with none showing pathologic findings that might indicate the need to restrict their participation in the sport.
Almost one-third (30%) of female athletes and 41% of male athletes exceeded the American Society of Echocardiography’s upper limit of normal for LV wall thickness, with a measure greater than 12 mm seen in 12% of men and 1% of women.
The majority (51% of females and 59% of males) exceeded normal ranges for body surface area–indexed LV mass, with 77% and 68%, respectively, having LV volumes above the normal range.
Dr. Baggish stressed in an interview, however, that these data tell a story about healthy hearts, not at-risk hearts.
“These are the healthiest, highest-performing elite soccer players that we have in the United States, and this is really a look at how adaptive the heart can be, how much it can grow and change in size, shape, structure, and function in response to sport,” said Dr. Baggish.
The mean age of screened athletes was 20 years (range, 15-40 years). The majority of the female players were White (71%), whereas the male players were more evenly divided between Black (34%), Hispanic (33%), and White (32%).
Screening was performed at U.S. Soccer training sites by experienced clinicians affiliated with the Massachusetts General Hospital cardiovascular performance program.
Interestingly, the study debunks the idea that women, on average, have smaller chamber sizes. “When we did body-size correction, the men and women actually looked pretty similar with respect to their ability to adapt to strenuous exercise,” noted Dr. Baggish.
They did see, however, that women were more likely than men to have abnormal ECG findings. Male athletes showed a higher prevalence of “normal” training-related ECG findings, whereas female athletes were more likely to have abnormal ECG patterns (11.5% vs. 0.0% in the male cohort), most often pathologic T-wave inversions (TWI) confined to the anterior precordial lead distribution.
“This is important because ECGs are the most common screening tool used and we wanted to alert people to the fact that these women who showed some abnormalities on ECG went on to have a total healthy-looking echo, so a false-positive ECG is something to consider,” said Dr. Baggish.
This excess in anterior TWIs has been seen in previous studies and is thought to be benign, although the mechanism remains unclear. Four of the nine female athletes with abnormal ECG findings on initial evaluation had normalized on repeat testing 2-4 years later. Serial data were available in only a subset of athletes.
Clarity needed after COVID
The data, published recently in JAMA Cardiology, are particularly valuable these days given concern over the effects of COVID-19 on the heart and return-to-play recommendations.
“Athletes who have had COVID are being sent for echocardiograms before they can return to play to check for COVID-induced heart disease – which is real – but what we’re seeing is that there’s confusion out there in terms of what is a COVID-related abnormality and what is a normal, adapted athletic heart,” said Dr. Baggish.
“In this paper, we provide a dataset of normal values – generated before COVID was on anyone’s radar – to let cardiologists know what’s ‘big good’ and not ‘big bad.’ ”
More sport-specific data needed
“Although these numbers are still small, this dataset is an important step forward in our understanding of athletic adaptations,” said Matthew Martinez, MD, in an interview. “Many factors impact physiologic athletic changes, and the study aids in our understanding of gender- and sport-specific changes in athletes.”
Dr. Martinez, who is the director of sports cardiology at Atlantic Health–Morristown (N.J.) Medical Center and the Gagnon Cardiovascular Institute, also in Morristown, and the chair of Sports and Exercise Cardiology Section Leadership Council for the American College of Cardiology, noted the relatively young mean age of screened athletes.
“The data represent collegiate-age athletes with some older groups mixed in, but it does not represent older established elite athlete changes,” he said.
Mean age was 21 years in the female players but only 18 years in the males because the men’s senior national team failed to qualify for the World Cup during the study period and was therefore not screened. The authors acknowledged the “dearth of older men in the cohort.”
There is, overall, little age-, sport-, and sex-specific normative data for differentiating training-related cardiovascular adaptations from potentially pathologic phenotypes, wrote the authors.
It exists for men playing in the National Football League and for both sexes participating in the National Basketball Association, but most other studies have mixed the sports and focused mainly on men. That said, Dr. Baggish does not consider these data to be applicable to all elite athletes.
“Soccer is kind of in a league of its own with respect to the mixed amount of explosive or resistant and aerobic work that these athletes have to do, and also it’s the most popular sport in the world, so we really wanted to focus on them,” said Dr. Baggish.
Although the findings are perhaps applicable to athletes from other team sports characterized by explosive spurts of high-intensity activity – like hockey, lacrosse, and field hockey – he would not suggest they be applied to, say, long-distance runners, cyclists, or other sports that require a similar type of aerobic output.
Dr. Baggish reported no relevant conflict of interest. Dr. Martinez is league cardiologist for Major League Soccer.
A version of this article first appeared on Medscape.com.
Elite American soccer players have, on average, larger, thicker, and heavier hearts than the general population, according to a new study that provides clinicians with normative echocardiogram and electrocardiogram (ECG) cutoffs to use when assessing the heart health of competitive athletes.
To provide these age- and sex-specific reference values, a team from Massachusetts General Hospital, Boston, led by Timothy W. Churchill, MD, and Aaron L. Baggish, MD, analyzed data from 122 female and 116 male soccer players from the American national teams preparing for World Cup play and undergoing FIFA-mandated preparticipation screening.
The athletes frequently exceeded normal echocardiographic ranges for left ventricular (LV) mass, volume, and wall thickness – structural cardiac parameters responsive to exercise-induced remodeling – but with none showing pathologic findings that might indicate the need to restrict their participation in the sport.
Almost one-third (30%) of female athletes and 41% of male athletes exceeded the American Society of Echocardiography’s upper limit of normal for LV wall thickness, with a measure greater than 12 mm seen in 12% of men and 1% of women.
The majority (51% of females and 59% of males) exceeded normal ranges for body surface area–indexed LV mass, with 77% and 68%, respectively, having LV volumes above the normal range.
Dr. Baggish stressed in an interview, however, that these data tell a story about healthy hearts, not at-risk hearts.
“These are the healthiest, highest-performing elite soccer players that we have in the United States, and this is really a look at how adaptive the heart can be, how much it can grow and change in size, shape, structure, and function in response to sport,” said Dr. Baggish.
The mean age of screened athletes was 20 years (range, 15-40 years). The majority of the female players were White (71%), whereas the male players were more evenly divided between Black (34%), Hispanic (33%), and White (32%).
Screening was performed at U.S. Soccer training sites by experienced clinicians affiliated with the Massachusetts General Hospital cardiovascular performance program.
Interestingly, the study debunks the idea that women, on average, have smaller chamber sizes. “When we did body-size correction, the men and women actually looked pretty similar with respect to their ability to adapt to strenuous exercise,” noted Dr. Baggish.
They did see, however, that women were more likely than men to have abnormal ECG findings. Male athletes showed a higher prevalence of “normal” training-related ECG findings, whereas female athletes were more likely to have abnormal ECG patterns (11.5% vs. 0.0% in the male cohort), most often pathologic T-wave inversions (TWI) confined to the anterior precordial lead distribution.
“This is important because ECGs are the most common screening tool used and we wanted to alert people to the fact that these women who showed some abnormalities on ECG went on to have a total healthy-looking echo, so a false-positive ECG is something to consider,” said Dr. Baggish.
This excess in anterior TWIs has been seen in previous studies and is thought to be benign, although the mechanism remains unclear. Four of the nine female athletes with abnormal ECG findings on initial evaluation had normalized on repeat testing 2-4 years later. Serial data were available in only a subset of athletes.
Clarity needed after COVID
The data, published recently in JAMA Cardiology, are particularly valuable these days given concern over the effects of COVID-19 on the heart and return-to-play recommendations.
“Athletes who have had COVID are being sent for echocardiograms before they can return to play to check for COVID-induced heart disease – which is real – but what we’re seeing is that there’s confusion out there in terms of what is a COVID-related abnormality and what is a normal, adapted athletic heart,” said Dr. Baggish.
“In this paper, we provide a dataset of normal values – generated before COVID was on anyone’s radar – to let cardiologists know what’s ‘big good’ and not ‘big bad.’ ”
More sport-specific data needed
“Although these numbers are still small, this dataset is an important step forward in our understanding of athletic adaptations,” said Matthew Martinez, MD, in an interview. “Many factors impact physiologic athletic changes, and the study aids in our understanding of gender- and sport-specific changes in athletes.”
Dr. Martinez, who is the director of sports cardiology at Atlantic Health–Morristown (N.J.) Medical Center and the Gagnon Cardiovascular Institute, also in Morristown, and the chair of Sports and Exercise Cardiology Section Leadership Council for the American College of Cardiology, noted the relatively young mean age of screened athletes.
“The data represent collegiate-age athletes with some older groups mixed in, but it does not represent older established elite athlete changes,” he said.
Mean age was 21 years in the female players but only 18 years in the males because the men’s senior national team failed to qualify for the World Cup during the study period and was therefore not screened. The authors acknowledged the “dearth of older men in the cohort.”
There is, overall, little age-, sport-, and sex-specific normative data for differentiating training-related cardiovascular adaptations from potentially pathologic phenotypes, wrote the authors.
It exists for men playing in the National Football League and for both sexes participating in the National Basketball Association, but most other studies have mixed the sports and focused mainly on men. That said, Dr. Baggish does not consider these data to be applicable to all elite athletes.
“Soccer is kind of in a league of its own with respect to the mixed amount of explosive or resistant and aerobic work that these athletes have to do, and also it’s the most popular sport in the world, so we really wanted to focus on them,” said Dr. Baggish.
Although the findings are perhaps applicable to athletes from other team sports characterized by explosive spurts of high-intensity activity – like hockey, lacrosse, and field hockey – he would not suggest they be applied to, say, long-distance runners, cyclists, or other sports that require a similar type of aerobic output.
Dr. Baggish reported no relevant conflict of interest. Dr. Martinez is league cardiologist for Major League Soccer.
A version of this article first appeared on Medscape.com.
COVID-19 case fatality doubled in heart transplant patients
Heart transplant recipients infected with SARS-CoV-2 are about twice as likely to die from COVID-19 and should be immediately referred to a transplant center for care, according to transplant experts from Northern Italy.
In a COVID Rapid Report published Dec. 9 in JACC Heart Failure, a group led by Tomaso Bottio, MD, PhD, from the University of Padua, Italy, presented findings on 47 heart transplant recipients who tested positive for SARS-Cov-2 between Feb. 21 and June 30.
The investigators found a case fatality rate of 29.7%, compared with 15.4% in the general population. Prevalence of infection was also much higher at 18 cases (vs. 7) per 1,000 population.
“In our opinion, prompt referral to a heart transplant center is crucial for immunosuppressive therapy optimization and cardiologic follow-up,” Dr. Bottio said in an interview.
Beyond the need for careful adjustment of immunosuppression, graft function should be assessed to “avoid acute rejection or decompensation,” he added.
Dr. Bottio and colleagues tracked COVID-19 cases from among the 2,676 heart transplant recipients alive before the onset of the pandemic at seven heart transplant centers in Northern Italy.
Of the 47 recipients who contracted SARS-CoV-2, 38 required hospitalization while 9 remained at home and 14 died. Mean length of stay in hospital was 17.8 days, much longer in survivors than nonsurvivors (23.2 days vs. 8.5 days; P < .001).
Nonsurvivors were significantly older than survivors (72 vs. 58 years; P = .002). Nonsurvivors were also more likely to present with diabetes (P = .04), extra-cardiac arteriopathy (P = .04), previous percutaneous coronary intervention (P = .04), more allograft vasculopathy (P = .04), and more symptoms of heart failure (P = .02).
Although the authors said the high case fatality rate was, unfortunately, expected, they did not expect so many patients to do well at home.
“What most surprised us was the proportion of a- or pauci-symptomatic heart transplanted patients who did well being treated at home without any therapy modifications,” Dr. Bottio shared. They were also surprised to see there were no cases of graft failure caused by infection-related myocarditis.
These findings from Northern Italy are not dissimilar from the 25% case fatality rate seen in a cohort of heart transplant recipients who caught COVID-19 in New York City early in the pandemic.
In another study, this time looking at a wider group of solid organ transplant recipients with SARS-CoV-2 infection at two centers during the first 3 weeks of the outbreak in New York City, 16 of 90 patients (18%) died.
Treatment recommendations?
Recognizing that there is no randomized trial data informing the treatment of this vulnerable patient population, Dr. Bottio and colleagues suggested that, based on their experience, no change in immunosuppression is needed in those who are “pauci-symptomatic” (mildly symptomatic).
“On the other hand, in hospitalized patients a partial reduction in immunosuppressive therapy avoiding full discontinuation and risk of graft rejection seems to be a common strategy in facing the viral infection,” he said. “In addition, the introduction of corticosteroids could help to suspend the onset of the inflammatory cascade responsible for severe forms of the disease.”
Antibiotic prophylaxis appears to be “fundamental,” he added, particularly in hospitalized patients, but “the role of specific antiviral therapies is still not fully understood in our population.”
Since July 1, they’ve seen an additional six patients with a positive test for SARS-CoV-2. Five were asymptomatic and quarantined at home without changing their immunosuppressive therapy. One patient was hospitalized for pneumonia and had immunosuppressive therapy reduced.
Dr. Bottio and the study coauthors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Heart transplant recipients infected with SARS-CoV-2 are about twice as likely to die from COVID-19 and should be immediately referred to a transplant center for care, according to transplant experts from Northern Italy.
In a COVID Rapid Report published Dec. 9 in JACC Heart Failure, a group led by Tomaso Bottio, MD, PhD, from the University of Padua, Italy, presented findings on 47 heart transplant recipients who tested positive for SARS-Cov-2 between Feb. 21 and June 30.
The investigators found a case fatality rate of 29.7%, compared with 15.4% in the general population. Prevalence of infection was also much higher at 18 cases (vs. 7) per 1,000 population.
“In our opinion, prompt referral to a heart transplant center is crucial for immunosuppressive therapy optimization and cardiologic follow-up,” Dr. Bottio said in an interview.
Beyond the need for careful adjustment of immunosuppression, graft function should be assessed to “avoid acute rejection or decompensation,” he added.
Dr. Bottio and colleagues tracked COVID-19 cases from among the 2,676 heart transplant recipients alive before the onset of the pandemic at seven heart transplant centers in Northern Italy.
Of the 47 recipients who contracted SARS-CoV-2, 38 required hospitalization while 9 remained at home and 14 died. Mean length of stay in hospital was 17.8 days, much longer in survivors than nonsurvivors (23.2 days vs. 8.5 days; P < .001).
Nonsurvivors were significantly older than survivors (72 vs. 58 years; P = .002). Nonsurvivors were also more likely to present with diabetes (P = .04), extra-cardiac arteriopathy (P = .04), previous percutaneous coronary intervention (P = .04), more allograft vasculopathy (P = .04), and more symptoms of heart failure (P = .02).
Although the authors said the high case fatality rate was, unfortunately, expected, they did not expect so many patients to do well at home.
“What most surprised us was the proportion of a- or pauci-symptomatic heart transplanted patients who did well being treated at home without any therapy modifications,” Dr. Bottio shared. They were also surprised to see there were no cases of graft failure caused by infection-related myocarditis.
These findings from Northern Italy are not dissimilar from the 25% case fatality rate seen in a cohort of heart transplant recipients who caught COVID-19 in New York City early in the pandemic.
In another study, this time looking at a wider group of solid organ transplant recipients with SARS-CoV-2 infection at two centers during the first 3 weeks of the outbreak in New York City, 16 of 90 patients (18%) died.
Treatment recommendations?
Recognizing that there is no randomized trial data informing the treatment of this vulnerable patient population, Dr. Bottio and colleagues suggested that, based on their experience, no change in immunosuppression is needed in those who are “pauci-symptomatic” (mildly symptomatic).
“On the other hand, in hospitalized patients a partial reduction in immunosuppressive therapy avoiding full discontinuation and risk of graft rejection seems to be a common strategy in facing the viral infection,” he said. “In addition, the introduction of corticosteroids could help to suspend the onset of the inflammatory cascade responsible for severe forms of the disease.”
Antibiotic prophylaxis appears to be “fundamental,” he added, particularly in hospitalized patients, but “the role of specific antiviral therapies is still not fully understood in our population.”
Since July 1, they’ve seen an additional six patients with a positive test for SARS-CoV-2. Five were asymptomatic and quarantined at home without changing their immunosuppressive therapy. One patient was hospitalized for pneumonia and had immunosuppressive therapy reduced.
Dr. Bottio and the study coauthors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Heart transplant recipients infected with SARS-CoV-2 are about twice as likely to die from COVID-19 and should be immediately referred to a transplant center for care, according to transplant experts from Northern Italy.
In a COVID Rapid Report published Dec. 9 in JACC Heart Failure, a group led by Tomaso Bottio, MD, PhD, from the University of Padua, Italy, presented findings on 47 heart transplant recipients who tested positive for SARS-Cov-2 between Feb. 21 and June 30.
The investigators found a case fatality rate of 29.7%, compared with 15.4% in the general population. Prevalence of infection was also much higher at 18 cases (vs. 7) per 1,000 population.
“In our opinion, prompt referral to a heart transplant center is crucial for immunosuppressive therapy optimization and cardiologic follow-up,” Dr. Bottio said in an interview.
Beyond the need for careful adjustment of immunosuppression, graft function should be assessed to “avoid acute rejection or decompensation,” he added.
Dr. Bottio and colleagues tracked COVID-19 cases from among the 2,676 heart transplant recipients alive before the onset of the pandemic at seven heart transplant centers in Northern Italy.
Of the 47 recipients who contracted SARS-CoV-2, 38 required hospitalization while 9 remained at home and 14 died. Mean length of stay in hospital was 17.8 days, much longer in survivors than nonsurvivors (23.2 days vs. 8.5 days; P < .001).
Nonsurvivors were significantly older than survivors (72 vs. 58 years; P = .002). Nonsurvivors were also more likely to present with diabetes (P = .04), extra-cardiac arteriopathy (P = .04), previous percutaneous coronary intervention (P = .04), more allograft vasculopathy (P = .04), and more symptoms of heart failure (P = .02).
Although the authors said the high case fatality rate was, unfortunately, expected, they did not expect so many patients to do well at home.
