Cardiology News

Cardiac injury caused by COVID-19 may be much less common than suggested previously, a new study has found.

The study examined cardiac MRI scans in 31 patients before and after having COVID-19 infection and found no new evidence of myocardial injury in the post-COVID scans relative to the pre-COVID scans.

“To the best of our knowledge this is the first cardiac MRI study to assess myocardial injury pre- and post-COVID-19,” the authors stated.

They say that while this study cannot rule out the possibility of rare events of COVID-19–induced myocardial injury, “the complete absence of de novo late gadolinium enhancement lesions after COVID-19 in this cohort indicates that outside special circumstances, COVID-19–induced myocardial injury may be much less common than suggested by previous studies.”

The study was published online in JACC: Cardiovascular Imaging.

Coauthor Till F. Althoff, MD, Cardiovascular Institute, Clínic–University Hospital Barcelona, said in an interview that previous reports have found a high rate of cardiac lesions in patients undergoing imaging after having had COVID-19 infection.

“In some reports, this has been as high as 80% of patients even though they have not had severe COVID disease. These reports have been interpreted as showing the majority of patients have some COVID-induced cardiac damage, which is an alarming message,” he commented.

However, he pointed out that the patients in these reports did not undergo a cardiac MRI scan before they had COVID-19 so it wasn’t known whether these cardiac lesions were present before infection or not.

To try and gain more accurate information, the current study examined cardiac MRI scans in the same patients before and after they had COVID-19.

The researchers, from an arrhythmia unit, made use of the fact that all their patients have cardiac MRI data, so they used their large registry of patients in whom cardiac MRI had been performed, and cross referenced this to a health care database to identify those patients who had confirmed COVID-19 after they obtaining a cardiac scan at the arrhythmia unit. They then conducted another cardiac MRI scan in the 31 patients identified a median of 5 months after their COVID-19 infection.

“These 31 patients had a cardiac MRI scan pre-COVID and post COVID using exactly the same scanner with identical sequences, so the scans were absolutely comparable,” Dr. Althoff noted.

Of these 31 patients, 7 had been hospitalized at the time of acute presentation with COVID-19, of whom 2 required intensive care. Most patients (29) had been symptomatic, but none reported cardiac symptoms.

Results showed that, on the post–COVID-19 scan, late gadolinium enhancement lesions indicative of residual myocardial injury were encountered in 15 of the 31 patients (48%), which the researchers said is in line with previous reports.

However, intraindividual comparison with the pre–COVID-19 cardiac MRI scans showed all these lesions were preexisting with identical localization, pattern, and transmural distribution, and thus not COVID-19 related.

Quantitative analyses, performed independently, detected no increase in the size of individual lesions nor in the global left ventricular late gadolinium enhancement extent.

Comparison of pre- and post COVID-19 imaging sequences did not show any differences in ventricular functional or structural parameters.

“While this study only has 31 patients, the fact that we are conducting intra-individual comparisons, which rules out bias, means that we don’t need a large number of patients for reliable results,” Dr. Althoff said.

“These types of lesions are normal to see. We know that individuals without cardiac disease have these types of lesions, and they are not necessarily an indication of any specific pathology. I was kind of surprised by the interpretation of previous data, which is why we did the current study,” he added.

Dr. Althoff acknowledged that some cardiac injury may have been seen if much larger numbers of patients had been included. “But I think we can say from this data that COVID-induced cardiac damage is much less of an issue than we may have previously thought,” he added.

He also noted that most of the patients in this study had mild COVID-19, so the results cannot be extrapolated to severe COVID-19 infection.

However, Dr. Althoff pointed out that all the patients already had atrial fibrillation, so would have been at higher risk of cardiac injury from COVID-19.

“These patients had preexisting cardiac risk factors, and thus they would have been more susceptible to both a more severe course of COVID and an increased risk of myocardial damage due to COVID. The fact that we don’t find any myocardial injury due to COVID in this group is even more reassuring. The general population will be at even lower risk,” he commented.

“I think we can say that, in COVID patients who do not have any cardiac symptoms, our study suggests that the incidence of cardiac injury is very low,” Dr. Althoff said.

“Even in patients with severe COVID and myocardial involvement reflected by increased troponin levels, I wouldn’t be sure that they have any residual cardiac injury. While it has been reported that cardiac lesions have been found in such patients, pre-COVID MRI scans were not available so we don’t know if they were there before,” he added.

“We do not know the true incidence of cardiac injury after COVID, but I think we can say from this data that it is definitely not anywhere near the 40%-50% or even greater that some of the previous reports have suggested,” he stated.

Dr. Althoff suggested that, based on these data, some of the recommendations based on previous reports such the need for follow-up cardiac scans and caution about partaking in sports again after COVID-19 infection, are probably not necessary.

“Our data suggest that these concerns are unfounded, and we need to step back a bit and stop alarming patients about the risk of cardiac damage after COVID,” he said. “Yes, if patients have cardiac symptoms during or after COVID infection they should get checked out, but I do not think we need to do a cardiac risk assessment in patients without cardiac symptoms in COVID.”

This work is supported in part by grants from Instituto de Salud Carlos III, the Spanish government, Madrid, and Fundació la Marató de TV3 in Catalonia. Dr. Althoff has received research grants for investigator-initiated trials from Biosense Webster.

A version of this article first appeared on Medscape.com.

Cardiac injury caused by COVID-19 may be much less common than suggested previously, a new study has found.

The study examined cardiac MRI scans in 31 patients before and after having COVID-19 infection and found no new evidence of myocardial injury in the post-COVID scans relative to the pre-COVID scans.

“To the best of our knowledge this is the first cardiac MRI study to assess myocardial injury pre- and post-COVID-19,” the authors stated.

They say that while this study cannot rule out the possibility of rare events of COVID-19–induced myocardial injury, “the complete absence of de novo late gadolinium enhancement lesions after COVID-19 in this cohort indicates that outside special circumstances, COVID-19–induced myocardial injury may be much less common than suggested by previous studies.”

The study was published online in JACC: Cardiovascular Imaging.

Coauthor Till F. Althoff, MD, Cardiovascular Institute, Clínic–University Hospital Barcelona, said in an interview that previous reports have found a high rate of cardiac lesions in patients undergoing imaging after having had COVID-19 infection.

“In some reports, this has been as high as 80% of patients even though they have not had severe COVID disease. These reports have been interpreted as showing the majority of patients have some COVID-induced cardiac damage, which is an alarming message,” he commented.

However, he pointed out that the patients in these reports did not undergo a cardiac MRI scan before they had COVID-19 so it wasn’t known whether these cardiac lesions were present before infection or not.

To try and gain more accurate information, the current study examined cardiac MRI scans in the same patients before and after they had COVID-19.

The researchers, from an arrhythmia unit, made use of the fact that all their patients have cardiac MRI data, so they used their large registry of patients in whom cardiac MRI had been performed, and cross referenced this to a health care database to identify those patients who had confirmed COVID-19 after they obtaining a cardiac scan at the arrhythmia unit. They then conducted another cardiac MRI scan in the 31 patients identified a median of 5 months after their COVID-19 infection.

“These 31 patients had a cardiac MRI scan pre-COVID and post COVID using exactly the same scanner with identical sequences, so the scans were absolutely comparable,” Dr. Althoff noted.

Of these 31 patients, 7 had been hospitalized at the time of acute presentation with COVID-19, of whom 2 required intensive care. Most patients (29) had been symptomatic, but none reported cardiac symptoms.

Results showed that, on the post–COVID-19 scan, late gadolinium enhancement lesions indicative of residual myocardial injury were encountered in 15 of the 31 patients (48%), which the researchers said is in line with previous reports.

However, intraindividual comparison with the pre–COVID-19 cardiac MRI scans showed all these lesions were preexisting with identical localization, pattern, and transmural distribution, and thus not COVID-19 related.

Quantitative analyses, performed independently, detected no increase in the size of individual lesions nor in the global left ventricular late gadolinium enhancement extent.

Comparison of pre- and post COVID-19 imaging sequences did not show any differences in ventricular functional or structural parameters.

“While this study only has 31 patients, the fact that we are conducting intra-individual comparisons, which rules out bias, means that we don’t need a large number of patients for reliable results,” Dr. Althoff said.

“These types of lesions are normal to see. We know that individuals without cardiac disease have these types of lesions, and they are not necessarily an indication of any specific pathology. I was kind of surprised by the interpretation of previous data, which is why we did the current study,” he added.

Dr. Althoff acknowledged that some cardiac injury may have been seen if much larger numbers of patients had been included. “But I think we can say from this data that COVID-induced cardiac damage is much less of an issue than we may have previously thought,” he added.

He also noted that most of the patients in this study had mild COVID-19, so the results cannot be extrapolated to severe COVID-19 infection.

However, Dr. Althoff pointed out that all the patients already had atrial fibrillation, so would have been at higher risk of cardiac injury from COVID-19.

“These patients had preexisting cardiac risk factors, and thus they would have been more susceptible to both a more severe course of COVID and an increased risk of myocardial damage due to COVID. The fact that we don’t find any myocardial injury due to COVID in this group is even more reassuring. The general population will be at even lower risk,” he commented.

“I think we can say that, in COVID patients who do not have any cardiac symptoms, our study suggests that the incidence of cardiac injury is very low,” Dr. Althoff said.

“Even in patients with severe COVID and myocardial involvement reflected by increased troponin levels, I wouldn’t be sure that they have any residual cardiac injury. While it has been reported that cardiac lesions have been found in such patients, pre-COVID MRI scans were not available so we don’t know if they were there before,” he added.

“We do not know the true incidence of cardiac injury after COVID, but I think we can say from this data that it is definitely not anywhere near the 40%-50% or even greater that some of the previous reports have suggested,” he stated.

Dr. Althoff suggested that, based on these data, some of the recommendations based on previous reports such the need for follow-up cardiac scans and caution about partaking in sports again after COVID-19 infection, are probably not necessary.

“Our data suggest that these concerns are unfounded, and we need to step back a bit and stop alarming patients about the risk of cardiac damage after COVID,” he said. “Yes, if patients have cardiac symptoms during or after COVID infection they should get checked out, but I do not think we need to do a cardiac risk assessment in patients without cardiac symptoms in COVID.”

This work is supported in part by grants from Instituto de Salud Carlos III, the Spanish government, Madrid, and Fundació la Marató de TV3 in Catalonia. Dr. Althoff has received research grants for investigator-initiated trials from Biosense Webster.

A version of this article first appeared on Medscape.com.

Cardiac injury caused by COVID-19 may be much less common than suggested previously, a new study has found.

The study examined cardiac MRI scans in 31 patients before and after having COVID-19 infection and found no new evidence of myocardial injury in the post-COVID scans relative to the pre-COVID scans.

“To the best of our knowledge this is the first cardiac MRI study to assess myocardial injury pre- and post-COVID-19,” the authors stated.

They say that while this study cannot rule out the possibility of rare events of COVID-19–induced myocardial injury, “the complete absence of de novo late gadolinium enhancement lesions after COVID-19 in this cohort indicates that outside special circumstances, COVID-19–induced myocardial injury may be much less common than suggested by previous studies.”

The study was published online in JACC: Cardiovascular Imaging.

Coauthor Till F. Althoff, MD, Cardiovascular Institute, Clínic–University Hospital Barcelona, said in an interview that previous reports have found a high rate of cardiac lesions in patients undergoing imaging after having had COVID-19 infection.

“In some reports, this has been as high as 80% of patients even though they have not had severe COVID disease. These reports have been interpreted as showing the majority of patients have some COVID-induced cardiac damage, which is an alarming message,” he commented.

However, he pointed out that the patients in these reports did not undergo a cardiac MRI scan before they had COVID-19 so it wasn’t known whether these cardiac lesions were present before infection or not.

To try and gain more accurate information, the current study examined cardiac MRI scans in the same patients before and after they had COVID-19.

The researchers, from an arrhythmia unit, made use of the fact that all their patients have cardiac MRI data, so they used their large registry of patients in whom cardiac MRI had been performed, and cross referenced this to a health care database to identify those patients who had confirmed COVID-19 after they obtaining a cardiac scan at the arrhythmia unit. They then conducted another cardiac MRI scan in the 31 patients identified a median of 5 months after their COVID-19 infection.

“These 31 patients had a cardiac MRI scan pre-COVID and post COVID using exactly the same scanner with identical sequences, so the scans were absolutely comparable,” Dr. Althoff noted.

Of these 31 patients, 7 had been hospitalized at the time of acute presentation with COVID-19, of whom 2 required intensive care. Most patients (29) had been symptomatic, but none reported cardiac symptoms.

Results showed that, on the post–COVID-19 scan, late gadolinium enhancement lesions indicative of residual myocardial injury were encountered in 15 of the 31 patients (48%), which the researchers said is in line with previous reports.

However, intraindividual comparison with the pre–COVID-19 cardiac MRI scans showed all these lesions were preexisting with identical localization, pattern, and transmural distribution, and thus not COVID-19 related.

Quantitative analyses, performed independently, detected no increase in the size of individual lesions nor in the global left ventricular late gadolinium enhancement extent.

Comparison of pre- and post COVID-19 imaging sequences did not show any differences in ventricular functional or structural parameters.

“While this study only has 31 patients, the fact that we are conducting intra-individual comparisons, which rules out bias, means that we don’t need a large number of patients for reliable results,” Dr. Althoff said.

“These types of lesions are normal to see. We know that individuals without cardiac disease have these types of lesions, and they are not necessarily an indication of any specific pathology. I was kind of surprised by the interpretation of previous data, which is why we did the current study,” he added.

Dr. Althoff acknowledged that some cardiac injury may have been seen if much larger numbers of patients had been included. “But I think we can say from this data that COVID-induced cardiac damage is much less of an issue than we may have previously thought,” he added.

He also noted that most of the patients in this study had mild COVID-19, so the results cannot be extrapolated to severe COVID-19 infection.

However, Dr. Althoff pointed out that all the patients already had atrial fibrillation, so would have been at higher risk of cardiac injury from COVID-19.

“These patients had preexisting cardiac risk factors, and thus they would have been more susceptible to both a more severe course of COVID and an increased risk of myocardial damage due to COVID. The fact that we don’t find any myocardial injury due to COVID in this group is even more reassuring. The general population will be at even lower risk,” he commented.

“I think we can say that, in COVID patients who do not have any cardiac symptoms, our study suggests that the incidence of cardiac injury is very low,” Dr. Althoff said.

“Even in patients with severe COVID and myocardial involvement reflected by increased troponin levels, I wouldn’t be sure that they have any residual cardiac injury. While it has been reported that cardiac lesions have been found in such patients, pre-COVID MRI scans were not available so we don’t know if they were there before,” he added.

“We do not know the true incidence of cardiac injury after COVID, but I think we can say from this data that it is definitely not anywhere near the 40%-50% or even greater that some of the previous reports have suggested,” he stated.

Dr. Althoff suggested that, based on these data, some of the recommendations based on previous reports such the need for follow-up cardiac scans and caution about partaking in sports again after COVID-19 infection, are probably not necessary.

“Our data suggest that these concerns are unfounded, and we need to step back a bit and stop alarming patients about the risk of cardiac damage after COVID,” he said. “Yes, if patients have cardiac symptoms during or after COVID infection they should get checked out, but I do not think we need to do a cardiac risk assessment in patients without cardiac symptoms in COVID.”

This work is supported in part by grants from Instituto de Salud Carlos III, the Spanish government, Madrid, and Fundació la Marató de TV3 in Catalonia. Dr. Althoff has received research grants for investigator-initiated trials from Biosense Webster.

A version of this article first appeared on Medscape.com.

Seven former patients have filed malpractice complaints against an interventional cardiologist based in Indianapolis, alleging he performed unnecessary cardiac procedures that led to physical and emotional harm.

The medical records for one patient, 70-year-old John Pflum, of Noblesville, Ind., show that Edward Harlamert, MD, performed 44 heart catheterizations and inserted at least 41 stents between 2004 and 2013, according to an investigation by WTHR 13News in Indianapolis that was published Dec. 14.

The news outlet asked four cardiologists to review and comment on John Pflum’s medical records.

“There is not a single scenario I can think of where doing this level of stents and angiograms would be justified or make sense. I have never seen this happen in the course of my medical training or my medical career,” Payal Kohli, MD, cardiologist and medical director of Cherry Creek Heart in Denver, told 13News.

Sunil Rao, MD, director of interventional cardiology at NYU Langone Health and president of the Society for Cardiovascular Angioplasty and Interventions, who also reviewed Mr. Pflum’s medical records for 13News, said he’s “never seen a patient who has gotten this many procedures.”

Dr. Rao said that on the basis of what he saw in the records and in the images, there were several deviations from the standard of care.

Two other independent cardiologists who spoke with 13News voiced similar opinions.

Mr. Pflum was “getting cathed almost every month. That’s not how it’s done,” Morton Rinder, MD, an interventional cardiologist at St. Luke’s Hospital near St. Louis, told 13News.

Dr. Rinder has been hired as a medical consultant for the attorneys who filed Mr. Pflum’s malpractice complaint against Dr. Harlamert.

Cardiologists who reviewed the catheterization films for 13News said some of Mr. Pflum’s heart blockages met the 70% threshold to warrant consideration of a stent, while others clearly did not. In-stent restenosis occurred in several of the implanted stents, requiring a second open heart surgery.

In a statement, Dr. Harlamert’s attorneys told 13News that Dr. Harlamert has “always been committed to providing quality care to patients” and that he treated his cardiology patients “based on their unique circumstances, his expertise, and the tools available.

“Because of stringent privacy laws and pending litigation, a response to a local news story is not the proper forum to present a picture of any particular treatment decision, especially when that picture may be incomplete at this time,” the statement reads.
 

A version of this article first appeared on Medscape.com.

Seven former patients have filed malpractice complaints against an interventional cardiologist based in Indianapolis, alleging he performed unnecessary cardiac procedures that led to physical and emotional harm.

The medical records for one patient, 70-year-old John Pflum, of Noblesville, Ind., show that Edward Harlamert, MD, performed 44 heart catheterizations and inserted at least 41 stents between 2004 and 2013, according to an investigation by WTHR 13News in Indianapolis that was published Dec. 14.

The news outlet asked four cardiologists to review and comment on John Pflum’s medical records.

“There is not a single scenario I can think of where doing this level of stents and angiograms would be justified or make sense. I have never seen this happen in the course of my medical training or my medical career,” Payal Kohli, MD, cardiologist and medical director of Cherry Creek Heart in Denver, told 13News.

Sunil Rao, MD, director of interventional cardiology at NYU Langone Health and president of the Society for Cardiovascular Angioplasty and Interventions, who also reviewed Mr. Pflum’s medical records for 13News, said he’s “never seen a patient who has gotten this many procedures.”

Dr. Rao said that on the basis of what he saw in the records and in the images, there were several deviations from the standard of care.

Two other independent cardiologists who spoke with 13News voiced similar opinions.

Mr. Pflum was “getting cathed almost every month. That’s not how it’s done,” Morton Rinder, MD, an interventional cardiologist at St. Luke’s Hospital near St. Louis, told 13News.

Dr. Rinder has been hired as a medical consultant for the attorneys who filed Mr. Pflum’s malpractice complaint against Dr. Harlamert.

