Arrhythmias & EP

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.

The chance of surviving a cardiac arrest varies widely across hospitals in the United States, even when the arrest occurs in the highly controlled setting of a cardiac catheterization lab, a new study indicates.

Among 4,787 patients who arrested in the cath lab at 231 hospitals in the Get With The Guidelines (GWTG) Resuscitation registry, only about one-third survived to discharge. The median risk-adjusted survival rate (RASR) for all hospitals was 36%.

When stratified by RASR tertiles, however, median survival rates were 20%, 36%, and 52% for hospitals in the lowest, middle, and highest tertiles.

The odds of survival differed by 71% in similar patients presenting at two randomly selected hospitals (median odds ratio, 1.71; 95% confidence interval, 1.52-1.87).

“The good news is that cardiac arrests in the cath lab are relatively infrequent, but the bad news is that they still occur and the outcomes are, in general, pretty dismal,” senior author Deepak L. Bhatt, MD, MPH, said in an interview. “So anything that we can do as hospitals [and] health care systems to improve the care of these patients could go a long way.”

Hospital and patient factors

Possible explanations for the wide disparity in survival are the small number of cardiac arrests in the cath lab, the increasing complexity of cases, and the fact that patients are often very sick and may experience a problem during a procedure, or both, Dr. Bhatt suggested. Cath labs also vary in how they handle resuscitative efforts and access to advanced mechanical support devices, such as extracorporeal membrane oxygenation (ECMO).

“It’s not available in every cath lab and, even in hospitals that have it, they may not have a given ECMO circuit available at the exact time the patient’s having a cardiac arrest,” he said. “That’s one example of something that can make, in my opinion, a big difference in whether a patient lives or dies if they’re having a cardiac arrest but may not always be easily deployed.”

When the investigators looked specifically at hospital-level factors, only yearly volume of cardiac arrests in the cath lab was significantly associated with risk-adjusted survival (P < .01), whereas hospital size, rural or urban setting, teaching status, and geographic location were not.

In multivariate adjusted analyses, factors associated with survival to discharge included age (OR, 0.78), Black race (OR, 0.68), respiratory insufficiency (OR, 0.75), and initial cardiac arrest rhythm (OR, 3.32).

The median hospital RASR was 27% higher for ventricular tachycardia or ventricular fibrillation arrests than for arrests with a nonshockable rhythm of asystole and pulseless electrical activity (55% vs. 28%).

Notably, hospitals in the lowest tertile of risk-adjusted survival rates had a higher prevalence of non-White patients, renal and respiratory comorbidity, and arrest with nonshockable rhythm.

“We want to make sure as we’re contemplating whether to resuscitate a patient or how aggressively to resuscitate, that we aren’t letting any of our own biases, whether they have to do with race or potentially sex and gender, interfere with more objective assessments of whether the patient can in fact be saved or not,” Dr. Bhatt said.

Reached for comment, Srihari S. Naidu, MD, who chaired the writing group for the Society for Cardiovascular Angiography and Interventions’ (SCAI) consensus statement on cardiogenic shock and co-authored its document on best practices in the cardiac cath lab, said the findings show that survival in the cath lab is higher than that seen in-hospital. “Still, there’s a lot of room for improvement,” he said.

He was particularly struck by the variability in survival. “Underprivileged individuals, so those who are non-White populations and have respiratory and renal problems, they seem to have a worse survival and that makes sense – patients with comorbidities – but it feeds into the issue of, ‘Are we treating our population similarly in terms of their baseline race and ethnicity as a gap in care?’ ”

Better survival at hospitals with high volumes likely reflects more experience in handling these events, a rapid response and personnel to help with resuscitation, and overall better critical care and cath lab environment, said Dr. Naidu, director of the cardiac cath lab at Westchester Medical Center and professor of medicine at New York Medical College, both in Valhalla, N.Y.

“So that leads into two things,” he said. “One is that probably we should be working on having all high-risk patients go to centers of excellence. So, for example, [for] patients in shock, patients with STEMI, regionalization of care to the high-volume cath labs that are experienced in cardiac arrest and critical care management may be a way to go.”

“Second, if experience counts, can that experience be simulated through drills and simulations in the cath lab?” Dr. Naidu said. “Should all cath labs have drills where we have a cardiac arrest patient, and how would we respond to that? Who’s going to do the compressions? Where’s the mechanical support device? What are the things we need to have a seamless cardiac arrest protocol for arrests during the cath lab?”

Dr. Bhatt and colleagues acknowledge that despite adjustment for many key variables, the study lacked procedural details that may affect survival and information related to resuscitation efforts.

“We really do need to focus more research efforts, potentially more in the way of quality-improvement efforts, to try and help patients get these sorts of patients who are in dire straits to the cath lab but hopefully also through the hospital discharge and back home,” Dr. Bhatt said.

In an editorial accompanying the study, Matthew L. Tomey, MD, Icahn School of Medicine at Mount Sinai, New York, writes that the “findings and limitations of this study together sound a call to action.”

He also signaled the need for more research and for registries and reporting instruments to capture variables particular to in-laboratory cardiac arrest and resuscitation in the cardiac cath lab. “A necessary first step is the development of consensus data elements for supplemental reporting in cases of ILCA,” such as indication for cath lab presentation, timing of arrest relative to procedure, and cause of arrest.

