Cardiology

Medtronic has stopped the sale of its Heartware Ventricular Assist Device (HVAD) system and is advising that physicians cease implanting the device because problems with an internal pump can lead to death or serious injuries.

“There is an increased risk of neurological adverse events and mortality associated with the internal pump,” the U.S. Food and Drug Administration announced today.

There is also a potential for the internal pump to stop, and there may be delay or failure to restart. “Both problems may lead to death or serious injuries,” the agency said.

Between January 2009 and April 22, 2021, Medtronic received a total of 106 complaints involving delay or failure to restart with the HVAD pump. Of these, 26 complaints involved HVAD devices operating under normal conditions (dual stator mode) and 80 involved devices operating in a back-up mode (single stator mode) that allows for continued pump function if electrical continuity between the pump and controller is interrupted.

Of the 26 complaints that occurred under normal conditions, four resulted in patient death and five led to urgent explant. Of the 80 complaints that occurred in single stator mode, 10 deaths and eight explants were reported to Medtronic, according to an urgent medical device communication letter issued by the company today.

“Considering these findings and given the availability of alternative devices such as the Abbott HeartMate 3, Medtronic has made the decision to stop the distribution and sale of the HVAD System,” the letter says. “Medtronic advises that there be no further implantations of the HVAD System.”

Medtronic undertook a previous recall of the Heartware HVAD system in February, focusing on batteries, power, datalink cables, and other peripheral equipment, because of the “risk of wear and tear of the connector plugs (power sources, data cable, and alarm adapter), which could cause damage to the controller port metal pins (for example, bent pins).” The FDA deemed that recall Class I, the most serious category of safety alert, in April.

The company noted that patients who currently have an HVAD implant “may require support for many years,” and that it is moving as quickly as possible to create a plan to guide the ongoing support for patients, caregivers, and health care professionals.

In response to the restart failure issue and evolving data about neurologic risks associated with the HVAD pump, Medtronic said it engaged an Independent Practitioner Quality Panel (IPQP), composed of cardiologists, surgeons, and VAD coordinators, to advise on recommendations for appropriate patient management. Based on information collected to date and IPQP input, Medtronic is recommending that physicians continue following best clinical practices and manage patients implanted with the HVAD pump according to the recommendations in the Instructions for Use (IFU).

“Prophylactic explant of the HVAD™ device is not recommended, as risks associated with explantation may outweigh the potential benefits,” the letter says. “The decision regarding explant and exchange of the HVAD™ pump should be made by physicians on a case-by-case basis, considering the patient’s clinical condition and surgical risks. If a physician determines that pump exchange is appropriate, we recommend exchanging to an alternative commercial LVAD.”

For patients in urgent need of an LVAD, Medtronic said physicians should use an alternative commercial LVAD or, if one is not available, that “a Patient Information form is required to be completed by you and your patient to acknowledge the risks of an HVAD implant prior to implanting your HVAD inventory.”

Today’s letter also provides recommendations on blood pressure management goals and anticoagulation. For any other questions or concerns, physicians should contact the Medtronic Office of Medical Affairs at: atrs.mcsmedicalaffairs@medtronic.com.

Medtronic issued another urgent letter in December 2020, warning physicians that a subset of HVAD devices included an internal pump component from three specific lots that increased the risk for restart failure. At that time, the company had not been able to pinpoint a root cause of the pump restart failure.

Consistent with the December 2020 notice, the rate of failure among pumps outside of the subset of three specific lots currently remains at about 0.4%, according to today’s notice.

Although Medtronic has identified the root cause and mitigations for pumps within the three specific lots, it has not been able to identify a root cause of the other restart failures reported with the HVAD pumps, the company said.

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

Medtronic has stopped the sale of its Heartware Ventricular Assist Device (HVAD) system and is advising that physicians cease implanting the device because problems with an internal pump can lead to death or serious injuries.

“There is an increased risk of neurological adverse events and mortality associated with the internal pump,” the U.S. Food and Drug Administration announced today.

There is also a potential for the internal pump to stop, and there may be delay or failure to restart. “Both problems may lead to death or serious injuries,” the agency said.

Between January 2009 and April 22, 2021, Medtronic received a total of 106 complaints involving delay or failure to restart with the HVAD pump. Of these, 26 complaints involved HVAD devices operating under normal conditions (dual stator mode) and 80 involved devices operating in a back-up mode (single stator mode) that allows for continued pump function if electrical continuity between the pump and controller is interrupted.

Of the 26 complaints that occurred under normal conditions, four resulted in patient death and five led to urgent explant. Of the 80 complaints that occurred in single stator mode, 10 deaths and eight explants were reported to Medtronic, according to an urgent medical device communication letter issued by the company today.

“Considering these findings and given the availability of alternative devices such as the Abbott HeartMate 3, Medtronic has made the decision to stop the distribution and sale of the HVAD System,” the letter says. “Medtronic advises that there be no further implantations of the HVAD System.”

Medtronic undertook a previous recall of the Heartware HVAD system in February, focusing on batteries, power, datalink cables, and other peripheral equipment, because of the “risk of wear and tear of the connector plugs (power sources, data cable, and alarm adapter), which could cause damage to the controller port metal pins (for example, bent pins).” The FDA deemed that recall Class I, the most serious category of safety alert, in April.

The company noted that patients who currently have an HVAD implant “may require support for many years,” and that it is moving as quickly as possible to create a plan to guide the ongoing support for patients, caregivers, and health care professionals.

In response to the restart failure issue and evolving data about neurologic risks associated with the HVAD pump, Medtronic said it engaged an Independent Practitioner Quality Panel (IPQP), composed of cardiologists, surgeons, and VAD coordinators, to advise on recommendations for appropriate patient management. Based on information collected to date and IPQP input, Medtronic is recommending that physicians continue following best clinical practices and manage patients implanted with the HVAD pump according to the recommendations in the Instructions for Use (IFU).

“Prophylactic explant of the HVAD™ device is not recommended, as risks associated with explantation may outweigh the potential benefits,” the letter says. “The decision regarding explant and exchange of the HVAD™ pump should be made by physicians on a case-by-case basis, considering the patient’s clinical condition and surgical risks. If a physician determines that pump exchange is appropriate, we recommend exchanging to an alternative commercial LVAD.”

For patients in urgent need of an LVAD, Medtronic said physicians should use an alternative commercial LVAD or, if one is not available, that “a Patient Information form is required to be completed by you and your patient to acknowledge the risks of an HVAD implant prior to implanting your HVAD inventory.”

Today’s letter also provides recommendations on blood pressure management goals and anticoagulation. For any other questions or concerns, physicians should contact the Medtronic Office of Medical Affairs at: atrs.mcsmedicalaffairs@medtronic.com.

Medtronic issued another urgent letter in December 2020, warning physicians that a subset of HVAD devices included an internal pump component from three specific lots that increased the risk for restart failure. At that time, the company had not been able to pinpoint a root cause of the pump restart failure.

Consistent with the December 2020 notice, the rate of failure among pumps outside of the subset of three specific lots currently remains at about 0.4%, according to today’s notice.

Although Medtronic has identified the root cause and mitigations for pumps within the three specific lots, it has not been able to identify a root cause of the other restart failures reported with the HVAD pumps, the company said.

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

Medtronic has stopped the sale of its Heartware Ventricular Assist Device (HVAD) system and is advising that physicians cease implanting the device because problems with an internal pump can lead to death or serious injuries.

“There is an increased risk of neurological adverse events and mortality associated with the internal pump,” the U.S. Food and Drug Administration announced today.

There is also a potential for the internal pump to stop, and there may be delay or failure to restart. “Both problems may lead to death or serious injuries,” the agency said.

Between January 2009 and April 22, 2021, Medtronic received a total of 106 complaints involving delay or failure to restart with the HVAD pump. Of these, 26 complaints involved HVAD devices operating under normal conditions (dual stator mode) and 80 involved devices operating in a back-up mode (single stator mode) that allows for continued pump function if electrical continuity between the pump and controller is interrupted.

Of the 26 complaints that occurred under normal conditions, four resulted in patient death and five led to urgent explant. Of the 80 complaints that occurred in single stator mode, 10 deaths and eight explants were reported to Medtronic, according to an urgent medical device communication letter issued by the company today.

“Considering these findings and given the availability of alternative devices such as the Abbott HeartMate 3, Medtronic has made the decision to stop the distribution and sale of the HVAD System,” the letter says. “Medtronic advises that there be no further implantations of the HVAD System.”

Medtronic undertook a previous recall of the Heartware HVAD system in February, focusing on batteries, power, datalink cables, and other peripheral equipment, because of the “risk of wear and tear of the connector plugs (power sources, data cable, and alarm adapter), which could cause damage to the controller port metal pins (for example, bent pins).” The FDA deemed that recall Class I, the most serious category of safety alert, in April.

The company noted that patients who currently have an HVAD implant “may require support for many years,” and that it is moving as quickly as possible to create a plan to guide the ongoing support for patients, caregivers, and health care professionals.

In response to the restart failure issue and evolving data about neurologic risks associated with the HVAD pump, Medtronic said it engaged an Independent Practitioner Quality Panel (IPQP), composed of cardiologists, surgeons, and VAD coordinators, to advise on recommendations for appropriate patient management. Based on information collected to date and IPQP input, Medtronic is recommending that physicians continue following best clinical practices and manage patients implanted with the HVAD pump according to the recommendations in the Instructions for Use (IFU).

“Prophylactic explant of the HVAD™ device is not recommended, as risks associated with explantation may outweigh the potential benefits,” the letter says. “The decision regarding explant and exchange of the HVAD™ pump should be made by physicians on a case-by-case basis, considering the patient’s clinical condition and surgical risks. If a physician determines that pump exchange is appropriate, we recommend exchanging to an alternative commercial LVAD.”

For patients in urgent need of an LVAD, Medtronic said physicians should use an alternative commercial LVAD or, if one is not available, that “a Patient Information form is required to be completed by you and your patient to acknowledge the risks of an HVAD implant prior to implanting your HVAD inventory.”

Today’s letter also provides recommendations on blood pressure management goals and anticoagulation. For any other questions or concerns, physicians should contact the Medtronic Office of Medical Affairs at: atrs.mcsmedicalaffairs@medtronic.com.

Medtronic issued another urgent letter in December 2020, warning physicians that a subset of HVAD devices included an internal pump component from three specific lots that increased the risk for restart failure. At that time, the company had not been able to pinpoint a root cause of the pump restart failure.

Consistent with the December 2020 notice, the rate of failure among pumps outside of the subset of three specific lots currently remains at about 0.4%, according to today’s notice.

Although Medtronic has identified the root cause and mitigations for pumps within the three specific lots, it has not been able to identify a root cause of the other restart failures reported with the HVAD pumps, the company said.

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

College athletes who have recently recovered from COVID-19 infection show cardiac abnormalities on electrocardiography.

In a small study of ECGs on National Collegiate Athletic Association Division II athletes, those who had been infected with COVID-19 had a prolonged PR interval, compared with matched athletes who had not been infected.

The study was presented at the 2021 Virtual American College of Sports Medicine Annual Meeting & World Congresses.

“The NCAA was requiring athletes to have an ECG for return to play after noting there could be some myocardial abnormalities following COVID-19 infection,” lead author Frank Wyatt, EdD, a sports physiologist and professor at Midwestern State University in Wichita Falls, Tex., told this news organization.

“Our head athletic trainer asked me if I could do ECGs on our COVID-19–recovered athletes, and I decided to do a matched pair–design study to see how our infected and noninfected athletes compared,” Dr. Wyatt said.

Research in the general population has suggested that COVID-19 can cause damage not only to the lungs, but also to the myocardium, he said. “Recent literature suggests COVID-19 is actually infusing itself into the cells of the myocardium and killing those cells, much the way it did in the lung, and possibly kidney and liver, so it’s going after those organs as well, not just the lungs.”

Dr. Wyatt presented results of ECGs that were done in seven COVID-infected athletes and in seven controls, who were free of infection.

The athletes’ recovery from COVID-19 infection was documented after two negative tests.

All subjects were matched by sport, gender, ethnicity, and anthropometry. Investigators obtained ECG recordings 2-4 weeks after the infected athletes had their recovery documented.

Study participants engaged in football, basketball, soccer, and volleyball, and Dr. Wyatt and associates were blinded as to their infected or control status.

Participants self-reported their ethnicity. Most were White or African American.

The main abnormality found was a prolonged PR interval. In the athletes who were recovered from COVID-19, the mean PR interval was 183.6 milliseconds (± 32.4 ms), compared with 141.7 ms (± 22.7 ms) among the controls.
 

Baseline ECGs for all young athletes?

Dr. Wyatt said he would like to see ECGs done at baseline as part of the physical exam NCAA athletes have to undergo at the start of each season. But that would be expensive.

“It has been suggested that they all need to have ECGs for baseline information, but they don’t do it because of money. If we had that baseline data on these athletes it would really give us a better picture of whether there was damage or not,” he said. “At our small university, if I wasn’t available to do these ECGs, our athletic department would then have to go to the cardiologist to do them, and that is tremendously expensive. It has also been suggested that high school athletes get ECGs as a preliminary test when they start their season, and I think that is warranted as well as for the NCAA athletes, but because of the expense, they’re not doing it.”

Dr. Wyatt has continued to do ECGs on athletes who have survived COVID-19 and to date has ECG data on 70 athletes. He plans further comparisons between the infected and noninfected athletes.

“We want to see if we can solidify the results we presented at ACSM. We had small numbers, so our follow up is to see if we can statistically show in a more robust manner whether or not there was widespread abnormality in the athletes who got infected. They were only 2-4 weeks post infected, and I don’t know what the long-term effects are going to be,” he said.
 

May be an important finding

“This may be an important finding, but needs many more athletes, as there were only seven in each group,” commented Curt J. Daniels, MD, director of the sports cardiology program and professor at Ohio State University Wexner Medical Center, Columbus.

“Plus, it will need some imaging correlate and recovery ECGs to see if this effect of PR interval prolongation correlates with myocardial changes and whether it persists or resolves,” added Dr. Daniels, who was not part of the study. “But I do find this interesting. ... I agree we are looking for any ECG sign that might help tell us who needs a cardiac MRI. The Big Ten COVID-19 Cardiac Registry has 1,597 ECGs on post COVID athletes we are analyzing, but preliminarily did not see any changes.”

Dr. Wyatt and Dr. Daniels reported no relevant financial relationships.

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

College athletes who have recently recovered from COVID-19 infection show cardiac abnormalities on electrocardiography.

In a small study of ECGs on National Collegiate Athletic Association Division II athletes, those who had been infected with COVID-19 had a prolonged PR interval, compared with matched athletes who had not been infected.

The study was presented at the 2021 Virtual American College of Sports Medicine Annual Meeting & World Congresses.

“The NCAA was requiring athletes to have an ECG for return to play after noting there could be some myocardial abnormalities following COVID-19 infection,” lead author Frank Wyatt, EdD, a sports physiologist and professor at Midwestern State University in Wichita Falls, Tex., told this news organization.

“Our head athletic trainer asked me if I could do ECGs on our COVID-19–recovered athletes, and I decided to do a matched pair–design study to see how our infected and noninfected athletes compared,” Dr. Wyatt said.

Research in the general population has suggested that COVID-19 can cause damage not only to the lungs, but also to the myocardium, he said. “Recent literature suggests COVID-19 is actually infusing itself into the cells of the myocardium and killing those cells, much the way it did in the lung, and possibly kidney and liver, so it’s going after those organs as well, not just the lungs.”

Dr. Wyatt presented results of ECGs that were done in seven COVID-infected athletes and in seven controls, who were free of infection.

The athletes’ recovery from COVID-19 infection was documented after two negative tests.

All subjects were matched by sport, gender, ethnicity, and anthropometry. Investigators obtained ECG recordings 2-4 weeks after the infected athletes had their recovery documented.

Study participants engaged in football, basketball, soccer, and volleyball, and Dr. Wyatt and associates were blinded as to their infected or control status.

Participants self-reported their ethnicity. Most were White or African American.

The main abnormality found was a prolonged PR interval. In the athletes who were recovered from COVID-19, the mean PR interval was 183.6 milliseconds (± 32.4 ms), compared with 141.7 ms (± 22.7 ms) among the controls.
 

Baseline ECGs for all young athletes?

Dr. Wyatt said he would like to see ECGs done at baseline as part of the physical exam NCAA athletes have to undergo at the start of each season. But that would be expensive.

“It has been suggested that they all need to have ECGs for baseline information, but they don’t do it because of money. If we had that baseline data on these athletes it would really give us a better picture of whether there was damage or not,” he said. “At our small university, if I wasn’t available to do these ECGs, our athletic department would then have to go to the cardiologist to do them, and that is tremendously expensive. It has also been suggested that high school athletes get ECGs as a preliminary test when they start their season, and I think that is warranted as well as for the NCAA athletes, but because of the expense, they’re not doing it.”

Dr. Wyatt has continued to do ECGs on athletes who have survived COVID-19 and to date has ECG data on 70 athletes. He plans further comparisons between the infected and noninfected athletes.

“We want to see if we can solidify the results we presented at ACSM. We had small numbers, so our follow up is to see if we can statistically show in a more robust manner whether or not there was widespread abnormality in the athletes who got infected. They were only 2-4 weeks post infected, and I don’t know what the long-term effects are going to be,” he said.
 

May be an important finding

“This may be an important finding, but needs many more athletes, as there were only seven in each group,” commented Curt J. Daniels, MD, director of the sports cardiology program and professor at Ohio State University Wexner Medical Center, Columbus.

“Plus, it will need some imaging correlate and recovery ECGs to see if this effect of PR interval prolongation correlates with myocardial changes and whether it persists or resolves,” added Dr. Daniels, who was not part of the study. “But I do find this interesting. ... I agree we are looking for any ECG sign that might help tell us who needs a cardiac MRI. The Big Ten COVID-19 Cardiac Registry has 1,597 ECGs on post COVID athletes we are analyzing, but preliminarily did not see any changes.”

Dr. Wyatt and Dr. Daniels reported no relevant financial relationships.

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

College athletes who have recently recovered from COVID-19 infection show cardiac abnormalities on electrocardiography.

