Arrhythmias & EP

LONDON — Updated guidelines for the management of atrial fibrillation released by the European Society of Cardiology are revamping the approach to care for this complex, multifactorial disease.

The identification and treatment of comorbidities and risk factors are the initial and central components of patient management, and are crucial for all other aspects of care for patients with atrial fibrillation (AF), Isabelle Van Gelder, MD, PhD, professor of cardiology at the University Medical Center in Groningen, the Netherlands, explained at the European Society of Cardiology (ESC) Congress.

It is not just appropriate to place the same emphasis on the control of comorbidities as on the rhythm disturbance, it is critical, said Dr. Van Gelder, who served as chair of the ESC-AF guidelines task force.

Comorbidities are the drivers of both the onset and recurrence of atrial fibrillation, and a dynamic approach to comorbidities is “central for the success of AF management.”
 

Class I Recommendation

In fact, on the basis of overwhelming evidence, a class I recommendation has been issued for a large number of goals in the comorbidity and risk factor management step of atrial fibrillation management, including those for hypertension, components of heart failure, obesity, diabetes, alcohol consumption, and exercise.

Sodium-glucose cotransporter-2 (SGLT2) inhibitors “should be offered to all patients with AF,” according to Dr. Van Gelder, who identified this as a new class I recommendation.

Patients who are not managed aggressively for the listed comorbidities ultimately face “treatment failure, poor patient outcomes, and a waste of healthcare resources,” she said.

Control of sleep apnea is also noted as a key target, although Van Gelder acknowledged that the supporting evidence only allows for a class IIb recommendation.

Control of comorbidities is not a new idea. In the 2023 joint guideline, led by a consortium of professional groups, including the American Heart Association (AHA) and the American College of Cardiology (ACC), the control of comorbidities, including most of those identified in the new ESC guidelines, was second in a list of 10 key take-home messages.

However, the new ESC guidelines have prioritized comorbidity management by listing it first in each of the specific patient-care pathways developed to define optimized care. 

These pathways, defined in algorithms for newly diagnosed AF, paroxysmal AF, and persistent AF, always start with the assessment of comorbidities, followed by step A — avoiding stroke — largely with anticoagulation.

Direct oral anticoagulants should be used, “except in those with a mechanical valve or mitral stenosis,” Dr. Van Gelder said. This includes, essentially, all patients with a CHA2DS2-VASc score of 2 or greater, and it should be “considered” in those with a score of 1. 

The ESC framework has been identified with the acronym AF-CARE, in which the C stands for comorbidities.

In the A step of the framework, identifying and treating all modifiable bleeding risk factors in AF patients is a class I recommendation. On the basis of a class III recommendation, she cautioned against withholding anticoagulants because of CHA2DS2-VASc risk factors alone. Rather, Dr. Van Gelder called the decision to administer or withhold anticoagulation — like all decisions — one that should be individualized in consultation with the patient.

For reducing AF symptoms and rhythm control, the specific pathways diverge for newly diagnosed AF, paroxysmal AF, and persistent AF. Like all of the guidelines, the specific options for symptom management and AF ablation are color coded, with green signifying level 1 evidence.

The evaluation and dynamic reassessment step refers to the need to periodically assess patients for new modifiable risk factors related to comorbidities, risk for stroke, risk for bleeding, and risk for AF. 

The management of risk factors for AF has long been emphasized in guidelines, but a previous focus on AF with attention to comorbidities has been replaced by a focus on comorbidities with an expectation of more durable AF control. The success of this pivot is based on multidisciplinary care, chosen in collaboration with the patient, to reduce or eliminate the triggers of AF and the risks of its complications.
 

Pathways Are Appropriate for All Patients

A very important recommendation — and this is new — is “to treat all our patients with atrial fibrillation, whether they are young or old, men or women, Black or White, or at high or low risk, according to our patient-centered integrated AF-CARE approach,” Dr. Van Gelder said.

The changes reflect a shared appreciation for the tight relation between the control of comorbidities and the control of AF, according to José A. Joglar, MD, professor of cardiac electrophysiologic research at the University of Texas Southwestern Medical Center in Dallas. Dr. Joglar was chair of the writing committee for the joint 2023 AF guidelines released by the AHA, ACC, the American College of Clinical Pharmacy, and the Heart Rhythm Society.

“It is increasingly clear that AF in many cases is the consequence of underlying risk factors and comorbidities, which cannot be separated from AF alone,” Dr. Joglar explained in an interview.

This was placed first “to emphasize the importance of viewing AFib as a complex disease that requires a holistic, multidisciplinary approach to care, as opposed to being viewed just as a rhythm abnormality,” he said.
 

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

LONDON — Updated guidelines for the management of atrial fibrillation released by the European Society of Cardiology are revamping the approach to care for this complex, multifactorial disease.

The identification and treatment of comorbidities and risk factors are the initial and central components of patient management, and are crucial for all other aspects of care for patients with atrial fibrillation (AF), Isabelle Van Gelder, MD, PhD, professor of cardiology at the University Medical Center in Groningen, the Netherlands, explained at the European Society of Cardiology (ESC) Congress.

It is not just appropriate to place the same emphasis on the control of comorbidities as on the rhythm disturbance, it is critical, said Dr. Van Gelder, who served as chair of the ESC-AF guidelines task force.

Comorbidities are the drivers of both the onset and recurrence of atrial fibrillation, and a dynamic approach to comorbidities is “central for the success of AF management.”
 

Class I Recommendation

In fact, on the basis of overwhelming evidence, a class I recommendation has been issued for a large number of goals in the comorbidity and risk factor management step of atrial fibrillation management, including those for hypertension, components of heart failure, obesity, diabetes, alcohol consumption, and exercise.

Sodium-glucose cotransporter-2 (SGLT2) inhibitors “should be offered to all patients with AF,” according to Dr. Van Gelder, who identified this as a new class I recommendation.

Patients who are not managed aggressively for the listed comorbidities ultimately face “treatment failure, poor patient outcomes, and a waste of healthcare resources,” she said.

Control of sleep apnea is also noted as a key target, although Van Gelder acknowledged that the supporting evidence only allows for a class IIb recommendation.

Control of comorbidities is not a new idea. In the 2023 joint guideline, led by a consortium of professional groups, including the American Heart Association (AHA) and the American College of Cardiology (ACC), the control of comorbidities, including most of those identified in the new ESC guidelines, was second in a list of 10 key take-home messages.

However, the new ESC guidelines have prioritized comorbidity management by listing it first in each of the specific patient-care pathways developed to define optimized care. 

These pathways, defined in algorithms for newly diagnosed AF, paroxysmal AF, and persistent AF, always start with the assessment of comorbidities, followed by step A — avoiding stroke — largely with anticoagulation.

Direct oral anticoagulants should be used, “except in those with a mechanical valve or mitral stenosis,” Dr. Van Gelder said. This includes, essentially, all patients with a CHA2DS2-VASc score of 2 or greater, and it should be “considered” in those with a score of 1. 

The ESC framework has been identified with the acronym AF-CARE, in which the C stands for comorbidities.

In the A step of the framework, identifying and treating all modifiable bleeding risk factors in AF patients is a class I recommendation. On the basis of a class III recommendation, she cautioned against withholding anticoagulants because of CHA2DS2-VASc risk factors alone. Rather, Dr. Van Gelder called the decision to administer or withhold anticoagulation — like all decisions — one that should be individualized in consultation with the patient.

For reducing AF symptoms and rhythm control, the specific pathways diverge for newly diagnosed AF, paroxysmal AF, and persistent AF. Like all of the guidelines, the specific options for symptom management and AF ablation are color coded, with green signifying level 1 evidence.

The evaluation and dynamic reassessment step refers to the need to periodically assess patients for new modifiable risk factors related to comorbidities, risk for stroke, risk for bleeding, and risk for AF. 

The management of risk factors for AF has long been emphasized in guidelines, but a previous focus on AF with attention to comorbidities has been replaced by a focus on comorbidities with an expectation of more durable AF control. The success of this pivot is based on multidisciplinary care, chosen in collaboration with the patient, to reduce or eliminate the triggers of AF and the risks of its complications.
 

Pathways Are Appropriate for All Patients

A very important recommendation — and this is new — is “to treat all our patients with atrial fibrillation, whether they are young or old, men or women, Black or White, or at high or low risk, according to our patient-centered integrated AF-CARE approach,” Dr. Van Gelder said.

The changes reflect a shared appreciation for the tight relation between the control of comorbidities and the control of AF, according to José A. Joglar, MD, professor of cardiac electrophysiologic research at the University of Texas Southwestern Medical Center in Dallas. Dr. Joglar was chair of the writing committee for the joint 2023 AF guidelines released by the AHA, ACC, the American College of Clinical Pharmacy, and the Heart Rhythm Society.

“It is increasingly clear that AF in many cases is the consequence of underlying risk factors and comorbidities, which cannot be separated from AF alone,” Dr. Joglar explained in an interview.

This was placed first “to emphasize the importance of viewing AFib as a complex disease that requires a holistic, multidisciplinary approach to care, as opposed to being viewed just as a rhythm abnormality,” he said.
 

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

LONDON — Updated guidelines for the management of atrial fibrillation released by the European Society of Cardiology are revamping the approach to care for this complex, multifactorial disease.

The identification and treatment of comorbidities and risk factors are the initial and central components of patient management, and are crucial for all other aspects of care for patients with atrial fibrillation (AF), Isabelle Van Gelder, MD, PhD, professor of cardiology at the University Medical Center in Groningen, the Netherlands, explained at the European Society of Cardiology (ESC) Congress.

It is not just appropriate to place the same emphasis on the control of comorbidities as on the rhythm disturbance, it is critical, said Dr. Van Gelder, who served as chair of the ESC-AF guidelines task force.

Comorbidities are the drivers of both the onset and recurrence of atrial fibrillation, and a dynamic approach to comorbidities is “central for the success of AF management.”
 

Class I Recommendation

In fact, on the basis of overwhelming evidence, a class I recommendation has been issued for a large number of goals in the comorbidity and risk factor management step of atrial fibrillation management, including those for hypertension, components of heart failure, obesity, diabetes, alcohol consumption, and exercise.

Sodium-glucose cotransporter-2 (SGLT2) inhibitors “should be offered to all patients with AF,” according to Dr. Van Gelder, who identified this as a new class I recommendation.

Patients who are not managed aggressively for the listed comorbidities ultimately face “treatment failure, poor patient outcomes, and a waste of healthcare resources,” she said.

Control of sleep apnea is also noted as a key target, although Van Gelder acknowledged that the supporting evidence only allows for a class IIb recommendation.

Control of comorbidities is not a new idea. In the 2023 joint guideline, led by a consortium of professional groups, including the American Heart Association (AHA) and the American College of Cardiology (ACC), the control of comorbidities, including most of those identified in the new ESC guidelines, was second in a list of 10 key take-home messages.

However, the new ESC guidelines have prioritized comorbidity management by listing it first in each of the specific patient-care pathways developed to define optimized care. 

These pathways, defined in algorithms for newly diagnosed AF, paroxysmal AF, and persistent AF, always start with the assessment of comorbidities, followed by step A — avoiding stroke — largely with anticoagulation.

Direct oral anticoagulants should be used, “except in those with a mechanical valve or mitral stenosis,” Dr. Van Gelder said. This includes, essentially, all patients with a CHA2DS2-VASc score of 2 or greater, and it should be “considered” in those with a score of 1. 

The ESC framework has been identified with the acronym AF-CARE, in which the C stands for comorbidities.

In the A step of the framework, identifying and treating all modifiable bleeding risk factors in AF patients is a class I recommendation. On the basis of a class III recommendation, she cautioned against withholding anticoagulants because of CHA2DS2-VASc risk factors alone. Rather, Dr. Van Gelder called the decision to administer or withhold anticoagulation — like all decisions — one that should be individualized in consultation with the patient.

For reducing AF symptoms and rhythm control, the specific pathways diverge for newly diagnosed AF, paroxysmal AF, and persistent AF. Like all of the guidelines, the specific options for symptom management and AF ablation are color coded, with green signifying level 1 evidence.

The evaluation and dynamic reassessment step refers to the need to periodically assess patients for new modifiable risk factors related to comorbidities, risk for stroke, risk for bleeding, and risk for AF. 

The management of risk factors for AF has long been emphasized in guidelines, but a previous focus on AF with attention to comorbidities has been replaced by a focus on comorbidities with an expectation of more durable AF control. The success of this pivot is based on multidisciplinary care, chosen in collaboration with the patient, to reduce or eliminate the triggers of AF and the risks of its complications.
 

Pathways Are Appropriate for All Patients

A very important recommendation — and this is new — is “to treat all our patients with atrial fibrillation, whether they are young or old, men or women, Black or White, or at high or low risk, according to our patient-centered integrated AF-CARE approach,” Dr. Van Gelder said.

The changes reflect a shared appreciation for the tight relation between the control of comorbidities and the control of AF, according to José A. Joglar, MD, professor of cardiac electrophysiologic research at the University of Texas Southwestern Medical Center in Dallas. Dr. Joglar was chair of the writing committee for the joint 2023 AF guidelines released by the AHA, ACC, the American College of Clinical Pharmacy, and the Heart Rhythm Society.

“It is increasingly clear that AF in many cases is the consequence of underlying risk factors and comorbidities, which cannot be separated from AF alone,” Dr. Joglar explained in an interview.

This was placed first “to emphasize the importance of viewing AFib as a complex disease that requires a holistic, multidisciplinary approach to care, as opposed to being viewed just as a rhythm abnormality,” he said.
 

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

A patient who developed atrial fibrillation resulting from the failure to adjust the levothyroxine dose after rapid, significant weight loss while on the antiobesity drug tirzepatide (Zepbound) serves as a key reminder in managing patients experiencing rapid weight loss, either from antiobesity medications or any other means: Patients taking medications with weight-based dosing need to have their doses closely monitored.

“Failing to monitor and adjust dosing of these [and other] medications during a period of rapid weight loss may lead to supratherapeutic — even toxic — levels, as was seen in this [case],” underscore the authors of an editorial regarding the Teachable Moment case, published in JAMA Internal Medicine.

Toxicities from excessive doses can have a range of detrimental effects. In terms of thyroid medicine, the failure to adjust levothyroxine treatment for hypothyroidism in cases of rapid weight loss can lead to thyrotoxicosis, and in older patients in particular, a resulting thyrotropin level < 0.1 mIU/L is associated with as much as a threefold increased risk for atrial fibrillation, as observed in the report. 
 

Case Demonstrates Risks

The case involved a 62-year-old man with obesity, hypothyroidism, and type 1 diabetes who presented to the emergency department with palpitations, excessive sweating, confusion, fever, and hand tremors. Upon being diagnosed with atrial fibrillation, the patient was immediately treated. 

His medical history revealed the underlying culprit: Six months earlier, the patient had started treatment with the gastric inhibitory polypeptide (GIP)/glucagon-like peptide (GLP) 1 dual agonist tirzepatide. As is typical with the drug, the patient’s weight quickly plummeted, dropping from a starting body mass index of 44.4 down to 31.2 after 6 months and a decrease in body weight from 132 kg to 93 kg (a loss of 39 kg [approximately 86 lb]).

Despite the substantial change in body weight, his initial dose of 200 µg of levothyroxine, received for hypothyroidism, was not adjusted.

When he was prescribed tirzepatide, 2.5 mg weekly, for obesity, the patient had been recommended to increase the dose every 4 weeks as tolerated and, importantly, to have a follow-up visit in a month. But because he lived in different states seasonally, the follow-up never occurred.

Upon his emergency department visit, the patient’s thyrotropin level had dropped from 1.9 mIU/L at the first visit 6 months earlier to 0.001 mIU/L (well within the atrial fibrillation risk range), and his free thyroxine level (fT4) was 7.26 ng/ dL — substantially outside of the normal range of about 0.9-1.7 ng/dL for adults. 

“The patient had 4-times higher fT4 levels of the upper limit,” first author Kagan E. Karakus, MD, of the Barbara Davis Center for Diabetes, University of Colorado Anschutz Medical Campus, Aurora, told this news organization. “That is why he had experienced the adverse event of atrial fibrillation.”
 

Thyrotoxicosis Symptoms Can Be ‘Insidious,’ Levothyroxine Should Be Monitored

Although tirzepatide has not been approved by the US Food and Drug Administration for the treatment of type 1 diabetes, obesity is on the rise among patients with this disorder and recent research has shown a more than 10% reduction in body weight in 6 months and significant reductions in A1c with various doses. 