Cardiologists who reviewed the catheterization films for 13News said some of Mr. Pflum’s heart blockages met the 70% threshold to warrant consideration of a stent, while others clearly did not. In-stent restenosis occurred in several of the implanted stents, requiring a second open heart surgery.

In a statement, Dr. Harlamert’s attorneys told 13News that Dr. Harlamert has “always been committed to providing quality care to patients” and that he treated his cardiology patients “based on their unique circumstances, his expertise, and the tools available.

“Because of stringent privacy laws and pending litigation, a response to a local news story is not the proper forum to present a picture of any particular treatment decision, especially when that picture may be incomplete at this time,” the statement reads.
 

A version of this article first appeared on Medscape.com.

Seven former patients have filed malpractice complaints against an interventional cardiologist based in Indianapolis, alleging he performed unnecessary cardiac procedures that led to physical and emotional harm.

The medical records for one patient, 70-year-old John Pflum, of Noblesville, Ind., show that Edward Harlamert, MD, performed 44 heart catheterizations and inserted at least 41 stents between 2004 and 2013, according to an investigation by WTHR 13News in Indianapolis that was published Dec. 14.

The news outlet asked four cardiologists to review and comment on John Pflum’s medical records.

“There is not a single scenario I can think of where doing this level of stents and angiograms would be justified or make sense. I have never seen this happen in the course of my medical training or my medical career,” Payal Kohli, MD, cardiologist and medical director of Cherry Creek Heart in Denver, told 13News.

Sunil Rao, MD, director of interventional cardiology at NYU Langone Health and president of the Society for Cardiovascular Angioplasty and Interventions, who also reviewed Mr. Pflum’s medical records for 13News, said he’s “never seen a patient who has gotten this many procedures.”

Dr. Rao said that on the basis of what he saw in the records and in the images, there were several deviations from the standard of care.

Two other independent cardiologists who spoke with 13News voiced similar opinions.

Mr. Pflum was “getting cathed almost every month. That’s not how it’s done,” Morton Rinder, MD, an interventional cardiologist at St. Luke’s Hospital near St. Louis, told 13News.

Dr. Rinder has been hired as a medical consultant for the attorneys who filed Mr. Pflum’s malpractice complaint against Dr. Harlamert.

Cardiologists who reviewed the catheterization films for 13News said some of Mr. Pflum’s heart blockages met the 70% threshold to warrant consideration of a stent, while others clearly did not. In-stent restenosis occurred in several of the implanted stents, requiring a second open heart surgery.

In a statement, Dr. Harlamert’s attorneys told 13News that Dr. Harlamert has “always been committed to providing quality care to patients” and that he treated his cardiology patients “based on their unique circumstances, his expertise, and the tools available.

“Because of stringent privacy laws and pending litigation, a response to a local news story is not the proper forum to present a picture of any particular treatment decision, especially when that picture may be incomplete at this time,” the statement reads.
 

A version of this article first appeared on Medscape.com.

CHICAGO – Black patients with heart failure with reduced ejection fraction (HFrEF) may receive more benefit from treatment with a sodium-glucose cotransporter-2 (SGLT2) inhibitor than do White patients, according to a new report.

A secondary analysis of data collected from the pivotal trials that assessed the SGLT2 inhibitor empagliflozin in patients with HFrEF, EMPEROR-Reduced, and in patients with heart failure with preserved ejection fraction (HFpEF), EMPEROR-Preserved, was presented by Subodh Verma, MD, PhD, at the American Heart Association scientific sessions.

Mitchel L. Zoler/MDedge News

The “hypothesis-generating” analysis of data from EMPEROR-Reduced showed “a suggestion of a greater benefit of empagliflozin” in Black, compared with White patients, for the study’s primary endpoint (cardiovascular death or hospitalization for heart failure) as well as for first and total hospitalizations for heart failure, he reported.

However, a similar but separate analysis that compared Black and White patients with heart failure who received treatment with a second agent, dapagliflozin, from the same SGLT2-inhibitor class did not show any suggestion of heterogeneity in the drug’s effect based on race.
 

Race-linked heterogeneity in empagliflozin’s effect

In EMPEROR-Reduced, which randomized 3,730 patients with heart failure and a left ventricular ejection fraction of 40% or less, treatment of White patients with empagliflozin (Jardiance) produced a nonsignificant 16% relative reduction in the rate of the primary endpoint, compared with placebo, during a median 16-month follow-up.

By contrast, among Black patients, treatment with empagliflozin produced a significant 56% reduction in the primary endpoint, compared with placebo-treated patients, a significant heterogeneity (P = .02) in effect between the two race subgroups, said Dr. Verma, a cardiac surgeon and professor at the University of Toronto.

The analysis he reported used combined data from EMPEROR-Reduced and the companion trial EMPEROR-Preserved, which randomized 5,988 patients with heart failure and a left ventricular ejection fraction greater than 40% to treatment with either empagliflozin or placebo and followed them for a median of 26 months.

To assess the effects of the randomized treatments in the two racial subgroups, Dr. Verma and associates used pooled data from both trials, but only from the 3,502 patients enrolled in the Americas, which included 3,024 White patients and 478 Black patients. Analysis of the patients in this subgroup who were randomized to placebo showed a significantly excess rate of the primary outcome among Blacks, who tallied 49% more of the primary outcome events during follow-up than did White patients, Dr. Verma reported. The absolute rate of the primary outcome without empagliflozin treatment was 13.15 events/100 patient-years of follow-up in White patients and 20.83 events/100 patient-years in Black patients.

The impact of empagliflozin was not statistically heterogeneous in the total pool of patients that included both those with HFrEF and those with HFpEF. The drug reduced the primary outcome incidence by a significant 20% in White patients, and by a significant 44% among Black patients.

But this point-estimate difference in efficacy, when coupled with the underlying difference in risk for an event between the two racial groups, meant that the number-needed-to-treat to prevent one primary outcome event was 42 among White patients and 12 among Black patients.
 

Race-linked treatment responses only in HFrEF

This suggestion of an imbalance in treatment efficacy was especially apparent among patients with HFrEF. In addition to the heterogeneity for the primary outcome, the Black and White subgroups also showed significantly divergent results for the outcomes of first hospitalization for heart failure, with a nonsignificant 21% relative reduction with empagliflozin treatment in Whites but a significant 65% relative cut in this endpoint with empagliflozin in Blacks, and for total hospitalizations for heart failure, which showed a similar level of significant heterogeneity between the two race subgroups.

In contrast, the patients with HFpEF showed no signal at all for heterogeneous outcome rates between Black and White subgroups.

One other study outcome, change in symptom burden measured by the Kansas City Cardiomyopathy Questionnaire (KCCQ), also showed suggestion of a race-based imbalance. The adjusted mean difference from baseline in the KCCQ clinical summary score was 1.50 points higher with empagliflozin treatment, compared with placebo among all White patients (those with HFrEF and those with HFpEF), and compared with a 5.25-point increase with empagliflozin over placebo among all Black patients with heart failure in the pooled American EMPEROR dataset, a difference between White and Black patients that just missed significance (P = .06). Again, this difference was especially notable and significant among the patients with HFrEF, where the adjusted mean difference in KCCQ was a 0.77-point increase in White patients and a 6.71-point increase among Black patients (P = .043),

These results also appeared in a report published simultaneously with Dr. Verma’s talk.

But two other analyses that assessed a possible race-based difference in empagliflozin’s effect on renal protection and on functional status showed no suggestion of heterogeneity.

Dr. Verma stressed caution about the limitations of these analyses because they involved a relatively small number of Black patients, and were possibly subject to unadjusted confounding from differences in baseline characteristics between the Black and White patients.

Black patients also had a number-needed-to-treat advantage with dapagliflozin

The finding that Black patients with heart failure potentially get more bang for the buck from treatment with an SGLT2 inhibitor by having a lower number needed to treat also showed up in a separate report at the meeting that assessed the treatment effect from dapagliflozin (Farxiga) in Black and White patients in a pooled analysis of the DAPA-HF pivotal trial of patients with HFrEF and the DELIVER pivotal trial of patients with HFpEF. The pooled cohort included a total of 11,007, but for the analysis by race the investigators also limited their focus to patients from the Americas with 2,626 White patients and 381 Black patients.

Mitchel L. Zoler/MDedge News

Assessment of the effect of dapagliflozin on the primary outcome of cardiovascular death or hospitalization for heart failure among all patients, both those with HFrEF and those with HFpEF, again showed that event rates among patients treated with placebo were significantly higher in Black, compared with White patients, and this led to a difference in the number needed to treat to prevent one primary outcome event of 12 in Blacks and 17 in Whites, Jawad H. Butt, MD said in a talk at the meeting.

Although treatment with dapagliflozin reduced the rate of the primary outcome in this subgroup of patients from the DAPA-HF trial and the DELIVER trial by similar rates in Black and White patients, event rates were higher in the Black patients resulting in “greater benefit in absolute terms” for Black patients, explained Dr. Butt, a cardiologist at Rigshospitalet in Copenhagen.

But in contrast to the empagliflozin findings reported by Dr. Verma, the combined data from the dapagliflozin trials showed no suggestion of heterogeneity in the beneficial effect of dapagliflozin based on left ventricular ejection fraction. In the Black patients, for example, the relative benefit from dapagliflozin on the primary outcome was consistent across the full spectrum of patients with HFrEF and HFpEF.

EMPEROR-Reduced and EMPEROR-Preserved were sponsored by Boehringer Ingelheim and Lilly, the companies that jointly market empagliflozin (Jardiance). The DAPA-HF and DELIVER trials were sponsored by AstraZeneca, the company that markets dapagliflozin (Farxiga). Dr. Verma has received honoraria, research support, or both from AstraZeneca, Boehringer Ingelheim, and Lilly, and from numerous other companies. Dr. Butt has been a consultant to and received travel grants from AstraZeneca, honoraria from Novartis, and has been an adviser to Bayer.




 

CHICAGO – Black patients with heart failure with reduced ejection fraction (HFrEF) may receive more benefit from treatment with a sodium-glucose cotransporter-2 (SGLT2) inhibitor than do White patients, according to a new report.

A secondary analysis of data collected from the pivotal trials that assessed the SGLT2 inhibitor empagliflozin in patients with HFrEF, EMPEROR-Reduced, and in patients with heart failure with preserved ejection fraction (HFpEF), EMPEROR-Preserved, was presented by Subodh Verma, MD, PhD, at the American Heart Association scientific sessions.

Mitchel L. Zoler/MDedge News

The “hypothesis-generating” analysis of data from EMPEROR-Reduced showed “a suggestion of a greater benefit of empagliflozin” in Black, compared with White patients, for the study’s primary endpoint (cardiovascular death or hospitalization for heart failure) as well as for first and total hospitalizations for heart failure, he reported.

However, a similar but separate analysis that compared Black and White patients with heart failure who received treatment with a second agent, dapagliflozin, from the same SGLT2-inhibitor class did not show any suggestion of heterogeneity in the drug’s effect based on race.
 

Race-linked heterogeneity in empagliflozin’s effect

In EMPEROR-Reduced, which randomized 3,730 patients with heart failure and a left ventricular ejection fraction of 40% or less, treatment of White patients with empagliflozin (Jardiance) produced a nonsignificant 16% relative reduction in the rate of the primary endpoint, compared with placebo, during a median 16-month follow-up.

By contrast, among Black patients, treatment with empagliflozin produced a significant 56% reduction in the primary endpoint, compared with placebo-treated patients, a significant heterogeneity (P = .02) in effect between the two race subgroups, said Dr. Verma, a cardiac surgeon and professor at the University of Toronto.

The analysis he reported used combined data from EMPEROR-Reduced and the companion trial EMPEROR-Preserved, which randomized 5,988 patients with heart failure and a left ventricular ejection fraction greater than 40% to treatment with either empagliflozin or placebo and followed them for a median of 26 months.

To assess the effects of the randomized treatments in the two racial subgroups, Dr. Verma and associates used pooled data from both trials, but only from the 3,502 patients enrolled in the Americas, which included 3,024 White patients and 478 Black patients. Analysis of the patients in this subgroup who were randomized to placebo showed a significantly excess rate of the primary outcome among Blacks, who tallied 49% more of the primary outcome events during follow-up than did White patients, Dr. Verma reported. The absolute rate of the primary outcome without empagliflozin treatment was 13.15 events/100 patient-years of follow-up in White patients and 20.83 events/100 patient-years in Black patients.

The impact of empagliflozin was not statistically heterogeneous in the total pool of patients that included both those with HFrEF and those with HFpEF. The drug reduced the primary outcome incidence by a significant 20% in White patients, and by a significant 44% among Black patients.

But this point-estimate difference in efficacy, when coupled with the underlying difference in risk for an event between the two racial groups, meant that the number-needed-to-treat to prevent one primary outcome event was 42 among White patients and 12 among Black patients.
 

Race-linked treatment responses only in HFrEF

This suggestion of an imbalance in treatment efficacy was especially apparent among patients with HFrEF. In addition to the heterogeneity for the primary outcome, the Black and White subgroups also showed significantly divergent results for the outcomes of first hospitalization for heart failure, with a nonsignificant 21% relative reduction with empagliflozin treatment in Whites but a significant 65% relative cut in this endpoint with empagliflozin in Blacks, and for total hospitalizations for heart failure, which showed a similar level of significant heterogeneity between the two race subgroups.

In contrast, the patients with HFpEF showed no signal at all for heterogeneous outcome rates between Black and White subgroups.

One other study outcome, change in symptom burden measured by the Kansas City Cardiomyopathy Questionnaire (KCCQ), also showed suggestion of a race-based imbalance. The adjusted mean difference from baseline in the KCCQ clinical summary score was 1.50 points higher with empagliflozin treatment, compared with placebo among all White patients (those with HFrEF and those with HFpEF), and compared with a 5.25-point increase with empagliflozin over placebo among all Black patients with heart failure in the pooled American EMPEROR dataset, a difference between White and Black patients that just missed significance (P = .06). Again, this difference was especially notable and significant among the patients with HFrEF, where the adjusted mean difference in KCCQ was a 0.77-point increase in White patients and a 6.71-point increase among Black patients (P = .043),

These results also appeared in a report published simultaneously with Dr. Verma’s talk.

But two other analyses that assessed a possible race-based difference in empagliflozin’s effect on renal protection and on functional status showed no suggestion of heterogeneity.

Dr. Verma stressed caution about the limitations of these analyses because they involved a relatively small number of Black patients, and were possibly subject to unadjusted confounding from differences in baseline characteristics between the Black and White patients.

Black patients also had a number-needed-to-treat advantage with dapagliflozin

The finding that Black patients with heart failure potentially get more bang for the buck from treatment with an SGLT2 inhibitor by having a lower number needed to treat also showed up in a separate report at the meeting that assessed the treatment effect from dapagliflozin (Farxiga) in Black and White patients in a pooled analysis of the DAPA-HF pivotal trial of patients with HFrEF and the DELIVER pivotal trial of patients with HFpEF. The pooled cohort included a total of 11,007, but for the analysis by race the investigators also limited their focus to patients from the Americas with 2,626 White patients and 381 Black patients.

Mitchel L. Zoler/MDedge News

Assessment of the effect of dapagliflozin on the primary outcome of cardiovascular death or hospitalization for heart failure among all patients, both those with HFrEF and those with HFpEF, again showed that event rates among patients treated with placebo were significantly higher in Black, compared with White patients, and this led to a difference in the number needed to treat to prevent one primary outcome event of 12 in Blacks and 17 in Whites, Jawad H. Butt, MD said in a talk at the meeting.

Although treatment with dapagliflozin reduced the rate of the primary outcome in this subgroup of patients from the DAPA-HF trial and the DELIVER trial by similar rates in Black and White patients, event rates were higher in the Black patients resulting in “greater benefit in absolute terms” for Black patients, explained Dr. Butt, a cardiologist at Rigshospitalet in Copenhagen.

But in contrast to the empagliflozin findings reported by Dr. Verma, the combined data from the dapagliflozin trials showed no suggestion of heterogeneity in the beneficial effect of dapagliflozin based on left ventricular ejection fraction. In the Black patients, for example, the relative benefit from dapagliflozin on the primary outcome was consistent across the full spectrum of patients with HFrEF and HFpEF.

EMPEROR-Reduced and EMPEROR-Preserved were sponsored by Boehringer Ingelheim and Lilly, the companies that jointly market empagliflozin (Jardiance). The DAPA-HF and DELIVER trials were sponsored by AstraZeneca, the company that markets dapagliflozin (Farxiga). Dr. Verma has received honoraria, research support, or both from AstraZeneca, Boehringer Ingelheim, and Lilly, and from numerous other companies. Dr. Butt has been a consultant to and received travel grants from AstraZeneca, honoraria from Novartis, and has been an adviser to Bayer.




 

CHICAGO – Black patients with heart failure with reduced ejection fraction (HFrEF) may receive more benefit from treatment with a sodium-glucose cotransporter-2 (SGLT2) inhibitor than do White patients, according to a new report.

A secondary analysis of data collected from the pivotal trials that assessed the SGLT2 inhibitor empagliflozin in patients with HFrEF, EMPEROR-Reduced, and in patients with heart failure with preserved ejection fraction (HFpEF), EMPEROR-Preserved, was presented by Subodh Verma, MD, PhD, at the American Heart Association scientific sessions.

Mitchel L. Zoler/MDedge News

The “hypothesis-generating” analysis of data from EMPEROR-Reduced showed “a suggestion of a greater benefit of empagliflozin” in Black, compared with White patients, for the study’s primary endpoint (cardiovascular death or hospitalization for heart failure) as well as for first and total hospitalizations for heart failure, he reported.

However, a similar but separate analysis that compared Black and White patients with heart failure who received treatment with a second agent, dapagliflozin, from the same SGLT2-inhibitor class did not show any suggestion of heterogeneity in the drug’s effect based on race.
 

Race-linked heterogeneity in empagliflozin’s effect

In EMPEROR-Reduced, which randomized 3,730 patients with heart failure and a left ventricular ejection fraction of 40% or less, treatment of White patients with empagliflozin (Jardiance) produced a nonsignificant 16% relative reduction in the rate of the primary endpoint, compared with placebo, during a median 16-month follow-up.

By contrast, among Black patients, treatment with empagliflozin produced a significant 56% reduction in the primary endpoint, compared with placebo-treated patients, a significant heterogeneity (P = .02) in effect between the two race subgroups, said Dr. Verma, a cardiac surgeon and professor at the University of Toronto.

The analysis he reported used combined data from EMPEROR-Reduced and the companion trial EMPEROR-Preserved, which randomized 5,988 patients with heart failure and a left ventricular ejection fraction greater than 40% to treatment with either empagliflozin or placebo and followed them for a median of 26 months.

To assess the effects of the randomized treatments in the two racial subgroups, Dr. Verma and associates used pooled data from both trials, but only from the 3,502 patients enrolled in the Americas, which included 3,024 White patients and 478 Black patients. Analysis of the patients in this subgroup who were randomized to placebo showed a significantly excess rate of the primary outcome among Blacks, who tallied 49% more of the primary outcome events during follow-up than did White patients, Dr. Verma reported. The absolute rate of the primary outcome without empagliflozin treatment was 13.15 events/100 patient-years of follow-up in White patients and 20.83 events/100 patient-years in Black patients.