“What most surprised us was the proportion of a- or pauci-symptomatic heart transplanted patients who did well being treated at home without any therapy modifications,” Dr. Bottio shared. They were also surprised to see there were no cases of graft failure caused by infection-related myocarditis.
These findings from Northern Italy are not dissimilar from the 25% case fatality rate seen in a cohort of heart transplant recipients who caught COVID-19 in New York City early in the pandemic.
In another study, this time looking at a wider group of solid organ transplant recipients with SARS-CoV-2 infection at two centers during the first 3 weeks of the outbreak in New York City, 16 of 90 patients (18%) died.
Treatment recommendations?
Recognizing that there is no randomized trial data informing the treatment of this vulnerable patient population, Dr. Bottio and colleagues suggested that, based on their experience, no change in immunosuppression is needed in those who are “pauci-symptomatic” (mildly symptomatic).
“On the other hand, in hospitalized patients a partial reduction in immunosuppressive therapy avoiding full discontinuation and risk of graft rejection seems to be a common strategy in facing the viral infection,” he said. “In addition, the introduction of corticosteroids could help to suspend the onset of the inflammatory cascade responsible for severe forms of the disease.”
Antibiotic prophylaxis appears to be “fundamental,” he added, particularly in hospitalized patients, but “the role of specific antiviral therapies is still not fully understood in our population.”
Since July 1, they’ve seen an additional six patients with a positive test for SARS-CoV-2. Five were asymptomatic and quarantined at home without changing their immunosuppressive therapy. One patient was hospitalized for pneumonia and had immunosuppressive therapy reduced.
Dr. Bottio and the study coauthors have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Myocarditis rare, macrophage infiltration common at COVID autopsy
An international autopsy study of 21 patients who died from COVID-19 has shown the presence of multifocal lymphocytic myocarditis in three patients (14%). In an additional six patients, focally increased interstitial T-lymphocytes within the myocardium were noted, with only focal or no myocyte injury.
However, increased interstitial macrophage infiltration, possibly related to cytokine infiltration, was seen in 86% of patients.
“One way to think about this is that, if these patients were having biopsies and not autopsies, there would be myocardial injury in the patients with myocarditis, even after they recovered. But with interstitial macrophages, there may or may not be any injury,” said cardiovascular pathologist James R. Stone, MD, PhD, Massachusetts General Hospital, Boston.
Dr. Stone and colleagues from Mass General, two hospitals in Italy, the University of Amsterdam, and the Mayo Clinic in Rochester, Minn., conducted the autopsies in March and April. The results were published in the October 14 issue of the European Heart Journal.
Their technique was rigorous: a median of 20 full-thickness blocks of myocardium were examined histologically (range, 5-29 blocks).
The presence of myocarditis, defined by the presence of multiple foci of inflammation with associated myocyte injury, was determined, and the inflammatory cell composition analyzed by immunohistochemistry.
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“I think one of the take-homes from this study is that you have to do a thorough sampling of the heart in order to exclude myocardial injury. You cannot exclude myocarditis with just a biopsy or two,” said Dr. Stone in an interview.
“We looked at multiple different sections of tissue preserved in paraffin for every case and found only 14% had myocarditis. The vast majority of autopsies done on patients dying from COVID-19 have short-changed the autopsy and not been done in a way to exclude myocarditis,” he added.
For all patients, COVID-19 was the underlying cause of death, but the mechanisms of death were acute respiratory distress syndrome in 15, viral pneumonia in 4, cardiogenic shock in 1, and cardiac arrest in 1. Seven patients had a history of cardiovascular disease, including atrial fibrillation in four, coronary artery disease in three, left ventricular hypertrophy in one, and previous valve replacement in one. A total of 16 had hypertension, 7 had diabetes mellitus, and 1 had chronic obstructive pulmonary disease. In four cases, mild pericarditis was present. Acute myocyte injury in the right ventricle, most probably from strain or overload, was also present in four cases.
A nonsignificant trend was seen toward higher serum troponin levels in the patients with myocarditis compared with those without myocarditis. There were no reports of disrupted coronary artery plaques, coronary artery aneurysms, or large pulmonary emboli.
Macrophage infiltration rather than myocarditis, myocardial injury?
The study sheds more light on previous cardiac magnetic resonance (CMR) imaging findings that have suggested that many patients who recover from COVID-19 show signs suggestive of myocarditis. These earlier studies include a recent one in competitive athletes and the earlier Puntmann and colleagues study of relatively young COVID-19 patients, which showed ongoing myocardial involvement in a majority of patients.
“It would not surprise me if some or all of the cardiac MR changes seen in some of these recent imaging studies are due to the macrophages,” said Dr. Stone.
“What we saw was not a routine pathology by any means. It was a huge amount of macrophages, higher that what we saw in SARS and more similar to a study published in 2007 that looked at patients with bacterial sepsis,” said Dr. Stone.
In an older study of SARS patients, 35% had the virus detected in myocardial tissue by polymerase chain reaction. In that subset, the degree of myocardial macrophage infiltrate was comparable to that seen in 86% of the COVID-19 cases described in this series.
Another possibility is that the macrophage infiltration reflects underlying disease rather than COVID-19. All but one of the patients had known underlying medical conditions associated with cardiac remodeling, said Nikolaos G. Frangogiannis, MD, a cardiologist who studies the mechanisms of cardiac injury, repair, and remodeling.
Frangogiannis, from Albert Einstein College of Medicine, New York, wrote an editorial that accompanied the autopsy study.
“The problem with this finding of increased macrophage infiltration is that it’s very hard to interpret because as we age, and especially in a less healthy population, the numbers and the density of macrophages in the heart increase, so it’s impossible to interpret as an effect of the infection itself unless you have an appropriate control population that matches the same characteristics, which is almost impossible to ask for,” he said.
“I’ve observed since the beginning of the pandemic that there seemed to be some people who wanted every single case to be myocarditis and others who had a bias toward not wanting COVID-19 to be a cause of myocarditis. I think what we’re seeing is it’s not either/or for anything with this virus, it’s a bit of everything,” said Dr. Stone.
Dr. Stone and Dr. Frangogiannis reported no conflict of interest.
A version of this article originally appeared on Medscape.com.
An international autopsy study of 21 patients who died from COVID-19 has shown the presence of multifocal lymphocytic myocarditis in three patients (14%). In an additional six patients, focally increased interstitial T-lymphocytes within the myocardium were noted, with only focal or no myocyte injury.
However, increased interstitial macrophage infiltration, possibly related to cytokine infiltration, was seen in 86% of patients.
“One way to think about this is that, if these patients were having biopsies and not autopsies, there would be myocardial injury in the patients with myocarditis, even after they recovered. But with interstitial macrophages, there may or may not be any injury,” said cardiovascular pathologist James R. Stone, MD, PhD, Massachusetts General Hospital, Boston.
Dr. Stone and colleagues from Mass General, two hospitals in Italy, the University of Amsterdam, and the Mayo Clinic in Rochester, Minn., conducted the autopsies in March and April. The results were published in the October 14 issue of the European Heart Journal.
Their technique was rigorous: a median of 20 full-thickness blocks of myocardium were examined histologically (range, 5-29 blocks).
The presence of myocarditis, defined by the presence of multiple foci of inflammation with associated myocyte injury, was determined, and the inflammatory cell composition analyzed by immunohistochemistry.
[embed:render:related:node:226328]
“I think one of the take-homes from this study is that you have to do a thorough sampling of the heart in order to exclude myocardial injury. You cannot exclude myocarditis with just a biopsy or two,” said Dr. Stone in an interview.
“We looked at multiple different sections of tissue preserved in paraffin for every case and found only 14% had myocarditis. The vast majority of autopsies done on patients dying from COVID-19 have short-changed the autopsy and not been done in a way to exclude myocarditis,” he added.
For all patients, COVID-19 was the underlying cause of death, but the mechanisms of death were acute respiratory distress syndrome in 15, viral pneumonia in 4, cardiogenic shock in 1, and cardiac arrest in 1. Seven patients had a history of cardiovascular disease, including atrial fibrillation in four, coronary artery disease in three, left ventricular hypertrophy in one, and previous valve replacement in one. A total of 16 had hypertension, 7 had diabetes mellitus, and 1 had chronic obstructive pulmonary disease. In four cases, mild pericarditis was present. Acute myocyte injury in the right ventricle, most probably from strain or overload, was also present in four cases.
A nonsignificant trend was seen toward higher serum troponin levels in the patients with myocarditis compared with those without myocarditis. There were no reports of disrupted coronary artery plaques, coronary artery aneurysms, or large pulmonary emboli.
Macrophage infiltration rather than myocarditis, myocardial injury?
The study sheds more light on previous cardiac magnetic resonance (CMR) imaging findings that have suggested that many patients who recover from COVID-19 show signs suggestive of myocarditis. These earlier studies include a recent one in competitive athletes and the earlier Puntmann and colleagues study of relatively young COVID-19 patients, which showed ongoing myocardial involvement in a majority of patients.
“It would not surprise me if some or all of the cardiac MR changes seen in some of these recent imaging studies are due to the macrophages,” said Dr. Stone.
“What we saw was not a routine pathology by any means. It was a huge amount of macrophages, higher that what we saw in SARS and more similar to a study published in 2007 that looked at patients with bacterial sepsis,” said Dr. Stone.
In an older study of SARS patients, 35% had the virus detected in myocardial tissue by polymerase chain reaction. In that subset, the degree of myocardial macrophage infiltrate was comparable to that seen in 86% of the COVID-19 cases described in this series.
Another possibility is that the macrophage infiltration reflects underlying disease rather than COVID-19. All but one of the patients had known underlying medical conditions associated with cardiac remodeling, said Nikolaos G. Frangogiannis, MD, a cardiologist who studies the mechanisms of cardiac injury, repair, and remodeling.
Frangogiannis, from Albert Einstein College of Medicine, New York, wrote an editorial that accompanied the autopsy study.
“The problem with this finding of increased macrophage infiltration is that it’s very hard to interpret because as we age, and especially in a less healthy population, the numbers and the density of macrophages in the heart increase, so it’s impossible to interpret as an effect of the infection itself unless you have an appropriate control population that matches the same characteristics, which is almost impossible to ask for,” he said.
“I’ve observed since the beginning of the pandemic that there seemed to be some people who wanted every single case to be myocarditis and others who had a bias toward not wanting COVID-19 to be a cause of myocarditis. I think what we’re seeing is it’s not either/or for anything with this virus, it’s a bit of everything,” said Dr. Stone.
Dr. Stone and Dr. Frangogiannis reported no conflict of interest.
A version of this article originally appeared on Medscape.com.
An international autopsy study of 21 patients who died from COVID-19 has shown the presence of multifocal lymphocytic myocarditis in three patients (14%). In an additional six patients, focally increased interstitial T-lymphocytes within the myocardium were noted, with only focal or no myocyte injury.
However, increased interstitial macrophage infiltration, possibly related to cytokine infiltration, was seen in 86% of patients.
“One way to think about this is that, if these patients were having biopsies and not autopsies, there would be myocardial injury in the patients with myocarditis, even after they recovered. But with interstitial macrophages, there may or may not be any injury,” said cardiovascular pathologist James R. Stone, MD, PhD, Massachusetts General Hospital, Boston.
Dr. Stone and colleagues from Mass General, two hospitals in Italy, the University of Amsterdam, and the Mayo Clinic in Rochester, Minn., conducted the autopsies in March and April. The results were published in the October 14 issue of the European Heart Journal.
Their technique was rigorous: a median of 20 full-thickness blocks of myocardium were examined histologically (range, 5-29 blocks).
The presence of myocarditis, defined by the presence of multiple foci of inflammation with associated myocyte injury, was determined, and the inflammatory cell composition analyzed by immunohistochemistry.
[embed:render:related:node:226328]
“I think one of the take-homes from this study is that you have to do a thorough sampling of the heart in order to exclude myocardial injury. You cannot exclude myocarditis with just a biopsy or two,” said Dr. Stone in an interview.
“We looked at multiple different sections of tissue preserved in paraffin for every case and found only 14% had myocarditis. The vast majority of autopsies done on patients dying from COVID-19 have short-changed the autopsy and not been done in a way to exclude myocarditis,” he added.
For all patients, COVID-19 was the underlying cause of death, but the mechanisms of death were acute respiratory distress syndrome in 15, viral pneumonia in 4, cardiogenic shock in 1, and cardiac arrest in 1. Seven patients had a history of cardiovascular disease, including atrial fibrillation in four, coronary artery disease in three, left ventricular hypertrophy in one, and previous valve replacement in one. A total of 16 had hypertension, 7 had diabetes mellitus, and 1 had chronic obstructive pulmonary disease. In four cases, mild pericarditis was present. Acute myocyte injury in the right ventricle, most probably from strain or overload, was also present in four cases.
A nonsignificant trend was seen toward higher serum troponin levels in the patients with myocarditis compared with those without myocarditis. There were no reports of disrupted coronary artery plaques, coronary artery aneurysms, or large pulmonary emboli.
Macrophage infiltration rather than myocarditis, myocardial injury?
The study sheds more light on previous cardiac magnetic resonance (CMR) imaging findings that have suggested that many patients who recover from COVID-19 show signs suggestive of myocarditis. These earlier studies include a recent one in competitive athletes and the earlier Puntmann and colleagues study of relatively young COVID-19 patients, which showed ongoing myocardial involvement in a majority of patients.
“It would not surprise me if some or all of the cardiac MR changes seen in some of these recent imaging studies are due to the macrophages,” said Dr. Stone.
“What we saw was not a routine pathology by any means. It was a huge amount of macrophages, higher that what we saw in SARS and more similar to a study published in 2007 that looked at patients with bacterial sepsis,” said Dr. Stone.
In an older study of SARS patients, 35% had the virus detected in myocardial tissue by polymerase chain reaction. In that subset, the degree of myocardial macrophage infiltrate was comparable to that seen in 86% of the COVID-19 cases described in this series.
Another possibility is that the macrophage infiltration reflects underlying disease rather than COVID-19. All but one of the patients had known underlying medical conditions associated with cardiac remodeling, said Nikolaos G. Frangogiannis, MD, a cardiologist who studies the mechanisms of cardiac injury, repair, and remodeling.
Frangogiannis, from Albert Einstein College of Medicine, New York, wrote an editorial that accompanied the autopsy study.
“The problem with this finding of increased macrophage infiltration is that it’s very hard to interpret because as we age, and especially in a less healthy population, the numbers and the density of macrophages in the heart increase, so it’s impossible to interpret as an effect of the infection itself unless you have an appropriate control population that matches the same characteristics, which is almost impossible to ask for,” he said.
“I’ve observed since the beginning of the pandemic that there seemed to be some people who wanted every single case to be myocarditis and others who had a bias toward not wanting COVID-19 to be a cause of myocarditis. I think what we’re seeing is it’s not either/or for anything with this virus, it’s a bit of everything,” said Dr. Stone.
Dr. Stone and Dr. Frangogiannis reported no conflict of interest.
A version of this article originally appeared on Medscape.com.
Proinflammatory dietary pattern linked to higher CV risk
Dietary patterns with higher inflammatory potential were significantly associated with a higher incidence of cardiovascular disease (CVD) and stroke in a new pooled analysis of three prospective cohort studies.
The analysis included 210,145 U.S. women and men followed for up to 32 years in the Nurses’ Health Studies I and II and the Health Professionals Follow-up Study.
After adjustment for use of anti-inflammatory medications and CVD risk factors, those whose dietary pattern ranked in the highest quintile of inflammatory potential had a 38% higher risk of CVD (hazard ratio comparing highest with lowest quintiles, 1.38), a 46% higher risk of coronary heart disease (HR, 1.46), and a 28% higher risk of stroke (HR, 1.28) (all P for trend < .001).
Jun Li, MD, PhD, and colleagues at Harvard School of Public Health and Harvard Medical School, Boston, published the findings of their study in the Nov. 10 issue of the Journal of the American College of Cardiology.
The inflammatory potential of a diet was assessed using a food-based, dietary index called the “empirical dietary inflammatory pattern” or EDIP.
In an interview, Dr. Li explained that the EDIP was developed 4 years ago by many of the same authors involved with this study, including nutrition heavyweights Walter C. Willett, MD, DrPH, and Frank B. Hu, MD, PhD, both from Harvard.
“We summarized all the foods people eat into 39 defined food groups and did a reduced-rank regression analysis that looked at these 39 food groups and three inflammatory markers – interleukin-6, C-reactive protein, and tumor necrosis factor–alpha receptor 2. We found 18 food groups that are most predictive of these biomarkers, and the EDIP was calculated as the weighted sum of these 18 food groups.”
Individuals who had higher intakes of green-leafy vegetables (kale, spinach, arugula), dark-yellow vegetables (pumpkin, yellow peppers, carrots), whole grains, fruits, tea, coffee and wine had lower long-term CVD risk than those with higher intakes of red meat, processed meat, organ meat, refined carbohydrates, and sweetened beverages.
The associations were consistent across cohorts and between sexes and remained significant in multiple sensitivity analysis that adjusted for alcohol consumption, smoking pack-years, use of lipid-lowering and antihypertensive medications, sodium intake, and blood pressure.
In a secondary analysis, diets with higher inflammatory potential were also associated with significantly higher biomarker levels indicative of more systemic, vascular, and metabolic inflammation, as well as less favorable lipid profiles.
“We wanted to be able to provide guidance on dietary patterns and food combinations,” said Dr. Li. “If you tell people to eat more polyunsaturated fats instead of saturated fat or trans fat, most people don’t know what foods are higher and lower in those nutrients. Also, many foods have different nutrients – some of which are good and some of which are bad – so we wanted to help people find the foods with the higher proportion of healthy nutrients rather than point out specific nutrients to avoid.”
Researchers used prospectively gathered data from the Nurses’ Health Studies I and II starting from 1984 and from the Health Professionals Follow-up Study. After excluding participants with missing diet information or previously diagnosed heart disease, stroke or cancer, over 210,000 participants were included in the analysis. Participants completed a survey every 4 years to ascertain dietary intake.
Prevention, not treatment
In an editorial comment, Ramon Estruch, MD, PhD, from the Hospital Clinic in Barcelona, and colleagues suggested that it might be time for better dietary guidelines.