Of note, in the current case, although the patient’s levothyroxine dose was not adjusted, his insulin dose was gradually self-decreased during his tirzepatide treatment to prevent hypoglycemia.

“If insulin treatment is excessive in diabetes, it causes hypoglycemia, [and] people with type 1 diabetes will recognize the signs of hypoglycemia related to excessive insulin earlier,” Dr. Karakus said.

If symptoms appear, patients can reduce their insulin doses on their own; however, the symptoms of thyrotoxicosis caused by excessive levothyroxine can be more insidious compared with hypoglycemia, he explained. 

“Although patients can change their insulin doses, they cannot change the levothyroxine doses since it requires a blood test [thyroid-stimulating hormone; TSH] and a new prescription of the new dose.”

The key lesson is that “following levothyroxine treatment initiation or dose adjustment, 4-6 weeks is the optimal duration to recheck [the] thyrotropin level and adjust the dose as needed,” Dr. Karakus said.
 

Key Medications to Monitor

Other common outpatient medications that should be closely monitored in patients experiencing rapid weight loss, by any method, range from anticoagulants, anticonvulsants, and antituberculosis drugs to antibiotics and antifungals, the authors note.

Of note, medications with a narrow therapeutic index include phenytoin, warfarin, lithium carbonate, digoxin theophylline, tacrolimus, valproic acid, carbamazepine, and cyclosporine.

The failure to make necessary dose adjustments “is seen more often since the newer antiobesity drugs reduce a great amount of weight within months, almost as rapidly as bariatric surgery,” Dr. Karakus said.

“It is very important for physicians to be aware of the weight-based medications and narrow therapeutic index medications since their doses should be adjusted carefully, especially during weight loss,” he added.

Furthermore, “the patient should also know that weight reduction medication may cause adverse effects like nausea, vomiting and also may affect metabolism of other medications such that some medication doses should be adjusted regularly.”

In the editorial published with the study, Tyrone A. Johnson, MD, of the Department of Medicine, University of California, San Francisco, and colleagues note that the need for close monitoring is particularly important with older patients, who, in addition to having a higher likelihood of comorbidities, commonly have polypharmacy that could increase the potential for adverse effects.

Another key area concern is the emergence of direct-to-consumer avenues for GLP-1/GIP agonists for the many who either cannot afford or do not have access to the drugs, providing further opportunities for treatment without appropriate clinical oversight, they add.

Overall, the case “highlights the potential dangers underlying under-supervised prescribing of GLP-1/GIP receptor agonists and affirms the need for strong partnerships between patients and their clinicians during their use,” they wrote. 

“These medications are best used in collaboration with continuity care teams, in context of a patient’s entire health, and in comprehensive risk-benefit assessment throughout the entire duration of treatment.”
 

A Caveat: Subclinical Levothyroxine Dosing

Commenting on the study, Matthew Ettleson, MD, a clinical instructor of medicine in the Section of Endocrinology, Diabetes, & Metabolism, University of Chicago, noted the important caveat that patients with hypothyroidism are commonly on subclinical doses, with varying dose adjustment needs.

“The patient in the case was clearly on a replacement level dose. However, many patients are on low doses of levothyroxine (75 µg or lower) for subclinical hypothyroidism, and, in general, I think the risks are lower with patients with subclinical hypothyroidism on lower doses of levothyroxine,” he told this news organization.

Because of that, “frequent TSH monitoring may be excessive in this population,” he said. “I would hesitate to empirically lower the dose with weight loss, unless it was clear that the patient was unlikely to follow up.

“Checking TSH at a more frequent interval and adjusting the dose accordingly should be adequate to prevent situations like this case.”

Dr. Karakus, Dr. Ettleson, and the editorial authors had no relevant disclosures to report.
 

A version of this article appeared on Medscape.com.

A patient who developed atrial fibrillation resulting from the failure to adjust the levothyroxine dose after rapid, significant weight loss while on the antiobesity drug tirzepatide (Zepbound) serves as a key reminder in managing patients experiencing rapid weight loss, either from antiobesity medications or any other means: Patients taking medications with weight-based dosing need to have their doses closely monitored.

“Failing to monitor and adjust dosing of these [and other] medications during a period of rapid weight loss may lead to supratherapeutic — even toxic — levels, as was seen in this [case],” underscore the authors of an editorial regarding the Teachable Moment case, published in JAMA Internal Medicine.

Toxicities from excessive doses can have a range of detrimental effects. In terms of thyroid medicine, the failure to adjust levothyroxine treatment for hypothyroidism in cases of rapid weight loss can lead to thyrotoxicosis, and in older patients in particular, a resulting thyrotropin level < 0.1 mIU/L is associated with as much as a threefold increased risk for atrial fibrillation, as observed in the report. 
 

Case Demonstrates Risks

The case involved a 62-year-old man with obesity, hypothyroidism, and type 1 diabetes who presented to the emergency department with palpitations, excessive sweating, confusion, fever, and hand tremors. Upon being diagnosed with atrial fibrillation, the patient was immediately treated. 

His medical history revealed the underlying culprit: Six months earlier, the patient had started treatment with the gastric inhibitory polypeptide (GIP)/glucagon-like peptide (GLP) 1 dual agonist tirzepatide. As is typical with the drug, the patient’s weight quickly plummeted, dropping from a starting body mass index of 44.4 down to 31.2 after 6 months and a decrease in body weight from 132 kg to 93 kg (a loss of 39 kg [approximately 86 lb]).

Despite the substantial change in body weight, his initial dose of 200 µg of levothyroxine, received for hypothyroidism, was not adjusted.

When he was prescribed tirzepatide, 2.5 mg weekly, for obesity, the patient had been recommended to increase the dose every 4 weeks as tolerated and, importantly, to have a follow-up visit in a month. But because he lived in different states seasonally, the follow-up never occurred.

Upon his emergency department visit, the patient’s thyrotropin level had dropped from 1.9 mIU/L at the first visit 6 months earlier to 0.001 mIU/L (well within the atrial fibrillation risk range), and his free thyroxine level (fT4) was 7.26 ng/ dL — substantially outside of the normal range of about 0.9-1.7 ng/dL for adults. 

“The patient had 4-times higher fT4 levels of the upper limit,” first author Kagan E. Karakus, MD, of the Barbara Davis Center for Diabetes, University of Colorado Anschutz Medical Campus, Aurora, told this news organization. “That is why he had experienced the adverse event of atrial fibrillation.”
 

Thyrotoxicosis Symptoms Can Be ‘Insidious,’ Levothyroxine Should Be Monitored

Although tirzepatide has not been approved by the US Food and Drug Administration for the treatment of type 1 diabetes, obesity is on the rise among patients with this disorder and recent research has shown a more than 10% reduction in body weight in 6 months and significant reductions in A1c with various doses. 

Of note, in the current case, although the patient’s levothyroxine dose was not adjusted, his insulin dose was gradually self-decreased during his tirzepatide treatment to prevent hypoglycemia.

“If insulin treatment is excessive in diabetes, it causes hypoglycemia, [and] people with type 1 diabetes will recognize the signs of hypoglycemia related to excessive insulin earlier,” Dr. Karakus said.

If symptoms appear, patients can reduce their insulin doses on their own; however, the symptoms of thyrotoxicosis caused by excessive levothyroxine can be more insidious compared with hypoglycemia, he explained. 

“Although patients can change their insulin doses, they cannot change the levothyroxine doses since it requires a blood test [thyroid-stimulating hormone; TSH] and a new prescription of the new dose.”

The key lesson is that “following levothyroxine treatment initiation or dose adjustment, 4-6 weeks is the optimal duration to recheck [the] thyrotropin level and adjust the dose as needed,” Dr. Karakus said.
 

Key Medications to Monitor

Other common outpatient medications that should be closely monitored in patients experiencing rapid weight loss, by any method, range from anticoagulants, anticonvulsants, and antituberculosis drugs to antibiotics and antifungals, the authors note.

Of note, medications with a narrow therapeutic index include phenytoin, warfarin, lithium carbonate, digoxin theophylline, tacrolimus, valproic acid, carbamazepine, and cyclosporine.

The failure to make necessary dose adjustments “is seen more often since the newer antiobesity drugs reduce a great amount of weight within months, almost as rapidly as bariatric surgery,” Dr. Karakus said.

“It is very important for physicians to be aware of the weight-based medications and narrow therapeutic index medications since their doses should be adjusted carefully, especially during weight loss,” he added.

Furthermore, “the patient should also know that weight reduction medication may cause adverse effects like nausea, vomiting and also may affect metabolism of other medications such that some medication doses should be adjusted regularly.”

In the editorial published with the study, Tyrone A. Johnson, MD, of the Department of Medicine, University of California, San Francisco, and colleagues note that the need for close monitoring is particularly important with older patients, who, in addition to having a higher likelihood of comorbidities, commonly have polypharmacy that could increase the potential for adverse effects.

Another key area concern is the emergence of direct-to-consumer avenues for GLP-1/GIP agonists for the many who either cannot afford or do not have access to the drugs, providing further opportunities for treatment without appropriate clinical oversight, they add.

Overall, the case “highlights the potential dangers underlying under-supervised prescribing of GLP-1/GIP receptor agonists and affirms the need for strong partnerships between patients and their clinicians during their use,” they wrote. 

“These medications are best used in collaboration with continuity care teams, in context of a patient’s entire health, and in comprehensive risk-benefit assessment throughout the entire duration of treatment.”
 

A Caveat: Subclinical Levothyroxine Dosing

Commenting on the study, Matthew Ettleson, MD, a clinical instructor of medicine in the Section of Endocrinology, Diabetes, & Metabolism, University of Chicago, noted the important caveat that patients with hypothyroidism are commonly on subclinical doses, with varying dose adjustment needs.

“The patient in the case was clearly on a replacement level dose. However, many patients are on low doses of levothyroxine (75 µg or lower) for subclinical hypothyroidism, and, in general, I think the risks are lower with patients with subclinical hypothyroidism on lower doses of levothyroxine,” he told this news organization.

Because of that, “frequent TSH monitoring may be excessive in this population,” he said. “I would hesitate to empirically lower the dose with weight loss, unless it was clear that the patient was unlikely to follow up.

“Checking TSH at a more frequent interval and adjusting the dose accordingly should be adequate to prevent situations like this case.”

Dr. Karakus, Dr. Ettleson, and the editorial authors had no relevant disclosures to report.
 

A version of this article appeared on Medscape.com.

A patient who developed atrial fibrillation resulting from the failure to adjust the levothyroxine dose after rapid, significant weight loss while on the antiobesity drug tirzepatide (Zepbound) serves as a key reminder in managing patients experiencing rapid weight loss, either from antiobesity medications or any other means: Patients taking medications with weight-based dosing need to have their doses closely monitored.

“Failing to monitor and adjust dosing of these [and other] medications during a period of rapid weight loss may lead to supratherapeutic — even toxic — levels, as was seen in this [case],” underscore the authors of an editorial regarding the Teachable Moment case, published in JAMA Internal Medicine.

Toxicities from excessive doses can have a range of detrimental effects. In terms of thyroid medicine, the failure to adjust levothyroxine treatment for hypothyroidism in cases of rapid weight loss can lead to thyrotoxicosis, and in older patients in particular, a resulting thyrotropin level < 0.1 mIU/L is associated with as much as a threefold increased risk for atrial fibrillation, as observed in the report. 
 

Case Demonstrates Risks

The case involved a 62-year-old man with obesity, hypothyroidism, and type 1 diabetes who presented to the emergency department with palpitations, excessive sweating, confusion, fever, and hand tremors. Upon being diagnosed with atrial fibrillation, the patient was immediately treated. 

His medical history revealed the underlying culprit: Six months earlier, the patient had started treatment with the gastric inhibitory polypeptide (GIP)/glucagon-like peptide (GLP) 1 dual agonist tirzepatide. As is typical with the drug, the patient’s weight quickly plummeted, dropping from a starting body mass index of 44.4 down to 31.2 after 6 months and a decrease in body weight from 132 kg to 93 kg (a loss of 39 kg [approximately 86 lb]).

Despite the substantial change in body weight, his initial dose of 200 µg of levothyroxine, received for hypothyroidism, was not adjusted.

When he was prescribed tirzepatide, 2.5 mg weekly, for obesity, the patient had been recommended to increase the dose every 4 weeks as tolerated and, importantly, to have a follow-up visit in a month. But because he lived in different states seasonally, the follow-up never occurred.

Upon his emergency department visit, the patient’s thyrotropin level had dropped from 1.9 mIU/L at the first visit 6 months earlier to 0.001 mIU/L (well within the atrial fibrillation risk range), and his free thyroxine level (fT4) was 7.26 ng/ dL — substantially outside of the normal range of about 0.9-1.7 ng/dL for adults. 

“The patient had 4-times higher fT4 levels of the upper limit,” first author Kagan E. Karakus, MD, of the Barbara Davis Center for Diabetes, University of Colorado Anschutz Medical Campus, Aurora, told this news organization. “That is why he had experienced the adverse event of atrial fibrillation.”
 

Thyrotoxicosis Symptoms Can Be ‘Insidious,’ Levothyroxine Should Be Monitored

Although tirzepatide has not been approved by the US Food and Drug Administration for the treatment of type 1 diabetes, obesity is on the rise among patients with this disorder and recent research has shown a more than 10% reduction in body weight in 6 months and significant reductions in A1c with various doses. 

Of note, in the current case, although the patient’s levothyroxine dose was not adjusted, his insulin dose was gradually self-decreased during his tirzepatide treatment to prevent hypoglycemia.

“If insulin treatment is excessive in diabetes, it causes hypoglycemia, [and] people with type 1 diabetes will recognize the signs of hypoglycemia related to excessive insulin earlier,” Dr. Karakus said.

If symptoms appear, patients can reduce their insulin doses on their own; however, the symptoms of thyrotoxicosis caused by excessive levothyroxine can be more insidious compared with hypoglycemia, he explained. 

“Although patients can change their insulin doses, they cannot change the levothyroxine doses since it requires a blood test [thyroid-stimulating hormone; TSH] and a new prescription of the new dose.”

The key lesson is that “following levothyroxine treatment initiation or dose adjustment, 4-6 weeks is the optimal duration to recheck [the] thyrotropin level and adjust the dose as needed,” Dr. Karakus said.
 

Key Medications to Monitor

Other common outpatient medications that should be closely monitored in patients experiencing rapid weight loss, by any method, range from anticoagulants, anticonvulsants, and antituberculosis drugs to antibiotics and antifungals, the authors note.

Of note, medications with a narrow therapeutic index include phenytoin, warfarin, lithium carbonate, digoxin theophylline, tacrolimus, valproic acid, carbamazepine, and cyclosporine.

The failure to make necessary dose adjustments “is seen more often since the newer antiobesity drugs reduce a great amount of weight within months, almost as rapidly as bariatric surgery,” Dr. Karakus said.

“It is very important for physicians to be aware of the weight-based medications and narrow therapeutic index medications since their doses should be adjusted carefully, especially during weight loss,” he added.

Furthermore, “the patient should also know that weight reduction medication may cause adverse effects like nausea, vomiting and also may affect metabolism of other medications such that some medication doses should be adjusted regularly.”

In the editorial published with the study, Tyrone A. Johnson, MD, of the Department of Medicine, University of California, San Francisco, and colleagues note that the need for close monitoring is particularly important with older patients, who, in addition to having a higher likelihood of comorbidities, commonly have polypharmacy that could increase the potential for adverse effects.

Another key area concern is the emergence of direct-to-consumer avenues for GLP-1/GIP agonists for the many who either cannot afford or do not have access to the drugs, providing further opportunities for treatment without appropriate clinical oversight, they add.

Overall, the case “highlights the potential dangers underlying under-supervised prescribing of GLP-1/GIP receptor agonists and affirms the need for strong partnerships between patients and their clinicians during their use,” they wrote. 

“These medications are best used in collaboration with continuity care teams, in context of a patient’s entire health, and in comprehensive risk-benefit assessment throughout the entire duration of treatment.”
 

A Caveat: Subclinical Levothyroxine Dosing

Commenting on the study, Matthew Ettleson, MD, a clinical instructor of medicine in the Section of Endocrinology, Diabetes, & Metabolism, University of Chicago, noted the important caveat that patients with hypothyroidism are commonly on subclinical doses, with varying dose adjustment needs.

“The patient in the case was clearly on a replacement level dose. However, many patients are on low doses of levothyroxine (75 µg or lower) for subclinical hypothyroidism, and, in general, I think the risks are lower with patients with subclinical hypothyroidism on lower doses of levothyroxine,” he told this news organization.