Dr. Bhatt reported numerous relationships with industry. Dr. Naidu and Dr. Tomey report having no relevant financial relationships.

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

The chance of surviving a cardiac arrest varies widely across hospitals in the United States, even when the arrest occurs in the highly controlled setting of a cardiac catheterization lab, a new study indicates.

Among 4,787 patients who arrested in the cath lab at 231 hospitals in the Get With The Guidelines (GWTG) Resuscitation registry, only about one-third survived to discharge. The median risk-adjusted survival rate (RASR) for all hospitals was 36%.

When stratified by RASR tertiles, however, median survival rates were 20%, 36%, and 52% for hospitals in the lowest, middle, and highest tertiles.

The odds of survival differed by 71% in similar patients presenting at two randomly selected hospitals (median odds ratio, 1.71; 95% confidence interval, 1.52-1.87).

“The good news is that cardiac arrests in the cath lab are relatively infrequent, but the bad news is that they still occur and the outcomes are, in general, pretty dismal,” senior author Deepak L. Bhatt, MD, MPH, said in an interview. “So anything that we can do as hospitals [and] health care systems to improve the care of these patients could go a long way.”

Hospital and patient factors

Possible explanations for the wide disparity in survival are the small number of cardiac arrests in the cath lab, the increasing complexity of cases, and the fact that patients are often very sick and may experience a problem during a procedure, or both, Dr. Bhatt suggested. Cath labs also vary in how they handle resuscitative efforts and access to advanced mechanical support devices, such as extracorporeal membrane oxygenation (ECMO).

“It’s not available in every cath lab and, even in hospitals that have it, they may not have a given ECMO circuit available at the exact time the patient’s having a cardiac arrest,” he said. “That’s one example of something that can make, in my opinion, a big difference in whether a patient lives or dies if they’re having a cardiac arrest but may not always be easily deployed.”

When the investigators looked specifically at hospital-level factors, only yearly volume of cardiac arrests in the cath lab was significantly associated with risk-adjusted survival (P < .01), whereas hospital size, rural or urban setting, teaching status, and geographic location were not.

In multivariate adjusted analyses, factors associated with survival to discharge included age (OR, 0.78), Black race (OR, 0.68), respiratory insufficiency (OR, 0.75), and initial cardiac arrest rhythm (OR, 3.32).

The median hospital RASR was 27% higher for ventricular tachycardia or ventricular fibrillation arrests than for arrests with a nonshockable rhythm of asystole and pulseless electrical activity (55% vs. 28%).

Notably, hospitals in the lowest tertile of risk-adjusted survival rates had a higher prevalence of non-White patients, renal and respiratory comorbidity, and arrest with nonshockable rhythm.

“We want to make sure as we’re contemplating whether to resuscitate a patient or how aggressively to resuscitate, that we aren’t letting any of our own biases, whether they have to do with race or potentially sex and gender, interfere with more objective assessments of whether the patient can in fact be saved or not,” Dr. Bhatt said.

Reached for comment, Srihari S. Naidu, MD, who chaired the writing group for the Society for Cardiovascular Angiography and Interventions’ (SCAI) consensus statement on cardiogenic shock and co-authored its document on best practices in the cardiac cath lab, said the findings show that survival in the cath lab is higher than that seen in-hospital. “Still, there’s a lot of room for improvement,” he said.

He was particularly struck by the variability in survival. “Underprivileged individuals, so those who are non-White populations and have respiratory and renal problems, they seem to have a worse survival and that makes sense – patients with comorbidities – but it feeds into the issue of, ‘Are we treating our population similarly in terms of their baseline race and ethnicity as a gap in care?’ ”

Better survival at hospitals with high volumes likely reflects more experience in handling these events, a rapid response and personnel to help with resuscitation, and overall better critical care and cath lab environment, said Dr. Naidu, director of the cardiac cath lab at Westchester Medical Center and professor of medicine at New York Medical College, both in Valhalla, N.Y.

“So that leads into two things,” he said. “One is that probably we should be working on having all high-risk patients go to centers of excellence. So, for example, [for] patients in shock, patients with STEMI, regionalization of care to the high-volume cath labs that are experienced in cardiac arrest and critical care management may be a way to go.”

“Second, if experience counts, can that experience be simulated through drills and simulations in the cath lab?” Dr. Naidu said. “Should all cath labs have drills where we have a cardiac arrest patient, and how would we respond to that? Who’s going to do the compressions? Where’s the mechanical support device? What are the things we need to have a seamless cardiac arrest protocol for arrests during the cath lab?”

Dr. Bhatt and colleagues acknowledge that despite adjustment for many key variables, the study lacked procedural details that may affect survival and information related to resuscitation efforts.

“We really do need to focus more research efforts, potentially more in the way of quality-improvement efforts, to try and help patients get these sorts of patients who are in dire straits to the cath lab but hopefully also through the hospital discharge and back home,” Dr. Bhatt said.

In an editorial accompanying the study, Matthew L. Tomey, MD, Icahn School of Medicine at Mount Sinai, New York, writes that the “findings and limitations of this study together sound a call to action.”

