Arrhythmias & EP

One year ago, as the sun was setting on a late fall day, Andrés Snitcofsky, a 40-year-old designer from Buenos Aires, Argentina, heard harrowing cries for help. It was the niece and the wife of one of his neighbors: a man in his 60s who the women had found “passed out” in the bedroom. While they were all waiting for the ambulance, Mr. Snitcofsky went over, tilted the man’s head back, and confirmed that he wasn’t breathing, that he wasn’t choking. And then he started chest compressions, just like he’d learned in a CPR class he’d taken 2 decades earlier. “I did CPR for 5 minutes straight until a friend of the victim came in and asked me to stop, telling me that the man had probably been dead for 2 or 3 hours already. But I had no idea because I’d never seen a dead body before,” Mr. Snitcofsky told this news organization. A few minutes later, the ambulance arrived. The doctor confirmed that there was nothing more that could be done.

Mr. Snitcofsky went home. Nobody had asked for his name or address or phone number. … And it wasn’t because they already knew who he was. In fact, there wasn’t any sort of relationship there. Mr. Snitcofsky had only known his neighbors by sight. His actions that day, however, “did not come without a cost. It took me weeks – months, actually – to put myself together again,” he said. The things he saw, the things he heard, everything about that night played over and over in his head. “I had trouble sleeping. I would play out different scenarios in my head. I questioned myself. I second-guessed myself, criticized myself. It’s like some taboo subject. There’s no one to share the experience with, no one who gets it. But with time, I was able to process the event.

“For 2 months, I talked to my psychologist about it all,” he continued. “That really helped me a lot. In addition to therapy, I reached out to a couple I know – they’re both physicians – and to a firefighter who teaches CPR. Their insight and guidance allowed me to get to a point where I was able to understand that what I did was a good thing and that what I did was all that could have been done. But anyone who finds themselves in the position of having to do CPR – they’re going to be affected in many, many ways. It goes beyond the euphoria of seeing a person come back to life. Of that, I’m quite certain.”

We’ve all seen campaigns encouraging people to learn CPR and to be prepared if the need arises. But in training the public (and even health care professionals), not much, if anything, is said about the “collateral damage”: the psychological and emotional consequences of carrying out the procedure. These especially come into play when you don’t know whether the person survived, when your efforts weren’t able to reverse the sudden cardiac arrest, or when the person you gave CPR to was a loved one – a case that may entail immediate therapeutic interventions to minimize or prevent the risk of suffering long-lasting trauma.

In May 2020, popular American activist and educator Kristin Flanary saw someone suffering cardiac arrest. She stepped in and started doing CPR. And she continued doing CPR … for 10 long minutes. The person she was trying to save was her 34-year-old husband, ophthalmologist and comedian Will Flanary. On Twitter, where she’s known as Lady Glaucomflecken, Ms. Flanary recently shared the following message, putting the topic of CPR and automated external defibrillator training front and center.

“Yes, everyone should learn #CPRandAED. But if we are going to ask people to perform such a brutal task, it’s imperative that we also provide them with the info and resources they need to process it mentally and emotionally. It’s traumatic and life changing. It’s irresponsible and unethical to ask people to help in such a brutal and traumatic way and then neglect to help them in return.” In less than a month, the tweet has racked up over 200,000 views.
 

Doing one’s duty

There are many people who work to promote CPR and strengthen the other links in the chain of survival for out-of-hospital sudden cardiac arrest, such as prompt access to and delivery of early defibrillation. According to them, any negative psychological impact of intervening is temporary and, when compared with the satisfaction of having done one’s duty, quite insignificant – even if the efforts to save a person’s life are not successful.

“In 99.9% of cases, people who have performed CPR feel a sense of satisfaction, even happiness, knowing that they’ve helped. The individuals I’ve spoken with, I’ve never heard any of them say that they felt worse after the event or that they needed to see a psychologist,” said Mario Fitz Maurice, MD, director of the Arrhythmia Council of the Argentine Society of Cardiology and head of Electrophysiology at Rivadavia Hospital in Buenos Aires. He went on to tell this news organization, “Of course, some degree of fear, sadness, or melancholy can remain afterward. But it seems to me, and there are reports saying as much, that, in the end, what stands out in the person’s mind is the fact that they tried to save a life. And for them, there’s joy in knowing this.”

Dr. Fitz Maurice, who is also the director of the National Arrhythmia Institute in Buenos Aires, pointed out that the kind of person who takes CPR classes “has a profile that’s going to allow them to be psychologically involved; they’re the caring person, the one who’s ready and willing to help people.” And he added that, at his hospital, if they can identify the individuals or first responders who have done CPR on a patient, the protocol is to always contact them to offer psychological care and assistance. “But in 99% of cases, they don’t even understand why we’re calling them, they’re extremely happy to have taken part.”

Some studies, though, paint a much different picture, one that shows that providing CPR can be emotionally challenging and have consequences in terms of one’s family and work life. A qualitative study published in 2016 looked into the experiences of 20 lay rescuers in Norway – five were health educated – who had provided CPR to 18 out-of-hospital cardiac arrest (OHCA) victims, 66% of whom survived. The time from experiencing the OHCA incident to participating in the interview ranged from 6 days to 13 years (median 5.5 years). Several participants reported the OHCA incident as a “shocking and terrifying” experience. Tiredness, exhaustion, confusion, and feeling alone about the OHCA experience were individual reactions that could vary in time from days to months. Anxiety and insomnia were also experienced following the incident.

Some lay rescuers described the influence on work and family life, and a few of them described deep sorrow, even several years after the incident. Overall, they reported repetitive self-criticism regarding whether they could have carried out anything else to achieve a better outcome for the cardiac arrest victim. All of them wanted to be informed about the outcome. And four of the lay rescuers needed professional counseling to process the OHCA experience.

In 2020, another qualitative study was conducted, this time in Taiwan. There were nine participants, none of whom were health professionals. Each had provided initial CPR and defibrillation with AED in public locations. Event-to-interview duration was within 1 year and 1-2 years. The major findings from the study were the following:

• The lay rescuers possessed helping traits and high motivation.  
• The lay rescuers reported certain aspects of rescue reality that differed much from prior training and expectations, including difficulty in the depth of chest compression, and uncertainties in real emergency situations.
• The lay rescuers gained positive personal fulfillment in sharing their experience and receiving positive feedback from others, and were willing to help next time, although they experienced a short-term negative psychological impact from the event.
“Measures should be taken to increase [a] layperson’s confidence and situation awareness, to reduce training-reality discrepancy, and to build up a support system to avoid negative psychological effects.” This was the conclusion of the study team, which was led by Matthew Huei-Ming Ma, MD, PhD. A professor in the department of emergency medicine at National Taiwan University in Taipei, he is also on the board of directors of the Resuscitation Council of Asia.

Potential trauma

In recalling his experience, Mr. Snitcofsky said, “The hardest part of it all was the moment that I stopped giving CPR, that moment of letting go. This became the image that kept coming back to me, the traumatic moment I hadn’t thought about.”

Psychiatrist Daniel Mosca, MD, is the founder and former president of the Argentine Society of Trauma Psychology. He is also the coordinator of the human factors team at the City of Buenos Aires Emergency Medical Care System. “Any event has the potential to be traumatic, all the more so when it’s an event where you come face to face with death and uncertainty. But how a rescuer reacts will depend on their psychological makeup.” Of the individuals who were held for months or years in the jungle as hostages of the Revolutionary Armed Forces of Colombia, “only” half developed symptoms of posttraumatic stress disorder.

Dr. Mosca believes that a comment by Frank Ochberg, MD, speaks to this finding. “In many cases, peritraumatic symptoms are a normal person’s normal response to an abnormal situation.” For a lot of people who have found themselves having to perform CPR, the symptoms associated with the initial acute stress reaction will resolve on their own in 30-90 days. “But if this doesn’t happen, and those symptoms persist, psychotherapeutic or pharmacological intervention will be necessary,” he noted.

“In CPR classes, it would be good for the instructors to talk about the warning signs that people should look out for in themselves and their fellow rescuers. So, for example, insomnia, anxiety, a heightened state of alertness, feeling disconnected from reality,” Dr. Mosca told this news organization.

“Another thing that can help rescuers is letting them know what happened to the person they gave CPR to. This way, they can get closure,” suggested Manlio Márquez Murillo, MD, a cardiologist and electrophysiologist in Mexico. He is also the coordinator of the Alliance Against Sudden Cardiac Death at the Interamerican Society of Cardiology.

“Medical and nursing societies would have to develop a brief protocol or performance standard. The goal would be to ensure that rescuers are asked for their contact information and that someone gets in touch to debrief them and to offer them care. Next would come the treatment part, to resolve any remaining aftereffects,” said in an interview.

For example, a three-stage Lay Responder Support Model (LRSM) was developed and implemented as part of a lay responder support program established in 2014 by the Peel Regional Council in Ontario. The LRSM identifies and engages individuals who witnessed or participated directly or indirectly in an OHCA, inviting them to participate in a debriefing session facilitated by a trained practitioner. Held 24-48 hours post event, the debriefing allows lay responders to contextualize their reaction to the event. The conversation also serves as an opportunity for them to fully articulate their concerns, questions, and thoughts. The facilitator can communicate stress reduction techniques and address psychological first aid needs as they emerge. Approximately 1 week post event, a secondary follow-up occurs. If the lay responder communicates a continuing struggle with symptoms impacting and interfering with everyday life, the facilitator offers a coordinated or facilitated referral for mental health support.

In an article published in the Journal of Cardiac Failure. Ms. Flanary speaks about the three kinds of language that anyone who was either forced to or inspired to perform CPR can use to help process their trauma: words that explain what happened, words that name (eg, “forgotten patients”), and words that validate the experience and allow the person to articulate their feelings. The tools and technologies that organizations and health care professionals provide can help the healing process. Empathy and compassion, too, have a place.

But there are virtually no standardized and proactive initiatives of this kind in much of the world, including Latin America. So, most people who just happened to be in the right place at the right time find that they have to navigate the “after” part all on their own.
 

Other obstacles

Dr. Márquez Murillo finds it unfortunate that countries in the region have yet to enact “Good Samaritan” laws. If individuals render aid to someone suffering cardiac arrest, then these laws would ensure that they will not be held liable in any way. This is the case in Argentina and Uruguay. So, the fear of things turning into a legal matter may be holding people back from taking action; that fear could also create additional stress for those who end up stepping in to help.

Even with the legal safeguards, exceptional circumstances may arise where rescuers find themselves facing unexpected emotional challenges. In Argentina, Virginia Pérez Antonelli, the 17-year-old who tried in vain to save the life of Fernando Báez Sosa, had to testify at the trial of the eight defendants accused of brutally beating him in January 2020. The press, the public – the attention of an entire country – was focused on her. She had to respond to the defense attorneys who were able to ask whether she was sure that she performed the CPR maneuvers correctly. And a few weeks ago, a medical examiner hired by the defense suggested that “the CPR may have made the situation worse” for the victim. An indignant Dr. Fitz Maurice responded on Twitter: “CPR SAVES LIVES!! Let’s not let a CHEAP AND BASELESS argument destroy all the work that’s been done…!”

Of course, there are consequences that are beyond our control and others that can, in fact, be anticipated and planned for. Dr. Fitz Maurice brought up a preventive approach: Make CPR second nature, teach it in schools, help people overcome their fears. “Cardiac deaths are 200 times more frequent than deaths resulting from fires – and we practice fire drills a lot more than we practice CPR,” he told this news organization. In a society where there is widespread training on the procedure, where people regularly practice the technique, those who have had the experience of giving someone CPR will feel less alone, will be better understood by others.

“On the other hand, beyond the initial impact and the lack of a formal support system, the medium- and long-term outcome for those who acted is also psychologically and emotionally favorable,” said Jorge Bombau, MD, an obstetrician/gynecologist in Buenos Aires. After Dr. Bombau’s 14-year-old son Beltrán suddenly died during a school sports tournament, Dr. Bombau became a prominent advocate spreading the word about CPR.

“I don’t know anyone who regrets doing CPR,” he told this news organization. “There may be a brief period when the person feels distressed or depressed, when they have trouble sleeping. But it’s been proven that doing a good deed improves one’s mood. And what better deed is there than trying to save someone’s life? Whether their efforts were successful or in vain, that person has, at the end of the day, done something meaningful and worthwhile.”

Mr. Snitcofsky shares this sentiment. For several months now, he’s been feeling he’s “in a good place.” And he’s been actively promoting CPR on social media. As he recently posted on Twitter, “I’m here to retweet everything that has to do with getting us all to become familiar with how to do CPR and working up the courage to do it. The training takes no more than a few hours.

“I want to know that, if I ever have an out-of-hospital sudden cardiac arrest, there will be neighbors, friends, or family members around who know how to do CPR. Every person who knows how to do CPR can persuade others, and those of us who’ve had to do CPR in real life are even better candidates for persuading others. And if one day a person ends up needing CPR, I want to step in again and make up for lost time. Here’s hoping it’ll do the job,” he concluded.

It’s the same for Matías Alonso, a journalist in Buenos Aires. On New Year’s Eve 15 years ago, he was at a family dinner when, a few minutes before midnight, he found himself giving CPR to his stepmother’s father. “Unfortunately, he passed away, but I continued doing CPR on him until the ambulance arrived. For some time, I felt a little guilty for not taking charge of the situation from the beginning, and because I had this idea in my head that more people pulled through and recovered. But afterwards, they really thanked me a lot. And that helped me realize that I’d done something. I didn’t stand still when faced with the inevitability of death. I understood that it was good to have tried,” Mr. Alonso told this news organization. “And next time … hopefully there won’t be a next time … but I’m more prepared, and I now know how I can do better.”

Mr. Alonso, Mr. Snitcofsky, Dr. Fitz Maurice, Dr. Mosca, Dr. Bombau, and Dr. Márquez Murillo disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com. This article was translated from Medscape Spanish.

One year ago, as the sun was setting on a late fall day, Andrés Snitcofsky, a 40-year-old designer from Buenos Aires, Argentina, heard harrowing cries for help. It was the niece and the wife of one of his neighbors: a man in his 60s who the women had found “passed out” in the bedroom. While they were all waiting for the ambulance, Mr. Snitcofsky went over, tilted the man’s head back, and confirmed that he wasn’t breathing, that he wasn’t choking. And then he started chest compressions, just like he’d learned in a CPR class he’d taken 2 decades earlier. “I did CPR for 5 minutes straight until a friend of the victim came in and asked me to stop, telling me that the man had probably been dead for 2 or 3 hours already. But I had no idea because I’d never seen a dead body before,” Mr. Snitcofsky told this news organization. A few minutes later, the ambulance arrived. The doctor confirmed that there was nothing more that could be done.

Mr. Snitcofsky went home. Nobody had asked for his name or address or phone number. … And it wasn’t because they already knew who he was. In fact, there wasn’t any sort of relationship there. Mr. Snitcofsky had only known his neighbors by sight. His actions that day, however, “did not come without a cost. It took me weeks – months, actually – to put myself together again,” he said. The things he saw, the things he heard, everything about that night played over and over in his head. “I had trouble sleeping. I would play out different scenarios in my head. I questioned myself. I second-guessed myself, criticized myself. It’s like some taboo subject. There’s no one to share the experience with, no one who gets it. But with time, I was able to process the event.

“For 2 months, I talked to my psychologist about it all,” he continued. “That really helped me a lot. In addition to therapy, I reached out to a couple I know – they’re both physicians – and to a firefighter who teaches CPR. Their insight and guidance allowed me to get to a point where I was able to understand that what I did was a good thing and that what I did was all that could have been done. But anyone who finds themselves in the position of having to do CPR – they’re going to be affected in many, many ways. It goes beyond the euphoria of seeing a person come back to life. Of that, I’m quite certain.”

We’ve all seen campaigns encouraging people to learn CPR and to be prepared if the need arises. But in training the public (and even health care professionals), not much, if anything, is said about the “collateral damage”: the psychological and emotional consequences of carrying out the procedure. These especially come into play when you don’t know whether the person survived, when your efforts weren’t able to reverse the sudden cardiac arrest, or when the person you gave CPR to was a loved one – a case that may entail immediate therapeutic interventions to minimize or prevent the risk of suffering long-lasting trauma.

In May 2020, popular American activist and educator Kristin Flanary saw someone suffering cardiac arrest. She stepped in and started doing CPR. And she continued doing CPR … for 10 long minutes. The person she was trying to save was her 34-year-old husband, ophthalmologist and comedian Will Flanary. On Twitter, where she’s known as Lady Glaucomflecken, Ms. Flanary recently shared the following message, putting the topic of CPR and automated external defibrillator training front and center.

“Yes, everyone should learn #CPRandAED. But if we are going to ask people to perform such a brutal task, it’s imperative that we also provide them with the info and resources they need to process it mentally and emotionally. It’s traumatic and life changing. It’s irresponsible and unethical to ask people to help in such a brutal and traumatic way and then neglect to help them in return.” In less than a month, the tweet has racked up over 200,000 views.
 

Doing one’s duty

There are many people who work to promote CPR and strengthen the other links in the chain of survival for out-of-hospital sudden cardiac arrest, such as prompt access to and delivery of early defibrillation. According to them, any negative psychological impact of intervening is temporary and, when compared with the satisfaction of having done one’s duty, quite insignificant – even if the efforts to save a person’s life are not successful.

“In 99.9% of cases, people who have performed CPR feel a sense of satisfaction, even happiness, knowing that they’ve helped. The individuals I’ve spoken with, I’ve never heard any of them say that they felt worse after the event or that they needed to see a psychologist,” said Mario Fitz Maurice, MD, director of the Arrhythmia Council of the Argentine Society of Cardiology and head of Electrophysiology at Rivadavia Hospital in Buenos Aires. He went on to tell this news organization, “Of course, some degree of fear, sadness, or melancholy can remain afterward. But it seems to me, and there are reports saying as much, that, in the end, what stands out in the person’s mind is the fact that they tried to save a life. And for them, there’s joy in knowing this.”

Dr. Fitz Maurice, who is also the director of the National Arrhythmia Institute in Buenos Aires, pointed out that the kind of person who takes CPR classes “has a profile that’s going to allow them to be psychologically involved; they’re the caring person, the one who’s ready and willing to help people.” And he added that, at his hospital, if they can identify the individuals or first responders who have done CPR on a patient, the protocol is to always contact them to offer psychological care and assistance. “But in 99% of cases, they don’t even understand why we’re calling them, they’re extremely happy to have taken part.”

Some studies, though, paint a much different picture, one that shows that providing CPR can be emotionally challenging and have consequences in terms of one’s family and work life. A qualitative study published in 2016 looked into the experiences of 20 lay rescuers in Norway – five were health educated – who had provided CPR to 18 out-of-hospital cardiac arrest (OHCA) victims, 66% of whom survived. The time from experiencing the OHCA incident to participating in the interview ranged from 6 days to 13 years (median 5.5 years). Several participants reported the OHCA incident as a “shocking and terrifying” experience. Tiredness, exhaustion, confusion, and feeling alone about the OHCA experience were individual reactions that could vary in time from days to months. Anxiety and insomnia were also experienced following the incident.

Some lay rescuers described the influence on work and family life, and a few of them described deep sorrow, even several years after the incident. Overall, they reported repetitive self-criticism regarding whether they could have carried out anything else to achieve a better outcome for the cardiac arrest victim. All of them wanted to be informed about the outcome. And four of the lay rescuers needed professional counseling to process the OHCA experience.