Because of that, “frequent TSH monitoring may be excessive in this population,” he said. “I would hesitate to empirically lower the dose with weight loss, unless it was clear that the patient was unlikely to follow up.

“Checking TSH at a more frequent interval and adjusting the dose accordingly should be adequate to prevent situations like this case.”

Dr. Karakus, Dr. Ettleson, and the editorial authors had no relevant disclosures to report.
 

A version of this article appeared on Medscape.com.

Rapid eye movement (REM) sleep, deep sleep, and sleep irregularity were significantly associated with increased risk for a range of chronic diseases, based on a new study of > 6000 individuals. 

“Most of what we think we know about sleep patterns in adults comes from either self-report surveys, which are widely used but have all sorts of problems with over- and under-estimating sleep duration and quality, or single-night sleep studies,” corresponding author Evan L. Brittain, MD, of Vanderbilt University, Nashville, Tennessee, said in an interview. 

The single-night study yields the highest quality data but is limited by extrapolating a single night’s sleep to represent habitual sleep patterns, which is often not the case, he said. In the current study, published in Nature Medicine, “we had a unique opportunity to understand sleep using a large cohort of individuals using wearable devices that measure sleep duration, quality, and variability. The All of Us Research Program is the first to link wearables data to the electronic health record at scale and allowed us to study long-term, real-world sleep behavior,” Dr. Brittain said.

The timing of the study is important because the American Heart Association now recognizes sleep as a key component of heart health, and public awareness of the value of sleep is increasing, he added. 

The researchers reviewed objectively measured, longitudinal sleep data from 6785 adults who used commercial wearable devices (Fitbit) linked to electronic health record data in the All of Us Research Program. The median age of the participants was 50.2 years, 71% were women, and 84% self-identified as White individuals. The median period of sleep monitoring was 4.5 years.

REM sleep and deep sleep were inversely associated with the odds of incident heart rhythm and heart rate abnormalities. Each percent increase in REM sleep was associated with a reduced incidence of atrial fibrillation (odds ratio [OR], 0.86), atrial flutter (OR, 0.78), and sinoatrial node dysfunction/bradycardia (OR, 0.72). A higher percentage of deep sleep was associated with reduced odds of atrial fibrillation (OR, 0.87), major depressive disorder (OR, 0.93), and anxiety disorder (OR, 0.94). 

Increased irregular sleep was significantly associated with increased odds of incident obesity (OR, 1.49), hyperlipidemia (OR, 1.39), and hypertension (OR, 1.56), as well as major depressive disorder (OR, 1.75), anxiety disorder (OR, 1.55), and bipolar disorder (OR, 2.27). 

The researchers also identified J-shaped associations between average daily sleep duration and hypertension (P for nonlinearity = .003), as well as major depressive disorder and generalized anxiety disorder (both P < .001). 

The study was limited by several factors including the relatively young, White, and female study population. However, the results illustrate how sleep stages, duration, and regularity are associated with chronic disease development, and may inform evidence-based recommendations on healthy sleeping habits, the researchers wrote.
 

Findings Support Need for Sleep Consistency 

“The biggest surprise for me was the impact of sleep variability of health,” Dr. Brittain told this news organization. “The more your sleep duration varies, the higher your risk of numerous chronic diseases across the entire spectrum of organ systems. Sleep duration and quality were also important but that was less surprising,” he said. 

The clinical implications of the findings are that sleep duration, quality, and variability are all important, said Dr. Brittain. “To me, the easiest finding to translate into the clinic is the importance of reducing the variability of sleep duration as much as possible,” he said. For patients, that means explaining that they need to go to sleep and wake up at roughly the same time night to night, he said. 

“Commercial wearable devices are not perfect compared with research grade devices, but our study showed that they nonetheless collect clinically relevant information,” Dr. Brittain added. “For patients who own a device, I have adopted the practice of reviewing my patients’ sleep and activity data which gives objective insight into behavior that is not always accurate through routine questioning,” he said.

As for other limitations, “Our cohort was limited to individuals who already owned a Fitbit; not surprisingly, these individuals differ from a random sample of the community in important ways, both demographic and behavioral, and our findings need to be validated in a more diverse population,” said Dr. Brittain. 

Looking ahead, “we are interested in using commercial devices as a tool for sleep interventions to test the impact of improving sleep hygiene on chronic disease incidence, severity, and progression,” he said.
 

Device Data Will Evolve to Inform Patient Care

“With the increasing use of commercial wearable devices, it is crucial to identify and understand the data they can collect,” said Arianne K. Baldomero, MD, a pulmonologist and assistant professor of medicine at the University of Minnesota, Minneapolis, in an interview. “This study specifically analyzed sleep data from Fitbit devices among participants in the All of Us Research Program to assess sleep patterns and their association with chronic disease risk,” said Dr. Baldomero, who was not involved in the study. 

The significant relationships between sleep patterns and risk for chronic diseases were not surprising, said Dr. Baldomero. The findings of an association between shorter sleep duration and greater sleep irregularity with obesity and sleep apnea validated previous studies in large-scale population surveys, she said. Findings from the current study also reflect data from the literature on sleep duration associated with hypertension, major depressive disorder, and generalized anxiety findings, she added.

“This study reinforces the importance of adequate sleep, typically around 7 hours per night, and suggests that insufficient or poor-quality sleep may be associated with chronic diseases,” Dr. Baldomero told this news organization. “Pulmonologists should remain vigilant about sleep-related issues, and consider further investigation and referrals to sleep specialty clinics for patients suspected of having sleep disturbances,” she said.

“What remains unclear is whether abnormal sleep patterns are a cause or an effect of chronic diseases,” Dr. Baldomero noted. “Additionally, it is essential to ensure that these devices accurately capture sleep patterns and continue to validate their data against gold standard measures of sleep disturbances,” she said.

The study was based on work that was partially funded by an unrestricted gift from Google, and the study itself was supported by National Institutes of Health. Dr. Brittain disclosed received research funds unrelated to this work from United Therapeutics. Dr. Baldomero had no financial conflicts to disclose.

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

Rapid eye movement (REM) sleep, deep sleep, and sleep irregularity were significantly associated with increased risk for a range of chronic diseases, based on a new study of > 6000 individuals. 

“Most of what we think we know about sleep patterns in adults comes from either self-report surveys, which are widely used but have all sorts of problems with over- and under-estimating sleep duration and quality, or single-night sleep studies,” corresponding author Evan L. Brittain, MD, of Vanderbilt University, Nashville, Tennessee, said in an interview. 

The single-night study yields the highest quality data but is limited by extrapolating a single night’s sleep to represent habitual sleep patterns, which is often not the case, he said. In the current study, published in Nature Medicine, “we had a unique opportunity to understand sleep using a large cohort of individuals using wearable devices that measure sleep duration, quality, and variability. The All of Us Research Program is the first to link wearables data to the electronic health record at scale and allowed us to study long-term, real-world sleep behavior,” Dr. Brittain said.

The timing of the study is important because the American Heart Association now recognizes sleep as a key component of heart health, and public awareness of the value of sleep is increasing, he added. 

The researchers reviewed objectively measured, longitudinal sleep data from 6785 adults who used commercial wearable devices (Fitbit) linked to electronic health record data in the All of Us Research Program. The median age of the participants was 50.2 years, 71% were women, and 84% self-identified as White individuals. The median period of sleep monitoring was 4.5 years.

REM sleep and deep sleep were inversely associated with the odds of incident heart rhythm and heart rate abnormalities. Each percent increase in REM sleep was associated with a reduced incidence of atrial fibrillation (odds ratio [OR], 0.86), atrial flutter (OR, 0.78), and sinoatrial node dysfunction/bradycardia (OR, 0.72). A higher percentage of deep sleep was associated with reduced odds of atrial fibrillation (OR, 0.87), major depressive disorder (OR, 0.93), and anxiety disorder (OR, 0.94). 

Increased irregular sleep was significantly associated with increased odds of incident obesity (OR, 1.49), hyperlipidemia (OR, 1.39), and hypertension (OR, 1.56), as well as major depressive disorder (OR, 1.75), anxiety disorder (OR, 1.55), and bipolar disorder (OR, 2.27). 

The researchers also identified J-shaped associations between average daily sleep duration and hypertension (P for nonlinearity = .003), as well as major depressive disorder and generalized anxiety disorder (both P < .001). 

The study was limited by several factors including the relatively young, White, and female study population. However, the results illustrate how sleep stages, duration, and regularity are associated with chronic disease development, and may inform evidence-based recommendations on healthy sleeping habits, the researchers wrote.
 

Findings Support Need for Sleep Consistency 

“The biggest surprise for me was the impact of sleep variability of health,” Dr. Brittain told this news organization. “The more your sleep duration varies, the higher your risk of numerous chronic diseases across the entire spectrum of organ systems. Sleep duration and quality were also important but that was less surprising,” he said. 

The clinical implications of the findings are that sleep duration, quality, and variability are all important, said Dr. Brittain. “To me, the easiest finding to translate into the clinic is the importance of reducing the variability of sleep duration as much as possible,” he said. For patients, that means explaining that they need to go to sleep and wake up at roughly the same time night to night, he said. 

“Commercial wearable devices are not perfect compared with research grade devices, but our study showed that they nonetheless collect clinically relevant information,” Dr. Brittain added. “For patients who own a device, I have adopted the practice of reviewing my patients’ sleep and activity data which gives objective insight into behavior that is not always accurate through routine questioning,” he said.

As for other limitations, “Our cohort was limited to individuals who already owned a Fitbit; not surprisingly, these individuals differ from a random sample of the community in important ways, both demographic and behavioral, and our findings need to be validated in a more diverse population,” said Dr. Brittain. 

Looking ahead, “we are interested in using commercial devices as a tool for sleep interventions to test the impact of improving sleep hygiene on chronic disease incidence, severity, and progression,” he said.
 

Device Data Will Evolve to Inform Patient Care

“With the increasing use of commercial wearable devices, it is crucial to identify and understand the data they can collect,” said Arianne K. Baldomero, MD, a pulmonologist and assistant professor of medicine at the University of Minnesota, Minneapolis, in an interview. “This study specifically analyzed sleep data from Fitbit devices among participants in the All of Us Research Program to assess sleep patterns and their association with chronic disease risk,” said Dr. Baldomero, who was not involved in the study. 

The significant relationships between sleep patterns and risk for chronic diseases were not surprising, said Dr. Baldomero. The findings of an association between shorter sleep duration and greater sleep irregularity with obesity and sleep apnea validated previous studies in large-scale population surveys, she said. Findings from the current study also reflect data from the literature on sleep duration associated with hypertension, major depressive disorder, and generalized anxiety findings, she added.

“This study reinforces the importance of adequate sleep, typically around 7 hours per night, and suggests that insufficient or poor-quality sleep may be associated with chronic diseases,” Dr. Baldomero told this news organization. “Pulmonologists should remain vigilant about sleep-related issues, and consider further investigation and referrals to sleep specialty clinics for patients suspected of having sleep disturbances,” she said.

“What remains unclear is whether abnormal sleep patterns are a cause or an effect of chronic diseases,” Dr. Baldomero noted. “Additionally, it is essential to ensure that these devices accurately capture sleep patterns and continue to validate their data against gold standard measures of sleep disturbances,” she said.

The study was based on work that was partially funded by an unrestricted gift from Google, and the study itself was supported by National Institutes of Health. Dr. Brittain disclosed received research funds unrelated to this work from United Therapeutics. Dr. Baldomero had no financial conflicts to disclose.

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

Rapid eye movement (REM) sleep, deep sleep, and sleep irregularity were significantly associated with increased risk for a range of chronic diseases, based on a new study of > 6000 individuals. 

“Most of what we think we know about sleep patterns in adults comes from either self-report surveys, which are widely used but have all sorts of problems with over- and under-estimating sleep duration and quality, or single-night sleep studies,” corresponding author Evan L. Brittain, MD, of Vanderbilt University, Nashville, Tennessee, said in an interview. 

The single-night study yields the highest quality data but is limited by extrapolating a single night’s sleep to represent habitual sleep patterns, which is often not the case, he said. In the current study, published in Nature Medicine, “we had a unique opportunity to understand sleep using a large cohort of individuals using wearable devices that measure sleep duration, quality, and variability. The All of Us Research Program is the first to link wearables data to the electronic health record at scale and allowed us to study long-term, real-world sleep behavior,” Dr. Brittain said.

The timing of the study is important because the American Heart Association now recognizes sleep as a key component of heart health, and public awareness of the value of sleep is increasing, he added. 

The researchers reviewed objectively measured, longitudinal sleep data from 6785 adults who used commercial wearable devices (Fitbit) linked to electronic health record data in the All of Us Research Program. The median age of the participants was 50.2 years, 71% were women, and 84% self-identified as White individuals. The median period of sleep monitoring was 4.5 years.

REM sleep and deep sleep were inversely associated with the odds of incident heart rhythm and heart rate abnormalities. Each percent increase in REM sleep was associated with a reduced incidence of atrial fibrillation (odds ratio [OR], 0.86), atrial flutter (OR, 0.78), and sinoatrial node dysfunction/bradycardia (OR, 0.72). A higher percentage of deep sleep was associated with reduced odds of atrial fibrillation (OR, 0.87), major depressive disorder (OR, 0.93), and anxiety disorder (OR, 0.94). 

Increased irregular sleep was significantly associated with increased odds of incident obesity (OR, 1.49), hyperlipidemia (OR, 1.39), and hypertension (OR, 1.56), as well as major depressive disorder (OR, 1.75), anxiety disorder (OR, 1.55), and bipolar disorder (OR, 2.27). 

The researchers also identified J-shaped associations between average daily sleep duration and hypertension (P for nonlinearity = .003), as well as major depressive disorder and generalized anxiety disorder (both P < .001). 

The study was limited by several factors including the relatively young, White, and female study population. However, the results illustrate how sleep stages, duration, and regularity are associated with chronic disease development, and may inform evidence-based recommendations on healthy sleeping habits, the researchers wrote.
 

Findings Support Need for Sleep Consistency 

“The biggest surprise for me was the impact of sleep variability of health,” Dr. Brittain told this news organization. “The more your sleep duration varies, the higher your risk of numerous chronic diseases across the entire spectrum of organ systems. Sleep duration and quality were also important but that was less surprising,” he said. 

The clinical implications of the findings are that sleep duration, quality, and variability are all important, said Dr. Brittain. “To me, the easiest finding to translate into the clinic is the importance of reducing the variability of sleep duration as much as possible,” he said. For patients, that means explaining that they need to go to sleep and wake up at roughly the same time night to night, he said. 

“Commercial wearable devices are not perfect compared with research grade devices, but our study showed that they nonetheless collect clinically relevant information,” Dr. Brittain added. “For patients who own a device, I have adopted the practice of reviewing my patients’ sleep and activity data which gives objective insight into behavior that is not always accurate through routine questioning,” he said.

As for other limitations, “Our cohort was limited to individuals who already owned a Fitbit; not surprisingly, these individuals differ from a random sample of the community in important ways, both demographic and behavioral, and our findings need to be validated in a more diverse population,” said Dr. Brittain. 

Looking ahead, “we are interested in using commercial devices as a tool for sleep interventions to test the impact of improving sleep hygiene on chronic disease incidence, severity, and progression,” he said.
 

Device Data Will Evolve to Inform Patient Care

“With the increasing use of commercial wearable devices, it is crucial to identify and understand the data they can collect,” said Arianne K. Baldomero, MD, a pulmonologist and assistant professor of medicine at the University of Minnesota, Minneapolis, in an interview. “This study specifically analyzed sleep data from Fitbit devices among participants in the All of Us Research Program to assess sleep patterns and their association with chronic disease risk,” said Dr. Baldomero, who was not involved in the study. 

The significant relationships between sleep patterns and risk for chronic diseases were not surprising, said Dr. Baldomero. The findings of an association between shorter sleep duration and greater sleep irregularity with obesity and sleep apnea validated previous studies in large-scale population surveys, she said. Findings from the current study also reflect data from the literature on sleep duration associated with hypertension, major depressive disorder, and generalized anxiety findings, she added.

“This study reinforces the importance of adequate sleep, typically around 7 hours per night, and suggests that insufficient or poor-quality sleep may be associated with chronic diseases,” Dr. Baldomero told this news organization. “Pulmonologists should remain vigilant about sleep-related issues, and consider further investigation and referrals to sleep specialty clinics for patients suspected of having sleep disturbances,” she said.