He also signaled the need for more research and for registries and reporting instruments to capture variables particular to in-laboratory cardiac arrest and resuscitation in the cardiac cath lab. “A necessary first step is the development of consensus data elements for supplemental reporting in cases of ILCA,” such as indication for cath lab presentation, timing of arrest relative to procedure, and cause of arrest.

Dr. Bhatt reported numerous relationships with industry. Dr. Naidu and Dr. Tomey report having no relevant financial relationships.

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

The chance of surviving a cardiac arrest varies widely across hospitals in the United States, even when the arrest occurs in the highly controlled setting of a cardiac catheterization lab, a new study indicates.

Among 4,787 patients who arrested in the cath lab at 231 hospitals in the Get With The Guidelines (GWTG) Resuscitation registry, only about one-third survived to discharge. The median risk-adjusted survival rate (RASR) for all hospitals was 36%.

When stratified by RASR tertiles, however, median survival rates were 20%, 36%, and 52% for hospitals in the lowest, middle, and highest tertiles.

The odds of survival differed by 71% in similar patients presenting at two randomly selected hospitals (median odds ratio, 1.71; 95% confidence interval, 1.52-1.87).

“The good news is that cardiac arrests in the cath lab are relatively infrequent, but the bad news is that they still occur and the outcomes are, in general, pretty dismal,” senior author Deepak L. Bhatt, MD, MPH, said in an interview. “So anything that we can do as hospitals [and] health care systems to improve the care of these patients could go a long way.”

Hospital and patient factors

Possible explanations for the wide disparity in survival are the small number of cardiac arrests in the cath lab, the increasing complexity of cases, and the fact that patients are often very sick and may experience a problem during a procedure, or both, Dr. Bhatt suggested. Cath labs also vary in how they handle resuscitative efforts and access to advanced mechanical support devices, such as extracorporeal membrane oxygenation (ECMO).

“It’s not available in every cath lab and, even in hospitals that have it, they may not have a given ECMO circuit available at the exact time the patient’s having a cardiac arrest,” he said. “That’s one example of something that can make, in my opinion, a big difference in whether a patient lives or dies if they’re having a cardiac arrest but may not always be easily deployed.”

When the investigators looked specifically at hospital-level factors, only yearly volume of cardiac arrests in the cath lab was significantly associated with risk-adjusted survival (P < .01), whereas hospital size, rural or urban setting, teaching status, and geographic location were not.

In multivariate adjusted analyses, factors associated with survival to discharge included age (OR, 0.78), Black race (OR, 0.68), respiratory insufficiency (OR, 0.75), and initial cardiac arrest rhythm (OR, 3.32).

The median hospital RASR was 27% higher for ventricular tachycardia or ventricular fibrillation arrests than for arrests with a nonshockable rhythm of asystole and pulseless electrical activity (55% vs. 28%).

Notably, hospitals in the lowest tertile of risk-adjusted survival rates had a higher prevalence of non-White patients, renal and respiratory comorbidity, and arrest with nonshockable rhythm.

“We want to make sure as we’re contemplating whether to resuscitate a patient or how aggressively to resuscitate, that we aren’t letting any of our own biases, whether they have to do with race or potentially sex and gender, interfere with more objective assessments of whether the patient can in fact be saved or not,” Dr. Bhatt said.

Reached for comment, Srihari S. Naidu, MD, who chaired the writing group for the Society for Cardiovascular Angiography and Interventions’ (SCAI) consensus statement on cardiogenic shock and co-authored its document on best practices in the cardiac cath lab, said the findings show that survival in the cath lab is higher than that seen in-hospital. “Still, there’s a lot of room for improvement,” he said.

He was particularly struck by the variability in survival. “Underprivileged individuals, so those who are non-White populations and have respiratory and renal problems, they seem to have a worse survival and that makes sense – patients with comorbidities – but it feeds into the issue of, ‘Are we treating our population similarly in terms of their baseline race and ethnicity as a gap in care?’ ”

Better survival at hospitals with high volumes likely reflects more experience in handling these events, a rapid response and personnel to help with resuscitation, and overall better critical care and cath lab environment, said Dr. Naidu, director of the cardiac cath lab at Westchester Medical Center and professor of medicine at New York Medical College, both in Valhalla, N.Y.

“So that leads into two things,” he said. “One is that probably we should be working on having all high-risk patients go to centers of excellence. So, for example, [for] patients in shock, patients with STEMI, regionalization of care to the high-volume cath labs that are experienced in cardiac arrest and critical care management may be a way to go.”

“Second, if experience counts, can that experience be simulated through drills and simulations in the cath lab?” Dr. Naidu said. “Should all cath labs have drills where we have a cardiac arrest patient, and how would we respond to that? Who’s going to do the compressions? Where’s the mechanical support device? What are the things we need to have a seamless cardiac arrest protocol for arrests during the cath lab?”

Dr. Bhatt and colleagues acknowledge that despite adjustment for many key variables, the study lacked procedural details that may affect survival and information related to resuscitation efforts.

“We really do need to focus more research efforts, potentially more in the way of quality-improvement efforts, to try and help patients get these sorts of patients who are in dire straits to the cath lab but hopefully also through the hospital discharge and back home,” Dr. Bhatt said.