The impact of empagliflozin was not statistically heterogeneous in the total pool of patients that included both those with HFrEF and those with HFpEF. The drug reduced the primary outcome incidence by a significant 20% in White patients, and by a significant 44% among Black patients.

But this point-estimate difference in efficacy, when coupled with the underlying difference in risk for an event between the two racial groups, meant that the number-needed-to-treat to prevent one primary outcome event was 42 among White patients and 12 among Black patients.
 

Race-linked treatment responses only in HFrEF

This suggestion of an imbalance in treatment efficacy was especially apparent among patients with HFrEF. In addition to the heterogeneity for the primary outcome, the Black and White subgroups also showed significantly divergent results for the outcomes of first hospitalization for heart failure, with a nonsignificant 21% relative reduction with empagliflozin treatment in Whites but a significant 65% relative cut in this endpoint with empagliflozin in Blacks, and for total hospitalizations for heart failure, which showed a similar level of significant heterogeneity between the two race subgroups.

In contrast, the patients with HFpEF showed no signal at all for heterogeneous outcome rates between Black and White subgroups.

One other study outcome, change in symptom burden measured by the Kansas City Cardiomyopathy Questionnaire (KCCQ), also showed suggestion of a race-based imbalance. The adjusted mean difference from baseline in the KCCQ clinical summary score was 1.50 points higher with empagliflozin treatment, compared with placebo among all White patients (those with HFrEF and those with HFpEF), and compared with a 5.25-point increase with empagliflozin over placebo among all Black patients with heart failure in the pooled American EMPEROR dataset, a difference between White and Black patients that just missed significance (P = .06). Again, this difference was especially notable and significant among the patients with HFrEF, where the adjusted mean difference in KCCQ was a 0.77-point increase in White patients and a 6.71-point increase among Black patients (P = .043),

These results also appeared in a report published simultaneously with Dr. Verma’s talk.

But two other analyses that assessed a possible race-based difference in empagliflozin’s effect on renal protection and on functional status showed no suggestion of heterogeneity.

Dr. Verma stressed caution about the limitations of these analyses because they involved a relatively small number of Black patients, and were possibly subject to unadjusted confounding from differences in baseline characteristics between the Black and White patients.

Black patients also had a number-needed-to-treat advantage with dapagliflozin

The finding that Black patients with heart failure potentially get more bang for the buck from treatment with an SGLT2 inhibitor by having a lower number needed to treat also showed up in a separate report at the meeting that assessed the treatment effect from dapagliflozin (Farxiga) in Black and White patients in a pooled analysis of the DAPA-HF pivotal trial of patients with HFrEF and the DELIVER pivotal trial of patients with HFpEF. The pooled cohort included a total of 11,007, but for the analysis by race the investigators also limited their focus to patients from the Americas with 2,626 White patients and 381 Black patients.

Mitchel L. Zoler/MDedge News

Assessment of the effect of dapagliflozin on the primary outcome of cardiovascular death or hospitalization for heart failure among all patients, both those with HFrEF and those with HFpEF, again showed that event rates among patients treated with placebo were significantly higher in Black, compared with White patients, and this led to a difference in the number needed to treat to prevent one primary outcome event of 12 in Blacks and 17 in Whites, Jawad H. Butt, MD said in a talk at the meeting.

Although treatment with dapagliflozin reduced the rate of the primary outcome in this subgroup of patients from the DAPA-HF trial and the DELIVER trial by similar rates in Black and White patients, event rates were higher in the Black patients resulting in “greater benefit in absolute terms” for Black patients, explained Dr. Butt, a cardiologist at Rigshospitalet in Copenhagen.

But in contrast to the empagliflozin findings reported by Dr. Verma, the combined data from the dapagliflozin trials showed no suggestion of heterogeneity in the beneficial effect of dapagliflozin based on left ventricular ejection fraction. In the Black patients, for example, the relative benefit from dapagliflozin on the primary outcome was consistent across the full spectrum of patients with HFrEF and HFpEF.

EMPEROR-Reduced and EMPEROR-Preserved were sponsored by Boehringer Ingelheim and Lilly, the companies that jointly market empagliflozin (Jardiance). The DAPA-HF and DELIVER trials were sponsored by AstraZeneca, the company that markets dapagliflozin (Farxiga). Dr. Verma has received honoraria, research support, or both from AstraZeneca, Boehringer Ingelheim, and Lilly, and from numerous other companies. Dr. Butt has been a consultant to and received travel grants from AstraZeneca, honoraria from Novartis, and has been an adviser to Bayer.




 

A re-evaluation of cardiovascular risk management guidelines intended for use by rheumatologists may be warranted based on findings from a recently published population-based study of the risks for 12 different cardiovascular disease outcomes in patients with autoimmune diseases.

“The notion that patients with rheumatic diseases are at increased risk of developing cardiovascular diseases has been ongoing for many years,” Nathalie Conrad, PhD, and coauthors wrote in a viewpoint article in Annals of the Rheumatic Diseases.

This has “sparked much debate concerning whether and when to initiate cardiovascular prevention therapies,” they said.

Dr. Conrad was first author on the population-based study published in The Lancet in August 2022 that used linked primary and secondary care records from datasets in the U.K. Clinical Practice Research Datalink involving individuals who were recently diagnosed with any of 19 different autoimmune diseases during an 18-year period stretching from 2000 to 2017 but free of cardiovascular disease until at least 12 months after incident autoimmune disease. “Every single autoimmune disorder we looked at was associated with increased cardiovascular risk,” Dr. Conrad, of the department of public health and primary care at Catholic University Leuven (Belgium), said in an interview.

Not only was the risk for cardiovascular disease increased for people with rheumatic diseases by an average of 68%, compared with people without rheumatic diseases, but also the whole spectrum of cardiovascular disorders was seen.

“We saw increases in thromboembolic diseases, degenerative heart diseases, and heart inflammation,” Dr. Conrad said.
 

Large datasets examined

The idea for the epidemiologic study came from mounting evidence for cardiovascular disease risk among people with autoimmune diseases but not enough to support the design of specific prevention measures.

Dr. Conrad’s Lancet study examined electronic health records of 446,449 individuals with autoimmune diseases and matched them to 2,102,830 individuals without autoimmune disease. This included 160,217 individuals with seven rheumatic diseases: rheumatoid arthritis, polymyalgia rheumatica, vasculitis, systemic lupus erythematosus, Sjögren’s syndrome, ankylosing spondylitis, and systemic sclerosis.

In addition to looking for any evidence of cardiovascular disease, Dr. Conrad and coauthors looked at 12 specific outcomes: atherosclerotic diseases, peripheral arterial disease, stroke or transient ischemic attack, heart failure, valve disorders, thromboembolic disease, atrial fibrillation or flutter, conduction system disease, supraventricular arrhythmias, aortic aneurysm, myocarditis and pericarditis, and infective endocarditis.
 

CV risk in rheumatic diseases

As might be expected, “greater magnitudes of risk” were seen for individuals with systemic lupus erythematosus and systemic sclerosis than for people in the general population, with the chances of cardiovascular disease being two to four times higher. But what perhaps wasn’t expected was that all rheumatic diseases carried an increased risk for heart or vascular-related problems.

Furthermore, the increased risk could not solely be accounted for by the presence of traditional risk factors, such as blood pressure, smoking, or obesity.

“The background here is that any context of systemic inflammation would be predicted to lead to an increased vascular risk,” Iain McInnes, MD, PhD, professor of medicine and rheumatology at the University of Glasgow, said in an interview. Dr. McInnes was a coauthor of the viewpoint article in Annals of the Rheumatic Diseases.

“The implication is that there may well be increased vascular risk across the whole range of immune-mediated inflammatory diseases,” he added. “We should not, however, infer the magnitude of risk will be the same for each disease.”

What is more intriguing, Dr. McInnes said, is that “we don’t know yet whether there’s one final common pathway that leads to the blood vessel being damaged or whether different diseases might contribute different pathways.”

He added: “A question for the future is to see what are those mechanisms that drive risk across different diseases? And the reason that matters, of course, is that we might want to think about the effectiveness of different therapeutic interventions.”
 

Determining cardiovascular risk

Dr. Conrad and associates in their viewpoint article suggested that an update to the European Alliance of Associations for Rheumatology guidelines for cardiovascular risk management of rheumatic and musculoskeletal diseases (RMDs) could tailor cardiovascular risk scores to certain diseases.

They suggested that the guidelines could consider a risk multiplier of 2.5 for systemic sclerosis, 2.0 for lupus, and 1.5 for any other rheumatic disease.

“We argue that [EULAR] recommendations should consider this new evidence of poorer cardiovascular health in numerous RMDs and envisage cardiovascular screening and associated prevention measures,” Dr. Conrad said.

While they recognize that risk multipliers aren’t perfect, “they are the best available option until personalized risk prediction tools are developed specifically for patients with RMDs.”
 

Addressing cardiovascular risk

As a former president of EULAR, Dr. McInnes was keen to point out that “EULAR’s recommendations are evidence based and are rigorously built on [standard operating procedures] that work and have stood the test of time. I’m quite sure that the members of relevant EULAR task forces will be looking at these data, but they’ll be looking at the whole range of literature to see whether change is necessary.”

Good-quality inflammatory disease control will certainly contribute to reducing vascular risk, “but we should not make the assumption that it will be sufficient,” he cautioned. “We still have to be very careful in addressing so called conventional risk factors, but in particular thinking about obesity and cardiometabolic syndrome to be sure that when those are present, that we detect them and we treat them appropriately.”

As to who is best placed to manage a patient’s cardiovascular risk profile, Dr. McInnes said: “I think the rheumatologist has a responsibility to make sure that as much of the patient’s disease spectrum is being treated as possible.”

“As a rheumatologist, I would like to know that those elements of a patient’s disease presentation are being addressed,” whether that is by a primary care physician, cardiologist, diabetologist, or other specialist involved in the optimal management of the patient.

Dr. Conrad acknowledged receiving support from the European Union’s Horizon 2020 Program, the European Society for Cardiology, and grant funding paid to her institution from the Belgian-based Research Foundation Flounders. She also acknowledged receipt of royalties in regard to the intellectual property of a home-monitoring system for heart failure paid to Oxford University Innovation. Dr. McInnes acknowledged financial relationships with many pharmaceutical companies.

*This article was updated 12/30/2022.

A re-evaluation of cardiovascular risk management guidelines intended for use by rheumatologists may be warranted based on findings from a recently published population-based study of the risks for 12 different cardiovascular disease outcomes in patients with autoimmune diseases.

“The notion that patients with rheumatic diseases are at increased risk of developing cardiovascular diseases has been ongoing for many years,” Nathalie Conrad, PhD, and coauthors wrote in a viewpoint article in Annals of the Rheumatic Diseases.

This has “sparked much debate concerning whether and when to initiate cardiovascular prevention therapies,” they said.

Dr. Conrad was first author on the population-based study published in The Lancet in August 2022 that used linked primary and secondary care records from datasets in the U.K. Clinical Practice Research Datalink involving individuals who were recently diagnosed with any of 19 different autoimmune diseases during an 18-year period stretching from 2000 to 2017 but free of cardiovascular disease until at least 12 months after incident autoimmune disease. “Every single autoimmune disorder we looked at was associated with increased cardiovascular risk,” Dr. Conrad, of the department of public health and primary care at Catholic University Leuven (Belgium), said in an interview.

Not only was the risk for cardiovascular disease increased for people with rheumatic diseases by an average of 68%, compared with people without rheumatic diseases, but also the whole spectrum of cardiovascular disorders was seen.

“We saw increases in thromboembolic diseases, degenerative heart diseases, and heart inflammation,” Dr. Conrad said.
 

Large datasets examined

The idea for the epidemiologic study came from mounting evidence for cardiovascular disease risk among people with autoimmune diseases but not enough to support the design of specific prevention measures.

Dr. Conrad’s Lancet study examined electronic health records of 446,449 individuals with autoimmune diseases and matched them to 2,102,830 individuals without autoimmune disease. This included 160,217 individuals with seven rheumatic diseases: rheumatoid arthritis, polymyalgia rheumatica, vasculitis, systemic lupus erythematosus, Sjögren’s syndrome, ankylosing spondylitis, and systemic sclerosis.

In addition to looking for any evidence of cardiovascular disease, Dr. Conrad and coauthors looked at 12 specific outcomes: atherosclerotic diseases, peripheral arterial disease, stroke or transient ischemic attack, heart failure, valve disorders, thromboembolic disease, atrial fibrillation or flutter, conduction system disease, supraventricular arrhythmias, aortic aneurysm, myocarditis and pericarditis, and infective endocarditis.
 

CV risk in rheumatic diseases

As might be expected, “greater magnitudes of risk” were seen for individuals with systemic lupus erythematosus and systemic sclerosis than for people in the general population, with the chances of cardiovascular disease being two to four times higher. But what perhaps wasn’t expected was that all rheumatic diseases carried an increased risk for heart or vascular-related problems.

Furthermore, the increased risk could not solely be accounted for by the presence of traditional risk factors, such as blood pressure, smoking, or obesity.

“The background here is that any context of systemic inflammation would be predicted to lead to an increased vascular risk,” Iain McInnes, MD, PhD, professor of medicine and rheumatology at the University of Glasgow, said in an interview. Dr. McInnes was a coauthor of the viewpoint article in Annals of the Rheumatic Diseases.

“The implication is that there may well be increased vascular risk across the whole range of immune-mediated inflammatory diseases,” he added. “We should not, however, infer the magnitude of risk will be the same for each disease.”

What is more intriguing, Dr. McInnes said, is that “we don’t know yet whether there’s one final common pathway that leads to the blood vessel being damaged or whether different diseases might contribute different pathways.”

He added: “A question for the future is to see what are those mechanisms that drive risk across different diseases? And the reason that matters, of course, is that we might want to think about the effectiveness of different therapeutic interventions.”
 

Determining cardiovascular risk

Dr. Conrad and associates in their viewpoint article suggested that an update to the European Alliance of Associations for Rheumatology guidelines for cardiovascular risk management of rheumatic and musculoskeletal diseases (RMDs) could tailor cardiovascular risk scores to certain diseases.

They suggested that the guidelines could consider a risk multiplier of 2.5 for systemic sclerosis, 2.0 for lupus, and 1.5 for any other rheumatic disease.

“We argue that [EULAR] recommendations should consider this new evidence of poorer cardiovascular health in numerous RMDs and envisage cardiovascular screening and associated prevention measures,” Dr. Conrad said.

While they recognize that risk multipliers aren’t perfect, “they are the best available option until personalized risk prediction tools are developed specifically for patients with RMDs.”
 

Addressing cardiovascular risk

As a former president of EULAR, Dr. McInnes was keen to point out that “EULAR’s recommendations are evidence based and are rigorously built on [standard operating procedures] that work and have stood the test of time. I’m quite sure that the members of relevant EULAR task forces will be looking at these data, but they’ll be looking at the whole range of literature to see whether change is necessary.”

Good-quality inflammatory disease control will certainly contribute to reducing vascular risk, “but we should not make the assumption that it will be sufficient,” he cautioned. “We still have to be very careful in addressing so called conventional risk factors, but in particular thinking about obesity and cardiometabolic syndrome to be sure that when those are present, that we detect them and we treat them appropriately.”

As to who is best placed to manage a patient’s cardiovascular risk profile, Dr. McInnes said: “I think the rheumatologist has a responsibility to make sure that as much of the patient’s disease spectrum is being treated as possible.”

“As a rheumatologist, I would like to know that those elements of a patient’s disease presentation are being addressed,” whether that is by a primary care physician, cardiologist, diabetologist, or other specialist involved in the optimal management of the patient.

Dr. Conrad acknowledged receiving support from the European Union’s Horizon 2020 Program, the European Society for Cardiology, and grant funding paid to her institution from the Belgian-based Research Foundation Flounders. She also acknowledged receipt of royalties in regard to the intellectual property of a home-monitoring system for heart failure paid to Oxford University Innovation. Dr. McInnes acknowledged financial relationships with many pharmaceutical companies.

*This article was updated 12/30/2022.

A re-evaluation of cardiovascular risk management guidelines intended for use by rheumatologists may be warranted based on findings from a recently published population-based study of the risks for 12 different cardiovascular disease outcomes in patients with autoimmune diseases.

“The notion that patients with rheumatic diseases are at increased risk of developing cardiovascular diseases has been ongoing for many years,” Nathalie Conrad, PhD, and coauthors wrote in a viewpoint article in Annals of the Rheumatic Diseases.

This has “sparked much debate concerning whether and when to initiate cardiovascular prevention therapies,” they said.

Dr. Conrad was first author on the population-based study published in The Lancet in August 2022 that used linked primary and secondary care records from datasets in the U.K. Clinical Practice Research Datalink involving individuals who were recently diagnosed with any of 19 different autoimmune diseases during an 18-year period stretching from 2000 to 2017 but free of cardiovascular disease until at least 12 months after incident autoimmune disease. “Every single autoimmune disorder we looked at was associated with increased cardiovascular risk,” Dr. Conrad, of the department of public health and primary care at Catholic University Leuven (Belgium), said in an interview.

Not only was the risk for cardiovascular disease increased for people with rheumatic diseases by an average of 68%, compared with people without rheumatic diseases, but also the whole spectrum of cardiovascular disorders was seen.

“We saw increases in thromboembolic diseases, degenerative heart diseases, and heart inflammation,” Dr. Conrad said.
 

Large datasets examined

The idea for the epidemiologic study came from mounting evidence for cardiovascular disease risk among people with autoimmune diseases but not enough to support the design of specific prevention measures.

Dr. Conrad’s Lancet study examined electronic health records of 446,449 individuals with autoimmune diseases and matched them to 2,102,830 individuals without autoimmune disease. This included 160,217 individuals with seven rheumatic diseases: rheumatoid arthritis, polymyalgia rheumatica, vasculitis, systemic lupus erythematosus, Sjögren’s syndrome, ankylosing spondylitis, and systemic sclerosis.

In addition to looking for any evidence of cardiovascular disease, Dr. Conrad and coauthors looked at 12 specific outcomes: atherosclerotic diseases, peripheral arterial disease, stroke or transient ischemic attack, heart failure, valve disorders, thromboembolic disease, atrial fibrillation or flutter, conduction system disease, supraventricular arrhythmias, aortic aneurysm, myocarditis and pericarditis, and infective endocarditis.
 

CV risk in rheumatic diseases

As might be expected, “greater magnitudes of risk” were seen for individuals with systemic lupus erythematosus and systemic sclerosis than for people in the general population, with the chances of cardiovascular disease being two to four times higher. But what perhaps wasn’t expected was that all rheumatic diseases carried an increased risk for heart or vascular-related problems.

Furthermore, the increased risk could not solely be accounted for by the presence of traditional risk factors, such as blood pressure, smoking, or obesity.

“The background here is that any context of systemic inflammation would be predicted to lead to an increased vascular risk,” Iain McInnes, MD, PhD, professor of medicine and rheumatology at the University of Glasgow, said in an interview. Dr. McInnes was a coauthor of the viewpoint article in Annals of the Rheumatic Diseases.