“A better knowledge of health protection provided by different foods and dietary patterns, mainly their anti-inflammatory properties, should provide the basis for designing even healthier dietary patterns to protect against heart disease,” the editorialists wrote.
They added extra-virgin olive oil, fatty fish, and tomatoes to the list of foods with “established anti-inflammatory activity.”
In a comment, Dr. Estruch said the findings of this new study are confirmatory of the PREDIMED trial, which showed a reduction in risk of major CV events in individuals at high cardiovascular risk assigned to an anti-inflammatory Mediterranean diet pattern supplemented with extra-virgin olive oil or nuts as compared with those assigned to a reduced-fat diet.
“The study of Jun Li et al. confirms that an anti-inflammatory diet is useful to prevent cardiovascular events and, more important, that healthy dietary patterns may be even healthier if subjects increase consumption of foods with the highest anti-inflammatory potential,” he said, adding that “mechanistic explanations add plausibility to the results of observational studies.”
Dr. Estruch was the principal investigator of PREDIMED. This trial was originally published in 2013 and then retracted and republished in 2018, with some required corrections, but the results had not materially changed.
Dr. Li is supported by grants from the National Institute of Diabetes and Digestive and Kidney Diseases and Boston Nutrition Obesity Research Center. Dr. Estruch disclosed no financial relationships relevant to the contents of this article.
A version of this article originally appeared on Medscape.com.
Dietary patterns with higher inflammatory potential were significantly associated with a higher incidence of cardiovascular disease (CVD) and stroke in a new pooled analysis of three prospective cohort studies.
The analysis included 210,145 U.S. women and men followed for up to 32 years in the Nurses’ Health Studies I and II and the Health Professionals Follow-up Study.
After adjustment for use of anti-inflammatory medications and CVD risk factors, those whose dietary pattern ranked in the highest quintile of inflammatory potential had a 38% higher risk of CVD (hazard ratio comparing highest with lowest quintiles, 1.38), a 46% higher risk of coronary heart disease (HR, 1.46), and a 28% higher risk of stroke (HR, 1.28) (all P for trend < .001).
Jun Li, MD, PhD, and colleagues at Harvard School of Public Health and Harvard Medical School, Boston, published the findings of their study in the Nov. 10 issue of the Journal of the American College of Cardiology.
The inflammatory potential of a diet was assessed using a food-based, dietary index called the “empirical dietary inflammatory pattern” or EDIP.
In an interview, Dr. Li explained that the EDIP was developed 4 years ago by many of the same authors involved with this study, including nutrition heavyweights Walter C. Willett, MD, DrPH, and Frank B. Hu, MD, PhD, both from Harvard.
“We summarized all the foods people eat into 39 defined food groups and did a reduced-rank regression analysis that looked at these 39 food groups and three inflammatory markers – interleukin-6, C-reactive protein, and tumor necrosis factor–alpha receptor 2. We found 18 food groups that are most predictive of these biomarkers, and the EDIP was calculated as the weighted sum of these 18 food groups.”
Individuals who had higher intakes of green-leafy vegetables (kale, spinach, arugula), dark-yellow vegetables (pumpkin, yellow peppers, carrots), whole grains, fruits, tea, coffee and wine had lower long-term CVD risk than those with higher intakes of red meat, processed meat, organ meat, refined carbohydrates, and sweetened beverages.
The associations were consistent across cohorts and between sexes and remained significant in multiple sensitivity analysis that adjusted for alcohol consumption, smoking pack-years, use of lipid-lowering and antihypertensive medications, sodium intake, and blood pressure.
In a secondary analysis, diets with higher inflammatory potential were also associated with significantly higher biomarker levels indicative of more systemic, vascular, and metabolic inflammation, as well as less favorable lipid profiles.
“We wanted to be able to provide guidance on dietary patterns and food combinations,” said Dr. Li. “If you tell people to eat more polyunsaturated fats instead of saturated fat or trans fat, most people don’t know what foods are higher and lower in those nutrients. Also, many foods have different nutrients – some of which are good and some of which are bad – so we wanted to help people find the foods with the higher proportion of healthy nutrients rather than point out specific nutrients to avoid.”
Researchers used prospectively gathered data from the Nurses’ Health Studies I and II starting from 1984 and from the Health Professionals Follow-up Study. After excluding participants with missing diet information or previously diagnosed heart disease, stroke or cancer, over 210,000 participants were included in the analysis. Participants completed a survey every 4 years to ascertain dietary intake.
Prevention, not treatment
In an editorial comment, Ramon Estruch, MD, PhD, from the Hospital Clinic in Barcelona, and colleagues suggested that it might be time for better dietary guidelines.
“A better knowledge of health protection provided by different foods and dietary patterns, mainly their anti-inflammatory properties, should provide the basis for designing even healthier dietary patterns to protect against heart disease,” the editorialists wrote.
They added extra-virgin olive oil, fatty fish, and tomatoes to the list of foods with “established anti-inflammatory activity.”
In a comment, Dr. Estruch said the findings of this new study are confirmatory of the PREDIMED trial, which showed a reduction in risk of major CV events in individuals at high cardiovascular risk assigned to an anti-inflammatory Mediterranean diet pattern supplemented with extra-virgin olive oil or nuts as compared with those assigned to a reduced-fat diet.
“The study of Jun Li et al. confirms that an anti-inflammatory diet is useful to prevent cardiovascular events and, more important, that healthy dietary patterns may be even healthier if subjects increase consumption of foods with the highest anti-inflammatory potential,” he said, adding that “mechanistic explanations add plausibility to the results of observational studies.”
Dr. Estruch was the principal investigator of PREDIMED. This trial was originally published in 2013 and then retracted and republished in 2018, with some required corrections, but the results had not materially changed.
Dr. Li is supported by grants from the National Institute of Diabetes and Digestive and Kidney Diseases and Boston Nutrition Obesity Research Center. Dr. Estruch disclosed no financial relationships relevant to the contents of this article.
A version of this article originally appeared on Medscape.com.
Dietary patterns with higher inflammatory potential were significantly associated with a higher incidence of cardiovascular disease (CVD) and stroke in a new pooled analysis of three prospective cohort studies.
The analysis included 210,145 U.S. women and men followed for up to 32 years in the Nurses’ Health Studies I and II and the Health Professionals Follow-up Study.
After adjustment for use of anti-inflammatory medications and CVD risk factors, those whose dietary pattern ranked in the highest quintile of inflammatory potential had a 38% higher risk of CVD (hazard ratio comparing highest with lowest quintiles, 1.38), a 46% higher risk of coronary heart disease (HR, 1.46), and a 28% higher risk of stroke (HR, 1.28) (all P for trend < .001).
Jun Li, MD, PhD, and colleagues at Harvard School of Public Health and Harvard Medical School, Boston, published the findings of their study in the Nov. 10 issue of the Journal of the American College of Cardiology.
The inflammatory potential of a diet was assessed using a food-based, dietary index called the “empirical dietary inflammatory pattern” or EDIP.
In an interview, Dr. Li explained that the EDIP was developed 4 years ago by many of the same authors involved with this study, including nutrition heavyweights Walter C. Willett, MD, DrPH, and Frank B. Hu, MD, PhD, both from Harvard.
“We summarized all the foods people eat into 39 defined food groups and did a reduced-rank regression analysis that looked at these 39 food groups and three inflammatory markers – interleukin-6, C-reactive protein, and tumor necrosis factor–alpha receptor 2. We found 18 food groups that are most predictive of these biomarkers, and the EDIP was calculated as the weighted sum of these 18 food groups.”
Individuals who had higher intakes of green-leafy vegetables (kale, spinach, arugula), dark-yellow vegetables (pumpkin, yellow peppers, carrots), whole grains, fruits, tea, coffee and wine had lower long-term CVD risk than those with higher intakes of red meat, processed meat, organ meat, refined carbohydrates, and sweetened beverages.
The associations were consistent across cohorts and between sexes and remained significant in multiple sensitivity analysis that adjusted for alcohol consumption, smoking pack-years, use of lipid-lowering and antihypertensive medications, sodium intake, and blood pressure.
In a secondary analysis, diets with higher inflammatory potential were also associated with significantly higher biomarker levels indicative of more systemic, vascular, and metabolic inflammation, as well as less favorable lipid profiles.
“We wanted to be able to provide guidance on dietary patterns and food combinations,” said Dr. Li. “If you tell people to eat more polyunsaturated fats instead of saturated fat or trans fat, most people don’t know what foods are higher and lower in those nutrients. Also, many foods have different nutrients – some of which are good and some of which are bad – so we wanted to help people find the foods with the higher proportion of healthy nutrients rather than point out specific nutrients to avoid.”
Researchers used prospectively gathered data from the Nurses’ Health Studies I and II starting from 1984 and from the Health Professionals Follow-up Study. After excluding participants with missing diet information or previously diagnosed heart disease, stroke or cancer, over 210,000 participants were included in the analysis. Participants completed a survey every 4 years to ascertain dietary intake.
Prevention, not treatment
In an editorial comment, Ramon Estruch, MD, PhD, from the Hospital Clinic in Barcelona, and colleagues suggested that it might be time for better dietary guidelines.
“A better knowledge of health protection provided by different foods and dietary patterns, mainly their anti-inflammatory properties, should provide the basis for designing even healthier dietary patterns to protect against heart disease,” the editorialists wrote.
They added extra-virgin olive oil, fatty fish, and tomatoes to the list of foods with “established anti-inflammatory activity.”
In a comment, Dr. Estruch said the findings of this new study are confirmatory of the PREDIMED trial, which showed a reduction in risk of major CV events in individuals at high cardiovascular risk assigned to an anti-inflammatory Mediterranean diet pattern supplemented with extra-virgin olive oil or nuts as compared with those assigned to a reduced-fat diet.
“The study of Jun Li et al. confirms that an anti-inflammatory diet is useful to prevent cardiovascular events and, more important, that healthy dietary patterns may be even healthier if subjects increase consumption of foods with the highest anti-inflammatory potential,” he said, adding that “mechanistic explanations add plausibility to the results of observational studies.”
Dr. Estruch was the principal investigator of PREDIMED. This trial was originally published in 2013 and then retracted and republished in 2018, with some required corrections, but the results had not materially changed.
Dr. Li is supported by grants from the National Institute of Diabetes and Digestive and Kidney Diseases and Boston Nutrition Obesity Research Center. Dr. Estruch disclosed no financial relationships relevant to the contents of this article.
A version of this article originally appeared on Medscape.com.
ACC expert consensus on post-TAVR arrhythmias
The American College of Cardiology (ACC) has released a new Expert Consensus Decision Pathway (ECDP) on the management of conduction disturbances after transcatheter aortic valve replacement (TAVR).
The document provides guidance to clinicians in identifying and managing this common complication of TAVR, covering the pre-TAVR, periprocedural and post-TAVR periods.
“Conduction disturbances after TAVR are common and there is currently heterogeneity in how they’re managed, ranging from a casual observational approach to invasive electrophysiological studies and preemptive pacemaker implantation,” said writing committee chair Scott Lilly, MD, PhD, from the Ohio State Wexner Medical Center in Columbus.
“We felt this kind of collaborative effort to review what little research there is on this topic and come to [an] expert consensus was long overdue,” he added.
The document was published online Oct. 21 in the Journal of the American College of Cardiology.
Dr. Lilly stressed in an interview that this effort is an ECDP and not a guideline “because there is not data out there to solidly stand on and say, ‘This is the way we should do things.’ “
His hope is that this document will generate more discussion on this topic and spur some (probably National Institutes of Health–sponsored) clinical trials to better guide practice.
Not uncommon and not decreasing
Complete heart block requiring permanent pacemaker (PPM) implantation is seen in about 15% of patients within 30 days after TAVR. While this is a clear indication for PPM, there is no consensus on the management of less severe conduction disturbances such as new bundle branch or transient complete atrioventricular (AV) heart block.
Unlike the rates of bleeding, vascular injury, and stroke, which have decreased over time, the rates of in-hospital PPM implantation after TAVR have not changed significantly since commercialization in 2012. This is a concern because TAVR is increasingly used in younger, lower-risk patients.
“The pacemaker rate really hasn’t improved at a clip we would like to see if it was going to be a durable technology,” Dr. Lilly said.
Consensus regarding a reasonable strategy to manage cardiac conduction disturbances after TAVR has been elusive. This is a result of several things: a dearth of adequately powered, randomized controlled trials; the often transient nature of the conduction disturbances; evolving technologies; and the interplay of cardiology subspecialties involved.
The 2013 European Society of Cardiology guidelines address pacing post-TAVR, but do not provide in-depth discussion on the topic. This is the first effort sponsored by a cardiovascular society in the United States to review the existing data and experience and propose evidence-based expert guidance.
Pre-TAVR assessment
Pre-TAVR assessment should consider the patient’s risk for postprocedure conduction disturbances, the authors said. Since bradyarrythmias and aortic stenosis may present similarly (fatigue, lightheadedness, and syncope being hallmarks of both), a careful history is needed to determine if bradyarrhythmia is present.
An electrocardiogram (ECG) or ambulatory rhythm monitoring may identify baseline conduction abnormalities and help predict the need for post-TAVR PPM.
“In this section, we underscored some of the literature that has raised awareness about the presence of preexisting arrhythmias in TAVR patients and suggest that monitoring in selected patients before the procedure is reasonable, particularly those presenting with syncope or lightheadedness,” said Dr. Lilly.
Intraprocedural management
On the day of the procedure, patients determined to have elevated risk for complete AV heart block require careful perioperative ECG and hemodynamic monitoring. Regardless of preexisting risk, said the authors that all patients should be monitored on a telemetry unit during the procedure with ability to do emergency pacing if necessary.
“In the periprocedural section, we address the role of electrophysiological studies for identifying patients at high-risk of subsequent heart block,” said Dr. Lilly. “That’s a practice that’s occurring at a number of centers, but the data out there is insufficient to establish it as a pacemaker indication. Routine EP testing for patients deemed at risk for conduction disturbances after TAVR is not guideline-based and more research is needed.”
The document also outlines the effects of medications and anesthesia on postprocedure conduction abnormalities.
Post-TAVR management
The authors define post-TAVR management as continuing through 30-days after discharge.
The ECDP carefully outlines which patients can be discharged without monitoring and those for whom outpatient monitoring can be considered.
“If I’m going to pick one thing from this section, it’s the monitoring piece. A lot of patients that have a conduction disturbance right after TAVR – but you’re not sure if it’s going to progress and require a pacemaker – might stay in the hospital for an extended time waiting to see if the heart holds up,” reported Dr. Lilly.
“But a number of centers are now discharging people at 1 or 2 days, which begs the question: What do you do with these folks? Our group has published data showing that 30-day monitoring in select patients is a safe approach,” said Dr. Lilly.
There are shortcomings, however, in existing data, and recommendations will likely change as more data are collected, he explained.
As well, there remains uncertainty in how conduction block should be managed after TAVR, and clinical judgment is “foundational” in this, wrote the authors.
“This document is meant to help programs deal with these situations right now, acknowledging full and well, that really good randomized clinical data is not available,” said Dr. Lilly.
Dr. Lilly has disclosed no relevant financial relationships. The work of the writing committee was supported exclusively by the American College of Cardiology without commercial support.
A version of this article originally appeared on Medscape.com.
The American College of Cardiology (ACC) has released a new Expert Consensus Decision Pathway (ECDP) on the management of conduction disturbances after transcatheter aortic valve replacement (TAVR).
The document provides guidance to clinicians in identifying and managing this common complication of TAVR, covering the pre-TAVR, periprocedural and post-TAVR periods.
“Conduction disturbances after TAVR are common and there is currently heterogeneity in how they’re managed, ranging from a casual observational approach to invasive electrophysiological studies and preemptive pacemaker implantation,” said writing committee chair Scott Lilly, MD, PhD, from the Ohio State Wexner Medical Center in Columbus.
“We felt this kind of collaborative effort to review what little research there is on this topic and come to [an] expert consensus was long overdue,” he added.
The document was published online Oct. 21 in the Journal of the American College of Cardiology.
Dr. Lilly stressed in an interview that this effort is an ECDP and not a guideline “because there is not data out there to solidly stand on and say, ‘This is the way we should do things.’ “
His hope is that this document will generate more discussion on this topic and spur some (probably National Institutes of Health–sponsored) clinical trials to better guide practice.
Not uncommon and not decreasing
Complete heart block requiring permanent pacemaker (PPM) implantation is seen in about 15% of patients within 30 days after TAVR. While this is a clear indication for PPM, there is no consensus on the management of less severe conduction disturbances such as new bundle branch or transient complete atrioventricular (AV) heart block.
Unlike the rates of bleeding, vascular injury, and stroke, which have decreased over time, the rates of in-hospital PPM implantation after TAVR have not changed significantly since commercialization in 2012. This is a concern because TAVR is increasingly used in younger, lower-risk patients.
“The pacemaker rate really hasn’t improved at a clip we would like to see if it was going to be a durable technology,” Dr. Lilly said.
Consensus regarding a reasonable strategy to manage cardiac conduction disturbances after TAVR has been elusive. This is a result of several things: a dearth of adequately powered, randomized controlled trials; the often transient nature of the conduction disturbances; evolving technologies; and the interplay of cardiology subspecialties involved.
The 2013 European Society of Cardiology guidelines address pacing post-TAVR, but do not provide in-depth discussion on the topic. This is the first effort sponsored by a cardiovascular society in the United States to review the existing data and experience and propose evidence-based expert guidance.
Pre-TAVR assessment
Pre-TAVR assessment should consider the patient’s risk for postprocedure conduction disturbances, the authors said. Since bradyarrythmias and aortic stenosis may present similarly (fatigue, lightheadedness, and syncope being hallmarks of both), a careful history is needed to determine if bradyarrhythmia is present.
An electrocardiogram (ECG) or ambulatory rhythm monitoring may identify baseline conduction abnormalities and help predict the need for post-TAVR PPM.