In an editorial accompanying the study, Matthew L. Tomey, MD, Icahn School of Medicine at Mount Sinai, New York, writes that the “findings and limitations of this study together sound a call to action.”

He also signaled the need for more research and for registries and reporting instruments to capture variables particular to in-laboratory cardiac arrest and resuscitation in the cardiac cath lab. “A necessary first step is the development of consensus data elements for supplemental reporting in cases of ILCA,” such as indication for cath lab presentation, timing of arrest relative to procedure, and cause of arrest.

Dr. Bhatt reported numerous relationships with industry. Dr. Naidu and Dr. Tomey report having no relevant financial relationships.

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

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

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

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

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

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

The study was published online in JAMA Cardiology.
 

No significant differences

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

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

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

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

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

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

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

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

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

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

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

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

U.S. in worse shape

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The study was published online in JAMA Cardiology.
 

No significant differences

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

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

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

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

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

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

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

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

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

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

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

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

U.S. in worse shape

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The study was published online in JAMA Cardiology.
 

No significant differences

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

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

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

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

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

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

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

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

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

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

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

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

U.S. in worse shape

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

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

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

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

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

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

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

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

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

CHICAGO – Extended follow-up of patients with heart failure enrolled in the RAFT trial strengthens the case for starting treatment early with a cardiac resynchronization therapy plus defibrillation (CRT-D) device in appropriate patients.

RAFT, which compared CRT-D with treatment with an implantable cardioverter defibrillator (ICD) alone, showed that the early survival benefit produced by CRT-D during an average 40-month follow-up in the original trial persisted during an additional mean follow-up of about 5 years. This result strengthens the case for starting treatment early with a CRT-D device in appropriate patients with heart failure.

Mitchel L. Zoler/MDedge News

During extended follow-up of more than half of the enrolled patients, out to an average of 7.6 years overall and to an average of 12.9 years among survivors, patients who received a CRT-D device had a significant 21% relative reduction in their rate of all-cause mortality compared with randomized patients who received an ICD and no cardiac resynchronization, John L. Sapp, MD, reported at the American Heart Association scientific sessions.

The primary results of RAFT were first reported in 2010.

This magnitude of a survival benefit among the patients originally randomized to CRT is “dramatic,” given that many of the comparator patients who initially received no CRT likely crossed over to receive a CRT-D device once the initial, randomized 4 years of the study finished, commented Lynne W. Stevenson, MD, director of cardiomyopathy and the Lisa M. Jacobson Professor of Cardiology at Vanderbilt University Medical Center in Nashville, Tenn., who was not involved with the study.

‘CRT can remap heart failure trajectory’

The new findings “strengthen our conviction that CRT can remap the trajectory” of selected patients with heart failure, and that “candidates for CRT should be vigorously identified,” Dr. Stevenson said in an interview.

She also noted that the benefit with extended follow-up was “strikingly parallel” to that seen at 12 years after the addition of an ACE inhibitor for mild heart failure during the 4 years of the landmark SOLVD trial. The new RAFT extended follow-up, as well as the 12-year follow-up of the SOLVD trial, “support the concept that longer follow-up reveals vital information not provided by the relatively short randomized trial period,” she said.

“The new data say ‘don’t delay starting CRT in appropriate patients with heart failure,’ and ‘don’t think of CRT as just a treatment that makes patients feel better.’

 

“The totality of these data shows that CRT also treats the underlying heart muscle weakness, which helps patients live longer. Previous data showed that patients with left bundle branch block eligible for CRT are unlikely to respond well to the usual, recommended heart medications so it is important to start treatment with CRT-D early,” declared Dr. Stevenson, who cochaired the session where Dr. Sapp gave his report.

RAFT randomized 1,798 patients with New York Heart Association (NYHA) class II or III heart failure, a left ventricular ejection fraction of 30% or less, and an intrinsic QRS duration of at least 120 msec to receive either a CRT-D or ICD device. The study’s primary endpoint was death from any cause or hospitalization for heart failure. After an average 40 months of randomized follow-up, the primary endpoint occurred in 40% of the patients with an ICD and in 33% of those with a CRT-D device, a significant 25% relative reduction linked with CRT-D use. Both endpoint components contributed to the combined result significantly and to about the same extent, and the incremental benefit from CRT-D was significant for patients with NYHA class II heart failure as well as for those with class III.

However, prespecified subgroup analyses showed that the incremental benefit from CRT-D was significantly limited to patients with an intrinsic QRS duration of at least 150 msec, while in those with a duration of 120-149 msec CRT-D had a neutral effect compared with ICD. The same pattern also appeared when the analysis split patients into those with a left bundle branch block, who significantly benefited from CRT-D, but the initial benefit was not apparent in patients with right bundle branch block.

A study subgroup with extended follow-up

The new, extended follow-up analysis presented by Dr. Sapp included 1,050 of the original 1,798 patients (58%) enrolled at any of eight participating Canadian centers that each enrolled at least 100 patients and followed them through the end of 2021 (the full study cohort came from 34 centers, including 10 centers outside Canada). This subgroup included 520 patients randomized to receive CRT-D and 530 who received an ICD. Although this was a post hoc subgroup analysis, the CRT-D and ICD arms matched closely in all measured baseline characteristics.