“The implication is that there may well be increased vascular risk across the whole range of immune-mediated inflammatory diseases,” he added. “We should not, however, infer the magnitude of risk will be the same for each disease.”

What is more intriguing, Dr. McInnes said, is that “we don’t know yet whether there’s one final common pathway that leads to the blood vessel being damaged or whether different diseases might contribute different pathways.”

He added: “A question for the future is to see what are those mechanisms that drive risk across different diseases? And the reason that matters, of course, is that we might want to think about the effectiveness of different therapeutic interventions.”
 

Determining cardiovascular risk

Dr. Conrad and associates in their viewpoint article suggested that an update to the European Alliance of Associations for Rheumatology guidelines for cardiovascular risk management of rheumatic and musculoskeletal diseases (RMDs) could tailor cardiovascular risk scores to certain diseases.

They suggested that the guidelines could consider a risk multiplier of 2.5 for systemic sclerosis, 2.0 for lupus, and 1.5 for any other rheumatic disease.

“We argue that [EULAR] recommendations should consider this new evidence of poorer cardiovascular health in numerous RMDs and envisage cardiovascular screening and associated prevention measures,” Dr. Conrad said.

While they recognize that risk multipliers aren’t perfect, “they are the best available option until personalized risk prediction tools are developed specifically for patients with RMDs.”
 

Addressing cardiovascular risk

As a former president of EULAR, Dr. McInnes was keen to point out that “EULAR’s recommendations are evidence based and are rigorously built on [standard operating procedures] that work and have stood the test of time. I’m quite sure that the members of relevant EULAR task forces will be looking at these data, but they’ll be looking at the whole range of literature to see whether change is necessary.”

Good-quality inflammatory disease control will certainly contribute to reducing vascular risk, “but we should not make the assumption that it will be sufficient,” he cautioned. “We still have to be very careful in addressing so called conventional risk factors, but in particular thinking about obesity and cardiometabolic syndrome to be sure that when those are present, that we detect them and we treat them appropriately.”

As to who is best placed to manage a patient’s cardiovascular risk profile, Dr. McInnes said: “I think the rheumatologist has a responsibility to make sure that as much of the patient’s disease spectrum is being treated as possible.”

“As a rheumatologist, I would like to know that those elements of a patient’s disease presentation are being addressed,” whether that is by a primary care physician, cardiologist, diabetologist, or other specialist involved in the optimal management of the patient.

Dr. Conrad acknowledged receiving support from the European Union’s Horizon 2020 Program, the European Society for Cardiology, and grant funding paid to her institution from the Belgian-based Research Foundation Flounders. She also acknowledged receipt of royalties in regard to the intellectual property of a home-monitoring system for heart failure paid to Oxford University Innovation. Dr. McInnes acknowledged financial relationships with many pharmaceutical companies.

*This article was updated 12/30/2022.

High levels of lipoprotein(a) increase the risk for incident cardiovascular disease (CVD) for hypertensive individuals but not for those without hypertension, a new MESA analysis suggests.

There are ways to test for statistical interaction, “in this case, multiplicative interaction between Lp(a) and hypertension, which suggests that Lp(a) is actually modifying the effect between blood pressure and cardiovascular disease. It’s not simply additive,” senior author Michael D. Shapiro, DO, Wake Forest University, Winston-Salem, N.C., told this news organization.

“So that’s new and I don’t think anybody’s looked at that before.”

Although Lp(a) is recognized as an independent cause of atherosclerotic CVD (ASCVD), the significance of Lp(a) in hypertension has been “virtually untapped,” he noted. A recent prospective study reported that elevated CVD risk was present only in individuals with Lp(a) ≥ 30 mg/dL and hypertension but it included only Chinese participants with stable coronary artery disease.

The current analysis, published online in the journal Hypertension, included 6,674 participants in the ongoing Multi-Ethnic Study of Atherosclerosis (MESA), all free of baseline ASCVD, who were recruited from six communities in the United States and had measured baseline Lp(a), blood pressure, and CVD events data over follow-up from 2000 to 2018.

Participants were stratified into four groups based on the presence or absence of hypertension (defined as 140/90 mm Hg or higher or the use of antihypertensive drugs) and an Lp(a) threshold of 50 mg/dL, as recommended by the American College of Cardiology/American Heart Association cholesterol guideline for consideration as an ASCVD risk-enhancing factor.

Slightly more than half of participants were female (52.8%), 38.6% were White, 27.5% were African American, 22.1% were Hispanic, and 11.9% were Chinese American.

According to the researchers, 809 participants had a CVD event over an average follow-up of 13.9 years, including 7.7% of group 1 with Lp(a) < 50 mg/dL and no hypertension, 8.0% of group 2 with Lp(a) ≥ 50 mg/dL and no hypertension, 16.2% of group 3 with Lp(a) < 50 mg/dL and hypertension, and 18.8% of group 4 with Lp(a) ≥ 50 mg/dL and hypertension.

When compared with group 1 in a fully adjusted Cox proportional model, participants with elevated Lp(a) and no hypertension (group 2) did not have an increased risk of CVD events (hazard ratio [HR], 1.09; 95% confidence interval [CI], 0.79-1.50).

CVD risk, however, was significantly higher in group 3 with normal Lp(a) and hypertension (HR, 1.66; 95% CI, 1.39-1.98) and group 4 with elevated Lp(a) and hypertension (HR, 2.07, 95% CI, 1.63-2.62).

Among all participants with hypertension (groups 3 and 4), Lp(a) was associated with a significant increase in CVD risk (HR, 1.24, 95% CI, 1.01-1.53).

“What I think is interesting here is that in the absence of hypertension, we didn’t really see an increased risk despite having an elevated Lp(a),” said Dr. Shapiro. “What it may indicate is that really for Lp(a) to be associated with risk, there may already need to be some kind of arterial damage that allows the Lp(a) to have its atherogenic impact.

“In other words, in individuals who have totally normal arterial walls, potentially, maybe that is protective enough against Lp(a) that in the absence of any other injurious factor, maybe it’s not an issue,” he said. “That’s a big hypothesis-generating [statement], but hypertension is certainly one of those risk factors that’s known to cause endothelial injury and endothelial dysfunction.”

Dr. Shapiro pointed out that when first measured in MESA, Lp(a) was measured in 4,600 participants who were not on statins, which is important because statins can increase Lp(a) levels.

“When you look just at those participants, those 4,600, you actually do see a relationship between Lp(a) and cardiovascular disease,” he said. “When you look at the whole population, including the 17% who are baseline populations, even when you adjust for statin therapy, we fail to see that, at least in the long-term follow up.”

Nevertheless, he cautioned that hypertension is just one of many traditional cardiovascular risk factors that could affect the relationship between Lp(a) and CVD risk. “I don’t want to suggest that we believe there’s something specifically magical about hypertension and Lp(a). If we chose, say, diabetes or smoking or another traditional risk factor, we may or may not have seen kind of similar results.”

When the investigators stratified the analyses by sex and race/ethnicity, they found that Lp(a) was not associated with CVD risk, regardless of hypertension status. In Black participants, however, greater CVD risk was seen when both elevated Lp(a) and hypertension were present (HR, 2.07, 95% CI, 1.34-3.21; P = .001).

Asked whether the results support one-time universal screening for Lp(a), which is almost exclusively genetically determined, Dr. Shapiro said he supports screening but that this was a secondary analysis and its numbers were modest. He added that median Lp(a) level is higher in African Americans than any other racial/ethnic group but the “most recent data has clarified that, per any absolute level of Lp(a), it appears to confer the same absolute risk in any racial or ethnic group.”

The authors acknowledge that differential loss to follow-up could have resulted in selection bias in the study and that there were relatively few CVD events in group 2, which may have limited the ability to detect differences in groups without hypertension, particularly in the subgroup analyses. Other limitations are the potential for residual confounding and participants may have developed hypertension during follow-up, resulting in misclassification bias.

Further research is needed to better understand the mechanistic link between Lp(a), hypertension, and CVD, Dr. Shapiro said. Further insights also should be provided by the ongoing phase 3 Lp(a) HORIZON trial evaluating the effect of Lp(a) lowering with the investigational antisense drug, pelacarsen, on cardiovascular events in 8,324 patients with established CVD and elevated Lp(a). The study is expected to be completed in May 2025.

The study was supported by contracts from the National Heart, Lung, and Blood Institute and by grants from the National Center for Advanced Translational Sciences. Dr. Shapiro reports participating in scientific advisory boards with Amgen, Novartis, and Novo Nordisk, and consulting for Regeneron.

A version of this article first appeared on Medscape.com.

High levels of lipoprotein(a) increase the risk for incident cardiovascular disease (CVD) for hypertensive individuals but not for those without hypertension, a new MESA analysis suggests.

There are ways to test for statistical interaction, “in this case, multiplicative interaction between Lp(a) and hypertension, which suggests that Lp(a) is actually modifying the effect between blood pressure and cardiovascular disease. It’s not simply additive,” senior author Michael D. Shapiro, DO, Wake Forest University, Winston-Salem, N.C., told this news organization.

“So that’s new and I don’t think anybody’s looked at that before.”

Although Lp(a) is recognized as an independent cause of atherosclerotic CVD (ASCVD), the significance of Lp(a) in hypertension has been “virtually untapped,” he noted. A recent prospective study reported that elevated CVD risk was present only in individuals with Lp(a) ≥ 30 mg/dL and hypertension but it included only Chinese participants with stable coronary artery disease.

The current analysis, published online in the journal Hypertension, included 6,674 participants in the ongoing Multi-Ethnic Study of Atherosclerosis (MESA), all free of baseline ASCVD, who were recruited from six communities in the United States and had measured baseline Lp(a), blood pressure, and CVD events data over follow-up from 2000 to 2018.

Participants were stratified into four groups based on the presence or absence of hypertension (defined as 140/90 mm Hg or higher or the use of antihypertensive drugs) and an Lp(a) threshold of 50 mg/dL, as recommended by the American College of Cardiology/American Heart Association cholesterol guideline for consideration as an ASCVD risk-enhancing factor.

Slightly more than half of participants were female (52.8%), 38.6% were White, 27.5% were African American, 22.1% were Hispanic, and 11.9% were Chinese American.

According to the researchers, 809 participants had a CVD event over an average follow-up of 13.9 years, including 7.7% of group 1 with Lp(a) < 50 mg/dL and no hypertension, 8.0% of group 2 with Lp(a) ≥ 50 mg/dL and no hypertension, 16.2% of group 3 with Lp(a) < 50 mg/dL and hypertension, and 18.8% of group 4 with Lp(a) ≥ 50 mg/dL and hypertension.

When compared with group 1 in a fully adjusted Cox proportional model, participants with elevated Lp(a) and no hypertension (group 2) did not have an increased risk of CVD events (hazard ratio [HR], 1.09; 95% confidence interval [CI], 0.79-1.50).

CVD risk, however, was significantly higher in group 3 with normal Lp(a) and hypertension (HR, 1.66; 95% CI, 1.39-1.98) and group 4 with elevated Lp(a) and hypertension (HR, 2.07, 95% CI, 1.63-2.62).

Among all participants with hypertension (groups 3 and 4), Lp(a) was associated with a significant increase in CVD risk (HR, 1.24, 95% CI, 1.01-1.53).

“What I think is interesting here is that in the absence of hypertension, we didn’t really see an increased risk despite having an elevated Lp(a),” said Dr. Shapiro. “What it may indicate is that really for Lp(a) to be associated with risk, there may already need to be some kind of arterial damage that allows the Lp(a) to have its atherogenic impact.

“In other words, in individuals who have totally normal arterial walls, potentially, maybe that is protective enough against Lp(a) that in the absence of any other injurious factor, maybe it’s not an issue,” he said. “That’s a big hypothesis-generating [statement], but hypertension is certainly one of those risk factors that’s known to cause endothelial injury and endothelial dysfunction.”

Dr. Shapiro pointed out that when first measured in MESA, Lp(a) was measured in 4,600 participants who were not on statins, which is important because statins can increase Lp(a) levels.

“When you look just at those participants, those 4,600, you actually do see a relationship between Lp(a) and cardiovascular disease,” he said. “When you look at the whole population, including the 17% who are baseline populations, even when you adjust for statin therapy, we fail to see that, at least in the long-term follow up.”

Nevertheless, he cautioned that hypertension is just one of many traditional cardiovascular risk factors that could affect the relationship between Lp(a) and CVD risk. “I don’t want to suggest that we believe there’s something specifically magical about hypertension and Lp(a). If we chose, say, diabetes or smoking or another traditional risk factor, we may or may not have seen kind of similar results.”

When the investigators stratified the analyses by sex and race/ethnicity, they found that Lp(a) was not associated with CVD risk, regardless of hypertension status. In Black participants, however, greater CVD risk was seen when both elevated Lp(a) and hypertension were present (HR, 2.07, 95% CI, 1.34-3.21; P = .001).

Asked whether the results support one-time universal screening for Lp(a), which is almost exclusively genetically determined, Dr. Shapiro said he supports screening but that this was a secondary analysis and its numbers were modest. He added that median Lp(a) level is higher in African Americans than any other racial/ethnic group but the “most recent data has clarified that, per any absolute level of Lp(a), it appears to confer the same absolute risk in any racial or ethnic group.”

The authors acknowledge that differential loss to follow-up could have resulted in selection bias in the study and that there were relatively few CVD events in group 2, which may have limited the ability to detect differences in groups without hypertension, particularly in the subgroup analyses. Other limitations are the potential for residual confounding and participants may have developed hypertension during follow-up, resulting in misclassification bias.

Further research is needed to better understand the mechanistic link between Lp(a), hypertension, and CVD, Dr. Shapiro said. Further insights also should be provided by the ongoing phase 3 Lp(a) HORIZON trial evaluating the effect of Lp(a) lowering with the investigational antisense drug, pelacarsen, on cardiovascular events in 8,324 patients with established CVD and elevated Lp(a). The study is expected to be completed in May 2025.

The study was supported by contracts from the National Heart, Lung, and Blood Institute and by grants from the National Center for Advanced Translational Sciences. Dr. Shapiro reports participating in scientific advisory boards with Amgen, Novartis, and Novo Nordisk, and consulting for Regeneron.

A version of this article first appeared on Medscape.com.

High levels of lipoprotein(a) increase the risk for incident cardiovascular disease (CVD) for hypertensive individuals but not for those without hypertension, a new MESA analysis suggests.

There are ways to test for statistical interaction, “in this case, multiplicative interaction between Lp(a) and hypertension, which suggests that Lp(a) is actually modifying the effect between blood pressure and cardiovascular disease. It’s not simply additive,” senior author Michael D. Shapiro, DO, Wake Forest University, Winston-Salem, N.C., told this news organization.

“So that’s new and I don’t think anybody’s looked at that before.”

Although Lp(a) is recognized as an independent cause of atherosclerotic CVD (ASCVD), the significance of Lp(a) in hypertension has been “virtually untapped,” he noted. A recent prospective study reported that elevated CVD risk was present only in individuals with Lp(a) ≥ 30 mg/dL and hypertension but it included only Chinese participants with stable coronary artery disease.

The current analysis, published online in the journal Hypertension, included 6,674 participants in the ongoing Multi-Ethnic Study of Atherosclerosis (MESA), all free of baseline ASCVD, who were recruited from six communities in the United States and had measured baseline Lp(a), blood pressure, and CVD events data over follow-up from 2000 to 2018.

Participants were stratified into four groups based on the presence or absence of hypertension (defined as 140/90 mm Hg or higher or the use of antihypertensive drugs) and an Lp(a) threshold of 50 mg/dL, as recommended by the American College of Cardiology/American Heart Association cholesterol guideline for consideration as an ASCVD risk-enhancing factor.

Slightly more than half of participants were female (52.8%), 38.6% were White, 27.5% were African American, 22.1% were Hispanic, and 11.9% were Chinese American.

According to the researchers, 809 participants had a CVD event over an average follow-up of 13.9 years, including 7.7% of group 1 with Lp(a) < 50 mg/dL and no hypertension, 8.0% of group 2 with Lp(a) ≥ 50 mg/dL and no hypertension, 16.2% of group 3 with Lp(a) < 50 mg/dL and hypertension, and 18.8% of group 4 with Lp(a) ≥ 50 mg/dL and hypertension.

When compared with group 1 in a fully adjusted Cox proportional model, participants with elevated Lp(a) and no hypertension (group 2) did not have an increased risk of CVD events (hazard ratio [HR], 1.09; 95% confidence interval [CI], 0.79-1.50).

CVD risk, however, was significantly higher in group 3 with normal Lp(a) and hypertension (HR, 1.66; 95% CI, 1.39-1.98) and group 4 with elevated Lp(a) and hypertension (HR, 2.07, 95% CI, 1.63-2.62).

Among all participants with hypertension (groups 3 and 4), Lp(a) was associated with a significant increase in CVD risk (HR, 1.24, 95% CI, 1.01-1.53).

“What I think is interesting here is that in the absence of hypertension, we didn’t really see an increased risk despite having an elevated Lp(a),” said Dr. Shapiro. “What it may indicate is that really for Lp(a) to be associated with risk, there may already need to be some kind of arterial damage that allows the Lp(a) to have its atherogenic impact.

“In other words, in individuals who have totally normal arterial walls, potentially, maybe that is protective enough against Lp(a) that in the absence of any other injurious factor, maybe it’s not an issue,” he said. “That’s a big hypothesis-generating [statement], but hypertension is certainly one of those risk factors that’s known to cause endothelial injury and endothelial dysfunction.”

Dr. Shapiro pointed out that when first measured in MESA, Lp(a) was measured in 4,600 participants who were not on statins, which is important because statins can increase Lp(a) levels.

“When you look just at those participants, those 4,600, you actually do see a relationship between Lp(a) and cardiovascular disease,” he said. “When you look at the whole population, including the 17% who are baseline populations, even when you adjust for statin therapy, we fail to see that, at least in the long-term follow up.”

Nevertheless, he cautioned that hypertension is just one of many traditional cardiovascular risk factors that could affect the relationship between Lp(a) and CVD risk. “I don’t want to suggest that we believe there’s something specifically magical about hypertension and Lp(a). If we chose, say, diabetes or smoking or another traditional risk factor, we may or may not have seen kind of similar results.”

When the investigators stratified the analyses by sex and race/ethnicity, they found that Lp(a) was not associated with CVD risk, regardless of hypertension status. In Black participants, however, greater CVD risk was seen when both elevated Lp(a) and hypertension were present (HR, 2.07, 95% CI, 1.34-3.21; P = .001).

Asked whether the results support one-time universal screening for Lp(a), which is almost exclusively genetically determined, Dr. Shapiro said he supports screening but that this was a secondary analysis and its numbers were modest. He added that median Lp(a) level is higher in African Americans than any other racial/ethnic group but the “most recent data has clarified that, per any absolute level of Lp(a), it appears to confer the same absolute risk in any racial or ethnic group.”

The authors acknowledge that differential loss to follow-up could have resulted in selection bias in the study and that there were relatively few CVD events in group 2, which may have limited the ability to detect differences in groups without hypertension, particularly in the subgroup analyses. Other limitations are the potential for residual confounding and participants may have developed hypertension during follow-up, resulting in misclassification bias.