In 2020, another qualitative study was conducted, this time in Taiwan. There were nine participants, none of whom were health professionals. Each had provided initial CPR and defibrillation with AED in public locations. Event-to-interview duration was within 1 year and 1-2 years. The major findings from the study were the following:

• The lay rescuers possessed helping traits and high motivation.  
• The lay rescuers reported certain aspects of rescue reality that differed much from prior training and expectations, including difficulty in the depth of chest compression, and uncertainties in real emergency situations.
• The lay rescuers gained positive personal fulfillment in sharing their experience and receiving positive feedback from others, and were willing to help next time, although they experienced a short-term negative psychological impact from the event.
“Measures should be taken to increase [a] layperson’s confidence and situation awareness, to reduce training-reality discrepancy, and to build up a support system to avoid negative psychological effects.” This was the conclusion of the study team, which was led by Matthew Huei-Ming Ma, MD, PhD. A professor in the department of emergency medicine at National Taiwan University in Taipei, he is also on the board of directors of the Resuscitation Council of Asia.

Potential trauma

In recalling his experience, Mr. Snitcofsky said, “The hardest part of it all was the moment that I stopped giving CPR, that moment of letting go. This became the image that kept coming back to me, the traumatic moment I hadn’t thought about.”

Psychiatrist Daniel Mosca, MD, is the founder and former president of the Argentine Society of Trauma Psychology. He is also the coordinator of the human factors team at the City of Buenos Aires Emergency Medical Care System. “Any event has the potential to be traumatic, all the more so when it’s an event where you come face to face with death and uncertainty. But how a rescuer reacts will depend on their psychological makeup.” Of the individuals who were held for months or years in the jungle as hostages of the Revolutionary Armed Forces of Colombia, “only” half developed symptoms of posttraumatic stress disorder.

Dr. Mosca believes that a comment by Frank Ochberg, MD, speaks to this finding. “In many cases, peritraumatic symptoms are a normal person’s normal response to an abnormal situation.” For a lot of people who have found themselves having to perform CPR, the symptoms associated with the initial acute stress reaction will resolve on their own in 30-90 days. “But if this doesn’t happen, and those symptoms persist, psychotherapeutic or pharmacological intervention will be necessary,” he noted.

“In CPR classes, it would be good for the instructors to talk about the warning signs that people should look out for in themselves and their fellow rescuers. So, for example, insomnia, anxiety, a heightened state of alertness, feeling disconnected from reality,” Dr. Mosca told this news organization.

“Another thing that can help rescuers is letting them know what happened to the person they gave CPR to. This way, they can get closure,” suggested Manlio Márquez Murillo, MD, a cardiologist and electrophysiologist in Mexico. He is also the coordinator of the Alliance Against Sudden Cardiac Death at the Interamerican Society of Cardiology.

“Medical and nursing societies would have to develop a brief protocol or performance standard. The goal would be to ensure that rescuers are asked for their contact information and that someone gets in touch to debrief them and to offer them care. Next would come the treatment part, to resolve any remaining aftereffects,” said in an interview.

For example, a three-stage Lay Responder Support Model (LRSM) was developed and implemented as part of a lay responder support program established in 2014 by the Peel Regional Council in Ontario. The LRSM identifies and engages individuals who witnessed or participated directly or indirectly in an OHCA, inviting them to participate in a debriefing session facilitated by a trained practitioner. Held 24-48 hours post event, the debriefing allows lay responders to contextualize their reaction to the event. The conversation also serves as an opportunity for them to fully articulate their concerns, questions, and thoughts. The facilitator can communicate stress reduction techniques and address psychological first aid needs as they emerge. Approximately 1 week post event, a secondary follow-up occurs. If the lay responder communicates a continuing struggle with symptoms impacting and interfering with everyday life, the facilitator offers a coordinated or facilitated referral for mental health support.

In an article published in the Journal of Cardiac Failure. Ms. Flanary speaks about the three kinds of language that anyone who was either forced to or inspired to perform CPR can use to help process their trauma: words that explain what happened, words that name (eg, “forgotten patients”), and words that validate the experience and allow the person to articulate their feelings. The tools and technologies that organizations and health care professionals provide can help the healing process. Empathy and compassion, too, have a place.

But there are virtually no standardized and proactive initiatives of this kind in much of the world, including Latin America. So, most people who just happened to be in the right place at the right time find that they have to navigate the “after” part all on their own.
 

Other obstacles

Dr. Márquez Murillo finds it unfortunate that countries in the region have yet to enact “Good Samaritan” laws. If individuals render aid to someone suffering cardiac arrest, then these laws would ensure that they will not be held liable in any way. This is the case in Argentina and Uruguay. So, the fear of things turning into a legal matter may be holding people back from taking action; that fear could also create additional stress for those who end up stepping in to help.

Even with the legal safeguards, exceptional circumstances may arise where rescuers find themselves facing unexpected emotional challenges. In Argentina, Virginia Pérez Antonelli, the 17-year-old who tried in vain to save the life of Fernando Báez Sosa, had to testify at the trial of the eight defendants accused of brutally beating him in January 2020. The press, the public – the attention of an entire country – was focused on her. She had to respond to the defense attorneys who were able to ask whether she was sure that she performed the CPR maneuvers correctly. And a few weeks ago, a medical examiner hired by the defense suggested that “the CPR may have made the situation worse” for the victim. An indignant Dr. Fitz Maurice responded on Twitter: “CPR SAVES LIVES!! Let’s not let a CHEAP AND BASELESS argument destroy all the work that’s been done…!”

Of course, there are consequences that are beyond our control and others that can, in fact, be anticipated and planned for. Dr. Fitz Maurice brought up a preventive approach: Make CPR second nature, teach it in schools, help people overcome their fears. “Cardiac deaths are 200 times more frequent than deaths resulting from fires – and we practice fire drills a lot more than we practice CPR,” he told this news organization. In a society where there is widespread training on the procedure, where people regularly practice the technique, those who have had the experience of giving someone CPR will feel less alone, will be better understood by others.

“On the other hand, beyond the initial impact and the lack of a formal support system, the medium- and long-term outcome for those who acted is also psychologically and emotionally favorable,” said Jorge Bombau, MD, an obstetrician/gynecologist in Buenos Aires. After Dr. Bombau’s 14-year-old son Beltrán suddenly died during a school sports tournament, Dr. Bombau became a prominent advocate spreading the word about CPR.

“I don’t know anyone who regrets doing CPR,” he told this news organization. “There may be a brief period when the person feels distressed or depressed, when they have trouble sleeping. But it’s been proven that doing a good deed improves one’s mood. And what better deed is there than trying to save someone’s life? Whether their efforts were successful or in vain, that person has, at the end of the day, done something meaningful and worthwhile.”

Mr. Snitcofsky shares this sentiment. For several months now, he’s been feeling he’s “in a good place.” And he’s been actively promoting CPR on social media. As he recently posted on Twitter, “I’m here to retweet everything that has to do with getting us all to become familiar with how to do CPR and working up the courage to do it. The training takes no more than a few hours.

“I want to know that, if I ever have an out-of-hospital sudden cardiac arrest, there will be neighbors, friends, or family members around who know how to do CPR. Every person who knows how to do CPR can persuade others, and those of us who’ve had to do CPR in real life are even better candidates for persuading others. And if one day a person ends up needing CPR, I want to step in again and make up for lost time. Here’s hoping it’ll do the job,” he concluded.

It’s the same for Matías Alonso, a journalist in Buenos Aires. On New Year’s Eve 15 years ago, he was at a family dinner when, a few minutes before midnight, he found himself giving CPR to his stepmother’s father. “Unfortunately, he passed away, but I continued doing CPR on him until the ambulance arrived. For some time, I felt a little guilty for not taking charge of the situation from the beginning, and because I had this idea in my head that more people pulled through and recovered. But afterwards, they really thanked me a lot. And that helped me realize that I’d done something. I didn’t stand still when faced with the inevitability of death. I understood that it was good to have tried,” Mr. Alonso told this news organization. “And next time … hopefully there won’t be a next time … but I’m more prepared, and I now know how I can do better.”

Mr. Alonso, Mr. Snitcofsky, Dr. Fitz Maurice, Dr. Mosca, Dr. Bombau, and Dr. Márquez Murillo disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com. This article was translated from Medscape Spanish.

One year ago, as the sun was setting on a late fall day, Andrés Snitcofsky, a 40-year-old designer from Buenos Aires, Argentina, heard harrowing cries for help. It was the niece and the wife of one of his neighbors: a man in his 60s who the women had found “passed out” in the bedroom. While they were all waiting for the ambulance, Mr. Snitcofsky went over, tilted the man’s head back, and confirmed that he wasn’t breathing, that he wasn’t choking. And then he started chest compressions, just like he’d learned in a CPR class he’d taken 2 decades earlier. “I did CPR for 5 minutes straight until a friend of the victim came in and asked me to stop, telling me that the man had probably been dead for 2 or 3 hours already. But I had no idea because I’d never seen a dead body before,” Mr. Snitcofsky told this news organization. A few minutes later, the ambulance arrived. The doctor confirmed that there was nothing more that could be done.

Mr. Snitcofsky went home. Nobody had asked for his name or address or phone number. … And it wasn’t because they already knew who he was. In fact, there wasn’t any sort of relationship there. Mr. Snitcofsky had only known his neighbors by sight. His actions that day, however, “did not come without a cost. It took me weeks – months, actually – to put myself together again,” he said. The things he saw, the things he heard, everything about that night played over and over in his head. “I had trouble sleeping. I would play out different scenarios in my head. I questioned myself. I second-guessed myself, criticized myself. It’s like some taboo subject. There’s no one to share the experience with, no one who gets it. But with time, I was able to process the event.

“For 2 months, I talked to my psychologist about it all,” he continued. “That really helped me a lot. In addition to therapy, I reached out to a couple I know – they’re both physicians – and to a firefighter who teaches CPR. Their insight and guidance allowed me to get to a point where I was able to understand that what I did was a good thing and that what I did was all that could have been done. But anyone who finds themselves in the position of having to do CPR – they’re going to be affected in many, many ways. It goes beyond the euphoria of seeing a person come back to life. Of that, I’m quite certain.”

We’ve all seen campaigns encouraging people to learn CPR and to be prepared if the need arises. But in training the public (and even health care professionals), not much, if anything, is said about the “collateral damage”: the psychological and emotional consequences of carrying out the procedure. These especially come into play when you don’t know whether the person survived, when your efforts weren’t able to reverse the sudden cardiac arrest, or when the person you gave CPR to was a loved one – a case that may entail immediate therapeutic interventions to minimize or prevent the risk of suffering long-lasting trauma.

In May 2020, popular American activist and educator Kristin Flanary saw someone suffering cardiac arrest. She stepped in and started doing CPR. And she continued doing CPR … for 10 long minutes. The person she was trying to save was her 34-year-old husband, ophthalmologist and comedian Will Flanary. On Twitter, where she’s known as Lady Glaucomflecken, Ms. Flanary recently shared the following message, putting the topic of CPR and automated external defibrillator training front and center.

“Yes, everyone should learn #CPRandAED. But if we are going to ask people to perform such a brutal task, it’s imperative that we also provide them with the info and resources they need to process it mentally and emotionally. It’s traumatic and life changing. It’s irresponsible and unethical to ask people to help in such a brutal and traumatic way and then neglect to help them in return.” In less than a month, the tweet has racked up over 200,000 views.
 

Doing one’s duty

There are many people who work to promote CPR and strengthen the other links in the chain of survival for out-of-hospital sudden cardiac arrest, such as prompt access to and delivery of early defibrillation. According to them, any negative psychological impact of intervening is temporary and, when compared with the satisfaction of having done one’s duty, quite insignificant – even if the efforts to save a person’s life are not successful.

“In 99.9% of cases, people who have performed CPR feel a sense of satisfaction, even happiness, knowing that they’ve helped. The individuals I’ve spoken with, I’ve never heard any of them say that they felt worse after the event or that they needed to see a psychologist,” said Mario Fitz Maurice, MD, director of the Arrhythmia Council of the Argentine Society of Cardiology and head of Electrophysiology at Rivadavia Hospital in Buenos Aires. He went on to tell this news organization, “Of course, some degree of fear, sadness, or melancholy can remain afterward. But it seems to me, and there are reports saying as much, that, in the end, what stands out in the person’s mind is the fact that they tried to save a life. And for them, there’s joy in knowing this.”

Dr. Fitz Maurice, who is also the director of the National Arrhythmia Institute in Buenos Aires, pointed out that the kind of person who takes CPR classes “has a profile that’s going to allow them to be psychologically involved; they’re the caring person, the one who’s ready and willing to help people.” And he added that, at his hospital, if they can identify the individuals or first responders who have done CPR on a patient, the protocol is to always contact them to offer psychological care and assistance. “But in 99% of cases, they don’t even understand why we’re calling them, they’re extremely happy to have taken part.”

Some studies, though, paint a much different picture, one that shows that providing CPR can be emotionally challenging and have consequences in terms of one’s family and work life. A qualitative study published in 2016 looked into the experiences of 20 lay rescuers in Norway – five were health educated – who had provided CPR to 18 out-of-hospital cardiac arrest (OHCA) victims, 66% of whom survived. The time from experiencing the OHCA incident to participating in the interview ranged from 6 days to 13 years (median 5.5 years). Several participants reported the OHCA incident as a “shocking and terrifying” experience. Tiredness, exhaustion, confusion, and feeling alone about the OHCA experience were individual reactions that could vary in time from days to months. Anxiety and insomnia were also experienced following the incident.

Some lay rescuers described the influence on work and family life, and a few of them described deep sorrow, even several years after the incident. Overall, they reported repetitive self-criticism regarding whether they could have carried out anything else to achieve a better outcome for the cardiac arrest victim. All of them wanted to be informed about the outcome. And four of the lay rescuers needed professional counseling to process the OHCA experience.

In 2020, another qualitative study was conducted, this time in Taiwan. There were nine participants, none of whom were health professionals. Each had provided initial CPR and defibrillation with AED in public locations. Event-to-interview duration was within 1 year and 1-2 years. The major findings from the study were the following:

• The lay rescuers possessed helping traits and high motivation.  
• The lay rescuers reported certain aspects of rescue reality that differed much from prior training and expectations, including difficulty in the depth of chest compression, and uncertainties in real emergency situations.
• The lay rescuers gained positive personal fulfillment in sharing their experience and receiving positive feedback from others, and were willing to help next time, although they experienced a short-term negative psychological impact from the event.
“Measures should be taken to increase [a] layperson’s confidence and situation awareness, to reduce training-reality discrepancy, and to build up a support system to avoid negative psychological effects.” This was the conclusion of the study team, which was led by Matthew Huei-Ming Ma, MD, PhD. A professor in the department of emergency medicine at National Taiwan University in Taipei, he is also on the board of directors of the Resuscitation Council of Asia.

Potential trauma

In recalling his experience, Mr. Snitcofsky said, “The hardest part of it all was the moment that I stopped giving CPR, that moment of letting go. This became the image that kept coming back to me, the traumatic moment I hadn’t thought about.”

Psychiatrist Daniel Mosca, MD, is the founder and former president of the Argentine Society of Trauma Psychology. He is also the coordinator of the human factors team at the City of Buenos Aires Emergency Medical Care System. “Any event has the potential to be traumatic, all the more so when it’s an event where you come face to face with death and uncertainty. But how a rescuer reacts will depend on their psychological makeup.” Of the individuals who were held for months or years in the jungle as hostages of the Revolutionary Armed Forces of Colombia, “only” half developed symptoms of posttraumatic stress disorder.

Dr. Mosca believes that a comment by Frank Ochberg, MD, speaks to this finding. “In many cases, peritraumatic symptoms are a normal person’s normal response to an abnormal situation.” For a lot of people who have found themselves having to perform CPR, the symptoms associated with the initial acute stress reaction will resolve on their own in 30-90 days. “But if this doesn’t happen, and those symptoms persist, psychotherapeutic or pharmacological intervention will be necessary,” he noted.

“In CPR classes, it would be good for the instructors to talk about the warning signs that people should look out for in themselves and their fellow rescuers. So, for example, insomnia, anxiety, a heightened state of alertness, feeling disconnected from reality,” Dr. Mosca told this news organization.

“Another thing that can help rescuers is letting them know what happened to the person they gave CPR to. This way, they can get closure,” suggested Manlio Márquez Murillo, MD, a cardiologist and electrophysiologist in Mexico. He is also the coordinator of the Alliance Against Sudden Cardiac Death at the Interamerican Society of Cardiology.

“Medical and nursing societies would have to develop a brief protocol or performance standard. The goal would be to ensure that rescuers are asked for their contact information and that someone gets in touch to debrief them and to offer them care. Next would come the treatment part, to resolve any remaining aftereffects,” said in an interview.

For example, a three-stage Lay Responder Support Model (LRSM) was developed and implemented as part of a lay responder support program established in 2014 by the Peel Regional Council in Ontario. The LRSM identifies and engages individuals who witnessed or participated directly or indirectly in an OHCA, inviting them to participate in a debriefing session facilitated by a trained practitioner. Held 24-48 hours post event, the debriefing allows lay responders to contextualize their reaction to the event. The conversation also serves as an opportunity for them to fully articulate their concerns, questions, and thoughts. The facilitator can communicate stress reduction techniques and address psychological first aid needs as they emerge. Approximately 1 week post event, a secondary follow-up occurs. If the lay responder communicates a continuing struggle with symptoms impacting and interfering with everyday life, the facilitator offers a coordinated or facilitated referral for mental health support.

In an article published in the Journal of Cardiac Failure. Ms. Flanary speaks about the three kinds of language that anyone who was either forced to or inspired to perform CPR can use to help process their trauma: words that explain what happened, words that name (eg, “forgotten patients”), and words that validate the experience and allow the person to articulate their feelings. The tools and technologies that organizations and health care professionals provide can help the healing process. Empathy and compassion, too, have a place.

But there are virtually no standardized and proactive initiatives of this kind in much of the world, including Latin America. So, most people who just happened to be in the right place at the right time find that they have to navigate the “after” part all on their own.
 

Other obstacles

Dr. Márquez Murillo finds it unfortunate that countries in the region have yet to enact “Good Samaritan” laws. If individuals render aid to someone suffering cardiac arrest, then these laws would ensure that they will not be held liable in any way. This is the case in Argentina and Uruguay. So, the fear of things turning into a legal matter may be holding people back from taking action; that fear could also create additional stress for those who end up stepping in to help.

Even with the legal safeguards, exceptional circumstances may arise where rescuers find themselves facing unexpected emotional challenges. In Argentina, Virginia Pérez Antonelli, the 17-year-old who tried in vain to save the life of Fernando Báez Sosa, had to testify at the trial of the eight defendants accused of brutally beating him in January 2020. The press, the public – the attention of an entire country – was focused on her. She had to respond to the defense attorneys who were able to ask whether she was sure that she performed the CPR maneuvers correctly. And a few weeks ago, a medical examiner hired by the defense suggested that “the CPR may have made the situation worse” for the victim. An indignant Dr. Fitz Maurice responded on Twitter: “CPR SAVES LIVES!! Let’s not let a CHEAP AND BASELESS argument destroy all the work that’s been done…!”

Of course, there are consequences that are beyond our control and others that can, in fact, be anticipated and planned for. Dr. Fitz Maurice brought up a preventive approach: Make CPR second nature, teach it in schools, help people overcome their fears. “Cardiac deaths are 200 times more frequent than deaths resulting from fires – and we practice fire drills a lot more than we practice CPR,” he told this news organization. In a society where there is widespread training on the procedure, where people regularly practice the technique, those who have had the experience of giving someone CPR will feel less alone, will be better understood by others.

“On the other hand, beyond the initial impact and the lack of a formal support system, the medium- and long-term outcome for those who acted is also psychologically and emotionally favorable,” said Jorge Bombau, MD, an obstetrician/gynecologist in Buenos Aires. After Dr. Bombau’s 14-year-old son Beltrán suddenly died during a school sports tournament, Dr. Bombau became a prominent advocate spreading the word about CPR.

“I don’t know anyone who regrets doing CPR,” he told this news organization. “There may be a brief period when the person feels distressed or depressed, when they have trouble sleeping. But it’s been proven that doing a good deed improves one’s mood. And what better deed is there than trying to save someone’s life? Whether their efforts were successful or in vain, that person has, at the end of the day, done something meaningful and worthwhile.”