The prespecified primary outcome of this follow-up analysis was the rate of all-cause mortality. Because of their longer disease trajectory, this pared-down study cohort included many more patients with NYHA class II function, 803, and in this subgroup CRT-D exerted a significant 23% incremental reduction in mortality compared with ICD treatment. CRT-D also produced a 17% relative reduction in long-term mortality among patients with NYHA class III function at baseline, but this point estimate of relative benefit was not significant in this subgroup of just 247 patients, said Dr. Sapp, a cardiologist and professor at Dalhousie University & Nova Scotia Health in Halifax.

Based on the original RAFT results from 2010, as well as on evidence from several other trials, the current heart failure management guideline from the AHA, the American College of Cardiology, and the Heart Failure Society of America give the highest level of recommendation, level 1, for CRT in patients with a left ventricular ejection fraction of 35% or less, sinus rhythm with left bundle branch block, a QRS duration of at least 150 msec, and NYHA class II, III, or ambulatory IV symptoms while on guideline-directed medical therapy.

The guideline also gives class 2a (“can be useful”) or 2b (“may be considered”) recommendation for certain other heart failure patients, including those with a QRS duration of 120-149 msec, a left ventricular ejection fraction as high as 50%, no left bundle branch block, or NYHA class I symptoms.

Don’t wait to start CRT

Although this 2022 guideline, as well as earlier versions that had roughly similar recommendations for CRT for about a decade, have led to “common” use of CRT in appropriate patients in U.S. practice, “it has not been used as much as it should be, in part because there’s been a feeling that CRT mostly treats symptoms and so perhaps you can wait” to start it, said Dr. Stevenson.

The findings from the new, extended follow-up RAFT analysis give increased urgency to starting CRT “as soon as possible” in appropriate patients with heart failure, even before they stabilize on guideline-directed medical therapy, said Dr. Stevenson. She also downplayed any ambiguity in the RAFT findings about optimal medical therapy, which during the RAFT study included traditional triple therapy at a time before treatment with sacubitril/valsartan (Entresto) and sodium-glucose cotransporter 2 (SGLT2) inhibitors became recommended.

“There is no reason to think that these treatments will negate the benefit of CRT for patients with heart failure with reduced ejection fraction and a wide left bundle branch block,” Dr. Stevenson said.

She also believes that the extended follow-up results, which showed clear efficacy for CRT-D in patients with NYHA class II function, support the case for upgrading the current 2b recommendation for using CRT treatment in patients with NYHA class I function and ischemic heart failure to a 2a recommendation regardless of whether or not patients have coronary artery disease. “The difference between class I and class II depends more on a patient’s lifestyle rather than on the severity of their heart failure,” Dr. Stevenson noted. “The RAFT study results encourage us to reexamine the clinical class and timing for CRT” in the current heart failure guideline.

RAFT received partial sponsorship from Medtronic. Dr. Sapp has been a consultant to Abbott, Biosense Webster, Medtronic, and Varian and has received research funding from Abbott and Biosense Webster. Dr. Stevenson had no disclosures.

CHICAGO – Extended follow-up of patients with heart failure enrolled in the RAFT trial strengthens the case for starting treatment early with a cardiac resynchronization therapy plus defibrillation (CRT-D) device in appropriate patients.

RAFT, which compared CRT-D with treatment with an implantable cardioverter defibrillator (ICD) alone, showed that the early survival benefit produced by CRT-D during an average 40-month follow-up in the original trial persisted during an additional mean follow-up of about 5 years. This result strengthens the case for starting treatment early with a CRT-D device in appropriate patients with heart failure.

Mitchel L. Zoler/MDedge News

During extended follow-up of more than half of the enrolled patients, out to an average of 7.6 years overall and to an average of 12.9 years among survivors, patients who received a CRT-D device had a significant 21% relative reduction in their rate of all-cause mortality compared with randomized patients who received an ICD and no cardiac resynchronization, John L. Sapp, MD, reported at the American Heart Association scientific sessions.

The primary results of RAFT were first reported in 2010.

This magnitude of a survival benefit among the patients originally randomized to CRT is “dramatic,” given that many of the comparator patients who initially received no CRT likely crossed over to receive a CRT-D device once the initial, randomized 4 years of the study finished, commented Lynne W. Stevenson, MD, director of cardiomyopathy and the Lisa M. Jacobson Professor of Cardiology at Vanderbilt University Medical Center in Nashville, Tenn., who was not involved with the study.

‘CRT can remap heart failure trajectory’

The new findings “strengthen our conviction that CRT can remap the trajectory” of selected patients with heart failure, and that “candidates for CRT should be vigorously identified,” Dr. Stevenson said in an interview.

She also noted that the benefit with extended follow-up was “strikingly parallel” to that seen at 12 years after the addition of an ACE inhibitor for mild heart failure during the 4 years of the landmark SOLVD trial. The new RAFT extended follow-up, as well as the 12-year follow-up of the SOLVD trial, “support the concept that longer follow-up reveals vital information not provided by the relatively short randomized trial period,” she said.