Further research is needed to better understand the mechanistic link between Lp(a), hypertension, and CVD, Dr. Shapiro said. Further insights also should be provided by the ongoing phase 3 Lp(a) HORIZON trial evaluating the effect of Lp(a) lowering with the investigational antisense drug, pelacarsen, on cardiovascular events in 8,324 patients with established CVD and elevated Lp(a). The study is expected to be completed in May 2025.

The study was supported by contracts from the National Heart, Lung, and Blood Institute and by grants from the National Center for Advanced Translational Sciences. Dr. Shapiro reports participating in scientific advisory boards with Amgen, Novartis, and Novo Nordisk, and consulting for Regeneron.

A version of this article first appeared on Medscape.com.

Dispatching trained volunteer responders via smartphones to retrieve automated external defibrillators for patients in out-of-hospital cardiac arrest (OHCA) did not significantly increase bystander AED use in a randomized clinical trial in Sweden.

Most patients in OHCA can be saved if cardiopulmonary resuscitation and defibrillation are initiated within minutes, but despite the “substantial” public availability of AEDs and widespread CPR training among the Swedish public, use rates of both are low, Mattias Ringh, MD, PhD, of Karolinska Institutet in Stockholm, and colleagues wrote.

A previous study by the team showed that dispatching volunteer responders via a smartphone app significantly increased bystander CPR. The current study, called the Swedish AED and Mobile Bystander Activation (SAMBA) trial, aimed to see whether dispatching volunteer responders to collect a nearby AED would increase bystander AED use. A control group of volunteer responders was instructed to go straight to the scene and start CPR.

“The results showed that the volunteer responders were first to provide treatment with both CPR and AEDs in a large proportion of cases in both groups, thereby creating a ‘statistical’ dilutional effect,” Dr. Ringh said in an interview. In effect, the control arm also became an active arm.

“But if we agree that treatment with AEDs and CPR is saving lives, then dispatching volunteer responders is doing just that, although we could not fully measure the effect in our study,” he added.

The study was published online in JAMA Cardiology.
 

No significant differences

The SAMBA trial assessed outcomes of the smartphone dispatch system (Heartrunner), which is triggered at emergency dispatch centers in response to suspected OHCAs at the same time that an ambulance with advanced life support equipment is dispatched.

The volunteer responder system locates a maximum of 30 volunteer responders within a 1.3-km radius from the suspected out-of-hospital cardiac arrest, the researchers explained in their report. Volunteer responders are requested via their smartphone application to accept or decline the alert. If they accept an alert, the volunteer responders receive map-aided route directions to the location of the suspected arrest.

In patients allocated to intervention in this study, four of five of all volunteer responders who accepted the alert received instructions to collect the nearest available AED and then go directly to the patient with suspected out-of-hospital cardiac arrest, the authors noted. Route directions to the scene of the cardiac arrest and the AED were displayed on their smartphones. One of the 5 volunteer responders, closest to the arrest, was dispatched to go directly to initiate CPR.

In patients allocated to the control group, all volunteer responders who accepted the alert were instructed to go directly to the patient with suspected out-of-hospital cardiac arrest to perform CPR. No route directions to or locations of AEDs were displayed.

The study was conducted in Stockholm and in Västra Götaland from 2018 to 2020. At the start of the study, there were 3,123 AEDs and 24,493 volunteer responders in Stockholm and 3,195 AEDs and 19,117 volunteer responders in Västra Götaland.

Post-randomization exclusions included patients without OHCA, those with OHCAs not treated by emergency medical services, and those with OHCAs witnessed by EMS.

The primary outcome was overall bystander AED attachment before the arrival of EMS, including those attached by the volunteer responders but also by lay volunteers who did not use the smartphone app.

Volunteer responders were activated for 947 individuals with OHCA; 461 patients were randomized to the intervention group and 486 to the control group. In both groups, the patients’ median age was 73 and about 65% were men.

Attachment of the AED before the arrival of EMS or first responders occurred in 61 patients (13.2%) in the intervention group versus 46 (9.5%) in the control group (P = .08). However, the majority of all AEDs were attached by lay volunteers who were not volunteer responders using the smartphone app (37 in the intervention arm vs. 28 in the control arm), the researchers noted.

No significant differences were seen in secondary outcomes, which included bystander CPR (69% vs. 71.6%, respectively) and defibrillation before EMS arrival (3.7% vs. 3.9%) between groups.

Among the volunteer responders using the app, crossover was 11% and compliance to instructions was 31%. Overall, volunteer responders attached 38% of all bystander-attached AEDs and provided 45% of all bystander defibrillations and 43% of all bystander CPR.

Going forward, Dr. Ringh and colleagues will be further analyzing the results to understand how to better optimize the logistical challenges involved with smartphone dispatch to OHCA patients. “In the longer term, investigating the impact on survival is also warranted,” he concluded.
 

U.S. in worse shape

In a comment, Christopher Calandrella, DO, chair of emergency medicine at Long Island Jewish Forest Hills,, New York, part of Northwell Health, said: “Significant data are available to support the importance of prompt initiation of CPR and defibrillation for OHCA, and although this study did not demonstrate a meaningful increase in use of AEDs with the trial system, layperson CPR was initiated in approximately 70% of cases in the cohort as a whole. Because of this, I believe it is evident that patients still benefit from a system that encourages bystanders to provide aid prior to the arrival of EMS.”

Nevertheless, he noted, “despite the training of volunteers in applying an AED, overall, only a small percentage of patients in either group had placement and use of the device. While the reasons likely are multifactorial, it may be in part due to the significant stress and anxiety associated with OHCA.”

Additional research would be helpful, he said. “Future studies focusing on more rural areas with lower population density and limited availability of AEDs may be beneficial. Expanding the research outside of Europe to other countries would be useful. Next-phase trials looking at 30-day survival in these patients would also be important.”

Currently in the United States, research is underway to evaluate the use of smartphones to improve in-hospital cardiac arrests, he added, “but no nationwide programs are in place for OHCA.”

Similarly, Kevin G. Volpp, MD, PhD, and Benjamin S. Abella, MD, MPhil, both of the University of Pennsylvania, Philadelphia, wrote in a related editorial: “It is sobering to recognize that, in the U.S., it may be nearly impossible to even test an idea like this, given the lack of a supporting data infrastructure.”

Although there is an app in the United States to link OHCA events to bystander response, they noted, less than half of eligible 911 centers have linked to it.

“Furthermore, the bystander CPR rate in the U.S. is less than 35%, only about half of the Swedish rate, indicating far fewer people are trained in CPR and comfortable performing it in the U.S.,” they wrote. “A wealthy country like the U.S. should be able to develop a far more effective approach to preventing millions of ... families from having a loved one die of OHCA in the decade to come.”

The study was funded by unrestricted grant from the Swedish Heart-Lung Foundation and Stockholm County. The authors, editorialists, and Dr. Calandrella disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Dispatching trained volunteer responders via smartphones to retrieve automated external defibrillators for patients in out-of-hospital cardiac arrest (OHCA) did not significantly increase bystander AED use in a randomized clinical trial in Sweden.

Most patients in OHCA can be saved if cardiopulmonary resuscitation and defibrillation are initiated within minutes, but despite the “substantial” public availability of AEDs and widespread CPR training among the Swedish public, use rates of both are low, Mattias Ringh, MD, PhD, of Karolinska Institutet in Stockholm, and colleagues wrote.

A previous study by the team showed that dispatching volunteer responders via a smartphone app significantly increased bystander CPR. The current study, called the Swedish AED and Mobile Bystander Activation (SAMBA) trial, aimed to see whether dispatching volunteer responders to collect a nearby AED would increase bystander AED use. A control group of volunteer responders was instructed to go straight to the scene and start CPR.

“The results showed that the volunteer responders were first to provide treatment with both CPR and AEDs in a large proportion of cases in both groups, thereby creating a ‘statistical’ dilutional effect,” Dr. Ringh said in an interview. In effect, the control arm also became an active arm.

“But if we agree that treatment with AEDs and CPR is saving lives, then dispatching volunteer responders is doing just that, although we could not fully measure the effect in our study,” he added.

The study was published online in JAMA Cardiology.
 

No significant differences

The SAMBA trial assessed outcomes of the smartphone dispatch system (Heartrunner), which is triggered at emergency dispatch centers in response to suspected OHCAs at the same time that an ambulance with advanced life support equipment is dispatched.

The volunteer responder system locates a maximum of 30 volunteer responders within a 1.3-km radius from the suspected out-of-hospital cardiac arrest, the researchers explained in their report. Volunteer responders are requested via their smartphone application to accept or decline the alert. If they accept an alert, the volunteer responders receive map-aided route directions to the location of the suspected arrest.

In patients allocated to intervention in this study, four of five of all volunteer responders who accepted the alert received instructions to collect the nearest available AED and then go directly to the patient with suspected out-of-hospital cardiac arrest, the authors noted. Route directions to the scene of the cardiac arrest and the AED were displayed on their smartphones. One of the 5 volunteer responders, closest to the arrest, was dispatched to go directly to initiate CPR.

In patients allocated to the control group, all volunteer responders who accepted the alert were instructed to go directly to the patient with suspected out-of-hospital cardiac arrest to perform CPR. No route directions to or locations of AEDs were displayed.

The study was conducted in Stockholm and in Västra Götaland from 2018 to 2020. At the start of the study, there were 3,123 AEDs and 24,493 volunteer responders in Stockholm and 3,195 AEDs and 19,117 volunteer responders in Västra Götaland.

Post-randomization exclusions included patients without OHCA, those with OHCAs not treated by emergency medical services, and those with OHCAs witnessed by EMS.

The primary outcome was overall bystander AED attachment before the arrival of EMS, including those attached by the volunteer responders but also by lay volunteers who did not use the smartphone app.

Volunteer responders were activated for 947 individuals with OHCA; 461 patients were randomized to the intervention group and 486 to the control group. In both groups, the patients’ median age was 73 and about 65% were men.

Attachment of the AED before the arrival of EMS or first responders occurred in 61 patients (13.2%) in the intervention group versus 46 (9.5%) in the control group (P = .08). However, the majority of all AEDs were attached by lay volunteers who were not volunteer responders using the smartphone app (37 in the intervention arm vs. 28 in the control arm), the researchers noted.

No significant differences were seen in secondary outcomes, which included bystander CPR (69% vs. 71.6%, respectively) and defibrillation before EMS arrival (3.7% vs. 3.9%) between groups.

Among the volunteer responders using the app, crossover was 11% and compliance to instructions was 31%. Overall, volunteer responders attached 38% of all bystander-attached AEDs and provided 45% of all bystander defibrillations and 43% of all bystander CPR.

Going forward, Dr. Ringh and colleagues will be further analyzing the results to understand how to better optimize the logistical challenges involved with smartphone dispatch to OHCA patients. “In the longer term, investigating the impact on survival is also warranted,” he concluded.
 

U.S. in worse shape

In a comment, Christopher Calandrella, DO, chair of emergency medicine at Long Island Jewish Forest Hills,, New York, part of Northwell Health, said: “Significant data are available to support the importance of prompt initiation of CPR and defibrillation for OHCA, and although this study did not demonstrate a meaningful increase in use of AEDs with the trial system, layperson CPR was initiated in approximately 70% of cases in the cohort as a whole. Because of this, I believe it is evident that patients still benefit from a system that encourages bystanders to provide aid prior to the arrival of EMS.”

Nevertheless, he noted, “despite the training of volunteers in applying an AED, overall, only a small percentage of patients in either group had placement and use of the device. While the reasons likely are multifactorial, it may be in part due to the significant stress and anxiety associated with OHCA.”

Additional research would be helpful, he said. “Future studies focusing on more rural areas with lower population density and limited availability of AEDs may be beneficial. Expanding the research outside of Europe to other countries would be useful. Next-phase trials looking at 30-day survival in these patients would also be important.”

Currently in the United States, research is underway to evaluate the use of smartphones to improve in-hospital cardiac arrests, he added, “but no nationwide programs are in place for OHCA.”

Similarly, Kevin G. Volpp, MD, PhD, and Benjamin S. Abella, MD, MPhil, both of the University of Pennsylvania, Philadelphia, wrote in a related editorial: “It is sobering to recognize that, in the U.S., it may be nearly impossible to even test an idea like this, given the lack of a supporting data infrastructure.”

Although there is an app in the United States to link OHCA events to bystander response, they noted, less than half of eligible 911 centers have linked to it.

“Furthermore, the bystander CPR rate in the U.S. is less than 35%, only about half of the Swedish rate, indicating far fewer people are trained in CPR and comfortable performing it in the U.S.,” they wrote. “A wealthy country like the U.S. should be able to develop a far more effective approach to preventing millions of ... families from having a loved one die of OHCA in the decade to come.”

The study was funded by unrestricted grant from the Swedish Heart-Lung Foundation and Stockholm County. The authors, editorialists, and Dr. Calandrella disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Dispatching trained volunteer responders via smartphones to retrieve automated external defibrillators for patients in out-of-hospital cardiac arrest (OHCA) did not significantly increase bystander AED use in a randomized clinical trial in Sweden.

Most patients in OHCA can be saved if cardiopulmonary resuscitation and defibrillation are initiated within minutes, but despite the “substantial” public availability of AEDs and widespread CPR training among the Swedish public, use rates of both are low, Mattias Ringh, MD, PhD, of Karolinska Institutet in Stockholm, and colleagues wrote.

A previous study by the team showed that dispatching volunteer responders via a smartphone app significantly increased bystander CPR. The current study, called the Swedish AED and Mobile Bystander Activation (SAMBA) trial, aimed to see whether dispatching volunteer responders to collect a nearby AED would increase bystander AED use. A control group of volunteer responders was instructed to go straight to the scene and start CPR.

“The results showed that the volunteer responders were first to provide treatment with both CPR and AEDs in a large proportion of cases in both groups, thereby creating a ‘statistical’ dilutional effect,” Dr. Ringh said in an interview. In effect, the control arm also became an active arm.

“But if we agree that treatment with AEDs and CPR is saving lives, then dispatching volunteer responders is doing just that, although we could not fully measure the effect in our study,” he added.

The study was published online in JAMA Cardiology.
 

No significant differences

The SAMBA trial assessed outcomes of the smartphone dispatch system (Heartrunner), which is triggered at emergency dispatch centers in response to suspected OHCAs at the same time that an ambulance with advanced life support equipment is dispatched.

The volunteer responder system locates a maximum of 30 volunteer responders within a 1.3-km radius from the suspected out-of-hospital cardiac arrest, the researchers explained in their report. Volunteer responders are requested via their smartphone application to accept or decline the alert. If they accept an alert, the volunteer responders receive map-aided route directions to the location of the suspected arrest.

In patients allocated to intervention in this study, four of five of all volunteer responders who accepted the alert received instructions to collect the nearest available AED and then go directly to the patient with suspected out-of-hospital cardiac arrest, the authors noted. Route directions to the scene of the cardiac arrest and the AED were displayed on their smartphones. One of the 5 volunteer responders, closest to the arrest, was dispatched to go directly to initiate CPR.

In patients allocated to the control group, all volunteer responders who accepted the alert were instructed to go directly to the patient with suspected out-of-hospital cardiac arrest to perform CPR. No route directions to or locations of AEDs were displayed.

The study was conducted in Stockholm and in Västra Götaland from 2018 to 2020. At the start of the study, there were 3,123 AEDs and 24,493 volunteer responders in Stockholm and 3,195 AEDs and 19,117 volunteer responders in Västra Götaland.

Post-randomization exclusions included patients without OHCA, those with OHCAs not treated by emergency medical services, and those with OHCAs witnessed by EMS.

The primary outcome was overall bystander AED attachment before the arrival of EMS, including those attached by the volunteer responders but also by lay volunteers who did not use the smartphone app.

Volunteer responders were activated for 947 individuals with OHCA; 461 patients were randomized to the intervention group and 486 to the control group. In both groups, the patients’ median age was 73 and about 65% were men.

Attachment of the AED before the arrival of EMS or first responders occurred in 61 patients (13.2%) in the intervention group versus 46 (9.5%) in the control group (P = .08). However, the majority of all AEDs were attached by lay volunteers who were not volunteer responders using the smartphone app (37 in the intervention arm vs. 28 in the control arm), the researchers noted.

No significant differences were seen in secondary outcomes, which included bystander CPR (69% vs. 71.6%, respectively) and defibrillation before EMS arrival (3.7% vs. 3.9%) between groups.

Among the volunteer responders using the app, crossover was 11% and compliance to instructions was 31%. Overall, volunteer responders attached 38% of all bystander-attached AEDs and provided 45% of all bystander defibrillations and 43% of all bystander CPR.

Going forward, Dr. Ringh and colleagues will be further analyzing the results to understand how to better optimize the logistical challenges involved with smartphone dispatch to OHCA patients. “In the longer term, investigating the impact on survival is also warranted,” he concluded.
 

U.S. in worse shape

In a comment, Christopher Calandrella, DO, chair of emergency medicine at Long Island Jewish Forest Hills,, New York, part of Northwell Health, said: “Significant data are available to support the importance of prompt initiation of CPR and defibrillation for OHCA, and although this study did not demonstrate a meaningful increase in use of AEDs with the trial system, layperson CPR was initiated in approximately 70% of cases in the cohort as a whole. Because of this, I believe it is evident that patients still benefit from a system that encourages bystanders to provide aid prior to the arrival of EMS.”

Nevertheless, he noted, “despite the training of volunteers in applying an AED, overall, only a small percentage of patients in either group had placement and use of the device. While the reasons likely are multifactorial, it may be in part due to the significant stress and anxiety associated with OHCA.”

Additional research would be helpful, he said. “Future studies focusing on more rural areas with lower population density and limited availability of AEDs may be beneficial. Expanding the research outside of Europe to other countries would be useful. Next-phase trials looking at 30-day survival in these patients would also be important.”

Currently in the United States, research is underway to evaluate the use of smartphones to improve in-hospital cardiac arrests, he added, “but no nationwide programs are in place for OHCA.”

Similarly, Kevin G. Volpp, MD, PhD, and Benjamin S. Abella, MD, MPhil, both of the University of Pennsylvania, Philadelphia, wrote in a related editorial: “It is sobering to recognize that, in the U.S., it may be nearly impossible to even test an idea like this, given the lack of a supporting data infrastructure.”

Although there is an app in the United States to link OHCA events to bystander response, they noted, less than half of eligible 911 centers have linked to it.

“Furthermore, the bystander CPR rate in the U.S. is less than 35%, only about half of the Swedish rate, indicating far fewer people are trained in CPR and comfortable performing it in the U.S.,” they wrote. “A wealthy country like the U.S. should be able to develop a far more effective approach to preventing millions of ... families from having a loved one die of OHCA in the decade to come.”

The study was funded by unrestricted grant from the Swedish Heart-Lung Foundation and Stockholm County. The authors, editorialists, and Dr. Calandrella disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Women with preexisting ischemic heart disease without another cardiac diagnosis have a higher risk of severe maternal morbidity and mortality than women with no cardiac disease, a new study suggests.

However, after adjustment for other comorbidities, the risk associated with isolated preexisting ischemic heart disease without additional evidence of cardiomyopathy was relatively similar to that of other low-risk cardiac diseases.