“What remains unclear is whether abnormal sleep patterns are a cause or an effect of chronic diseases,” Dr. Baldomero noted. “Additionally, it is essential to ensure that these devices accurately capture sleep patterns and continue to validate their data against gold standard measures of sleep disturbances,” she said.

The study was based on work that was partially funded by an unrestricted gift from Google, and the study itself was supported by National Institutes of Health. Dr. Brittain disclosed received research funds unrelated to this work from United Therapeutics. Dr. Baldomero had no financial conflicts to disclose.

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

Hyperkalemia tends to cause panic in healthcare professionals, and rightfully so. On a good day, it causes weakness in the legs; on a bad day, it causes cardiac arrest.

It makes sense that a high potassium level causes clinicians to feel a bit jumpy. This anxiety tends to result in treating the issue by overly restricting potassium in the diet. The problem with this method is that it should be temporary but often isn’t. There are only a few concerns that justify long-term potassium restriction.

As a dietitian, I have seen numerous patients with varying disease states who are terrified of potassium because they were never properly educated on the situation that required restriction or were never notified that their potassium was corrected. 

I’ve seen patients whose potassium level hasn’t been elevated in years refuse banana bread because they were told that they could never eat a banana again. I’ve worked with patients who continued to needlessly restrict, which eventually led to hypokalemia.

Not only does this indicate ineffective education — banana bread is actually a low-potassium food at about 80 mg per slice — but also poor follow-up. 

Potassium has been designated by the United States Department of Agriculture as a nutrient of public health concern due to its underconsumption in the general population. Although there is concern in the public health community that the current guidelines for potassium intake (3500-4700 mg/d) are unattainable, with some professionals arguing for lowering the standard, there remains significant deficiency in the general population. This deficiency has also been connected to increasing rates of hypertension and cardiovascular disease. 
 

Nondietary Causes of Hyperkalemia 

There are many causes of hyperkalemia, of which excessive potassium intake is only one, and an uncommon one at that. A high potassium level should resolve during the course of treatment for metabolic acidosis, hyperglycemia, and dehydration. We may also see resolution with medication changes. But the question remains: Are we relaying this information to patients?

Renal insufficiency is a common cause of hyperkalemia, but it is also a common cause of chronic constipation that can cause hyperkalemia as well. Are we addressing bowel movements with these patients? I often work with patients who aren’t having their bowel movements addressed until the patient themselves voices discomfort. 

Depending upon the urgency of treatment, potassium restriction may be the most effective and efficient way to address an acutely elevated value. However, long-term potassium restriction may not be an appropriate intervention for all patients, even those with kidney conditions.

As a dietitian, I have seen many patients who overly restrict dietary potassium because they had one elevated value. These patients tend to view potassium as the enemy because they were never educated on the actual cause of their hyperkalemia. They were simply given a list of high-potassium foods and told to avoid them. A lack of follow-up education may cause them to avoid those foods forever. 
 

Benefits of Potassium

The problem with this perpetual avoidance of high potassium foods is that a potassium-rich diet has been shown to be exceptionally beneficial. 

Potassium exists in many forms in the Western diet: as a preservative and additive, a salt substitute, and naturally occurring in both animal and plant products. My concern regarding blanket potassium restriction is that potassium-rich plant and animal products can actually be beneficial, even to those with kidney and heart conditions who are most often advised to restrict its intake. 

Adequate potassium intake can: 

• Decrease blood pressure by increasing urinary excretion of sodium
• Improve nephrolithiasis by decreasing urinary excretion of calcium
• Decrease incidence of metabolic acidosis by providing precursors to bicarbonate that facilitate excretion of potassium
• Increase bone density in postmenopausal women
• Decrease risk for stroke and cardiovascular disease in the general population

One study found that metabolic acidosis can be corrected in patients with stage 4 chronic kidney disease, without hyperkalemia, by increasing fruit and vegetable intake when compared with those treated with bicarbonate alone, thus preserving kidney function.

Do I suggest encouraging a patient with acute hyperkalemia to eat a banana? Of course not. But I would suggest finding ways to work with patients who have chronic hyperkalemia to increase intake of potassium-rich plant foods to maintain homeostasis while liberalizing diet and preventing progression of chronic kidney disease. 
 

When to Refer to a Dietitian

In patients for whom a potassium-restricted diet is a necessary long-term treatment of hyperkalemia, education with a registered dietitian can be beneficial. A registered dietitian has the time and expertise to address the areas in the diet where excessive potassium exists without forfeiting other nutritional benefits that come from whole foods like fruits, vegetables, lean protein, legumes, nuts, and seeds in a way that is both realistic and helpful. A dietitian can work with patients to reduce intake of potassium-containing salt substitutes, preservatives, and other additives while still encouraging a whole-food diet rich in antioxidants, fiber, and healthy fats.

Dietitians also provide education on serving size and methods to reduce potassium content of food.

For example, tomatoes are a high-potassium food at 300+ mg per medium-sized tomato. But how often does a patient eat a whole tomato? A slice of tomato on a sandwich or a handful of cherry tomatoes in a salad are actually low in potassium per serving and can provide additional nutrients like vitamin C, beta-carotene, and antioxidants like lycopene, which is linked to a decreased incidence of prostate cancer.

By incorporating the assistance of a registered dietitian into the treatment of chronic hyperkalemia, we can develop individualized restrictions that are realistic for the patient and tailored to their nutritional needs to promote optimal health and thus encourage continued compliance. 

Ms. Winfree is a renal dietitian in private practice in Mary Esther, Florida. She disclosed no relevant conflicts of interest.

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

Hyperkalemia tends to cause panic in healthcare professionals, and rightfully so. On a good day, it causes weakness in the legs; on a bad day, it causes cardiac arrest.

It makes sense that a high potassium level causes clinicians to feel a bit jumpy. This anxiety tends to result in treating the issue by overly restricting potassium in the diet. The problem with this method is that it should be temporary but often isn’t. There are only a few concerns that justify long-term potassium restriction.

As a dietitian, I have seen numerous patients with varying disease states who are terrified of potassium because they were never properly educated on the situation that required restriction or were never notified that their potassium was corrected. 

I’ve seen patients whose potassium level hasn’t been elevated in years refuse banana bread because they were told that they could never eat a banana again. I’ve worked with patients who continued to needlessly restrict, which eventually led to hypokalemia.

Not only does this indicate ineffective education — banana bread is actually a low-potassium food at about 80 mg per slice — but also poor follow-up. 

Potassium has been designated by the United States Department of Agriculture as a nutrient of public health concern due to its underconsumption in the general population. Although there is concern in the public health community that the current guidelines for potassium intake (3500-4700 mg/d) are unattainable, with some professionals arguing for lowering the standard, there remains significant deficiency in the general population. This deficiency has also been connected to increasing rates of hypertension and cardiovascular disease. 
 

Nondietary Causes of Hyperkalemia 

There are many causes of hyperkalemia, of which excessive potassium intake is only one, and an uncommon one at that. A high potassium level should resolve during the course of treatment for metabolic acidosis, hyperglycemia, and dehydration. We may also see resolution with medication changes. But the question remains: Are we relaying this information to patients?

Renal insufficiency is a common cause of hyperkalemia, but it is also a common cause of chronic constipation that can cause hyperkalemia as well. Are we addressing bowel movements with these patients? I often work with patients who aren’t having their bowel movements addressed until the patient themselves voices discomfort. 

Depending upon the urgency of treatment, potassium restriction may be the most effective and efficient way to address an acutely elevated value. However, long-term potassium restriction may not be an appropriate intervention for all patients, even those with kidney conditions.

As a dietitian, I have seen many patients who overly restrict dietary potassium because they had one elevated value. These patients tend to view potassium as the enemy because they were never educated on the actual cause of their hyperkalemia. They were simply given a list of high-potassium foods and told to avoid them. A lack of follow-up education may cause them to avoid those foods forever. 
 

Benefits of Potassium

The problem with this perpetual avoidance of high potassium foods is that a potassium-rich diet has been shown to be exceptionally beneficial. 

Potassium exists in many forms in the Western diet: as a preservative and additive, a salt substitute, and naturally occurring in both animal and plant products. My concern regarding blanket potassium restriction is that potassium-rich plant and animal products can actually be beneficial, even to those with kidney and heart conditions who are most often advised to restrict its intake. 

Adequate potassium intake can: 

• Decrease blood pressure by increasing urinary excretion of sodium
• Improve nephrolithiasis by decreasing urinary excretion of calcium
• Decrease incidence of metabolic acidosis by providing precursors to bicarbonate that facilitate excretion of potassium
• Increase bone density in postmenopausal women
• Decrease risk for stroke and cardiovascular disease in the general population

One study found that metabolic acidosis can be corrected in patients with stage 4 chronic kidney disease, without hyperkalemia, by increasing fruit and vegetable intake when compared with those treated with bicarbonate alone, thus preserving kidney function.

Do I suggest encouraging a patient with acute hyperkalemia to eat a banana? Of course not. But I would suggest finding ways to work with patients who have chronic hyperkalemia to increase intake of potassium-rich plant foods to maintain homeostasis while liberalizing diet and preventing progression of chronic kidney disease. 
 

When to Refer to a Dietitian

In patients for whom a potassium-restricted diet is a necessary long-term treatment of hyperkalemia, education with a registered dietitian can be beneficial. A registered dietitian has the time and expertise to address the areas in the diet where excessive potassium exists without forfeiting other nutritional benefits that come from whole foods like fruits, vegetables, lean protein, legumes, nuts, and seeds in a way that is both realistic and helpful. A dietitian can work with patients to reduce intake of potassium-containing salt substitutes, preservatives, and other additives while still encouraging a whole-food diet rich in antioxidants, fiber, and healthy fats.

Dietitians also provide education on serving size and methods to reduce potassium content of food.

For example, tomatoes are a high-potassium food at 300+ mg per medium-sized tomato. But how often does a patient eat a whole tomato? A slice of tomato on a sandwich or a handful of cherry tomatoes in a salad are actually low in potassium per serving and can provide additional nutrients like vitamin C, beta-carotene, and antioxidants like lycopene, which is linked to a decreased incidence of prostate cancer.

By incorporating the assistance of a registered dietitian into the treatment of chronic hyperkalemia, we can develop individualized restrictions that are realistic for the patient and tailored to their nutritional needs to promote optimal health and thus encourage continued compliance. 

Ms. Winfree is a renal dietitian in private practice in Mary Esther, Florida. She disclosed no relevant conflicts of interest.

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

Hyperkalemia tends to cause panic in healthcare professionals, and rightfully so. On a good day, it causes weakness in the legs; on a bad day, it causes cardiac arrest.

It makes sense that a high potassium level causes clinicians to feel a bit jumpy. This anxiety tends to result in treating the issue by overly restricting potassium in the diet. The problem with this method is that it should be temporary but often isn’t. There are only a few concerns that justify long-term potassium restriction.

As a dietitian, I have seen numerous patients with varying disease states who are terrified of potassium because they were never properly educated on the situation that required restriction or were never notified that their potassium was corrected. 

I’ve seen patients whose potassium level hasn’t been elevated in years refuse banana bread because they were told that they could never eat a banana again. I’ve worked with patients who continued to needlessly restrict, which eventually led to hypokalemia.

Not only does this indicate ineffective education — banana bread is actually a low-potassium food at about 80 mg per slice — but also poor follow-up. 

Potassium has been designated by the United States Department of Agriculture as a nutrient of public health concern due to its underconsumption in the general population. Although there is concern in the public health community that the current guidelines for potassium intake (3500-4700 mg/d) are unattainable, with some professionals arguing for lowering the standard, there remains significant deficiency in the general population. This deficiency has also been connected to increasing rates of hypertension and cardiovascular disease. 
 

Nondietary Causes of Hyperkalemia 

There are many causes of hyperkalemia, of which excessive potassium intake is only one, and an uncommon one at that. A high potassium level should resolve during the course of treatment for metabolic acidosis, hyperglycemia, and dehydration. We may also see resolution with medication changes. But the question remains: Are we relaying this information to patients?

Renal insufficiency is a common cause of hyperkalemia, but it is also a common cause of chronic constipation that can cause hyperkalemia as well. Are we addressing bowel movements with these patients? I often work with patients who aren’t having their bowel movements addressed until the patient themselves voices discomfort. 

Depending upon the urgency of treatment, potassium restriction may be the most effective and efficient way to address an acutely elevated value. However, long-term potassium restriction may not be an appropriate intervention for all patients, even those with kidney conditions.

As a dietitian, I have seen many patients who overly restrict dietary potassium because they had one elevated value. These patients tend to view potassium as the enemy because they were never educated on the actual cause of their hyperkalemia. They were simply given a list of high-potassium foods and told to avoid them. A lack of follow-up education may cause them to avoid those foods forever. 
 

Benefits of Potassium

The problem with this perpetual avoidance of high potassium foods is that a potassium-rich diet has been shown to be exceptionally beneficial. 

Potassium exists in many forms in the Western diet: as a preservative and additive, a salt substitute, and naturally occurring in both animal and plant products. My concern regarding blanket potassium restriction is that potassium-rich plant and animal products can actually be beneficial, even to those with kidney and heart conditions who are most often advised to restrict its intake. 

Adequate potassium intake can: 

• Decrease blood pressure by increasing urinary excretion of sodium
• Improve nephrolithiasis by decreasing urinary excretion of calcium
• Decrease incidence of metabolic acidosis by providing precursors to bicarbonate that facilitate excretion of potassium
• Increase bone density in postmenopausal women
• Decrease risk for stroke and cardiovascular disease in the general population

One study found that metabolic acidosis can be corrected in patients with stage 4 chronic kidney disease, without hyperkalemia, by increasing fruit and vegetable intake when compared with those treated with bicarbonate alone, thus preserving kidney function.

Do I suggest encouraging a patient with acute hyperkalemia to eat a banana? Of course not. But I would suggest finding ways to work with patients who have chronic hyperkalemia to increase intake of potassium-rich plant foods to maintain homeostasis while liberalizing diet and preventing progression of chronic kidney disease. 
 

When to Refer to a Dietitian

In patients for whom a potassium-restricted diet is a necessary long-term treatment of hyperkalemia, education with a registered dietitian can be beneficial. A registered dietitian has the time and expertise to address the areas in the diet where excessive potassium exists without forfeiting other nutritional benefits that come from whole foods like fruits, vegetables, lean protein, legumes, nuts, and seeds in a way that is both realistic and helpful. A dietitian can work with patients to reduce intake of potassium-containing salt substitutes, preservatives, and other additives while still encouraging a whole-food diet rich in antioxidants, fiber, and healthy fats.

Dietitians also provide education on serving size and methods to reduce potassium content of food.

For example, tomatoes are a high-potassium food at 300+ mg per medium-sized tomato. But how often does a patient eat a whole tomato? A slice of tomato on a sandwich or a handful of cherry tomatoes in a salad are actually low in potassium per serving and can provide additional nutrients like vitamin C, beta-carotene, and antioxidants like lycopene, which is linked to a decreased incidence of prostate cancer.

By incorporating the assistance of a registered dietitian into the treatment of chronic hyperkalemia, we can develop individualized restrictions that are realistic for the patient and tailored to their nutritional needs to promote optimal health and thus encourage continued compliance. 

Ms. Winfree is a renal dietitian in private practice in Mary Esther, Florida. She disclosed no relevant conflicts of interest.

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

My field of electrophysiology is abuzz with excitement over the new technology of pulsed field ablation (PFA). It dominated 2024’s heart rhythm meetings, and it dominates my private electrophysiologist chat groups. My Google alert for “AF ablation” most often includes notices on PFA and the expansion of the atrial fibrillation ablation market. 

Yet, the excitement does not match the empirical data. 

Despite having strong brains, electrophysiologists adopt new things as if we were emotional shoppers. Our neighbor buys a sports car and we think we need the same car. Left atrial appendage occlusion and subcutaneous defibrillators were past examples. 

The most recent example of soft thinking (especially in the United States) is the enthusiasm and early adoption of first-generation PFA systems for the treatment of AF. 

Readers of cardiac news (including some of my patients) might think PFA has solved the AF puzzle. It has not.

A true breakthrough in AF would be to find its cause. PFA is simply another way to destroy (ablate) cardiac myocytes. PFA uses electrical energy (think shocks) to create pores in the cell membranes of myocytes. It’s delivered through various types of catheters. 