In a small study of ECGs on National Collegiate Athletic Association Division II athletes, those who had been infected with COVID-19 had a prolonged PR interval, compared with matched athletes who had not been infected.

The study was presented at the 2021 Virtual American College of Sports Medicine Annual Meeting & World Congresses.

“The NCAA was requiring athletes to have an ECG for return to play after noting there could be some myocardial abnormalities following COVID-19 infection,” lead author Frank Wyatt, EdD, a sports physiologist and professor at Midwestern State University in Wichita Falls, Tex., told this news organization.

“Our head athletic trainer asked me if I could do ECGs on our COVID-19–recovered athletes, and I decided to do a matched pair–design study to see how our infected and noninfected athletes compared,” Dr. Wyatt said.

Research in the general population has suggested that COVID-19 can cause damage not only to the lungs, but also to the myocardium, he said. “Recent literature suggests COVID-19 is actually infusing itself into the cells of the myocardium and killing those cells, much the way it did in the lung, and possibly kidney and liver, so it’s going after those organs as well, not just the lungs.”

Dr. Wyatt presented results of ECGs that were done in seven COVID-infected athletes and in seven controls, who were free of infection.

The athletes’ recovery from COVID-19 infection was documented after two negative tests.

All subjects were matched by sport, gender, ethnicity, and anthropometry. Investigators obtained ECG recordings 2-4 weeks after the infected athletes had their recovery documented.

Study participants engaged in football, basketball, soccer, and volleyball, and Dr. Wyatt and associates were blinded as to their infected or control status.

Participants self-reported their ethnicity. Most were White or African American.

The main abnormality found was a prolonged PR interval. In the athletes who were recovered from COVID-19, the mean PR interval was 183.6 milliseconds (± 32.4 ms), compared with 141.7 ms (± 22.7 ms) among the controls.
 

Baseline ECGs for all young athletes?

Dr. Wyatt said he would like to see ECGs done at baseline as part of the physical exam NCAA athletes have to undergo at the start of each season. But that would be expensive.

“It has been suggested that they all need to have ECGs for baseline information, but they don’t do it because of money. If we had that baseline data on these athletes it would really give us a better picture of whether there was damage or not,” he said. “At our small university, if I wasn’t available to do these ECGs, our athletic department would then have to go to the cardiologist to do them, and that is tremendously expensive. It has also been suggested that high school athletes get ECGs as a preliminary test when they start their season, and I think that is warranted as well as for the NCAA athletes, but because of the expense, they’re not doing it.”

Dr. Wyatt has continued to do ECGs on athletes who have survived COVID-19 and to date has ECG data on 70 athletes. He plans further comparisons between the infected and noninfected athletes.

“We want to see if we can solidify the results we presented at ACSM. We had small numbers, so our follow up is to see if we can statistically show in a more robust manner whether or not there was widespread abnormality in the athletes who got infected. They were only 2-4 weeks post infected, and I don’t know what the long-term effects are going to be,” he said.
 

May be an important finding

“This may be an important finding, but needs many more athletes, as there were only seven in each group,” commented Curt J. Daniels, MD, director of the sports cardiology program and professor at Ohio State University Wexner Medical Center, Columbus.

“Plus, it will need some imaging correlate and recovery ECGs to see if this effect of PR interval prolongation correlates with myocardial changes and whether it persists or resolves,” added Dr. Daniels, who was not part of the study. “But I do find this interesting. ... I agree we are looking for any ECG sign that might help tell us who needs a cardiac MRI. The Big Ten COVID-19 Cardiac Registry has 1,597 ECGs on post COVID athletes we are analyzing, but preliminarily did not see any changes.”

Dr. Wyatt and Dr. Daniels reported no relevant financial relationships.

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

Taking more steps each day, in short spurts or longer bouts, was associated with a longer life in women older than 60 years, according to data from more than 16,000 participants in the ongoing Women’s Health Study.

The American Heart Association recommends at least 150 minutes per week of moderate physical activity, 75 minutes of vigorous physical activity, or a combination of both as fitness guidelines for adults. Walking is a safe and easy way for many adults to follow these guidelines, according to Christopher C. Moore, MS, a PhD candidate at the University of North Carolina at Chapel Hill.

The popularity of step counts reflect that they are simple and objective, and “focusing on steps can help promote an active lifestyle,” he said. Data on the impact of sporadic steps accumulated outside of longer bouts of activity on health outcomes are limited; however, technology advances in the form of fitness apps and wearable devices make it possible for researchers to track and measure the benefits of short periods of activity as well as longer periods.

In a study presented at the Epidemiology and Prevention/Lifestyle and Cardiometabolic Health meeting, sponsored by the AHA, Mr. Moore and colleagues assessed data from women older than 60 years who used wearable step-counting devices to measure their daily steps and walking patterns.

The study population included 16,732 women enrolled in the Women’s Health Study, a longstanding study of heart disease, cancer, and disease prevention among women in the United States. The participants wore waist step counters 4-7 days a week during 2011-2015. The average of the women was 72 years; 96% were non-Hispanic White, and the average BMI was 26 kg/m².

The researchers divided the total number of steps for each study participant into two groups: “bouted” steps, defined as 10 minutes or longer bouts of walking with few interruptions; and “sporadic” steps, defined as short spurts of walking during regular daily activities such as housework, taking the stairs, or walking to or from a car.

A total of 804 deaths occurred during an average of 6 years of follow-up. Each initial increase of 1,000 steps including sporadic or bouted steps was associated with a 28% decrease in death, compared with no daily steps (hazard ratio, 0.72).

Each increasing quartile of sporadic steps was linked with higher total steps per day, Mr. Moore said. “Initial increase in sporadic steps corresponded to the greatest reductions in mortality,” with a HR of 0.69 per additional sporadic steps below 3,200 per day, and the impact on reduced mortality plateaued at about 4,500 sporadic steps per day.

In further analysis, the researchers also found a roughly 32% decrease in death in participants who took more than 2,000 steps daily in uninterrupted bouts (HR, 0.69).

The study findings were limited by several factors, including the relatively short follow-up period and number of events, the assessment of steps at a single time point, and the mostly homogeneous population, Mr. Moore noted. Additional research is needed to assess whether the results are generalizable to men, younger women, and diverse racial and ethnic groups.

However, the results may have implications for public health messaging, he emphasized. The message is that, to impact longevity, the total volume of steps is more important than the type of activity through which they are accumulated.

“You can accumulate your steps through longer bouts of purposeful activity or through everyday behaviors such as walking to your car, taking the stairs, and doing housework,” Mr. Moore concluded.

Find a friend, both of you benefit

On the basis of this study and other available evidence, more steps daily are recommended for everyone, Nieca Goldberg, MD, a cardiologist at New York University Langone Health, said in an interview.

“You can increase minutes of walking and frequency of walking,” she said.

Dr. Goldberg emphasized that you don’t need a fancy app or wearable device to up your steps. She offered some tips to help overcome barriers to putting one foot in front of the other. “Take the steps instead of the elevator. Park your car farther from your destination so you can walk.” Also, you can help yourself and help a friend to better health. “Get a walking buddy so you can encourage each other to walk,” Dr. Goldberg added.

Mr. Moore and Dr. Goldberg had no financial conflicts to disclose. The Women’s Health Study is funded by Brigham and Women’s Hospital; the National Heart, Lung, and Blood Institute; and the National Cancer Institute. Mr. Moore was funded by a grant from the NHLBI but had no other financial conflicts to disclose.

Taking more steps each day, in short spurts or longer bouts, was associated with a longer life in women older than 60 years, according to data from more than 16,000 participants in the ongoing Women’s Health Study.

The American Heart Association recommends at least 150 minutes per week of moderate physical activity, 75 minutes of vigorous physical activity, or a combination of both as fitness guidelines for adults. Walking is a safe and easy way for many adults to follow these guidelines, according to Christopher C. Moore, MS, a PhD candidate at the University of North Carolina at Chapel Hill.

The popularity of step counts reflect that they are simple and objective, and “focusing on steps can help promote an active lifestyle,” he said. Data on the impact of sporadic steps accumulated outside of longer bouts of activity on health outcomes are limited; however, technology advances in the form of fitness apps and wearable devices make it possible for researchers to track and measure the benefits of short periods of activity as well as longer periods.

In a study presented at the Epidemiology and Prevention/Lifestyle and Cardiometabolic Health meeting, sponsored by the AHA, Mr. Moore and colleagues assessed data from women older than 60 years who used wearable step-counting devices to measure their daily steps and walking patterns.

The study population included 16,732 women enrolled in the Women’s Health Study, a longstanding study of heart disease, cancer, and disease prevention among women in the United States. The participants wore waist step counters 4-7 days a week during 2011-2015. The average of the women was 72 years; 96% were non-Hispanic White, and the average BMI was 26 kg/m².

The researchers divided the total number of steps for each study participant into two groups: “bouted” steps, defined as 10 minutes or longer bouts of walking with few interruptions; and “sporadic” steps, defined as short spurts of walking during regular daily activities such as housework, taking the stairs, or walking to or from a car.

A total of 804 deaths occurred during an average of 6 years of follow-up. Each initial increase of 1,000 steps including sporadic or bouted steps was associated with a 28% decrease in death, compared with no daily steps (hazard ratio, 0.72).

Each increasing quartile of sporadic steps was linked with higher total steps per day, Mr. Moore said. “Initial increase in sporadic steps corresponded to the greatest reductions in mortality,” with a HR of 0.69 per additional sporadic steps below 3,200 per day, and the impact on reduced mortality plateaued at about 4,500 sporadic steps per day.

In further analysis, the researchers also found a roughly 32% decrease in death in participants who took more than 2,000 steps daily in uninterrupted bouts (HR, 0.69).

The study findings were limited by several factors, including the relatively short follow-up period and number of events, the assessment of steps at a single time point, and the mostly homogeneous population, Mr. Moore noted. Additional research is needed to assess whether the results are generalizable to men, younger women, and diverse racial and ethnic groups.

However, the results may have implications for public health messaging, he emphasized. The message is that, to impact longevity, the total volume of steps is more important than the type of activity through which they are accumulated.

“You can accumulate your steps through longer bouts of purposeful activity or through everyday behaviors such as walking to your car, taking the stairs, and doing housework,” Mr. Moore concluded.

Find a friend, both of you benefit

On the basis of this study and other available evidence, more steps daily are recommended for everyone, Nieca Goldberg, MD, a cardiologist at New York University Langone Health, said in an interview.

“You can increase minutes of walking and frequency of walking,” she said.

Dr. Goldberg emphasized that you don’t need a fancy app or wearable device to up your steps. She offered some tips to help overcome barriers to putting one foot in front of the other. “Take the steps instead of the elevator. Park your car farther from your destination so you can walk.” Also, you can help yourself and help a friend to better health. “Get a walking buddy so you can encourage each other to walk,” Dr. Goldberg added.

Mr. Moore and Dr. Goldberg had no financial conflicts to disclose. The Women’s Health Study is funded by Brigham and Women’s Hospital; the National Heart, Lung, and Blood Institute; and the National Cancer Institute. Mr. Moore was funded by a grant from the NHLBI but had no other financial conflicts to disclose.

Taking more steps each day, in short spurts or longer bouts, was associated with a longer life in women older than 60 years, according to data from more than 16,000 participants in the ongoing Women’s Health Study.

The American Heart Association recommends at least 150 minutes per week of moderate physical activity, 75 minutes of vigorous physical activity, or a combination of both as fitness guidelines for adults. Walking is a safe and easy way for many adults to follow these guidelines, according to Christopher C. Moore, MS, a PhD candidate at the University of North Carolina at Chapel Hill.

The popularity of step counts reflect that they are simple and objective, and “focusing on steps can help promote an active lifestyle,” he said. Data on the impact of sporadic steps accumulated outside of longer bouts of activity on health outcomes are limited; however, technology advances in the form of fitness apps and wearable devices make it possible for researchers to track and measure the benefits of short periods of activity as well as longer periods.

In a study presented at the Epidemiology and Prevention/Lifestyle and Cardiometabolic Health meeting, sponsored by the AHA, Mr. Moore and colleagues assessed data from women older than 60 years who used wearable step-counting devices to measure their daily steps and walking patterns.

The study population included 16,732 women enrolled in the Women’s Health Study, a longstanding study of heart disease, cancer, and disease prevention among women in the United States. The participants wore waist step counters 4-7 days a week during 2011-2015. The average of the women was 72 years; 96% were non-Hispanic White, and the average BMI was 26 kg/m².

The researchers divided the total number of steps for each study participant into two groups: “bouted” steps, defined as 10 minutes or longer bouts of walking with few interruptions; and “sporadic” steps, defined as short spurts of walking during regular daily activities such as housework, taking the stairs, or walking to or from a car.

A total of 804 deaths occurred during an average of 6 years of follow-up. Each initial increase of 1,000 steps including sporadic or bouted steps was associated with a 28% decrease in death, compared with no daily steps (hazard ratio, 0.72).

Each increasing quartile of sporadic steps was linked with higher total steps per day, Mr. Moore said. “Initial increase in sporadic steps corresponded to the greatest reductions in mortality,” with a HR of 0.69 per additional sporadic steps below 3,200 per day, and the impact on reduced mortality plateaued at about 4,500 sporadic steps per day.

In further analysis, the researchers also found a roughly 32% decrease in death in participants who took more than 2,000 steps daily in uninterrupted bouts (HR, 0.69).

The study findings were limited by several factors, including the relatively short follow-up period and number of events, the assessment of steps at a single time point, and the mostly homogeneous population, Mr. Moore noted. Additional research is needed to assess whether the results are generalizable to men, younger women, and diverse racial and ethnic groups.

However, the results may have implications for public health messaging, he emphasized. The message is that, to impact longevity, the total volume of steps is more important than the type of activity through which they are accumulated.

“You can accumulate your steps through longer bouts of purposeful activity or through everyday behaviors such as walking to your car, taking the stairs, and doing housework,” Mr. Moore concluded.

Find a friend, both of you benefit

On the basis of this study and other available evidence, more steps daily are recommended for everyone, Nieca Goldberg, MD, a cardiologist at New York University Langone Health, said in an interview.

“You can increase minutes of walking and frequency of walking,” she said.

Dr. Goldberg emphasized that you don’t need a fancy app or wearable device to up your steps. She offered some tips to help overcome barriers to putting one foot in front of the other. “Take the steps instead of the elevator. Park your car farther from your destination so you can walk.” Also, you can help yourself and help a friend to better health. “Get a walking buddy so you can encourage each other to walk,” Dr. Goldberg added.

Mr. Moore and Dr. Goldberg had no financial conflicts to disclose. The Women’s Health Study is funded by Brigham and Women’s Hospital; the National Heart, Lung, and Blood Institute; and the National Cancer Institute. Mr. Moore was funded by a grant from the NHLBI but had no other financial conflicts to disclose.

Anti–apolipoprotein A-I (apo A-I) antibodies are common in nonalcoholic fatty liver disease and may not only drive its development but also underlie the link between NAFLD and cardiovascular disease, suggests a novel analysis.

Conducting a clinical analysis and a series of experiments, Sabrina Pagano, PhD, diagnostic department, Geneva University Hospital, and colleagues looked for anti–apo A-I antibodies in patients with NAFLD and then examined their impact on hepatic cells and inflammatory markers.

They found that nearly half of 137 patients with NAFLD were seropositive, and that the antibodies were associated with increased lipid accumulation in the liver, altered triglyceride metabolism, and proinflammatory effects on liver cells.

“We hypothesize that anti–apo A-I IgG may be a potential driver in the development of NAFLD, and further studies are needed to support anti–apo A-I IgG as a possible link between NAFLD and cardiovascular disease,” Dr. Pagano said.

The research was presented at the European Atherosclerosis Society 2021 Virtual Congress.

Asked whether anti–apo A-I antibodies could represent a potential treatment target for NAFLD, Dr. Pagano said in an interview that they have “already developed a peptide that is recognized by the antibodies in order to try to reverse the anti–apo A-I deleterious effect.”

While this was successful in vitro, “unfortunately we didn’t observe ... the peptide reverse of these anti–apo A-I effects in mice, so ... for the moment it’s a little early,” to say whether it represents a promising target.

Approached for comment, Maciej Banach, MD, PhD, full professor of cardiology, Polish Mother’s Memorial Hospital Research Institute, Lodz, said that the results are “very interesting and encouraging.”

He said that his own global burden of disease analysis, which is set to be published soon, showed that the worldwide prevalence of NAFLD is 11%, “representing almost 900 million cases,” and a more than 33% increase in prevalence in the past 30 years.

Consequently, any “attempt to have effective, especially early, diagnosis and treatment,” is highly anticipated.

Dr. Banach said the findings from the experimental analyses are “very interesting and promising,” especially regarding the proinflammatory effects of anti–apo A-I antibodies.

However, he underlined that the clinical part, looking at antibody seropositivity in patients with NAFLD, was limited by the lack of a control group, and there was no indication as to what treatment the patients received, despite it being clear that many were obese.

Dr. Banach also believes that, taking into account the patient characteristics, it is likely that most of the patients had the more severe nonalcoholic steatohepatitis, and “it would be additionally useful to see the autoantibodies levels both in NASH and NAFLD.”

Nevertheless, the clinical utility of measuring anti–apo A-I antibodies is limited at this stage.

He said that the lack of “good, easy, and cheap diagnostic methods based on both laboratory and imaging data” for NAFLD means it would be difficult to determine whether assessing antibody seropositivity “might be indeed an added value.”
 

Independent predictors

Dr. Pagano explained that anti–apo A-I antibodies, which target the major protein fraction of HDL cholesterol, are independent predictors of cardiovascular events in high-risk populations.

They are also independently associated with cardiovascular disease in the general population, as well as atherosclerotic plaque vulnerability in both mice and humans.

She said that apo A-I antibodies have a metabolic role in vivo, and have been shown in vitro to disrupt cholesterol metabolism, promoting foam cell formation.

Studies have also indicated they play a role in hepatic fibrosis, predicting the development of cirrhosis in individuals with chronic hepatitis C infection.