Mr. Snitcofsky shares this sentiment. For several months now, he’s been feeling he’s “in a good place.” And he’s been actively promoting CPR on social media. As he recently posted on Twitter, “I’m here to retweet everything that has to do with getting us all to become familiar with how to do CPR and working up the courage to do it. The training takes no more than a few hours.

“I want to know that, if I ever have an out-of-hospital sudden cardiac arrest, there will be neighbors, friends, or family members around who know how to do CPR. Every person who knows how to do CPR can persuade others, and those of us who’ve had to do CPR in real life are even better candidates for persuading others. And if one day a person ends up needing CPR, I want to step in again and make up for lost time. Here’s hoping it’ll do the job,” he concluded.

It’s the same for Matías Alonso, a journalist in Buenos Aires. On New Year’s Eve 15 years ago, he was at a family dinner when, a few minutes before midnight, he found himself giving CPR to his stepmother’s father. “Unfortunately, he passed away, but I continued doing CPR on him until the ambulance arrived. For some time, I felt a little guilty for not taking charge of the situation from the beginning, and because I had this idea in my head that more people pulled through and recovered. But afterwards, they really thanked me a lot. And that helped me realize that I’d done something. I didn’t stand still when faced with the inevitability of death. I understood that it was good to have tried,” Mr. Alonso told this news organization. “And next time … hopefully there won’t be a next time … but I’m more prepared, and I now know how I can do better.”

Mr. Alonso, Mr. Snitcofsky, Dr. Fitz Maurice, Dr. Mosca, Dr. Bombau, and Dr. Márquez Murillo disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com. This article was translated from Medscape Spanish.

Evidence supporting medications that slow the heart rate (HR), notably beta-blockers, is overwhelming in heart failure (HF) with reduced ejection fraction. Underwhelming, however, is clinical trial support for such agents in patients with HF with preserved ejection fraction (HFpEF).
 

Indeed, at least for some such patients, a treatment that modestly accelerates resting HR may be a more promising strategy, suggests an early line of research that challenges prevalent thinking about HFpEF therapy.

In a small, randomized test of the idea, patients with HFpEF and standard pacemakers set to a backup resting HR a bit higher than a standard of care 60 bpm, usually to about 75 bpm, reaped important quality of life benefits.

More strikingly, their natriuretic peptide levels and burden of atrial fibrillation (AFib) fell significantly, the latter by 27% over 1 year.

The trial enrolled only HFpEF patients with pacemakers previously implanted for sick sinus syndrome or atrioventricular block. But researchers say their 107-patient study called myPACE – if confirmed in larger, multicenter trials – lays the groundwork for a device therapy that is broadly useful, potentially, in patients with “preclinical or overt” HFpEF.

Indeed, some of the intervention’s “quite substantial” benefits rivaled or surpassed what his group has observed with available HFpEF drug therapies, including the sodium-glucose cotransporter 2 inhibitors, observed Markus Meyer, MD, PhD, University of Minnesota, Minneapolis.

Moreover, the study may be “the first to show that, with this approach, we can actually also reduce atrial fibrillation,” he said in an interview.

Dr. Meyer said his group is “confident” that the HR-modulation strategy will be successful in appropriate clinical trials and that “pacemakers, in the end, will become a treatment modality for HFpEF.”

Meyer is senior author on the trial’s publication in JAMA Cardiology in JAMA Cardiology (2023 Feb 1. doi: 10.1001/jamacardio.2022.5320), with lead author Margaret Infeld, MD, University of Vermont, Burlington.

The trial entered pacemaker patients with HFpEF of stage B or C – that is, either asymptomatic with structural disease or fully symptomatic. But, Dr. Meyer said, “we saw that the treatment effect was much more pronounced in the patients who had overt heart failure with preserved ejection fraction.”
 

Challenging beta-blocker dogma

The study, the report states, “contradicts canonical thinking” by suggesting HFpEF patients may benefit from a higher resting heart rate, which would presumably shorten diastolic filling time. It also “may help reduce the overprescription of beta-blockers to allow higher heart rates in this population.”

Indeed, Dr. Meyer observed, no one really knows whether beta-blockers work in HFpEF, “because they really have never been studied in a sufficiently powered randomized controlled trial.”

The current study “basically rewrites what we know about the pathophysiology of this form of clinical heart failure,” said Michael R. Zile, MD, Medical University of South Carolina and Veterans Affairs Medical Center, both in Charleston, who was not part of the trial or report.

Previously in HFpEF, Dr. Zile said in an interview, “everybody thought you needed to make diastole longer to give the ventricle a longer time to fill. And none of that really made any sense. It was just sort of accepted as dogma.”

The idea led to widespread use of beta-blockers in HFpEF but “turned out just not to be true.” Indeed, European and North American guidelines, Dr. Zile observed, “have all taken beta-blockers out of the equation for HFpEF” except for treating comorbidities that can be associated with HFpEF, like hypertension or AFib.

Many patients with HFpEF and chronotropic incompetence could be provided with standard pacemakers with primarily conduction-system pacing but are not getting them, he observed.

The current study might help change that. No one is suggesting, based on the current study, “that we start putting pacemakers in every single patient with HFpEF,” Dr. Zile said. Still, for HFpEF patients already with a pacemaker, the study provides “reasonable assurance” that its criteria for elevated resting HR may well improve symptoms.

Moreover, it suggests such pacemakers, programmed as in the study, might potentially give a boost to HFpEF patients without chronotropic incompetence but with persisting symptoms despite guideline-directed drug therapy. That’s certainly worth exploring in further trials, Dr. Zile said.
 

How the study worked

The single-center trial entered 107 participants with HFpEF and pacemakers set, at baseline, to a backup resting HR of 60 bpm; their age averaged 75 and 48% were women. Only patients with devices for atrial pacing, conduction-system pacing, or biventricular pacing – which are unlikely to promote ventricular dyssynchrony – were included.

They were randomly assigned, double-blind, to have their devices set to an accelerated backup rate or to be continued at 60 bpm. The backup resting rate set for the intervention group’s 50 patients was individualized based on height and other factors; the median was 75 bpm.

Scores on the Minnesota Living with Heart Failure Questionnaire, the primary endpoint, improved in the intervention group, compared with baseline, by about 11 points after 1 month and by 15 points after 1 year (P < .001).

The scores in the usual-care group deteriorated by half a point and by 3.5 points at 1 month and 1 year (P = .03), respectively.

Consistent advantages for the accelerated-HR strategy were evident throughout the major secondary endpoints. For example, levels of N-terminal pro-B-type natriuretic peptide fell an average 109 pg/dL after 1 month in the accelerated-HR group and rose a mean of 128 pg/dL in the usual-care group (P = .02).

Mean daily pacemaker-monitored activity level rose by 47 minutes by 1 year in the accelerated-HR group, compared with a drop of 22 minutes for those assigned to the standard-care rate (P < .001).

AFib was detected in 18% of intervention patients at the 1-year follow-up, down from 31% at baseline. Their risk ratio for AFib at 1 year was 0.73 (95% confidence interval, 0.55-0.99, P = .04), compared with the control group.

In other patients with HFpEF “we have done pacing studies where we just ramped up the pacing rate, and we see that these pressures in the left atrium actually drop immediately,” Dr. Meyer said. It’s that “unburdening of the atria,” he added, that probably leads to the reduction in AFib.

Dr. Meyer reported holding a patent for pacemakers for HFpEF licensed to Medtronic. Dr. Zile said he consults for Medtronic and has no other relevant financial relationships.

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

Evidence supporting medications that slow the heart rate (HR), notably beta-blockers, is overwhelming in heart failure (HF) with reduced ejection fraction. Underwhelming, however, is clinical trial support for such agents in patients with HF with preserved ejection fraction (HFpEF).
 

Indeed, at least for some such patients, a treatment that modestly accelerates resting HR may be a more promising strategy, suggests an early line of research that challenges prevalent thinking about HFpEF therapy.

In a small, randomized test of the idea, patients with HFpEF and standard pacemakers set to a backup resting HR a bit higher than a standard of care 60 bpm, usually to about 75 bpm, reaped important quality of life benefits.

More strikingly, their natriuretic peptide levels and burden of atrial fibrillation (AFib) fell significantly, the latter by 27% over 1 year.

The trial enrolled only HFpEF patients with pacemakers previously implanted for sick sinus syndrome or atrioventricular block. But researchers say their 107-patient study called myPACE – if confirmed in larger, multicenter trials – lays the groundwork for a device therapy that is broadly useful, potentially, in patients with “preclinical or overt” HFpEF.

Indeed, some of the intervention’s “quite substantial” benefits rivaled or surpassed what his group has observed with available HFpEF drug therapies, including the sodium-glucose cotransporter 2 inhibitors, observed Markus Meyer, MD, PhD, University of Minnesota, Minneapolis.

Moreover, the study may be “the first to show that, with this approach, we can actually also reduce atrial fibrillation,” he said in an interview.

Dr. Meyer said his group is “confident” that the HR-modulation strategy will be successful in appropriate clinical trials and that “pacemakers, in the end, will become a treatment modality for HFpEF.”

Meyer is senior author on the trial’s publication in JAMA Cardiology in JAMA Cardiology (2023 Feb 1. doi: 10.1001/jamacardio.2022.5320), with lead author Margaret Infeld, MD, University of Vermont, Burlington.

The trial entered pacemaker patients with HFpEF of stage B or C – that is, either asymptomatic with structural disease or fully symptomatic. But, Dr. Meyer said, “we saw that the treatment effect was much more pronounced in the patients who had overt heart failure with preserved ejection fraction.”
 

Challenging beta-blocker dogma

The study, the report states, “contradicts canonical thinking” by suggesting HFpEF patients may benefit from a higher resting heart rate, which would presumably shorten diastolic filling time. It also “may help reduce the overprescription of beta-blockers to allow higher heart rates in this population.”

Indeed, Dr. Meyer observed, no one really knows whether beta-blockers work in HFpEF, “because they really have never been studied in a sufficiently powered randomized controlled trial.”

The current study “basically rewrites what we know about the pathophysiology of this form of clinical heart failure,” said Michael R. Zile, MD, Medical University of South Carolina and Veterans Affairs Medical Center, both in Charleston, who was not part of the trial or report.

Previously in HFpEF, Dr. Zile said in an interview, “everybody thought you needed to make diastole longer to give the ventricle a longer time to fill. And none of that really made any sense. It was just sort of accepted as dogma.”

The idea led to widespread use of beta-blockers in HFpEF but “turned out just not to be true.” Indeed, European and North American guidelines, Dr. Zile observed, “have all taken beta-blockers out of the equation for HFpEF” except for treating comorbidities that can be associated with HFpEF, like hypertension or AFib.

Many patients with HFpEF and chronotropic incompetence could be provided with standard pacemakers with primarily conduction-system pacing but are not getting them, he observed.

The current study might help change that. No one is suggesting, based on the current study, “that we start putting pacemakers in every single patient with HFpEF,” Dr. Zile said. Still, for HFpEF patients already with a pacemaker, the study provides “reasonable assurance” that its criteria for elevated resting HR may well improve symptoms.

Moreover, it suggests such pacemakers, programmed as in the study, might potentially give a boost to HFpEF patients without chronotropic incompetence but with persisting symptoms despite guideline-directed drug therapy. That’s certainly worth exploring in further trials, Dr. Zile said.
 

How the study worked

The single-center trial entered 107 participants with HFpEF and pacemakers set, at baseline, to a backup resting HR of 60 bpm; their age averaged 75 and 48% were women. Only patients with devices for atrial pacing, conduction-system pacing, or biventricular pacing – which are unlikely to promote ventricular dyssynchrony – were included.

They were randomly assigned, double-blind, to have their devices set to an accelerated backup rate or to be continued at 60 bpm. The backup resting rate set for the intervention group’s 50 patients was individualized based on height and other factors; the median was 75 bpm.

Scores on the Minnesota Living with Heart Failure Questionnaire, the primary endpoint, improved in the intervention group, compared with baseline, by about 11 points after 1 month and by 15 points after 1 year (P < .001).

The scores in the usual-care group deteriorated by half a point and by 3.5 points at 1 month and 1 year (P = .03), respectively.

Consistent advantages for the accelerated-HR strategy were evident throughout the major secondary endpoints. For example, levels of N-terminal pro-B-type natriuretic peptide fell an average 109 pg/dL after 1 month in the accelerated-HR group and rose a mean of 128 pg/dL in the usual-care group (P = .02).

Mean daily pacemaker-monitored activity level rose by 47 minutes by 1 year in the accelerated-HR group, compared with a drop of 22 minutes for those assigned to the standard-care rate (P < .001).

AFib was detected in 18% of intervention patients at the 1-year follow-up, down from 31% at baseline. Their risk ratio for AFib at 1 year was 0.73 (95% confidence interval, 0.55-0.99, P = .04), compared with the control group.

In other patients with HFpEF “we have done pacing studies where we just ramped up the pacing rate, and we see that these pressures in the left atrium actually drop immediately,” Dr. Meyer said. It’s that “unburdening of the atria,” he added, that probably leads to the reduction in AFib.

Dr. Meyer reported holding a patent for pacemakers for HFpEF licensed to Medtronic. Dr. Zile said he consults for Medtronic and has no other relevant financial relationships.

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

Evidence supporting medications that slow the heart rate (HR), notably beta-blockers, is overwhelming in heart failure (HF) with reduced ejection fraction. Underwhelming, however, is clinical trial support for such agents in patients with HF with preserved ejection fraction (HFpEF).
 

Indeed, at least for some such patients, a treatment that modestly accelerates resting HR may be a more promising strategy, suggests an early line of research that challenges prevalent thinking about HFpEF therapy.

In a small, randomized test of the idea, patients with HFpEF and standard pacemakers set to a backup resting HR a bit higher than a standard of care 60 bpm, usually to about 75 bpm, reaped important quality of life benefits.

More strikingly, their natriuretic peptide levels and burden of atrial fibrillation (AFib) fell significantly, the latter by 27% over 1 year.

The trial enrolled only HFpEF patients with pacemakers previously implanted for sick sinus syndrome or atrioventricular block. But researchers say their 107-patient study called myPACE – if confirmed in larger, multicenter trials – lays the groundwork for a device therapy that is broadly useful, potentially, in patients with “preclinical or overt” HFpEF.

Indeed, some of the intervention’s “quite substantial” benefits rivaled or surpassed what his group has observed with available HFpEF drug therapies, including the sodium-glucose cotransporter 2 inhibitors, observed Markus Meyer, MD, PhD, University of Minnesota, Minneapolis.

Moreover, the study may be “the first to show that, with this approach, we can actually also reduce atrial fibrillation,” he said in an interview.

Dr. Meyer said his group is “confident” that the HR-modulation strategy will be successful in appropriate clinical trials and that “pacemakers, in the end, will become a treatment modality for HFpEF.”

Meyer is senior author on the trial’s publication in JAMA Cardiology in JAMA Cardiology (2023 Feb 1. doi: 10.1001/jamacardio.2022.5320), with lead author Margaret Infeld, MD, University of Vermont, Burlington.

The trial entered pacemaker patients with HFpEF of stage B or C – that is, either asymptomatic with structural disease or fully symptomatic. But, Dr. Meyer said, “we saw that the treatment effect was much more pronounced in the patients who had overt heart failure with preserved ejection fraction.”
 

Challenging beta-blocker dogma

The study, the report states, “contradicts canonical thinking” by suggesting HFpEF patients may benefit from a higher resting heart rate, which would presumably shorten diastolic filling time. It also “may help reduce the overprescription of beta-blockers to allow higher heart rates in this population.”

Indeed, Dr. Meyer observed, no one really knows whether beta-blockers work in HFpEF, “because they really have never been studied in a sufficiently powered randomized controlled trial.”

The current study “basically rewrites what we know about the pathophysiology of this form of clinical heart failure,” said Michael R. Zile, MD, Medical University of South Carolina and Veterans Affairs Medical Center, both in Charleston, who was not part of the trial or report.

Previously in HFpEF, Dr. Zile said in an interview, “everybody thought you needed to make diastole longer to give the ventricle a longer time to fill. And none of that really made any sense. It was just sort of accepted as dogma.”

The idea led to widespread use of beta-blockers in HFpEF but “turned out just not to be true.” Indeed, European and North American guidelines, Dr. Zile observed, “have all taken beta-blockers out of the equation for HFpEF” except for treating comorbidities that can be associated with HFpEF, like hypertension or AFib.

Many patients with HFpEF and chronotropic incompetence could be provided with standard pacemakers with primarily conduction-system pacing but are not getting them, he observed.

The current study might help change that. No one is suggesting, based on the current study, “that we start putting pacemakers in every single patient with HFpEF,” Dr. Zile said. Still, for HFpEF patients already with a pacemaker, the study provides “reasonable assurance” that its criteria for elevated resting HR may well improve symptoms.

Moreover, it suggests such pacemakers, programmed as in the study, might potentially give a boost to HFpEF patients without chronotropic incompetence but with persisting symptoms despite guideline-directed drug therapy. That’s certainly worth exploring in further trials, Dr. Zile said.
 

How the study worked

The single-center trial entered 107 participants with HFpEF and pacemakers set, at baseline, to a backup resting HR of 60 bpm; their age averaged 75 and 48% were women. Only patients with devices for atrial pacing, conduction-system pacing, or biventricular pacing – which are unlikely to promote ventricular dyssynchrony – were included.

They were randomly assigned, double-blind, to have their devices set to an accelerated backup rate or to be continued at 60 bpm. The backup resting rate set for the intervention group’s 50 patients was individualized based on height and other factors; the median was 75 bpm.

Scores on the Minnesota Living with Heart Failure Questionnaire, the primary endpoint, improved in the intervention group, compared with baseline, by about 11 points after 1 month and by 15 points after 1 year (P < .001).

The scores in the usual-care group deteriorated by half a point and by 3.5 points at 1 month and 1 year (P = .03), respectively.

Consistent advantages for the accelerated-HR strategy were evident throughout the major secondary endpoints. For example, levels of N-terminal pro-B-type natriuretic peptide fell an average 109 pg/dL after 1 month in the accelerated-HR group and rose a mean of 128 pg/dL in the usual-care group (P = .02).

Mean daily pacemaker-monitored activity level rose by 47 minutes by 1 year in the accelerated-HR group, compared with a drop of 22 minutes for those assigned to the standard-care rate (P < .001).

AFib was detected in 18% of intervention patients at the 1-year follow-up, down from 31% at baseline. Their risk ratio for AFib at 1 year was 0.73 (95% confidence interval, 0.55-0.99, P = .04), compared with the control group.

In other patients with HFpEF “we have done pacing studies where we just ramped up the pacing rate, and we see that these pressures in the left atrium actually drop immediately,” Dr. Meyer said. It’s that “unburdening of the atria,” he added, that probably leads to the reduction in AFib.

Dr. Meyer reported holding a patent for pacemakers for HFpEF licensed to Medtronic. Dr. Zile said he consults for Medtronic and has no other relevant financial relationships.

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

Functions like sensing and pacing in implantable cardioverter defibrillators (ICDs) tend to resist interference from the energy fields generated by MRI, as long as device programming is properly adjusted before the scan.

That applies even to patients with older “legacy” devices implanted before the 2015 advent of MRI-conditional ICDs despite, in practice, prevalent but misguided resistance to obtaining MRI scans in such cases.

Less is known whether such non–MRI-conditional devices, once exposed to MRI, will then reliably deliver antiarrhythmic shocks or antitachycardia pacing (ATP) when needed.

A new cohort study has tried to fill in some of that knowledge gap. It showed no evidence of an excess risk for death or ICD failure to deliver therapy within about 2 years of clinically indicated MRI scans in 629 patients with non–MRI-conditional devices.