“In this section, we underscored some of the literature that has raised awareness about the presence of preexisting arrhythmias in TAVR patients and suggest that monitoring in selected patients before the procedure is reasonable, particularly those presenting with syncope or lightheadedness,” said Dr. Lilly.
Intraprocedural management
On the day of the procedure, patients determined to have elevated risk for complete AV heart block require careful perioperative ECG and hemodynamic monitoring. Regardless of preexisting risk, said the authors that all patients should be monitored on a telemetry unit during the procedure with ability to do emergency pacing if necessary.
“In the periprocedural section, we address the role of electrophysiological studies for identifying patients at high-risk of subsequent heart block,” said Dr. Lilly. “That’s a practice that’s occurring at a number of centers, but the data out there is insufficient to establish it as a pacemaker indication. Routine EP testing for patients deemed at risk for conduction disturbances after TAVR is not guideline-based and more research is needed.”
The document also outlines the effects of medications and anesthesia on postprocedure conduction abnormalities.
Post-TAVR management
The authors define post-TAVR management as continuing through 30-days after discharge.
The ECDP carefully outlines which patients can be discharged without monitoring and those for whom outpatient monitoring can be considered.
“If I’m going to pick one thing from this section, it’s the monitoring piece. A lot of patients that have a conduction disturbance right after TAVR – but you’re not sure if it’s going to progress and require a pacemaker – might stay in the hospital for an extended time waiting to see if the heart holds up,” reported Dr. Lilly.
“But a number of centers are now discharging people at 1 or 2 days, which begs the question: What do you do with these folks? Our group has published data showing that 30-day monitoring in select patients is a safe approach,” said Dr. Lilly.
There are shortcomings, however, in existing data, and recommendations will likely change as more data are collected, he explained.
As well, there remains uncertainty in how conduction block should be managed after TAVR, and clinical judgment is “foundational” in this, wrote the authors.
“This document is meant to help programs deal with these situations right now, acknowledging full and well, that really good randomized clinical data is not available,” said Dr. Lilly.
Dr. Lilly has disclosed no relevant financial relationships. The work of the writing committee was supported exclusively by the American College of Cardiology without commercial support.
A version of this article originally appeared on Medscape.com.
The American College of Cardiology (ACC) has released a new Expert Consensus Decision Pathway (ECDP) on the management of conduction disturbances after transcatheter aortic valve replacement (TAVR).
The document provides guidance to clinicians in identifying and managing this common complication of TAVR, covering the pre-TAVR, periprocedural and post-TAVR periods.
“Conduction disturbances after TAVR are common and there is currently heterogeneity in how they’re managed, ranging from a casual observational approach to invasive electrophysiological studies and preemptive pacemaker implantation,” said writing committee chair Scott Lilly, MD, PhD, from the Ohio State Wexner Medical Center in Columbus.
“We felt this kind of collaborative effort to review what little research there is on this topic and come to [an] expert consensus was long overdue,” he added.
The document was published online Oct. 21 in the Journal of the American College of Cardiology.
Dr. Lilly stressed in an interview that this effort is an ECDP and not a guideline “because there is not data out there to solidly stand on and say, ‘This is the way we should do things.’ “
His hope is that this document will generate more discussion on this topic and spur some (probably National Institutes of Health–sponsored) clinical trials to better guide practice.
Not uncommon and not decreasing
Complete heart block requiring permanent pacemaker (PPM) implantation is seen in about 15% of patients within 30 days after TAVR. While this is a clear indication for PPM, there is no consensus on the management of less severe conduction disturbances such as new bundle branch or transient complete atrioventricular (AV) heart block.
Unlike the rates of bleeding, vascular injury, and stroke, which have decreased over time, the rates of in-hospital PPM implantation after TAVR have not changed significantly since commercialization in 2012. This is a concern because TAVR is increasingly used in younger, lower-risk patients.
“The pacemaker rate really hasn’t improved at a clip we would like to see if it was going to be a durable technology,” Dr. Lilly said.
Consensus regarding a reasonable strategy to manage cardiac conduction disturbances after TAVR has been elusive. This is a result of several things: a dearth of adequately powered, randomized controlled trials; the often transient nature of the conduction disturbances; evolving technologies; and the interplay of cardiology subspecialties involved.
The 2013 European Society of Cardiology guidelines address pacing post-TAVR, but do not provide in-depth discussion on the topic. This is the first effort sponsored by a cardiovascular society in the United States to review the existing data and experience and propose evidence-based expert guidance.
Pre-TAVR assessment
Pre-TAVR assessment should consider the patient’s risk for postprocedure conduction disturbances, the authors said. Since bradyarrythmias and aortic stenosis may present similarly (fatigue, lightheadedness, and syncope being hallmarks of both), a careful history is needed to determine if bradyarrhythmia is present.
An electrocardiogram (ECG) or ambulatory rhythm monitoring may identify baseline conduction abnormalities and help predict the need for post-TAVR PPM.
“In this section, we underscored some of the literature that has raised awareness about the presence of preexisting arrhythmias in TAVR patients and suggest that monitoring in selected patients before the procedure is reasonable, particularly those presenting with syncope or lightheadedness,” said Dr. Lilly.
Intraprocedural management
On the day of the procedure, patients determined to have elevated risk for complete AV heart block require careful perioperative ECG and hemodynamic monitoring. Regardless of preexisting risk, said the authors that all patients should be monitored on a telemetry unit during the procedure with ability to do emergency pacing if necessary.
“In the periprocedural section, we address the role of electrophysiological studies for identifying patients at high-risk of subsequent heart block,” said Dr. Lilly. “That’s a practice that’s occurring at a number of centers, but the data out there is insufficient to establish it as a pacemaker indication. Routine EP testing for patients deemed at risk for conduction disturbances after TAVR is not guideline-based and more research is needed.”
The document also outlines the effects of medications and anesthesia on postprocedure conduction abnormalities.
Post-TAVR management
The authors define post-TAVR management as continuing through 30-days after discharge.
The ECDP carefully outlines which patients can be discharged without monitoring and those for whom outpatient monitoring can be considered.
“If I’m going to pick one thing from this section, it’s the monitoring piece. A lot of patients that have a conduction disturbance right after TAVR – but you’re not sure if it’s going to progress and require a pacemaker – might stay in the hospital for an extended time waiting to see if the heart holds up,” reported Dr. Lilly.
“But a number of centers are now discharging people at 1 or 2 days, which begs the question: What do you do with these folks? Our group has published data showing that 30-day monitoring in select patients is a safe approach,” said Dr. Lilly.
There are shortcomings, however, in existing data, and recommendations will likely change as more data are collected, he explained.
As well, there remains uncertainty in how conduction block should be managed after TAVR, and clinical judgment is “foundational” in this, wrote the authors.
“This document is meant to help programs deal with these situations right now, acknowledging full and well, that really good randomized clinical data is not available,” said Dr. Lilly.
Dr. Lilly has disclosed no relevant financial relationships. The work of the writing committee was supported exclusively by the American College of Cardiology without commercial support.
A version of this article originally appeared on Medscape.com.
Higher serum omega-3 tied to better outcome after STEMI
Regular consumption of foods rich in omega-3 fatty acids was associated with improved prognosis after ST-segment myocardial infarction (STEMI) in a new observational study.
The prospective study, which involved 944 patients with STEMI who underwent primary percutaneous coronary intervention (PCI), showed that plasma levels of fatty acids at the time of the STEMI were inversely associated with both incident major adverse cardiovascular events (MACE) and cardiovascular readmissions (adjusted hazard ratio, 0.76 and 0.74 for 1-SD increase; for both, P < .05).
No association was seen for the endpoint of all-cause mortality.
“What we showed is that your consumption of fish and other sources of omega-3 fatty acids before the heart attack impacts your prognosis after the heart attack. It’s a novel approach because it’s not primary prevention or secondary prevention,” said Aleix Sala-Vila, PharmD, PhD, from the Institut Hospital del Mar d’Investigacions Mèdiques (IMIM) in Barcelona, Spain.
Sala-Vila, co–senior author Antoni Bayés-Genís, MD, PhD, Heart Universitari Germans Trias I Pujol, Barcelona, and first author Iolanda Lázaro, PhD, also from IMIM, reported their findings online Oct. 26 in the Journal of the American College of Cardiology.
It has been established that dietary omega-3 eicosapentaenoic acid (EPA) has cardioprotective properties, but observational studies and randomized trials of EPA intake have yielded disparate findings.
This study avoided the usual traps of nutritional epidemiology research – self-reported food diaries and intake questionnaires. For this study, the researchers measured tissue levels of EPA and alpha-linolenic acid (ALA) by measuring serum phosphatidylcholine (PC) levels, which reflect dietary intake during the previous 3 or 4 weeks.
This technique, said Sala-Vila, not only provides a more reliable measure of fatty acid intake over time but also avoids measurement errors related to fatty acid content variation.
For example, “The EPA content of a piece of fish eaten in January could be very different from one eaten in June,” explained Sala-Vila.
That said, he acknowledged that this technique, which uses gas chromatography, does not at present have a clear clinical application. “It’s quite difficult just to convert levels of serum-PC EPA into consumption of fatty fish. We feel that the best advice at this point is that given by the American Heart Association to eat two servings of fatty fish a week.”
EPA and ALA: Partners in prevention?
In addition to the findings regarding EPA, the researchers also found that serum-PC ALA was inversely related to all-cause mortality after STEMI (HR, 0.65 for 1-SD increase; P < .05).
A trend was seen for an association between ALA and lower risk for incident MACE (P = .093).
ALA is readily available from inexpensive plant sources (eg, chia seeds, flax seeds, walnuts, soy beans) and has been associated with lower all-cause mortality in high-risk individuals.
This omega-3 fatty acid is often given short shrift in the fatty acid world because of the seven-step enzymatic process needed to convert it into more beneficial forms.
“We know that the conversion of ALA to EPA or DHA [docohexaenoic acid] is marginal, but we decided to include it in the study because we feel that this fatty acid is becoming more important because there are some issues with fish consumption – people are concerned about pollutants and sustainability, and some just don’t like it,” explained Sala-Vila.
“We were shocked to see that the marine-derived and vegetable-derived fatty acids don’t appear to compete, but rather they act synergistically,” said Sala-Villa. The researchers suggested that marine and vegetable omega-3 fatty acids may act as “partners in prevention.”
“We are not metabolically adapted to converting ALA to EPA, but despite this, there is a large body of evidence showing that one way to increase the status of EPA and DHA in our membranes is by eating these sources of fatty acids,” said Sala-Vila.
For almost 20 years, Sala-Vila has been studying how the consumption of foods rich in omega-3 affects disease. Two of his current projects involve studying levels of ALA in red blood cell membranes as a risk factor for ischemic stroke and omega-3 status in individuals with cognitive impairment who are at high risk for Alzheimer’s disease.
Applicable to all patients with atherosclerosis
In comments to theheart.org | Medscape Cardiology, Deepak Bhatt, MD, called the study “terrific,” adding that the effort is “as good as it gets” for observational nutrition research.
“I think one has to view these findings in the larger universe of what is really a revolution in omega-3 fatty acid research,” said Bhatt.
This universe, he said, includes a wealth of observational research showing the benefits of omega-3s, two outcome trials – JELIS and REDUCE-IT – that showed the benefits of EPA supplementation, and two imaging studies – EVAPORATE and CHERRY – that showed favorable effects of EPA on the vasculature.
REDUCE-IT, for which Bhatt served as principal investigator, showed that treatment with icosapent ethyl (Vascepa), a high-dose purified form of EPA, led to a 25% relative risk reduction in MACE in an at-risk Western population.
The results, said Bhatt, who co-wrote an editorial that accompanies the current Sala-Vila article, “likely apply to all patients with atherosclerosis or who are at high risk for it” and supports the practice of counseling patients to increase their intake of food rich in omega-3 fatty acids.
The field may be due for a shake-up, he noted. At next month’s American Heart Association meeting, the results of another trial of another prescription-grade EPA/DHA supplement will be presented, and they are expected to be negative.
AstraZeneca announced in January 2020 the early closure of the STRENGTH trial of Epanova after an interim analysis showed a low likelihood of their product demonstrating benefit in the enrolled population.
Epanova is a fish-oil derived mixture of free fatty acids, primarily EPA and DHA. It is approved in the United States and is indicated as an adjunct to diet to reduce triglyceride levels in adults with severe (≥500 mg/dL) hypertriglyceridemia. This indication is not affected by the data from the STRENGTH trial, according to a company press release.
Sala-Vila has received grants and support from the California Walnut Commission, including a grant to support part of this study. Bayés-Genís and Bhatt have relationships with a number of companies.
This article first appeared on Medscape.com.
Regular consumption of foods rich in omega-3 fatty acids was associated with improved prognosis after ST-segment myocardial infarction (STEMI) in a new observational study.
The prospective study, which involved 944 patients with STEMI who underwent primary percutaneous coronary intervention (PCI), showed that plasma levels of fatty acids at the time of the STEMI were inversely associated with both incident major adverse cardiovascular events (MACE) and cardiovascular readmissions (adjusted hazard ratio, 0.76 and 0.74 for 1-SD increase; for both, P < .05).
No association was seen for the endpoint of all-cause mortality.
“What we showed is that your consumption of fish and other sources of omega-3 fatty acids before the heart attack impacts your prognosis after the heart attack. It’s a novel approach because it’s not primary prevention or secondary prevention,” said Aleix Sala-Vila, PharmD, PhD, from the Institut Hospital del Mar d’Investigacions Mèdiques (IMIM) in Barcelona, Spain.
Sala-Vila, co–senior author Antoni Bayés-Genís, MD, PhD, Heart Universitari Germans Trias I Pujol, Barcelona, and first author Iolanda Lázaro, PhD, also from IMIM, reported their findings online Oct. 26 in the Journal of the American College of Cardiology.
It has been established that dietary omega-3 eicosapentaenoic acid (EPA) has cardioprotective properties, but observational studies and randomized trials of EPA intake have yielded disparate findings.
This study avoided the usual traps of nutritional epidemiology research – self-reported food diaries and intake questionnaires. For this study, the researchers measured tissue levels of EPA and alpha-linolenic acid (ALA) by measuring serum phosphatidylcholine (PC) levels, which reflect dietary intake during the previous 3 or 4 weeks.
This technique, said Sala-Vila, not only provides a more reliable measure of fatty acid intake over time but also avoids measurement errors related to fatty acid content variation.
For example, “The EPA content of a piece of fish eaten in January could be very different from one eaten in June,” explained Sala-Vila.
That said, he acknowledged that this technique, which uses gas chromatography, does not at present have a clear clinical application. “It’s quite difficult just to convert levels of serum-PC EPA into consumption of fatty fish. We feel that the best advice at this point is that given by the American Heart Association to eat two servings of fatty fish a week.”
EPA and ALA: Partners in prevention?
In addition to the findings regarding EPA, the researchers also found that serum-PC ALA was inversely related to all-cause mortality after STEMI (HR, 0.65 for 1-SD increase; P < .05).
A trend was seen for an association between ALA and lower risk for incident MACE (P = .093).
ALA is readily available from inexpensive plant sources (eg, chia seeds, flax seeds, walnuts, soy beans) and has been associated with lower all-cause mortality in high-risk individuals.
This omega-3 fatty acid is often given short shrift in the fatty acid world because of the seven-step enzymatic process needed to convert it into more beneficial forms.
“We know that the conversion of ALA to EPA or DHA [docohexaenoic acid] is marginal, but we decided to include it in the study because we feel that this fatty acid is becoming more important because there are some issues with fish consumption – people are concerned about pollutants and sustainability, and some just don’t like it,” explained Sala-Vila.
“We were shocked to see that the marine-derived and vegetable-derived fatty acids don’t appear to compete, but rather they act synergistically,” said Sala-Villa. The researchers suggested that marine and vegetable omega-3 fatty acids may act as “partners in prevention.”
“We are not metabolically adapted to converting ALA to EPA, but despite this, there is a large body of evidence showing that one way to increase the status of EPA and DHA in our membranes is by eating these sources of fatty acids,” said Sala-Vila.
For almost 20 years, Sala-Vila has been studying how the consumption of foods rich in omega-3 affects disease. Two of his current projects involve studying levels of ALA in red blood cell membranes as a risk factor for ischemic stroke and omega-3 status in individuals with cognitive impairment who are at high risk for Alzheimer’s disease.
Applicable to all patients with atherosclerosis
In comments to theheart.org | Medscape Cardiology, Deepak Bhatt, MD, called the study “terrific,” adding that the effort is “as good as it gets” for observational nutrition research.
“I think one has to view these findings in the larger universe of what is really a revolution in omega-3 fatty acid research,” said Bhatt.
This universe, he said, includes a wealth of observational research showing the benefits of omega-3s, two outcome trials – JELIS and REDUCE-IT – that showed the benefits of EPA supplementation, and two imaging studies – EVAPORATE and CHERRY – that showed favorable effects of EPA on the vasculature.
REDUCE-IT, for which Bhatt served as principal investigator, showed that treatment with icosapent ethyl (Vascepa), a high-dose purified form of EPA, led to a 25% relative risk reduction in MACE in an at-risk Western population.
The results, said Bhatt, who co-wrote an editorial that accompanies the current Sala-Vila article, “likely apply to all patients with atherosclerosis or who are at high risk for it” and supports the practice of counseling patients to increase their intake of food rich in omega-3 fatty acids.
The field may be due for a shake-up, he noted. At next month’s American Heart Association meeting, the results of another trial of another prescription-grade EPA/DHA supplement will be presented, and they are expected to be negative.
AstraZeneca announced in January 2020 the early closure of the STRENGTH trial of Epanova after an interim analysis showed a low likelihood of their product demonstrating benefit in the enrolled population.
Epanova is a fish-oil derived mixture of free fatty acids, primarily EPA and DHA. It is approved in the United States and is indicated as an adjunct to diet to reduce triglyceride levels in adults with severe (≥500 mg/dL) hypertriglyceridemia. This indication is not affected by the data from the STRENGTH trial, according to a company press release.
Sala-Vila has received grants and support from the California Walnut Commission, including a grant to support part of this study. Bayés-Genís and Bhatt have relationships with a number of companies.
This article first appeared on Medscape.com.