The team therefore set out to determine the presence of anti–apo A-I antibodies in individuals with NAFLD, defined here as fatty acid levels greater than 5% of liver weight, as well as their effect on hepatic cells.

Working with colleagues at Magna Græcia University of Catanzaro (Italy), they obtained serum samples from 137 patients with NAFLD confirmed on ultrasound.

The patients had an average age of 49 years, and 48.9% were male. The median body mass index was 31.8 kg/m². Cholesterol levels were typically in the intermediate range.

They found that 46% of the participants had anti–apo A-I IgG antibodies, “which is quite high when compared with the 15%-20% positivity that we retrieved from the general population,” Dr. Pagano said.

To explore the link between high anti–apo A-I antibodies and NAFLD, the team studied hepatic cells, treating them with anti–apo A-I IgG antibodies or control IgG antibodies, or leaving them untreated, for 24 hours.

This revealed that anti–apo A-I IgG antibodies were associated with a significant increase in liquid droplet content in hepatic cells, compared with both cells treated with control IgG (P = .0008), and untreated cells (P = .0002).

Next, the team immunized apo E knockout mice with anti–apo A-I or control IgG antibodies. After 16 weeks, they found there was a significant increase in liver lipid content in mice given anti–apo A-I antibodies versus those treated with controls (P = .03).

They then asked whether anti–apo A-I antibodies could affect triglyceride metabolism. They examined the expression of the transcription factor sterol regulatory element binding protein (SREBP) and regulation of the triglyceride and cholesterol pathways.

Treating hepatic cells again for 24 hours with anti–apo A-I IgG antibodies or control IgG antibodies, or leaving them untreated, showed that anti–apo A-I antibodies were associated with “dramatic” increases in the active form of SREBP.

They also found that expression of two key enzymes in the triglyceride pathway, fatty acid synthetase and glycerol phosphate acyltransferase, was substantially decreased in the presence anti–apo A-I antibodies.

In both experiments, the untreated hepatic cells and those exposed to control IgG antibodies showed no significant changes.

“These results suggest that negative feedback ... turns off these enzymes, probably due to the lipid overload that is found in the cells after 24 hours of anti–apo A-I treatment,” Dr. Pagano said.

Finally, the researchers observed that anti–apo A-I, but not control antibodies, were associated with increases in inflammatory markers in liver cells.

Specifically, exposure to the antibodies was linked to an approximately 10-fold increase in interleukin-6 levels, as well as an approximate 25-fold increase in IL-8, and around a 7-fold increase in tumor necrosis factor–alpha.

Dr. Pagano suggested that the inflammatory effects are “probably mediated by binding anti–apo A-I antibodies to toll-like receptor 2, which has been previously described in macrophages.”

No funding was declared. The study authors disclosed no relevant financial relationships.

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

Anti–apolipoprotein A-I (apo A-I) antibodies are common in nonalcoholic fatty liver disease and may not only drive its development but also underlie the link between NAFLD and cardiovascular disease, suggests a novel analysis.

Conducting a clinical analysis and a series of experiments, Sabrina Pagano, PhD, diagnostic department, Geneva University Hospital, and colleagues looked for anti–apo A-I antibodies in patients with NAFLD and then examined their impact on hepatic cells and inflammatory markers.

They found that nearly half of 137 patients with NAFLD were seropositive, and that the antibodies were associated with increased lipid accumulation in the liver, altered triglyceride metabolism, and proinflammatory effects on liver cells.

“We hypothesize that anti–apo A-I IgG may be a potential driver in the development of NAFLD, and further studies are needed to support anti–apo A-I IgG as a possible link between NAFLD and cardiovascular disease,” Dr. Pagano said.

The research was presented at the European Atherosclerosis Society 2021 Virtual Congress.

Asked whether anti–apo A-I antibodies could represent a potential treatment target for NAFLD, Dr. Pagano said in an interview that they have “already developed a peptide that is recognized by the antibodies in order to try to reverse the anti–apo A-I deleterious effect.”

While this was successful in vitro, “unfortunately we didn’t observe ... the peptide reverse of these anti–apo A-I effects in mice, so ... for the moment it’s a little early,” to say whether it represents a promising target.

Approached for comment, Maciej Banach, MD, PhD, full professor of cardiology, Polish Mother’s Memorial Hospital Research Institute, Lodz, said that the results are “very interesting and encouraging.”

He said that his own global burden of disease analysis, which is set to be published soon, showed that the worldwide prevalence of NAFLD is 11%, “representing almost 900 million cases,” and a more than 33% increase in prevalence in the past 30 years.

Consequently, any “attempt to have effective, especially early, diagnosis and treatment,” is highly anticipated.

Dr. Banach said the findings from the experimental analyses are “very interesting and promising,” especially regarding the proinflammatory effects of anti–apo A-I antibodies.

However, he underlined that the clinical part, looking at antibody seropositivity in patients with NAFLD, was limited by the lack of a control group, and there was no indication as to what treatment the patients received, despite it being clear that many were obese.

Dr. Banach also believes that, taking into account the patient characteristics, it is likely that most of the patients had the more severe nonalcoholic steatohepatitis, and “it would be additionally useful to see the autoantibodies levels both in NASH and NAFLD.”

Nevertheless, the clinical utility of measuring anti–apo A-I antibodies is limited at this stage.

He said that the lack of “good, easy, and cheap diagnostic methods based on both laboratory and imaging data” for NAFLD means it would be difficult to determine whether assessing antibody seropositivity “might be indeed an added value.”
 

Independent predictors

Dr. Pagano explained that anti–apo A-I antibodies, which target the major protein fraction of HDL cholesterol, are independent predictors of cardiovascular events in high-risk populations.

They are also independently associated with cardiovascular disease in the general population, as well as atherosclerotic plaque vulnerability in both mice and humans.

She said that apo A-I antibodies have a metabolic role in vivo, and have been shown in vitro to disrupt cholesterol metabolism, promoting foam cell formation.

Studies have also indicated they play a role in hepatic fibrosis, predicting the development of cirrhosis in individuals with chronic hepatitis C infection.

The team therefore set out to determine the presence of anti–apo A-I antibodies in individuals with NAFLD, defined here as fatty acid levels greater than 5% of liver weight, as well as their effect on hepatic cells.

Working with colleagues at Magna Græcia University of Catanzaro (Italy), they obtained serum samples from 137 patients with NAFLD confirmed on ultrasound.

The patients had an average age of 49 years, and 48.9% were male. The median body mass index was 31.8 kg/m². Cholesterol levels were typically in the intermediate range.

They found that 46% of the participants had anti–apo A-I IgG antibodies, “which is quite high when compared with the 15%-20% positivity that we retrieved from the general population,” Dr. Pagano said.

To explore the link between high anti–apo A-I antibodies and NAFLD, the team studied hepatic cells, treating them with anti–apo A-I IgG antibodies or control IgG antibodies, or leaving them untreated, for 24 hours.

This revealed that anti–apo A-I IgG antibodies were associated with a significant increase in liquid droplet content in hepatic cells, compared with both cells treated with control IgG (P = .0008), and untreated cells (P = .0002).

Next, the team immunized apo E knockout mice with anti–apo A-I or control IgG antibodies. After 16 weeks, they found there was a significant increase in liver lipid content in mice given anti–apo A-I antibodies versus those treated with controls (P = .03).

They then asked whether anti–apo A-I antibodies could affect triglyceride metabolism. They examined the expression of the transcription factor sterol regulatory element binding protein (SREBP) and regulation of the triglyceride and cholesterol pathways.

Treating hepatic cells again for 24 hours with anti–apo A-I IgG antibodies or control IgG antibodies, or leaving them untreated, showed that anti–apo A-I antibodies were associated with “dramatic” increases in the active form of SREBP.

They also found that expression of two key enzymes in the triglyceride pathway, fatty acid synthetase and glycerol phosphate acyltransferase, was substantially decreased in the presence anti–apo A-I antibodies.

In both experiments, the untreated hepatic cells and those exposed to control IgG antibodies showed no significant changes.

“These results suggest that negative feedback ... turns off these enzymes, probably due to the lipid overload that is found in the cells after 24 hours of anti–apo A-I treatment,” Dr. Pagano said.

Finally, the researchers observed that anti–apo A-I, but not control antibodies, were associated with increases in inflammatory markers in liver cells.

Specifically, exposure to the antibodies was linked to an approximately 10-fold increase in interleukin-6 levels, as well as an approximate 25-fold increase in IL-8, and around a 7-fold increase in tumor necrosis factor–alpha.

Dr. Pagano suggested that the inflammatory effects are “probably mediated by binding anti–apo A-I antibodies to toll-like receptor 2, which has been previously described in macrophages.”

No funding was declared. The study authors disclosed no relevant financial relationships.

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

Anti–apolipoprotein A-I (apo A-I) antibodies are common in nonalcoholic fatty liver disease and may not only drive its development but also underlie the link between NAFLD and cardiovascular disease, suggests a novel analysis.

Conducting a clinical analysis and a series of experiments, Sabrina Pagano, PhD, diagnostic department, Geneva University Hospital, and colleagues looked for anti–apo A-I antibodies in patients with NAFLD and then examined their impact on hepatic cells and inflammatory markers.

They found that nearly half of 137 patients with NAFLD were seropositive, and that the antibodies were associated with increased lipid accumulation in the liver, altered triglyceride metabolism, and proinflammatory effects on liver cells.

“We hypothesize that anti–apo A-I IgG may be a potential driver in the development of NAFLD, and further studies are needed to support anti–apo A-I IgG as a possible link between NAFLD and cardiovascular disease,” Dr. Pagano said.

The research was presented at the European Atherosclerosis Society 2021 Virtual Congress.

Asked whether anti–apo A-I antibodies could represent a potential treatment target for NAFLD, Dr. Pagano said in an interview that they have “already developed a peptide that is recognized by the antibodies in order to try to reverse the anti–apo A-I deleterious effect.”

While this was successful in vitro, “unfortunately we didn’t observe ... the peptide reverse of these anti–apo A-I effects in mice, so ... for the moment it’s a little early,” to say whether it represents a promising target.

Approached for comment, Maciej Banach, MD, PhD, full professor of cardiology, Polish Mother’s Memorial Hospital Research Institute, Lodz, said that the results are “very interesting and encouraging.”

He said that his own global burden of disease analysis, which is set to be published soon, showed that the worldwide prevalence of NAFLD is 11%, “representing almost 900 million cases,” and a more than 33% increase in prevalence in the past 30 years.

Consequently, any “attempt to have effective, especially early, diagnosis and treatment,” is highly anticipated.

Dr. Banach said the findings from the experimental analyses are “very interesting and promising,” especially regarding the proinflammatory effects of anti–apo A-I antibodies.

However, he underlined that the clinical part, looking at antibody seropositivity in patients with NAFLD, was limited by the lack of a control group, and there was no indication as to what treatment the patients received, despite it being clear that many were obese.

Dr. Banach also believes that, taking into account the patient characteristics, it is likely that most of the patients had the more severe nonalcoholic steatohepatitis, and “it would be additionally useful to see the autoantibodies levels both in NASH and NAFLD.”

Nevertheless, the clinical utility of measuring anti–apo A-I antibodies is limited at this stage.

He said that the lack of “good, easy, and cheap diagnostic methods based on both laboratory and imaging data” for NAFLD means it would be difficult to determine whether assessing antibody seropositivity “might be indeed an added value.”
 

Independent predictors

Dr. Pagano explained that anti–apo A-I antibodies, which target the major protein fraction of HDL cholesterol, are independent predictors of cardiovascular events in high-risk populations.

They are also independently associated with cardiovascular disease in the general population, as well as atherosclerotic plaque vulnerability in both mice and humans.

She said that apo A-I antibodies have a metabolic role in vivo, and have been shown in vitro to disrupt cholesterol metabolism, promoting foam cell formation.

Studies have also indicated they play a role in hepatic fibrosis, predicting the development of cirrhosis in individuals with chronic hepatitis C infection.

The team therefore set out to determine the presence of anti–apo A-I antibodies in individuals with NAFLD, defined here as fatty acid levels greater than 5% of liver weight, as well as their effect on hepatic cells.

Working with colleagues at Magna Græcia University of Catanzaro (Italy), they obtained serum samples from 137 patients with NAFLD confirmed on ultrasound.

The patients had an average age of 49 years, and 48.9% were male. The median body mass index was 31.8 kg/m². Cholesterol levels were typically in the intermediate range.

They found that 46% of the participants had anti–apo A-I IgG antibodies, “which is quite high when compared with the 15%-20% positivity that we retrieved from the general population,” Dr. Pagano said.

To explore the link between high anti–apo A-I antibodies and NAFLD, the team studied hepatic cells, treating them with anti–apo A-I IgG antibodies or control IgG antibodies, or leaving them untreated, for 24 hours.

This revealed that anti–apo A-I IgG antibodies were associated with a significant increase in liquid droplet content in hepatic cells, compared with both cells treated with control IgG (P = .0008), and untreated cells (P = .0002).

Next, the team immunized apo E knockout mice with anti–apo A-I or control IgG antibodies. After 16 weeks, they found there was a significant increase in liver lipid content in mice given anti–apo A-I antibodies versus those treated with controls (P = .03).

They then asked whether anti–apo A-I antibodies could affect triglyceride metabolism. They examined the expression of the transcription factor sterol regulatory element binding protein (SREBP) and regulation of the triglyceride and cholesterol pathways.

Treating hepatic cells again for 24 hours with anti–apo A-I IgG antibodies or control IgG antibodies, or leaving them untreated, showed that anti–apo A-I antibodies were associated with “dramatic” increases in the active form of SREBP.

They also found that expression of two key enzymes in the triglyceride pathway, fatty acid synthetase and glycerol phosphate acyltransferase, was substantially decreased in the presence anti–apo A-I antibodies.

In both experiments, the untreated hepatic cells and those exposed to control IgG antibodies showed no significant changes.

“These results suggest that negative feedback ... turns off these enzymes, probably due to the lipid overload that is found in the cells after 24 hours of anti–apo A-I treatment,” Dr. Pagano said.

Finally, the researchers observed that anti–apo A-I, but not control antibodies, were associated with increases in inflammatory markers in liver cells.

Specifically, exposure to the antibodies was linked to an approximately 10-fold increase in interleukin-6 levels, as well as an approximate 25-fold increase in IL-8, and around a 7-fold increase in tumor necrosis factor–alpha.

Dr. Pagano suggested that the inflammatory effects are “probably mediated by binding anti–apo A-I antibodies to toll-like receptor 2, which has been previously described in macrophages.”

No funding was declared. The study authors disclosed no relevant financial relationships.

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

Although recent trial results have established the sodium glucose cotransporter 2 inhibitors dapagliflozin and empagliflozin as a key new part of the recommended multidrug treatment regimen for patients with heart failure with reduced ejection fraction, the current U.S. cost for dapagliflozin means it has merely “intermediate” value when it comes to cost-effectiveness.

adventtr/iStock/Getty Images Plus

A typical regimen with dapagliflozin to treat patients with heart failure with reduced ejection fraction (HFrEF) costs about $474/month or roughly $5,700/year based on Medicare pricing. After factoring in the incremental clinical benefits producing by dapagliflozin seen in the DAPA-HF pivotal trial that helped establish its role, this price produces a cost per quality-adjusted life-year (QALY) gain of about $84,000, which puts dapagliflozin squarely in the intermediate range for value set in 2014 by a task force of the American College of Cardiology and the American Heart Association.

This cost-effectiveness value depends largely on the proven efficacy of dapagliflozin (Farxiga) for decreasing the incidence of cardiovascular death among treated patients with HFrEF, and puts the drug’s value roughly on par with another agent recently approved to treat such patients, sacubitril/valsartan (Entresto), which carries a cost-effectiveness value of about $45,000/QALY.

The U.S. cost per QALY for dapagliflozin treatment of patients with HFrEF dwarfed the value numbers calculated for several other countries that were generally one-tenth this size. This disparity stemmed from both the relatively high price for dapagliflozin in the U.S. compared with other countries – nearly tenfold higher – and relatively higher costs for all types of U.S. medical care, Justin T. Parizo, MD, and coauthors said in a recent report. But the cost, and hence the cost per QALY, of dapagliflozin may soon drop because certain patents on the drug expired in October 2020, added Dr. Parizo, a cardiologist at Stanford (Calif.) University, and associates. Despite the expired patents, as of June 2021 no generic form of dapagliflozin appeared available for U.S. sale.
 

Medicare patients pay about $1,630/year out-of-pocket

“A key caveat” to this finding for dapagliflozin is that being cost-effective “is not by itself a mandate for routine clinical use,” Derek S. Chew, MD, and Daniel B. Mark, MD, said in an editorial that accompanied the report.

A major stumbling block for widespread U.S. prescribing of dapagliflozin to patients with HFrEF is its overall price tag for U.S. patients, estimated at $12 billion/year, as well as an out-of-pocket annual cost for individual Medicare patients of roughly $1,630/year. Adding this out-of-pocket cost to the copay for sacubitril/valsartan and two other much less expensive drug classes that together form the current mainstay, quadruple-drug regimen for HFrEF treatment means a potential annual cost paid by each Medicare patient of about $3,000, wrote Dr. Chew, a cardiologist, and Dr. Mark, a cardiologist and professor, both at Duke University, Durham, N.C.

They cited the precedent of the “unexpectedly slow” and “anemic” uptake of sacubitril/valsartan since its U.S. approval in 2015, a cost-effective agent with “comparable clinical effectiveness” to dapagliflozin. “Even with full inclusion [of sacubitril/valsartan] on formularies and elimination of preapproval requirements, use remains very low, and patient-borne out-of-pocket costs may be a key factor,” wrote Dr. Chew and Dr. Mark. They cited a results from a study that showed abandonment of new prescriptions at retail U.S. pharmacies spiked to a 60% rate when out-of-pocket cost exceeded $500.
 

More than what patients ‘can afford or are willing to spend’

The estimated $3,000-plus total out-of-pocket cost currently borne by some Medicare beneficiaries with HFrEF who have to shell out for both sacubitril/valsartan and dapagliflozin “appears to substantially exceed what many patients with heart failure can afford or are willing to spend,” wrote Dr. Chew and Dr. Mark.