The findings, published online in the Annals of Internal Medicine, come with caveats. For example, they’re based on the experience of one, albeit major, center and on MRIs that were for varied indications using 1.5-tesla equipment only.

Despite such safety evidence for appropriately adjusted non–MRI-conditional ICDs, many patients with the devices don›t receive clinically indicated MRI scans due to “perceived risk” that the ICDs won’t then reliably deliver appropriate therapy, observe the authors, led by Joshua Ra, MD, University of California, San Francisco.

Any such risks are “largely theoretical,” but may still explain “why some institutions are shying away from offering MRI exams” to patients with non–MRI-conditional ICDs, Dr. Ra told this news organization.

Many such hospitals refer such patients to more experienced centers, creating “significant logistical barriers in terms of patient access to these MRIs,” he said. “That seems to still be prevalent, unfortunately.”

The current findings “provide another layer of reassurance” that MRI scans in patients with non–MRI-conditional ICDs don’t impair a device’s ability to deliver shocks or ATP, Dr. Ra said.

The cohort consisted of 629 patients with non–MRI-conditional ICDs who underwent 813 clinically indicated MRI exams from 2003 to early 2015 at Johns Hopkins University, Baltimore.

Scans performed within 4 weeks of device implantation were excluded because, the report notes, that’s when spontaneous lead dislodgements or changes to device parameters are most likely to occur. Also excluded were patients with permanent epicardial leads, abandoned leads, or subcutaneous ICD lead systems, the report states.

Still, Dr. Ra said, the cohort is fairly representative of “the modern patient population” of non–MRI-conditional ICD recipients.

A total of 4,177 arrhythmia episodes were documented during a median 2.2 years between scans and last device interrogation prior to pulse-generator change-out or lead exchange.

Of note, Dr. Ra observed, the arrhythmias were confirmed in only 85% of the cohort. Most of the remainder were referral patients who were lost to follow-up whose devices were unavailable for interrogation.

Device therapy terminated “nearly all” documented spontaneous arrhythmias in that 85% of patients, the report states. They included 757 episodes of ventricular tachycardia (VT) or ventricular fibrillation (VF), including 130 that were shocked and the remainder that were managed with ATP. There were also 105 supraventricular tachycardias, all successfully terminated with shocks.

There were no cases of VT or VF detection delay from undersensing or instances of syncope because of “abnormalities” in device detection of arrhythmias, the report states.

Of the 210 known deaths, which occurred a median 1.7 years after the scan, about half were noncardiac and more than a third were cardiac but nonarrhythmic.

Ten patients died from arrhythmia-related cardiac causes, representing 5% of deaths; but 7% of deaths were of undetermined cause.

“No direct relationship of deaths attributable to prior MRI exposure was found or reported,” the report states.

The researchers informally compared outcomes between older and more recently implanted non–MRI-conditional ICDs, the latter presumably with more modern design features. Their data, based on device interrogations, Dr. Ra said, “seem to suggest there were no differences.”

The study was supported by Johns Hopkins University and the National Institutes of Health. Author disclosures are available at apconline.org.

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

Functions like sensing and pacing in implantable cardioverter defibrillators (ICDs) tend to resist interference from the energy fields generated by MRI, as long as device programming is properly adjusted before the scan.

That applies even to patients with older “legacy” devices implanted before the 2015 advent of MRI-conditional ICDs despite, in practice, prevalent but misguided resistance to obtaining MRI scans in such cases.

Less is known whether such non–MRI-conditional devices, once exposed to MRI, will then reliably deliver antiarrhythmic shocks or antitachycardia pacing (ATP) when needed.

A new cohort study has tried to fill in some of that knowledge gap. It showed no evidence of an excess risk for death or ICD failure to deliver therapy within about 2 years of clinically indicated MRI scans in 629 patients with non–MRI-conditional devices.

The findings, published online in the Annals of Internal Medicine, come with caveats. For example, they’re based on the experience of one, albeit major, center and on MRIs that were for varied indications using 1.5-tesla equipment only.

Despite such safety evidence for appropriately adjusted non–MRI-conditional ICDs, many patients with the devices don›t receive clinically indicated MRI scans due to “perceived risk” that the ICDs won’t then reliably deliver appropriate therapy, observe the authors, led by Joshua Ra, MD, University of California, San Francisco.

Any such risks are “largely theoretical,” but may still explain “why some institutions are shying away from offering MRI exams” to patients with non–MRI-conditional ICDs, Dr. Ra told this news organization.

Many such hospitals refer such patients to more experienced centers, creating “significant logistical barriers in terms of patient access to these MRIs,” he said. “That seems to still be prevalent, unfortunately.”

The current findings “provide another layer of reassurance” that MRI scans in patients with non–MRI-conditional ICDs don’t impair a device’s ability to deliver shocks or ATP, Dr. Ra said.

The cohort consisted of 629 patients with non–MRI-conditional ICDs who underwent 813 clinically indicated MRI exams from 2003 to early 2015 at Johns Hopkins University, Baltimore.

Scans performed within 4 weeks of device implantation were excluded because, the report notes, that’s when spontaneous lead dislodgements or changes to device parameters are most likely to occur. Also excluded were patients with permanent epicardial leads, abandoned leads, or subcutaneous ICD lead systems, the report states.

Still, Dr. Ra said, the cohort is fairly representative of “the modern patient population” of non–MRI-conditional ICD recipients.

A total of 4,177 arrhythmia episodes were documented during a median 2.2 years between scans and last device interrogation prior to pulse-generator change-out or lead exchange.

Of note, Dr. Ra observed, the arrhythmias were confirmed in only 85% of the cohort. Most of the remainder were referral patients who were lost to follow-up whose devices were unavailable for interrogation.

Device therapy terminated “nearly all” documented spontaneous arrhythmias in that 85% of patients, the report states. They included 757 episodes of ventricular tachycardia (VT) or ventricular fibrillation (VF), including 130 that were shocked and the remainder that were managed with ATP. There were also 105 supraventricular tachycardias, all successfully terminated with shocks.

There were no cases of VT or VF detection delay from undersensing or instances of syncope because of “abnormalities” in device detection of arrhythmias, the report states.

Of the 210 known deaths, which occurred a median 1.7 years after the scan, about half were noncardiac and more than a third were cardiac but nonarrhythmic.

Ten patients died from arrhythmia-related cardiac causes, representing 5% of deaths; but 7% of deaths were of undetermined cause.

“No direct relationship of deaths attributable to prior MRI exposure was found or reported,” the report states.

The researchers informally compared outcomes between older and more recently implanted non–MRI-conditional ICDs, the latter presumably with more modern design features. Their data, based on device interrogations, Dr. Ra said, “seem to suggest there were no differences.”

The study was supported by Johns Hopkins University and the National Institutes of Health. Author disclosures are available at apconline.org.

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

Functions like sensing and pacing in implantable cardioverter defibrillators (ICDs) tend to resist interference from the energy fields generated by MRI, as long as device programming is properly adjusted before the scan.

That applies even to patients with older “legacy” devices implanted before the 2015 advent of MRI-conditional ICDs despite, in practice, prevalent but misguided resistance to obtaining MRI scans in such cases.

Less is known whether such non–MRI-conditional devices, once exposed to MRI, will then reliably deliver antiarrhythmic shocks or antitachycardia pacing (ATP) when needed.

A new cohort study has tried to fill in some of that knowledge gap. It showed no evidence of an excess risk for death or ICD failure to deliver therapy within about 2 years of clinically indicated MRI scans in 629 patients with non–MRI-conditional devices.

The findings, published online in the Annals of Internal Medicine, come with caveats. For example, they’re based on the experience of one, albeit major, center and on MRIs that were for varied indications using 1.5-tesla equipment only.

Despite such safety evidence for appropriately adjusted non–MRI-conditional ICDs, many patients with the devices don›t receive clinically indicated MRI scans due to “perceived risk” that the ICDs won’t then reliably deliver appropriate therapy, observe the authors, led by Joshua Ra, MD, University of California, San Francisco.

Any such risks are “largely theoretical,” but may still explain “why some institutions are shying away from offering MRI exams” to patients with non–MRI-conditional ICDs, Dr. Ra told this news organization.

Many such hospitals refer such patients to more experienced centers, creating “significant logistical barriers in terms of patient access to these MRIs,” he said. “That seems to still be prevalent, unfortunately.”

The current findings “provide another layer of reassurance” that MRI scans in patients with non–MRI-conditional ICDs don’t impair a device’s ability to deliver shocks or ATP, Dr. Ra said.

The cohort consisted of 629 patients with non–MRI-conditional ICDs who underwent 813 clinically indicated MRI exams from 2003 to early 2015 at Johns Hopkins University, Baltimore.

Scans performed within 4 weeks of device implantation were excluded because, the report notes, that’s when spontaneous lead dislodgements or changes to device parameters are most likely to occur. Also excluded were patients with permanent epicardial leads, abandoned leads, or subcutaneous ICD lead systems, the report states.

Still, Dr. Ra said, the cohort is fairly representative of “the modern patient population” of non–MRI-conditional ICD recipients.

A total of 4,177 arrhythmia episodes were documented during a median 2.2 years between scans and last device interrogation prior to pulse-generator change-out or lead exchange.

Of note, Dr. Ra observed, the arrhythmias were confirmed in only 85% of the cohort. Most of the remainder were referral patients who were lost to follow-up whose devices were unavailable for interrogation.

Device therapy terminated “nearly all” documented spontaneous arrhythmias in that 85% of patients, the report states. They included 757 episodes of ventricular tachycardia (VT) or ventricular fibrillation (VF), including 130 that were shocked and the remainder that were managed with ATP. There were also 105 supraventricular tachycardias, all successfully terminated with shocks.

There were no cases of VT or VF detection delay from undersensing or instances of syncope because of “abnormalities” in device detection of arrhythmias, the report states.

Of the 210 known deaths, which occurred a median 1.7 years after the scan, about half were noncardiac and more than a third were cardiac but nonarrhythmic.

Ten patients died from arrhythmia-related cardiac causes, representing 5% of deaths; but 7% of deaths were of undetermined cause.

“No direct relationship of deaths attributable to prior MRI exposure was found or reported,” the report states.

The researchers informally compared outcomes between older and more recently implanted non–MRI-conditional ICDs, the latter presumably with more modern design features. Their data, based on device interrogations, Dr. Ra said, “seem to suggest there were no differences.”

The study was supported by Johns Hopkins University and the National Institutes of Health. Author disclosures are available at apconline.org.

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

Cardiovascular-related deaths increased dramatically in 2020, marking the largest single-year increase since 2015 and surpassing the previous record from 2003, according to the American Heart Association’s 2023 Statistical Update.

During the first year of the COVID-19 pandemic, the largest increases in cardiovascular disease (CVD) deaths were seen among Asian, Black, and Hispanic people.

“We thought we had been improving as a country with respect to CVD deaths over the past few decades,” Connie Tsao, MD, chair of the AHA Statistical Update writing committee, told this news organization.

Since 2020, however, those trends have changed. Dr. Tsao, a staff cardiologist at Beth Israel Deaconess Medical Center and assistant professor of medicine at Harvard Medical School, both in Boston, noted the firsthand experience that many clinicians had in seeing the shift.

“We observed this sharp rise in age-adjusted CVD deaths, which corresponds to the COVID-19 pandemic,” she said. “Those of us health care providers knew from the overfull hospitals and ICUs that clearly COVID took a toll, particularly in those with cardiovascular risk factors.”

The AHA Statistical Update was published online in the journal Circulation.
 

Data on deaths

Each year, the American Heart Association and National Institutes of Health report the latest statistics related to heart disease, stroke, and cardiovascular risk factors. The 2023 update includes additional information about pandemic-related data.

Overall, the number of people who died from cardiovascular disease increased during the first year of the pandemic, rising from 876,613 in 2019 to 928,741 in 2020. This topped the previous high of 910,000 in 2003.

In addition, the age-adjusted mortality rate increased for the first time in several years, Dr. Tsao said, by a “fairly substantial” 4.6%. The age-adjusted mortality rate incorporates the variability in the aging population from year to year, accounting for higher death rates among older people.

“Even though our total number of deaths has been slowly increasing over the past decade, we have seen a decline each year in our age-adjusted rates – until 2020,” she said. “I think that is very indicative of what has been going on within our country – and the world – in light of people of all ages being impacted by the COVID-19 pandemic, especially before vaccines were available to slow the spread.”

The largest increases in CVD-related deaths occurred among Asian, Black, and Hispanic people, who were most heavily affected during the first year of the pandemic.

“People from communities of color were among those most highly impacted, especially early on, often due to a disproportionate burden of cardiovascular risk factors, such as hypertension and obesity,” Michelle Albert, MD, MPH, president of AHA and a professor of medicine at the University of California, San Francisco, said in a statement.

Dr. Albert, who is also the director of UCSF’s Center for the Study of Adversity and Cardiovascular Disease, does research on health equity and noted the disparities seen in the 2020 numbers. “Additionally, there are socioeconomic considerations, as well as the ongoing impact of structural racism on multiple factors, including limiting the ability to access quality health care,” she said.
 

Additional considerations

In a special commentary, the Statistical Update writing committee pointed to the need to track data for other underrepresented communities, including LGBTQ people and those living in rural or urban areas. The authors outlined several ways to better understand the effects of identity and social determinants of health, as well as strategies to reduce cardiovascular-related disparities.

“This year’s writing group made a concerted effort to gather information on specific social factors related to health risk and outcomes, including sexual orientation, gender identity, urbanization, and socioeconomic position,” Dr. Tsao said. “However, the data are lacking because these communities are grossly underrepresented in clinical and epidemiological research.”

For the next several years, the AHA Statistical Update will likely include more insights about the effects of the COVID-19 pandemic, as well as ongoing disparities.

“For sure, we will be continuing to see the effects of the pandemic for years to come,” Dr. Tsao said. “Recognition of the disparities in outcomes among vulnerable groups should be a call to action among health care providers and researchers, administration, and policy leaders to investigate the reasons and make changes to reverse these trends.”

The statistical update was prepared by a volunteer writing group on behalf of the American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee.

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

Cardiovascular-related deaths increased dramatically in 2020, marking the largest single-year increase since 2015 and surpassing the previous record from 2003, according to the American Heart Association’s 2023 Statistical Update.

During the first year of the COVID-19 pandemic, the largest increases in cardiovascular disease (CVD) deaths were seen among Asian, Black, and Hispanic people.

“We thought we had been improving as a country with respect to CVD deaths over the past few decades,” Connie Tsao, MD, chair of the AHA Statistical Update writing committee, told this news organization.

Since 2020, however, those trends have changed. Dr. Tsao, a staff cardiologist at Beth Israel Deaconess Medical Center and assistant professor of medicine at Harvard Medical School, both in Boston, noted the firsthand experience that many clinicians had in seeing the shift.

“We observed this sharp rise in age-adjusted CVD deaths, which corresponds to the COVID-19 pandemic,” she said. “Those of us health care providers knew from the overfull hospitals and ICUs that clearly COVID took a toll, particularly in those with cardiovascular risk factors.”

The AHA Statistical Update was published online in the journal Circulation.
 

Data on deaths

Each year, the American Heart Association and National Institutes of Health report the latest statistics related to heart disease, stroke, and cardiovascular risk factors. The 2023 update includes additional information about pandemic-related data.

Overall, the number of people who died from cardiovascular disease increased during the first year of the pandemic, rising from 876,613 in 2019 to 928,741 in 2020. This topped the previous high of 910,000 in 2003.

In addition, the age-adjusted mortality rate increased for the first time in several years, Dr. Tsao said, by a “fairly substantial” 4.6%. The age-adjusted mortality rate incorporates the variability in the aging population from year to year, accounting for higher death rates among older people.

“Even though our total number of deaths has been slowly increasing over the past decade, we have seen a decline each year in our age-adjusted rates – until 2020,” she said. “I think that is very indicative of what has been going on within our country – and the world – in light of people of all ages being impacted by the COVID-19 pandemic, especially before vaccines were available to slow the spread.”

The largest increases in CVD-related deaths occurred among Asian, Black, and Hispanic people, who were most heavily affected during the first year of the pandemic.

“People from communities of color were among those most highly impacted, especially early on, often due to a disproportionate burden of cardiovascular risk factors, such as hypertension and obesity,” Michelle Albert, MD, MPH, president of AHA and a professor of medicine at the University of California, San Francisco, said in a statement.

Dr. Albert, who is also the director of UCSF’s Center for the Study of Adversity and Cardiovascular Disease, does research on health equity and noted the disparities seen in the 2020 numbers. “Additionally, there are socioeconomic considerations, as well as the ongoing impact of structural racism on multiple factors, including limiting the ability to access quality health care,” she said.
 

Additional considerations

In a special commentary, the Statistical Update writing committee pointed to the need to track data for other underrepresented communities, including LGBTQ people and those living in rural or urban areas. The authors outlined several ways to better understand the effects of identity and social determinants of health, as well as strategies to reduce cardiovascular-related disparities.

“This year’s writing group made a concerted effort to gather information on specific social factors related to health risk and outcomes, including sexual orientation, gender identity, urbanization, and socioeconomic position,” Dr. Tsao said. “However, the data are lacking because these communities are grossly underrepresented in clinical and epidemiological research.”

For the next several years, the AHA Statistical Update will likely include more insights about the effects of the COVID-19 pandemic, as well as ongoing disparities.

“For sure, we will be continuing to see the effects of the pandemic for years to come,” Dr. Tsao said. “Recognition of the disparities in outcomes among vulnerable groups should be a call to action among health care providers and researchers, administration, and policy leaders to investigate the reasons and make changes to reverse these trends.”

The statistical update was prepared by a volunteer writing group on behalf of the American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee.

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

Cardiovascular-related deaths increased dramatically in 2020, marking the largest single-year increase since 2015 and surpassing the previous record from 2003, according to the American Heart Association’s 2023 Statistical Update.

During the first year of the COVID-19 pandemic, the largest increases in cardiovascular disease (CVD) deaths were seen among Asian, Black, and Hispanic people.

“We thought we had been improving as a country with respect to CVD deaths over the past few decades,” Connie Tsao, MD, chair of the AHA Statistical Update writing committee, told this news organization.

Since 2020, however, those trends have changed. Dr. Tsao, a staff cardiologist at Beth Israel Deaconess Medical Center and assistant professor of medicine at Harvard Medical School, both in Boston, noted the firsthand experience that many clinicians had in seeing the shift.

“We observed this sharp rise in age-adjusted CVD deaths, which corresponds to the COVID-19 pandemic,” she said. “Those of us health care providers knew from the overfull hospitals and ICUs that clearly COVID took a toll, particularly in those with cardiovascular risk factors.”

The AHA Statistical Update was published online in the journal Circulation.
 

Data on deaths

Each year, the American Heart Association and National Institutes of Health report the latest statistics related to heart disease, stroke, and cardiovascular risk factors. The 2023 update includes additional information about pandemic-related data.

Overall, the number of people who died from cardiovascular disease increased during the first year of the pandemic, rising from 876,613 in 2019 to 928,741 in 2020. This topped the previous high of 910,000 in 2003.

In addition, the age-adjusted mortality rate increased for the first time in several years, Dr. Tsao said, by a “fairly substantial” 4.6%. The age-adjusted mortality rate incorporates the variability in the aging population from year to year, accounting for higher death rates among older people.

“Even though our total number of deaths has been slowly increasing over the past decade, we have seen a decline each year in our age-adjusted rates – until 2020,” she said. “I think that is very indicative of what has been going on within our country – and the world – in light of people of all ages being impacted by the COVID-19 pandemic, especially before vaccines were available to slow the spread.”

The largest increases in CVD-related deaths occurred among Asian, Black, and Hispanic people, who were most heavily affected during the first year of the pandemic.