“The new data say ‘don’t delay starting CRT in appropriate patients with heart failure,’ and ‘don’t think of CRT as just a treatment that makes patients feel better.’

 

“The totality of these data shows that CRT also treats the underlying heart muscle weakness, which helps patients live longer. Previous data showed that patients with left bundle branch block eligible for CRT are unlikely to respond well to the usual, recommended heart medications so it is important to start treatment with CRT-D early,” declared Dr. Stevenson, who cochaired the session where Dr. Sapp gave his report.

RAFT randomized 1,798 patients with New York Heart Association (NYHA) class II or III heart failure, a left ventricular ejection fraction of 30% or less, and an intrinsic QRS duration of at least 120 msec to receive either a CRT-D or ICD device. The study’s primary endpoint was death from any cause or hospitalization for heart failure. After an average 40 months of randomized follow-up, the primary endpoint occurred in 40% of the patients with an ICD and in 33% of those with a CRT-D device, a significant 25% relative reduction linked with CRT-D use. Both endpoint components contributed to the combined result significantly and to about the same extent, and the incremental benefit from CRT-D was significant for patients with NYHA class II heart failure as well as for those with class III.

However, prespecified subgroup analyses showed that the incremental benefit from CRT-D was significantly limited to patients with an intrinsic QRS duration of at least 150 msec, while in those with a duration of 120-149 msec CRT-D had a neutral effect compared with ICD. The same pattern also appeared when the analysis split patients into those with a left bundle branch block, who significantly benefited from CRT-D, but the initial benefit was not apparent in patients with right bundle branch block.

A study subgroup with extended follow-up

The new, extended follow-up analysis presented by Dr. Sapp included 1,050 of the original 1,798 patients (58%) enrolled at any of eight participating Canadian centers that each enrolled at least 100 patients and followed them through the end of 2021 (the full study cohort came from 34 centers, including 10 centers outside Canada). This subgroup included 520 patients randomized to receive CRT-D and 530 who received an ICD. Although this was a post hoc subgroup analysis, the CRT-D and ICD arms matched closely in all measured baseline characteristics.

The prespecified primary outcome of this follow-up analysis was the rate of all-cause mortality. Because of their longer disease trajectory, this pared-down study cohort included many more patients with NYHA class II function, 803, and in this subgroup CRT-D exerted a significant 23% incremental reduction in mortality compared with ICD treatment. CRT-D also produced a 17% relative reduction in long-term mortality among patients with NYHA class III function at baseline, but this point estimate of relative benefit was not significant in this subgroup of just 247 patients, said Dr. Sapp, a cardiologist and professor at Dalhousie University & Nova Scotia Health in Halifax.

Based on the original RAFT results from 2010, as well as on evidence from several other trials, the current heart failure management guideline from the AHA, the American College of Cardiology, and the Heart Failure Society of America give the highest level of recommendation, level 1, for CRT in patients with a left ventricular ejection fraction of 35% or less, sinus rhythm with left bundle branch block, a QRS duration of at least 150 msec, and NYHA class II, III, or ambulatory IV symptoms while on guideline-directed medical therapy.

The guideline also gives class 2a (“can be useful”) or 2b (“may be considered”) recommendation for certain other heart failure patients, including those with a QRS duration of 120-149 msec, a left ventricular ejection fraction as high as 50%, no left bundle branch block, or NYHA class I symptoms.

Don’t wait to start CRT

Although this 2022 guideline, as well as earlier versions that had roughly similar recommendations for CRT for about a decade, have led to “common” use of CRT in appropriate patients in U.S. practice, “it has not been used as much as it should be, in part because there’s been a feeling that CRT mostly treats symptoms and so perhaps you can wait” to start it, said Dr. Stevenson.

The findings from the new, extended follow-up RAFT analysis give increased urgency to starting CRT “as soon as possible” in appropriate patients with heart failure, even before they stabilize on guideline-directed medical therapy, said Dr. Stevenson. She also downplayed any ambiguity in the RAFT findings about optimal medical therapy, which during the RAFT study included traditional triple therapy at a time before treatment with sacubitril/valsartan (Entresto) and sodium-glucose cotransporter 2 (SGLT2) inhibitors became recommended.

“There is no reason to think that these treatments will negate the benefit of CRT for patients with heart failure with reduced ejection fraction and a wide left bundle branch block,” Dr. Stevenson said.

She also believes that the extended follow-up results, which showed clear efficacy for CRT-D in patients with NYHA class II function, support the case for upgrading the current 2b recommendation for using CRT treatment in patients with NYHA class I function and ischemic heart failure to a 2a recommendation regardless of whether or not patients have coronary artery disease. “The difference between class I and class II depends more on a patient’s lifestyle rather than on the severity of their heart failure,” Dr. Stevenson noted. “The RAFT study results encourage us to reexamine the clinical class and timing for CRT” in the current heart failure guideline.

RAFT received partial sponsorship from Medtronic. Dr. Sapp has been a consultant to Abbott, Biosense Webster, Medtronic, and Varian and has received research funding from Abbott and Biosense Webster. Dr. Stevenson had no disclosures.