The main theoretical advantage of PFA is cardioselectivity, which is possible because myocytes have lower thresholds for irreversible electroporation than surrounding tissues. The dose of electrical energy that ablates cardiac tissue does not affect surrounding tissues. Cardioselectivity decreases the chance of the most feared complication of standard AF ablation, thermal damage to the esophagus, which is often fatal. The esophagus lies immediately behind the posterior wall of the left atrium and can be inadvertently injured during thermal ablation. 

The challenge in assessing this potential advantage is that thermal esophageal damage is, thankfully, exceedingly rare. Its incidence is in the range of 1 in 10,000 AF ablations. But it might be even lower than that in contemporary practice, because knowledge of esophageal injury has led to innovations that probably have reduced its incidence even further. 

Proponents of PFA would rightly point to the fact that not having to worry about esophageal injury allows operators to add posterior wall ablation to the normal pulmonary vein isolation lesion set. This ability, they would argue, is likely to improve AF ablation outcomes. The problem is that the strongest and most recent trial of posterior wall isolation (with radiofrequency ablation) did not show better outcomes. A more recent observational analysis also showed no benefit to posterior wall isolation (using PFA) over pulmonary vein isolation alone. 
 

What About PFA Efficacy?

I’ve long spoken and written about the lack of progress in AF ablation. In 1998, the first report on ablation of AF showed a 62% arrhythmia-free rate. Two decades later, in the carefully chosen labs treating patients in the CABANA trial, arrhythmia-free rates after AF ablation remain unchanged. We have improved our speed and ability to isolate pulmonary veins, but this has not increased our success in eliminating AF. The reason, I believe, is that we have made little to no progress in understanding the pathophysiology of AF. 

The Food and Drug Administration regulatory trial called ADVENT randomly assigned more than 600 patients to thermal ablation or PFA, and the primary endpoint of ablation success was nearly identical. Single-center studies, observational registries, and single-arm studies have all shown similar efficacy of PFA and thermal ablation. 

Proponents of PFA might argue that these early studies used first-generation PFA systems, and iteration will lead to better efficacy. Perhaps, but we’ve had 20 years of iteration of thermal ablation, and its efficacy has not budged. 
 

What About PFA Safety?

In the ADVENT randomized trial, safety results were similar, though the one death, caused by cardiac perforation and tamponade, occurred in the PFA arm. In the MANIFEST-17K multinational survey of PFA ablation, safety events were in the range reported with thermal ablation. PFA still involves placing catheters in the heart, and complications such as tamponade, stroke, and vascular damage occur. 

The large MANIFEST-17K survey also exposed two PFA-specific complications: coronary artery spasm, which can occur when PFA is delivered close to coronary arteries; and hemolysis-related kidney failure — severe enough to require dialysis in five patients. Supporters of PFA speculate that hemolysis occurs because electrical energy within the atrium can shred red blood cells. Their solution is to strive for good contact and use hydration. The irony of this latter fix is that one of the best advances in thermal ablation has been catheters that deliver less fluid and less need for diuresis after the procedure. 

No PFA study has shown a decreased incidence of thermal damage to the esophagus with PFA ablation. Of course, this is because it is such a low-incidence event. 

One of my concerns with PFA is brain safety. PFA creates substantial microbubbles in the left atrium, which can then travel north to the brain. In a small series from ADVENT, three patients had brain lesions after PFA vs none with thermal ablation. PFA proponents wrote that brain safety was important to study, but few patients have been systematically studied with brain MRI scans. Asymptomatic brain lesions have been noted after many arterial procedures. The clinical significance of these is not known. As a new technology, and one that creates substantial microbubbles in the left atrium, I agree with the PFA proponents that brain safety should be thoroughly studied — before widespread adoption. 
 

What About Speed and Cost? 

Observational studies from European labs report fast procedure times. I have seen PFA procedures in Europe; they’re fast — typically under an hour. A standard thermal ablation takes me about 60-70 minutes.

I am not sure that US operators can duplicate European procedural times. In the ADVENT regulatory trial, the mean procedure time was 105 minutes and that was in experienced US centers. While this still represents early experience with PFA, the culture of US AF ablation entails far more mapping and extra catheters than I have seen used in European labs. 

Cost is a major issue. It’s hard to sort out exact costs in the United States, but a PFA catheter costs approximately threefold more than a standard ablation catheter. A recent study from Liverpool, England, found that PFA ablation was faster but more expensive than standard thermal ablation because of higher PFA equipment prices. For better or worse, US patients are not directly affected by the higher procedural costs. But the fact remains that PFA adds more costs to the healthcare system. 
 

What Drives the Enthusiasm for First-Generation PFA? 

So why all the enthusiasm? It’s surely not the empirical data. Evidence thus far shows no obvious advantage in safety or efficacy. European use of PFA does seem to reduce procedure time. But in many electrophysiology labs in the United States, the rate-limiting step for AF ablation is not time in the lab but having enough staff to turn rooms around.

The main factor driving early acceptance of PFA relates to basic human nature. It is the fear of missing out. Marketing works on consumers, and it surely works on doctors. Companies that make PFA systems sponsor key opinion leaders to discuss PFA. These companies have beautiful booths in the expo of our meetings; they host dinners and talks. When a hospital in a city does PFA, the other hospitals feel the urge to keep up. It’s hard to be a Top Person in electrophysiology and not be a PFA user. 

One of my favorite comments came from a key opinion leader. He told me that he advised his administration to buy a PFA system, promote that they have it, and keep it in the closet until better systems are released. 

Iteration in the medical device field is tricky. There are negatives to being too harsh on first-generation systems. Early cardiac resynchronization tools, for instance, were horrible. Now CRT is transformative in selected patients with heart failure. 

It’s possible (but not certain) that electrical ablative therapy will iterate and surpass thermal ablation in the future. Maybe. 

But for now, the enthusiasm for PFA far outstrips its evidence. Until better evidence emerges, I will be a slow adopter. And I hope that our field gathers evidence before widespread adoption makes it impossible to do proper studies. 
 

Dr. Mandrola, clinical electrophysiologist, Baptist Medical Associates, Louisville, Kentucky, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

My field of electrophysiology is abuzz with excitement over the new technology of pulsed field ablation (PFA). It dominated 2024’s heart rhythm meetings, and it dominates my private electrophysiologist chat groups. My Google alert for “AF ablation” most often includes notices on PFA and the expansion of the atrial fibrillation ablation market. 

Yet, the excitement does not match the empirical data. 

Despite having strong brains, electrophysiologists adopt new things as if we were emotional shoppers. Our neighbor buys a sports car and we think we need the same car. Left atrial appendage occlusion and subcutaneous defibrillators were past examples. 

The most recent example of soft thinking (especially in the United States) is the enthusiasm and early adoption of first-generation PFA systems for the treatment of AF. 

Readers of cardiac news (including some of my patients) might think PFA has solved the AF puzzle. It has not.

A true breakthrough in AF would be to find its cause. PFA is simply another way to destroy (ablate) cardiac myocytes. PFA uses electrical energy (think shocks) to create pores in the cell membranes of myocytes. It’s delivered through various types of catheters. 

The main theoretical advantage of PFA is cardioselectivity, which is possible because myocytes have lower thresholds for irreversible electroporation than surrounding tissues. The dose of electrical energy that ablates cardiac tissue does not affect surrounding tissues. Cardioselectivity decreases the chance of the most feared complication of standard AF ablation, thermal damage to the esophagus, which is often fatal. The esophagus lies immediately behind the posterior wall of the left atrium and can be inadvertently injured during thermal ablation. 

The challenge in assessing this potential advantage is that thermal esophageal damage is, thankfully, exceedingly rare. Its incidence is in the range of 1 in 10,000 AF ablations. But it might be even lower than that in contemporary practice, because knowledge of esophageal injury has led to innovations that probably have reduced its incidence even further. 

Proponents of PFA would rightly point to the fact that not having to worry about esophageal injury allows operators to add posterior wall ablation to the normal pulmonary vein isolation lesion set. This ability, they would argue, is likely to improve AF ablation outcomes. The problem is that the strongest and most recent trial of posterior wall isolation (with radiofrequency ablation) did not show better outcomes. A more recent observational analysis also showed no benefit to posterior wall isolation (using PFA) over pulmonary vein isolation alone. 
 

What About PFA Efficacy?

I’ve long spoken and written about the lack of progress in AF ablation. In 1998, the first report on ablation of AF showed a 62% arrhythmia-free rate. Two decades later, in the carefully chosen labs treating patients in the CABANA trial, arrhythmia-free rates after AF ablation remain unchanged. We have improved our speed and ability to isolate pulmonary veins, but this has not increased our success in eliminating AF. The reason, I believe, is that we have made little to no progress in understanding the pathophysiology of AF. 

The Food and Drug Administration regulatory trial called ADVENT randomly assigned more than 600 patients to thermal ablation or PFA, and the primary endpoint of ablation success was nearly identical. Single-center studies, observational registries, and single-arm studies have all shown similar efficacy of PFA and thermal ablation. 

Proponents of PFA might argue that these early studies used first-generation PFA systems, and iteration will lead to better efficacy. Perhaps, but we’ve had 20 years of iteration of thermal ablation, and its efficacy has not budged. 
 

What About PFA Safety?

In the ADVENT randomized trial, safety results were similar, though the one death, caused by cardiac perforation and tamponade, occurred in the PFA arm. In the MANIFEST-17K multinational survey of PFA ablation, safety events were in the range reported with thermal ablation. PFA still involves placing catheters in the heart, and complications such as tamponade, stroke, and vascular damage occur. 

The large MANIFEST-17K survey also exposed two PFA-specific complications: coronary artery spasm, which can occur when PFA is delivered close to coronary arteries; and hemolysis-related kidney failure — severe enough to require dialysis in five patients. Supporters of PFA speculate that hemolysis occurs because electrical energy within the atrium can shred red blood cells. Their solution is to strive for good contact and use hydration. The irony of this latter fix is that one of the best advances in thermal ablation has been catheters that deliver less fluid and less need for diuresis after the procedure. 

No PFA study has shown a decreased incidence of thermal damage to the esophagus with PFA ablation. Of course, this is because it is such a low-incidence event. 

One of my concerns with PFA is brain safety. PFA creates substantial microbubbles in the left atrium, which can then travel north to the brain. In a small series from ADVENT, three patients had brain lesions after PFA vs none with thermal ablation. PFA proponents wrote that brain safety was important to study, but few patients have been systematically studied with brain MRI scans. Asymptomatic brain lesions have been noted after many arterial procedures. The clinical significance of these is not known. As a new technology, and one that creates substantial microbubbles in the left atrium, I agree with the PFA proponents that brain safety should be thoroughly studied — before widespread adoption. 
 

What About Speed and Cost? 

Observational studies from European labs report fast procedure times. I have seen PFA procedures in Europe; they’re fast — typically under an hour. A standard thermal ablation takes me about 60-70 minutes.

I am not sure that US operators can duplicate European procedural times. In the ADVENT regulatory trial, the mean procedure time was 105 minutes and that was in experienced US centers. While this still represents early experience with PFA, the culture of US AF ablation entails far more mapping and extra catheters than I have seen used in European labs. 

Cost is a major issue. It’s hard to sort out exact costs in the United States, but a PFA catheter costs approximately threefold more than a standard ablation catheter. A recent study from Liverpool, England, found that PFA ablation was faster but more expensive than standard thermal ablation because of higher PFA equipment prices. For better or worse, US patients are not directly affected by the higher procedural costs. But the fact remains that PFA adds more costs to the healthcare system. 
 

What Drives the Enthusiasm for First-Generation PFA? 

So why all the enthusiasm? It’s surely not the empirical data. Evidence thus far shows no obvious advantage in safety or efficacy. European use of PFA does seem to reduce procedure time. But in many electrophysiology labs in the United States, the rate-limiting step for AF ablation is not time in the lab but having enough staff to turn rooms around.

The main factor driving early acceptance of PFA relates to basic human nature. It is the fear of missing out. Marketing works on consumers, and it surely works on doctors. Companies that make PFA systems sponsor key opinion leaders to discuss PFA. These companies have beautiful booths in the expo of our meetings; they host dinners and talks. When a hospital in a city does PFA, the other hospitals feel the urge to keep up. It’s hard to be a Top Person in electrophysiology and not be a PFA user. 

One of my favorite comments came from a key opinion leader. He told me that he advised his administration to buy a PFA system, promote that they have it, and keep it in the closet until better systems are released. 

Iteration in the medical device field is tricky. There are negatives to being too harsh on first-generation systems. Early cardiac resynchronization tools, for instance, were horrible. Now CRT is transformative in selected patients with heart failure. 

It’s possible (but not certain) that electrical ablative therapy will iterate and surpass thermal ablation in the future. Maybe. 

But for now, the enthusiasm for PFA far outstrips its evidence. Until better evidence emerges, I will be a slow adopter. And I hope that our field gathers evidence before widespread adoption makes it impossible to do proper studies. 
 

Dr. Mandrola, clinical electrophysiologist, Baptist Medical Associates, Louisville, Kentucky, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

My field of electrophysiology is abuzz with excitement over the new technology of pulsed field ablation (PFA). It dominated 2024’s heart rhythm meetings, and it dominates my private electrophysiologist chat groups. My Google alert for “AF ablation” most often includes notices on PFA and the expansion of the atrial fibrillation ablation market. 

Yet, the excitement does not match the empirical data. 

Despite having strong brains, electrophysiologists adopt new things as if we were emotional shoppers. Our neighbor buys a sports car and we think we need the same car. Left atrial appendage occlusion and subcutaneous defibrillators were past examples. 

The most recent example of soft thinking (especially in the United States) is the enthusiasm and early adoption of first-generation PFA systems for the treatment of AF. 

Readers of cardiac news (including some of my patients) might think PFA has solved the AF puzzle. It has not.

A true breakthrough in AF would be to find its cause. PFA is simply another way to destroy (ablate) cardiac myocytes. PFA uses electrical energy (think shocks) to create pores in the cell membranes of myocytes. It’s delivered through various types of catheters. 

The main theoretical advantage of PFA is cardioselectivity, which is possible because myocytes have lower thresholds for irreversible electroporation than surrounding tissues. The dose of electrical energy that ablates cardiac tissue does not affect surrounding tissues. Cardioselectivity decreases the chance of the most feared complication of standard AF ablation, thermal damage to the esophagus, which is often fatal. The esophagus lies immediately behind the posterior wall of the left atrium and can be inadvertently injured during thermal ablation. 

The challenge in assessing this potential advantage is that thermal esophageal damage is, thankfully, exceedingly rare. Its incidence is in the range of 1 in 10,000 AF ablations. But it might be even lower than that in contemporary practice, because knowledge of esophageal injury has led to innovations that probably have reduced its incidence even further. 

Proponents of PFA would rightly point to the fact that not having to worry about esophageal injury allows operators to add posterior wall ablation to the normal pulmonary vein isolation lesion set. This ability, they would argue, is likely to improve AF ablation outcomes. The problem is that the strongest and most recent trial of posterior wall isolation (with radiofrequency ablation) did not show better outcomes. A more recent observational analysis also showed no benefit to posterior wall isolation (using PFA) over pulmonary vein isolation alone. 
 

What About PFA Efficacy?

I’ve long spoken and written about the lack of progress in AF ablation. In 1998, the first report on ablation of AF showed a 62% arrhythmia-free rate. Two decades later, in the carefully chosen labs treating patients in the CABANA trial, arrhythmia-free rates after AF ablation remain unchanged. We have improved our speed and ability to isolate pulmonary veins, but this has not increased our success in eliminating AF. The reason, I believe, is that we have made little to no progress in understanding the pathophysiology of AF. 

The Food and Drug Administration regulatory trial called ADVENT randomly assigned more than 600 patients to thermal ablation or PFA, and the primary endpoint of ablation success was nearly identical. Single-center studies, observational registries, and single-arm studies have all shown similar efficacy of PFA and thermal ablation. 

Proponents of PFA might argue that these early studies used first-generation PFA systems, and iteration will lead to better efficacy. Perhaps, but we’ve had 20 years of iteration of thermal ablation, and its efficacy has not budged. 
 

What About PFA Safety?

In the ADVENT randomized trial, safety results were similar, though the one death, caused by cardiac perforation and tamponade, occurred in the PFA arm. In the MANIFEST-17K multinational survey of PFA ablation, safety events were in the range reported with thermal ablation. PFA still involves placing catheters in the heart, and complications such as tamponade, stroke, and vascular damage occur. 

The large MANIFEST-17K survey also exposed two PFA-specific complications: coronary artery spasm, which can occur when PFA is delivered close to coronary arteries; and hemolysis-related kidney failure — severe enough to require dialysis in five patients. Supporters of PFA speculate that hemolysis occurs because electrical energy within the atrium can shred red blood cells. Their solution is to strive for good contact and use hydration. The irony of this latter fix is that one of the best advances in thermal ablation has been catheters that deliver less fluid and less need for diuresis after the procedure. 