Dr. Parizo and coauthors developed their cost-effectiveness model for dapagliflozin in treating HFrEF using primarily data collected in the DAPA-HF trial, which proved the efficacy of the drug for reducing cardiovascular deaths or acute heart failure events that led to hospitalization or intravenous outpatient treatment in more than 4,700 randomized patients with HFrEF. The trial enrolled roughly similar numbers of patients with or without type 2 diabetes.

The model showed an overall incremental cost-effectiveness ratio of $83,650/QALY, which was about the same regardless of whether patients also had type 2 diabetes. On a more granular level, the cost-effectiveness value estimate was $78,483/QALY in patients with mild health-status impairment due to their heart failure, and $97,608/QALY in patients with moderate impairment, a finding that underscores the importance of starting dapagliflozin treatment early in the course of HFrEF when disease effects are less severe. The analysis could not address value in patients with more advanced heart failure and in New York Heart Association functional class IV because fewer than 1% of patients in DAPA-HF were in this category.

Drug cost was a major determinant of cost-effectiveness. A 50% drop in cost from the Medicare benchmark of $473.64/month resulted in an incremental cost-effectiveness ratio of about $45,000/QALY (putting it into the high-value category based on the 2014 ACC/AHA formula), while a 50% rise in price yielded a value of nearly $123,000/QALY (still in the intermediate range, which spans from $50,000/QALY to $150,000/QALY). No other cost parameters had a meaningful effect on the cost-effectiveness calculation. The analyses also showed that using the basic cost assumptions, treatment with dapagliflozin needs to persist and remain effective for at least 44 months to produce a cost per QALY that’s less than $150,000. The authors stressed that their analysis considered heart failure effects and did not account for added benefit from treatment with dapagliflozin on preservation of renal function.

While it’s indisputable that treatment with dapagliflozin decreases health care costs by, for example, reducing hospitalizations for heart failure, each hospitalization costs just over $12,000, according to the assumptions made by Dr. Parizo and coauthors. But given dapagliflozin’s impact on this outcome, this cost saving translates into about $500/patient during 18 months on treatment (the median duration of treatment in DAPA-HF), which means the savings barely counterbalances the current cost of dapagliflozin treatment for 1 month, noted Dr. Chew and Dr. Mark.

The DAPA-HF trial was sponsored by AstraZeneca, the company that markets dapagliflozin (Farxiga). Dr. Parizo had no disclosures and none of his coauthors had a relationship with AstraZeneca. Dr. Chew had no disclosures. Dr. Mark has received research grants from HeartFlow, Mayo Clinic, and Merck.

mzoler@mdedge.com

Although recent trial results have established the sodium glucose cotransporter 2 inhibitors dapagliflozin and empagliflozin as a key new part of the recommended multidrug treatment regimen for patients with heart failure with reduced ejection fraction, the current U.S. cost for dapagliflozin means it has merely “intermediate” value when it comes to cost-effectiveness.

adventtr/iStock/Getty Images Plus

A typical regimen with dapagliflozin to treat patients with heart failure with reduced ejection fraction (HFrEF) costs about $474/month or roughly $5,700/year based on Medicare pricing. After factoring in the incremental clinical benefits producing by dapagliflozin seen in the DAPA-HF pivotal trial that helped establish its role, this price produces a cost per quality-adjusted life-year (QALY) gain of about $84,000, which puts dapagliflozin squarely in the intermediate range for value set in 2014 by a task force of the American College of Cardiology and the American Heart Association.

This cost-effectiveness value depends largely on the proven efficacy of dapagliflozin (Farxiga) for decreasing the incidence of cardiovascular death among treated patients with HFrEF, and puts the drug’s value roughly on par with another agent recently approved to treat such patients, sacubitril/valsartan (Entresto), which carries a cost-effectiveness value of about $45,000/QALY.

The U.S. cost per QALY for dapagliflozin treatment of patients with HFrEF dwarfed the value numbers calculated for several other countries that were generally one-tenth this size. This disparity stemmed from both the relatively high price for dapagliflozin in the U.S. compared with other countries – nearly tenfold higher – and relatively higher costs for all types of U.S. medical care, Justin T. Parizo, MD, and coauthors said in a recent report. But the cost, and hence the cost per QALY, of dapagliflozin may soon drop because certain patents on the drug expired in October 2020, added Dr. Parizo, a cardiologist at Stanford (Calif.) University, and associates. Despite the expired patents, as of June 2021 no generic form of dapagliflozin appeared available for U.S. sale.
 

Medicare patients pay about $1,630/year out-of-pocket

“A key caveat” to this finding for dapagliflozin is that being cost-effective “is not by itself a mandate for routine clinical use,” Derek S. Chew, MD, and Daniel B. Mark, MD, said in an editorial that accompanied the report.

A major stumbling block for widespread U.S. prescribing of dapagliflozin to patients with HFrEF is its overall price tag for U.S. patients, estimated at $12 billion/year, as well as an out-of-pocket annual cost for individual Medicare patients of roughly $1,630/year. Adding this out-of-pocket cost to the copay for sacubitril/valsartan and two other much less expensive drug classes that together form the current mainstay, quadruple-drug regimen for HFrEF treatment means a potential annual cost paid by each Medicare patient of about $3,000, wrote Dr. Chew, a cardiologist, and Dr. Mark, a cardiologist and professor, both at Duke University, Durham, N.C.

They cited the precedent of the “unexpectedly slow” and “anemic” uptake of sacubitril/valsartan since its U.S. approval in 2015, a cost-effective agent with “comparable clinical effectiveness” to dapagliflozin. “Even with full inclusion [of sacubitril/valsartan] on formularies and elimination of preapproval requirements, use remains very low, and patient-borne out-of-pocket costs may be a key factor,” wrote Dr. Chew and Dr. Mark. They cited a results from a study that showed abandonment of new prescriptions at retail U.S. pharmacies spiked to a 60% rate when out-of-pocket cost exceeded $500.
 

More than what patients ‘can afford or are willing to spend’

The estimated $3,000-plus total out-of-pocket cost currently borne by some Medicare beneficiaries with HFrEF who have to shell out for both sacubitril/valsartan and dapagliflozin “appears to substantially exceed what many patients with heart failure can afford or are willing to spend,” wrote Dr. Chew and Dr. Mark.

Dr. Parizo and coauthors developed their cost-effectiveness model for dapagliflozin in treating HFrEF using primarily data collected in the DAPA-HF trial, which proved the efficacy of the drug for reducing cardiovascular deaths or acute heart failure events that led to hospitalization or intravenous outpatient treatment in more than 4,700 randomized patients with HFrEF. The trial enrolled roughly similar numbers of patients with or without type 2 diabetes.

The model showed an overall incremental cost-effectiveness ratio of $83,650/QALY, which was about the same regardless of whether patients also had type 2 diabetes. On a more granular level, the cost-effectiveness value estimate was $78,483/QALY in patients with mild health-status impairment due to their heart failure, and $97,608/QALY in patients with moderate impairment, a finding that underscores the importance of starting dapagliflozin treatment early in the course of HFrEF when disease effects are less severe. The analysis could not address value in patients with more advanced heart failure and in New York Heart Association functional class IV because fewer than 1% of patients in DAPA-HF were in this category.

Drug cost was a major determinant of cost-effectiveness. A 50% drop in cost from the Medicare benchmark of $473.64/month resulted in an incremental cost-effectiveness ratio of about $45,000/QALY (putting it into the high-value category based on the 2014 ACC/AHA formula), while a 50% rise in price yielded a value of nearly $123,000/QALY (still in the intermediate range, which spans from $50,000/QALY to $150,000/QALY). No other cost parameters had a meaningful effect on the cost-effectiveness calculation. The analyses also showed that using the basic cost assumptions, treatment with dapagliflozin needs to persist and remain effective for at least 44 months to produce a cost per QALY that’s less than $150,000. The authors stressed that their analysis considered heart failure effects and did not account for added benefit from treatment with dapagliflozin on preservation of renal function.

While it’s indisputable that treatment with dapagliflozin decreases health care costs by, for example, reducing hospitalizations for heart failure, each hospitalization costs just over $12,000, according to the assumptions made by Dr. Parizo and coauthors. But given dapagliflozin’s impact on this outcome, this cost saving translates into about $500/patient during 18 months on treatment (the median duration of treatment in DAPA-HF), which means the savings barely counterbalances the current cost of dapagliflozin treatment for 1 month, noted Dr. Chew and Dr. Mark.

The DAPA-HF trial was sponsored by AstraZeneca, the company that markets dapagliflozin (Farxiga). Dr. Parizo had no disclosures and none of his coauthors had a relationship with AstraZeneca. Dr. Chew had no disclosures. Dr. Mark has received research grants from HeartFlow, Mayo Clinic, and Merck.

mzoler@mdedge.com

Although recent trial results have established the sodium glucose cotransporter 2 inhibitors dapagliflozin and empagliflozin as a key new part of the recommended multidrug treatment regimen for patients with heart failure with reduced ejection fraction, the current U.S. cost for dapagliflozin means it has merely “intermediate” value when it comes to cost-effectiveness.

adventtr/iStock/Getty Images Plus

A typical regimen with dapagliflozin to treat patients with heart failure with reduced ejection fraction (HFrEF) costs about $474/month or roughly $5,700/year based on Medicare pricing. After factoring in the incremental clinical benefits producing by dapagliflozin seen in the DAPA-HF pivotal trial that helped establish its role, this price produces a cost per quality-adjusted life-year (QALY) gain of about $84,000, which puts dapagliflozin squarely in the intermediate range for value set in 2014 by a task force of the American College of Cardiology and the American Heart Association.

This cost-effectiveness value depends largely on the proven efficacy of dapagliflozin (Farxiga) for decreasing the incidence of cardiovascular death among treated patients with HFrEF, and puts the drug’s value roughly on par with another agent recently approved to treat such patients, sacubitril/valsartan (Entresto), which carries a cost-effectiveness value of about $45,000/QALY.

The U.S. cost per QALY for dapagliflozin treatment of patients with HFrEF dwarfed the value numbers calculated for several other countries that were generally one-tenth this size. This disparity stemmed from both the relatively high price for dapagliflozin in the U.S. compared with other countries – nearly tenfold higher – and relatively higher costs for all types of U.S. medical care, Justin T. Parizo, MD, and coauthors said in a recent report. But the cost, and hence the cost per QALY, of dapagliflozin may soon drop because certain patents on the drug expired in October 2020, added Dr. Parizo, a cardiologist at Stanford (Calif.) University, and associates. Despite the expired patents, as of June 2021 no generic form of dapagliflozin appeared available for U.S. sale.
 

Medicare patients pay about $1,630/year out-of-pocket

“A key caveat” to this finding for dapagliflozin is that being cost-effective “is not by itself a mandate for routine clinical use,” Derek S. Chew, MD, and Daniel B. Mark, MD, said in an editorial that accompanied the report.

A major stumbling block for widespread U.S. prescribing of dapagliflozin to patients with HFrEF is its overall price tag for U.S. patients, estimated at $12 billion/year, as well as an out-of-pocket annual cost for individual Medicare patients of roughly $1,630/year. Adding this out-of-pocket cost to the copay for sacubitril/valsartan and two other much less expensive drug classes that together form the current mainstay, quadruple-drug regimen for HFrEF treatment means a potential annual cost paid by each Medicare patient of about $3,000, wrote Dr. Chew, a cardiologist, and Dr. Mark, a cardiologist and professor, both at Duke University, Durham, N.C.

They cited the precedent of the “unexpectedly slow” and “anemic” uptake of sacubitril/valsartan since its U.S. approval in 2015, a cost-effective agent with “comparable clinical effectiveness” to dapagliflozin. “Even with full inclusion [of sacubitril/valsartan] on formularies and elimination of preapproval requirements, use remains very low, and patient-borne out-of-pocket costs may be a key factor,” wrote Dr. Chew and Dr. Mark. They cited a results from a study that showed abandonment of new prescriptions at retail U.S. pharmacies spiked to a 60% rate when out-of-pocket cost exceeded $500.
 

More than what patients ‘can afford or are willing to spend’

The estimated $3,000-plus total out-of-pocket cost currently borne by some Medicare beneficiaries with HFrEF who have to shell out for both sacubitril/valsartan and dapagliflozin “appears to substantially exceed what many patients with heart failure can afford or are willing to spend,” wrote Dr. Chew and Dr. Mark.

Dr. Parizo and coauthors developed their cost-effectiveness model for dapagliflozin in treating HFrEF using primarily data collected in the DAPA-HF trial, which proved the efficacy of the drug for reducing cardiovascular deaths or acute heart failure events that led to hospitalization or intravenous outpatient treatment in more than 4,700 randomized patients with HFrEF. The trial enrolled roughly similar numbers of patients with or without type 2 diabetes.

The model showed an overall incremental cost-effectiveness ratio of $83,650/QALY, which was about the same regardless of whether patients also had type 2 diabetes. On a more granular level, the cost-effectiveness value estimate was $78,483/QALY in patients with mild health-status impairment due to their heart failure, and $97,608/QALY in patients with moderate impairment, a finding that underscores the importance of starting dapagliflozin treatment early in the course of HFrEF when disease effects are less severe. The analysis could not address value in patients with more advanced heart failure and in New York Heart Association functional class IV because fewer than 1% of patients in DAPA-HF were in this category.

Drug cost was a major determinant of cost-effectiveness. A 50% drop in cost from the Medicare benchmark of $473.64/month resulted in an incremental cost-effectiveness ratio of about $45,000/QALY (putting it into the high-value category based on the 2014 ACC/AHA formula), while a 50% rise in price yielded a value of nearly $123,000/QALY (still in the intermediate range, which spans from $50,000/QALY to $150,000/QALY). No other cost parameters had a meaningful effect on the cost-effectiveness calculation. The analyses also showed that using the basic cost assumptions, treatment with dapagliflozin needs to persist and remain effective for at least 44 months to produce a cost per QALY that’s less than $150,000. The authors stressed that their analysis considered heart failure effects and did not account for added benefit from treatment with dapagliflozin on preservation of renal function.

While it’s indisputable that treatment with dapagliflozin decreases health care costs by, for example, reducing hospitalizations for heart failure, each hospitalization costs just over $12,000, according to the assumptions made by Dr. Parizo and coauthors. But given dapagliflozin’s impact on this outcome, this cost saving translates into about $500/patient during 18 months on treatment (the median duration of treatment in DAPA-HF), which means the savings barely counterbalances the current cost of dapagliflozin treatment for 1 month, noted Dr. Chew and Dr. Mark.

The DAPA-HF trial was sponsored by AstraZeneca, the company that markets dapagliflozin (Farxiga). Dr. Parizo had no disclosures and none of his coauthors had a relationship with AstraZeneca. Dr. Chew had no disclosures. Dr. Mark has received research grants from HeartFlow, Mayo Clinic, and Merck.

mzoler@mdedge.com

The keys to effective resuscitation in the hospital setting include effective compression and early defibrillation, according to Jessica Nave Allen, MD, FHM, a hospitalist with Emory University Hospital in Atlanta. She spoke about best practices in resuscitation medicine recently at SHM Converge, the annual conference of the Society of Hospital Medicine.

“We know CPR [cardiopulmonary resuscitation] and shocking are the two biggest determinants of outcomes, so really strive to make those chest compressions really high quality,” said Dr. Allen. She urged hospitalists to consider mechanical piston compressions and even “reverse CPR” when appropriate.

Dr. Allen offered several other tips about effective in-hospital resuscitation.
 

Don’t overcrowd the hospital room

There shouldn’t be more than eight people inside the room during a code, she said. If you’re the code leader, “make sure that somebody has already started high-quality chest compressions. You want to make sure that somebody is already on the airway. It’s usually two people, one person to actually hold the mask down to make sure there’s a good seal, and the other person to deliver the breaths.”

Two to three people should be assigned to chest compressions, Dr. Allen said, “and you need one or two nurses for medication delivery and grabbing things from the runners. And then you need to have a recorder and the code leader. Everyone else who’s not in one of those formalized roles needs to be outside the room. That includes the pharmacist, who usually stands at the door if you don’t have a code pharmacist at your institution.”

A helpful mnemonic for the resuscitation process is I(CA)RAMBO, which was developed at Tufts Medical Center and published in 2020, she said. The mnemonic stands for the following:

• I: Identify yourself as code leader.
• CA: Compression, Airway.
• R: Roles (assign roles in the resuscitation).
• A: Access (intravenous access is preferred to intraosseous, per the American Heart Association’s , unless intravenous access is unavailable, Dr. Allen noted).
• M: Monitor (make sure pads are placed correctly; turn the defibrillator on).
• B: Backboard.
• O: Oxygen.

Focus on high-quality chest compressions

The number of chest compressions must be 100-120 per minute, Dr. Allen said. You can time them to the beat of a song, such as “Stayin’ Alive,” or with a metronome, she said, “but whatever it is, you need to stay in that window.”

The correct compression depth is 2-2.4 inches. “That’s very difficult to do during the middle of a code, which is why it’s important to allow full recoil,” she said. “This doesn’t mean taking your hands off of the chest: You should actually never take your hands off of the chest. But you should allow the chest wall to return to its normal state. Also, make sure you aren’t off the chest for more for 10 seconds whenever you’re doing a rhythm check.”

Audiovisual feedback devices can provide insight into the quality of chest compressions. For example, some defibrillators are equipped with sensors that urge users to push harder and faster when appropriate. “Studies have shown that the quality of chest compressions goes up when you use these devices,” she said.
 

Don’t be afraid of mechanical chest compression

Although early research raised questions about the quality of resuscitation outcomes when mechanical piston chest compression devices are used, a 2015 systematic review and meta-analysis found that “man was equal to machine,” Dr. Allen said. “The bottom line is that these devices may be a reasonable alternative to conventional CPR in specific settings.”

American Heart Association guidelines state that mechanical compressions may be appropriate in certain specific situations “where the delivery of high-quality manual compressions may be challenging or dangerous for the provider.”

According to Dr. Allen, “there are times when it’s useful,” such as for a patient with COVID-19, in the cath lab, or in a medical helicopter.
 