CHICAGO – Extended follow-up of patients with heart failure enrolled in the RAFT trial strengthens the case for starting treatment early with a cardiac resynchronization therapy plus defibrillation (CRT-D) device in appropriate patients.

RAFT, which compared CRT-D with treatment with an implantable cardioverter defibrillator (ICD) alone, showed that the early survival benefit produced by CRT-D during an average 40-month follow-up in the original trial persisted during an additional mean follow-up of about 5 years. This result strengthens the case for starting treatment early with a CRT-D device in appropriate patients with heart failure.

Mitchel L. Zoler/MDedge News

During extended follow-up of more than half of the enrolled patients, out to an average of 7.6 years overall and to an average of 12.9 years among survivors, patients who received a CRT-D device had a significant 21% relative reduction in their rate of all-cause mortality compared with randomized patients who received an ICD and no cardiac resynchronization, John L. Sapp, MD, reported at the American Heart Association scientific sessions.

The primary results of RAFT were first reported in 2010.

This magnitude of a survival benefit among the patients originally randomized to CRT is “dramatic,” given that many of the comparator patients who initially received no CRT likely crossed over to receive a CRT-D device once the initial, randomized 4 years of the study finished, commented Lynne W. Stevenson, MD, director of cardiomyopathy and the Lisa M. Jacobson Professor of Cardiology at Vanderbilt University Medical Center in Nashville, Tenn., who was not involved with the study.

‘CRT can remap heart failure trajectory’

The new findings “strengthen our conviction that CRT can remap the trajectory” of selected patients with heart failure, and that “candidates for CRT should be vigorously identified,” Dr. Stevenson said in an interview.

She also noted that the benefit with extended follow-up was “strikingly parallel” to that seen at 12 years after the addition of an ACE inhibitor for mild heart failure during the 4 years of the landmark SOLVD trial. The new RAFT extended follow-up, as well as the 12-year follow-up of the SOLVD trial, “support the concept that longer follow-up reveals vital information not provided by the relatively short randomized trial period,” she said.

“The new data say ‘don’t delay starting CRT in appropriate patients with heart failure,’ and ‘don’t think of CRT as just a treatment that makes patients feel better.’

 

“The totality of these data shows that CRT also treats the underlying heart muscle weakness, which helps patients live longer. Previous data showed that patients with left bundle branch block eligible for CRT are unlikely to respond well to the usual, recommended heart medications so it is important to start treatment with CRT-D early,” declared Dr. Stevenson, who cochaired the session where Dr. Sapp gave his report.

RAFT randomized 1,798 patients with New York Heart Association (NYHA) class II or III heart failure, a left ventricular ejection fraction of 30% or less, and an intrinsic QRS duration of at least 120 msec to receive either a CRT-D or ICD device. The study’s primary endpoint was death from any cause or hospitalization for heart failure. After an average 40 months of randomized follow-up, the primary endpoint occurred in 40% of the patients with an ICD and in 33% of those with a CRT-D device, a significant 25% relative reduction linked with CRT-D use. Both endpoint components contributed to the combined result significantly and to about the same extent, and the incremental benefit from CRT-D was significant for patients with NYHA class II heart failure as well as for those with class III.

However, prespecified subgroup analyses showed that the incremental benefit from CRT-D was significantly limited to patients with an intrinsic QRS duration of at least 150 msec, while in those with a duration of 120-149 msec CRT-D had a neutral effect compared with ICD. The same pattern also appeared when the analysis split patients into those with a left bundle branch block, who significantly benefited from CRT-D, but the initial benefit was not apparent in patients with right bundle branch block.

A study subgroup with extended follow-up

The new, extended follow-up analysis presented by Dr. Sapp included 1,050 of the original 1,798 patients (58%) enrolled at any of eight participating Canadian centers that each enrolled at least 100 patients and followed them through the end of 2021 (the full study cohort came from 34 centers, including 10 centers outside Canada). This subgroup included 520 patients randomized to receive CRT-D and 530 who received an ICD. Although this was a post hoc subgroup analysis, the CRT-D and ICD arms matched closely in all measured baseline characteristics.

The prespecified primary outcome of this follow-up analysis was the rate of all-cause mortality. Because of their longer disease trajectory, this pared-down study cohort included many more patients with NYHA class II function, 803, and in this subgroup CRT-D exerted a significant 23% incremental reduction in mortality compared with ICD treatment. CRT-D also produced a 17% relative reduction in long-term mortality among patients with NYHA class III function at baseline, but this point estimate of relative benefit was not significant in this subgroup of just 247 patients, said Dr. Sapp, a cardiologist and professor at Dalhousie University & Nova Scotia Health in Halifax.

Based on the original RAFT results from 2010, as well as on evidence from several other trials, the current heart failure management guideline from the AHA, the American College of Cardiology, and the Heart Failure Society of America give the highest level of recommendation, level 1, for CRT in patients with a left ventricular ejection fraction of 35% or less, sinus rhythm with left bundle branch block, a QRS duration of at least 150 msec, and NYHA class II, III, or ambulatory IV symptoms while on guideline-directed medical therapy.