“These are reassuring findings,” lead author of the study, Anna E. Denoble, MD, Yale University, New Haven, Conn., told this news organization. “The risk is not zero. Women with preexisting ischemic heart disease are at a small increased risk compared to women without preexisting cardiac disease. But with good control of cardiovascular risk factors, these women have a good chance of a positive outcome.”

The study was published online in JACC: Advances.

“To our knowledge, this study provides the largest analysis to date examining the risk of severe morbidity and mortality among pregnant people with pre-existing ischemic heart disease,” the authors noted.

Dr. Denoble, a maternal and fetal medicine specialist, explained that in recent years, there has been an increase in the number of patients with preexisting ischemic heart disease who are considering pregnancy or who are pregnant when they present, but there is little information on outcomes for these patients.

The diagnosis of ischemic heart disease is not included in the main classification used for heart disease in pregnancy – the modified World Health Organization classification, Dr. Denoble noted. “This classification includes information on pregnancy outcomes in women with many cardiac conditions, including arrhythmias, congenital heart disease, heart failure, and aortic aneurysm, but ischemic heart disease is missing.”

She suggested this is probably because ischemic heart disease is regarded as a condition that occurs mainly in older people. “But we are seeing more and more women with ischemic heart disease who are pregnant or considering pregnancy. This could be because women are now often older when considering pregnancy, and also risk factors for ischemic heart disease, such as obesity and diabetes, are becoming more frequent in younger women.”

The researchers conducted the current study to investigate pregnancy outcomes for these women.

The retrospective cohort study analyzed data from the Nationwide Readmissions Database on women who had experienced a delivery hospitalization from Oct. 1, 2015, to Dec. 31, 2018. They compared outcomes for women with isolated preexisting ischemic heart disease with those of women who had no apparent cardiac condition and to those with mild or more severe cardiac conditions included in the mWHO classification after controlling for other comorbidities.

The primary outcome was severe maternal morbidity or death. Dr. Denoble explained that severe maternal morbidity includes mechanical ventilation, blood transfusion, and hysterectomy – the more severe maternal adverse outcomes of pregnancy.

Results showed that, of 11,556,136 delivery hospitalizations, 65,331 patients had another cardiac diagnosis, and 3,009 had ischemic heart disease alone. Patients with ischemic heart disease were older, and rates of diabetes and hypertension were higher.

In unadjusted analyses, adverse outcomes were more common among patients with ischemic heart disease alone than among patients with no cardiac disease and mild cardiac conditions (mWHO class I-II cardiac disease).

Of those with preexisting ischemic heart disease, 6.6% experienced severe maternal morbidity or death, compared with 1.5% of those without a cardiac disease (unadjusted relative risk vs. no cardiac disease, 4.3; 95% confidence interval, 3.5-5.2).

In comparison, 4.2% of women with mWHO I-II cardiac diseases and 23.1% of those with more severe mWHO II/III-IV cardiac diseases experienced severe maternal morbidity or death.

Similar differences were noted for nontransfusion severe maternal morbidity and mortality, as well as cardiac severe maternal morbidity and mortality.

After adjustment, ischemic heart disease alone was associated with a higher risk of severe maternal morbidity or death compared to no cardiac disease (adjusted RR, 1.51; 95% CI, 1.19-1.92).

In comparison, the aRR was 1.90 for WHO class I-II diseases and 5.87 (95% CI, 5.49-6.27) for more severe cardiac conditions defined as WHO II/III-IV diseases.

Risk for nontransfusion severe maternal morbidity or death (aRR, 1.60) and cardiac severe maternal morbidity or death (aRR, 2.98) were also higher for those with ischemic heart disease than for women without any cardiac disease.

There were no significant differences in preterm birth for those with preexisting ischemic heart disease compared to those with no cardiac disease after adjustment.

The risk of severe maternal morbidity and mortality, nontransfusion severe maternal morbidity and mortality, and cardiac severe maternal morbidity and mortality for ischemic heart disease alone most closely approximated that of mWHO class I or II cardiac diseases, the researchers said.

“We found that individuals with preexisting ischemic heart disease had a rate of severe maternal morbidity/mortality in the same range as those with other cardiac diagnoses in the mild cardiac disease classification (class I or II),” Dr. Denoble commented.

“This prognosis suggests it is very reasonable for these women to consider pregnancy. The risk of adverse outcomes is not so high that pregnancy is contraindicated,” she added.

Dr. Denoble said this information will be very helpful when counseling women with preexisting ischemic heart disease who are considering pregnancy. “These patients may need some extra monitoring, but in general, they have a high chance of a good outcome,” she noted.

“I would still advise these women to register with a high-risk obstetrics provider to have a baseline cardiovascular pregnancy evaluation. As long as that is reassuring, then further frequent intensive supervision may not be necessary,” she said.

However, the authors pointed out, “it is important to communicate to patients that while pregnancy may be considered low risk in the setting of pre-existing ischemic heart disease, 6.6% of patients with pre-existing ischemic heart disease alone did experience severe maternal morbidity or death during the delivery hospitalization.”

They added that other medical comorbidities should be factored into discussions regarding the risks of pregnancy.

The researchers also noted that the study was limited to evaluation of maternal outcomes occurring during the delivery hospitalization and that additional research that assesses rates of maternal adverse cardiac events and maternal morbidity occurring prior to or after the delivery hospitalization would be beneficial.

Future studies examining the potential gradation in risk associated with additional cardiac comorbidities in individuals with preexisting ischemic heart disease would also be worthwhile, they added.

The study was supported by funding from the National Institutes of Health and the Foundation for Women and Girls with Blood Disorders. The authors disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Women with preexisting ischemic heart disease without another cardiac diagnosis have a higher risk of severe maternal morbidity and mortality than women with no cardiac disease, a new study suggests.

However, after adjustment for other comorbidities, the risk associated with isolated preexisting ischemic heart disease without additional evidence of cardiomyopathy was relatively similar to that of other low-risk cardiac diseases.

“These are reassuring findings,” lead author of the study, Anna E. Denoble, MD, Yale University, New Haven, Conn., told this news organization. “The risk is not zero. Women with preexisting ischemic heart disease are at a small increased risk compared to women without preexisting cardiac disease. But with good control of cardiovascular risk factors, these women have a good chance of a positive outcome.”

The study was published online in JACC: Advances.

“To our knowledge, this study provides the largest analysis to date examining the risk of severe morbidity and mortality among pregnant people with pre-existing ischemic heart disease,” the authors noted.

Dr. Denoble, a maternal and fetal medicine specialist, explained that in recent years, there has been an increase in the number of patients with preexisting ischemic heart disease who are considering pregnancy or who are pregnant when they present, but there is little information on outcomes for these patients.

The diagnosis of ischemic heart disease is not included in the main classification used for heart disease in pregnancy – the modified World Health Organization classification, Dr. Denoble noted. “This classification includes information on pregnancy outcomes in women with many cardiac conditions, including arrhythmias, congenital heart disease, heart failure, and aortic aneurysm, but ischemic heart disease is missing.”

She suggested this is probably because ischemic heart disease is regarded as a condition that occurs mainly in older people. “But we are seeing more and more women with ischemic heart disease who are pregnant or considering pregnancy. This could be because women are now often older when considering pregnancy, and also risk factors for ischemic heart disease, such as obesity and diabetes, are becoming more frequent in younger women.”

The researchers conducted the current study to investigate pregnancy outcomes for these women.

The retrospective cohort study analyzed data from the Nationwide Readmissions Database on women who had experienced a delivery hospitalization from Oct. 1, 2015, to Dec. 31, 2018. They compared outcomes for women with isolated preexisting ischemic heart disease with those of women who had no apparent cardiac condition and to those with mild or more severe cardiac conditions included in the mWHO classification after controlling for other comorbidities.

The primary outcome was severe maternal morbidity or death. Dr. Denoble explained that severe maternal morbidity includes mechanical ventilation, blood transfusion, and hysterectomy – the more severe maternal adverse outcomes of pregnancy.

Results showed that, of 11,556,136 delivery hospitalizations, 65,331 patients had another cardiac diagnosis, and 3,009 had ischemic heart disease alone. Patients with ischemic heart disease were older, and rates of diabetes and hypertension were higher.

In unadjusted analyses, adverse outcomes were more common among patients with ischemic heart disease alone than among patients with no cardiac disease and mild cardiac conditions (mWHO class I-II cardiac disease).

Of those with preexisting ischemic heart disease, 6.6% experienced severe maternal morbidity or death, compared with 1.5% of those without a cardiac disease (unadjusted relative risk vs. no cardiac disease, 4.3; 95% confidence interval, 3.5-5.2).

In comparison, 4.2% of women with mWHO I-II cardiac diseases and 23.1% of those with more severe mWHO II/III-IV cardiac diseases experienced severe maternal morbidity or death.

Similar differences were noted for nontransfusion severe maternal morbidity and mortality, as well as cardiac severe maternal morbidity and mortality.

After adjustment, ischemic heart disease alone was associated with a higher risk of severe maternal morbidity or death compared to no cardiac disease (adjusted RR, 1.51; 95% CI, 1.19-1.92).

In comparison, the aRR was 1.90 for WHO class I-II diseases and 5.87 (95% CI, 5.49-6.27) for more severe cardiac conditions defined as WHO II/III-IV diseases.

Risk for nontransfusion severe maternal morbidity or death (aRR, 1.60) and cardiac severe maternal morbidity or death (aRR, 2.98) were also higher for those with ischemic heart disease than for women without any cardiac disease.

There were no significant differences in preterm birth for those with preexisting ischemic heart disease compared to those with no cardiac disease after adjustment.

The risk of severe maternal morbidity and mortality, nontransfusion severe maternal morbidity and mortality, and cardiac severe maternal morbidity and mortality for ischemic heart disease alone most closely approximated that of mWHO class I or II cardiac diseases, the researchers said.

“We found that individuals with preexisting ischemic heart disease had a rate of severe maternal morbidity/mortality in the same range as those with other cardiac diagnoses in the mild cardiac disease classification (class I or II),” Dr. Denoble commented.

“This prognosis suggests it is very reasonable for these women to consider pregnancy. The risk of adverse outcomes is not so high that pregnancy is contraindicated,” she added.

Dr. Denoble said this information will be very helpful when counseling women with preexisting ischemic heart disease who are considering pregnancy. “These patients may need some extra monitoring, but in general, they have a high chance of a good outcome,” she noted.

“I would still advise these women to register with a high-risk obstetrics provider to have a baseline cardiovascular pregnancy evaluation. As long as that is reassuring, then further frequent intensive supervision may not be necessary,” she said.

However, the authors pointed out, “it is important to communicate to patients that while pregnancy may be considered low risk in the setting of pre-existing ischemic heart disease, 6.6% of patients with pre-existing ischemic heart disease alone did experience severe maternal morbidity or death during the delivery hospitalization.”

They added that other medical comorbidities should be factored into discussions regarding the risks of pregnancy.

The researchers also noted that the study was limited to evaluation of maternal outcomes occurring during the delivery hospitalization and that additional research that assesses rates of maternal adverse cardiac events and maternal morbidity occurring prior to or after the delivery hospitalization would be beneficial.

Future studies examining the potential gradation in risk associated with additional cardiac comorbidities in individuals with preexisting ischemic heart disease would also be worthwhile, they added.

The study was supported by funding from the National Institutes of Health and the Foundation for Women and Girls with Blood Disorders. The authors disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Women with preexisting ischemic heart disease without another cardiac diagnosis have a higher risk of severe maternal morbidity and mortality than women with no cardiac disease, a new study suggests.

However, after adjustment for other comorbidities, the risk associated with isolated preexisting ischemic heart disease without additional evidence of cardiomyopathy was relatively similar to that of other low-risk cardiac diseases.

“These are reassuring findings,” lead author of the study, Anna E. Denoble, MD, Yale University, New Haven, Conn., told this news organization. “The risk is not zero. Women with preexisting ischemic heart disease are at a small increased risk compared to women without preexisting cardiac disease. But with good control of cardiovascular risk factors, these women have a good chance of a positive outcome.”

The study was published online in JACC: Advances.

“To our knowledge, this study provides the largest analysis to date examining the risk of severe morbidity and mortality among pregnant people with pre-existing ischemic heart disease,” the authors noted.

Dr. Denoble, a maternal and fetal medicine specialist, explained that in recent years, there has been an increase in the number of patients with preexisting ischemic heart disease who are considering pregnancy or who are pregnant when they present, but there is little information on outcomes for these patients.

The diagnosis of ischemic heart disease is not included in the main classification used for heart disease in pregnancy – the modified World Health Organization classification, Dr. Denoble noted. “This classification includes information on pregnancy outcomes in women with many cardiac conditions, including arrhythmias, congenital heart disease, heart failure, and aortic aneurysm, but ischemic heart disease is missing.”

She suggested this is probably because ischemic heart disease is regarded as a condition that occurs mainly in older people. “But we are seeing more and more women with ischemic heart disease who are pregnant or considering pregnancy. This could be because women are now often older when considering pregnancy, and also risk factors for ischemic heart disease, such as obesity and diabetes, are becoming more frequent in younger women.”

The researchers conducted the current study to investigate pregnancy outcomes for these women.

The retrospective cohort study analyzed data from the Nationwide Readmissions Database on women who had experienced a delivery hospitalization from Oct. 1, 2015, to Dec. 31, 2018. They compared outcomes for women with isolated preexisting ischemic heart disease with those of women who had no apparent cardiac condition and to those with mild or more severe cardiac conditions included in the mWHO classification after controlling for other comorbidities.

The primary outcome was severe maternal morbidity or death. Dr. Denoble explained that severe maternal morbidity includes mechanical ventilation, blood transfusion, and hysterectomy – the more severe maternal adverse outcomes of pregnancy.

Results showed that, of 11,556,136 delivery hospitalizations, 65,331 patients had another cardiac diagnosis, and 3,009 had ischemic heart disease alone. Patients with ischemic heart disease were older, and rates of diabetes and hypertension were higher.

In unadjusted analyses, adverse outcomes were more common among patients with ischemic heart disease alone than among patients with no cardiac disease and mild cardiac conditions (mWHO class I-II cardiac disease).

Of those with preexisting ischemic heart disease, 6.6% experienced severe maternal morbidity or death, compared with 1.5% of those without a cardiac disease (unadjusted relative risk vs. no cardiac disease, 4.3; 95% confidence interval, 3.5-5.2).

In comparison, 4.2% of women with mWHO I-II cardiac diseases and 23.1% of those with more severe mWHO II/III-IV cardiac diseases experienced severe maternal morbidity or death.

Similar differences were noted for nontransfusion severe maternal morbidity and mortality, as well as cardiac severe maternal morbidity and mortality.

After adjustment, ischemic heart disease alone was associated with a higher risk of severe maternal morbidity or death compared to no cardiac disease (adjusted RR, 1.51; 95% CI, 1.19-1.92).

In comparison, the aRR was 1.90 for WHO class I-II diseases and 5.87 (95% CI, 5.49-6.27) for more severe cardiac conditions defined as WHO II/III-IV diseases.

Risk for nontransfusion severe maternal morbidity or death (aRR, 1.60) and cardiac severe maternal morbidity or death (aRR, 2.98) were also higher for those with ischemic heart disease than for women without any cardiac disease.

There were no significant differences in preterm birth for those with preexisting ischemic heart disease compared to those with no cardiac disease after adjustment.

The risk of severe maternal morbidity and mortality, nontransfusion severe maternal morbidity and mortality, and cardiac severe maternal morbidity and mortality for ischemic heart disease alone most closely approximated that of mWHO class I or II cardiac diseases, the researchers said.

“We found that individuals with preexisting ischemic heart disease had a rate of severe maternal morbidity/mortality in the same range as those with other cardiac diagnoses in the mild cardiac disease classification (class I or II),” Dr. Denoble commented.

“This prognosis suggests it is very reasonable for these women to consider pregnancy. The risk of adverse outcomes is not so high that pregnancy is contraindicated,” she added.

Dr. Denoble said this information will be very helpful when counseling women with preexisting ischemic heart disease who are considering pregnancy. “These patients may need some extra monitoring, but in general, they have a high chance of a good outcome,” she noted.

“I would still advise these women to register with a high-risk obstetrics provider to have a baseline cardiovascular pregnancy evaluation. As long as that is reassuring, then further frequent intensive supervision may not be necessary,” she said.

However, the authors pointed out, “it is important to communicate to patients that while pregnancy may be considered low risk in the setting of pre-existing ischemic heart disease, 6.6% of patients with pre-existing ischemic heart disease alone did experience severe maternal morbidity or death during the delivery hospitalization.”

They added that other medical comorbidities should be factored into discussions regarding the risks of pregnancy.

The researchers also noted that the study was limited to evaluation of maternal outcomes occurring during the delivery hospitalization and that additional research that assesses rates of maternal adverse cardiac events and maternal morbidity occurring prior to or after the delivery hospitalization would be beneficial.

Future studies examining the potential gradation in risk associated with additional cardiac comorbidities in individuals with preexisting ischemic heart disease would also be worthwhile, they added.

The study was supported by funding from the National Institutes of Health and the Foundation for Women and Girls with Blood Disorders. The authors disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

LISBON – Efforts are underway to better identify which individuals with so-called “prediabetes” are at greatest risk for developing type 2 diabetes and subsequent complications, and therefore merit more intensive intervention.

“Prediabetes” is the term coined to refer to either “impaired fasting glucose (IFG)” or “impaired glucose tolerance (IGT),” both denoting levels of elevated glycemia that don’t meet the thresholds for diabetes. It’s a heterogeneous group overall, and despite its name, not everyone with prediabetes will progress to develop type 2 diabetes.

There have been major increases in prediabetes in the United States and globally over the past 2 decades, epidemiologist Elizabeth Selvin, PhD, said at the recent IDF World Diabetes Congress 2022.

She noted that the concept of “prediabetes” has been controversial, previously dubbed a “dubious diagnosis” and a “boon for Pharma” in a 2019 Science article.

Others have said it’s “not a medical condition” and that it’s “an artificial category with virtually zero clinical relevance” in a press statement issued for a 2014 BMJ article.

“I don’t agree with these statements entirely but I think they speak to the confusion and tremendous controversy around the concept of prediabetes ... I think instead of calling prediabetes a ‘dubious diagnosis’ we should think of it as an opportunity,” said Dr. Selvin, of Johns Hopkins University Bloomberg School of Public Health, Baltimore.

She proposes trying to home in on those with highest risk of developing type 2 diabetes, which she suggests could be achieved by using a combination of elevated fasting glucose and an elevated A1c, although she stresses that this isn’t in any official guidance.

With the appropriate definition, people who are truly at risk for progression to type 2 diabetes can be identified so that lifestyle factors and cardiovascular risk can be addressed, and weight loss efforts implemented.

“Prevention of weight gain is ... important. That message often gets lost. Even if we can’t get people to lose weight, preventing [further] weight gain is important,” she noted.

Asked to comment, Sue Kirkman, MD, told this news organization, “The term prediabetes – or IFG or IGT or any of the ‘intermediate’ terms – is pragmatic in a way. It helps clinicians and patients understand that they are in a higher-risk category and might need intervention and likely need ongoing monitoring. But like many other risk factors [such as] blood pressure, [high] BMI, etc., the risk is not dichotomous but a continuum.