“People from communities of color were among those most highly impacted, especially early on, often due to a disproportionate burden of cardiovascular risk factors, such as hypertension and obesity,” Michelle Albert, MD, MPH, president of AHA and a professor of medicine at the University of California, San Francisco, said in a statement.

Dr. Albert, who is also the director of UCSF’s Center for the Study of Adversity and Cardiovascular Disease, does research on health equity and noted the disparities seen in the 2020 numbers. “Additionally, there are socioeconomic considerations, as well as the ongoing impact of structural racism on multiple factors, including limiting the ability to access quality health care,” she said.
 

Additional considerations

In a special commentary, the Statistical Update writing committee pointed to the need to track data for other underrepresented communities, including LGBTQ people and those living in rural or urban areas. The authors outlined several ways to better understand the effects of identity and social determinants of health, as well as strategies to reduce cardiovascular-related disparities.

“This year’s writing group made a concerted effort to gather information on specific social factors related to health risk and outcomes, including sexual orientation, gender identity, urbanization, and socioeconomic position,” Dr. Tsao said. “However, the data are lacking because these communities are grossly underrepresented in clinical and epidemiological research.”

For the next several years, the AHA Statistical Update will likely include more insights about the effects of the COVID-19 pandemic, as well as ongoing disparities.

“For sure, we will be continuing to see the effects of the pandemic for years to come,” Dr. Tsao said. “Recognition of the disparities in outcomes among vulnerable groups should be a call to action among health care providers and researchers, administration, and policy leaders to investigate the reasons and make changes to reverse these trends.”

The statistical update was prepared by a volunteer writing group on behalf of the American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee.

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

Five factors underlie the ongoing overdiagnosis and misdiagnosis of long QT syndrome (LQTS), including temporary QT prolongation following vasovagal syncope, a “pseudo”-positive genetic test result, family history of sudden cardiac death, transient QT prolongation, and misinterpretation of the QTc interval, a new study suggests.

Awareness of these characteristics, which led to a diagnostic reversal in 290 of 1,841 (16%) patients, could reduce the burden of overdiagnosis on the health care system and on patients and families, senior author Michael J. Ackerman, MD, PhD, of Mayo Clinic, Rochester, Minn., and colleagues conclude.

“The findings are a disturbing and disappointing sequel to the paper we published about LQTS overdiagnosis back in 2007, which showed that 2 out of every 5 patients who came to Mayo Clinic for a second opinion left without the diagnosis,” Dr. Ackerman told this news organization.

To date, Dr. Ackerman has reversed the diagnosis for 350 patients, he said.

The consequences of an LQTS diagnosis are “profound,” he noted, including years of unnecessary drug therapy, implantation of a cardioverter defibrillator, disqualification from competitive sports, and emotional stress to the individual and family.

By pointing out the five biggest mistakes his team has seen, he said, “we hope to equip the diagnostician with the means to challenge and assess the veracity of a LQTS diagnosis.”

The study was published online in the Journal of the American College of Cardiology.
 

Time to do better

Dr. Ackerman and colleagues analyzed electronic medical records on 290 of 1,841 (16%) patients who presented with an outside diagnosis of LQTS but subsequently were dismissed as having normal findings. The mean age of these patients at their first Mayo Clinic evaluation was 22, 60% were female, and the mean QTc interval was 427 ±25 milliseconds.

Overall, 38% of misdiagnoses were the result of misinterpretation of clinical factors; 29%, to diagnostic test misinterpretations; 17%, to an apparently positive genetic test in the context of a weak or absent phenotype; and 16%, to a family history of false LQTS or of sudden cardiac or sudden unexplained death.

More specifically, the most common cause of an LQTS misdiagnosis was QT prolongation following vasovagal syncope, which was misinterpreted as LQTS-attributed syncope.

The second most common cause was an apparently positive genetic test for an LQTS gene that turned out to be a benign or likely benign variant.

The third most common cause was an LQTS diagnosis based solely on a family history of sudden unexplained death (26 patients), QT prolongation (11 patients), or sudden cardiac arrest (9 patients).

The fourth most common cause was an isolated event of QT prolongation (44 patients). The transient QT prolongation was observed under myriad conditions unrelated to LQTS. Yet, 31 patients received a diagnosis based solely on the event.

The fifth most common cause was inclusion of the U-wave in the calculation of the QTc interval (40 patients), leading to an inaccurate interpretation of the electrocardiogram.

Dr. Ackerman noted that these LQTS diagnoses were given by heart-rhythm specialists, and most patients self-referred for a second opinion because a family member questioned the diagnosis after doing their own research.

“It’s time that we step up to the plate and do better,” Dr. Ackerman said. The team’s evaluation of the impact of the misdiagnosis on the patients’ lifestyle and quality of life showed that 45% had been restricted from competitive sports (and subsequently resumed sports activity with no adverse events); 80% had been started on beta-blockers (the drugs were discontinued in 84% as a result of the Mayo Clinic evaluation, whereas 16% opted to continue); and 10 of 22 patients (45%) who received an implanted cardioverter device underwent an extraction of the device without complications.

The authors conclude: “Although missing a patient who truly has LQTS can lead to a tragic outcome, the implications of overdiagnosed LQTS are not trivial and are potentially tragic as well.”
 

‘Tricky diagnosis’

LQTS specialist Peter Aziz, MD, director of pediatric electrophysiology at the Cleveland Clinic, agreed with these findings.

“Most of us ‘channelopathists’ who see LQTS for a living have a good grasp of the disease, but it can be elusive for others,” he said in an interview. “This is a tricky diagnosis. There are ends of the spectrum where people for sure don’t have it and people for sure do. Most clinicians are able to identify that.”

However, he added, “A lot of patients fall into that gray area where it may not be clear at first, even to an expert. But the expert knows how to do a comprehensive evaluation, examining episodes and symptoms and understanding whether they are relevant to LQTS or completely red herrings, and feeling confident about how they calculate the acute interval on an electrocardiogram.”

“All of these may seem mundane, but without the experience, clinicians are vulnerable to miscalculations,” he said. “That’s why our bias, as channelopathists, is that every patient who has a suspected diagnosis or is being treated for LQTS really should see an expert.”

Similarly, Arthur A.M. Wilde, MD, PhD, of the University of Amsterdam, and Peter J. Schwartz, MD, of IRCCS Istituto Auxologico Italiano, Milan, write in a related editorial that it “has to be kept in mind that both diagnostic scores and risk scores are dynamic and can be modified by time and by appropriate therapy.

“Therefore, to make hasty diagnosis of a disease that requires life-long treatment is inappropriate, especially when this is done without the support of adequate, specific experience.”

No commercial funding or relevant financial relationships were reported.

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

Five factors underlie the ongoing overdiagnosis and misdiagnosis of long QT syndrome (LQTS), including temporary QT prolongation following vasovagal syncope, a “pseudo”-positive genetic test result, family history of sudden cardiac death, transient QT prolongation, and misinterpretation of the QTc interval, a new study suggests.

Awareness of these characteristics, which led to a diagnostic reversal in 290 of 1,841 (16%) patients, could reduce the burden of overdiagnosis on the health care system and on patients and families, senior author Michael J. Ackerman, MD, PhD, of Mayo Clinic, Rochester, Minn., and colleagues conclude.

“The findings are a disturbing and disappointing sequel to the paper we published about LQTS overdiagnosis back in 2007, which showed that 2 out of every 5 patients who came to Mayo Clinic for a second opinion left without the diagnosis,” Dr. Ackerman told this news organization.

To date, Dr. Ackerman has reversed the diagnosis for 350 patients, he said.

The consequences of an LQTS diagnosis are “profound,” he noted, including years of unnecessary drug therapy, implantation of a cardioverter defibrillator, disqualification from competitive sports, and emotional stress to the individual and family.

By pointing out the five biggest mistakes his team has seen, he said, “we hope to equip the diagnostician with the means to challenge and assess the veracity of a LQTS diagnosis.”

The study was published online in the Journal of the American College of Cardiology.
 

Time to do better

Dr. Ackerman and colleagues analyzed electronic medical records on 290 of 1,841 (16%) patients who presented with an outside diagnosis of LQTS but subsequently were dismissed as having normal findings. The mean age of these patients at their first Mayo Clinic evaluation was 22, 60% were female, and the mean QTc interval was 427 ±25 milliseconds.

Overall, 38% of misdiagnoses were the result of misinterpretation of clinical factors; 29%, to diagnostic test misinterpretations; 17%, to an apparently positive genetic test in the context of a weak or absent phenotype; and 16%, to a family history of false LQTS or of sudden cardiac or sudden unexplained death.

More specifically, the most common cause of an LQTS misdiagnosis was QT prolongation following vasovagal syncope, which was misinterpreted as LQTS-attributed syncope.

The second most common cause was an apparently positive genetic test for an LQTS gene that turned out to be a benign or likely benign variant.

The third most common cause was an LQTS diagnosis based solely on a family history of sudden unexplained death (26 patients), QT prolongation (11 patients), or sudden cardiac arrest (9 patients).

The fourth most common cause was an isolated event of QT prolongation (44 patients). The transient QT prolongation was observed under myriad conditions unrelated to LQTS. Yet, 31 patients received a diagnosis based solely on the event.

The fifth most common cause was inclusion of the U-wave in the calculation of the QTc interval (40 patients), leading to an inaccurate interpretation of the electrocardiogram.

Dr. Ackerman noted that these LQTS diagnoses were given by heart-rhythm specialists, and most patients self-referred for a second opinion because a family member questioned the diagnosis after doing their own research.

“It’s time that we step up to the plate and do better,” Dr. Ackerman said. The team’s evaluation of the impact of the misdiagnosis on the patients’ lifestyle and quality of life showed that 45% had been restricted from competitive sports (and subsequently resumed sports activity with no adverse events); 80% had been started on beta-blockers (the drugs were discontinued in 84% as a result of the Mayo Clinic evaluation, whereas 16% opted to continue); and 10 of 22 patients (45%) who received an implanted cardioverter device underwent an extraction of the device without complications.

The authors conclude: “Although missing a patient who truly has LQTS can lead to a tragic outcome, the implications of overdiagnosed LQTS are not trivial and are potentially tragic as well.”
 

‘Tricky diagnosis’

LQTS specialist Peter Aziz, MD, director of pediatric electrophysiology at the Cleveland Clinic, agreed with these findings.

“Most of us ‘channelopathists’ who see LQTS for a living have a good grasp of the disease, but it can be elusive for others,” he said in an interview. “This is a tricky diagnosis. There are ends of the spectrum where people for sure don’t have it and people for sure do. Most clinicians are able to identify that.”

However, he added, “A lot of patients fall into that gray area where it may not be clear at first, even to an expert. But the expert knows how to do a comprehensive evaluation, examining episodes and symptoms and understanding whether they are relevant to LQTS or completely red herrings, and feeling confident about how they calculate the acute interval on an electrocardiogram.”

“All of these may seem mundane, but without the experience, clinicians are vulnerable to miscalculations,” he said. “That’s why our bias, as channelopathists, is that every patient who has a suspected diagnosis or is being treated for LQTS really should see an expert.”

Similarly, Arthur A.M. Wilde, MD, PhD, of the University of Amsterdam, and Peter J. Schwartz, MD, of IRCCS Istituto Auxologico Italiano, Milan, write in a related editorial that it “has to be kept in mind that both diagnostic scores and risk scores are dynamic and can be modified by time and by appropriate therapy.

“Therefore, to make hasty diagnosis of a disease that requires life-long treatment is inappropriate, especially when this is done without the support of adequate, specific experience.”

No commercial funding or relevant financial relationships were reported.

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

Five factors underlie the ongoing overdiagnosis and misdiagnosis of long QT syndrome (LQTS), including temporary QT prolongation following vasovagal syncope, a “pseudo”-positive genetic test result, family history of sudden cardiac death, transient QT prolongation, and misinterpretation of the QTc interval, a new study suggests.

Awareness of these characteristics, which led to a diagnostic reversal in 290 of 1,841 (16%) patients, could reduce the burden of overdiagnosis on the health care system and on patients and families, senior author Michael J. Ackerman, MD, PhD, of Mayo Clinic, Rochester, Minn., and colleagues conclude.

“The findings are a disturbing and disappointing sequel to the paper we published about LQTS overdiagnosis back in 2007, which showed that 2 out of every 5 patients who came to Mayo Clinic for a second opinion left without the diagnosis,” Dr. Ackerman told this news organization.

To date, Dr. Ackerman has reversed the diagnosis for 350 patients, he said.

The consequences of an LQTS diagnosis are “profound,” he noted, including years of unnecessary drug therapy, implantation of a cardioverter defibrillator, disqualification from competitive sports, and emotional stress to the individual and family.

By pointing out the five biggest mistakes his team has seen, he said, “we hope to equip the diagnostician with the means to challenge and assess the veracity of a LQTS diagnosis.”

The study was published online in the Journal of the American College of Cardiology.
 

Time to do better

Dr. Ackerman and colleagues analyzed electronic medical records on 290 of 1,841 (16%) patients who presented with an outside diagnosis of LQTS but subsequently were dismissed as having normal findings. The mean age of these patients at their first Mayo Clinic evaluation was 22, 60% were female, and the mean QTc interval was 427 ±25 milliseconds.

Overall, 38% of misdiagnoses were the result of misinterpretation of clinical factors; 29%, to diagnostic test misinterpretations; 17%, to an apparently positive genetic test in the context of a weak or absent phenotype; and 16%, to a family history of false LQTS or of sudden cardiac or sudden unexplained death.

More specifically, the most common cause of an LQTS misdiagnosis was QT prolongation following vasovagal syncope, which was misinterpreted as LQTS-attributed syncope.

The second most common cause was an apparently positive genetic test for an LQTS gene that turned out to be a benign or likely benign variant.

The third most common cause was an LQTS diagnosis based solely on a family history of sudden unexplained death (26 patients), QT prolongation (11 patients), or sudden cardiac arrest (9 patients).

The fourth most common cause was an isolated event of QT prolongation (44 patients). The transient QT prolongation was observed under myriad conditions unrelated to LQTS. Yet, 31 patients received a diagnosis based solely on the event.

The fifth most common cause was inclusion of the U-wave in the calculation of the QTc interval (40 patients), leading to an inaccurate interpretation of the electrocardiogram.

Dr. Ackerman noted that these LQTS diagnoses were given by heart-rhythm specialists, and most patients self-referred for a second opinion because a family member questioned the diagnosis after doing their own research.

“It’s time that we step up to the plate and do better,” Dr. Ackerman said. The team’s evaluation of the impact of the misdiagnosis on the patients’ lifestyle and quality of life showed that 45% had been restricted from competitive sports (and subsequently resumed sports activity with no adverse events); 80% had been started on beta-blockers (the drugs were discontinued in 84% as a result of the Mayo Clinic evaluation, whereas 16% opted to continue); and 10 of 22 patients (45%) who received an implanted cardioverter device underwent an extraction of the device without complications.

The authors conclude: “Although missing a patient who truly has LQTS can lead to a tragic outcome, the implications of overdiagnosed LQTS are not trivial and are potentially tragic as well.”
 

‘Tricky diagnosis’

LQTS specialist Peter Aziz, MD, director of pediatric electrophysiology at the Cleveland Clinic, agreed with these findings.

“Most of us ‘channelopathists’ who see LQTS for a living have a good grasp of the disease, but it can be elusive for others,” he said in an interview. “This is a tricky diagnosis. There are ends of the spectrum where people for sure don’t have it and people for sure do. Most clinicians are able to identify that.”

However, he added, “A lot of patients fall into that gray area where it may not be clear at first, even to an expert. But the expert knows how to do a comprehensive evaluation, examining episodes and symptoms and understanding whether they are relevant to LQTS or completely red herrings, and feeling confident about how they calculate the acute interval on an electrocardiogram.”

“All of these may seem mundane, but without the experience, clinicians are vulnerable to miscalculations,” he said. “That’s why our bias, as channelopathists, is that every patient who has a suspected diagnosis or is being treated for LQTS really should see an expert.”

Similarly, Arthur A.M. Wilde, MD, PhD, of the University of Amsterdam, and Peter J. Schwartz, MD, of IRCCS Istituto Auxologico Italiano, Milan, write in a related editorial that it “has to be kept in mind that both diagnostic scores and risk scores are dynamic and can be modified by time and by appropriate therapy.

“Therefore, to make hasty diagnosis of a disease that requires life-long treatment is inappropriate, especially when this is done without the support of adequate, specific experience.”

No commercial funding or relevant financial relationships were reported.

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

A new study has identified differences in the brain present in patients with the cardiac disorder Takotsubo syndrome versus control scans, which may lead to new therapeutic targets.

Takotsubo syndrome is an acute heart failure cardiomyopathy mimicking an acute myocardial infarction in its presentation, but on investigation, no obstructive coronary disease is present. The syndrome, which mainly affects women, typically occurs in the aftermath of intense emotional or physical stress and has become known as “broken heart syndrome.”

The mechanism by which emotional processing in the context of stress leads to significant cardiac injury and acute left ventricular dysfunction is not understood. So, the current study examined both structural and functional effects in the brain in patients with Takotsubo syndrome to shed more light on the issue.

“The abnormalities in the thalamus-amygdala-insula and basal ganglia support the concept of involvement of higher-level function centers in Takotsubo syndrome, and interventions aimed at modulating these may be of benefit,” the authors conclude.

The study was published online in JACC: Heart Failure.

Lead author Hilal Khan, MB BCh, BAO, from the University of Aberdeen (Scotland), explained to this news organization that patients with Takotsubo syndrome have a substantial drop in heart function and show an apical ballooning of the heart.

It is a relatively newly defined condition and was first described in 1990 in Japan, and so named because the heart was thought to resemble the Takotsubo pot used by Japanese fishermen to trap octopus.

Although uncommon, the condition is not rare. Dr. Khan estimates that about 1 in 20 women with suspected MI turn out to have Takotsubo syndrome, with cases increasing in times of global stress such as in the recent pandemic.

While patients tend to recover in a few weeks and the pumping function of the heart usually returns to normal, there are some long-term cardiac complications including a reduction in global longitudinal strain, and patients have similar long-term outcomes as those with MI.  

“It is believed that these cardiac changes may be triggered by changes in the brain caused by emotional stress, so we wanted to look at this more closely,” Dr. Khan said.  

There have been a couple of studies published previously looking at brain changes in Takotsubo syndrome, but they haven’t reported patients in the acute stage of the condition and they haven’t compared the patients to controls, he noted.

For the current study, the researchers looked at brain scans for 25 acute Takotsubo patients and in 25 controls matched for age, gender, comorbidities, and medications. All the patients and controls were examined using the same MRI scanner in the same hospital.

“This is the largest structural and functional brain study of acute Takotsubo syndrome patients compared with matched control subjects,” Dr. Khan said.

The researchers looked at many different factors including brain volume in different regions, cortical thickness, small-vessel disease, and functional and structural connectivity to try and obtain a complete holistic view of the brain.

Key findings were that patients with Takotsubo syndrome had smaller brain volumes, compared with matched controls, driven by a reduction in brain surface area. In contrast, the insula and thalamus regions were larger.

“A reduction in brain volume could be caused by inflammation; this is often seen in depression,” Dr. Khan commented.  

The researchers also found that certain areas of the brain had a reduction in functional connectivity, particularly the thalamus – the central autonomic area of the brain, which regulates the autonomic nervous system – and also the insula region, which is also involved in the autonomic regulation of the heart.

They suggest that there may be a loss of parasympathetic inhibition in Takotsubo syndrome, which would fit the theory that Takotsubo brings with it a surge of catecholamines, which could injure the heart.

Reduced functional connectivity was also seen in parts of the basal ganglia, abnormalities of which have been associated with an increased risk of both arrhythmias, and in the amygdala, similar to patients with a tendency to catastrophize events.

The other observation was that there appeared to be an increase in structural connectivity in certain areas of the brain. 