Move quickly to defibrillation

“Most of us know that you want to shock as early as possible in shockable rhythms,” Dr. Allen said. Support, she said, comes from a 2008 study that linked delayed defibrillation to lower survival rates. “We want to shock as soon as possible, because your chances of surviving go down for every minute you wait.”

Take special care for patients with confirmed or suspected COVID-19

“Not surprisingly, the goals here are to minimize exposure to staff,” Dr. Allen said.

Put on personal protective equipment before entering the room even if care is delayed, she advised, and reduce the number of staff members in the room below the typical maximum of eight. “In COVID, it should be a maximum of six, and some institutions have even gotten it down to four where the code leaders are outside the room with an iPad.”

Use mechanical compression devices, she advised, and place patients on ventilators as soon as possible. She added: “Use a HEPA [high-efficiency particulate air] filter for all your airway modalities.”

CPR may be challenging in some cases, such as when a large, intubated patient is prone and cannot be quickly or safely flipped over. In those cases, consider posterior chest compressions, also known as reverse CPR, at vertebral positions T7-T10. “We have done reverse CPR on several COVID patients throughout the Emory system,” she said.
 

Debrief right after codes

“You really want to debrief with the code team,” Dr. Allen said. “If you don’t already have a policy in place at your institution, you should help come up with one where you sit down with the team and talk about what could you have done better as a group. It’s not a time to place blame. It’s a time to learn.”

Dr. Allen has disclosed no relevant financial relationships.

This article was updated 7/26/21.

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

The keys to effective resuscitation in the hospital setting include effective compression and early defibrillation, according to Jessica Nave Allen, MD, FHM, a hospitalist with Emory University Hospital in Atlanta. She spoke about best practices in resuscitation medicine recently at SHM Converge, the annual conference of the Society of Hospital Medicine.

“We know CPR [cardiopulmonary resuscitation] and shocking are the two biggest determinants of outcomes, so really strive to make those chest compressions really high quality,” said Dr. Allen. She urged hospitalists to consider mechanical piston compressions and even “reverse CPR” when appropriate.

Dr. Allen offered several other tips about effective in-hospital resuscitation.
 

Don’t overcrowd the hospital room

There shouldn’t be more than eight people inside the room during a code, she said. If you’re the code leader, “make sure that somebody has already started high-quality chest compressions. You want to make sure that somebody is already on the airway. It’s usually two people, one person to actually hold the mask down to make sure there’s a good seal, and the other person to deliver the breaths.”

Two to three people should be assigned to chest compressions, Dr. Allen said, “and you need one or two nurses for medication delivery and grabbing things from the runners. And then you need to have a recorder and the code leader. Everyone else who’s not in one of those formalized roles needs to be outside the room. That includes the pharmacist, who usually stands at the door if you don’t have a code pharmacist at your institution.”

A helpful mnemonic for the resuscitation process is I(CA)RAMBO, which was developed at Tufts Medical Center and published in 2020, she said. The mnemonic stands for the following:

• I: Identify yourself as code leader.
• CA: Compression, Airway.
• R: Roles (assign roles in the resuscitation).
• A: Access (intravenous access is preferred to intraosseous, per the American Heart Association’s , unless intravenous access is unavailable, Dr. Allen noted).
• M: Monitor (make sure pads are placed correctly; turn the defibrillator on).
• B: Backboard.
• O: Oxygen.

Focus on high-quality chest compressions

The number of chest compressions must be 100-120 per minute, Dr. Allen said. You can time them to the beat of a song, such as “Stayin’ Alive,” or with a metronome, she said, “but whatever it is, you need to stay in that window.”

The correct compression depth is 2-2.4 inches. “That’s very difficult to do during the middle of a code, which is why it’s important to allow full recoil,” she said. “This doesn’t mean taking your hands off of the chest: You should actually never take your hands off of the chest. But you should allow the chest wall to return to its normal state. Also, make sure you aren’t off the chest for more for 10 seconds whenever you’re doing a rhythm check.”

Audiovisual feedback devices can provide insight into the quality of chest compressions. For example, some defibrillators are equipped with sensors that urge users to push harder and faster when appropriate. “Studies have shown that the quality of chest compressions goes up when you use these devices,” she said.
 

Don’t be afraid of mechanical chest compression

Although early research raised questions about the quality of resuscitation outcomes when mechanical piston chest compression devices are used, a 2015 systematic review and meta-analysis found that “man was equal to machine,” Dr. Allen said. “The bottom line is that these devices may be a reasonable alternative to conventional CPR in specific settings.”

American Heart Association guidelines state that mechanical compressions may be appropriate in certain specific situations “where the delivery of high-quality manual compressions may be challenging or dangerous for the provider.”

According to Dr. Allen, “there are times when it’s useful,” such as for a patient with COVID-19, in the cath lab, or in a medical helicopter.
 

Move quickly to defibrillation

“Most of us know that you want to shock as early as possible in shockable rhythms,” Dr. Allen said. Support, she said, comes from a 2008 study that linked delayed defibrillation to lower survival rates. “We want to shock as soon as possible, because your chances of surviving go down for every minute you wait.”

Take special care for patients with confirmed or suspected COVID-19

“Not surprisingly, the goals here are to minimize exposure to staff,” Dr. Allen said.

Put on personal protective equipment before entering the room even if care is delayed, she advised, and reduce the number of staff members in the room below the typical maximum of eight. “In COVID, it should be a maximum of six, and some institutions have even gotten it down to four where the code leaders are outside the room with an iPad.”

Use mechanical compression devices, she advised, and place patients on ventilators as soon as possible. She added: “Use a HEPA [high-efficiency particulate air] filter for all your airway modalities.”

CPR may be challenging in some cases, such as when a large, intubated patient is prone and cannot be quickly or safely flipped over. In those cases, consider posterior chest compressions, also known as reverse CPR, at vertebral positions T7-T10. “We have done reverse CPR on several COVID patients throughout the Emory system,” she said.
 

Debrief right after codes

“You really want to debrief with the code team,” Dr. Allen said. “If you don’t already have a policy in place at your institution, you should help come up with one where you sit down with the team and talk about what could you have done better as a group. It’s not a time to place blame. It’s a time to learn.”

Dr. Allen has disclosed no relevant financial relationships.

This article was updated 7/26/21.

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

The keys to effective resuscitation in the hospital setting include effective compression and early defibrillation, according to Jessica Nave Allen, MD, FHM, a hospitalist with Emory University Hospital in Atlanta. She spoke about best practices in resuscitation medicine recently at SHM Converge, the annual conference of the Society of Hospital Medicine.

“We know CPR [cardiopulmonary resuscitation] and shocking are the two biggest determinants of outcomes, so really strive to make those chest compressions really high quality,” said Dr. Allen. She urged hospitalists to consider mechanical piston compressions and even “reverse CPR” when appropriate.

Dr. Allen offered several other tips about effective in-hospital resuscitation.
 

Don’t overcrowd the hospital room

There shouldn’t be more than eight people inside the room during a code, she said. If you’re the code leader, “make sure that somebody has already started high-quality chest compressions. You want to make sure that somebody is already on the airway. It’s usually two people, one person to actually hold the mask down to make sure there’s a good seal, and the other person to deliver the breaths.”

Two to three people should be assigned to chest compressions, Dr. Allen said, “and you need one or two nurses for medication delivery and grabbing things from the runners. And then you need to have a recorder and the code leader. Everyone else who’s not in one of those formalized roles needs to be outside the room. That includes the pharmacist, who usually stands at the door if you don’t have a code pharmacist at your institution.”

A helpful mnemonic for the resuscitation process is I(CA)RAMBO, which was developed at Tufts Medical Center and published in 2020, she said. The mnemonic stands for the following:

• I: Identify yourself as code leader.
• CA: Compression, Airway.
• R: Roles (assign roles in the resuscitation).
• A: Access (intravenous access is preferred to intraosseous, per the American Heart Association’s , unless intravenous access is unavailable, Dr. Allen noted).
• M: Monitor (make sure pads are placed correctly; turn the defibrillator on).
• B: Backboard.
• O: Oxygen.

Focus on high-quality chest compressions

The number of chest compressions must be 100-120 per minute, Dr. Allen said. You can time them to the beat of a song, such as “Stayin’ Alive,” or with a metronome, she said, “but whatever it is, you need to stay in that window.”

The correct compression depth is 2-2.4 inches. “That’s very difficult to do during the middle of a code, which is why it’s important to allow full recoil,” she said. “This doesn’t mean taking your hands off of the chest: You should actually never take your hands off of the chest. But you should allow the chest wall to return to its normal state. Also, make sure you aren’t off the chest for more for 10 seconds whenever you’re doing a rhythm check.”

Audiovisual feedback devices can provide insight into the quality of chest compressions. For example, some defibrillators are equipped with sensors that urge users to push harder and faster when appropriate. “Studies have shown that the quality of chest compressions goes up when you use these devices,” she said.
 

Don’t be afraid of mechanical chest compression

Although early research raised questions about the quality of resuscitation outcomes when mechanical piston chest compression devices are used, a 2015 systematic review and meta-analysis found that “man was equal to machine,” Dr. Allen said. “The bottom line is that these devices may be a reasonable alternative to conventional CPR in specific settings.”

American Heart Association guidelines state that mechanical compressions may be appropriate in certain specific situations “where the delivery of high-quality manual compressions may be challenging or dangerous for the provider.”

According to Dr. Allen, “there are times when it’s useful,” such as for a patient with COVID-19, in the cath lab, or in a medical helicopter.
 

Move quickly to defibrillation

“Most of us know that you want to shock as early as possible in shockable rhythms,” Dr. Allen said. Support, she said, comes from a 2008 study that linked delayed defibrillation to lower survival rates. “We want to shock as soon as possible, because your chances of surviving go down for every minute you wait.”

Take special care for patients with confirmed or suspected COVID-19

“Not surprisingly, the goals here are to minimize exposure to staff,” Dr. Allen said.

Put on personal protective equipment before entering the room even if care is delayed, she advised, and reduce the number of staff members in the room below the typical maximum of eight. “In COVID, it should be a maximum of six, and some institutions have even gotten it down to four where the code leaders are outside the room with an iPad.”

Use mechanical compression devices, she advised, and place patients on ventilators as soon as possible. She added: “Use a HEPA [high-efficiency particulate air] filter for all your airway modalities.”

CPR may be challenging in some cases, such as when a large, intubated patient is prone and cannot be quickly or safely flipped over. In those cases, consider posterior chest compressions, also known as reverse CPR, at vertebral positions T7-T10. “We have done reverse CPR on several COVID patients throughout the Emory system,” she said.
 

Debrief right after codes

“You really want to debrief with the code team,” Dr. Allen said. “If you don’t already have a policy in place at your institution, you should help come up with one where you sit down with the team and talk about what could you have done better as a group. It’s not a time to place blame. It’s a time to learn.”

Dr. Allen has disclosed no relevant financial relationships.

This article was updated 7/26/21.

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

People with prediabetes, defined by having a hemoglobin A1c of 5.7%-6.4%, had a significantly increased rate of atherosclerotic cardiovascular disease events and incident chronic kidney disease in a study of nearly 337,000 people included in the UK Biobank database.

The findings suggest that people with prediabetes have “heightened risk even without progression to type 2 diabetes,” Michael C. Honigberg, MD, said at the annual scientific sessions of the American College of Cardiology.

“Hemoglobin A1c may be better considered as a continuous measure of risk rather than dichotomized” as either less than 6.5%, or 6.5% or higher, the usual threshold defining people with type 2 diabetes, said Dr. Honigberg, a cardiologist at Massachusetts General Hospital in Boston.
 

‘Prediabetes is not a benign entity’

“Our findings reinforce the notion that A1c represents a continuum of risk, with elevated risks observed, especially for atherosclerotic cardiovascular disease [ASCVD], at levels where some clinicians wouldn’t think twice about them. Prediabetes is not a benign entity in the middle-aged population we studied,” Dr. Honigberg said in an interview. “Risks are higher in individuals with type 2 diabetes,” he stressed, “however, prediabetes is so much more common that it appears to confer similar cardio, renal, and metabolic risks at a population level.”

Results from prior observational studies also showed elevated incidence rate of cardiovascular disease events in people with prediabetes, including a 2010 report based on data from about 11,000 U.S. residents, and in a more recent meta-analysis of 129 studies involving more than 10 million people. The new report by Dr. Honigberg “is the first to comprehensively evaluate diverse cardio-renal-metabolic outcomes across a range of A1c levels using a very large, contemporary database,” he noted. In addition, most prior reports did not include chronic kidney disease as an examined outcome.

The primary endpoint examined in the new analysis was the combined incidence during a median follow-up of just over 11 years of ASCVD events (coronary artery disease, ischemic stroke, or peripheral artery disease), CKD, or heart failure among 336,709 adults in the UK Biobank who at baseline had none of these conditions nor type 1 diabetes.

The vast majority, 82%, were normoglycemic at baseline, based on having an A1c of less than 5.7%; 14% had prediabetes, with an A1c of 5.7%-6.4%; and 4% had type 2 diabetes based on an A1c of at least 6.5% or on insulin treatment. Patients averaged about 57 years of age, slightly more than half were women, and average body mass index was in the overweight category except for those with type 2 diabetes.

The primary endpoint, the combined incidence of ASCVD, CKD, and heart failure, was 24% among those with type 2 diabetes, 14% in those with prediabetes, and 8% in those who were normoglycemic at entry. Concurrently with the report, the results appeared online. Most of these events involved ASCVD, which occurred in 11% of those in the prediabetes subgroup (roughly four-fifths of the events in this subgroup), and in 17% of those with type 2 diabetes (nearly three-quarters of the events in this subgroup).

In an analysis that adjusted for more than a dozen demographic and clinical factors, the presence of prediabetes linked with significant increases in the incidence rate of all three outcomes compared with people who were normoglycemic at baseline. The analysis also identified an A1c level of 5.0% as linked with the lowest incidence of each of the three adverse outcomes. And a very granular analysis suggested that a significantly elevated risk for ASCVD first appeared when A1c levels were in the range of 5.4%-5.7%; a significantly increased incidence of CKD became apparent once A1c was in the range of 6.2%-6.5%; and a significantly increased incidence of heart failure began to manifest once A1c levels reached at least 7.0%.

Need for comprehensive cardiometabolic risk management

The findings “highlight the importance of identifying and comprehensively managing cardiometabolic risk in people with prediabetes, including dietary modification, exercise, weight loss and obesity management, smoking cessation, and attention to hypertension and hypercholesterolemia,” Dr. Honigberg said. While these data cannot address the appropriateness of using novel drug interventions in people with prediabetes, they suggest that people with prediabetes should be the focus of future prevention trials testing agents such as sodium-glucose cotransporter 2 inhibitors.

“These data help us discuss risk with patients [with prediabetes], and reemphasize the importance of guideline-directed preventive care,” said Vijay Nambi, MD, PhD, a preventive cardiologist and lipid specialist at Baylor College of Medicine and the Michael E. DeBakey VA Medical Center in Houston, who was not involved with the study.

An additional analysis reported by Dr. Honigberg examined the risk among people with prediabetes who also were current or former smokers and in the top tertile of the prediabetes study population for systolic blood pressure, high non-HDL cholesterol, and C-reactive protein (a marker of inflammation). This very high-risk subgroup of people with prediabetes had incidence rates for ASCVD events and for heart failure that tracked identically to those with type 2 diabetes. However. the incidence rate for CKD in these high-risk people with prediabetes remained below that of patients with type 2 diabetes.

Dr. Honigberg had no disclosures. Dr. Nambi has received research funding from Amgen, Merck, and Roche.

mzoler@mdedge.com

People with prediabetes, defined by having a hemoglobin A1c of 5.7%-6.4%, had a significantly increased rate of atherosclerotic cardiovascular disease events and incident chronic kidney disease in a study of nearly 337,000 people included in the UK Biobank database.

The findings suggest that people with prediabetes have “heightened risk even without progression to type 2 diabetes,” Michael C. Honigberg, MD, said at the annual scientific sessions of the American College of Cardiology.

“Hemoglobin A1c may be better considered as a continuous measure of risk rather than dichotomized” as either less than 6.5%, or 6.5% or higher, the usual threshold defining people with type 2 diabetes, said Dr. Honigberg, a cardiologist at Massachusetts General Hospital in Boston.
 

‘Prediabetes is not a benign entity’

“Our findings reinforce the notion that A1c represents a continuum of risk, with elevated risks observed, especially for atherosclerotic cardiovascular disease [ASCVD], at levels where some clinicians wouldn’t think twice about them. Prediabetes is not a benign entity in the middle-aged population we studied,” Dr. Honigberg said in an interview. “Risks are higher in individuals with type 2 diabetes,” he stressed, “however, prediabetes is so much more common that it appears to confer similar cardio, renal, and metabolic risks at a population level.”

Results from prior observational studies also showed elevated incidence rate of cardiovascular disease events in people with prediabetes, including a 2010 report based on data from about 11,000 U.S. residents, and in a more recent meta-analysis of 129 studies involving more than 10 million people. The new report by Dr. Honigberg “is the first to comprehensively evaluate diverse cardio-renal-metabolic outcomes across a range of A1c levels using a very large, contemporary database,” he noted. In addition, most prior reports did not include chronic kidney disease as an examined outcome.

The primary endpoint examined in the new analysis was the combined incidence during a median follow-up of just over 11 years of ASCVD events (coronary artery disease, ischemic stroke, or peripheral artery disease), CKD, or heart failure among 336,709 adults in the UK Biobank who at baseline had none of these conditions nor type 1 diabetes.

The vast majority, 82%, were normoglycemic at baseline, based on having an A1c of less than 5.7%; 14% had prediabetes, with an A1c of 5.7%-6.4%; and 4% had type 2 diabetes based on an A1c of at least 6.5% or on insulin treatment. Patients averaged about 57 years of age, slightly more than half were women, and average body mass index was in the overweight category except for those with type 2 diabetes.