No PFA study has shown a decreased incidence of thermal damage to the esophagus with PFA ablation. Of course, this is because it is such a low-incidence event. 

One of my concerns with PFA is brain safety. PFA creates substantial microbubbles in the left atrium, which can then travel north to the brain. In a small series from ADVENT, three patients had brain lesions after PFA vs none with thermal ablation. PFA proponents wrote that brain safety was important to study, but few patients have been systematically studied with brain MRI scans. Asymptomatic brain lesions have been noted after many arterial procedures. The clinical significance of these is not known. As a new technology, and one that creates substantial microbubbles in the left atrium, I agree with the PFA proponents that brain safety should be thoroughly studied — before widespread adoption. 
 

What About Speed and Cost? 

Observational studies from European labs report fast procedure times. I have seen PFA procedures in Europe; they’re fast — typically under an hour. A standard thermal ablation takes me about 60-70 minutes.

I am not sure that US operators can duplicate European procedural times. In the ADVENT regulatory trial, the mean procedure time was 105 minutes and that was in experienced US centers. While this still represents early experience with PFA, the culture of US AF ablation entails far more mapping and extra catheters than I have seen used in European labs. 

Cost is a major issue. It’s hard to sort out exact costs in the United States, but a PFA catheter costs approximately threefold more than a standard ablation catheter. A recent study from Liverpool, England, found that PFA ablation was faster but more expensive than standard thermal ablation because of higher PFA equipment prices. For better or worse, US patients are not directly affected by the higher procedural costs. But the fact remains that PFA adds more costs to the healthcare system. 
 

What Drives the Enthusiasm for First-Generation PFA? 

So why all the enthusiasm? It’s surely not the empirical data. Evidence thus far shows no obvious advantage in safety or efficacy. European use of PFA does seem to reduce procedure time. But in many electrophysiology labs in the United States, the rate-limiting step for AF ablation is not time in the lab but having enough staff to turn rooms around.

The main factor driving early acceptance of PFA relates to basic human nature. It is the fear of missing out. Marketing works on consumers, and it surely works on doctors. Companies that make PFA systems sponsor key opinion leaders to discuss PFA. These companies have beautiful booths in the expo of our meetings; they host dinners and talks. When a hospital in a city does PFA, the other hospitals feel the urge to keep up. It’s hard to be a Top Person in electrophysiology and not be a PFA user. 

One of my favorite comments came from a key opinion leader. He told me that he advised his administration to buy a PFA system, promote that they have it, and keep it in the closet until better systems are released. 

Iteration in the medical device field is tricky. There are negatives to being too harsh on first-generation systems. Early cardiac resynchronization tools, for instance, were horrible. Now CRT is transformative in selected patients with heart failure. 

It’s possible (but not certain) that electrical ablative therapy will iterate and surpass thermal ablation in the future. Maybe. 

But for now, the enthusiasm for PFA far outstrips its evidence. Until better evidence emerges, I will be a slow adopter. And I hope that our field gathers evidence before widespread adoption makes it impossible to do proper studies. 
 

Dr. Mandrola, clinical electrophysiologist, Baptist Medical Associates, Louisville, Kentucky, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

TOPLINE:

Lowering the dose of edoxaban to 30 mg in patients 80 years of age and older with atrial fibrillation (AF) reduces major bleeding events without increasing ischemic events.

METHODOLOGY:

• Researchers conducted a parallel design, double-blind clinical trial of 21,105 patients with AF.
• Nearly 3000 patients aged 80 years and older were included in the secondary analysis, focusing on edoxaban, 60 mg vs 30 mg, and edoxaban 30 mg vs warfarin.
• The primary outcome was a composite of death, stroke or systemic embolism, and major bleeding, with secondary outcomes including ischemic stroke and all-cause death.
• People were excluded from the study if they had moderate or severe mitral stenosis, a mechanical heart valve, a high risk for bleeding, or were on antiplatelet drugs.

TAKEAWAY:

• Participants without dose-reduction criteria who received edoxaban 30 mg had lower rates of major bleeding than those who received 60 mg (hazard ratio [HR], 1.57; 95% CI, 1.04-2.38; P = .03).
• Rates of major gastrointestinal hemorrhage were higher with edoxaban 60 mg than with 30 mg (HR, 2.24; 95% CI, 1.29-3.90; P = .004).
• People who took edoxaban 30 mg had a 17% lower risk for all-cause death than those who received warfarin (HR, 0.83; 95% CI, 0.70-1.00; P = .046).
• In a little over 2400 participants with or without dose-reduction criteria, those receiving edoxaban 30 mg had the lower risk for major bleeding (HR, 0.59; 95% CI, 0.45-0.77; P < .001) and death (HR, 0.83; 95% CI, 0.70-1.00; P = .046); risk for stroke or systemic embolism was comparable between the two drugs.

IN PRACTICE:

“These data suggest that lower-dose anticoagulants, such as edoxaban, 30 mg once daily, may be considered in all patients 80 years and older with AF irrespective of dose-reduction criteria,” the study authors wrote.

SOURCE:

The study was led by André Zimerman, MD, PhD, of Brigham and Women’s Hospital and the Department of Medicine at Harvard Medical School in Boston. It was published online in JAMA Cardiology. The study was funded by Daiichi Sankyo for the TIMI Study Group.

LIMITATIONS:

The study did not adjust for multiple comparisons, increasing the risk for type I and type II errors. Additionally, the trial participants may represent a more compliant subset of the target population, which could influence the results.

DISCLOSURES:

Various authors reported receiving grants, consultant fees, and consulting fees from AstraZeneca, Merck, Novartis, Amgen, Boehringer Ingelheim/Lilly, and Cardurion Pharmaceuticals, among others.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Lowering the dose of edoxaban to 30 mg in patients 80 years of age and older with atrial fibrillation (AF) reduces major bleeding events without increasing ischemic events.

METHODOLOGY:

• Researchers conducted a parallel design, double-blind clinical trial of 21,105 patients with AF.
• Nearly 3000 patients aged 80 years and older were included in the secondary analysis, focusing on edoxaban, 60 mg vs 30 mg, and edoxaban 30 mg vs warfarin.
• The primary outcome was a composite of death, stroke or systemic embolism, and major bleeding, with secondary outcomes including ischemic stroke and all-cause death.
• People were excluded from the study if they had moderate or severe mitral stenosis, a mechanical heart valve, a high risk for bleeding, or were on antiplatelet drugs.

TAKEAWAY:

• Participants without dose-reduction criteria who received edoxaban 30 mg had lower rates of major bleeding than those who received 60 mg (hazard ratio [HR], 1.57; 95% CI, 1.04-2.38; P = .03).
• Rates of major gastrointestinal hemorrhage were higher with edoxaban 60 mg than with 30 mg (HR, 2.24; 95% CI, 1.29-3.90; P = .004).
• People who took edoxaban 30 mg had a 17% lower risk for all-cause death than those who received warfarin (HR, 0.83; 95% CI, 0.70-1.00; P = .046).
• In a little over 2400 participants with or without dose-reduction criteria, those receiving edoxaban 30 mg had the lower risk for major bleeding (HR, 0.59; 95% CI, 0.45-0.77; P < .001) and death (HR, 0.83; 95% CI, 0.70-1.00; P = .046); risk for stroke or systemic embolism was comparable between the two drugs.

IN PRACTICE:

“These data suggest that lower-dose anticoagulants, such as edoxaban, 30 mg once daily, may be considered in all patients 80 years and older with AF irrespective of dose-reduction criteria,” the study authors wrote.

SOURCE:

The study was led by André Zimerman, MD, PhD, of Brigham and Women’s Hospital and the Department of Medicine at Harvard Medical School in Boston. It was published online in JAMA Cardiology. The study was funded by Daiichi Sankyo for the TIMI Study Group.

LIMITATIONS:

The study did not adjust for multiple comparisons, increasing the risk for type I and type II errors. Additionally, the trial participants may represent a more compliant subset of the target population, which could influence the results.

DISCLOSURES:

Various authors reported receiving grants, consultant fees, and consulting fees from AstraZeneca, Merck, Novartis, Amgen, Boehringer Ingelheim/Lilly, and Cardurion Pharmaceuticals, among others.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Lowering the dose of edoxaban to 30 mg in patients 80 years of age and older with atrial fibrillation (AF) reduces major bleeding events without increasing ischemic events.

METHODOLOGY:

• Researchers conducted a parallel design, double-blind clinical trial of 21,105 patients with AF.
• Nearly 3000 patients aged 80 years and older were included in the secondary analysis, focusing on edoxaban, 60 mg vs 30 mg, and edoxaban 30 mg vs warfarin.
• The primary outcome was a composite of death, stroke or systemic embolism, and major bleeding, with secondary outcomes including ischemic stroke and all-cause death.
• People were excluded from the study if they had moderate or severe mitral stenosis, a mechanical heart valve, a high risk for bleeding, or were on antiplatelet drugs.

TAKEAWAY:

• Participants without dose-reduction criteria who received edoxaban 30 mg had lower rates of major bleeding than those who received 60 mg (hazard ratio [HR], 1.57; 95% CI, 1.04-2.38; P = .03).
• Rates of major gastrointestinal hemorrhage were higher with edoxaban 60 mg than with 30 mg (HR, 2.24; 95% CI, 1.29-3.90; P = .004).
• People who took edoxaban 30 mg had a 17% lower risk for all-cause death than those who received warfarin (HR, 0.83; 95% CI, 0.70-1.00; P = .046).
• In a little over 2400 participants with or without dose-reduction criteria, those receiving edoxaban 30 mg had the lower risk for major bleeding (HR, 0.59; 95% CI, 0.45-0.77; P < .001) and death (HR, 0.83; 95% CI, 0.70-1.00; P = .046); risk for stroke or systemic embolism was comparable between the two drugs.

IN PRACTICE:

“These data suggest that lower-dose anticoagulants, such as edoxaban, 30 mg once daily, may be considered in all patients 80 years and older with AF irrespective of dose-reduction criteria,” the study authors wrote.

SOURCE:

The study was led by André Zimerman, MD, PhD, of Brigham and Women’s Hospital and the Department of Medicine at Harvard Medical School in Boston. It was published online in JAMA Cardiology. The study was funded by Daiichi Sankyo for the TIMI Study Group.

LIMITATIONS:

The study did not adjust for multiple comparisons, increasing the risk for type I and type II errors. Additionally, the trial participants may represent a more compliant subset of the target population, which could influence the results.

DISCLOSURES:

Various authors reported receiving grants, consultant fees, and consulting fees from AstraZeneca, Merck, Novartis, Amgen, Boehringer Ingelheim/Lilly, and Cardurion Pharmaceuticals, among others.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

New-onset atrial fibrillation (AF) is associated with a substantially higher risk for all-cause dementia in patients with type 2 diabetes (T2D).

METHODOLOGY:

• Studies suggest a potential link between AF and dementia in the broader population, but evidence is scarce in people with diabetes, who are at increased risk for both conditions.
• This longitudinal observational study assessed the association between new-onset AF and dementia in 22,989 patients with T2D (median age at enrollment, 61.0 years; 62.3% men; 86.3% White individuals).
• New-onset AF was identified through hospital admission records using the International Classification of Diseases – 9th Revision (ICD-9) and ICD-10 codes, and dementia cases were identified using an algorithm developed by the UK Biobank.
• Time-varying Cox proportional hazard regression models were used to determine the association between incident dementia and new-onset AF.

TAKEAWAY:

• Over a median follow-up duration of about 12 years, 844 patients developed all-cause dementia, 342 were diagnosed with Alzheimer’s disease, and 246 had vascular dementia.
• Patients with incident AF had a higher risk of developing all-cause dementia (hazard ratio [HR], 2.15; 95% CI, 1.80-2.57), Alzheimer’s disease (HR, 1.44; 95% CI, 1.06-1.96), and vascular dementia (HR, 3.11; 95% CI, 2.32-4.17) than those without incident AF.
• The results are independent of common dementia risk factors, such as sociodemographic characteristics and lifestyle factors.
• The mean time intervals from the onset of AF to all-cause dementia, Alzheimer’s disease and vascular dementia were 2.95, 2.81, and 3.37 years, respectively.

IN PRACTICE:

“AF is a significant risk factor for dementia in patients with type 2 diabetes, suggesting the importance of timely and effective treatment of AF, such as early rhythm control strategies and anticoagulant use, in preventing dementia among this demographic,” the authors wrote.
 

SOURCE:

The study, led by Ying Zhou, PhD, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China, was published online in Diabetes, Obesity and Metabolism.

LIMITATIONS:

The study could not explore the link between different AF subtypes and dementia owing to its small sample size. The effects of AF treatment on the risk for dementia in patients with type 2 diabetes were not considered because of lack of information. The mostly White study population limits the generalizability of the findings to other races and ethnicities.

DISCLOSURES:

The study was supported by the National Social Science Fund of China. The authors declared no conflicts of interest.

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

TOPLINE:

New-onset atrial fibrillation (AF) is associated with a substantially higher risk for all-cause dementia in patients with type 2 diabetes (T2D).

METHODOLOGY:

• Studies suggest a potential link between AF and dementia in the broader population, but evidence is scarce in people with diabetes, who are at increased risk for both conditions.
• This longitudinal observational study assessed the association between new-onset AF and dementia in 22,989 patients with T2D (median age at enrollment, 61.0 years; 62.3% men; 86.3% White individuals).
• New-onset AF was identified through hospital admission records using the International Classification of Diseases – 9th Revision (ICD-9) and ICD-10 codes, and dementia cases were identified using an algorithm developed by the UK Biobank.
• Time-varying Cox proportional hazard regression models were used to determine the association between incident dementia and new-onset AF.

TAKEAWAY:

• Over a median follow-up duration of about 12 years, 844 patients developed all-cause dementia, 342 were diagnosed with Alzheimer’s disease, and 246 had vascular dementia.
• Patients with incident AF had a higher risk of developing all-cause dementia (hazard ratio [HR], 2.15; 95% CI, 1.80-2.57), Alzheimer’s disease (HR, 1.44; 95% CI, 1.06-1.96), and vascular dementia (HR, 3.11; 95% CI, 2.32-4.17) than those without incident AF.
• The results are independent of common dementia risk factors, such as sociodemographic characteristics and lifestyle factors.
• The mean time intervals from the onset of AF to all-cause dementia, Alzheimer’s disease and vascular dementia were 2.95, 2.81, and 3.37 years, respectively.

IN PRACTICE:

“AF is a significant risk factor for dementia in patients with type 2 diabetes, suggesting the importance of timely and effective treatment of AF, such as early rhythm control strategies and anticoagulant use, in preventing dementia among this demographic,” the authors wrote.
 

SOURCE:

The study, led by Ying Zhou, PhD, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China, was published online in Diabetes, Obesity and Metabolism.

LIMITATIONS:

The study could not explore the link between different AF subtypes and dementia owing to its small sample size. The effects of AF treatment on the risk for dementia in patients with type 2 diabetes were not considered because of lack of information. The mostly White study population limits the generalizability of the findings to other races and ethnicities.

DISCLOSURES:

The study was supported by the National Social Science Fund of China. The authors declared no conflicts of interest.

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

TOPLINE:

New-onset atrial fibrillation (AF) is associated with a substantially higher risk for all-cause dementia in patients with type 2 diabetes (T2D).

METHODOLOGY:

• Studies suggest a potential link between AF and dementia in the broader population, but evidence is scarce in people with diabetes, who are at increased risk for both conditions.
• This longitudinal observational study assessed the association between new-onset AF and dementia in 22,989 patients with T2D (median age at enrollment, 61.0 years; 62.3% men; 86.3% White individuals).
• New-onset AF was identified through hospital admission records using the International Classification of Diseases – 9th Revision (ICD-9) and ICD-10 codes, and dementia cases were identified using an algorithm developed by the UK Biobank.
• Time-varying Cox proportional hazard regression models were used to determine the association between incident dementia and new-onset AF.

TAKEAWAY:

• Over a median follow-up duration of about 12 years, 844 patients developed all-cause dementia, 342 were diagnosed with Alzheimer’s disease, and 246 had vascular dementia.
• Patients with incident AF had a higher risk of developing all-cause dementia (hazard ratio [HR], 2.15; 95% CI, 1.80-2.57), Alzheimer’s disease (HR, 1.44; 95% CI, 1.06-1.96), and vascular dementia (HR, 3.11; 95% CI, 2.32-4.17) than those without incident AF.
• The results are independent of common dementia risk factors, such as sociodemographic characteristics and lifestyle factors.
• The mean time intervals from the onset of AF to all-cause dementia, Alzheimer’s disease and vascular dementia were 2.95, 2.81, and 3.37 years, respectively.