“Structural pathways seem to be increased but functional connectivity was reduced, so while physical pathways are enhanced, they don’t seem to be doing anything,” Dr. Khan said. “We don’t know why this occurs, or if this has happened over time and made the brain and heart more vulnerable in some way.”

One possibility is that ,under a significant emotional stress, the brain may divert function from some areas to others to be able to cope, and that this results in reduced functioning in areas of the brain responsible for regulating the heart, Dr. Khan suggested.  

“We believe this study confirms that the brain is involved in Takotsubo syndrome, and we have identified markers in the brain that may be contributing to the condition,” he said.

The researchers are planning to further study these markers and whether it might be possible to modulate these changes with various interventions such as exercise or mindfulness.

“We believe there is some interface between the brain changes and the impact on the heart. We don’t think it is just the release of catecholamines that causes damage to the heart. We think there is something else happening as well,” Dr. Khan commented.  

It is also possible that the hearts of patients with Takotsubo syndrome are predisposed in some way and more vulnerable to this condition occurring. 

“It will be important to obtain a greater understanding of the triggers and identify people who may be vulnerable,” Dr. Khan noted. “Around 10% of individuals who experience Takotsubo syndrome will have a recurrence, so we need to try and develop preventative strategies to reduce this.”

He suggested that possible preventive or therapeutic approaches may involve interventions such as exercise or mindfulness.

This work was supported by National Health Service Grampian Endowment. The authors report no relevant financial relationships.

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

A new study has identified differences in the brain present in patients with the cardiac disorder Takotsubo syndrome versus control scans, which may lead to new therapeutic targets.

Takotsubo syndrome is an acute heart failure cardiomyopathy mimicking an acute myocardial infarction in its presentation, but on investigation, no obstructive coronary disease is present. The syndrome, which mainly affects women, typically occurs in the aftermath of intense emotional or physical stress and has become known as “broken heart syndrome.”

The mechanism by which emotional processing in the context of stress leads to significant cardiac injury and acute left ventricular dysfunction is not understood. So, the current study examined both structural and functional effects in the brain in patients with Takotsubo syndrome to shed more light on the issue.

“The abnormalities in the thalamus-amygdala-insula and basal ganglia support the concept of involvement of higher-level function centers in Takotsubo syndrome, and interventions aimed at modulating these may be of benefit,” the authors conclude.

The study was published online in JACC: Heart Failure.

Lead author Hilal Khan, MB BCh, BAO, from the University of Aberdeen (Scotland), explained to this news organization that patients with Takotsubo syndrome have a substantial drop in heart function and show an apical ballooning of the heart.

It is a relatively newly defined condition and was first described in 1990 in Japan, and so named because the heart was thought to resemble the Takotsubo pot used by Japanese fishermen to trap octopus.

Although uncommon, the condition is not rare. Dr. Khan estimates that about 1 in 20 women with suspected MI turn out to have Takotsubo syndrome, with cases increasing in times of global stress such as in the recent pandemic.

While patients tend to recover in a few weeks and the pumping function of the heart usually returns to normal, there are some long-term cardiac complications including a reduction in global longitudinal strain, and patients have similar long-term outcomes as those with MI.  

“It is believed that these cardiac changes may be triggered by changes in the brain caused by emotional stress, so we wanted to look at this more closely,” Dr. Khan said.  

There have been a couple of studies published previously looking at brain changes in Takotsubo syndrome, but they haven’t reported patients in the acute stage of the condition and they haven’t compared the patients to controls, he noted.

For the current study, the researchers looked at brain scans for 25 acute Takotsubo patients and in 25 controls matched for age, gender, comorbidities, and medications. All the patients and controls were examined using the same MRI scanner in the same hospital.

“This is the largest structural and functional brain study of acute Takotsubo syndrome patients compared with matched control subjects,” Dr. Khan said.

The researchers looked at many different factors including brain volume in different regions, cortical thickness, small-vessel disease, and functional and structural connectivity to try and obtain a complete holistic view of the brain.

Key findings were that patients with Takotsubo syndrome had smaller brain volumes, compared with matched controls, driven by a reduction in brain surface area. In contrast, the insula and thalamus regions were larger.

“A reduction in brain volume could be caused by inflammation; this is often seen in depression,” Dr. Khan commented.  

The researchers also found that certain areas of the brain had a reduction in functional connectivity, particularly the thalamus – the central autonomic area of the brain, which regulates the autonomic nervous system – and also the insula region, which is also involved in the autonomic regulation of the heart.

They suggest that there may be a loss of parasympathetic inhibition in Takotsubo syndrome, which would fit the theory that Takotsubo brings with it a surge of catecholamines, which could injure the heart.

Reduced functional connectivity was also seen in parts of the basal ganglia, abnormalities of which have been associated with an increased risk of both arrhythmias, and in the amygdala, similar to patients with a tendency to catastrophize events.

The other observation was that there appeared to be an increase in structural connectivity in certain areas of the brain. 

“Structural pathways seem to be increased but functional connectivity was reduced, so while physical pathways are enhanced, they don’t seem to be doing anything,” Dr. Khan said. “We don’t know why this occurs, or if this has happened over time and made the brain and heart more vulnerable in some way.”

One possibility is that ,under a significant emotional stress, the brain may divert function from some areas to others to be able to cope, and that this results in reduced functioning in areas of the brain responsible for regulating the heart, Dr. Khan suggested.  

“We believe this study confirms that the brain is involved in Takotsubo syndrome, and we have identified markers in the brain that may be contributing to the condition,” he said.

The researchers are planning to further study these markers and whether it might be possible to modulate these changes with various interventions such as exercise or mindfulness.

“We believe there is some interface between the brain changes and the impact on the heart. We don’t think it is just the release of catecholamines that causes damage to the heart. We think there is something else happening as well,” Dr. Khan commented.  

It is also possible that the hearts of patients with Takotsubo syndrome are predisposed in some way and more vulnerable to this condition occurring. 

“It will be important to obtain a greater understanding of the triggers and identify people who may be vulnerable,” Dr. Khan noted. “Around 10% of individuals who experience Takotsubo syndrome will have a recurrence, so we need to try and develop preventative strategies to reduce this.”

He suggested that possible preventive or therapeutic approaches may involve interventions such as exercise or mindfulness.

This work was supported by National Health Service Grampian Endowment. The authors report no relevant financial relationships.

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

A new study has identified differences in the brain present in patients with the cardiac disorder Takotsubo syndrome versus control scans, which may lead to new therapeutic targets.

Takotsubo syndrome is an acute heart failure cardiomyopathy mimicking an acute myocardial infarction in its presentation, but on investigation, no obstructive coronary disease is present. The syndrome, which mainly affects women, typically occurs in the aftermath of intense emotional or physical stress and has become known as “broken heart syndrome.”

The mechanism by which emotional processing in the context of stress leads to significant cardiac injury and acute left ventricular dysfunction is not understood. So, the current study examined both structural and functional effects in the brain in patients with Takotsubo syndrome to shed more light on the issue.

“The abnormalities in the thalamus-amygdala-insula and basal ganglia support the concept of involvement of higher-level function centers in Takotsubo syndrome, and interventions aimed at modulating these may be of benefit,” the authors conclude.

The study was published online in JACC: Heart Failure.

Lead author Hilal Khan, MB BCh, BAO, from the University of Aberdeen (Scotland), explained to this news organization that patients with Takotsubo syndrome have a substantial drop in heart function and show an apical ballooning of the heart.

It is a relatively newly defined condition and was first described in 1990 in Japan, and so named because the heart was thought to resemble the Takotsubo pot used by Japanese fishermen to trap octopus.

Although uncommon, the condition is not rare. Dr. Khan estimates that about 1 in 20 women with suspected MI turn out to have Takotsubo syndrome, with cases increasing in times of global stress such as in the recent pandemic.

While patients tend to recover in a few weeks and the pumping function of the heart usually returns to normal, there are some long-term cardiac complications including a reduction in global longitudinal strain, and patients have similar long-term outcomes as those with MI.  

“It is believed that these cardiac changes may be triggered by changes in the brain caused by emotional stress, so we wanted to look at this more closely,” Dr. Khan said.  

There have been a couple of studies published previously looking at brain changes in Takotsubo syndrome, but they haven’t reported patients in the acute stage of the condition and they haven’t compared the patients to controls, he noted.

For the current study, the researchers looked at brain scans for 25 acute Takotsubo patients and in 25 controls matched for age, gender, comorbidities, and medications. All the patients and controls were examined using the same MRI scanner in the same hospital.

“This is the largest structural and functional brain study of acute Takotsubo syndrome patients compared with matched control subjects,” Dr. Khan said.

The researchers looked at many different factors including brain volume in different regions, cortical thickness, small-vessel disease, and functional and structural connectivity to try and obtain a complete holistic view of the brain.

Key findings were that patients with Takotsubo syndrome had smaller brain volumes, compared with matched controls, driven by a reduction in brain surface area. In contrast, the insula and thalamus regions were larger.

“A reduction in brain volume could be caused by inflammation; this is often seen in depression,” Dr. Khan commented.  

The researchers also found that certain areas of the brain had a reduction in functional connectivity, particularly the thalamus – the central autonomic area of the brain, which regulates the autonomic nervous system – and also the insula region, which is also involved in the autonomic regulation of the heart.

They suggest that there may be a loss of parasympathetic inhibition in Takotsubo syndrome, which would fit the theory that Takotsubo brings with it a surge of catecholamines, which could injure the heart.

Reduced functional connectivity was also seen in parts of the basal ganglia, abnormalities of which have been associated with an increased risk of both arrhythmias, and in the amygdala, similar to patients with a tendency to catastrophize events.

The other observation was that there appeared to be an increase in structural connectivity in certain areas of the brain. 

“Structural pathways seem to be increased but functional connectivity was reduced, so while physical pathways are enhanced, they don’t seem to be doing anything,” Dr. Khan said. “We don’t know why this occurs, or if this has happened over time and made the brain and heart more vulnerable in some way.”

One possibility is that ,under a significant emotional stress, the brain may divert function from some areas to others to be able to cope, and that this results in reduced functioning in areas of the brain responsible for regulating the heart, Dr. Khan suggested.  

“We believe this study confirms that the brain is involved in Takotsubo syndrome, and we have identified markers in the brain that may be contributing to the condition,” he said.

The researchers are planning to further study these markers and whether it might be possible to modulate these changes with various interventions such as exercise or mindfulness.

“We believe there is some interface between the brain changes and the impact on the heart. We don’t think it is just the release of catecholamines that causes damage to the heart. We think there is something else happening as well,” Dr. Khan commented.  

It is also possible that the hearts of patients with Takotsubo syndrome are predisposed in some way and more vulnerable to this condition occurring. 

“It will be important to obtain a greater understanding of the triggers and identify people who may be vulnerable,” Dr. Khan noted. “Around 10% of individuals who experience Takotsubo syndrome will have a recurrence, so we need to try and develop preventative strategies to reduce this.”

He suggested that possible preventive or therapeutic approaches may involve interventions such as exercise or mindfulness.

This work was supported by National Health Service Grampian Endowment. The authors report no relevant financial relationships.

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

Atrial dysfunction, widely considered a marker or consequence of other heart diseases, is a relevant clinical entity, which is why it is justified to define atrial failure or insufficiency as “a new syndrome that all cardiologists should be aware of,” said Adrián Baranchuk, MD, PhD, professor of medicine at Queen’s University, Kingston, Ont., during the 2022 48th Argentine Congress of Cardiology in Buenos Aires.

“The atria are like the heart’s silly sisters and can fail just like the ventricle fails. Understanding their function and dysfunction helps us to understand heart failure. And as electrophysiologists and clinical cardiologists, we have to embrace this concept and understand it in depth,” Dr. Baranchuk, president-elect of the Inter-American Society of Cardiology, said in an interview.

The specialist first proposed atrial failure as an entity or syndrome in early 2020 in an article in the Journal of the American College of Cardiology. His four collaborators included the experienced Eugene Braunwald, MD, from Brigham and Women’s Hospital, Boston, and Antoni Bayés de Luna, PhD, from the department of medicine of the autonomous University of Barcelona.
 

Pathology despite function

“In many patients with heart failure, the pump function is preserved, but what causes the pathology? For the last 5-10 years, attention has been focused on the ventricle: whether it contracts poorly or whether it contracts properly and relaxes poorly. However, we have also seen patients in whom the ventricle contracts properly and relaxes properly. Where else can we look? We started looking at atrial contraction, especially the left atrium,” recalled Dr. Baranchuk.

He and his colleagues proposed the following consensus definition of atrial failure or insufficiency: any atrial dysfunction (anatomical, mechanical, electrical, and rheological, including blood homeostasis) that causes impaired function, heart symptoms, and a worsening of quality of life (or life expectancy) in the absence of significant valvular or ventricular abnormalities.

In his presentation, recorded and projected by video from Canada, Dr. Baranchuk pointed out that there are two large groups of causes of atrial failure: one that has to do with electrical disorders of atrial and interatrial contraction and another related to the progressive development of fibrosis, which gradually leads to dyssynchrony in interatrial contraction, pump failure, and impaired atrial function as a reservoir and as a conduit.

“In turn, these mechanisms trigger neurohormonal alterations that perpetuate atrial failure, so it is not just a matter of progressive fibrosis, which is very difficult to treat, but also of constant neurohormonal activation that guarantees that these phenomena never resolve,” said Dr. Baranchuk. The manifestations or end point of this cascade of events are the known ones: stroke, ischemia, and heart failure.
 

New entity necessary?

Defining atrial failure or insufficiency as a clinical entity not only restores the hierarchy of the atria in cardiac function, which was already postulated by William Harvey in 1628, but also enables new lines of research that would eventually allow timely preventive interventions.

One key is early recognition of partial or total interatrial block by analyzing the characteristics of the P wave on the electrocardiogram, which could serve to prevent progression to atrial fibrillation. Left atrial enlargement can also be detected by echocardiography.

“When the contractile impairment is severe and you are in atrial fibrillation, all that remains is to apply patches. The strategy is to correct risk factors beforehand, such as high blood pressure, sleep apnea, or high-dose alcohol consumption, as well as tirelessly searching for atrial fibrillation, with Holter electrocardiograms, continuous monitoring devices, such as Apple Watch, KardiaMobile, or an implantable loop recorder,” Dr. Baranchuk said in an interview.

Two ongoing or planned studies, ARCADIA and AMIABLE, will seek to determine whether anticoagulation in patients with elevated cardiovascular risk scores and any of these atrial disorders that have not yet led to atrial fibrillation could reduce the incidence of stroke.

The strategy has a rational basis. In a subanalysis of raw data from the NAVIGATE ESUS study in patients with embolic stroke of unknown cause, Dr. Baranchuk estimated that the presence of interatrial block was a tenfold higher predictor of the risk of experiencing a second stroke. Another 2018 observational study in which he participated found that in outpatients with heart failure, advanced interatrial block approximately tripled the risk of developing atrial fibrillation and ischemic stroke.

For Dr. Baranchuk, other questions that still need to be answered include whether drugs used for heart failure with preserved ejection fraction can be useful in primary atrial failure or whether specific drugs can be repositioned or developed to suppress or slow the process of fibrosis. “From generating the clinical concept, many lines of research are enabled.”

“The concept of atrial failure is very interesting and opens our eyes to treatments,” another speaker at the session, Alejo Tronconi, MD, a cardiologist and electrophysiologist at the Cardiovascular Institute of the South, Cipolletti, Argentina, said in an interview.

“It is necessary to cut circuits that have been extensively studied in heart failure models, and now we are beginning to see their participation in atrial dysfunction,” he said.

Dr. Baranchuk and Dr. Tronconi declared no relevant financial conflict of interest.

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

Atrial dysfunction, widely considered a marker or consequence of other heart diseases, is a relevant clinical entity, which is why it is justified to define atrial failure or insufficiency as “a new syndrome that all cardiologists should be aware of,” said Adrián Baranchuk, MD, PhD, professor of medicine at Queen’s University, Kingston, Ont., during the 2022 48th Argentine Congress of Cardiology in Buenos Aires.

“The atria are like the heart’s silly sisters and can fail just like the ventricle fails. Understanding their function and dysfunction helps us to understand heart failure. And as electrophysiologists and clinical cardiologists, we have to embrace this concept and understand it in depth,” Dr. Baranchuk, president-elect of the Inter-American Society of Cardiology, said in an interview.

The specialist first proposed atrial failure as an entity or syndrome in early 2020 in an article in the Journal of the American College of Cardiology. His four collaborators included the experienced Eugene Braunwald, MD, from Brigham and Women’s Hospital, Boston, and Antoni Bayés de Luna, PhD, from the department of medicine of the autonomous University of Barcelona.
 

Pathology despite function

“In many patients with heart failure, the pump function is preserved, but what causes the pathology? For the last 5-10 years, attention has been focused on the ventricle: whether it contracts poorly or whether it contracts properly and relaxes poorly. However, we have also seen patients in whom the ventricle contracts properly and relaxes properly. Where else can we look? We started looking at atrial contraction, especially the left atrium,” recalled Dr. Baranchuk.

He and his colleagues proposed the following consensus definition of atrial failure or insufficiency: any atrial dysfunction (anatomical, mechanical, electrical, and rheological, including blood homeostasis) that causes impaired function, heart symptoms, and a worsening of quality of life (or life expectancy) in the absence of significant valvular or ventricular abnormalities.

In his presentation, recorded and projected by video from Canada, Dr. Baranchuk pointed out that there are two large groups of causes of atrial failure: one that has to do with electrical disorders of atrial and interatrial contraction and another related to the progressive development of fibrosis, which gradually leads to dyssynchrony in interatrial contraction, pump failure, and impaired atrial function as a reservoir and as a conduit.

“In turn, these mechanisms trigger neurohormonal alterations that perpetuate atrial failure, so it is not just a matter of progressive fibrosis, which is very difficult to treat, but also of constant neurohormonal activation that guarantees that these phenomena never resolve,” said Dr. Baranchuk. The manifestations or end point of this cascade of events are the known ones: stroke, ischemia, and heart failure.
 

New entity necessary?

Defining atrial failure or insufficiency as a clinical entity not only restores the hierarchy of the atria in cardiac function, which was already postulated by William Harvey in 1628, but also enables new lines of research that would eventually allow timely preventive interventions.

One key is early recognition of partial or total interatrial block by analyzing the characteristics of the P wave on the electrocardiogram, which could serve to prevent progression to atrial fibrillation. Left atrial enlargement can also be detected by echocardiography.

“When the contractile impairment is severe and you are in atrial fibrillation, all that remains is to apply patches. The strategy is to correct risk factors beforehand, such as high blood pressure, sleep apnea, or high-dose alcohol consumption, as well as tirelessly searching for atrial fibrillation, with Holter electrocardiograms, continuous monitoring devices, such as Apple Watch, KardiaMobile, or an implantable loop recorder,” Dr. Baranchuk said in an interview.

Two ongoing or planned studies, ARCADIA and AMIABLE, will seek to determine whether anticoagulation in patients with elevated cardiovascular risk scores and any of these atrial disorders that have not yet led to atrial fibrillation could reduce the incidence of stroke.

The strategy has a rational basis. In a subanalysis of raw data from the NAVIGATE ESUS study in patients with embolic stroke of unknown cause, Dr. Baranchuk estimated that the presence of interatrial block was a tenfold higher predictor of the risk of experiencing a second stroke. Another 2018 observational study in which he participated found that in outpatients with heart failure, advanced interatrial block approximately tripled the risk of developing atrial fibrillation and ischemic stroke.

For Dr. Baranchuk, other questions that still need to be answered include whether drugs used for heart failure with preserved ejection fraction can be useful in primary atrial failure or whether specific drugs can be repositioned or developed to suppress or slow the process of fibrosis. “From generating the clinical concept, many lines of research are enabled.”

“The concept of atrial failure is very interesting and opens our eyes to treatments,” another speaker at the session, Alejo Tronconi, MD, a cardiologist and electrophysiologist at the Cardiovascular Institute of the South, Cipolletti, Argentina, said in an interview.