The primary endpoint, the combined incidence of ASCVD, CKD, and heart failure, was 24% among those with type 2 diabetes, 14% in those with prediabetes, and 8% in those who were normoglycemic at entry. Concurrently with the report, the results appeared online. Most of these events involved ASCVD, which occurred in 11% of those in the prediabetes subgroup (roughly four-fifths of the events in this subgroup), and in 17% of those with type 2 diabetes (nearly three-quarters of the events in this subgroup).

In an analysis that adjusted for more than a dozen demographic and clinical factors, the presence of prediabetes linked with significant increases in the incidence rate of all three outcomes compared with people who were normoglycemic at baseline. The analysis also identified an A1c level of 5.0% as linked with the lowest incidence of each of the three adverse outcomes. And a very granular analysis suggested that a significantly elevated risk for ASCVD first appeared when A1c levels were in the range of 5.4%-5.7%; a significantly increased incidence of CKD became apparent once A1c was in the range of 6.2%-6.5%; and a significantly increased incidence of heart failure began to manifest once A1c levels reached at least 7.0%.

Need for comprehensive cardiometabolic risk management

The findings “highlight the importance of identifying and comprehensively managing cardiometabolic risk in people with prediabetes, including dietary modification, exercise, weight loss and obesity management, smoking cessation, and attention to hypertension and hypercholesterolemia,” Dr. Honigberg said. While these data cannot address the appropriateness of using novel drug interventions in people with prediabetes, they suggest that people with prediabetes should be the focus of future prevention trials testing agents such as sodium-glucose cotransporter 2 inhibitors.

“These data help us discuss risk with patients [with prediabetes], and reemphasize the importance of guideline-directed preventive care,” said Vijay Nambi, MD, PhD, a preventive cardiologist and lipid specialist at Baylor College of Medicine and the Michael E. DeBakey VA Medical Center in Houston, who was not involved with the study.

An additional analysis reported by Dr. Honigberg examined the risk among people with prediabetes who also were current or former smokers and in the top tertile of the prediabetes study population for systolic blood pressure, high non-HDL cholesterol, and C-reactive protein (a marker of inflammation). This very high-risk subgroup of people with prediabetes had incidence rates for ASCVD events and for heart failure that tracked identically to those with type 2 diabetes. However. the incidence rate for CKD in these high-risk people with prediabetes remained below that of patients with type 2 diabetes.

Dr. Honigberg had no disclosures. Dr. Nambi has received research funding from Amgen, Merck, and Roche.

mzoler@mdedge.com

People with prediabetes, defined by having a hemoglobin A1c of 5.7%-6.4%, had a significantly increased rate of atherosclerotic cardiovascular disease events and incident chronic kidney disease in a study of nearly 337,000 people included in the UK Biobank database.

The findings suggest that people with prediabetes have “heightened risk even without progression to type 2 diabetes,” Michael C. Honigberg, MD, said at the annual scientific sessions of the American College of Cardiology.

“Hemoglobin A1c may be better considered as a continuous measure of risk rather than dichotomized” as either less than 6.5%, or 6.5% or higher, the usual threshold defining people with type 2 diabetes, said Dr. Honigberg, a cardiologist at Massachusetts General Hospital in Boston.
 

‘Prediabetes is not a benign entity’

“Our findings reinforce the notion that A1c represents a continuum of risk, with elevated risks observed, especially for atherosclerotic cardiovascular disease [ASCVD], at levels where some clinicians wouldn’t think twice about them. Prediabetes is not a benign entity in the middle-aged population we studied,” Dr. Honigberg said in an interview. “Risks are higher in individuals with type 2 diabetes,” he stressed, “however, prediabetes is so much more common that it appears to confer similar cardio, renal, and metabolic risks at a population level.”

Results from prior observational studies also showed elevated incidence rate of cardiovascular disease events in people with prediabetes, including a 2010 report based on data from about 11,000 U.S. residents, and in a more recent meta-analysis of 129 studies involving more than 10 million people. The new report by Dr. Honigberg “is the first to comprehensively evaluate diverse cardio-renal-metabolic outcomes across a range of A1c levels using a very large, contemporary database,” he noted. In addition, most prior reports did not include chronic kidney disease as an examined outcome.

The primary endpoint examined in the new analysis was the combined incidence during a median follow-up of just over 11 years of ASCVD events (coronary artery disease, ischemic stroke, or peripheral artery disease), CKD, or heart failure among 336,709 adults in the UK Biobank who at baseline had none of these conditions nor type 1 diabetes.

The vast majority, 82%, were normoglycemic at baseline, based on having an A1c of less than 5.7%; 14% had prediabetes, with an A1c of 5.7%-6.4%; and 4% had type 2 diabetes based on an A1c of at least 6.5% or on insulin treatment. Patients averaged about 57 years of age, slightly more than half were women, and average body mass index was in the overweight category except for those with type 2 diabetes.

The primary endpoint, the combined incidence of ASCVD, CKD, and heart failure, was 24% among those with type 2 diabetes, 14% in those with prediabetes, and 8% in those who were normoglycemic at entry. Concurrently with the report, the results appeared online. Most of these events involved ASCVD, which occurred in 11% of those in the prediabetes subgroup (roughly four-fifths of the events in this subgroup), and in 17% of those with type 2 diabetes (nearly three-quarters of the events in this subgroup).

In an analysis that adjusted for more than a dozen demographic and clinical factors, the presence of prediabetes linked with significant increases in the incidence rate of all three outcomes compared with people who were normoglycemic at baseline. The analysis also identified an A1c level of 5.0% as linked with the lowest incidence of each of the three adverse outcomes. And a very granular analysis suggested that a significantly elevated risk for ASCVD first appeared when A1c levels were in the range of 5.4%-5.7%; a significantly increased incidence of CKD became apparent once A1c was in the range of 6.2%-6.5%; and a significantly increased incidence of heart failure began to manifest once A1c levels reached at least 7.0%.

Need for comprehensive cardiometabolic risk management

The findings “highlight the importance of identifying and comprehensively managing cardiometabolic risk in people with prediabetes, including dietary modification, exercise, weight loss and obesity management, smoking cessation, and attention to hypertension and hypercholesterolemia,” Dr. Honigberg said. While these data cannot address the appropriateness of using novel drug interventions in people with prediabetes, they suggest that people with prediabetes should be the focus of future prevention trials testing agents such as sodium-glucose cotransporter 2 inhibitors.

“These data help us discuss risk with patients [with prediabetes], and reemphasize the importance of guideline-directed preventive care,” said Vijay Nambi, MD, PhD, a preventive cardiologist and lipid specialist at Baylor College of Medicine and the Michael E. DeBakey VA Medical Center in Houston, who was not involved with the study.

An additional analysis reported by Dr. Honigberg examined the risk among people with prediabetes who also were current or former smokers and in the top tertile of the prediabetes study population for systolic blood pressure, high non-HDL cholesterol, and C-reactive protein (a marker of inflammation). This very high-risk subgroup of people with prediabetes had incidence rates for ASCVD events and for heart failure that tracked identically to those with type 2 diabetes. However. the incidence rate for CKD in these high-risk people with prediabetes remained below that of patients with type 2 diabetes.

Dr. Honigberg had no disclosures. Dr. Nambi has received research funding from Amgen, Merck, and Roche.

mzoler@mdedge.com

Myocarditis is present in a small percentage of competitive athletes after COVID-19 infection, even in those without symptoms, new research suggests.

In a cohort study of 1,597 competitive collegiate athletes undergoing comprehensive cardiovascular testing in the United States, the prevalence of clinical myocarditis based on a symptom-based screening strategy was only 0.31%.

But screening with cardiac MRI increased the prevalence of clinical and subclinical myocarditis by a factor of 7.4, to 2.3%, the authors reported.

The findings are published online May 27, 2021, in JAMA Cardiology.

“It was the largest study to evaluate college athletes who have had COVID with extensive cardiac testing, including MRI, and this gave us a very objective look at the cardiac findings, as they were not purely based upon a subjective evaluation of symptoms,” lead investigator Curt J. Daniels, MD, professor at Ohio State University Wexner Medical Center, Columbus, said in an interview.

“Unfortunately, our study showed that athletes can be asymptomatic, or at least not report symptoms. This is a very subjective feature, and we don’t know if they don’t report symptoms because they didn’t want to get tested. That is why we took a very objective approach,” Dr. Daniels said.

The finding that more than half of the asymptomatic athletes had myocarditis, or as the investigators called it, “subclinical myocarditis,” was a surprise, he acknowledged.

“More than half of the athletes found to have myocarditis reported no symptoms, and yes, that was a surprise, because prior to this study, the protocols that had been published stated that you had to have symptoms to even enter into the protocol for cardiac MRI. But, as our ... paper shows, if we had followed that protocol, we only would have found about 5 cases of myocarditis, as opposed to the total of 37 we found with cardiac MRI,” Dr. Daniels said.

In October 2020, the American College of Cardiology’s Sports and Exercise Council recommended that cardiac MRI be limited to athletes who exhibited symptoms as part of their guide to ensuring a safe return to play.

As reported by this news organization the council recommended a tiered approach to screening based on the presence of symptoms, followed by electrocardiography, injury biomarkers, and echocardiography. Any abnormalities detected were to be further characterized by the selective use of cardiac MRI.

At the time, there were relatively few data to support the recommendations, and all stakeholders called for larger datasets to better drive informed recommendations in the future.

In the current study, Dr. Daniels and associates conducted comprehensive cardiac screening – including ECG, troponin testing, echocardiography, and cardiac MRI – of 1,597 college athlete survivors of COVID-19.

The athletes were part of the Big Ten athletic conference, which consists of 13 major American universities.

AlexLMX/Getty Images

Cardiac MRI revealed that 37 (2.3%) of these athletes demonstrated diagnostic criteria for COVID-19 myocarditis; of these, 20 had no cardiovascular symptoms and had normal ECGs, echocardiography, and troponin test results.

“These patients would not have been identified without CMR imaging. If we were going according to the older protocol, we would not have made this discovery. Cardiac MRI is the most sensitive and specific test for myocardial inflammation, there is no argument about that,” Dr. Daniels said.

The catch is, cardiac MRI is expensive and often difficult to access, especially in remote, rural, or other underserviced areas.

“You can’t get an MRI for every person who has had COVID, it’s just not feasible,” Dr. Daniels said. “We are not advocating that everybody get an MRI. But we do hope that our study creates awareness among clinicians and athletes themselves that if you’ve had COVID, even if you’re asymptomatic, there may be some heart changes. So be aware when you start to exercise again, if you have any symptoms, pause and seek medical care.”
 

Kudos to the sports cardiology community

In an accompanying editorial, James E. Udelson, MD, Ethan J. Rowin, MD, and Barry J. Maron, MD, from the CardioVascular Center at Tufts Medical Center, Boston, applauded the sports cardiology community for its diligence in acquiring and publishing data about the post–COVID-19 prevalence of cardiac abnormalities in competitive athletes.

“It is a real tribute to the sports cardiology community. There has been an amazing growth of information, and they not only gathered this information, they analyzed and published it, starting out with a study of 29 or 30 athletes, and now thousands,” Dr. Udelson said in an interview.

At the start of the pandemic, it appeared that 15%-20% of athletes had myocarditis, and athletic conferences were discussing canceling sports events.

However, with greater numbers comes a more accurate picture of the extent of the problem.

“Once you get thousands of subjects in these studies, you can hone in on what the real number is, so now we understand that if you screen everybody with a cardiac MRI, 1%, 2%, or 3% will have some evidence of what looks like myocarditis,” he said.

Dr. Udelson agreed that doing cardiac imaging in everyone is not feasible.

“This study looked at a very large number of people who all had an MRI, but that doesn’t mean everyone should have them. If you just do an echo, an EKG, and a troponin test, and if everything is normal, which is kind of what current recommendations are, this paper tells us that we are going to miss one or two people out of a hundred, and that might be okay,” he said. “So, if you are at a huge university that has a large medical center and you want to screen all your athletes with MRI, great. But if you’re at a high school in a remote area, you know that the alternative, not having an MRI, isn’t so bad, either.”

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

Myocarditis is present in a small percentage of competitive athletes after COVID-19 infection, even in those without symptoms, new research suggests.

In a cohort study of 1,597 competitive collegiate athletes undergoing comprehensive cardiovascular testing in the United States, the prevalence of clinical myocarditis based on a symptom-based screening strategy was only 0.31%.

But screening with cardiac MRI increased the prevalence of clinical and subclinical myocarditis by a factor of 7.4, to 2.3%, the authors reported.

The findings are published online May 27, 2021, in JAMA Cardiology.

“It was the largest study to evaluate college athletes who have had COVID with extensive cardiac testing, including MRI, and this gave us a very objective look at the cardiac findings, as they were not purely based upon a subjective evaluation of symptoms,” lead investigator Curt J. Daniels, MD, professor at Ohio State University Wexner Medical Center, Columbus, said in an interview.

“Unfortunately, our study showed that athletes can be asymptomatic, or at least not report symptoms. This is a very subjective feature, and we don’t know if they don’t report symptoms because they didn’t want to get tested. That is why we took a very objective approach,” Dr. Daniels said.

The finding that more than half of the asymptomatic athletes had myocarditis, or as the investigators called it, “subclinical myocarditis,” was a surprise, he acknowledged.

“More than half of the athletes found to have myocarditis reported no symptoms, and yes, that was a surprise, because prior to this study, the protocols that had been published stated that you had to have symptoms to even enter into the protocol for cardiac MRI. But, as our ... paper shows, if we had followed that protocol, we only would have found about 5 cases of myocarditis, as opposed to the total of 37 we found with cardiac MRI,” Dr. Daniels said.

In October 2020, the American College of Cardiology’s Sports and Exercise Council recommended that cardiac MRI be limited to athletes who exhibited symptoms as part of their guide to ensuring a safe return to play.

As reported by this news organization the council recommended a tiered approach to screening based on the presence of symptoms, followed by electrocardiography, injury biomarkers, and echocardiography. Any abnormalities detected were to be further characterized by the selective use of cardiac MRI.

At the time, there were relatively few data to support the recommendations, and all stakeholders called for larger datasets to better drive informed recommendations in the future.

In the current study, Dr. Daniels and associates conducted comprehensive cardiac screening – including ECG, troponin testing, echocardiography, and cardiac MRI – of 1,597 college athlete survivors of COVID-19.

The athletes were part of the Big Ten athletic conference, which consists of 13 major American universities.

AlexLMX/Getty Images

Cardiac MRI revealed that 37 (2.3%) of these athletes demonstrated diagnostic criteria for COVID-19 myocarditis; of these, 20 had no cardiovascular symptoms and had normal ECGs, echocardiography, and troponin test results.

“These patients would not have been identified without CMR imaging. If we were going according to the older protocol, we would not have made this discovery. Cardiac MRI is the most sensitive and specific test for myocardial inflammation, there is no argument about that,” Dr. Daniels said.

The catch is, cardiac MRI is expensive and often difficult to access, especially in remote, rural, or other underserviced areas.

“You can’t get an MRI for every person who has had COVID, it’s just not feasible,” Dr. Daniels said. “We are not advocating that everybody get an MRI. But we do hope that our study creates awareness among clinicians and athletes themselves that if you’ve had COVID, even if you’re asymptomatic, there may be some heart changes. So be aware when you start to exercise again, if you have any symptoms, pause and seek medical care.”
 

Kudos to the sports cardiology community

In an accompanying editorial, James E. Udelson, MD, Ethan J. Rowin, MD, and Barry J. Maron, MD, from the CardioVascular Center at Tufts Medical Center, Boston, applauded the sports cardiology community for its diligence in acquiring and publishing data about the post–COVID-19 prevalence of cardiac abnormalities in competitive athletes.

“It is a real tribute to the sports cardiology community. There has been an amazing growth of information, and they not only gathered this information, they analyzed and published it, starting out with a study of 29 or 30 athletes, and now thousands,” Dr. Udelson said in an interview.

At the start of the pandemic, it appeared that 15%-20% of athletes had myocarditis, and athletic conferences were discussing canceling sports events.

However, with greater numbers comes a more accurate picture of the extent of the problem.

“Once you get thousands of subjects in these studies, you can hone in on what the real number is, so now we understand that if you screen everybody with a cardiac MRI, 1%, 2%, or 3% will have some evidence of what looks like myocarditis,” he said.

Dr. Udelson agreed that doing cardiac imaging in everyone is not feasible.

“This study looked at a very large number of people who all had an MRI, but that doesn’t mean everyone should have them. If you just do an echo, an EKG, and a troponin test, and if everything is normal, which is kind of what current recommendations are, this paper tells us that we are going to miss one or two people out of a hundred, and that might be okay,” he said. “So, if you are at a huge university that has a large medical center and you want to screen all your athletes with MRI, great. But if you’re at a high school in a remote area, you know that the alternative, not having an MRI, isn’t so bad, either.”

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

Myocarditis is present in a small percentage of competitive athletes after COVID-19 infection, even in those without symptoms, new research suggests.

In a cohort study of 1,597 competitive collegiate athletes undergoing comprehensive cardiovascular testing in the United States, the prevalence of clinical myocarditis based on a symptom-based screening strategy was only 0.31%.

But screening with cardiac MRI increased the prevalence of clinical and subclinical myocarditis by a factor of 7.4, to 2.3%, the authors reported.

The findings are published online May 27, 2021, in JAMA Cardiology.

“It was the largest study to evaluate college athletes who have had COVID with extensive cardiac testing, including MRI, and this gave us a very objective look at the cardiac findings, as they were not purely based upon a subjective evaluation of symptoms,” lead investigator Curt J. Daniels, MD, professor at Ohio State University Wexner Medical Center, Columbus, said in an interview.

“Unfortunately, our study showed that athletes can be asymptomatic, or at least not report symptoms. This is a very subjective feature, and we don’t know if they don’t report symptoms because they didn’t want to get tested. That is why we took a very objective approach,” Dr. Daniels said.

The finding that more than half of the asymptomatic athletes had myocarditis, or as the investigators called it, “subclinical myocarditis,” was a surprise, he acknowledged.

“More than half of the athletes found to have myocarditis reported no symptoms, and yes, that was a surprise, because prior to this study, the protocols that had been published stated that you had to have symptoms to even enter into the protocol for cardiac MRI. But, as our ... paper shows, if we had followed that protocol, we only would have found about 5 cases of myocarditis, as opposed to the total of 37 we found with cardiac MRI,” Dr. Daniels said.