“People at the low end of the ‘intermediate’ range are not going to have much more risk compared to people who are ‘normal,’ while those at the high end of the range have very high risk,” said Dr. Kirkman, of the University of North Carolina, Chapel Hill, and a coauthor of the American Diabetes Association’s diabetes and prediabetes classifications.

“So we lose information if we just lump everyone into a single category. For individual patients, we definitely need better ways to estimate and communicate their potential risk.”


 

Currently five definitions for prediabetes: Home in on risk

The problem, Dr. Selvin explained, is that currently there are five official definitions for “prediabetes” using cutoffs for hemoglobin A1c, fasting glucose, or an oral glucose tolerance test.

Each one identifies different numbers of people with differing risk levels, ranging from a prevalence of 4.3% of the middle-aged adult population with the International Expert Committee’s definition of A1c 6.0%-6.4% to 43.5% with the American Diabetes Association’s 100-125 mg/dL fasting glucose.

“That’s an enormous difference. No wonder people are confused about who has prediabetes and what we should do about it,” Dr. Selvin said, adding that the concern about overdiagnosing “prediabetes” is even greater for older populations, in whom “it’s incredibly common to have mildly elevated glucose.”  

Hence her proposal of what she sees as an evidence-based, “really easy solution” that clinicians can use now to better identify which patients with “intermediate hyperglycemia” to be most concerned about: Use a combination of fasting glucose above 100 mg/dL and an A1c greater than 5.7%.

“If you have both fasting glucose and hemoglobin A1c, you can use them together ... This is not codified in any guidelines. You won’t see this mentioned anywhere. The guidelines are silent on what to do when some people have an elevated fasting glucose but not an elevated A1c ... but I think a simple message is that if people have both an elevated fasting glucose and an elevated A1c, that’s a very high-risk group,” she said.

On the other hand, Dr. Kirkman pointed out, “most discrepancies are near the margins, as in one test is slightly elevated and one isn’t, so those people probably are at low risk.

“It may be that both being elevated means higher risk because they have more hyperglycemia ... so it seems reasonable, but only if it changes what you tell people.”

For example, Dr. Kirkman said, “I’d tell someone with A1c of 5.8% and fasting glucose of 99 mg/dL the same thing I’d tell someone with that A1c and a glucose of 104 mg/dL – that their risk is still pretty low – and I’d recommend healthy lifestyle and weight loss if overweight either way.”

However, she also said, “Certainly people with higher glucose or A1c are at much higher risk, and same for those with both.”
 

Tie “prediabetes” definition to risk, as cardiology scores do?

Dr. Selvin also believes that risk-based definitions of prediabetes are needed. Ideally, these would incorporate demographics and clinical factors such as age and body mass index. Other biomarkers could potentially be developed and validated for inclusion in the definition, such as C-reactive protein (CRP), lipids, or even genetic/proteomic information.  

Moreover, she thinks that the definition should be tied to clinical decision-making, as is the pooled cohort equation in cardiology.

“I think we could do something very similar in prediabetes,” she suggested, adding that even simply incorporating age and BMI into the definition could help further stratify the risk level until other predictors are validated.

Dr. Kirkman said, “The concept of risk scores a la cardiology is interesting, although we’d have to make them simple and also validate them against some outcome.”

Regarding the age issue, Dr. Kirkman noted that although age wasn’t a predictor of progression to type 2 diabetes in the placebo arm of the landmark Diabetes Prevention Program (DPP) trial, “I do agree that it’s a problem that many older folks have the label of prediabetes because of a mildly elevated A1c and we know that most will never get diabetes.”

And, she noted, in the DPP people with prediabetes who had a BMI over 35 kg/m² did have significantly higher progression rates than those with lower BMI, while women with a history of gestational diabetes mellitus are also known to be at particularly high risk.
 

Whom should we throw the kitchen sink at?

Some of this discussion, Dr. Kirkman said, “is really a philosophical one, especially when you consider that lifestyle intervention has benefits for almost everyone on many short- and long-term outcomes.”

“The question is probably whom we should ‘throw the kitchen sink at,’ who should get more scalable advice that might apply to everyone regardless of glycemic levels, and whether there’s some more intermediate group that needs more of a [National Diabetes Prevention Program] approach.”

Dr. Selvin’s group is now working on gathering data to inform development of a risk-based prediabetes definition. “We have a whole research effort in this area. I hope that with some really strong data on risk in prediabetes, that can help to solve the heterogeneity issue. I’m focused on bringing evidence to bear to change the guidelines.”

In the meantime, she told this news organization, “I think there are things we can do now to provide more guidance. I get a lot of feedback from people saying things like ‘my physician told me I have prediabetes but now I don’t’ or ‘I saw in my labs that my blood sugar is elevated but my doctor never said anything.’  That’s a communications issue where we can do a better job.”

The meeting was sponsored by the International Diabetes Federation.

Dr. Selvin is deputy editor of Diabetes Care and on the editorial board of Diabetologia. She receives funding from the NIH and the Foundation for the NIH, and royalties from UpToDate for sections related to screening, diagnosis, and laboratory testing for diabetes. Dr. Kirkman reports no relevant financial relationships.

A version of this article first appeared on Medscape.com.

LISBON – Efforts are underway to better identify which individuals with so-called “prediabetes” are at greatest risk for developing type 2 diabetes and subsequent complications, and therefore merit more intensive intervention.

“Prediabetes” is the term coined to refer to either “impaired fasting glucose (IFG)” or “impaired glucose tolerance (IGT),” both denoting levels of elevated glycemia that don’t meet the thresholds for diabetes. It’s a heterogeneous group overall, and despite its name, not everyone with prediabetes will progress to develop type 2 diabetes.

There have been major increases in prediabetes in the United States and globally over the past 2 decades, epidemiologist Elizabeth Selvin, PhD, said at the recent IDF World Diabetes Congress 2022.

She noted that the concept of “prediabetes” has been controversial, previously dubbed a “dubious diagnosis” and a “boon for Pharma” in a 2019 Science article.

Others have said it’s “not a medical condition” and that it’s “an artificial category with virtually zero clinical relevance” in a press statement issued for a 2014 BMJ article.

“I don’t agree with these statements entirely but I think they speak to the confusion and tremendous controversy around the concept of prediabetes ... I think instead of calling prediabetes a ‘dubious diagnosis’ we should think of it as an opportunity,” said Dr. Selvin, of Johns Hopkins University Bloomberg School of Public Health, Baltimore.

She proposes trying to home in on those with highest risk of developing type 2 diabetes, which she suggests could be achieved by using a combination of elevated fasting glucose and an elevated A1c, although she stresses that this isn’t in any official guidance.

With the appropriate definition, people who are truly at risk for progression to type 2 diabetes can be identified so that lifestyle factors and cardiovascular risk can be addressed, and weight loss efforts implemented.

“Prevention of weight gain is ... important. That message often gets lost. Even if we can’t get people to lose weight, preventing [further] weight gain is important,” she noted.

Asked to comment, Sue Kirkman, MD, told this news organization, “The term prediabetes – or IFG or IGT or any of the ‘intermediate’ terms – is pragmatic in a way. It helps clinicians and patients understand that they are in a higher-risk category and might need intervention and likely need ongoing monitoring. But like many other risk factors [such as] blood pressure, [high] BMI, etc., the risk is not dichotomous but a continuum.

“People at the low end of the ‘intermediate’ range are not going to have much more risk compared to people who are ‘normal,’ while those at the high end of the range have very high risk,” said Dr. Kirkman, of the University of North Carolina, Chapel Hill, and a coauthor of the American Diabetes Association’s diabetes and prediabetes classifications.

“So we lose information if we just lump everyone into a single category. For individual patients, we definitely need better ways to estimate and communicate their potential risk.”


 

Currently five definitions for prediabetes: Home in on risk

The problem, Dr. Selvin explained, is that currently there are five official definitions for “prediabetes” using cutoffs for hemoglobin A1c, fasting glucose, or an oral glucose tolerance test.

Each one identifies different numbers of people with differing risk levels, ranging from a prevalence of 4.3% of the middle-aged adult population with the International Expert Committee’s definition of A1c 6.0%-6.4% to 43.5% with the American Diabetes Association’s 100-125 mg/dL fasting glucose.

“That’s an enormous difference. No wonder people are confused about who has prediabetes and what we should do about it,” Dr. Selvin said, adding that the concern about overdiagnosing “prediabetes” is even greater for older populations, in whom “it’s incredibly common to have mildly elevated glucose.”  

Hence her proposal of what she sees as an evidence-based, “really easy solution” that clinicians can use now to better identify which patients with “intermediate hyperglycemia” to be most concerned about: Use a combination of fasting glucose above 100 mg/dL and an A1c greater than 5.7%.

“If you have both fasting glucose and hemoglobin A1c, you can use them together ... This is not codified in any guidelines. You won’t see this mentioned anywhere. The guidelines are silent on what to do when some people have an elevated fasting glucose but not an elevated A1c ... but I think a simple message is that if people have both an elevated fasting glucose and an elevated A1c, that’s a very high-risk group,” she said.

On the other hand, Dr. Kirkman pointed out, “most discrepancies are near the margins, as in one test is slightly elevated and one isn’t, so those people probably are at low risk.

“It may be that both being elevated means higher risk because they have more hyperglycemia ... so it seems reasonable, but only if it changes what you tell people.”

For example, Dr. Kirkman said, “I’d tell someone with A1c of 5.8% and fasting glucose of 99 mg/dL the same thing I’d tell someone with that A1c and a glucose of 104 mg/dL – that their risk is still pretty low – and I’d recommend healthy lifestyle and weight loss if overweight either way.”

However, she also said, “Certainly people with higher glucose or A1c are at much higher risk, and same for those with both.”
 

Tie “prediabetes” definition to risk, as cardiology scores do?

Dr. Selvin also believes that risk-based definitions of prediabetes are needed. Ideally, these would incorporate demographics and clinical factors such as age and body mass index. Other biomarkers could potentially be developed and validated for inclusion in the definition, such as C-reactive protein (CRP), lipids, or even genetic/proteomic information.  

Moreover, she thinks that the definition should be tied to clinical decision-making, as is the pooled cohort equation in cardiology.

“I think we could do something very similar in prediabetes,” she suggested, adding that even simply incorporating age and BMI into the definition could help further stratify the risk level until other predictors are validated.

Dr. Kirkman said, “The concept of risk scores a la cardiology is interesting, although we’d have to make them simple and also validate them against some outcome.”

Regarding the age issue, Dr. Kirkman noted that although age wasn’t a predictor of progression to type 2 diabetes in the placebo arm of the landmark Diabetes Prevention Program (DPP) trial, “I do agree that it’s a problem that many older folks have the label of prediabetes because of a mildly elevated A1c and we know that most will never get diabetes.”

And, she noted, in the DPP people with prediabetes who had a BMI over 35 kg/m² did have significantly higher progression rates than those with lower BMI, while women with a history of gestational diabetes mellitus are also known to be at particularly high risk.
 

Whom should we throw the kitchen sink at?

Some of this discussion, Dr. Kirkman said, “is really a philosophical one, especially when you consider that lifestyle intervention has benefits for almost everyone on many short- and long-term outcomes.”

“The question is probably whom we should ‘throw the kitchen sink at,’ who should get more scalable advice that might apply to everyone regardless of glycemic levels, and whether there’s some more intermediate group that needs more of a [National Diabetes Prevention Program] approach.”

Dr. Selvin’s group is now working on gathering data to inform development of a risk-based prediabetes definition. “We have a whole research effort in this area. I hope that with some really strong data on risk in prediabetes, that can help to solve the heterogeneity issue. I’m focused on bringing evidence to bear to change the guidelines.”

In the meantime, she told this news organization, “I think there are things we can do now to provide more guidance. I get a lot of feedback from people saying things like ‘my physician told me I have prediabetes but now I don’t’ or ‘I saw in my labs that my blood sugar is elevated but my doctor never said anything.’  That’s a communications issue where we can do a better job.”

The meeting was sponsored by the International Diabetes Federation.

Dr. Selvin is deputy editor of Diabetes Care and on the editorial board of Diabetologia. She receives funding from the NIH and the Foundation for the NIH, and royalties from UpToDate for sections related to screening, diagnosis, and laboratory testing for diabetes. Dr. Kirkman reports no relevant financial relationships.

A version of this article first appeared on Medscape.com.

LISBON – Efforts are underway to better identify which individuals with so-called “prediabetes” are at greatest risk for developing type 2 diabetes and subsequent complications, and therefore merit more intensive intervention.

“Prediabetes” is the term coined to refer to either “impaired fasting glucose (IFG)” or “impaired glucose tolerance (IGT),” both denoting levels of elevated glycemia that don’t meet the thresholds for diabetes. It’s a heterogeneous group overall, and despite its name, not everyone with prediabetes will progress to develop type 2 diabetes.

There have been major increases in prediabetes in the United States and globally over the past 2 decades, epidemiologist Elizabeth Selvin, PhD, said at the recent IDF World Diabetes Congress 2022.

She noted that the concept of “prediabetes” has been controversial, previously dubbed a “dubious diagnosis” and a “boon for Pharma” in a 2019 Science article.

Others have said it’s “not a medical condition” and that it’s “an artificial category with virtually zero clinical relevance” in a press statement issued for a 2014 BMJ article.

“I don’t agree with these statements entirely but I think they speak to the confusion and tremendous controversy around the concept of prediabetes ... I think instead of calling prediabetes a ‘dubious diagnosis’ we should think of it as an opportunity,” said Dr. Selvin, of Johns Hopkins University Bloomberg School of Public Health, Baltimore.

She proposes trying to home in on those with highest risk of developing type 2 diabetes, which she suggests could be achieved by using a combination of elevated fasting glucose and an elevated A1c, although she stresses that this isn’t in any official guidance.

With the appropriate definition, people who are truly at risk for progression to type 2 diabetes can be identified so that lifestyle factors and cardiovascular risk can be addressed, and weight loss efforts implemented.

“Prevention of weight gain is ... important. That message often gets lost. Even if we can’t get people to lose weight, preventing [further] weight gain is important,” she noted.

Asked to comment, Sue Kirkman, MD, told this news organization, “The term prediabetes – or IFG or IGT or any of the ‘intermediate’ terms – is pragmatic in a way. It helps clinicians and patients understand that they are in a higher-risk category and might need intervention and likely need ongoing monitoring. But like many other risk factors [such as] blood pressure, [high] BMI, etc., the risk is not dichotomous but a continuum.

“People at the low end of the ‘intermediate’ range are not going to have much more risk compared to people who are ‘normal,’ while those at the high end of the range have very high risk,” said Dr. Kirkman, of the University of North Carolina, Chapel Hill, and a coauthor of the American Diabetes Association’s diabetes and prediabetes classifications.

“So we lose information if we just lump everyone into a single category. For individual patients, we definitely need better ways to estimate and communicate their potential risk.”


 

Currently five definitions for prediabetes: Home in on risk

The problem, Dr. Selvin explained, is that currently there are five official definitions for “prediabetes” using cutoffs for hemoglobin A1c, fasting glucose, or an oral glucose tolerance test.

Each one identifies different numbers of people with differing risk levels, ranging from a prevalence of 4.3% of the middle-aged adult population with the International Expert Committee’s definition of A1c 6.0%-6.4% to 43.5% with the American Diabetes Association’s 100-125 mg/dL fasting glucose.

“That’s an enormous difference. No wonder people are confused about who has prediabetes and what we should do about it,” Dr. Selvin said, adding that the concern about overdiagnosing “prediabetes” is even greater for older populations, in whom “it’s incredibly common to have mildly elevated glucose.”  

Hence her proposal of what she sees as an evidence-based, “really easy solution” that clinicians can use now to better identify which patients with “intermediate hyperglycemia” to be most concerned about: Use a combination of fasting glucose above 100 mg/dL and an A1c greater than 5.7%.

“If you have both fasting glucose and hemoglobin A1c, you can use them together ... This is not codified in any guidelines. You won’t see this mentioned anywhere. The guidelines are silent on what to do when some people have an elevated fasting glucose but not an elevated A1c ... but I think a simple message is that if people have both an elevated fasting glucose and an elevated A1c, that’s a very high-risk group,” she said.

On the other hand, Dr. Kirkman pointed out, “most discrepancies are near the margins, as in one test is slightly elevated and one isn’t, so those people probably are at low risk.

“It may be that both being elevated means higher risk because they have more hyperglycemia ... so it seems reasonable, but only if it changes what you tell people.”

For example, Dr. Kirkman said, “I’d tell someone with A1c of 5.8% and fasting glucose of 99 mg/dL the same thing I’d tell someone with that A1c and a glucose of 104 mg/dL – that their risk is still pretty low – and I’d recommend healthy lifestyle and weight loss if overweight either way.”

However, she also said, “Certainly people with higher glucose or A1c are at much higher risk, and same for those with both.”
 

Tie “prediabetes” definition to risk, as cardiology scores do?

Dr. Selvin also believes that risk-based definitions of prediabetes are needed. Ideally, these would incorporate demographics and clinical factors such as age and body mass index. Other biomarkers could potentially be developed and validated for inclusion in the definition, such as C-reactive protein (CRP), lipids, or even genetic/proteomic information.  

Moreover, she thinks that the definition should be tied to clinical decision-making, as is the pooled cohort equation in cardiology.

“I think we could do something very similar in prediabetes,” she suggested, adding that even simply incorporating age and BMI into the definition could help further stratify the risk level until other predictors are validated.

Dr. Kirkman said, “The concept of risk scores a la cardiology is interesting, although we’d have to make them simple and also validate them against some outcome.”

Regarding the age issue, Dr. Kirkman noted that although age wasn’t a predictor of progression to type 2 diabetes in the placebo arm of the landmark Diabetes Prevention Program (DPP) trial, “I do agree that it’s a problem that many older folks have the label of prediabetes because of a mildly elevated A1c and we know that most will never get diabetes.”

And, she noted, in the DPP people with prediabetes who had a BMI over 35 kg/m² did have significantly higher progression rates than those with lower BMI, while women with a history of gestational diabetes mellitus are also known to be at particularly high risk.
 

Whom should we throw the kitchen sink at?

Some of this discussion, Dr. Kirkman said, “is really a philosophical one, especially when you consider that lifestyle intervention has benefits for almost everyone on many short- and long-term outcomes.”

“The question is probably whom we should ‘throw the kitchen sink at,’ who should get more scalable advice that might apply to everyone regardless of glycemic levels, and whether there’s some more intermediate group that needs more of a [National Diabetes Prevention Program] approach.”

Dr. Selvin’s group is now working on gathering data to inform development of a risk-based prediabetes definition. “We have a whole research effort in this area. I hope that with some really strong data on risk in prediabetes, that can help to solve the heterogeneity issue. I’m focused on bringing evidence to bear to change the guidelines.”

In the meantime, she told this news organization, “I think there are things we can do now to provide more guidance. I get a lot of feedback from people saying things like ‘my physician told me I have prediabetes but now I don’t’ or ‘I saw in my labs that my blood sugar is elevated but my doctor never said anything.’  That’s a communications issue where we can do a better job.”