“It is necessary to cut circuits that have been extensively studied in heart failure models, and now we are beginning to see their participation in atrial dysfunction,” he said.

Dr. Baranchuk and Dr. Tronconi declared no relevant financial conflict of interest.

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

Atrial dysfunction, widely considered a marker or consequence of other heart diseases, is a relevant clinical entity, which is why it is justified to define atrial failure or insufficiency as “a new syndrome that all cardiologists should be aware of,” said Adrián Baranchuk, MD, PhD, professor of medicine at Queen’s University, Kingston, Ont., during the 2022 48th Argentine Congress of Cardiology in Buenos Aires.

“The atria are like the heart’s silly sisters and can fail just like the ventricle fails. Understanding their function and dysfunction helps us to understand heart failure. And as electrophysiologists and clinical cardiologists, we have to embrace this concept and understand it in depth,” Dr. Baranchuk, president-elect of the Inter-American Society of Cardiology, said in an interview.

The specialist first proposed atrial failure as an entity or syndrome in early 2020 in an article in the Journal of the American College of Cardiology. His four collaborators included the experienced Eugene Braunwald, MD, from Brigham and Women’s Hospital, Boston, and Antoni Bayés de Luna, PhD, from the department of medicine of the autonomous University of Barcelona.
 

Pathology despite function

“In many patients with heart failure, the pump function is preserved, but what causes the pathology? For the last 5-10 years, attention has been focused on the ventricle: whether it contracts poorly or whether it contracts properly and relaxes poorly. However, we have also seen patients in whom the ventricle contracts properly and relaxes properly. Where else can we look? We started looking at atrial contraction, especially the left atrium,” recalled Dr. Baranchuk.

He and his colleagues proposed the following consensus definition of atrial failure or insufficiency: any atrial dysfunction (anatomical, mechanical, electrical, and rheological, including blood homeostasis) that causes impaired function, heart symptoms, and a worsening of quality of life (or life expectancy) in the absence of significant valvular or ventricular abnormalities.

In his presentation, recorded and projected by video from Canada, Dr. Baranchuk pointed out that there are two large groups of causes of atrial failure: one that has to do with electrical disorders of atrial and interatrial contraction and another related to the progressive development of fibrosis, which gradually leads to dyssynchrony in interatrial contraction, pump failure, and impaired atrial function as a reservoir and as a conduit.

“In turn, these mechanisms trigger neurohormonal alterations that perpetuate atrial failure, so it is not just a matter of progressive fibrosis, which is very difficult to treat, but also of constant neurohormonal activation that guarantees that these phenomena never resolve,” said Dr. Baranchuk. The manifestations or end point of this cascade of events are the known ones: stroke, ischemia, and heart failure.
 

New entity necessary?

Defining atrial failure or insufficiency as a clinical entity not only restores the hierarchy of the atria in cardiac function, which was already postulated by William Harvey in 1628, but also enables new lines of research that would eventually allow timely preventive interventions.

One key is early recognition of partial or total interatrial block by analyzing the characteristics of the P wave on the electrocardiogram, which could serve to prevent progression to atrial fibrillation. Left atrial enlargement can also be detected by echocardiography.

“When the contractile impairment is severe and you are in atrial fibrillation, all that remains is to apply patches. The strategy is to correct risk factors beforehand, such as high blood pressure, sleep apnea, or high-dose alcohol consumption, as well as tirelessly searching for atrial fibrillation, with Holter electrocardiograms, continuous monitoring devices, such as Apple Watch, KardiaMobile, or an implantable loop recorder,” Dr. Baranchuk said in an interview.

Two ongoing or planned studies, ARCADIA and AMIABLE, will seek to determine whether anticoagulation in patients with elevated cardiovascular risk scores and any of these atrial disorders that have not yet led to atrial fibrillation could reduce the incidence of stroke.

The strategy has a rational basis. In a subanalysis of raw data from the NAVIGATE ESUS study in patients with embolic stroke of unknown cause, Dr. Baranchuk estimated that the presence of interatrial block was a tenfold higher predictor of the risk of experiencing a second stroke. Another 2018 observational study in which he participated found that in outpatients with heart failure, advanced interatrial block approximately tripled the risk of developing atrial fibrillation and ischemic stroke.

For Dr. Baranchuk, other questions that still need to be answered include whether drugs used for heart failure with preserved ejection fraction can be useful in primary atrial failure or whether specific drugs can be repositioned or developed to suppress or slow the process of fibrosis. “From generating the clinical concept, many lines of research are enabled.”

“The concept of atrial failure is very interesting and opens our eyes to treatments,” another speaker at the session, Alejo Tronconi, MD, a cardiologist and electrophysiologist at the Cardiovascular Institute of the South, Cipolletti, Argentina, said in an interview.

“It is necessary to cut circuits that have been extensively studied in heart failure models, and now we are beginning to see their participation in atrial dysfunction,” he said.

Dr. Baranchuk and Dr. Tronconi declared no relevant financial conflict of interest.

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

Atropine is often considered a first-line intervention for unstable bradycardia. Unfortunately, atropine often fails when the bradycardia is not vagally induced and is not indicated for high-level atrioventricular blocks (for example, Mobitz II and third-degree AV block).

Transvenous pacing is typically the most effective therapy for unstable bradycardia but it is invasive, takes some time to perform, and is a procedure for which many acute care physicians lack comfort and significant experience. Transcutaneous pacing (TCP), on the other hand, is fast, easy to perform, and tends to be well tolerated by most patients when they receive appropriate doses of analgesia.

Unfortunately, TCP often fails to produce electrical or, more importantly, mechanical capture. Oftentimes when capture initially fails, the electrical current is increased in hopes of gaining capture but much to the discomfort of the patient. Increased body mass index can contribute to failure to capture, but what about TCP pad position? Despite recommendations for TCP in the United States and European resuscitation guidelines for many years, until now, no studies have evaluated optimal pad position for TCP. As a result, the default position for most clinicians using TCP has been the anterior-lateral (AL) position on the chest wall.

A study published in October 2022 compared the common AL position (anterior pad placed at the right upper chest and lateral pad placed over the left lower rib cage at the mid-axillary line) with the anterior-posterior (AP) position (anterior pad placed on the left chest over the apex of the heart and the posterior pad on the left mid-back area approximating the level of the mid-portion of the heart). The AP position has become more commonly used in defibrillating arrested hearts because it more accurately sends the current through the left ventricle. The concern with the AL position, especially in patients with large body habitus, is that the vector of the current may partially or entirely miss the left ventricle.

Moayedi and colleagues hypothesized that optimal TCP should employ pad placement that is similar to that used during optimal defibrillation attempts. They conducted a study comparing AL versus AP position during TCP and published their results in two parts, which will be discussed together.

The investigators evaluated 20 patients (6 women, 14 men) who had elective cardioversion of atrial fibrillation in the electrophysiology lab (Resuscitation. 2022 Dec;181:140-6). After successful cardioversion to sinus rhythm, the cardioversion pads were removed, and two new sets of pacer pads were placed on the patients’ chests. Pads were placed in both the AL and the AP positions, as previously described. Starting at a current output of 40 mA, the output was slowly increased on one set of pads until mechanical capture was obtained at the same rate as the pacer setting for at least 10 seconds. Pacing was then discontinued, but then the process was repeated using the second set of pads. The order in which the positions were tested (that is, AL tested first vs. AP tested first) was alternated. If capture was not obtained by 140 mA (the pacer’s maximum output), failure to capture was documented. Both positions were tested in all patients except for three cases where the second position was not tested because of inadequate analgesia.

The investigators found that 8 in 19 (42%) of the AL trials and 14 in 18 (78%) of the AP trials successfully captured. For the 17 participants who completed both trials, both positions captured in 8 in 17 (47%). AP but not AL was captured in 5 in 17 (29%); AL but not AP was captured in 0 cases. Neither position captured in 4 in 17 (24%). Of note, there was no association between successful capture and body mass index, chest circumference, or chest diameter. The AP position was more successful in both women and men, compared with the AL position. The investigators also found that, among the successful trials, the AP position tended to capture at lower currents than the AL position (93 mA vs. 126 mA).
 

In summary

TCP is a potentially lifesaving intervention in the treatment of patients with unstable bradycardia. Many of us who have attempted to perform TCP on unstable patients have frequently been disappointed with the results. In retrospect, however, I can recall that each time I have attempted this procedure, it has been using pads placed in the AL position.

Now for the first time we have data indicating that the standard AL position may be suboptimal, compared with the AP position. The study by Moayedi and colleagues is small, but the results are compelling, and the AP pad placement intuitively makes more sense. By using the AP pad placement, which provides greater likelihood of electrical current passing through the left ventricle, we should expect a greater likelihood of successful capture during attempts at TCP. In addition, we may anticipate lower analgesia needs if the AP position requires less current for success. Kudos to Moayedi and colleagues for performing a novel study of a critical procedure in acute care medicine.

Amal Mattu, MD, is a professor, vice chair of education, and codirector of the emergency cardiology fellowship in the department of emergency medicine at the University of Maryland, Baltimore. He had no disclosures. A version of this article first appeared on Medscape.com.

Atropine is often considered a first-line intervention for unstable bradycardia. Unfortunately, atropine often fails when the bradycardia is not vagally induced and is not indicated for high-level atrioventricular blocks (for example, Mobitz II and third-degree AV block).

Transvenous pacing is typically the most effective therapy for unstable bradycardia but it is invasive, takes some time to perform, and is a procedure for which many acute care physicians lack comfort and significant experience. Transcutaneous pacing (TCP), on the other hand, is fast, easy to perform, and tends to be well tolerated by most patients when they receive appropriate doses of analgesia.

Unfortunately, TCP often fails to produce electrical or, more importantly, mechanical capture. Oftentimes when capture initially fails, the electrical current is increased in hopes of gaining capture but much to the discomfort of the patient. Increased body mass index can contribute to failure to capture, but what about TCP pad position? Despite recommendations for TCP in the United States and European resuscitation guidelines for many years, until now, no studies have evaluated optimal pad position for TCP. As a result, the default position for most clinicians using TCP has been the anterior-lateral (AL) position on the chest wall.

A study published in October 2022 compared the common AL position (anterior pad placed at the right upper chest and lateral pad placed over the left lower rib cage at the mid-axillary line) with the anterior-posterior (AP) position (anterior pad placed on the left chest over the apex of the heart and the posterior pad on the left mid-back area approximating the level of the mid-portion of the heart). The AP position has become more commonly used in defibrillating arrested hearts because it more accurately sends the current through the left ventricle. The concern with the AL position, especially in patients with large body habitus, is that the vector of the current may partially or entirely miss the left ventricle.

Moayedi and colleagues hypothesized that optimal TCP should employ pad placement that is similar to that used during optimal defibrillation attempts. They conducted a study comparing AL versus AP position during TCP and published their results in two parts, which will be discussed together.

The investigators evaluated 20 patients (6 women, 14 men) who had elective cardioversion of atrial fibrillation in the electrophysiology lab (Resuscitation. 2022 Dec;181:140-6). After successful cardioversion to sinus rhythm, the cardioversion pads were removed, and two new sets of pacer pads were placed on the patients’ chests. Pads were placed in both the AL and the AP positions, as previously described. Starting at a current output of 40 mA, the output was slowly increased on one set of pads until mechanical capture was obtained at the same rate as the pacer setting for at least 10 seconds. Pacing was then discontinued, but then the process was repeated using the second set of pads. The order in which the positions were tested (that is, AL tested first vs. AP tested first) was alternated. If capture was not obtained by 140 mA (the pacer’s maximum output), failure to capture was documented. Both positions were tested in all patients except for three cases where the second position was not tested because of inadequate analgesia.

The investigators found that 8 in 19 (42%) of the AL trials and 14 in 18 (78%) of the AP trials successfully captured. For the 17 participants who completed both trials, both positions captured in 8 in 17 (47%). AP but not AL was captured in 5 in 17 (29%); AL but not AP was captured in 0 cases. Neither position captured in 4 in 17 (24%). Of note, there was no association between successful capture and body mass index, chest circumference, or chest diameter. The AP position was more successful in both women and men, compared with the AL position. The investigators also found that, among the successful trials, the AP position tended to capture at lower currents than the AL position (93 mA vs. 126 mA).
 

In summary

TCP is a potentially lifesaving intervention in the treatment of patients with unstable bradycardia. Many of us who have attempted to perform TCP on unstable patients have frequently been disappointed with the results. In retrospect, however, I can recall that each time I have attempted this procedure, it has been using pads placed in the AL position.

Now for the first time we have data indicating that the standard AL position may be suboptimal, compared with the AP position. The study by Moayedi and colleagues is small, but the results are compelling, and the AP pad placement intuitively makes more sense. By using the AP pad placement, which provides greater likelihood of electrical current passing through the left ventricle, we should expect a greater likelihood of successful capture during attempts at TCP. In addition, we may anticipate lower analgesia needs if the AP position requires less current for success. Kudos to Moayedi and colleagues for performing a novel study of a critical procedure in acute care medicine.

Amal Mattu, MD, is a professor, vice chair of education, and codirector of the emergency cardiology fellowship in the department of emergency medicine at the University of Maryland, Baltimore. He had no disclosures. A version of this article first appeared on Medscape.com.

Atropine is often considered a first-line intervention for unstable bradycardia. Unfortunately, atropine often fails when the bradycardia is not vagally induced and is not indicated for high-level atrioventricular blocks (for example, Mobitz II and third-degree AV block).

Transvenous pacing is typically the most effective therapy for unstable bradycardia but it is invasive, takes some time to perform, and is a procedure for which many acute care physicians lack comfort and significant experience. Transcutaneous pacing (TCP), on the other hand, is fast, easy to perform, and tends to be well tolerated by most patients when they receive appropriate doses of analgesia.

Unfortunately, TCP often fails to produce electrical or, more importantly, mechanical capture. Oftentimes when capture initially fails, the electrical current is increased in hopes of gaining capture but much to the discomfort of the patient. Increased body mass index can contribute to failure to capture, but what about TCP pad position? Despite recommendations for TCP in the United States and European resuscitation guidelines for many years, until now, no studies have evaluated optimal pad position for TCP. As a result, the default position for most clinicians using TCP has been the anterior-lateral (AL) position on the chest wall.

A study published in October 2022 compared the common AL position (anterior pad placed at the right upper chest and lateral pad placed over the left lower rib cage at the mid-axillary line) with the anterior-posterior (AP) position (anterior pad placed on the left chest over the apex of the heart and the posterior pad on the left mid-back area approximating the level of the mid-portion of the heart). The AP position has become more commonly used in defibrillating arrested hearts because it more accurately sends the current through the left ventricle. The concern with the AL position, especially in patients with large body habitus, is that the vector of the current may partially or entirely miss the left ventricle.

Moayedi and colleagues hypothesized that optimal TCP should employ pad placement that is similar to that used during optimal defibrillation attempts. They conducted a study comparing AL versus AP position during TCP and published their results in two parts, which will be discussed together.

The investigators evaluated 20 patients (6 women, 14 men) who had elective cardioversion of atrial fibrillation in the electrophysiology lab (Resuscitation. 2022 Dec;181:140-6). After successful cardioversion to sinus rhythm, the cardioversion pads were removed, and two new sets of pacer pads were placed on the patients’ chests. Pads were placed in both the AL and the AP positions, as previously described. Starting at a current output of 40 mA, the output was slowly increased on one set of pads until mechanical capture was obtained at the same rate as the pacer setting for at least 10 seconds. Pacing was then discontinued, but then the process was repeated using the second set of pads. The order in which the positions were tested (that is, AL tested first vs. AP tested first) was alternated. If capture was not obtained by 140 mA (the pacer’s maximum output), failure to capture was documented. Both positions were tested in all patients except for three cases where the second position was not tested because of inadequate analgesia.

The investigators found that 8 in 19 (42%) of the AL trials and 14 in 18 (78%) of the AP trials successfully captured. For the 17 participants who completed both trials, both positions captured in 8 in 17 (47%). AP but not AL was captured in 5 in 17 (29%); AL but not AP was captured in 0 cases. Neither position captured in 4 in 17 (24%). Of note, there was no association between successful capture and body mass index, chest circumference, or chest diameter. The AP position was more successful in both women and men, compared with the AL position. The investigators also found that, among the successful trials, the AP position tended to capture at lower currents than the AL position (93 mA vs. 126 mA).
 

In summary

TCP is a potentially lifesaving intervention in the treatment of patients with unstable bradycardia. Many of us who have attempted to perform TCP on unstable patients have frequently been disappointed with the results. In retrospect, however, I can recall that each time I have attempted this procedure, it has been using pads placed in the AL position.

Now for the first time we have data indicating that the standard AL position may be suboptimal, compared with the AP position. The study by Moayedi and colleagues is small, but the results are compelling, and the AP pad placement intuitively makes more sense. By using the AP pad placement, which provides greater likelihood of electrical current passing through the left ventricle, we should expect a greater likelihood of successful capture during attempts at TCP. In addition, we may anticipate lower analgesia needs if the AP position requires less current for success. Kudos to Moayedi and colleagues for performing a novel study of a critical procedure in acute care medicine.

Amal Mattu, MD, is a professor, vice chair of education, and codirector of the emergency cardiology fellowship in the department of emergency medicine at the University of Maryland, Baltimore. He had no disclosures. A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Hello. This is Dr. JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk with you about a recent report in JAMA Cardiology on atrial fibrillation (AF), sex differences, and modifiable risk factors.

We looked at these questions in our vitamin D and omega-3 trial VITAL in an ancillary study called VITAL Rhythm, led by Dr. Christine Albert at Cedars-Sinai. And this particular project was led by Dr. Hasan Siddiqi at Vanderbilt.

As you know, AF is the most common arrhythmia in the world, and it’s burgeoning in numbers, primarily because of the aging of the population. It’s also a major cause of stroke, heart failure, and cardiovascular mortality. Although women are known to have lower rates of AF than men, they’re also known to have a higher risk for cardiovascular complications and sequelae, such as higher risk for stroke and CVD mortality. Therefore, we thought that understanding sex differences in risk and modifiable risk factors for AF that could reduce the burden of disease would be important.

It’s known that greater height is a risk factor for AF, but the extent to which it explains the differences in AF risk between men and women isn’t really known. So we looked at these questions in the VITAL cohort. VITAL has more than 25,000 participants. It’s a large, diverse, nationwide cohort. About 51% are women, and all are aged 50 years or older, with a mean age of 67. All were free of known clinical cardiovascular disease at the start of the study.

AF reports were confirmed by medical records and also supplemented by Medicare CMS linkage for fuller ascertainment of outcomes. We had 900 incident cases of AF in the study, and we did see that women were less likely to be diagnosed with AF. They had a 32% lower risk – strongly statistically significant compared with men, with a P < .001. Women were also more likely to be symptomatic: About 77% of women vs. 63% of men had symptoms prior to or at diagnosis.

It was very interesting that adjustment for height eliminated the lower risk for AF in women compared with men. After accounting for height, there was not only no reduction in risk for AF among the women, there was actually a reversal of the association so that there was a slightly higher risk for AF in the women. Other risk factors for AF in the cohort included older age, higher body mass index, hypertension, and higher consumption of alcohol. We did not see an association between diabetes and higher risk for AF. We also saw no clear association with physical activity, although very strenuous physical activity has been linked to AF in some other studies.

We looked at the interventions of vitamin D (2,000 IU/day) and omega-3 fatty acids (460 mg/day of EPA and 380 mg/day of DHA) and found no association with AF, although some other studies have seen increased risk for AF with higher doses of the marine omega-3s > 1 g/day and certainly at doses of 4 g/day. So overall, the findings highlight the fact that many of the risk factors for AF do seem to be modifiable, and it is really important to identify and try to reduce these risk factors in order to reduce the burden of AF. This may be particularly important in women because women are more likely to have stroke and cardiovascular mortality in these adverse cardiovascular outcomes.