IN PRACTICE:

“AF is a significant risk factor for dementia in patients with type 2 diabetes, suggesting the importance of timely and effective treatment of AF, such as early rhythm control strategies and anticoagulant use, in preventing dementia among this demographic,” the authors wrote.
 

SOURCE:

The study, led by Ying Zhou, PhD, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China, was published online in Diabetes, Obesity and Metabolism.

LIMITATIONS:

The study could not explore the link between different AF subtypes and dementia owing to its small sample size. The effects of AF treatment on the risk for dementia in patients with type 2 diabetes were not considered because of lack of information. The mostly White study population limits the generalizability of the findings to other races and ethnicities.

DISCLOSURES:

The study was supported by the National Social Science Fund of China. The authors declared no conflicts of interest.

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

BOSTON — A Mediterranean diet with extra virgin olive oil (EVOO) significantly reduced the risk for tachyarrhythmia recurrence after atrial fibrillation (AF) ablation in patients with paroxysmal disease, but the diet had less of an impact on patients with persistent AF, a new study showed.

“An intervention with the Mediterranean diet with EVOO produced a nonsignificant reduction in any atrial tachycardia in a selected population after undergoing atrial fibrillation ablation, but this intervention produced a significant reduction in any atrial tachyarrhythmias in patients with paroxysmal AF,” said Maria Teresa Barrio-Lopez, MD, PhD, an electrophysiologist at University Hospital HM Monteprincipe in Madrid, Spain, who presented results from the PREDIMAR trial at the Heart Rhythm Society (HRS) 2024 annual meeting.

The PREDIMAR study enrolled 720 patients from the larger PREDIMED study, which showed that patients without AF at enrollment and who followed a Mediterranean diet enriched with EVOO had a 38% lower rate of incidental AF than control individuals.

PREDIMAR evaluated the impact of the diet on arrhythmia recurrence in patients after ablation. The patients were randomized in a 1:1 ratio to either the dietary intervention group or the control group.
 

PREDIMAR Study Results

The overall difference in the rate of AF recurrence in the 3-18 months after ablation between the dietary intervention and control groups was nonsignificant (34.8% vs 37.5%).

However, among the 431 patients with paroxysmal AF, 25.2% in the diet group and 34.7% in the control group had no tachyarrhythmia recurrence, which translates into a 31% lower risk in the diet group.

In this study, the diet was rich in fish, nuts, fruits, and vegetables and was complemented with EVOO. Participants were also permitted moderate wine consumption.

The intervention involved dietitians who remotely followed patients and made periodic telephone calls to encourage them to stay on the diet. Participants had weight and body measurements taken at baseline and at 3, 6, 12, and 18 months and underwent an ECG at 6, 12, and 18 months. Labs were obtained at baseline and at 12 months. Participants were also given educational materials throughout the intervention.

Average scores, based on a scale of 0-13, excluding an item for wine intake, were 7.8 in the diet group and 7.2 in the control group.

Daily average alcohol intake was higher in the diet group than in the control group (9.8 vs 8.2 g), but “the weight of the patient during the study didn’t change in any group,” Dr. Barrio-Lopez reported.

Baseline characteristics were similar in the two groups. About 60% were taking antiarrhythmic drugs, and about 84% were taking anticoagulants.
 

‘A Tour de Force’

PREDIMAR was “really a tour de force,” Christine Albert, MD, MPH, chair of cardiology at the Smidt Heart Institute at the Cedars-Sinai Medical Center in Los Angeles, California, said during a commentary presented at HRS. “We talk about how we’re going to do these dietary interventions and weight loss and all the risk-factor reduction, and they pulled it off with 700 individuals and also did it in a way that was very novel.”

This is the first large-scale dietary intervention trial of patients with AF. However, Dr. Albert noted later in an interview, the Mediterranean diet poses potential challenges for some people with AF.

“The Mediterranean diet recommends that people drink wine, but then there’s clear evidence that abstinence from alcohol actually reduces recurrences of atrial fibrillation, so even though there are a lot of things about the Mediterranean diet that are probably healthy and good for atrial fibrillation, that aspect of it might be working against the patient,” she explained.

The finding that patients in the Mediterranean diet group experienced no significant weight loss could be counterintuitive when it comes to preventing AF. But “you could adapt the diet for AF,” Dr. Albert said. You could “leave out the wine and focus more on weight loss if the patient is obese because those are also the pillars of what we’ve learned for patients with atrial fibrillation.”

Making weight loss a key component of the study could be significant for the American population. “At least in the United States, that’s a huge part of the risk factors for atrial fibrillation after ablation,” she said.

The remote follow-up component of the PREDIMAR study is also intriguing. “I think what’s most exciting about what they did is, they showed they can do all these things remotely,” Dr. Albert added.

Dr. Barrio-Lopez had no relevant financial relationships. Dr. Albert disclosed relationships with Abbott, Roche Diagnostics, St. Jude Medical, Boston Scientific, Medtronic, and Element Science.

A version of this article appeared on Medscape.com.

BOSTON — A Mediterranean diet with extra virgin olive oil (EVOO) significantly reduced the risk for tachyarrhythmia recurrence after atrial fibrillation (AF) ablation in patients with paroxysmal disease, but the diet had less of an impact on patients with persistent AF, a new study showed.

“An intervention with the Mediterranean diet with EVOO produced a nonsignificant reduction in any atrial tachycardia in a selected population after undergoing atrial fibrillation ablation, but this intervention produced a significant reduction in any atrial tachyarrhythmias in patients with paroxysmal AF,” said Maria Teresa Barrio-Lopez, MD, PhD, an electrophysiologist at University Hospital HM Monteprincipe in Madrid, Spain, who presented results from the PREDIMAR trial at the Heart Rhythm Society (HRS) 2024 annual meeting.

The PREDIMAR study enrolled 720 patients from the larger PREDIMED study, which showed that patients without AF at enrollment and who followed a Mediterranean diet enriched with EVOO had a 38% lower rate of incidental AF than control individuals.

PREDIMAR evaluated the impact of the diet on arrhythmia recurrence in patients after ablation. The patients were randomized in a 1:1 ratio to either the dietary intervention group or the control group.
 

PREDIMAR Study Results

The overall difference in the rate of AF recurrence in the 3-18 months after ablation between the dietary intervention and control groups was nonsignificant (34.8% vs 37.5%).

However, among the 431 patients with paroxysmal AF, 25.2% in the diet group and 34.7% in the control group had no tachyarrhythmia recurrence, which translates into a 31% lower risk in the diet group.

In this study, the diet was rich in fish, nuts, fruits, and vegetables and was complemented with EVOO. Participants were also permitted moderate wine consumption.

The intervention involved dietitians who remotely followed patients and made periodic telephone calls to encourage them to stay on the diet. Participants had weight and body measurements taken at baseline and at 3, 6, 12, and 18 months and underwent an ECG at 6, 12, and 18 months. Labs were obtained at baseline and at 12 months. Participants were also given educational materials throughout the intervention.

Average scores, based on a scale of 0-13, excluding an item for wine intake, were 7.8 in the diet group and 7.2 in the control group.

Daily average alcohol intake was higher in the diet group than in the control group (9.8 vs 8.2 g), but “the weight of the patient during the study didn’t change in any group,” Dr. Barrio-Lopez reported.

Baseline characteristics were similar in the two groups. About 60% were taking antiarrhythmic drugs, and about 84% were taking anticoagulants.
 

‘A Tour de Force’

PREDIMAR was “really a tour de force,” Christine Albert, MD, MPH, chair of cardiology at the Smidt Heart Institute at the Cedars-Sinai Medical Center in Los Angeles, California, said during a commentary presented at HRS. “We talk about how we’re going to do these dietary interventions and weight loss and all the risk-factor reduction, and they pulled it off with 700 individuals and also did it in a way that was very novel.”

This is the first large-scale dietary intervention trial of patients with AF. However, Dr. Albert noted later in an interview, the Mediterranean diet poses potential challenges for some people with AF.

“The Mediterranean diet recommends that people drink wine, but then there’s clear evidence that abstinence from alcohol actually reduces recurrences of atrial fibrillation, so even though there are a lot of things about the Mediterranean diet that are probably healthy and good for atrial fibrillation, that aspect of it might be working against the patient,” she explained.

The finding that patients in the Mediterranean diet group experienced no significant weight loss could be counterintuitive when it comes to preventing AF. But “you could adapt the diet for AF,” Dr. Albert said. You could “leave out the wine and focus more on weight loss if the patient is obese because those are also the pillars of what we’ve learned for patients with atrial fibrillation.”

Making weight loss a key component of the study could be significant for the American population. “At least in the United States, that’s a huge part of the risk factors for atrial fibrillation after ablation,” she said.

The remote follow-up component of the PREDIMAR study is also intriguing. “I think what’s most exciting about what they did is, they showed they can do all these things remotely,” Dr. Albert added.

Dr. Barrio-Lopez had no relevant financial relationships. Dr. Albert disclosed relationships with Abbott, Roche Diagnostics, St. Jude Medical, Boston Scientific, Medtronic, and Element Science.

A version of this article appeared on Medscape.com.

BOSTON — A Mediterranean diet with extra virgin olive oil (EVOO) significantly reduced the risk for tachyarrhythmia recurrence after atrial fibrillation (AF) ablation in patients with paroxysmal disease, but the diet had less of an impact on patients with persistent AF, a new study showed.

“An intervention with the Mediterranean diet with EVOO produced a nonsignificant reduction in any atrial tachycardia in a selected population after undergoing atrial fibrillation ablation, but this intervention produced a significant reduction in any atrial tachyarrhythmias in patients with paroxysmal AF,” said Maria Teresa Barrio-Lopez, MD, PhD, an electrophysiologist at University Hospital HM Monteprincipe in Madrid, Spain, who presented results from the PREDIMAR trial at the Heart Rhythm Society (HRS) 2024 annual meeting.

The PREDIMAR study enrolled 720 patients from the larger PREDIMED study, which showed that patients without AF at enrollment and who followed a Mediterranean diet enriched with EVOO had a 38% lower rate of incidental AF than control individuals.

PREDIMAR evaluated the impact of the diet on arrhythmia recurrence in patients after ablation. The patients were randomized in a 1:1 ratio to either the dietary intervention group or the control group.
 

PREDIMAR Study Results

The overall difference in the rate of AF recurrence in the 3-18 months after ablation between the dietary intervention and control groups was nonsignificant (34.8% vs 37.5%).

However, among the 431 patients with paroxysmal AF, 25.2% in the diet group and 34.7% in the control group had no tachyarrhythmia recurrence, which translates into a 31% lower risk in the diet group.

In this study, the diet was rich in fish, nuts, fruits, and vegetables and was complemented with EVOO. Participants were also permitted moderate wine consumption.

The intervention involved dietitians who remotely followed patients and made periodic telephone calls to encourage them to stay on the diet. Participants had weight and body measurements taken at baseline and at 3, 6, 12, and 18 months and underwent an ECG at 6, 12, and 18 months. Labs were obtained at baseline and at 12 months. Participants were also given educational materials throughout the intervention.

Average scores, based on a scale of 0-13, excluding an item for wine intake, were 7.8 in the diet group and 7.2 in the control group.

Daily average alcohol intake was higher in the diet group than in the control group (9.8 vs 8.2 g), but “the weight of the patient during the study didn’t change in any group,” Dr. Barrio-Lopez reported.

Baseline characteristics were similar in the two groups. About 60% were taking antiarrhythmic drugs, and about 84% were taking anticoagulants.
 

‘A Tour de Force’

PREDIMAR was “really a tour de force,” Christine Albert, MD, MPH, chair of cardiology at the Smidt Heart Institute at the Cedars-Sinai Medical Center in Los Angeles, California, said during a commentary presented at HRS. “We talk about how we’re going to do these dietary interventions and weight loss and all the risk-factor reduction, and they pulled it off with 700 individuals and also did it in a way that was very novel.”

This is the first large-scale dietary intervention trial of patients with AF. However, Dr. Albert noted later in an interview, the Mediterranean diet poses potential challenges for some people with AF.

“The Mediterranean diet recommends that people drink wine, but then there’s clear evidence that abstinence from alcohol actually reduces recurrences of atrial fibrillation, so even though there are a lot of things about the Mediterranean diet that are probably healthy and good for atrial fibrillation, that aspect of it might be working against the patient,” she explained.

The finding that patients in the Mediterranean diet group experienced no significant weight loss could be counterintuitive when it comes to preventing AF. But “you could adapt the diet for AF,” Dr. Albert said. You could “leave out the wine and focus more on weight loss if the patient is obese because those are also the pillars of what we’ve learned for patients with atrial fibrillation.”

Making weight loss a key component of the study could be significant for the American population. “At least in the United States, that’s a huge part of the risk factors for atrial fibrillation after ablation,” she said.

The remote follow-up component of the PREDIMAR study is also intriguing. “I think what’s most exciting about what they did is, they showed they can do all these things remotely,” Dr. Albert added.

Dr. Barrio-Lopez had no relevant financial relationships. Dr. Albert disclosed relationships with Abbott, Roche Diagnostics, St. Jude Medical, Boston Scientific, Medtronic, and Element Science.

A version of this article appeared on Medscape.com.

A few months ago, I posted a column on continuous positive airway pressure (CPAP) with the title, “CPAP Oversells and Underperforms.” To date, it has 299 likes and 90 comments, which are almost all negative. I’m glad to see that it’s generated interest, and I’d like to address some of the themes expressed in the posts.

Most comments were personal testimonies to the miracles of CPAP. These are important, and the point deserves emphasis. CPAP can provide significant improvements in daytime sleepiness and quality of life. I closed the original piece by acknowledging this important fact. Readers can be forgiven for missing it given that the title and text were otherwise disparaging of CPAP.

But several comments warrant a more in-depth discussion. The original piece focuses on CPAP and cardiovascular (CV) outcomes but made no mention of atrial fibrillation (AF) or ejection fraction (EF). The effects of CPAP on each are touted by cardiologists and PAP-pushers alike and are drivers of frequent referrals. It›s my fault for omitting them from the discussion.

AF is easy. The data is identical to all other things CPAP and CV. Based on biologic plausibility alone, the likelihood of a relationship between AF and obstructive sleep apnea (OSA) is similar to the odds that the Celtics raise an 18th banner come June. There’s hypoxia, intrathoracic pressure swings, sympathetic surges, and sleep state disruptions. It’s easy to get from there to arrhythmogenesis. There’s lots of observational noise, too, but no randomized proof that CPAP alters this relationship.

I found four randomized controlled trials (RCTs) that tested CPAP’s effect on AF. I’ll save you the suspense; they were all negative. One even found a signal for more adverse events in the CPAP group. These studies have several positive qualities: They enrolled patients with moderate to severe sleep apnea and high oxygen desaturation indices, adherence averaged more than 4 hours across all groups in all trials, and the methods for assessing the AF outcomes differed slightly. There’s also a lot not to like: The sample sizes were small, only one trial enrolled “sleepy” patients (as assessed by the Epworth Sleepiness Score), and follow-up was short.

To paraphrase Carl Sagan, “absence of evidence does not equal evidence of absence.” As a statistician would say, type II error cannot be excluded by these RCTs. In medicine, however, the burden of proof falls on demonstrating efficacy. If we treat before concluding that a therapy works, we risk wasting time, money, medical resources, and the most precious of patient commodities: the energy required for behavior change. In their response to letters to the editor, the authors of the third RCT summarize the CPAP, AF, and CV disease data far better than I ever could. They sound the same words of caution and come out against screening patients with AF for OSA. 

The story for CPAP’s effects on EF is similar though muddier. The American College of Cardiology (ACC)/American Heart Association (AHA) guidelines for heart failure cite a meta-analysis showing that CPAP improves left ventricular EF. In 2019, the American Academy of Sleep Medicine (AASM) CPAP guidelines included a systematic review and meta-analysis that found that CPAP has no effect on left ventricular EF in patients with or without heart failure.