In October 2020, the American College of Cardiology’s Sports and Exercise Council recommended that cardiac MRI be limited to athletes who exhibited symptoms as part of their guide to ensuring a safe return to play.

As reported by this news organization the council recommended a tiered approach to screening based on the presence of symptoms, followed by electrocardiography, injury biomarkers, and echocardiography. Any abnormalities detected were to be further characterized by the selective use of cardiac MRI.

At the time, there were relatively few data to support the recommendations, and all stakeholders called for larger datasets to better drive informed recommendations in the future.

In the current study, Dr. Daniels and associates conducted comprehensive cardiac screening – including ECG, troponin testing, echocardiography, and cardiac MRI – of 1,597 college athlete survivors of COVID-19.

The athletes were part of the Big Ten athletic conference, which consists of 13 major American universities.

AlexLMX/Getty Images

Cardiac MRI revealed that 37 (2.3%) of these athletes demonstrated diagnostic criteria for COVID-19 myocarditis; of these, 20 had no cardiovascular symptoms and had normal ECGs, echocardiography, and troponin test results.

“These patients would not have been identified without CMR imaging. If we were going according to the older protocol, we would not have made this discovery. Cardiac MRI is the most sensitive and specific test for myocardial inflammation, there is no argument about that,” Dr. Daniels said.

The catch is, cardiac MRI is expensive and often difficult to access, especially in remote, rural, or other underserviced areas.

“You can’t get an MRI for every person who has had COVID, it’s just not feasible,” Dr. Daniels said. “We are not advocating that everybody get an MRI. But we do hope that our study creates awareness among clinicians and athletes themselves that if you’ve had COVID, even if you’re asymptomatic, there may be some heart changes. So be aware when you start to exercise again, if you have any symptoms, pause and seek medical care.”
 

Kudos to the sports cardiology community

In an accompanying editorial, James E. Udelson, MD, Ethan J. Rowin, MD, and Barry J. Maron, MD, from the CardioVascular Center at Tufts Medical Center, Boston, applauded the sports cardiology community for its diligence in acquiring and publishing data about the post–COVID-19 prevalence of cardiac abnormalities in competitive athletes.

“It is a real tribute to the sports cardiology community. There has been an amazing growth of information, and they not only gathered this information, they analyzed and published it, starting out with a study of 29 or 30 athletes, and now thousands,” Dr. Udelson said in an interview.

At the start of the pandemic, it appeared that 15%-20% of athletes had myocarditis, and athletic conferences were discussing canceling sports events.

However, with greater numbers comes a more accurate picture of the extent of the problem.

“Once you get thousands of subjects in these studies, you can hone in on what the real number is, so now we understand that if you screen everybody with a cardiac MRI, 1%, 2%, or 3% will have some evidence of what looks like myocarditis,” he said.

Dr. Udelson agreed that doing cardiac imaging in everyone is not feasible.

“This study looked at a very large number of people who all had an MRI, but that doesn’t mean everyone should have them. If you just do an echo, an EKG, and a troponin test, and if everything is normal, which is kind of what current recommendations are, this paper tells us that we are going to miss one or two people out of a hundred, and that might be okay,” he said. “So, if you are at a huge university that has a large medical center and you want to screen all your athletes with MRI, great. But if you’re at a high school in a remote area, you know that the alternative, not having an MRI, isn’t so bad, either.”

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

Pericardial fat is associated with a heightened risk for heart failure, particularly in women, new research suggests.

In a prospective cohort study of nearly 7,000 individuals, excess pericardial fat was linked to a higher risk for heart failure, even after adjustment for established risk factors for heart failure.

Women with high pericardial fat volume (PFV), defined as more than 70 cm³ or 2.4 fluid ounces, had double the risk of developing heart failure. For men, high PFV, defined as more than 120 cm³ or 4.0 fluid ounces, was associated with a 50% increase in the risk for heart failure.

The findings were published in the Journal of the American College of Cardiology.

“People will ask why should they measure fat around the heart. Why can’t they just take the waist circumference or body mass index as a measure for increased risk?” lead author Satish Kenchaiah, MD, MPH, Icahn School of Medicine at Mount Sinai, New York, said in an interview.

“Yet, when we adjusted for waist circumference, hip circumference, waist to hip ratio, and other known variables, pericardial fat was still associated with an increased risk of heart failure. This tells me that it is not just overall fat in the body but something about its location around the heart that is playing a role,” Dr. Kenchaiah said.

“Now that we have found an association between any amount of fat around the pericardium and heart failure, it gives us an impetus to build future research on identifying how exactly these fat deposits influence the development of cardiomyopathy,” he said.

Dr. Kenchaiah and colleagues investigated the association of pericardial fat with incident heart failure by examining chest CT scans from 6,785 participants (3,584 women and 3,201 men aged 45-84 years) in the Multi-Ethnic Study of Atherosclerosis.

The participants were from four different ethnic groups: 38% were White; 28% were Black, 22% were Hispanic, and 12% were Chinese American. They were recruited between July 17, 2000, and Aug. 31, 2002, from six communities in the United States: Baltimore and Baltimore County; Chicago; Forsyth County, N.C.; Los Angeles County northern Manhattan and the Bronx, New York; and St. Paul, Minn.

All participants were free of cardiovascular disease at baseline.

The researchers followed participants for more than 17 years. During this time, 385 (5.7%; 164 women and 221 men) developed newly diagnosed heart failure.

In women, the hazard ratio for every 42 cm³ increase in PFV was 1.44 (95% confidence interval, 1.21-1.71; P < .001). In men, the HR was 1.13 (95% CI, 1.01-1.27; P = .03).

High PVF conferred a twofold greater risk for heart failure in women (HR, 2.06; 95% CI, 1.48-2.87; P < .001) and a 53% higher risk in men (HR, 1.53; 95% CI, 1.13-2.07; P = .006).

These associations remained significant after further adjustment for circulating markers of systemic inflammation (that is, C-reactive protein and interleukin-6), and abdominal subcutaneous or visceral fat.

They also found that the heightened risk persisted, even after adjustment for established risk factors for heart failure, such as age, cigarette smoking, alcohol consumption, sedentary lifestyle, high blood pressure, high blood sugar, high cholesterol, and myocardial infarction.

Results were similar among all of the ethnic groups studied.
 

A surprise finding

“The most surprising part of this study was that the risk for heart failure with increased pericardial fat does not seem to be explained by obesity and systemic inflammation alone,” Andreas P. Kalogeropoulos, MD, MPH, PhD, Stony Brook (N.Y.) University, said in an interview.

“If pericardial fat was merely a proxy for increased visceral fat, one would expect the association of pericardial fat with heart failure risk to go away after factoring in abdominal CT findings, which was not the case here. Also, accounting for inflammatory markers did not change things dramatically. However, we need to be careful here, as abdominal CT scans have not been done simultaneously with the pericardial fat scans in the study,” said Dr. Kalogeropoulos, who coauthored an accompanying editorial with Michael E. Hall, MD, University of Mississippi Medical Center, Jackson.

The other striking finding, although not entirely surprising, was the stronger association of pericardial fat with heart failure risk in women, he noted.

“Although several clues have been reported pointing to women being more sensitive to the adverse cardiac effects of pericardial fat, this is the first large prospective study to connect the dots and show much higher risk in women in a convincing way. For the record, this is the first prospective study to show the connection between pericardial fat and heart failure risk altogether,” Dr. Kalogeropoulos said.

“Obviously, we need to do more work to see how we can use the important findings of Kenchaiah and colleagues to reduce risk for heart failure among patients with increased pericardial fat, especially women. For starters, we would need a way to identify these patients,” he said. “In this aspect, it is encouraging that pericardial fat can be measured in low-radiation CT scans, similar to those used for coronary calcium, and that automation technology to speed up pericardial fat measurements is already in the pipeline.

“The next step would be to see what kind of interventions would reduce risk for heart failure in these patients,” he added. “Weight loss would be an obvious thing, but novel agents with favorable cardiometabolic effects, like newer antidiabetic medications, are intriguing options, too.”

The study was supported by the National Heart, Lung, and Blood Institute and the National Institutes of Health. Dr. Kenchaiah and Dr. Kalogeropoulos reported no relevant financial relationships.

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

Pericardial fat is associated with a heightened risk for heart failure, particularly in women, new research suggests.

In a prospective cohort study of nearly 7,000 individuals, excess pericardial fat was linked to a higher risk for heart failure, even after adjustment for established risk factors for heart failure.

Women with high pericardial fat volume (PFV), defined as more than 70 cm³ or 2.4 fluid ounces, had double the risk of developing heart failure. For men, high PFV, defined as more than 120 cm³ or 4.0 fluid ounces, was associated with a 50% increase in the risk for heart failure.

The findings were published in the Journal of the American College of Cardiology.

“People will ask why should they measure fat around the heart. Why can’t they just take the waist circumference or body mass index as a measure for increased risk?” lead author Satish Kenchaiah, MD, MPH, Icahn School of Medicine at Mount Sinai, New York, said in an interview.

“Yet, when we adjusted for waist circumference, hip circumference, waist to hip ratio, and other known variables, pericardial fat was still associated with an increased risk of heart failure. This tells me that it is not just overall fat in the body but something about its location around the heart that is playing a role,” Dr. Kenchaiah said.

“Now that we have found an association between any amount of fat around the pericardium and heart failure, it gives us an impetus to build future research on identifying how exactly these fat deposits influence the development of cardiomyopathy,” he said.

Dr. Kenchaiah and colleagues investigated the association of pericardial fat with incident heart failure by examining chest CT scans from 6,785 participants (3,584 women and 3,201 men aged 45-84 years) in the Multi-Ethnic Study of Atherosclerosis.

The participants were from four different ethnic groups: 38% were White; 28% were Black, 22% were Hispanic, and 12% were Chinese American. They were recruited between July 17, 2000, and Aug. 31, 2002, from six communities in the United States: Baltimore and Baltimore County; Chicago; Forsyth County, N.C.; Los Angeles County northern Manhattan and the Bronx, New York; and St. Paul, Minn.

All participants were free of cardiovascular disease at baseline.

The researchers followed participants for more than 17 years. During this time, 385 (5.7%; 164 women and 221 men) developed newly diagnosed heart failure.

In women, the hazard ratio for every 42 cm³ increase in PFV was 1.44 (95% confidence interval, 1.21-1.71; P < .001). In men, the HR was 1.13 (95% CI, 1.01-1.27; P = .03).

High PVF conferred a twofold greater risk for heart failure in women (HR, 2.06; 95% CI, 1.48-2.87; P < .001) and a 53% higher risk in men (HR, 1.53; 95% CI, 1.13-2.07; P = .006).

These associations remained significant after further adjustment for circulating markers of systemic inflammation (that is, C-reactive protein and interleukin-6), and abdominal subcutaneous or visceral fat.

They also found that the heightened risk persisted, even after adjustment for established risk factors for heart failure, such as age, cigarette smoking, alcohol consumption, sedentary lifestyle, high blood pressure, high blood sugar, high cholesterol, and myocardial infarction.

Results were similar among all of the ethnic groups studied.
 

A surprise finding

“The most surprising part of this study was that the risk for heart failure with increased pericardial fat does not seem to be explained by obesity and systemic inflammation alone,” Andreas P. Kalogeropoulos, MD, MPH, PhD, Stony Brook (N.Y.) University, said in an interview.

“If pericardial fat was merely a proxy for increased visceral fat, one would expect the association of pericardial fat with heart failure risk to go away after factoring in abdominal CT findings, which was not the case here. Also, accounting for inflammatory markers did not change things dramatically. However, we need to be careful here, as abdominal CT scans have not been done simultaneously with the pericardial fat scans in the study,” said Dr. Kalogeropoulos, who coauthored an accompanying editorial with Michael E. Hall, MD, University of Mississippi Medical Center, Jackson.

The other striking finding, although not entirely surprising, was the stronger association of pericardial fat with heart failure risk in women, he noted.

“Although several clues have been reported pointing to women being more sensitive to the adverse cardiac effects of pericardial fat, this is the first large prospective study to connect the dots and show much higher risk in women in a convincing way. For the record, this is the first prospective study to show the connection between pericardial fat and heart failure risk altogether,” Dr. Kalogeropoulos said.

“Obviously, we need to do more work to see how we can use the important findings of Kenchaiah and colleagues to reduce risk for heart failure among patients with increased pericardial fat, especially women. For starters, we would need a way to identify these patients,” he said. “In this aspect, it is encouraging that pericardial fat can be measured in low-radiation CT scans, similar to those used for coronary calcium, and that automation technology to speed up pericardial fat measurements is already in the pipeline.

“The next step would be to see what kind of interventions would reduce risk for heart failure in these patients,” he added. “Weight loss would be an obvious thing, but novel agents with favorable cardiometabolic effects, like newer antidiabetic medications, are intriguing options, too.”

The study was supported by the National Heart, Lung, and Blood Institute and the National Institutes of Health. Dr. Kenchaiah and Dr. Kalogeropoulos reported no relevant financial relationships.

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

Pericardial fat is associated with a heightened risk for heart failure, particularly in women, new research suggests.

In a prospective cohort study of nearly 7,000 individuals, excess pericardial fat was linked to a higher risk for heart failure, even after adjustment for established risk factors for heart failure.

Women with high pericardial fat volume (PFV), defined as more than 70 cm³ or 2.4 fluid ounces, had double the risk of developing heart failure. For men, high PFV, defined as more than 120 cm³ or 4.0 fluid ounces, was associated with a 50% increase in the risk for heart failure.

The findings were published in the Journal of the American College of Cardiology.

“People will ask why should they measure fat around the heart. Why can’t they just take the waist circumference or body mass index as a measure for increased risk?” lead author Satish Kenchaiah, MD, MPH, Icahn School of Medicine at Mount Sinai, New York, said in an interview.

“Yet, when we adjusted for waist circumference, hip circumference, waist to hip ratio, and other known variables, pericardial fat was still associated with an increased risk of heart failure. This tells me that it is not just overall fat in the body but something about its location around the heart that is playing a role,” Dr. Kenchaiah said.

“Now that we have found an association between any amount of fat around the pericardium and heart failure, it gives us an impetus to build future research on identifying how exactly these fat deposits influence the development of cardiomyopathy,” he said.

Dr. Kenchaiah and colleagues investigated the association of pericardial fat with incident heart failure by examining chest CT scans from 6,785 participants (3,584 women and 3,201 men aged 45-84 years) in the Multi-Ethnic Study of Atherosclerosis.

The participants were from four different ethnic groups: 38% were White; 28% were Black, 22% were Hispanic, and 12% were Chinese American. They were recruited between July 17, 2000, and Aug. 31, 2002, from six communities in the United States: Baltimore and Baltimore County; Chicago; Forsyth County, N.C.; Los Angeles County northern Manhattan and the Bronx, New York; and St. Paul, Minn.

All participants were free of cardiovascular disease at baseline.

The researchers followed participants for more than 17 years. During this time, 385 (5.7%; 164 women and 221 men) developed newly diagnosed heart failure.

In women, the hazard ratio for every 42 cm³ increase in PFV was 1.44 (95% confidence interval, 1.21-1.71; P < .001). In men, the HR was 1.13 (95% CI, 1.01-1.27; P = .03).

High PVF conferred a twofold greater risk for heart failure in women (HR, 2.06; 95% CI, 1.48-2.87; P < .001) and a 53% higher risk in men (HR, 1.53; 95% CI, 1.13-2.07; P = .006).

These associations remained significant after further adjustment for circulating markers of systemic inflammation (that is, C-reactive protein and interleukin-6), and abdominal subcutaneous or visceral fat.

They also found that the heightened risk persisted, even after adjustment for established risk factors for heart failure, such as age, cigarette smoking, alcohol consumption, sedentary lifestyle, high blood pressure, high blood sugar, high cholesterol, and myocardial infarction.

Results were similar among all of the ethnic groups studied.
 

A surprise finding

“The most surprising part of this study was that the risk for heart failure with increased pericardial fat does not seem to be explained by obesity and systemic inflammation alone,” Andreas P. Kalogeropoulos, MD, MPH, PhD, Stony Brook (N.Y.) University, said in an interview.

“If pericardial fat was merely a proxy for increased visceral fat, one would expect the association of pericardial fat with heart failure risk to go away after factoring in abdominal CT findings, which was not the case here. Also, accounting for inflammatory markers did not change things dramatically. However, we need to be careful here, as abdominal CT scans have not been done simultaneously with the pericardial fat scans in the study,” said Dr. Kalogeropoulos, who coauthored an accompanying editorial with Michael E. Hall, MD, University of Mississippi Medical Center, Jackson.

The other striking finding, although not entirely surprising, was the stronger association of pericardial fat with heart failure risk in women, he noted.

“Although several clues have been reported pointing to women being more sensitive to the adverse cardiac effects of pericardial fat, this is the first large prospective study to connect the dots and show much higher risk in women in a convincing way. For the record, this is the first prospective study to show the connection between pericardial fat and heart failure risk altogether,” Dr. Kalogeropoulos said.

“Obviously, we need to do more work to see how we can use the important findings of Kenchaiah and colleagues to reduce risk for heart failure among patients with increased pericardial fat, especially women. For starters, we would need a way to identify these patients,” he said. “In this aspect, it is encouraging that pericardial fat can be measured in low-radiation CT scans, similar to those used for coronary calcium, and that automation technology to speed up pericardial fat measurements is already in the pipeline.

“The next step would be to see what kind of interventions would reduce risk for heart failure in these patients,” he added. “Weight loss would be an obvious thing, but novel agents with favorable cardiometabolic effects, like newer antidiabetic medications, are intriguing options, too.”

The study was supported by the National Heart, Lung, and Blood Institute and the National Institutes of Health. Dr. Kenchaiah and Dr. Kalogeropoulos reported no relevant financial relationships.

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

The American Association of Clinical Endocrinology (AACE) has issued its first-ever official guidelines addressing the use of advanced technologies in the management of people with diabetes.