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

This transcript has been edited for clarity.

Hello. This is Dr. JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk with you about a recent report in JAMA Cardiology on atrial fibrillation (AF), sex differences, and modifiable risk factors.

We looked at these questions in our vitamin D and omega-3 trial VITAL in an ancillary study called VITAL Rhythm, led by Dr. Christine Albert at Cedars-Sinai. And this particular project was led by Dr. Hasan Siddiqi at Vanderbilt.

As you know, AF is the most common arrhythmia in the world, and it’s burgeoning in numbers, primarily because of the aging of the population. It’s also a major cause of stroke, heart failure, and cardiovascular mortality. Although women are known to have lower rates of AF than men, they’re also known to have a higher risk for cardiovascular complications and sequelae, such as higher risk for stroke and CVD mortality. Therefore, we thought that understanding sex differences in risk and modifiable risk factors for AF that could reduce the burden of disease would be important.

It’s known that greater height is a risk factor for AF, but the extent to which it explains the differences in AF risk between men and women isn’t really known. So we looked at these questions in the VITAL cohort. VITAL has more than 25,000 participants. It’s a large, diverse, nationwide cohort. About 51% are women, and all are aged 50 years or older, with a mean age of 67. All were free of known clinical cardiovascular disease at the start of the study.

AF reports were confirmed by medical records and also supplemented by Medicare CMS linkage for fuller ascertainment of outcomes. We had 900 incident cases of AF in the study, and we did see that women were less likely to be diagnosed with AF. They had a 32% lower risk – strongly statistically significant compared with men, with a P < .001. Women were also more likely to be symptomatic: About 77% of women vs. 63% of men had symptoms prior to or at diagnosis.

It was very interesting that adjustment for height eliminated the lower risk for AF in women compared with men. After accounting for height, there was not only no reduction in risk for AF among the women, there was actually a reversal of the association so that there was a slightly higher risk for AF in the women. Other risk factors for AF in the cohort included older age, higher body mass index, hypertension, and higher consumption of alcohol. We did not see an association between diabetes and higher risk for AF. We also saw no clear association with physical activity, although very strenuous physical activity has been linked to AF in some other studies.

We looked at the interventions of vitamin D (2,000 IU/day) and omega-3 fatty acids (460 mg/day of EPA and 380 mg/day of DHA) and found no association with AF, although some other studies have seen increased risk for AF with higher doses of the marine omega-3s > 1 g/day and certainly at doses of 4 g/day. So overall, the findings highlight the fact that many of the risk factors for AF do seem to be modifiable, and it is really important to identify and try to reduce these risk factors in order to reduce the burden of AF. This may be particularly important in women because women are more likely to have stroke and cardiovascular mortality in these adverse cardiovascular outcomes.

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

This transcript has been edited for clarity.

Hello. This is Dr. JoAnn Manson, professor of medicine at Harvard Medical School and Brigham and Women’s Hospital. I’d like to talk with you about a recent report in JAMA Cardiology on atrial fibrillation (AF), sex differences, and modifiable risk factors.

We looked at these questions in our vitamin D and omega-3 trial VITAL in an ancillary study called VITAL Rhythm, led by Dr. Christine Albert at Cedars-Sinai. And this particular project was led by Dr. Hasan Siddiqi at Vanderbilt.

As you know, AF is the most common arrhythmia in the world, and it’s burgeoning in numbers, primarily because of the aging of the population. It’s also a major cause of stroke, heart failure, and cardiovascular mortality. Although women are known to have lower rates of AF than men, they’re also known to have a higher risk for cardiovascular complications and sequelae, such as higher risk for stroke and CVD mortality. Therefore, we thought that understanding sex differences in risk and modifiable risk factors for AF that could reduce the burden of disease would be important.

It’s known that greater height is a risk factor for AF, but the extent to which it explains the differences in AF risk between men and women isn’t really known. So we looked at these questions in the VITAL cohort. VITAL has more than 25,000 participants. It’s a large, diverse, nationwide cohort. About 51% are women, and all are aged 50 years or older, with a mean age of 67. All were free of known clinical cardiovascular disease at the start of the study.

AF reports were confirmed by medical records and also supplemented by Medicare CMS linkage for fuller ascertainment of outcomes. We had 900 incident cases of AF in the study, and we did see that women were less likely to be diagnosed with AF. They had a 32% lower risk – strongly statistically significant compared with men, with a P < .001. Women were also more likely to be symptomatic: About 77% of women vs. 63% of men had symptoms prior to or at diagnosis.

It was very interesting that adjustment for height eliminated the lower risk for AF in women compared with men. After accounting for height, there was not only no reduction in risk for AF among the women, there was actually a reversal of the association so that there was a slightly higher risk for AF in the women. Other risk factors for AF in the cohort included older age, higher body mass index, hypertension, and higher consumption of alcohol. We did not see an association between diabetes and higher risk for AF. We also saw no clear association with physical activity, although very strenuous physical activity has been linked to AF in some other studies.

We looked at the interventions of vitamin D (2,000 IU/day) and omega-3 fatty acids (460 mg/day of EPA and 380 mg/day of DHA) and found no association with AF, although some other studies have seen increased risk for AF with higher doses of the marine omega-3s > 1 g/day and certainly at doses of 4 g/day. So overall, the findings highlight the fact that many of the risk factors for AF do seem to be modifiable, and it is really important to identify and try to reduce these risk factors in order to reduce the burden of AF. This may be particularly important in women because women are more likely to have stroke and cardiovascular mortality in these adverse cardiovascular outcomes.

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

The obvious first statement is that it’s neither wise nor appropriate to speculate on the specifics of Damar Hamlin’s cardiac event during a football game on Jan. 2 (including the possibility of commotio cordis) or his ongoing care. The public nature of his collapse induces intense curiosity but people with illness deserve privacy. Privacy in health care is in short supply. I disagree strongly with those who say his doctors ought to be giving public updates. That’s up to the family.

But there are important general concepts to consider about this incident. These include ...

Cardiac arrest can happen to anyone

People with structural heart disease or other chronic illnesses have a higher risk of arrhythmia, but the notion that athletes are immune from cardiac arrest is wrong. This sentence almost seems too obvious to write, but to this day, I hear clinicians express surprise that an athletic person has heart disease.

Survival turns on rapid and effective intervention

In the old days of electrophysiology, we used to test implantable cardioverter-defibrillators during an implant procedure by inducing ventricular fibrillation (VF) and watching the device convert it. Thankfully, trials have shown that this is no longer necessary for most implants.

When you induce VF In the EP lab, you learn quickly that a) it causes loss of consciousness in a matter of seconds, b) rapid defibrillation restores consciousness, often without the patients knowing or remembering they passed out, and c) the failure of the shock to terminate VF results in deterioration in a matter of 1-2 minutes. Even 1 minute in VF feels so long.

Need is an appropriate word in VF treatment

Clinicians often use the verb need. As in, this patient needs this pill or this procedure. It’s rarely appropriate.

But in the case of treating VF, patients truly need rapid defibrillation. Survival of out-of-hospital cardiac arrest is low because there just aren’t enough automated external defibrillators (AEDs) or people trained to use them. A study of patients who had out-of-hospital cardiac arrest in Denmark found that 30-day survival almost doubled (28.8% vs. 16.4%), when the nearest AED was accessible.

Bystanders must act

The public messages are simple: If a person loses consciousness in front of you, and is not breathing normally, assume it is a cardiac arrest, call 911 to get professional help, and start hands-only chest compressions. Don’t spend time checking for a pulse or trying to wake the person. If this is not a cardiac arrest, they will soon tell you to stop compressing their chest. Seconds matter.

Chest compressions are important but what is really needed is defibrillation. A crucial step in CPR is to send someone to get an AED and get the pads attached. If this is a shockable rhythm, deliver the shock. Hamlin’s collapse emphasizes the importance of the AED; without it, his survival to the hospital would have been unlikely.

Widespread preparticipation screening of young athletes remains a bad idea

Whenever cardiac arrest occurs in an athlete, in such a public way, people think about prevention. Surely it is better to prevent such an event than react to it, goes the thinking. The argument against this idea has four prongs:

The incidence of cardiac disease in a young athlete is extremely low, which sets up a situation where most “positive” tests are false positive. A false positive screening ECG or echocardiogram can create harm in multiple ways. One is the risk from downstream procedures, but worse is the inappropriate disqualification from sport. Healthwise, few harms could be greater than creating long-term fear of exercise in someone.

There is also the problem of false-negative screening tests. An ECG may be normal in the setting of hypertrophic cardiomyopathy. And a normal echocardiogram does not exclude arrhythmogenic right ventricular cardiomyopathy or other genetic causes of cardiac arrest. In a 2018 study from a major sports cardiology center in London, 6 of the 8 sudden cardiac deaths in their series were in athletes who had no detectable abnormalities on screening.

Even when disease is found, it’s not clear that prohibiting participation in sports prevents sudden death. Many previous class III recommendations against participation in sport now carry class II – may be considered – designations.

Finally, screening for any disease loses value as treatments improve. Public education regarding rapid intervention with CPR and AED use is the best treatment option. A great example is the case of Christian Erikson, a Danish soccer player who suffered cardiac arrest during a match at the European Championships in 2021 and was rapidly defibrillated on the field. Therapy was so effective that he was conscious and able to wave to fans on his way out of the stadium. He has now returned to elite competition.

Proponents of screening might oppose my take by saying that National Football League players are intensely screened. But this is different from widespread screening of high school and college athletes. It might sound harsh to say, but professional teams have dualities of interests in the health of their athletes given the million-dollar contracts.

What’s more, professional teams can afford to hire expert cardiologists to perform the testing. This would likely reduce the rate of false-positive findings, compared with screening in the community setting. I often have young people referred to me because of asymptomatic bradycardia found during athletic screening – an obviously normal finding.

Conclusions

As long as there are sports, there will be athletes who suffer cardiac arrest.

We can both hope for Hamlin’s full recovery and learn lessons to help reduce the rate of death from out-of-hospital cardiac arrest. This mostly involves education on how to help fellow humans and a public health commitment to access to AEDs.

John Mandrola, MD, practices cardiac electrophysiology in Louisville, Ky. and is a writer and podcaster for Medscape. He has disclosed no relevant financial relationships. A version of this article first appeared on Medscape.com.

The obvious first statement is that it’s neither wise nor appropriate to speculate on the specifics of Damar Hamlin’s cardiac event during a football game on Jan. 2 (including the possibility of commotio cordis) or his ongoing care. The public nature of his collapse induces intense curiosity but people with illness deserve privacy. Privacy in health care is in short supply. I disagree strongly with those who say his doctors ought to be giving public updates. That’s up to the family.

But there are important general concepts to consider about this incident. These include ...

Cardiac arrest can happen to anyone

People with structural heart disease or other chronic illnesses have a higher risk of arrhythmia, but the notion that athletes are immune from cardiac arrest is wrong. This sentence almost seems too obvious to write, but to this day, I hear clinicians express surprise that an athletic person has heart disease.

Survival turns on rapid and effective intervention

In the old days of electrophysiology, we used to test implantable cardioverter-defibrillators during an implant procedure by inducing ventricular fibrillation (VF) and watching the device convert it. Thankfully, trials have shown that this is no longer necessary for most implants.

When you induce VF In the EP lab, you learn quickly that a) it causes loss of consciousness in a matter of seconds, b) rapid defibrillation restores consciousness, often without the patients knowing or remembering they passed out, and c) the failure of the shock to terminate VF results in deterioration in a matter of 1-2 minutes. Even 1 minute in VF feels so long.

Need is an appropriate word in VF treatment

Clinicians often use the verb need. As in, this patient needs this pill or this procedure. It’s rarely appropriate.

But in the case of treating VF, patients truly need rapid defibrillation. Survival of out-of-hospital cardiac arrest is low because there just aren’t enough automated external defibrillators (AEDs) or people trained to use them. A study of patients who had out-of-hospital cardiac arrest in Denmark found that 30-day survival almost doubled (28.8% vs. 16.4%), when the nearest AED was accessible.

Bystanders must act

The public messages are simple: If a person loses consciousness in front of you, and is not breathing normally, assume it is a cardiac arrest, call 911 to get professional help, and start hands-only chest compressions. Don’t spend time checking for a pulse or trying to wake the person. If this is not a cardiac arrest, they will soon tell you to stop compressing their chest. Seconds matter.

Chest compressions are important but what is really needed is defibrillation. A crucial step in CPR is to send someone to get an AED and get the pads attached. If this is a shockable rhythm, deliver the shock. Hamlin’s collapse emphasizes the importance of the AED; without it, his survival to the hospital would have been unlikely.

Widespread preparticipation screening of young athletes remains a bad idea

Whenever cardiac arrest occurs in an athlete, in such a public way, people think about prevention. Surely it is better to prevent such an event than react to it, goes the thinking. The argument against this idea has four prongs:

The incidence of cardiac disease in a young athlete is extremely low, which sets up a situation where most “positive” tests are false positive. A false positive screening ECG or echocardiogram can create harm in multiple ways. One is the risk from downstream procedures, but worse is the inappropriate disqualification from sport. Healthwise, few harms could be greater than creating long-term fear of exercise in someone.

There is also the problem of false-negative screening tests. An ECG may be normal in the setting of hypertrophic cardiomyopathy. And a normal echocardiogram does not exclude arrhythmogenic right ventricular cardiomyopathy or other genetic causes of cardiac arrest. In a 2018 study from a major sports cardiology center in London, 6 of the 8 sudden cardiac deaths in their series were in athletes who had no detectable abnormalities on screening.

Even when disease is found, it’s not clear that prohibiting participation in sports prevents sudden death. Many previous class III recommendations against participation in sport now carry class II – may be considered – designations.

Finally, screening for any disease loses value as treatments improve. Public education regarding rapid intervention with CPR and AED use is the best treatment option. A great example is the case of Christian Erikson, a Danish soccer player who suffered cardiac arrest during a match at the European Championships in 2021 and was rapidly defibrillated on the field. Therapy was so effective that he was conscious and able to wave to fans on his way out of the stadium. He has now returned to elite competition.

Proponents of screening might oppose my take by saying that National Football League players are intensely screened. But this is different from widespread screening of high school and college athletes. It might sound harsh to say, but professional teams have dualities of interests in the health of their athletes given the million-dollar contracts.

What’s more, professional teams can afford to hire expert cardiologists to perform the testing. This would likely reduce the rate of false-positive findings, compared with screening in the community setting. I often have young people referred to me because of asymptomatic bradycardia found during athletic screening – an obviously normal finding.

Conclusions

As long as there are sports, there will be athletes who suffer cardiac arrest.

We can both hope for Hamlin’s full recovery and learn lessons to help reduce the rate of death from out-of-hospital cardiac arrest. This mostly involves education on how to help fellow humans and a public health commitment to access to AEDs.

John Mandrola, MD, practices cardiac electrophysiology in Louisville, Ky. and is a writer and podcaster for Medscape. He has disclosed no relevant financial relationships. A version of this article first appeared on Medscape.com.

The obvious first statement is that it’s neither wise nor appropriate to speculate on the specifics of Damar Hamlin’s cardiac event during a football game on Jan. 2 (including the possibility of commotio cordis) or his ongoing care. The public nature of his collapse induces intense curiosity but people with illness deserve privacy. Privacy in health care is in short supply. I disagree strongly with those who say his doctors ought to be giving public updates. That’s up to the family.

But there are important general concepts to consider about this incident. These include ...

Cardiac arrest can happen to anyone

People with structural heart disease or other chronic illnesses have a higher risk of arrhythmia, but the notion that athletes are immune from cardiac arrest is wrong. This sentence almost seems too obvious to write, but to this day, I hear clinicians express surprise that an athletic person has heart disease.

Survival turns on rapid and effective intervention

In the old days of electrophysiology, we used to test implantable cardioverter-defibrillators during an implant procedure by inducing ventricular fibrillation (VF) and watching the device convert it. Thankfully, trials have shown that this is no longer necessary for most implants.

When you induce VF In the EP lab, you learn quickly that a) it causes loss of consciousness in a matter of seconds, b) rapid defibrillation restores consciousness, often without the patients knowing or remembering they passed out, and c) the failure of the shock to terminate VF results in deterioration in a matter of 1-2 minutes. Even 1 minute in VF feels so long.

Need is an appropriate word in VF treatment

Clinicians often use the verb need. As in, this patient needs this pill or this procedure. It’s rarely appropriate.

But in the case of treating VF, patients truly need rapid defibrillation. Survival of out-of-hospital cardiac arrest is low because there just aren’t enough automated external defibrillators (AEDs) or people trained to use them. A study of patients who had out-of-hospital cardiac arrest in Denmark found that 30-day survival almost doubled (28.8% vs. 16.4%), when the nearest AED was accessible.

Bystanders must act

The public messages are simple: If a person loses consciousness in front of you, and is not breathing normally, assume it is a cardiac arrest, call 911 to get professional help, and start hands-only chest compressions. Don’t spend time checking for a pulse or trying to wake the person. If this is not a cardiac arrest, they will soon tell you to stop compressing their chest. Seconds matter.

Chest compressions are important but what is really needed is defibrillation. A crucial step in CPR is to send someone to get an AED and get the pads attached. If this is a shockable rhythm, deliver the shock. Hamlin’s collapse emphasizes the importance of the AED; without it, his survival to the hospital would have been unlikely.

Widespread preparticipation screening of young athletes remains a bad idea

Whenever cardiac arrest occurs in an athlete, in such a public way, people think about prevention. Surely it is better to prevent such an event than react to it, goes the thinking. The argument against this idea has four prongs:

The incidence of cardiac disease in a young athlete is extremely low, which sets up a situation where most “positive” tests are false positive. A false positive screening ECG or echocardiogram can create harm in multiple ways. One is the risk from downstream procedures, but worse is the inappropriate disqualification from sport. Healthwise, few harms could be greater than creating long-term fear of exercise in someone.

There is also the problem of false-negative screening tests. An ECG may be normal in the setting of hypertrophic cardiomyopathy. And a normal echocardiogram does not exclude arrhythmogenic right ventricular cardiomyopathy or other genetic causes of cardiac arrest. In a 2018 study from a major sports cardiology center in London, 6 of the 8 sudden cardiac deaths in their series were in athletes who had no detectable abnormalities on screening.

Even when disease is found, it’s not clear that prohibiting participation in sports prevents sudden death. Many previous class III recommendations against participation in sport now carry class II – may be considered – designations.

Finally, screening for any disease loses value as treatments improve. Public education regarding rapid intervention with CPR and AED use is the best treatment option. A great example is the case of Christian Erikson, a Danish soccer player who suffered cardiac arrest during a match at the European Championships in 2021 and was rapidly defibrillated on the field. Therapy was so effective that he was conscious and able to wave to fans on his way out of the stadium. He has now returned to elite competition.

Proponents of screening might oppose my take by saying that National Football League players are intensely screened. But this is different from widespread screening of high school and college athletes. It might sound harsh to say, but professional teams have dualities of interests in the health of their athletes given the million-dollar contracts.

What’s more, professional teams can afford to hire expert cardiologists to perform the testing. This would likely reduce the rate of false-positive findings, compared with screening in the community setting. I often have young people referred to me because of asymptomatic bradycardia found during athletic screening – an obviously normal finding.

Conclusions

As long as there are sports, there will be athletes who suffer cardiac arrest.

We can both hope for Hamlin’s full recovery and learn lessons to help reduce the rate of death from out-of-hospital cardiac arrest. This mostly involves education on how to help fellow humans and a public health commitment to access to AEDs.

John Mandrola, MD, practices cardiac electrophysiology in Louisville, Ky. and is a writer and podcaster for Medscape. He has disclosed no relevant financial relationships. A version of this article first appeared on Medscape.com.