The guideline also gives class 2a (“can be useful”) or 2b (“may be considered”) recommendation for certain other heart failure patients, including those with a QRS duration of 120-149 msec, a left ventricular ejection fraction as high as 50%, no left bundle branch block, or NYHA class I symptoms.

Don’t wait to start CRT

Although this 2022 guideline, as well as earlier versions that had roughly similar recommendations for CRT for about a decade, have led to “common” use of CRT in appropriate patients in U.S. practice, “it has not been used as much as it should be, in part because there’s been a feeling that CRT mostly treats symptoms and so perhaps you can wait” to start it, said Dr. Stevenson.

The findings from the new, extended follow-up RAFT analysis give increased urgency to starting CRT “as soon as possible” in appropriate patients with heart failure, even before they stabilize on guideline-directed medical therapy, said Dr. Stevenson. She also downplayed any ambiguity in the RAFT findings about optimal medical therapy, which during the RAFT study included traditional triple therapy at a time before treatment with sacubitril/valsartan (Entresto) and sodium-glucose cotransporter 2 (SGLT2) inhibitors became recommended.

“There is no reason to think that these treatments will negate the benefit of CRT for patients with heart failure with reduced ejection fraction and a wide left bundle branch block,” Dr. Stevenson said.

She also believes that the extended follow-up results, which showed clear efficacy for CRT-D in patients with NYHA class II function, support the case for upgrading the current 2b recommendation for using CRT treatment in patients with NYHA class I function and ischemic heart failure to a 2a recommendation regardless of whether or not patients have coronary artery disease. “The difference between class I and class II depends more on a patient’s lifestyle rather than on the severity of their heart failure,” Dr. Stevenson noted. “The RAFT study results encourage us to reexamine the clinical class and timing for CRT” in the current heart failure guideline.

RAFT received partial sponsorship from Medtronic. Dr. Sapp has been a consultant to Abbott, Biosense Webster, Medtronic, and Varian and has received research funding from Abbott and Biosense Webster. Dr. Stevenson had no disclosures.

The U.S. Food and Drug Administration issued a letter to health care providers describing a current shortage of Getinge intra-aortic balloon pump (IABP) catheters and other components.

Wikimedia Commons/FitzColinGerald/Creative Commons License

Earlier, the agency announced shortages of the company’s Maquet/Datascope IAB catheters, new Cardiosave IABP devices, and Cardiosave IABP parts. The new notification adds Getinge Maquet/Datascope IABP systems to the list.

The company’s letter explains that “ongoing supply chain issues have significantly impacted our ability to build intra-aortic balloon pumps, intra-aortic balloon catheters, and spare parts due to raw material shortages.”

It also offers guidance on maintaining Cardiosave Safety Disks and lithium-ion batteries in the face of the shortages. “In the event that you need a replacement pump while your IABP is undergoing service, please contact your local sales representative who may be able to assist with a temporary IABP.”

Providers are instructed to inform the company through its sales representatives “if you have any underutilized Maquet/Datascope IAB catheters or IABPs and are willing to share them with hospitals in need.”

The shortages are expected to continue into 2023, the FDA states in its letter.

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

The U.S. Food and Drug Administration issued a letter to health care providers describing a current shortage of Getinge intra-aortic balloon pump (IABP) catheters and other components.

Wikimedia Commons/FitzColinGerald/Creative Commons License

Earlier, the agency announced shortages of the company’s Maquet/Datascope IAB catheters, new Cardiosave IABP devices, and Cardiosave IABP parts. The new notification adds Getinge Maquet/Datascope IABP systems to the list.

The company’s letter explains that “ongoing supply chain issues have significantly impacted our ability to build intra-aortic balloon pumps, intra-aortic balloon catheters, and spare parts due to raw material shortages.”

It also offers guidance on maintaining Cardiosave Safety Disks and lithium-ion batteries in the face of the shortages. “In the event that you need a replacement pump while your IABP is undergoing service, please contact your local sales representative who may be able to assist with a temporary IABP.”

Providers are instructed to inform the company through its sales representatives “if you have any underutilized Maquet/Datascope IAB catheters or IABPs and are willing to share them with hospitals in need.”

The shortages are expected to continue into 2023, the FDA states in its letter.

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

The U.S. Food and Drug Administration issued a letter to health care providers describing a current shortage of Getinge intra-aortic balloon pump (IABP) catheters and other components.

Wikimedia Commons/FitzColinGerald/Creative Commons License

Earlier, the agency announced shortages of the company’s Maquet/Datascope IAB catheters, new Cardiosave IABP devices, and Cardiosave IABP parts. The new notification adds Getinge Maquet/Datascope IABP systems to the list.

The company’s letter explains that “ongoing supply chain issues have significantly impacted our ability to build intra-aortic balloon pumps, intra-aortic balloon catheters, and spare parts due to raw material shortages.”

It also offers guidance on maintaining Cardiosave Safety Disks and lithium-ion batteries in the face of the shortages. “In the event that you need a replacement pump while your IABP is undergoing service, please contact your local sales representative who may be able to assist with a temporary IABP.”

Providers are instructed to inform the company through its sales representatives “if you have any underutilized Maquet/Datascope IAB catheters or IABPs and are willing to share them with hospitals in need.”

The shortages are expected to continue into 2023, the FDA states in its letter.

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