They were presented on May 28 at the annual scientific & clinical congress of the American Association of Clinical Endocrinologists and simultaneously published in Endocrine Practice.

Previous AACE guidance on the clinical use of insulin pumps and CGM over the past decade has been published in the form of consensus or position statements rather than official evidence-based guidelines, task force cochair George Grunberger, MD, of the Grunberger Diabetes Institute, Bloomfield Hills, Mich., explained.

“There’s never really been, until now, hardcore evidence, [with] peer-reviewed, quality trials published in the literature to go after the evidence that is required for guidelines. ... This is not an opinion piece or position statement.”

The problem with that strict approach to “guidelines” is how quickly the diabetes technology field is evolving, he acknowledged. “It’s frustrating because we know what’s [coming up], but we can’t put it in a guideline because it hasn’t been published yet.”

In an AACE podcast, Dr. Grunberger said the guidelines will likely become a “living” document, along the lines of the American Diabetes Association’s annual Standards of Care, as “any cutoff date is arbitrary. More and more papers will be published on these technologies. ... This is certainly not a static field.”

In the meantime, task force cochair and author Jennifer Sherr, MD, PhD, a pediatric endocrinologist, said she hopes the guidelines will help to reduce insurance company barriers to use of the currently available technologies.

“I am very hopeful that these guidelines will also encourage payers to change their stance. And I think that we as a community can continue to advocate and inform them of these guidelines so they can appropriately change their coverage practices,” added Dr. Sherr, of Yale University, New Haven, Conn.
 

Recommendations address CGM, pumps, and connected systems

In the guidelines, CGM is “strongly recommended for all persons with diabetes treated with intensive insulin therapy, defined as three or more injections of insulin per day or the use of an insulin pump.” For those with diabetes who use CGM, “priority metrics” include a “time in range” of greater than 70% from 14 days of active use. Targets for mean glucose should be individualized, with glycemic variability 36% or lower.

Further specific CGM target metrics are given for people with type 1 diabetes, older/high risk individuals, and for pregnant women. The recommendations align with those issued in a 2019 joint consensus statement on CGM time-in-range endorsed by several organizations, including AACE.    

In response to an audience question about whether AACE is advising that time-in-range replace A1c for glycemia assessment, Dr. Sherr responded: “I think currently we’re not in a position where we can completely replace A1c with time in range. However, I’m hopeful that in future years we’ll see further data gathered ... to allow for that recommendation to occur.”

For now, she said, “What we really want to hone in on in the guidelines is that time-in-range and use of CGM truly allow clinicians to better understand how to optimize care for their persons with diabetes. It gives us a better picture. It’s not just a number of whether we’re hitting target. It tells us whether we need to attack time above range or time below range. So we really think it’s critical for clinical care.”

The document also provides specifics about real-time versus intermittently scanned CGM and use of diagnostic/professional CGM.

The “insulin delivery technologies” section covers use of connected pens, insulin pumps without CGM, insulin pumps with separate CGM, and the more advanced combined insulin pump-CGM systems including those with low-glucose suspend, predictive low-glucose suspend, and hybrid closed-loops (sometimes called the artificial pancreas).

In general, these automated insulin delivery systems (artificial pancreas), “are strongly recommended for all persons with [type 1 diabetes], since their use has been shown to increase time in range, especially in the overnight period, without causing an increased risk of hypoglycemia,” Dr. Sherr observed.
 

Other tech topics: Apps, telemedicine, and safety

The new guidelines say that “clinically validated” smartphone apps should be recommended to help teach or reinforce diabetes self-management skills and provide support and encouragement for healthy behaviors around food and exercise.

Dr. Grunberger pointed out: “As we know, there are tons of apps out there, and patients are using them. The problem is that very few of them have actually been validated in clinical trials in published peer-reviewed [journals].”

He recommended a joint statement on diabetes apps from the American Diabetes Association and the European Association for the Study of Diabetes that was initially discussed at the 2019 EASD meeting, as reported by this news organization, and subsequently published in January 2020 in Diabetes Care and Diabetologia.

“Telemedicine, including periodic phone calls, smartphone-web interactions ... by health care professionals ... is strongly recommended to treat persons with diabetes, provide diabetes education, remotely monitor glucose and/or insulin data to indicate the need for therapy adjustments, and improve diabetes-related outcomes/control with better engagement,” the document says.

Safety concerns addressed include the issue of certain medications interfering with CGM [readings] ... including acetaminophen, high-dose vitamin C, and hydroxyurea, as well as cautions about what to do in the event of device malfunction and assessing that the patient is sufficiently trained in proper device use. Criteria for insulin pump discontinuation are also given.
 

Implementation: Who will be prescribing? ‘This is not for amateurs’

A final section on implementation recommends that “initiation and use of diabetes technology should be implemented by health care professionals who are trained, committed, and experienced to prescribe and direct the use of these tools. Clinicians should have the infrastructure to support the needs of persons with diabetes using the technology.”

Dr. Grunberger commented: “I think the key is going to be who should be doing this? What is the role of a clinical endocrinologist in the future? What is our responsibility, [since] we don’t have the manpower and womanpower to take care of all these people as these technologies advance? It’s our responsibility to provide these hopefully valued recommendations as a resource for those who want to know more about it.”

However, he noted, “This is not for amateurs. If you want to actually use this in your practice, you need the infrastructure, the expertise, the training, the dedication, and the energy to be there for the patients all the time ... This clinical practice guideline is a foundation.”

Dr. Sherr added: “To me, it’s really thinking about ... changing our mindset from who is an appropriate candidate to who can benefit and how vast a group that entails ... I’m hopeful that we will see more technology use through continued conversations with our patients with diabetes, and hopefully through more clinicians being excited to be part of this revolution.”

Dr. Grunberger has reported being on speakers bureaus for Eli Lilly, Novo Nordisk, and Abbott. Dr. Sherr has reported being a consultant and speaker for Lilly and Medtronic Diabetes, a consultant for Insulet and Sanofi, and on advisory boards for Bigfoot Biomedical, Cecelia Health, Insulet, JDRF T1D fund, and Medtronic.

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

The American Association of Clinical Endocrinology (AACE) has issued its first-ever official guidelines addressing the use of advanced technologies in the management of people with diabetes.

They were presented on May 28 at the annual scientific & clinical congress of the American Association of Clinical Endocrinologists and simultaneously published in Endocrine Practice.

Previous AACE guidance on the clinical use of insulin pumps and CGM over the past decade has been published in the form of consensus or position statements rather than official evidence-based guidelines, task force cochair George Grunberger, MD, of the Grunberger Diabetes Institute, Bloomfield Hills, Mich., explained.

“There’s never really been, until now, hardcore evidence, [with] peer-reviewed, quality trials published in the literature to go after the evidence that is required for guidelines. ... This is not an opinion piece or position statement.”

The problem with that strict approach to “guidelines” is how quickly the diabetes technology field is evolving, he acknowledged. “It’s frustrating because we know what’s [coming up], but we can’t put it in a guideline because it hasn’t been published yet.”

In an AACE podcast, Dr. Grunberger said the guidelines will likely become a “living” document, along the lines of the American Diabetes Association’s annual Standards of Care, as “any cutoff date is arbitrary. More and more papers will be published on these technologies. ... This is certainly not a static field.”

In the meantime, task force cochair and author Jennifer Sherr, MD, PhD, a pediatric endocrinologist, said she hopes the guidelines will help to reduce insurance company barriers to use of the currently available technologies.

“I am very hopeful that these guidelines will also encourage payers to change their stance. And I think that we as a community can continue to advocate and inform them of these guidelines so they can appropriately change their coverage practices,” added Dr. Sherr, of Yale University, New Haven, Conn.
 

Recommendations address CGM, pumps, and connected systems

In the guidelines, CGM is “strongly recommended for all persons with diabetes treated with intensive insulin therapy, defined as three or more injections of insulin per day or the use of an insulin pump.” For those with diabetes who use CGM, “priority metrics” include a “time in range” of greater than 70% from 14 days of active use. Targets for mean glucose should be individualized, with glycemic variability 36% or lower.

Further specific CGM target metrics are given for people with type 1 diabetes, older/high risk individuals, and for pregnant women. The recommendations align with those issued in a 2019 joint consensus statement on CGM time-in-range endorsed by several organizations, including AACE.    

In response to an audience question about whether AACE is advising that time-in-range replace A1c for glycemia assessment, Dr. Sherr responded: “I think currently we’re not in a position where we can completely replace A1c with time in range. However, I’m hopeful that in future years we’ll see further data gathered ... to allow for that recommendation to occur.”

For now, she said, “What we really want to hone in on in the guidelines is that time-in-range and use of CGM truly allow clinicians to better understand how to optimize care for their persons with diabetes. It gives us a better picture. It’s not just a number of whether we’re hitting target. It tells us whether we need to attack time above range or time below range. So we really think it’s critical for clinical care.”

The document also provides specifics about real-time versus intermittently scanned CGM and use of diagnostic/professional CGM.

The “insulin delivery technologies” section covers use of connected pens, insulin pumps without CGM, insulin pumps with separate CGM, and the more advanced combined insulin pump-CGM systems including those with low-glucose suspend, predictive low-glucose suspend, and hybrid closed-loops (sometimes called the artificial pancreas).

In general, these automated insulin delivery systems (artificial pancreas), “are strongly recommended for all persons with [type 1 diabetes], since their use has been shown to increase time in range, especially in the overnight period, without causing an increased risk of hypoglycemia,” Dr. Sherr observed.
 

Other tech topics: Apps, telemedicine, and safety

The new guidelines say that “clinically validated” smartphone apps should be recommended to help teach or reinforce diabetes self-management skills and provide support and encouragement for healthy behaviors around food and exercise.

Dr. Grunberger pointed out: “As we know, there are tons of apps out there, and patients are using them. The problem is that very few of them have actually been validated in clinical trials in published peer-reviewed [journals].”

He recommended a joint statement on diabetes apps from the American Diabetes Association and the European Association for the Study of Diabetes that was initially discussed at the 2019 EASD meeting, as reported by this news organization, and subsequently published in January 2020 in Diabetes Care and Diabetologia.

“Telemedicine, including periodic phone calls, smartphone-web interactions ... by health care professionals ... is strongly recommended to treat persons with diabetes, provide diabetes education, remotely monitor glucose and/or insulin data to indicate the need for therapy adjustments, and improve diabetes-related outcomes/control with better engagement,” the document says.

Safety concerns addressed include the issue of certain medications interfering with CGM [readings] ... including acetaminophen, high-dose vitamin C, and hydroxyurea, as well as cautions about what to do in the event of device malfunction and assessing that the patient is sufficiently trained in proper device use. Criteria for insulin pump discontinuation are also given.
 

Implementation: Who will be prescribing? ‘This is not for amateurs’

A final section on implementation recommends that “initiation and use of diabetes technology should be implemented by health care professionals who are trained, committed, and experienced to prescribe and direct the use of these tools. Clinicians should have the infrastructure to support the needs of persons with diabetes using the technology.”

Dr. Grunberger commented: “I think the key is going to be who should be doing this? What is the role of a clinical endocrinologist in the future? What is our responsibility, [since] we don’t have the manpower and womanpower to take care of all these people as these technologies advance? It’s our responsibility to provide these hopefully valued recommendations as a resource for those who want to know more about it.”

However, he noted, “This is not for amateurs. If you want to actually use this in your practice, you need the infrastructure, the expertise, the training, the dedication, and the energy to be there for the patients all the time ... This clinical practice guideline is a foundation.”

Dr. Sherr added: “To me, it’s really thinking about ... changing our mindset from who is an appropriate candidate to who can benefit and how vast a group that entails ... I’m hopeful that we will see more technology use through continued conversations with our patients with diabetes, and hopefully through more clinicians being excited to be part of this revolution.”

Dr. Grunberger has reported being on speakers bureaus for Eli Lilly, Novo Nordisk, and Abbott. Dr. Sherr has reported being a consultant and speaker for Lilly and Medtronic Diabetes, a consultant for Insulet and Sanofi, and on advisory boards for Bigfoot Biomedical, Cecelia Health, Insulet, JDRF T1D fund, and Medtronic.

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

The American Association of Clinical Endocrinology (AACE) has issued its first-ever official guidelines addressing the use of advanced technologies in the management of people with diabetes.

They were presented on May 28 at the annual scientific & clinical congress of the American Association of Clinical Endocrinologists and simultaneously published in Endocrine Practice.

Previous AACE guidance on the clinical use of insulin pumps and CGM over the past decade has been published in the form of consensus or position statements rather than official evidence-based guidelines, task force cochair George Grunberger, MD, of the Grunberger Diabetes Institute, Bloomfield Hills, Mich., explained.

“There’s never really been, until now, hardcore evidence, [with] peer-reviewed, quality trials published in the literature to go after the evidence that is required for guidelines. ... This is not an opinion piece or position statement.”

The problem with that strict approach to “guidelines” is how quickly the diabetes technology field is evolving, he acknowledged. “It’s frustrating because we know what’s [coming up], but we can’t put it in a guideline because it hasn’t been published yet.”

In an AACE podcast, Dr. Grunberger said the guidelines will likely become a “living” document, along the lines of the American Diabetes Association’s annual Standards of Care, as “any cutoff date is arbitrary. More and more papers will be published on these technologies. ... This is certainly not a static field.”

In the meantime, task force cochair and author Jennifer Sherr, MD, PhD, a pediatric endocrinologist, said she hopes the guidelines will help to reduce insurance company barriers to use of the currently available technologies.

“I am very hopeful that these guidelines will also encourage payers to change their stance. And I think that we as a community can continue to advocate and inform them of these guidelines so they can appropriately change their coverage practices,” added Dr. Sherr, of Yale University, New Haven, Conn.
 

Recommendations address CGM, pumps, and connected systems

In the guidelines, CGM is “strongly recommended for all persons with diabetes treated with intensive insulin therapy, defined as three or more injections of insulin per day or the use of an insulin pump.” For those with diabetes who use CGM, “priority metrics” include a “time in range” of greater than 70% from 14 days of active use. Targets for mean glucose should be individualized, with glycemic variability 36% or lower.

Further specific CGM target metrics are given for people with type 1 diabetes, older/high risk individuals, and for pregnant women. The recommendations align with those issued in a 2019 joint consensus statement on CGM time-in-range endorsed by several organizations, including AACE.    

In response to an audience question about whether AACE is advising that time-in-range replace A1c for glycemia assessment, Dr. Sherr responded: “I think currently we’re not in a position where we can completely replace A1c with time in range. However, I’m hopeful that in future years we’ll see further data gathered ... to allow for that recommendation to occur.”

For now, she said, “What we really want to hone in on in the guidelines is that time-in-range and use of CGM truly allow clinicians to better understand how to optimize care for their persons with diabetes. It gives us a better picture. It’s not just a number of whether we’re hitting target. It tells us whether we need to attack time above range or time below range. So we really think it’s critical for clinical care.”

The document also provides specifics about real-time versus intermittently scanned CGM and use of diagnostic/professional CGM.

The “insulin delivery technologies” section covers use of connected pens, insulin pumps without CGM, insulin pumps with separate CGM, and the more advanced combined insulin pump-CGM systems including those with low-glucose suspend, predictive low-glucose suspend, and hybrid closed-loops (sometimes called the artificial pancreas).

In general, these automated insulin delivery systems (artificial pancreas), “are strongly recommended for all persons with [type 1 diabetes], since their use has been shown to increase time in range, especially in the overnight period, without causing an increased risk of hypoglycemia,” Dr. Sherr observed.
 

Other tech topics: Apps, telemedicine, and safety

The new guidelines say that “clinically validated” smartphone apps should be recommended to help teach or reinforce diabetes self-management skills and provide support and encouragement for healthy behaviors around food and exercise.

Dr. Grunberger pointed out: “As we know, there are tons of apps out there, and patients are using them. The problem is that very few of them have actually been validated in clinical trials in published peer-reviewed [journals].”

He recommended a joint statement on diabetes apps from the American Diabetes Association and the European Association for the Study of Diabetes that was initially discussed at the 2019 EASD meeting, as reported by this news organization, and subsequently published in January 2020 in Diabetes Care and Diabetologia.

“Telemedicine, including periodic phone calls, smartphone-web interactions ... by health care professionals ... is strongly recommended to treat persons with diabetes, provide diabetes education, remotely monitor glucose and/or insulin data to indicate the need for therapy adjustments, and improve diabetes-related outcomes/control with better engagement,” the document says.

Safety concerns addressed include the issue of certain medications interfering with CGM [readings] ... including acetaminophen, high-dose vitamin C, and hydroxyurea, as well as cautions about what to do in the event of device malfunction and assessing that the patient is sufficiently trained in proper device use. Criteria for insulin pump discontinuation are also given.
 

Implementation: Who will be prescribing? ‘This is not for amateurs’

A final section on implementation recommends that “initiation and use of diabetes technology should be implemented by health care professionals who are trained, committed, and experienced to prescribe and direct the use of these tools. Clinicians should have the infrastructure to support the needs of persons with diabetes using the technology.”

Dr. Grunberger commented: “I think the key is going to be who should be doing this? What is the role of a clinical endocrinologist in the future? What is our responsibility, [since] we don’t have the manpower and womanpower to take care of all these people as these technologies advance? It’s our responsibility to provide these hopefully valued recommendations as a resource for those who want to know more about it.”

However, he noted, “This is not for amateurs. If you want to actually use this in your practice, you need the infrastructure, the expertise, the training, the dedication, and the energy to be there for the patients all the time ... This clinical practice guideline is a foundation.”

Dr. Sherr added: “To me, it’s really thinking about ... changing our mindset from who is an appropriate candidate to who can benefit and how vast a group that entails ... I’m hopeful that we will see more technology use through continued conversations with our patients with diabetes, and hopefully through more clinicians being excited to be part of this revolution.”

Dr. Grunberger has reported being on speakers bureaus for Eli Lilly, Novo Nordisk, and Abbott. Dr. Sherr has reported being a consultant and speaker for Lilly and Medtronic Diabetes, a consultant for Insulet and Sanofi, and on advisory boards for Bigfoot Biomedical, Cecelia Health, Insulet, JDRF T1D fund, and Medtronic.

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