Regular consumption of foods rich in omega-3 fatty acids was associated with improved prognosis after ST-segment myocardial infarction (STEMI) in a new observational study.
The prospective study, which involved 944 patients with STEMI who underwent primary percutaneous coronary intervention (PCI), showed that plasma levels of fatty acids at the time of the STEMI were inversely associated with both incident major adverse cardiovascular events (MACE) and cardiovascular readmissions (adjusted hazard ratio, 0.76 and 0.74 for 1-SD increase; for both, P < .05).
No association was seen for the endpoint of all-cause mortality.
“What we showed is that your consumption of fish and other sources of omega-3 fatty acids before the heart attack impacts your prognosis after the heart attack. It’s a novel approach because it’s not primary prevention or secondary prevention,” said Aleix Sala-Vila, PharmD, PhD, from the Institut Hospital del Mar d’Investigacions Mèdiques (IMIM) in Barcelona, Spain.
Sala-Vila, co–senior author Antoni Bayés-Genís, MD, PhD, Heart Universitari Germans Trias I Pujol, Barcelona, and first author Iolanda Lázaro, PhD, also from IMIM, reported their findings online Oct. 26 in the Journal of the American College of Cardiology.
It has been established that dietary omega-3 eicosapentaenoic acid (EPA) has cardioprotective properties, but observational studies and randomized trials of EPA intake have yielded disparate findings.
This study avoided the usual traps of nutritional epidemiology research – self-reported food diaries and intake questionnaires. For this study, the researchers measured tissue levels of EPA and alpha-linolenic acid (ALA) by measuring serum phosphatidylcholine (PC) levels, which reflect dietary intake during the previous 3 or 4 weeks.
This technique, said Sala-Vila, not only provides a more reliable measure of fatty acid intake over time but also avoids measurement errors related to fatty acid content variation.
For example, “The EPA content of a piece of fish eaten in January could be very different from one eaten in June,” explained Sala-Vila.
That said, he acknowledged that this technique, which uses gas chromatography, does not at present have a clear clinical application. “It’s quite difficult just to convert levels of serum-PC EPA into consumption of fatty fish. We feel that the best advice at this point is that given by the American Heart Association to eat two servings of fatty fish a week.”
EPA and ALA: Partners in prevention?
In addition to the findings regarding EPA, the researchers also found that serum-PC ALA was inversely related to all-cause mortality after STEMI (HR, 0.65 for 1-SD increase; P < .05).
A trend was seen for an association between ALA and lower risk for incident MACE (P = .093).
ALA is readily available from inexpensive plant sources (eg, chia seeds, flax seeds, walnuts, soy beans) and has been associated with lower all-cause mortality in high-risk individuals.
This omega-3 fatty acid is often given short shrift in the fatty acid world because of the seven-step enzymatic process needed to convert it into more beneficial forms.
“We know that the conversion of ALA to EPA or DHA [docohexaenoic acid] is marginal, but we decided to include it in the study because we feel that this fatty acid is becoming more important because there are some issues with fish consumption – people are concerned about pollutants and sustainability, and some just don’t like it,” explained Sala-Vila.
“We were shocked to see that the marine-derived and vegetable-derived fatty acids don’t appear to compete, but rather they act synergistically,” said Sala-Villa. The researchers suggested that marine and vegetable omega-3 fatty acids may act as “partners in prevention.”
“We are not metabolically adapted to converting ALA to EPA, but despite this, there is a large body of evidence showing that one way to increase the status of EPA and DHA in our membranes is by eating these sources of fatty acids,” said Sala-Vila.
For almost 20 years, Sala-Vila has been studying how the consumption of foods rich in omega-3 affects disease. Two of his current projects involve studying levels of ALA in red blood cell membranes as a risk factor for ischemic stroke and omega-3 status in individuals with cognitive impairment who are at high risk for Alzheimer’s disease.
Applicable to all patients with atherosclerosis
In comments to theheart.org | Medscape Cardiology, Deepak Bhatt, MD, called the study “terrific,” adding that the effort is “as good as it gets” for observational nutrition research.
“I think one has to view these findings in the larger universe of what is really a revolution in omega-3 fatty acid research,” said Bhatt.
This universe, he said, includes a wealth of observational research showing the benefits of omega-3s, two outcome trials – JELIS and REDUCE-IT – that showed the benefits of EPA supplementation, and two imaging studies – EVAPORATE and CHERRY – that showed favorable effects of EPA on the vasculature.
REDUCE-IT, for which Bhatt served as principal investigator, showed that treatment with icosapent ethyl (Vascepa), a high-dose purified form of EPA, led to a 25% relative risk reduction in MACE in an at-risk Western population.
The results, said Bhatt, who co-wrote an editorial that accompanies the current Sala-Vila article, “likely apply to all patients with atherosclerosis or who are at high risk for it” and supports the practice of counseling patients to increase their intake of food rich in omega-3 fatty acids.
The field may be due for a shake-up, he noted. At next month’s American Heart Association meeting, the results of another trial of another prescription-grade EPA/DHA supplement will be presented, and they are expected to be negative.
AstraZeneca announced in January 2020 the early closure of the STRENGTH trial of Epanova after an interim analysis showed a low likelihood of their product demonstrating benefit in the enrolled population.
Epanova is a fish-oil derived mixture of free fatty acids, primarily EPA and DHA. It is approved in the United States and is indicated as an adjunct to diet to reduce triglyceride levels in adults with severe (≥500 mg/dL) hypertriglyceridemia. This indication is not affected by the data from the STRENGTH trial, according to a company press release.
Sala-Vila has received grants and support from the California Walnut Commission, including a grant to support part of this study. Bayés-Genís and Bhatt have relationships with a number of companies.
This article first appeared on Medscape.com.
Observational study again suggests lasting impact of COVID-19 on heart
A new study using cardiac magnetic resonance (CMR) imaging to examine the effects of novel coronavirus infection on the heart showed signs suggestive of myocarditis in 4 out of 26 competitive athletes who recovered from asymptomatic or mild cases of COVID-19.
While these and other similar findings are concerning, commentators are saying the results are preliminary and do not indicate widespread CMR screening is appropriate.
Two of the 4 patients showing signs of myocarditis in this series had no symptoms of COVID-19 but tested positive on routine testing. An additional 12 student athletes (46%) showed late gadolinium enhancement (LGE), of whom 8 (30.8%) had LGE without T2 elevation suggestive of prior myocardial injury.
An additional 12 student athletes (46%) showed late gadolinium enhancement (LGE), of whom 8 (31%) had LGE without T2 elevation suggestive of prior myocardial injury.
This finding, said Saurabh Rajpal, MBBS, MD, the study’s lead author, “could suggest prior myocardial injury or it could suggest athletic myocardial adaptation.”
In a research letter published in JAMA Cardiology, Rajpal and colleagues at Ohio State University in Columbus, described the findings of comprehensive CMR examinations in competitive athletes referred to the sport medicine clinic after testing positive for COVID-19 on reverse transcriptase-polymerase chain reaction between June and August 2020.
The university had made the decision in the spring to use CMR imaging as a screening tool for return to play, said Dr. Rajpal. While CMR is being used for research purposes, the American College of Cardiology’s recent “consensus expert opinion” statement on resumption of sport and exercise after COVID-19 infection does not require CMR imaging for resumption of competitive activity (JAMA Cardiol. 2020 May 13. doi:10.1001/jamacardio.2020.2136).
None of the athletes required hospitalization for their illness, and only 27% reported mild symptoms during the short-term infection, including sore throat, shortness of breath, myalgia, and fever.
On the day of CMR imaging, ECG and transthoracic echocardiography were performed, and serum troponin I was measured. There were no diagnostic ST/T wave changes, ventricular function and volumes were normal, and no athletes showed elevated serum troponin levels.
The updated Lake Louise Criteria were used to assess CMR findings consistent with myocarditis.
“I don’t think this is a COVID-specific issue. We have seen myocarditis after other viral infections; it’s just that COVID-19 is the most studied thus far, and with strenuous activity, inflammation in the heart can be risky,” Dr. Rajpal said in an interview. He added that more long-term and larger studies with control populations are needed.
His group is continuing to follow these athletes and has suggested that CMR “may provide an excellent risk-stratification assessment for myocarditis in athletes who have recovered from COVID-19 to guide safe competitive sports participation.”
Significance still unknown
Matthew Martinez, MD, the director of sports cardiology at Atlantic Health – Morristown (N.J.) Medical Center and the Gagnon Cardiovascular Institute, urged caution in making too much of the findings of this small study.
“We know that viruses cause myocardial damage and myocarditis. What we don’t know is how important these findings are. And in terms of risk, would we find the same phenomenon if we did this, say, in flu patients or in other age groups?” Dr. Martinez said in an interview.
“I haven’t seen all the images, but what I’d want to know is are these very subtle findings? Are these overt findings? Is this part of an active individual with symptoms? I need to know a little more data before I can tell if this influences the increased risk of sudden cardiac death that we often associate with myocarditis. I’m not sure how this should influence making decisions with regards to return to play.”
Dr. Martinez, who is the ACC’s chair of Sports and Exercise but was not an author of their recent guidance on return to sport, said that he is not routinely using CMR to assess athletes post-infection, as per the ACC’s recommendations.
“My approach is to evaluate anybody with a history of COVID infection and, first, determine whether it was an important infection with significant symptoms or not. And then, if they’re participating at a high level or are professional athletes, I would suggest an ECG, echo, and troponin. That’s our recommendation for the last several months and is still an appropriate way to evaluate that group.”
“In the presence of an abnormality or ongoing symptoms, I would ask for an MRI at that point,” said Dr. Martinez.
“We just don’t have much data on athletes with no symptoms to use to interpret these CMR findings and the study didn’t offer any controls. We don’t even know if these findings are new findings or old findings that have just been identified now,” he added.
New, updated recommendations from the ACC are coming soon, said Dr. Martinez. “I do not expect them to include CMR as first line.”
Cardiologists concerned about misinformation
This is at least the fourth study showing myocardial damage post-COVID-19 infection and there is concern in the medical community that the media has overstated the risks of heart damage, especially in athletes, and at the same time overstated the benefits of CMR.
In particular, Puntmann et al reported in July a 100-patient study that showed evidence of myocardial inflammation by CMR in 78% of patients recently recovered from a bout of COVID-19 (JAMA Cardiol. 2020 Jul 27; doi:10.1001/jamacardio.2020.3557).
“That paper is completely problematic,” John Mandrola, MD, of Baptists Medical Associates, Louisville, Ky., said in an interview. “It has the same overarching weaknesses [of other studies] that it’s observational and retrospective, but there were also numerical issues. So to me that paper is an interesting observation, but utterly unconvincing and preliminary,” said Dr. Mandrola.
Those limitations didn’t stop the study from garnering media attention, however. The Altmetric score (an attention score that tracks all mentions of an article in the media and on social media) for the Puntmann et al paper is approaching 13,000, including coverage from 276 news outlets and more than 19,000 tweets, putting it in the 99th percentile of all research outputs tracked by Altmetric to date.
To counter this, an “open letter” posted online just days before the Rajpal study published urging professional societies to “offer clear guidance discouraging CMR screening for COVID-19 related heart abnormalities in asymptomatic members of the general public.” The letter was signed by 51 clinicians, researchers, and imaging specialists from around the world.
Dr. Mandrola, one of the signatories, said: “This topic really scares people, and when it gets in the media like this, I think the leaders of these societies need to come out and say something really clear on major news networks letting people know that it’s just way too premature to start doing CMRs on every athlete that’s gotten this virus.”
“I understand that the current guidelines may be clear that CMR is not a first-line test for this indication, but when the media coverage is so extensive and so overblown, I wonder how much impact the guidelines will have in countering this fear that’s in the community,” he added.
Asked to comment on the letter, Dr. Rajpal said he agrees with the signatories that asymptomatic people from general population do not need routine cardiac MRI. “However, competitive athletes are a different story. Testing depends on risk assessment in specific population and competitive athletes as per our protocol will get enhanced cardiac workup including CMR for responsible and safe start of competitive sports. ... In the present scenario, while we get more data including control data, we will continue with our current protocol.”
Dr. Mandrola is Medscape Cardiology’s Chief Cardiology Consultant. MDedge is part of the Medscape Professional Network.
This article first appeared on Medscape.com.
A new study using cardiac magnetic resonance (CMR) imaging to examine the effects of novel coronavirus infection on the heart showed signs suggestive of myocarditis in 4 out of 26 competitive athletes who recovered from asymptomatic or mild cases of COVID-19.
While these and other similar findings are concerning, commentators are saying the results are preliminary and do not indicate widespread CMR screening is appropriate.
Two of the 4 patients showing signs of myocarditis in this series had no symptoms of COVID-19 but tested positive on routine testing. An additional 12 student athletes (46%) showed late gadolinium enhancement (LGE), of whom 8 (30.8%) had LGE without T2 elevation suggestive of prior myocardial injury.
An additional 12 student athletes (46%) showed late gadolinium enhancement (LGE), of whom 8 (31%) had LGE without T2 elevation suggestive of prior myocardial injury.
This finding, said Saurabh Rajpal, MBBS, MD, the study’s lead author, “could suggest prior myocardial injury or it could suggest athletic myocardial adaptation.”
In a research letter published in JAMA Cardiology, Rajpal and colleagues at Ohio State University in Columbus, described the findings of comprehensive CMR examinations in competitive athletes referred to the sport medicine clinic after testing positive for COVID-19 on reverse transcriptase-polymerase chain reaction between June and August 2020.
The university had made the decision in the spring to use CMR imaging as a screening tool for return to play, said Dr. Rajpal. While CMR is being used for research purposes, the American College of Cardiology’s recent “consensus expert opinion” statement on resumption of sport and exercise after COVID-19 infection does not require CMR imaging for resumption of competitive activity (JAMA Cardiol. 2020 May 13. doi:10.1001/jamacardio.2020.2136).
None of the athletes required hospitalization for their illness, and only 27% reported mild symptoms during the short-term infection, including sore throat, shortness of breath, myalgia, and fever.
On the day of CMR imaging, ECG and transthoracic echocardiography were performed, and serum troponin I was measured. There were no diagnostic ST/T wave changes, ventricular function and volumes were normal, and no athletes showed elevated serum troponin levels.
The updated Lake Louise Criteria were used to assess CMR findings consistent with myocarditis.
“I don’t think this is a COVID-specific issue. We have seen myocarditis after other viral infections; it’s just that COVID-19 is the most studied thus far, and with strenuous activity, inflammation in the heart can be risky,” Dr. Rajpal said in an interview. He added that more long-term and larger studies with control populations are needed.
His group is continuing to follow these athletes and has suggested that CMR “may provide an excellent risk-stratification assessment for myocarditis in athletes who have recovered from COVID-19 to guide safe competitive sports participation.”
Significance still unknown
Matthew Martinez, MD, the director of sports cardiology at Atlantic Health – Morristown (N.J.) Medical Center and the Gagnon Cardiovascular Institute, urged caution in making too much of the findings of this small study.
“We know that viruses cause myocardial damage and myocarditis. What we don’t know is how important these findings are. And in terms of risk, would we find the same phenomenon if we did this, say, in flu patients or in other age groups?” Dr. Martinez said in an interview.
“I haven’t seen all the images, but what I’d want to know is are these very subtle findings? Are these overt findings? Is this part of an active individual with symptoms? I need to know a little more data before I can tell if this influences the increased risk of sudden cardiac death that we often associate with myocarditis. I’m not sure how this should influence making decisions with regards to return to play.”
Dr. Martinez, who is the ACC’s chair of Sports and Exercise but was not an author of their recent guidance on return to sport, said that he is not routinely using CMR to assess athletes post-infection, as per the ACC’s recommendations.
“My approach is to evaluate anybody with a history of COVID infection and, first, determine whether it was an important infection with significant symptoms or not. And then, if they’re participating at a high level or are professional athletes, I would suggest an ECG, echo, and troponin. That’s our recommendation for the last several months and is still an appropriate way to evaluate that group.”
“In the presence of an abnormality or ongoing symptoms, I would ask for an MRI at that point,” said Dr. Martinez.
“We just don’t have much data on athletes with no symptoms to use to interpret these CMR findings and the study didn’t offer any controls. We don’t even know if these findings are new findings or old findings that have just been identified now,” he added.
New, updated recommendations from the ACC are coming soon, said Dr. Martinez. “I do not expect them to include CMR as first line.”
Cardiologists concerned about misinformation
This is at least the fourth study showing myocardial damage post-COVID-19 infection and there is concern in the medical community that the media has overstated the risks of heart damage, especially in athletes, and at the same time overstated the benefits of CMR.
In particular, Puntmann et al reported in July a 100-patient study that showed evidence of myocardial inflammation by CMR in 78% of patients recently recovered from a bout of COVID-19 (JAMA Cardiol. 2020 Jul 27; doi:10.1001/jamacardio.2020.3557).
“That paper is completely problematic,” John Mandrola, MD, of Baptists Medical Associates, Louisville, Ky., said in an interview. “It has the same overarching weaknesses [of other studies] that it’s observational and retrospective, but there were also numerical issues. So to me that paper is an interesting observation, but utterly unconvincing and preliminary,” said Dr. Mandrola.
Those limitations didn’t stop the study from garnering media attention, however. The Altmetric score (an attention score that tracks all mentions of an article in the media and on social media) for the Puntmann et al paper is approaching 13,000, including coverage from 276 news outlets and more than 19,000 tweets, putting it in the 99th percentile of all research outputs tracked by Altmetric to date.
To counter this, an “open letter” posted online just days before the Rajpal study published urging professional societies to “offer clear guidance discouraging CMR screening for COVID-19 related heart abnormalities in asymptomatic members of the general public.” The letter was signed by 51 clinicians, researchers, and imaging specialists from around the world.
Dr. Mandrola, one of the signatories, said: “This topic really scares people, and when it gets in the media like this, I think the leaders of these societies need to come out and say something really clear on major news networks letting people know that it’s just way too premature to start doing CMRs on every athlete that’s gotten this virus.”