The meeting was sponsored by the International Diabetes Federation.

Dr. Selvin is deputy editor of Diabetes Care and on the editorial board of Diabetologia. She receives funding from the NIH and the Foundation for the NIH, and royalties from UpToDate for sections related to screening, diagnosis, and laboratory testing for diabetes. Dr. Kirkman reports no relevant financial relationships.

A version of this article first appeared on Medscape.com.

More than a quarter of patients who were shot by assailants with guns had their injuries mislabeled as “unintentional” at hospital discharge, according to a review of more than 1,200 cases at three U.S. trauma centers.

These coding inaccuracies could distort our understanding of gun violence in the United States and make it seem like accidental shootings are more common than they really are, researchers reported in JAMA Network Open.

“The systematic error in intent classification is not widely known or acknowledged by researchers in this field,” Philip J. Cook, PhD, of Duke University, Durham, N.C., and Susan T. Parker, of the University of Michigan, Ann Arbor, wrote in an invited commentary about the new findings. “The bulk of all shootings, nonfatal and fatal together, are assaults, which is to say the result of one person intentionally shooting another. An accurate statistical portrait thus suggests that gun violence is predominantly a crime problem.”

In 2020, 79% of all homicides and 53% of all suicides involved firearms, the CDC reported. Gun violence is now the leading cause of death for children in the United States, government data show.

For the new study, Matthew Miller, MD, ScD, of Northeastern University and the Harvard Injury Control Research Center in Boston, and his colleagues examined how International Classification of Diseases (ICD) codes may misclassify the intent behind gunshot injuries.

Dr. Miller’s group looked at 1,227 incidents between 2008 and 2019 at three major trauma centers – Brigham and Women’s Hospital and Massachusetts General Hospital, both in Boston, and Harborview Medical Center in Seattle.

Of those shootings, 837 (68.2%) involved assaults, 168 (13.5%) were unintentional, 124 (9.9%) were deliberate self-harm, and 43 (3.4%) were instances of legal intervention, based on the researchers’ review of medical records.

ICD codes at discharge, however, labeled 581 cases (47.4%) as assaults and 432 (35.2%) as unintentional.

The researchers found that 234 of the 837 assaults (28%) and 9 of the 43 legal interventions (20.9%) were miscoded as unintentional. This problem occurred even when the “medical narrative explicitly indicated that the shooting was an act of interpersonal violence,” such as a drive-by shooting or an act of domestic violence, the researchers reported.

Hospital trauma registrars, who detail the circumstances surrounding injuries, were mostly in agreement with the researchers.

Medical coders “would likely have little trouble characterizing firearm injury intent accurately if incentives were created for them to do so,” the authors wrote.

Trends and interventions

Separately, researchers published studies showing that gun violence tends to affect various demographics differently, and that remediating abandoned houses could help reduce gun crime.

Lindsay Young, of the University of Cincinnati, and Henry Xiang, MD, PhD, director of the Center for Pediatric Trauma Research at Nationwide Children’s Hospital in Columbus, Ohio, analyzed rates of firearm deaths from 1981 to 2020.

They found that the rate of firearm-related homicide was five times higher among males than females, and the rate of suicide involving firearms was nearly seven times higher for men, they reported in PLOS ONE.

Black men were the group most affected by homicide, whereas White men were most affected by suicide, they found.

To see if fixing abandoned properties would improve health and reduce gun violence in low-income, Black neighborhoods in Philadelphia, Eugenia C. South, MD, of the University of Pennsylvania, Philadelphia, and colleagues conducted a randomized trial.

They randomly assigned abandoned properties in some areas to undergo full remediation (installing working windows and doors, cleaning trash, and weeding); trash cleanup and weeding only; or no intervention.

“Abandoned houses that were remediated showed substantial drops in nearby weapons violations (−8.43%), gun assaults (−13.12%), and to a lesser extent shootings (−6.96%),” the researchers reported.

The intervention targets effects of segregation that have resulted from “historical and ongoing government and private-sector policies” that lead to disinvestment in Black, urban communities, they wrote. Abandoned houses can be used to store firearms and for other illegal activity. They also can engender feelings of fear, neglect, and stress in communities, the researchers noted.

Dr. Miller’s study was funded by the National Collaborative on Gun Violence Research; coauthors disclosed corporate, government, and university grants. The full list of disclosures can be found with the original article. Editorialists Dr. Cook and Dr. Parker report no relevant financial relationships. Dr. South’s study was funded by the National Institutes of Health. Dr. South and some coauthors disclosed government grants.
 

A version of this article first appeared on Medscape.com.

More than a quarter of patients who were shot by assailants with guns had their injuries mislabeled as “unintentional” at hospital discharge, according to a review of more than 1,200 cases at three U.S. trauma centers.

These coding inaccuracies could distort our understanding of gun violence in the United States and make it seem like accidental shootings are more common than they really are, researchers reported in JAMA Network Open.

“The systematic error in intent classification is not widely known or acknowledged by researchers in this field,” Philip J. Cook, PhD, of Duke University, Durham, N.C., and Susan T. Parker, of the University of Michigan, Ann Arbor, wrote in an invited commentary about the new findings. “The bulk of all shootings, nonfatal and fatal together, are assaults, which is to say the result of one person intentionally shooting another. An accurate statistical portrait thus suggests that gun violence is predominantly a crime problem.”

In 2020, 79% of all homicides and 53% of all suicides involved firearms, the CDC reported. Gun violence is now the leading cause of death for children in the United States, government data show.

For the new study, Matthew Miller, MD, ScD, of Northeastern University and the Harvard Injury Control Research Center in Boston, and his colleagues examined how International Classification of Diseases (ICD) codes may misclassify the intent behind gunshot injuries.

Dr. Miller’s group looked at 1,227 incidents between 2008 and 2019 at three major trauma centers – Brigham and Women’s Hospital and Massachusetts General Hospital, both in Boston, and Harborview Medical Center in Seattle.

Of those shootings, 837 (68.2%) involved assaults, 168 (13.5%) were unintentional, 124 (9.9%) were deliberate self-harm, and 43 (3.4%) were instances of legal intervention, based on the researchers’ review of medical records.

ICD codes at discharge, however, labeled 581 cases (47.4%) as assaults and 432 (35.2%) as unintentional.

The researchers found that 234 of the 837 assaults (28%) and 9 of the 43 legal interventions (20.9%) were miscoded as unintentional. This problem occurred even when the “medical narrative explicitly indicated that the shooting was an act of interpersonal violence,” such as a drive-by shooting or an act of domestic violence, the researchers reported.

Hospital trauma registrars, who detail the circumstances surrounding injuries, were mostly in agreement with the researchers.

Medical coders “would likely have little trouble characterizing firearm injury intent accurately if incentives were created for them to do so,” the authors wrote.

Trends and interventions

Separately, researchers published studies showing that gun violence tends to affect various demographics differently, and that remediating abandoned houses could help reduce gun crime.

Lindsay Young, of the University of Cincinnati, and Henry Xiang, MD, PhD, director of the Center for Pediatric Trauma Research at Nationwide Children’s Hospital in Columbus, Ohio, analyzed rates of firearm deaths from 1981 to 2020.

They found that the rate of firearm-related homicide was five times higher among males than females, and the rate of suicide involving firearms was nearly seven times higher for men, they reported in PLOS ONE.

Black men were the group most affected by homicide, whereas White men were most affected by suicide, they found.

To see if fixing abandoned properties would improve health and reduce gun violence in low-income, Black neighborhoods in Philadelphia, Eugenia C. South, MD, of the University of Pennsylvania, Philadelphia, and colleagues conducted a randomized trial.

They randomly assigned abandoned properties in some areas to undergo full remediation (installing working windows and doors, cleaning trash, and weeding); trash cleanup and weeding only; or no intervention.

“Abandoned houses that were remediated showed substantial drops in nearby weapons violations (−8.43%), gun assaults (−13.12%), and to a lesser extent shootings (−6.96%),” the researchers reported.

The intervention targets effects of segregation that have resulted from “historical and ongoing government and private-sector policies” that lead to disinvestment in Black, urban communities, they wrote. Abandoned houses can be used to store firearms and for other illegal activity. They also can engender feelings of fear, neglect, and stress in communities, the researchers noted.

Dr. Miller’s study was funded by the National Collaborative on Gun Violence Research; coauthors disclosed corporate, government, and university grants. The full list of disclosures can be found with the original article. Editorialists Dr. Cook and Dr. Parker report no relevant financial relationships. Dr. South’s study was funded by the National Institutes of Health. Dr. South and some coauthors disclosed government grants.
 

A version of this article first appeared on Medscape.com.

More than a quarter of patients who were shot by assailants with guns had their injuries mislabeled as “unintentional” at hospital discharge, according to a review of more than 1,200 cases at three U.S. trauma centers.

These coding inaccuracies could distort our understanding of gun violence in the United States and make it seem like accidental shootings are more common than they really are, researchers reported in JAMA Network Open.

“The systematic error in intent classification is not widely known or acknowledged by researchers in this field,” Philip J. Cook, PhD, of Duke University, Durham, N.C., and Susan T. Parker, of the University of Michigan, Ann Arbor, wrote in an invited commentary about the new findings. “The bulk of all shootings, nonfatal and fatal together, are assaults, which is to say the result of one person intentionally shooting another. An accurate statistical portrait thus suggests that gun violence is predominantly a crime problem.”

In 2020, 79% of all homicides and 53% of all suicides involved firearms, the CDC reported. Gun violence is now the leading cause of death for children in the United States, government data show.

For the new study, Matthew Miller, MD, ScD, of Northeastern University and the Harvard Injury Control Research Center in Boston, and his colleagues examined how International Classification of Diseases (ICD) codes may misclassify the intent behind gunshot injuries.

Dr. Miller’s group looked at 1,227 incidents between 2008 and 2019 at three major trauma centers – Brigham and Women’s Hospital and Massachusetts General Hospital, both in Boston, and Harborview Medical Center in Seattle.

Of those shootings, 837 (68.2%) involved assaults, 168 (13.5%) were unintentional, 124 (9.9%) were deliberate self-harm, and 43 (3.4%) were instances of legal intervention, based on the researchers’ review of medical records.

ICD codes at discharge, however, labeled 581 cases (47.4%) as assaults and 432 (35.2%) as unintentional.

The researchers found that 234 of the 837 assaults (28%) and 9 of the 43 legal interventions (20.9%) were miscoded as unintentional. This problem occurred even when the “medical narrative explicitly indicated that the shooting was an act of interpersonal violence,” such as a drive-by shooting or an act of domestic violence, the researchers reported.

Hospital trauma registrars, who detail the circumstances surrounding injuries, were mostly in agreement with the researchers.

Medical coders “would likely have little trouble characterizing firearm injury intent accurately if incentives were created for them to do so,” the authors wrote.

Trends and interventions

Separately, researchers published studies showing that gun violence tends to affect various demographics differently, and that remediating abandoned houses could help reduce gun crime.

Lindsay Young, of the University of Cincinnati, and Henry Xiang, MD, PhD, director of the Center for Pediatric Trauma Research at Nationwide Children’s Hospital in Columbus, Ohio, analyzed rates of firearm deaths from 1981 to 2020.

They found that the rate of firearm-related homicide was five times higher among males than females, and the rate of suicide involving firearms was nearly seven times higher for men, they reported in PLOS ONE.

Black men were the group most affected by homicide, whereas White men were most affected by suicide, they found.

To see if fixing abandoned properties would improve health and reduce gun violence in low-income, Black neighborhoods in Philadelphia, Eugenia C. South, MD, of the University of Pennsylvania, Philadelphia, and colleagues conducted a randomized trial.

They randomly assigned abandoned properties in some areas to undergo full remediation (installing working windows and doors, cleaning trash, and weeding); trash cleanup and weeding only; or no intervention.

“Abandoned houses that were remediated showed substantial drops in nearby weapons violations (−8.43%), gun assaults (−13.12%), and to a lesser extent shootings (−6.96%),” the researchers reported.

The intervention targets effects of segregation that have resulted from “historical and ongoing government and private-sector policies” that lead to disinvestment in Black, urban communities, they wrote. Abandoned houses can be used to store firearms and for other illegal activity. They also can engender feelings of fear, neglect, and stress in communities, the researchers noted.

Dr. Miller’s study was funded by the National Collaborative on Gun Violence Research; coauthors disclosed corporate, government, and university grants. The full list of disclosures can be found with the original article. Editorialists Dr. Cook and Dr. Parker report no relevant financial relationships. Dr. South’s study was funded by the National Institutes of Health. Dr. South and some coauthors disclosed government grants.
 

A version of this article first appeared on Medscape.com.

The percentage of people in the U.S. getting the latest COVID-19 booster shot has crept up by single digits in the past couple months, despite health officials pleading for people to do so before the Christmas holiday. 

Now, a new poll shows why so few people are willing to roll up their sleeves again.

The most common reasons people give for not getting the latest booster shot is that they “don’t think they need one” (44%) and they “don’t think the benefits are worth it” (37%), according to poll results from the Kaiser Family Foundation. 

The data comes amid announcements by the Centers for Disease Control and Prevention that boosters reduced COVID-19 hospitalizations by up to 57% for U.S. adults and by up to 84% for people age 65 and older. Those figures are just the latest in a mountain of research reporting the public health benefits of COVID-19 vaccines.

Despite all of the statistical data, health officials’ recent vaccination campaigns have proven far from compelling. 

So far, just 15% of people age 12 and older have gotten the latest booster, and 36% of people age 65 and older have gotten it, the CDC’s vaccination trackershows.

Since the start of the pandemic, 1.1 million people in the U.S. have died from COVID-19, with the number of deaths currently rising by 400 per day, The New York Times COVID tracker shows.

Many experts continue to note the need for everyone to get booster shots regularly, but some advocate that perhaps a change in strategy is in order.

“What the administration should do is push for vaccinating people in high-risk groups, including those who are older, those who are immunocompromised and those who have comorbidities,” Paul Offitt, MD, director of the Vaccine Education Center at Children’s Hospital of Philadelphia, told CNN.

Federal regulators have announced they will meet Jan. 26 with a panel of vaccine advisors to examine the current recommended vaccination schedule as well as look at the effectiveness and composition of current vaccines and boosters, with an eye toward the make-up of next-generation shots.

Vaccines are the “best available protection” against hospitalization and death caused by COVID-19, said Peter Marks, MD, PhD, director of the FDA’s Center for Biologics Evaluation and Research, in a statement announcing the planned meeting.

“Since the initial authorizations of these vaccines, we have learned that protection wanes over time, especially as the virus rapidly mutates and new variants and subvariants emerge,” he said. “Therefore, it’s important to continue discussions about the optimal composition of COVID-19 vaccines for primary and booster vaccination, as well as the optimal interval for booster vaccination.”

A version of this article first appeared on WebMD.com.

The percentage of people in the U.S. getting the latest COVID-19 booster shot has crept up by single digits in the past couple months, despite health officials pleading for people to do so before the Christmas holiday. 

Now, a new poll shows why so few people are willing to roll up their sleeves again.

The most common reasons people give for not getting the latest booster shot is that they “don’t think they need one” (44%) and they “don’t think the benefits are worth it” (37%), according to poll results from the Kaiser Family Foundation. 

The data comes amid announcements by the Centers for Disease Control and Prevention that boosters reduced COVID-19 hospitalizations by up to 57% for U.S. adults and by up to 84% for people age 65 and older. Those figures are just the latest in a mountain of research reporting the public health benefits of COVID-19 vaccines.

Despite all of the statistical data, health officials’ recent vaccination campaigns have proven far from compelling. 

So far, just 15% of people age 12 and older have gotten the latest booster, and 36% of people age 65 and older have gotten it, the CDC’s vaccination trackershows.

Since the start of the pandemic, 1.1 million people in the U.S. have died from COVID-19, with the number of deaths currently rising by 400 per day, The New York Times COVID tracker shows.

Many experts continue to note the need for everyone to get booster shots regularly, but some advocate that perhaps a change in strategy is in order.

“What the administration should do is push for vaccinating people in high-risk groups, including those who are older, those who are immunocompromised and those who have comorbidities,” Paul Offitt, MD, director of the Vaccine Education Center at Children’s Hospital of Philadelphia, told CNN.

Federal regulators have announced they will meet Jan. 26 with a panel of vaccine advisors to examine the current recommended vaccination schedule as well as look at the effectiveness and composition of current vaccines and boosters, with an eye toward the make-up of next-generation shots.

Vaccines are the “best available protection” against hospitalization and death caused by COVID-19, said Peter Marks, MD, PhD, director of the FDA’s Center for Biologics Evaluation and Research, in a statement announcing the planned meeting.

“Since the initial authorizations of these vaccines, we have learned that protection wanes over time, especially as the virus rapidly mutates and new variants and subvariants emerge,” he said. “Therefore, it’s important to continue discussions about the optimal composition of COVID-19 vaccines for primary and booster vaccination, as well as the optimal interval for booster vaccination.”

A version of this article first appeared on WebMD.com.

The percentage of people in the U.S. getting the latest COVID-19 booster shot has crept up by single digits in the past couple months, despite health officials pleading for people to do so before the Christmas holiday. 

Now, a new poll shows why so few people are willing to roll up their sleeves again.

The most common reasons people give for not getting the latest booster shot is that they “don’t think they need one” (44%) and they “don’t think the benefits are worth it” (37%), according to poll results from the Kaiser Family Foundation. 

The data comes amid announcements by the Centers for Disease Control and Prevention that boosters reduced COVID-19 hospitalizations by up to 57% for U.S. adults and by up to 84% for people age 65 and older. Those figures are just the latest in a mountain of research reporting the public health benefits of COVID-19 vaccines.

Despite all of the statistical data, health officials’ recent vaccination campaigns have proven far from compelling. 

So far, just 15% of people age 12 and older have gotten the latest booster, and 36% of people age 65 and older have gotten it, the CDC’s vaccination trackershows.

Since the start of the pandemic, 1.1 million people in the U.S. have died from COVID-19, with the number of deaths currently rising by 400 per day, The New York Times COVID tracker shows.

Many experts continue to note the need for everyone to get booster shots regularly, but some advocate that perhaps a change in strategy is in order.

“What the administration should do is push for vaccinating people in high-risk groups, including those who are older, those who are immunocompromised and those who have comorbidities,” Paul Offitt, MD, director of the Vaccine Education Center at Children’s Hospital of Philadelphia, told CNN.

Federal regulators have announced they will meet Jan. 26 with a panel of vaccine advisors to examine the current recommended vaccination schedule as well as look at the effectiveness and composition of current vaccines and boosters, with an eye toward the make-up of next-generation shots.

Vaccines are the “best available protection” against hospitalization and death caused by COVID-19, said Peter Marks, MD, PhD, director of the FDA’s Center for Biologics Evaluation and Research, in a statement announcing the planned meeting.

“Since the initial authorizations of these vaccines, we have learned that protection wanes over time, especially as the virus rapidly mutates and new variants and subvariants emerge,” he said. “Therefore, it’s important to continue discussions about the optimal composition of COVID-19 vaccines for primary and booster vaccination, as well as the optimal interval for booster vaccination.”

A version of this article first appeared on WebMD.com.