There are a million reasons why two systematic reviews on the same topic might come to different conclusions. In this case, the included studies only partially overlap, and broadly speaking, it appears the authors made trade-offs. The review cited by the ACC/AHA had broader inclusion and significantly more patients and paid for it in heterogeneity (I2 in the 80%-90% range). The AASM analysis achieved 0% heterogeneity but limited inclusion to fewer than 100 patients. Across both, the improvement in EF was 2%- 5% at a minimally clinically important difference of 4%. Hardly convincing.

In summary, the road to negative trials and patient harm has always been paved with observational signal and biologic plausibility. Throw in some intellectual and academic bias, and you’ve created the perfect storm of therapeutic overconfidence. The cemetery for discarded medical therapies is crowded, but there’s room for CPAP, at least when it comes to using it to improve CV outcomes. 
 

Dr. Holley is a professor in the department of medicine, Uniformed Services University, Bethesda, Maryland, and a physician at Pulmonary/Sleep and Critical Care Medicine, MedStar Washington Hospital Center, Washington. He disclosed ties to Metapharm Inc., CHEST College, and WebMD.

A version of this article appeared on Medscape.com .

A few months ago, I posted a column on continuous positive airway pressure (CPAP) with the title, “CPAP Oversells and Underperforms.” To date, it has 299 likes and 90 comments, which are almost all negative. I’m glad to see that it’s generated interest, and I’d like to address some of the themes expressed in the posts.

Most comments were personal testimonies to the miracles of CPAP. These are important, and the point deserves emphasis. CPAP can provide significant improvements in daytime sleepiness and quality of life. I closed the original piece by acknowledging this important fact. Readers can be forgiven for missing it given that the title and text were otherwise disparaging of CPAP.

But several comments warrant a more in-depth discussion. The original piece focuses on CPAP and cardiovascular (CV) outcomes but made no mention of atrial fibrillation (AF) or ejection fraction (EF). The effects of CPAP on each are touted by cardiologists and PAP-pushers alike and are drivers of frequent referrals. It›s my fault for omitting them from the discussion.

AF is easy. The data is identical to all other things CPAP and CV. Based on biologic plausibility alone, the likelihood of a relationship between AF and obstructive sleep apnea (OSA) is similar to the odds that the Celtics raise an 18th banner come June. There’s hypoxia, intrathoracic pressure swings, sympathetic surges, and sleep state disruptions. It’s easy to get from there to arrhythmogenesis. There’s lots of observational noise, too, but no randomized proof that CPAP alters this relationship.

I found four randomized controlled trials (RCTs) that tested CPAP’s effect on AF. I’ll save you the suspense; they were all negative. One even found a signal for more adverse events in the CPAP group. These studies have several positive qualities: They enrolled patients with moderate to severe sleep apnea and high oxygen desaturation indices, adherence averaged more than 4 hours across all groups in all trials, and the methods for assessing the AF outcomes differed slightly. There’s also a lot not to like: The sample sizes were small, only one trial enrolled “sleepy” patients (as assessed by the Epworth Sleepiness Score), and follow-up was short.

To paraphrase Carl Sagan, “absence of evidence does not equal evidence of absence.” As a statistician would say, type II error cannot be excluded by these RCTs. In medicine, however, the burden of proof falls on demonstrating efficacy. If we treat before concluding that a therapy works, we risk wasting time, money, medical resources, and the most precious of patient commodities: the energy required for behavior change. In their response to letters to the editor, the authors of the third RCT summarize the CPAP, AF, and CV disease data far better than I ever could. They sound the same words of caution and come out against screening patients with AF for OSA. 

The story for CPAP’s effects on EF is similar though muddier. The American College of Cardiology (ACC)/American Heart Association (AHA) guidelines for heart failure cite a meta-analysis showing that CPAP improves left ventricular EF. In 2019, the American Academy of Sleep Medicine (AASM) CPAP guidelines included a systematic review and meta-analysis that found that CPAP has no effect on left ventricular EF in patients with or without heart failure.

There are a million reasons why two systematic reviews on the same topic might come to different conclusions. In this case, the included studies only partially overlap, and broadly speaking, it appears the authors made trade-offs. The review cited by the ACC/AHA had broader inclusion and significantly more patients and paid for it in heterogeneity (I2 in the 80%-90% range). The AASM analysis achieved 0% heterogeneity but limited inclusion to fewer than 100 patients. Across both, the improvement in EF was 2%- 5% at a minimally clinically important difference of 4%. Hardly convincing.

In summary, the road to negative trials and patient harm has always been paved with observational signal and biologic plausibility. Throw in some intellectual and academic bias, and you’ve created the perfect storm of therapeutic overconfidence. The cemetery for discarded medical therapies is crowded, but there’s room for CPAP, at least when it comes to using it to improve CV outcomes. 
 

Dr. Holley is a professor in the department of medicine, Uniformed Services University, Bethesda, Maryland, and a physician at Pulmonary/Sleep and Critical Care Medicine, MedStar Washington Hospital Center, Washington. He disclosed ties to Metapharm Inc., CHEST College, and WebMD.

A version of this article appeared on Medscape.com .

A few months ago, I posted a column on continuous positive airway pressure (CPAP) with the title, “CPAP Oversells and Underperforms.” To date, it has 299 likes and 90 comments, which are almost all negative. I’m glad to see that it’s generated interest, and I’d like to address some of the themes expressed in the posts.

Most comments were personal testimonies to the miracles of CPAP. These are important, and the point deserves emphasis. CPAP can provide significant improvements in daytime sleepiness and quality of life. I closed the original piece by acknowledging this important fact. Readers can be forgiven for missing it given that the title and text were otherwise disparaging of CPAP.

But several comments warrant a more in-depth discussion. The original piece focuses on CPAP and cardiovascular (CV) outcomes but made no mention of atrial fibrillation (AF) or ejection fraction (EF). The effects of CPAP on each are touted by cardiologists and PAP-pushers alike and are drivers of frequent referrals. It›s my fault for omitting them from the discussion.

AF is easy. The data is identical to all other things CPAP and CV. Based on biologic plausibility alone, the likelihood of a relationship between AF and obstructive sleep apnea (OSA) is similar to the odds that the Celtics raise an 18th banner come June. There’s hypoxia, intrathoracic pressure swings, sympathetic surges, and sleep state disruptions. It’s easy to get from there to arrhythmogenesis. There’s lots of observational noise, too, but no randomized proof that CPAP alters this relationship.

I found four randomized controlled trials (RCTs) that tested CPAP’s effect on AF. I’ll save you the suspense; they were all negative. One even found a signal for more adverse events in the CPAP group. These studies have several positive qualities: They enrolled patients with moderate to severe sleep apnea and high oxygen desaturation indices, adherence averaged more than 4 hours across all groups in all trials, and the methods for assessing the AF outcomes differed slightly. There’s also a lot not to like: The sample sizes were small, only one trial enrolled “sleepy” patients (as assessed by the Epworth Sleepiness Score), and follow-up was short.

To paraphrase Carl Sagan, “absence of evidence does not equal evidence of absence.” As a statistician would say, type II error cannot be excluded by these RCTs. In medicine, however, the burden of proof falls on demonstrating efficacy. If we treat before concluding that a therapy works, we risk wasting time, money, medical resources, and the most precious of patient commodities: the energy required for behavior change. In their response to letters to the editor, the authors of the third RCT summarize the CPAP, AF, and CV disease data far better than I ever could. They sound the same words of caution and come out against screening patients with AF for OSA. 

The story for CPAP’s effects on EF is similar though muddier. The American College of Cardiology (ACC)/American Heart Association (AHA) guidelines for heart failure cite a meta-analysis showing that CPAP improves left ventricular EF. In 2019, the American Academy of Sleep Medicine (AASM) CPAP guidelines included a systematic review and meta-analysis that found that CPAP has no effect on left ventricular EF in patients with or without heart failure.

There are a million reasons why two systematic reviews on the same topic might come to different conclusions. In this case, the included studies only partially overlap, and broadly speaking, it appears the authors made trade-offs. The review cited by the ACC/AHA had broader inclusion and significantly more patients and paid for it in heterogeneity (I2 in the 80%-90% range). The AASM analysis achieved 0% heterogeneity but limited inclusion to fewer than 100 patients. Across both, the improvement in EF was 2%- 5% at a minimally clinically important difference of 4%. Hardly convincing.

In summary, the road to negative trials and patient harm has always been paved with observational signal and biologic plausibility. Throw in some intellectual and academic bias, and you’ve created the perfect storm of therapeutic overconfidence. The cemetery for discarded medical therapies is crowded, but there’s room for CPAP, at least when it comes to using it to improve CV outcomes. 
 

Dr. Holley is a professor in the department of medicine, Uniformed Services University, Bethesda, Maryland, and a physician at Pulmonary/Sleep and Critical Care Medicine, MedStar Washington Hospital Center, Washington. He disclosed ties to Metapharm Inc., CHEST College, and WebMD.

A version of this article appeared on Medscape.com .

FROM BMJ

The lifetime risk of atrial fibrillation (AF) increased from 2000 to 2022 from one in four to one in three, a Danish population-based study of temporal trends found.

Heart failure was the most frequent complication linked to this arrhythmia, with a lifetime risk of two in five, twice that of stroke, according to investigators led by Nicklas Vinter, MD, PhD, a postdoctoral researcher at the Danish Center for Health Service Research in the Department of Clinical Medicine at Aalborg University, Denmark.

Published in BMJ, the study found the lifetime risks of post-AF stroke, ischemic stroke, and myocardial infarction improved only modestly over time and remained high, with virtually no improvement in the lifetime risk of heart failure.

Agata Lenczewska-Madsen, Regional Hospital Central Jutland

The Study

The cohort consisted of 3.5 million individuals (51.7% women) who did not have AF as of age 45 or older. These individuals were followed until incident AF, migration, death, or end of follow-up, whichever came first.

All 362,721 individuals with incident AF (53.6% men) but no prevalent complication were further followed over two time periods (2000-2010 and 2011-2020) until incident heart failure, stroke, or myocardial infarction.

Among the findings:

• Lifetime AF risk increased from 24.2% in 2000-2010 to 30.9% in 2011-2022, for a difference of 6.7% (95% confidence interval [CI], 6.5%-6.8%).
• Lifetime AF risk rose across all subgroups over time, with a larger increase in men and individuals with heart failure, myocardial infarction, stroke, diabetes, and chronic kidney disease.
• Lifetime risk of heart failure was 42.9% in 2000-2010 and 42.1% in 2011-2022, for a difference of −0.8% (95% CI, −3.8% to 2.2%).
• The lifetime risks of post-AF stroke and of myocardial infarction decreased slightly between the two periods, from 22.4% to 19.9% for stroke (difference −2.5%, 95% CI, −4.2% to −0.7%) and from 13.7% to 9.8% for myocardial infarction (−3.9%, 95% CI, −5.3% to −2.4%). No differential decrease between men and women emerged.

“Our novel quantification of the long-term downstream consequences of atrial fibrillation highlights the critical need for treatments to further decrease stroke risk as well as for heart failure prevention strategies among patients with atrial fibrillation,” the Danish researchers wrote.

Offering an outsider’s perspective, John P. Higgins, MD, MBA, MPhil, a sports cardiologist at McGovern Medical School at The University of Texas Health Science Center at Houston, said, “Think of atrial fibrillation as a barometer of underlying stress on the heart. When blood pressure is high, or a patient has underlying asymptomatic coronary artery disease or heart failure, they are more likely to have episodes of atrial fibrillation.”

University of Texas Health Science Center at Houston

Dr. Wu

FROM BMJ

The lifetime risk of atrial fibrillation (AF) increased from 2000 to 2022 from one in four to one in three, a Danish population-based study of temporal trends found.

Heart failure was the most frequent complication linked to this arrhythmia, with a lifetime risk of two in five, twice that of stroke, according to investigators led by Nicklas Vinter, MD, PhD, a postdoctoral researcher at the Danish Center for Health Service Research in the Department of Clinical Medicine at Aalborg University, Denmark.

Published in BMJ, the study found the lifetime risks of post-AF stroke, ischemic stroke, and myocardial infarction improved only modestly over time and remained high, with virtually no improvement in the lifetime risk of heart failure.

Agata Lenczewska-Madsen, Regional Hospital Central Jutland

The Study

The cohort consisted of 3.5 million individuals (51.7% women) who did not have AF as of age 45 or older. These individuals were followed until incident AF, migration, death, or end of follow-up, whichever came first.

All 362,721 individuals with incident AF (53.6% men) but no prevalent complication were further followed over two time periods (2000-2010 and 2011-2020) until incident heart failure, stroke, or myocardial infarction.

Among the findings:

• Lifetime AF risk increased from 24.2% in 2000-2010 to 30.9% in 2011-2022, for a difference of 6.7% (95% confidence interval [CI], 6.5%-6.8%).
• Lifetime AF risk rose across all subgroups over time, with a larger increase in men and individuals with heart failure, myocardial infarction, stroke, diabetes, and chronic kidney disease.
• Lifetime risk of heart failure was 42.9% in 2000-2010 and 42.1% in 2011-2022, for a difference of −0.8% (95% CI, −3.8% to 2.2%).
• The lifetime risks of post-AF stroke and of myocardial infarction decreased slightly between the two periods, from 22.4% to 19.9% for stroke (difference −2.5%, 95% CI, −4.2% to −0.7%) and from 13.7% to 9.8% for myocardial infarction (−3.9%, 95% CI, −5.3% to −2.4%). No differential decrease between men and women emerged.

“Our novel quantification of the long-term downstream consequences of atrial fibrillation highlights the critical need for treatments to further decrease stroke risk as well as for heart failure prevention strategies among patients with atrial fibrillation,” the Danish researchers wrote.

Offering an outsider’s perspective, John P. Higgins, MD, MBA, MPhil, a sports cardiologist at McGovern Medical School at The University of Texas Health Science Center at Houston, said, “Think of atrial fibrillation as a barometer of underlying stress on the heart. When blood pressure is high, or a patient has underlying asymptomatic coronary artery disease or heart failure, they are more likely to have episodes of atrial fibrillation.”

University of Texas Health Science Center at Houston

Dr. Wu

FROM BMJ

The lifetime risk of atrial fibrillation (AF) increased from 2000 to 2022 from one in four to one in three, a Danish population-based study of temporal trends found.

Heart failure was the most frequent complication linked to this arrhythmia, with a lifetime risk of two in five, twice that of stroke, according to investigators led by Nicklas Vinter, MD, PhD, a postdoctoral researcher at the Danish Center for Health Service Research in the Department of Clinical Medicine at Aalborg University, Denmark.

Published in BMJ, the study found the lifetime risks of post-AF stroke, ischemic stroke, and myocardial infarction improved only modestly over time and remained high, with virtually no improvement in the lifetime risk of heart failure.

Agata Lenczewska-Madsen, Regional Hospital Central Jutland

The Study

The cohort consisted of 3.5 million individuals (51.7% women) who did not have AF as of age 45 or older. These individuals were followed until incident AF, migration, death, or end of follow-up, whichever came first.

All 362,721 individuals with incident AF (53.6% men) but no prevalent complication were further followed over two time periods (2000-2010 and 2011-2020) until incident heart failure, stroke, or myocardial infarction.

Among the findings:

• Lifetime AF risk increased from 24.2% in 2000-2010 to 30.9% in 2011-2022, for a difference of 6.7% (95% confidence interval [CI], 6.5%-6.8%).
• Lifetime AF risk rose across all subgroups over time, with a larger increase in men and individuals with heart failure, myocardial infarction, stroke, diabetes, and chronic kidney disease.
• Lifetime risk of heart failure was 42.9% in 2000-2010 and 42.1% in 2011-2022, for a difference of −0.8% (95% CI, −3.8% to 2.2%).
• The lifetime risks of post-AF stroke and of myocardial infarction decreased slightly between the two periods, from 22.4% to 19.9% for stroke (difference −2.5%, 95% CI, −4.2% to −0.7%) and from 13.7% to 9.8% for myocardial infarction (−3.9%, 95% CI, −5.3% to −2.4%). No differential decrease between men and women emerged.

“Our novel quantification of the long-term downstream consequences of atrial fibrillation highlights the critical need for treatments to further decrease stroke risk as well as for heart failure prevention strategies among patients with atrial fibrillation,” the Danish researchers wrote.

Offering an outsider’s perspective, John P. Higgins, MD, MBA, MPhil, a sports cardiologist at McGovern Medical School at The University of Texas Health Science Center at Houston, said, “Think of atrial fibrillation as a barometer of underlying stress on the heart. When blood pressure is high, or a patient has underlying asymptomatic coronary artery disease or heart failure, they are more likely to have episodes of atrial fibrillation.”

University of Texas Health Science Center at Houston

Dr. Wu