“I understand that the current guidelines may be clear that CMR is not a first-line test for this indication, but when the media coverage is so extensive and so overblown, I wonder how much impact the guidelines will have in countering this fear that’s in the community,” he added.
Asked to comment on the letter, Dr. Rajpal said he agrees with the signatories that asymptomatic people from general population do not need routine cardiac MRI. “However, competitive athletes are a different story. Testing depends on risk assessment in specific population and competitive athletes as per our protocol will get enhanced cardiac workup including CMR for responsible and safe start of competitive sports. ... In the present scenario, while we get more data including control data, we will continue with our current protocol.”
Dr. Mandrola is Medscape Cardiology’s Chief Cardiology Consultant. MDedge is part of the Medscape Professional Network.
This article first appeared on Medscape.com.
A new study using cardiac magnetic resonance (CMR) imaging to examine the effects of novel coronavirus infection on the heart showed signs suggestive of myocarditis in 4 out of 26 competitive athletes who recovered from asymptomatic or mild cases of COVID-19.
While these and other similar findings are concerning, commentators are saying the results are preliminary and do not indicate widespread CMR screening is appropriate.
Two of the 4 patients showing signs of myocarditis in this series had no symptoms of COVID-19 but tested positive on routine testing. An additional 12 student athletes (46%) showed late gadolinium enhancement (LGE), of whom 8 (30.8%) had LGE without T2 elevation suggestive of prior myocardial injury.
An additional 12 student athletes (46%) showed late gadolinium enhancement (LGE), of whom 8 (31%) had LGE without T2 elevation suggestive of prior myocardial injury.
This finding, said Saurabh Rajpal, MBBS, MD, the study’s lead author, “could suggest prior myocardial injury or it could suggest athletic myocardial adaptation.”
In a research letter published in JAMA Cardiology, Rajpal and colleagues at Ohio State University in Columbus, described the findings of comprehensive CMR examinations in competitive athletes referred to the sport medicine clinic after testing positive for COVID-19 on reverse transcriptase-polymerase chain reaction between June and August 2020.
The university had made the decision in the spring to use CMR imaging as a screening tool for return to play, said Dr. Rajpal. While CMR is being used for research purposes, the American College of Cardiology’s recent “consensus expert opinion” statement on resumption of sport and exercise after COVID-19 infection does not require CMR imaging for resumption of competitive activity (JAMA Cardiol. 2020 May 13. doi:10.1001/jamacardio.2020.2136).
None of the athletes required hospitalization for their illness, and only 27% reported mild symptoms during the short-term infection, including sore throat, shortness of breath, myalgia, and fever.
On the day of CMR imaging, ECG and transthoracic echocardiography were performed, and serum troponin I was measured. There were no diagnostic ST/T wave changes, ventricular function and volumes were normal, and no athletes showed elevated serum troponin levels.
The updated Lake Louise Criteria were used to assess CMR findings consistent with myocarditis.
“I don’t think this is a COVID-specific issue. We have seen myocarditis after other viral infections; it’s just that COVID-19 is the most studied thus far, and with strenuous activity, inflammation in the heart can be risky,” Dr. Rajpal said in an interview. He added that more long-term and larger studies with control populations are needed.
His group is continuing to follow these athletes and has suggested that CMR “may provide an excellent risk-stratification assessment for myocarditis in athletes who have recovered from COVID-19 to guide safe competitive sports participation.”
Significance still unknown
Matthew Martinez, MD, the director of sports cardiology at Atlantic Health – Morristown (N.J.) Medical Center and the Gagnon Cardiovascular Institute, urged caution in making too much of the findings of this small study.
“We know that viruses cause myocardial damage and myocarditis. What we don’t know is how important these findings are. And in terms of risk, would we find the same phenomenon if we did this, say, in flu patients or in other age groups?” Dr. Martinez said in an interview.
“I haven’t seen all the images, but what I’d want to know is are these very subtle findings? Are these overt findings? Is this part of an active individual with symptoms? I need to know a little more data before I can tell if this influences the increased risk of sudden cardiac death that we often associate with myocarditis. I’m not sure how this should influence making decisions with regards to return to play.”
Dr. Martinez, who is the ACC’s chair of Sports and Exercise but was not an author of their recent guidance on return to sport, said that he is not routinely using CMR to assess athletes post-infection, as per the ACC’s recommendations.
“My approach is to evaluate anybody with a history of COVID infection and, first, determine whether it was an important infection with significant symptoms or not. And then, if they’re participating at a high level or are professional athletes, I would suggest an ECG, echo, and troponin. That’s our recommendation for the last several months and is still an appropriate way to evaluate that group.”
“In the presence of an abnormality or ongoing symptoms, I would ask for an MRI at that point,” said Dr. Martinez.
“We just don’t have much data on athletes with no symptoms to use to interpret these CMR findings and the study didn’t offer any controls. We don’t even know if these findings are new findings or old findings that have just been identified now,” he added.
New, updated recommendations from the ACC are coming soon, said Dr. Martinez. “I do not expect them to include CMR as first line.”
Cardiologists concerned about misinformation
This is at least the fourth study showing myocardial damage post-COVID-19 infection and there is concern in the medical community that the media has overstated the risks of heart damage, especially in athletes, and at the same time overstated the benefits of CMR.
In particular, Puntmann et al reported in July a 100-patient study that showed evidence of myocardial inflammation by CMR in 78% of patients recently recovered from a bout of COVID-19 (JAMA Cardiol. 2020 Jul 27; doi:10.1001/jamacardio.2020.3557).
“That paper is completely problematic,” John Mandrola, MD, of Baptists Medical Associates, Louisville, Ky., said in an interview. “It has the same overarching weaknesses [of other studies] that it’s observational and retrospective, but there were also numerical issues. So to me that paper is an interesting observation, but utterly unconvincing and preliminary,” said Dr. Mandrola.
Those limitations didn’t stop the study from garnering media attention, however. The Altmetric score (an attention score that tracks all mentions of an article in the media and on social media) for the Puntmann et al paper is approaching 13,000, including coverage from 276 news outlets and more than 19,000 tweets, putting it in the 99th percentile of all research outputs tracked by Altmetric to date.
To counter this, an “open letter” posted online just days before the Rajpal study published urging professional societies to “offer clear guidance discouraging CMR screening for COVID-19 related heart abnormalities in asymptomatic members of the general public.” The letter was signed by 51 clinicians, researchers, and imaging specialists from around the world.
Dr. Mandrola, one of the signatories, said: “This topic really scares people, and when it gets in the media like this, I think the leaders of these societies need to come out and say something really clear on major news networks letting people know that it’s just way too premature to start doing CMRs on every athlete that’s gotten this virus.”
“I understand that the current guidelines may be clear that CMR is not a first-line test for this indication, but when the media coverage is so extensive and so overblown, I wonder how much impact the guidelines will have in countering this fear that’s in the community,” he added.
Asked to comment on the letter, Dr. Rajpal said he agrees with the signatories that asymptomatic people from general population do not need routine cardiac MRI. “However, competitive athletes are a different story. Testing depends on risk assessment in specific population and competitive athletes as per our protocol will get enhanced cardiac workup including CMR for responsible and safe start of competitive sports. ... In the present scenario, while we get more data including control data, we will continue with our current protocol.”
Dr. Mandrola is Medscape Cardiology’s Chief Cardiology Consultant. MDedge is part of the Medscape Professional Network.
This article first appeared on Medscape.com.
Non-COVID-19 clinical trials grind to a halt during pandemic
The COVID-19 pandemic has created unique and unprecedented challenges for the clinical research world, with potentially long-lasting consequences.
A new analysis of the extent of disruption shows that the average rate of stopped trials nearly doubled during the first 5 months of 2020, compared with the 2 previous years.
“Typically, clinical research precedes clinical practice by several years, so this disruption we’re seeing now will be felt for many years to come,” said Mario Guadino, MD, of Weill Cornell Medicine, New York.
The analysis was published online July 31 in the Journal of the American College of Cardiology.
The researchers used Python software to query meta-data from all trials reported on ClinicalTrials.gov. Of 321,218 non-COVID-19 trials queried, 28,672 (8.9%) were reported as stopped, defined as a switch in trial status from “recruiting” to “active and not recruiting,” “completed,” “suspended,” “terminated,” or “withdrawn.”
The average rate of discontinuation was 638 trials/month from January 2017 to December 2019, rising to 1,147 trials/month between January 2020 and May 2020 (P < .001 for trend).
Once stopped (as opposed to paused), restarting a trial is a tricky prospect, said Dr. Guadino. “You can’t stop and restart a trial because it creates a lot of issues, so we should expect many of these stopped trials to never be completed.”
He said these figures likely represent an underestimate of the true impact of the pandemic because there is typically a delay in the updating of the status of a trial on ClinicalTrials.gov.
“We are likely looking only at the tip of the iceberg,” he added. “My impression is that the number of trials that will be affected and even canceled will be very high.”
As for cardiology trials, one of the report’s authors, Deepak Bhatt, MD, Brigham and Women’s Hospital, Boston, without naming specific trials, had this to say: “Several cardiovascular trials were paused, and some were permanently discontinued. It may be a while before we fully appreciate just how much information was lost and how much might be salvaged.”
He’s not worried, however, that upcoming cardiology meetings, which have moved online for the foreseeable future, might get a bit boring. “Fortunately, there is enough good work going on in the cardiovascular and cardiometabolic space that I believe there will still be ample randomized and observational data of high quality to present at the major meetings,” Dr. Bhatt said in an email.
The researchers found a weak correlation between the national population-adjusted numbers of COVID-19 cases and the proportion of non-COVID-19 trials stopped by country.
Even for trials that stopped recruiting for a period of time but are continuing, there are myriad issues involving compliance, data integrity, statistical interpretability, etc.
“Even if there is just a temporary disruption, that will most likely lead to reduced enrollment, missing follow-up visits, and protocol deviations, all things that would be red flags during normal times and impact the quality of the clinical trial,” said Dr. Guadino.
“And if your outcome of interest is mortality, well, how exactly do you measure that during a pandemic?” he added.
Stopped for lack of funding
Besides the logistical issues, another reason trials may be in jeopardy is funding. A warning early in the pandemic from the research community in Canada that funding was quickly drying up, leaving both jobs and data at risk, led to an aid package from the government to keep the lights on.
The National Institutes of Health (NIH), the Canadian Institutes of Health Research, and similar groups “have devoted large sums of money to research in COVID, which is of course very appropriate, but that clearly reduces the amount of funding that is available for other researchers,” said Dr. Guadino.
Some funding agencies around the world have canceled or put on hold all non-COVID-19 clinical trials still at the design state, Dr. Guadino said in an interview.
The NIH, he stressed, has not canceled funding and has been “extremely open and cooperative” in trying to help trialists navigate the many COVID-generated issues. They’ve even issued guidance on how to manage trials during COVID-19.
Of note, in the survey, the majority of the trials stopped (95.4%) had nongovernmental funding.
“The data are not very granular, so we’re only able to make some very simple, descriptive comments, but it does seem like the more fragile trials – those that are smaller and industry-funded – are the ones more likely to be disrupted,” said Dr. Guadino.
In some cases, he said, priorities have shifted to COVID-19. “If a small company is sponsoring a trial and they decide they want to sponsor something related to COVID, or they realize that because of the slow enrollment, the trial becomes too expensive to complete, they may opt to just abandon it,” said Dr. Guadino.
At what cost? It will take years to sort that out, he said.
This study received no funding. Dr. Guadino and Dr. Bhatt are both active trialists, participating in both industry- and government-sponsored clinical research.
A version of this article originally appeared on Medscape.com.
The COVID-19 pandemic has created unique and unprecedented challenges for the clinical research world, with potentially long-lasting consequences.
A new analysis of the extent of disruption shows that the average rate of stopped trials nearly doubled during the first 5 months of 2020, compared with the 2 previous years.
“Typically, clinical research precedes clinical practice by several years, so this disruption we’re seeing now will be felt for many years to come,” said Mario Guadino, MD, of Weill Cornell Medicine, New York.
The analysis was published online July 31 in the Journal of the American College of Cardiology.
The researchers used Python software to query meta-data from all trials reported on ClinicalTrials.gov. Of 321,218 non-COVID-19 trials queried, 28,672 (8.9%) were reported as stopped, defined as a switch in trial status from “recruiting” to “active and not recruiting,” “completed,” “suspended,” “terminated,” or “withdrawn.”
The average rate of discontinuation was 638 trials/month from January 2017 to December 2019, rising to 1,147 trials/month between January 2020 and May 2020 (P < .001 for trend).
Once stopped (as opposed to paused), restarting a trial is a tricky prospect, said Dr. Guadino. “You can’t stop and restart a trial because it creates a lot of issues, so we should expect many of these stopped trials to never be completed.”
He said these figures likely represent an underestimate of the true impact of the pandemic because there is typically a delay in the updating of the status of a trial on ClinicalTrials.gov.
“We are likely looking only at the tip of the iceberg,” he added. “My impression is that the number of trials that will be affected and even canceled will be very high.”
As for cardiology trials, one of the report’s authors, Deepak Bhatt, MD, Brigham and Women’s Hospital, Boston, without naming specific trials, had this to say: “Several cardiovascular trials were paused, and some were permanently discontinued. It may be a while before we fully appreciate just how much information was lost and how much might be salvaged.”
He’s not worried, however, that upcoming cardiology meetings, which have moved online for the foreseeable future, might get a bit boring. “Fortunately, there is enough good work going on in the cardiovascular and cardiometabolic space that I believe there will still be ample randomized and observational data of high quality to present at the major meetings,” Dr. Bhatt said in an email.
The researchers found a weak correlation between the national population-adjusted numbers of COVID-19 cases and the proportion of non-COVID-19 trials stopped by country.
Even for trials that stopped recruiting for a period of time but are continuing, there are myriad issues involving compliance, data integrity, statistical interpretability, etc.
“Even if there is just a temporary disruption, that will most likely lead to reduced enrollment, missing follow-up visits, and protocol deviations, all things that would be red flags during normal times and impact the quality of the clinical trial,” said Dr. Guadino.
“And if your outcome of interest is mortality, well, how exactly do you measure that during a pandemic?” he added.
Stopped for lack of funding
Besides the logistical issues, another reason trials may be in jeopardy is funding. A warning early in the pandemic from the research community in Canada that funding was quickly drying up, leaving both jobs and data at risk, led to an aid package from the government to keep the lights on.
The National Institutes of Health (NIH), the Canadian Institutes of Health Research, and similar groups “have devoted large sums of money to research in COVID, which is of course very appropriate, but that clearly reduces the amount of funding that is available for other researchers,” said Dr. Guadino.
Some funding agencies around the world have canceled or put on hold all non-COVID-19 clinical trials still at the design state, Dr. Guadino said in an interview.
The NIH, he stressed, has not canceled funding and has been “extremely open and cooperative” in trying to help trialists navigate the many COVID-generated issues. They’ve even issued guidance on how to manage trials during COVID-19.
Of note, in the survey, the majority of the trials stopped (95.4%) had nongovernmental funding.
“The data are not very granular, so we’re only able to make some very simple, descriptive comments, but it does seem like the more fragile trials – those that are smaller and industry-funded – are the ones more likely to be disrupted,” said Dr. Guadino.
In some cases, he said, priorities have shifted to COVID-19. “If a small company is sponsoring a trial and they decide they want to sponsor something related to COVID, or they realize that because of the slow enrollment, the trial becomes too expensive to complete, they may opt to just abandon it,” said Dr. Guadino.
At what cost? It will take years to sort that out, he said.
This study received no funding. Dr. Guadino and Dr. Bhatt are both active trialists, participating in both industry- and government-sponsored clinical research.
A version of this article originally appeared on Medscape.com.
The COVID-19 pandemic has created unique and unprecedented challenges for the clinical research world, with potentially long-lasting consequences.
A new analysis of the extent of disruption shows that the average rate of stopped trials nearly doubled during the first 5 months of 2020, compared with the 2 previous years.
“Typically, clinical research precedes clinical practice by several years, so this disruption we’re seeing now will be felt for many years to come,” said Mario Guadino, MD, of Weill Cornell Medicine, New York.
The analysis was published online July 31 in the Journal of the American College of Cardiology.
The researchers used Python software to query meta-data from all trials reported on ClinicalTrials.gov. Of 321,218 non-COVID-19 trials queried, 28,672 (8.9%) were reported as stopped, defined as a switch in trial status from “recruiting” to “active and not recruiting,” “completed,” “suspended,” “terminated,” or “withdrawn.”
The average rate of discontinuation was 638 trials/month from January 2017 to December 2019, rising to 1,147 trials/month between January 2020 and May 2020 (P < .001 for trend).
Once stopped (as opposed to paused), restarting a trial is a tricky prospect, said Dr. Guadino. “You can’t stop and restart a trial because it creates a lot of issues, so we should expect many of these stopped trials to never be completed.”
He said these figures likely represent an underestimate of the true impact of the pandemic because there is typically a delay in the updating of the status of a trial on ClinicalTrials.gov.
“We are likely looking only at the tip of the iceberg,” he added. “My impression is that the number of trials that will be affected and even canceled will be very high.”
As for cardiology trials, one of the report’s authors, Deepak Bhatt, MD, Brigham and Women’s Hospital, Boston, without naming specific trials, had this to say: “Several cardiovascular trials were paused, and some were permanently discontinued. It may be a while before we fully appreciate just how much information was lost and how much might be salvaged.”
He’s not worried, however, that upcoming cardiology meetings, which have moved online for the foreseeable future, might get a bit boring. “Fortunately, there is enough good work going on in the cardiovascular and cardiometabolic space that I believe there will still be ample randomized and observational data of high quality to present at the major meetings,” Dr. Bhatt said in an email.
The researchers found a weak correlation between the national population-adjusted numbers of COVID-19 cases and the proportion of non-COVID-19 trials stopped by country.
Even for trials that stopped recruiting for a period of time but are continuing, there are myriad issues involving compliance, data integrity, statistical interpretability, etc.
“Even if there is just a temporary disruption, that will most likely lead to reduced enrollment, missing follow-up visits, and protocol deviations, all things that would be red flags during normal times and impact the quality of the clinical trial,” said Dr. Guadino.
“And if your outcome of interest is mortality, well, how exactly do you measure that during a pandemic?” he added.
Stopped for lack of funding
Besides the logistical issues, another reason trials may be in jeopardy is funding. A warning early in the pandemic from the research community in Canada that funding was quickly drying up, leaving both jobs and data at risk, led to an aid package from the government to keep the lights on.
The National Institutes of Health (NIH), the Canadian Institutes of Health Research, and similar groups “have devoted large sums of money to research in COVID, which is of course very appropriate, but that clearly reduces the amount of funding that is available for other researchers,” said Dr. Guadino.
Some funding agencies around the world have canceled or put on hold all non-COVID-19 clinical trials still at the design state, Dr. Guadino said in an interview.
The NIH, he stressed, has not canceled funding and has been “extremely open and cooperative” in trying to help trialists navigate the many COVID-generated issues. They’ve even issued guidance on how to manage trials during COVID-19.
Of note, in the survey, the majority of the trials stopped (95.4%) had nongovernmental funding.
“The data are not very granular, so we’re only able to make some very simple, descriptive comments, but it does seem like the more fragile trials – those that are smaller and industry-funded – are the ones more likely to be disrupted,” said Dr. Guadino.
In some cases, he said, priorities have shifted to COVID-19. “If a small company is sponsoring a trial and they decide they want to sponsor something related to COVID, or they realize that because of the slow enrollment, the trial becomes too expensive to complete, they may opt to just abandon it,” said Dr. Guadino.
At what cost? It will take years to sort that out, he said.
This study received no funding. Dr. Guadino and Dr. Bhatt are both active trialists, participating in both industry- and government-sponsored clinical research.
A version of this article originally appeared on Medscape.com.
Antiaffirmative action paper blasted on Twitter now retracted
An article published in March in the Journal of the American Heart Association that raised a ruckus on #medtwitter this week has now been retracted.
It’s unclear what prompted the public explosion of anger, sadness, and recrimination that ultimately led to the retraction of this article – which flew almost completely under the radar when it first appeared online and in print – but it’s crystal clear why it might offend.
To many readers, the paper, written by Norman C. Wang, MD, MSc, an electrophysiologist at the University of Pittsburgh Medical Center, is a “racist” rant that relies on half-truths (J Am Heart Assoc. 2020 Mar 24. doi: 10.1161/JAHA.120.015959).
Officially, the article, “Diversity, Inclusion, and Equity: Evolution of Race and Ethnicity Considerations for the Cardiology Workforce in the United States of America From 1969 to 2019,” was retracted after the American Heart Association “became aware of serious concerns after publication. The author’s institution, the University of Pittsburgh Medical Center, has notified the Editor‐in‐Chief that the article contains many misconceptions and misquotes and that together those inaccuracies, misstatements, and selective misreading of source materials strip the paper of its scientific validity,” the retraction reads (J Am Heart Assoc. 2020 Aug 6. doi: 10.1161/JAHA.119.014602).
The journal will be publishing a detailed rebuttal, the notice adds: “This retraction notice will be updated with a link to the rebuttal when it publishes.”
“The Editor‐in‐Chief deeply regrets publishing the article and offers his apologies,” it further reads. “The American Heart Association and the Editor‐in‐Chief have determined that the best interest of the public and the research community will be served by issuing this notice of retraction. The author does not agree to the retraction.”
In the paper, Dr. Wang argues that affirmative action policies designed to increase minority representation in medical schools and cardiovascular training programs result in unqualified applicants being admitted, where they will struggle to succeed.
The article itself is a dense review of the topic of diversity, inclusion, and equity, aiming to “critically assess current paradigms, and to consider potential solutions to anticipated challenges,” according to its author. Supported by 108 references, Dr. Wang concludes with a lengthy quote from tennis great Arthur Ashe, an opponent of affirmative action who died in 1993.
Affirmative action, said Mr. Ashe, is “an insult to the people it intended to help.” Dr. Wang suggests that “racial and ethnic preferences for undergraduate and medical school admissions should be gradually rolled back with a target end year of 2028.”
He cites the $16 billion in federal funding that cardiovascular disease training programs receive every year to support graduate medical education in support of this contention.
#Medtwitter explodes
“My entire lived experience contradicts everything in that racist @JAHA_AHA article, as does the experience of so many others. So, I know it’s just a bad opinion piece passed off as ‘research’ that shouldn’t have been published. Still the damage has been done. We MUST do better,” tweeted Bryan A. Smith, MD, University of Chicago Medicine.
According to its Altmetric score, the article received very little attention back in March and April. There were three tweets referencing it, including one from JAHA announcing its publication. Since Aug. 2, an additional 390-odd Tweets from 347 Twitter users have been registered. None appear to be complimentary. Several days into the Twitter storm, the article was officially retracted.
“This article is shocking and makes me sad,” Martha Gulati, MD, University of Arizona, Phoenix, said in an interview. “We are all working so hard to make cardiology more inclusive and diverse, and this takes us like 1,000 steps backwards.”
For her part, Dr. Gulati would have liked a retraction earlier in the week. “The analysis was selective and incorrect, and the statements made intimate that minority trainees were selected based on affirmative action rather than their merits,” she said. It also suggested that their presence was representative of a decline in standards in cardiology programs that take underrepresented minorities (URMs).
Standard arguments against affirmative action
According to Dr. Wang, who did not respond to a request to comment for this article, allowing minority students into medical school with academic records that are weaker than their classmates sets them up for failure.
“Many do not complete their intended programs or do not attain academic success to be attractive candidates for subsequent educational programs or employment,” he wrote.
This is a standard argument of opponents to affirmative action, said Quinn Capers IV, MD. Dr. Capers, a longtime advocate for diversity in medicine, acknowledges that, “on average,” test scores for Blacks, Hispanics, and Native Americans tend to be lower than for White applicants for a wide range of reasons, many of which are related to systemic racism.
“This is the strongest weapon opponents to affirmative action have, and they keep coming back to it, but it’s out of step with how many in academic medicine feel,” said Dr. Capers, who is an interventional cardiologist and the vice dean for faculty affairs at Ohio State University, Columbus.
This is why, he added, most medical schools have embraced the Association of American Medical Colleges’ concept of “holistic review,” which judges potential physicians on their academic records, their personal experiences, and their individual attributes.
“Standardized tests and academic records are important, but so are the experiences one has gone through and the individual attributes they may have. How resilient are you? How compassionate? Our embrace of this more holistic approach, I believe, is helping many medical schools move toward having a more diverse class that is closer to reflecting the needs of our multicultural and multiracial society,” Dr. Capers said.
To be clear, Dr. Capers is not afraid of having a discussion on this topic and denies that the uproar against this article represents “cancel culture.”
“Hey, I love to debate and I’m not against hearing divisive voices, but then let’s have a debate and hear both sides. But there are several problems with the way they did this. No. 1, they called it a ‘white paper,’ which to most people means it reflects the views of the organization, not a specific individual, and, secondly, it’s more than an opinion piece in that he manipulates facts to make his points, with no chance for rebuttal.”
Several have also questioned how this paper, which is written by a nonexpert in the field, passed peer review.
The article contains some accurate historical references, said Dr. Capers, but intertwined with this history the author editorializes in a fashion that is “charged with racism.” In other places, Dr. Wang is just outright wrong, he added.
“I can also tell you that, in one place where he quotes me specifically, what he says is quite damaging and completely wrong. He quotes something we wrote but cuts off the final sentence, making it seem as though we acknowledged that we had to artificially rank minority applicants high, just so we could say we have a diverse fellowship program.
“It’s frankly very hard to believe that was an accident,” Dr. Capers added.
AHA backs away, promises investigation
The article has been disowned by all levels of the AHA leadership – past, present, and future.
In an Editor’s Note, Barry London, MD, PhD, the Editor in chief of the Journal of the American Heart Association, apologized for his role and the role of his staff in publishing the article.
“JAHA will support all efforts to correct this error, including but not limited to the publication of alternate viewpoints, which we solicited at the time of publication but have not yet been submitted to the journal. In addition, we will work to improve our peer review system to prevent future missteps of this type,” Dr. London wrote. “I can only hope that igniting a discussion around diversity in cardiology will ultimately fuel new ideas and lead to real advances.”
“I want to emphasize in the strongest possible terms that this paper does not represent the views of the AHA as an organization or its leadership. This paper should never have been published. A thorough investigation is rightly being conducted,” tweeted Mitchell S.V. Elkind, MD, MPhil, who took over the AHA presidency last month.
“Author’s views are racist and not consistent with my values nor AHA,” tweeted Robert Harrington, MD, immediate past president of the AHA. ‘Investigation is underway into how it made it through the editorial process. Like you, I want to know what happened. I am angry, frustrated and disappointed that this piece was published; expect review soon.’
“Agree with @HeartBobH. It is impossible not to hear and feel the hurt and pain out there on a very personal level, especially among our young colleagues. You are valued, and worthy. Please stay tuned and then help all of us work to be better,” tweeted Donald Lloyd-Jones, MD, president-elect of AHA.
A version of this article originally appeared on Medscape.com.
An article published in March in the Journal of the American Heart Association that raised a ruckus on #medtwitter this week has now been retracted.
It’s unclear what prompted the public explosion of anger, sadness, and recrimination that ultimately led to the retraction of this article – which flew almost completely under the radar when it first appeared online and in print – but it’s crystal clear why it might offend.
To many readers, the paper, written by Norman C. Wang, MD, MSc, an electrophysiologist at the University of Pittsburgh Medical Center, is a “racist” rant that relies on half-truths (J Am Heart Assoc. 2020 Mar 24. doi: 10.1161/JAHA.120.015959).
Officially, the article, “Diversity, Inclusion, and Equity: Evolution of Race and Ethnicity Considerations for the Cardiology Workforce in the United States of America From 1969 to 2019,” was retracted after the American Heart Association “became aware of serious concerns after publication. The author’s institution, the University of Pittsburgh Medical Center, has notified the Editor‐in‐Chief that the article contains many misconceptions and misquotes and that together those inaccuracies, misstatements, and selective misreading of source materials strip the paper of its scientific validity,” the retraction reads (J Am Heart Assoc. 2020 Aug 6. doi: 10.1161/JAHA.119.014602).
The journal will be publishing a detailed rebuttal, the notice adds: “This retraction notice will be updated with a link to the rebuttal when it publishes.”
“The Editor‐in‐Chief deeply regrets publishing the article and offers his apologies,” it further reads. “The American Heart Association and the Editor‐in‐Chief have determined that the best interest of the public and the research community will be served by issuing this notice of retraction. The author does not agree to the retraction.”
In the paper, Dr. Wang argues that affirmative action policies designed to increase minority representation in medical schools and cardiovascular training programs result in unqualified applicants being admitted, where they will struggle to succeed.
The article itself is a dense review of the topic of diversity, inclusion, and equity, aiming to “critically assess current paradigms, and to consider potential solutions to anticipated challenges,” according to its author. Supported by 108 references, Dr. Wang concludes with a lengthy quote from tennis great Arthur Ashe, an opponent of affirmative action who died in 1993.
Affirmative action, said Mr. Ashe, is “an insult to the people it intended to help.” Dr. Wang suggests that “racial and ethnic preferences for undergraduate and medical school admissions should be gradually rolled back with a target end year of 2028.”
He cites the $16 billion in federal funding that cardiovascular disease training programs receive every year to support graduate medical education in support of this contention.
#Medtwitter explodes
“My entire lived experience contradicts everything in that racist @JAHA_AHA article, as does the experience of so many others. So, I know it’s just a bad opinion piece passed off as ‘research’ that shouldn’t have been published. Still the damage has been done. We MUST do better,” tweeted Bryan A. Smith, MD, University of Chicago Medicine.
According to its Altmetric score, the article received very little attention back in March and April. There were three tweets referencing it, including one from JAHA announcing its publication. Since Aug. 2, an additional 390-odd Tweets from 347 Twitter users have been registered. None appear to be complimentary. Several days into the Twitter storm, the article was officially retracted.
“This article is shocking and makes me sad,” Martha Gulati, MD, University of Arizona, Phoenix, said in an interview. “We are all working so hard to make cardiology more inclusive and diverse, and this takes us like 1,000 steps backwards.”
For her part, Dr. Gulati would have liked a retraction earlier in the week. “The analysis was selective and incorrect, and the statements made intimate that minority trainees were selected based on affirmative action rather than their merits,” she said. It also suggested that their presence was representative of a decline in standards in cardiology programs that take underrepresented minorities (URMs).
Standard arguments against affirmative action
According to Dr. Wang, who did not respond to a request to comment for this article, allowing minority students into medical school with academic records that are weaker than their classmates sets them up for failure.
“Many do not complete their intended programs or do not attain academic success to be attractive candidates for subsequent educational programs or employment,” he wrote.
This is a standard argument of opponents to affirmative action, said Quinn Capers IV, MD. Dr. Capers, a longtime advocate for diversity in medicine, acknowledges that, “on average,” test scores for Blacks, Hispanics, and Native Americans tend to be lower than for White applicants for a wide range of reasons, many of which are related to systemic racism.
“This is the strongest weapon opponents to affirmative action have, and they keep coming back to it, but it’s out of step with how many in academic medicine feel,” said Dr. Capers, who is an interventional cardiologist and the vice dean for faculty affairs at Ohio State University, Columbus.
This is why, he added, most medical schools have embraced the Association of American Medical Colleges’ concept of “holistic review,” which judges potential physicians on their academic records, their personal experiences, and their individual attributes.
“Standardized tests and academic records are important, but so are the experiences one has gone through and the individual attributes they may have. How resilient are you? How compassionate? Our embrace of this more holistic approach, I believe, is helping many medical schools move toward having a more diverse class that is closer to reflecting the needs of our multicultural and multiracial society,” Dr. Capers said.
To be clear, Dr. Capers is not afraid of having a discussion on this topic and denies that the uproar against this article represents “cancel culture.”
“Hey, I love to debate and I’m not against hearing divisive voices, but then let’s have a debate and hear both sides. But there are several problems with the way they did this. No. 1, they called it a ‘white paper,’ which to most people means it reflects the views of the organization, not a specific individual, and, secondly, it’s more than an opinion piece in that he manipulates facts to make his points, with no chance for rebuttal.”
Several have also questioned how this paper, which is written by a nonexpert in the field, passed peer review.
The article contains some accurate historical references, said Dr. Capers, but intertwined with this history the author editorializes in a fashion that is “charged with racism.” In other places, Dr. Wang is just outright wrong, he added.
“I can also tell you that, in one place where he quotes me specifically, what he says is quite damaging and completely wrong. He quotes something we wrote but cuts off the final sentence, making it seem as though we acknowledged that we had to artificially rank minority applicants high, just so we could say we have a diverse fellowship program.
“It’s frankly very hard to believe that was an accident,” Dr. Capers added.
AHA backs away, promises investigation
The article has been disowned by all levels of the AHA leadership – past, present, and future.
In an Editor’s Note, Barry London, MD, PhD, the Editor in chief of the Journal of the American Heart Association, apologized for his role and the role of his staff in publishing the article.
“JAHA will support all efforts to correct this error, including but not limited to the publication of alternate viewpoints, which we solicited at the time of publication but have not yet been submitted to the journal. In addition, we will work to improve our peer review system to prevent future missteps of this type,” Dr. London wrote. “I can only hope that igniting a discussion around diversity in cardiology will ultimately fuel new ideas and lead to real advances.”
“I want to emphasize in the strongest possible terms that this paper does not represent the views of the AHA as an organization or its leadership. This paper should never have been published. A thorough investigation is rightly being conducted,” tweeted Mitchell S.V. Elkind, MD, MPhil, who took over the AHA presidency last month.
“Author’s views are racist and not consistent with my values nor AHA,” tweeted Robert Harrington, MD, immediate past president of the AHA. ‘Investigation is underway into how it made it through the editorial process. Like you, I want to know what happened. I am angry, frustrated and disappointed that this piece was published; expect review soon.’
“Agree with @HeartBobH. It is impossible not to hear and feel the hurt and pain out there on a very personal level, especially among our young colleagues. You are valued, and worthy. Please stay tuned and then help all of us work to be better,” tweeted Donald Lloyd-Jones, MD, president-elect of AHA.
A version of this article originally appeared on Medscape.com.
An article published in March in the Journal of the American Heart Association that raised a ruckus on #medtwitter this week has now been retracted.
It’s unclear what prompted the public explosion of anger, sadness, and recrimination that ultimately led to the retraction of this article – which flew almost completely under the radar when it first appeared online and in print – but it’s crystal clear why it might offend.
To many readers, the paper, written by Norman C. Wang, MD, MSc, an electrophysiologist at the University of Pittsburgh Medical Center, is a “racist” rant that relies on half-truths (J Am Heart Assoc. 2020 Mar 24. doi: 10.1161/JAHA.120.015959).
Officially, the article, “Diversity, Inclusion, and Equity: Evolution of Race and Ethnicity Considerations for the Cardiology Workforce in the United States of America From 1969 to 2019,” was retracted after the American Heart Association “became aware of serious concerns after publication. The author’s institution, the University of Pittsburgh Medical Center, has notified the Editor‐in‐Chief that the article contains many misconceptions and misquotes and that together those inaccuracies, misstatements, and selective misreading of source materials strip the paper of its scientific validity,” the retraction reads (J Am Heart Assoc. 2020 Aug 6. doi: 10.1161/JAHA.119.014602).
The journal will be publishing a detailed rebuttal, the notice adds: “This retraction notice will be updated with a link to the rebuttal when it publishes.”
“The Editor‐in‐Chief deeply regrets publishing the article and offers his apologies,” it further reads. “The American Heart Association and the Editor‐in‐Chief have determined that the best interest of the public and the research community will be served by issuing this notice of retraction. The author does not agree to the retraction.”
In the paper, Dr. Wang argues that affirmative action policies designed to increase minority representation in medical schools and cardiovascular training programs result in unqualified applicants being admitted, where they will struggle to succeed.
The article itself is a dense review of the topic of diversity, inclusion, and equity, aiming to “critically assess current paradigms, and to consider potential solutions to anticipated challenges,” according to its author. Supported by 108 references, Dr. Wang concludes with a lengthy quote from tennis great Arthur Ashe, an opponent of affirmative action who died in 1993.
Affirmative action, said Mr. Ashe, is “an insult to the people it intended to help.” Dr. Wang suggests that “racial and ethnic preferences for undergraduate and medical school admissions should be gradually rolled back with a target end year of 2028.”
He cites the $16 billion in federal funding that cardiovascular disease training programs receive every year to support graduate medical education in support of this contention.
#Medtwitter explodes
“My entire lived experience contradicts everything in that racist @JAHA_AHA article, as does the experience of so many others. So, I know it’s just a bad opinion piece passed off as ‘research’ that shouldn’t have been published. Still the damage has been done. We MUST do better,” tweeted Bryan A. Smith, MD, University of Chicago Medicine.
According to its Altmetric score, the article received very little attention back in March and April. There were three tweets referencing it, including one from JAHA announcing its publication. Since Aug. 2, an additional 390-odd Tweets from 347 Twitter users have been registered. None appear to be complimentary. Several days into the Twitter storm, the article was officially retracted.
“This article is shocking and makes me sad,” Martha Gulati, MD, University of Arizona, Phoenix, said in an interview. “We are all working so hard to make cardiology more inclusive and diverse, and this takes us like 1,000 steps backwards.”
For her part, Dr. Gulati would have liked a retraction earlier in the week. “The analysis was selective and incorrect, and the statements made intimate that minority trainees were selected based on affirmative action rather than their merits,” she said. It also suggested that their presence was representative of a decline in standards in cardiology programs that take underrepresented minorities (URMs).
Standard arguments against affirmative action
According to Dr. Wang, who did not respond to a request to comment for this article, allowing minority students into medical school with academic records that are weaker than their classmates sets them up for failure.
“Many do not complete their intended programs or do not attain academic success to be attractive candidates for subsequent educational programs or employment,” he wrote.
This is a standard argument of opponents to affirmative action, said Quinn Capers IV, MD. Dr. Capers, a longtime advocate for diversity in medicine, acknowledges that, “on average,” test scores for Blacks, Hispanics, and Native Americans tend to be lower than for White applicants for a wide range of reasons, many of which are related to systemic racism.
“This is the strongest weapon opponents to affirmative action have, and they keep coming back to it, but it’s out of step with how many in academic medicine feel,” said Dr. Capers, who is an interventional cardiologist and the vice dean for faculty affairs at Ohio State University, Columbus.
This is why, he added, most medical schools have embraced the Association of American Medical Colleges’ concept of “holistic review,” which judges potential physicians on their academic records, their personal experiences, and their individual attributes.
“Standardized tests and academic records are important, but so are the experiences one has gone through and the individual attributes they may have. How resilient are you? How compassionate? Our embrace of this more holistic approach, I believe, is helping many medical schools move toward having a more diverse class that is closer to reflecting the needs of our multicultural and multiracial society,” Dr. Capers said.
To be clear, Dr. Capers is not afraid of having a discussion on this topic and denies that the uproar against this article represents “cancel culture.”
“Hey, I love to debate and I’m not against hearing divisive voices, but then let’s have a debate and hear both sides. But there are several problems with the way they did this. No. 1, they called it a ‘white paper,’ which to most people means it reflects the views of the organization, not a specific individual, and, secondly, it’s more than an opinion piece in that he manipulates facts to make his points, with no chance for rebuttal.”
Several have also questioned how this paper, which is written by a nonexpert in the field, passed peer review.
The article contains some accurate historical references, said Dr. Capers, but intertwined with this history the author editorializes in a fashion that is “charged with racism.” In other places, Dr. Wang is just outright wrong, he added.
“I can also tell you that, in one place where he quotes me specifically, what he says is quite damaging and completely wrong. He quotes something we wrote but cuts off the final sentence, making it seem as though we acknowledged that we had to artificially rank minority applicants high, just so we could say we have a diverse fellowship program.
“It’s frankly very hard to believe that was an accident,” Dr. Capers added.
AHA backs away, promises investigation
The article has been disowned by all levels of the AHA leadership – past, present, and future.
In an Editor’s Note, Barry London, MD, PhD, the Editor in chief of the Journal of the American Heart Association, apologized for his role and the role of his staff in publishing the article.
“JAHA will support all efforts to correct this error, including but not limited to the publication of alternate viewpoints, which we solicited at the time of publication but have not yet been submitted to the journal. In addition, we will work to improve our peer review system to prevent future missteps of this type,” Dr. London wrote. “I can only hope that igniting a discussion around diversity in cardiology will ultimately fuel new ideas and lead to real advances.”
“I want to emphasize in the strongest possible terms that this paper does not represent the views of the AHA as an organization or its leadership. This paper should never have been published. A thorough investigation is rightly being conducted,” tweeted Mitchell S.V. Elkind, MD, MPhil, who took over the AHA presidency last month.
“Author’s views are racist and not consistent with my values nor AHA,” tweeted Robert Harrington, MD, immediate past president of the AHA. ‘Investigation is underway into how it made it through the editorial process. Like you, I want to know what happened. I am angry, frustrated and disappointed that this piece was published; expect review soon.’
“Agree with @HeartBobH. It is impossible not to hear and feel the hurt and pain out there on a very personal level, especially among our young colleagues. You are valued, and worthy. Please stay tuned and then help all of us work to be better,” tweeted Donald Lloyd-Jones, MD, president-elect of AHA.
A version of this article originally appeared on Medscape.com.
More U.S. cardiologists opting for larger practices
U.S. cardiologists are increasingly opting out of solo or small practices, and joining larger practices, according to a new analysis of U.S. data from 2013 and 2017.
In 2013, 34.2% of U.S. cardiologists worked in practices of five or fewer cardiologists. That number dropped to 27% by 2017. On the flip side, the proportion working in practices with 25 cardiologists or more rose from 26% in 2013 to 35.8% in 2017.
“This is a trend we’re seeing across health care – hospitals are merging and they’re acquiring physician practices, primary care doctors are joining larger practices, too – so to some extent it seems that cardiologists are just responding to changes in the market structure where they practice,” said Jose F. Figueroa, MD, MPH, of Harvard T.H. Chan School of Public Health and Brigham & Women’s Hospital, Boston.
Dr. Figueroa and colleagues published their findings as a research brief for the Aug. 4 issue of the Journal of the American College of Cardiology.
The average number of cardiologists in practice together rose from 3.6 in 2013 to 4.3 in 2017. This trend was less obvious in rural areas (2.05 to 2.20) than in urban areas (3.67 to 4.38).
The smallest change was seen in the mid-size practice tier. In 2013, 22.9% of cardiologists worked in a practice that included 11 to 24 cardiologists, and in 2017, the proportion was 23.2%.
To determine practices sizes, Dr. Figueroa and colleagues used publicly available data from 2013 and 2017 from the Centers for Medicare & Medicaid Services’ Physician Compare, a website that helps patients find and compare clinicians and groups enrolled in Medicare.
Market level variables were obtained from the Dartmouth Atlas Project, which uses CMS data to provide information and analysis about national, regional, and local health care markets, as well as hospitals and their affiliated physicians.
Market forces drive practice patterns
The investigators had no direct data from which to ascertain the reasons why cardiologists have tended to move from smaller to larger practices, but they did conduct a multivariable linear regression analysis to better understand possible market-level factors that may be influencing these trends.
What they found was that as hospital market concentration increased, practice sizes also increased. They found no association between any community-level and physician-level factors and changes in practice size.
So, for example, greater growth in the number of cardiologists in practice together was not associated with age or sex.
“It seems that cardiologists are responding to changes in the market structure where they practice, and in particular, to hospital market concentration. This is all in an effort basically to have more market power, which in part means better bargaining power when they’re negotiating with payers,” said Dr. Figueroa.
He also suggested that joining a large practice is almost a necessity these days given the administrative burdens imposed by value-based care initiatives and their attendant quality measure reporting.
“There are stringent requirements for electronic health records and a huge administrative burden related to requirements to ensure compliance and report on quality measures,” said Dr. Figueroa.
“And then there are also all of these new ‘alternative payment’ models to figure out, like accountable care organizations and bundled payments, so you can imagine that if you’re a solo practitioner, it would be really hard to manage all of these details yourself and still ensure you’re taking care of your patient.
“As a cardiologist you need to invest in a bunch of resources, including a workforce to help you manage all the quality measures and keeping track of patients, ensuring they all get their blood pressures checked on time, etc.,” he said.
Anecdotally, Dr. Figueroa suggests it’s also a quality-of-life decision for many cardiologists. “In terms of physician burnout, when you’re a solo practitioner or in a small practice, it’s really hard to go on vacation and find coverage.”
Larry Sobal, MBA, MHA, the CEO of the Heart and Vascular Institute of Wisconsin, agrees that this consolidation is in large part a reflection of the trend toward consolidation seen across the healthcare system.
“This is because hospitals that purchase cardiology practices often pursue a tactic of consolidating previously separate independent groups into one practice – either legally or virtually – for purposes of controlling cardiology market share,” he said in an interview.
But it also suits the younger cardiology workforce. “My experience has been that cardiologists graduating from fellowships increasingly want to subspecialize and are less likely to join smaller practices where they cannot focus on the area of their training. Positions that allow this type of subspecialization can most easily be found in larger practices.” said Mr. Sobal, cochair of the American College of Cardiology Management Publications Committee.
And if professional incentives aren’t enough, there is always money. While the study did not look at physician compensation by practice size, Mr. Sobal suspects physicians in larger practices have higher incomes.
Dr. Figueroa has disclosed no relevant financial relationships. Mr. Sobal is the CEO of a midsized cardiology practice (13 cardiologists).
A version of this article originally appeared on Medscape.com.
U.S. cardiologists are increasingly opting out of solo or small practices, and joining larger practices, according to a new analysis of U.S. data from 2013 and 2017.
In 2013, 34.2% of U.S. cardiologists worked in practices of five or fewer cardiologists. That number dropped to 27% by 2017. On the flip side, the proportion working in practices with 25 cardiologists or more rose from 26% in 2013 to 35.8% in 2017.
“This is a trend we’re seeing across health care – hospitals are merging and they’re acquiring physician practices, primary care doctors are joining larger practices, too – so to some extent it seems that cardiologists are just responding to changes in the market structure where they practice,” said Jose F. Figueroa, MD, MPH, of Harvard T.H. Chan School of Public Health and Brigham & Women’s Hospital, Boston.
Dr. Figueroa and colleagues published their findings as a research brief for the Aug. 4 issue of the Journal of the American College of Cardiology.
The average number of cardiologists in practice together rose from 3.6 in 2013 to 4.3 in 2017. This trend was less obvious in rural areas (2.05 to 2.20) than in urban areas (3.67 to 4.38).
The smallest change was seen in the mid-size practice tier. In 2013, 22.9% of cardiologists worked in a practice that included 11 to 24 cardiologists, and in 2017, the proportion was 23.2%.
To determine practices sizes, Dr. Figueroa and colleagues used publicly available data from 2013 and 2017 from the Centers for Medicare & Medicaid Services’ Physician Compare, a website that helps patients find and compare clinicians and groups enrolled in Medicare.
Market level variables were obtained from the Dartmouth Atlas Project, which uses CMS data to provide information and analysis about national, regional, and local health care markets, as well as hospitals and their affiliated physicians.
Market forces drive practice patterns
The investigators had no direct data from which to ascertain the reasons why cardiologists have tended to move from smaller to larger practices, but they did conduct a multivariable linear regression analysis to better understand possible market-level factors that may be influencing these trends.
What they found was that as hospital market concentration increased, practice sizes also increased. They found no association between any community-level and physician-level factors and changes in practice size.
So, for example, greater growth in the number of cardiologists in practice together was not associated with age or sex.
“It seems that cardiologists are responding to changes in the market structure where they practice, and in particular, to hospital market concentration. This is all in an effort basically to have more market power, which in part means better bargaining power when they’re negotiating with payers,” said Dr. Figueroa.
He also suggested that joining a large practice is almost a necessity these days given the administrative burdens imposed by value-based care initiatives and their attendant quality measure reporting.
“There are stringent requirements for electronic health records and a huge administrative burden related to requirements to ensure compliance and report on quality measures,” said Dr. Figueroa.
“And then there are also all of these new ‘alternative payment’ models to figure out, like accountable care organizations and bundled payments, so you can imagine that if you’re a solo practitioner, it would be really hard to manage all of these details yourself and still ensure you’re taking care of your patient.
“As a cardiologist you need to invest in a bunch of resources, including a workforce to help you manage all the quality measures and keeping track of patients, ensuring they all get their blood pressures checked on time, etc.,” he said.
Anecdotally, Dr. Figueroa suggests it’s also a quality-of-life decision for many cardiologists. “In terms of physician burnout, when you’re a solo practitioner or in a small practice, it’s really hard to go on vacation and find coverage.”
Larry Sobal, MBA, MHA, the CEO of the Heart and Vascular Institute of Wisconsin, agrees that this consolidation is in large part a reflection of the trend toward consolidation seen across the healthcare system.
“This is because hospitals that purchase cardiology practices often pursue a tactic of consolidating previously separate independent groups into one practice – either legally or virtually – for purposes of controlling cardiology market share,” he said in an interview.
But it also suits the younger cardiology workforce. “My experience has been that cardiologists graduating from fellowships increasingly want to subspecialize and are less likely to join smaller practices where they cannot focus on the area of their training. Positions that allow this type of subspecialization can most easily be found in larger practices.” said Mr. Sobal, cochair of the American College of Cardiology Management Publications Committee.
And if professional incentives aren’t enough, there is always money. While the study did not look at physician compensation by practice size, Mr. Sobal suspects physicians in larger practices have higher incomes.
Dr. Figueroa has disclosed no relevant financial relationships. Mr. Sobal is the CEO of a midsized cardiology practice (13 cardiologists).
A version of this article originally appeared on Medscape.com.
U.S. cardiologists are increasingly opting out of solo or small practices, and joining larger practices, according to a new analysis of U.S. data from 2013 and 2017.
In 2013, 34.2% of U.S. cardiologists worked in practices of five or fewer cardiologists. That number dropped to 27% by 2017. On the flip side, the proportion working in practices with 25 cardiologists or more rose from 26% in 2013 to 35.8% in 2017.
“This is a trend we’re seeing across health care – hospitals are merging and they’re acquiring physician practices, primary care doctors are joining larger practices, too – so to some extent it seems that cardiologists are just responding to changes in the market structure where they practice,” said Jose F. Figueroa, MD, MPH, of Harvard T.H. Chan School of Public Health and Brigham & Women’s Hospital, Boston.
Dr. Figueroa and colleagues published their findings as a research brief for the Aug. 4 issue of the Journal of the American College of Cardiology.
The average number of cardiologists in practice together rose from 3.6 in 2013 to 4.3 in 2017. This trend was less obvious in rural areas (2.05 to 2.20) than in urban areas (3.67 to 4.38).
The smallest change was seen in the mid-size practice tier. In 2013, 22.9% of cardiologists worked in a practice that included 11 to 24 cardiologists, and in 2017, the proportion was 23.2%.
To determine practices sizes, Dr. Figueroa and colleagues used publicly available data from 2013 and 2017 from the Centers for Medicare & Medicaid Services’ Physician Compare, a website that helps patients find and compare clinicians and groups enrolled in Medicare.
Market level variables were obtained from the Dartmouth Atlas Project, which uses CMS data to provide information and analysis about national, regional, and local health care markets, as well as hospitals and their affiliated physicians.
Market forces drive practice patterns
The investigators had no direct data from which to ascertain the reasons why cardiologists have tended to move from smaller to larger practices, but they did conduct a multivariable linear regression analysis to better understand possible market-level factors that may be influencing these trends.
What they found was that as hospital market concentration increased, practice sizes also increased. They found no association between any community-level and physician-level factors and changes in practice size.
So, for example, greater growth in the number of cardiologists in practice together was not associated with age or sex.
“It seems that cardiologists are responding to changes in the market structure where they practice, and in particular, to hospital market concentration. This is all in an effort basically to have more market power, which in part means better bargaining power when they’re negotiating with payers,” said Dr. Figueroa.
He also suggested that joining a large practice is almost a necessity these days given the administrative burdens imposed by value-based care initiatives and their attendant quality measure reporting.
“There are stringent requirements for electronic health records and a huge administrative burden related to requirements to ensure compliance and report on quality measures,” said Dr. Figueroa.
“And then there are also all of these new ‘alternative payment’ models to figure out, like accountable care organizations and bundled payments, so you can imagine that if you’re a solo practitioner, it would be really hard to manage all of these details yourself and still ensure you’re taking care of your patient.
“As a cardiologist you need to invest in a bunch of resources, including a workforce to help you manage all the quality measures and keeping track of patients, ensuring they all get their blood pressures checked on time, etc.,” he said.
Anecdotally, Dr. Figueroa suggests it’s also a quality-of-life decision for many cardiologists. “In terms of physician burnout, when you’re a solo practitioner or in a small practice, it’s really hard to go on vacation and find coverage.”
Larry Sobal, MBA, MHA, the CEO of the Heart and Vascular Institute of Wisconsin, agrees that this consolidation is in large part a reflection of the trend toward consolidation seen across the healthcare system.
“This is because hospitals that purchase cardiology practices often pursue a tactic of consolidating previously separate independent groups into one practice – either legally or virtually – for purposes of controlling cardiology market share,” he said in an interview.
But it also suits the younger cardiology workforce. “My experience has been that cardiologists graduating from fellowships increasingly want to subspecialize and are less likely to join smaller practices where they cannot focus on the area of their training. Positions that allow this type of subspecialization can most easily be found in larger practices.” said Mr. Sobal, cochair of the American College of Cardiology Management Publications Committee.
And if professional incentives aren’t enough, there is always money. While the study did not look at physician compensation by practice size, Mr. Sobal suspects physicians in larger practices have higher incomes.
Dr. Figueroa has disclosed no relevant financial relationships. Mr. Sobal is the CEO of a midsized cardiology practice (13 cardiologists).
A version of this article originally appeared on Medscape.com.
