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Pulsed Field Ablation for AF: Are US Electrophysiologists Too Easily Impressed?
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.
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.
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.
Lower Edoxaban Dose Cuts Bleeding Risk in Elderly Atrial Fibrillation Patients
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.
Study: AFib May Be Linked to Dementia in T2D
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.
Mediterranean Diet Lowers Tachyarrhythmia in Paroxysmal AF
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
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
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
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.
FROM HRS 2024
CPAP Underperforms: The Sequel
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.
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.
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.
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 .
Heart Failure the Most Common Complication of Atrial Fibrillation, Not Stroke
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.
“Our work provides novel lifetime risk estimates that are instrumental in facilitating effective risk communication between patients and their physicians,” Dr. Vinter said in an interview. “The knowledge of risks from a lifelong perspective may serve as a motivator for patients to commence or intensify preventive efforts.” AF patients could, for example, adopt healthier lifestyles or adhere to prescribed medications, Dr. Vinter explained.
“The substantial lifetime risk of heart failure following atrial fibrillation necessitates heightened attention to its prevention and early detection,” Dr. Vinter said. “Furthermore, the high lifetime risk of stroke remains a critical complication, which highlights the importance of continuous attention to the initiation and maintenance of oral anticoagulation therapy.”
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.”
According to Dr. Higgins, risk factors for AF are underappreciated in the United States and elsewhere, and primary care doctors need to be aware of them. “We should try to identify these risk factors and do primary prevention to improve risk factors to reduce the progression to heart failure and myocardial infarction and stroke. But lifelong prevention is even better, he added. “Doing things to prevent actually getting risk factors in the first place. So a healthy lifestyle including exercise, diet, hydration, sleep, relaxation, social contact, and a little sunlight might be the long-term keys and starting them at a young age, too.”
In an accompanying editorial, Jianhua Wu, PhD, a professor of biostatistics and health data science with the Wolfson Institute of Population Health at Queen Mary University of London, and a colleague, cited the study’s robust observational research and called the analysis noteworthy for its quantification of the long-term risks of post-AF sequelae. They cautioned, however, that its grouping into two 10-year periods (2000-2010 and 2011-2020) came at the cost of losing temporal resolution. They also called out the lack of reporting on the ethnic composition of the study population, a factor that influences lifetime AF risk, and the absence of subgroup analysis by socioeconomic status, which affects incidence and outcomes.
The editorialists noted that while interventions to prevent stroke dominated AF research and guidelines during the study time period, no evidence suggests these interventions can prevent incident heart failure. “Alignment of both randomised clinical trials and guidelines to better reflect the needs of the real-world population with atrial fibrillation is necessary because further improvements to patient prognosis are likely to require a broader perspective on atrial fibrillation management beyond prevention of stroke,” they wrote.
In the meantime this study “challenges research priorities and guideline design, and raises critical questions for the research and clinical communities about how the growing burden of atrial fibrillation can be stopped,” they wrote.
This work was supported by the Danish Cardiovascular Academy, which is funded by the Novo Nordisk Foundation, and The Danish Heart Foundation. Dr. Vinter has been an advisory board member and consultant for AstraZeneca and has an institutional research grant from BMS/Pfizer unrelated to the current study. He reported personal consulting fees from BMS and Pfizer. Other coauthors disclosed research support from and/or consulting work for private industry, as well as grants from not-for-profit research-funding organizations. Dr. Higgins had no competing interest to declare. The editorial writers had no relevant financial interests to declare. Dr. Wu is supported by Barts Charity.
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.
“Our work provides novel lifetime risk estimates that are instrumental in facilitating effective risk communication between patients and their physicians,” Dr. Vinter said in an interview. “The knowledge of risks from a lifelong perspective may serve as a motivator for patients to commence or intensify preventive efforts.” AF patients could, for example, adopt healthier lifestyles or adhere to prescribed medications, Dr. Vinter explained.
“The substantial lifetime risk of heart failure following atrial fibrillation necessitates heightened attention to its prevention and early detection,” Dr. Vinter said. “Furthermore, the high lifetime risk of stroke remains a critical complication, which highlights the importance of continuous attention to the initiation and maintenance of oral anticoagulation therapy.”
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.”
According to Dr. Higgins, risk factors for AF are underappreciated in the United States and elsewhere, and primary care doctors need to be aware of them. “We should try to identify these risk factors and do primary prevention to improve risk factors to reduce the progression to heart failure and myocardial infarction and stroke. But lifelong prevention is even better, he added. “Doing things to prevent actually getting risk factors in the first place. So a healthy lifestyle including exercise, diet, hydration, sleep, relaxation, social contact, and a little sunlight might be the long-term keys and starting them at a young age, too.”
In an accompanying editorial, Jianhua Wu, PhD, a professor of biostatistics and health data science with the Wolfson Institute of Population Health at Queen Mary University of London, and a colleague, cited the study’s robust observational research and called the analysis noteworthy for its quantification of the long-term risks of post-AF sequelae. They cautioned, however, that its grouping into two 10-year periods (2000-2010 and 2011-2020) came at the cost of losing temporal resolution. They also called out the lack of reporting on the ethnic composition of the study population, a factor that influences lifetime AF risk, and the absence of subgroup analysis by socioeconomic status, which affects incidence and outcomes.
The editorialists noted that while interventions to prevent stroke dominated AF research and guidelines during the study time period, no evidence suggests these interventions can prevent incident heart failure. “Alignment of both randomised clinical trials and guidelines to better reflect the needs of the real-world population with atrial fibrillation is necessary because further improvements to patient prognosis are likely to require a broader perspective on atrial fibrillation management beyond prevention of stroke,” they wrote.
In the meantime this study “challenges research priorities and guideline design, and raises critical questions for the research and clinical communities about how the growing burden of atrial fibrillation can be stopped,” they wrote.
This work was supported by the Danish Cardiovascular Academy, which is funded by the Novo Nordisk Foundation, and The Danish Heart Foundation. Dr. Vinter has been an advisory board member and consultant for AstraZeneca and has an institutional research grant from BMS/Pfizer unrelated to the current study. He reported personal consulting fees from BMS and Pfizer. Other coauthors disclosed research support from and/or consulting work for private industry, as well as grants from not-for-profit research-funding organizations. Dr. Higgins had no competing interest to declare. The editorial writers had no relevant financial interests to declare. Dr. Wu is supported by Barts Charity.
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.
“Our work provides novel lifetime risk estimates that are instrumental in facilitating effective risk communication between patients and their physicians,” Dr. Vinter said in an interview. “The knowledge of risks from a lifelong perspective may serve as a motivator for patients to commence or intensify preventive efforts.” AF patients could, for example, adopt healthier lifestyles or adhere to prescribed medications, Dr. Vinter explained.
“The substantial lifetime risk of heart failure following atrial fibrillation necessitates heightened attention to its prevention and early detection,” Dr. Vinter said. “Furthermore, the high lifetime risk of stroke remains a critical complication, which highlights the importance of continuous attention to the initiation and maintenance of oral anticoagulation therapy.”
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.”
According to Dr. Higgins, risk factors for AF are underappreciated in the United States and elsewhere, and primary care doctors need to be aware of them. “We should try to identify these risk factors and do primary prevention to improve risk factors to reduce the progression to heart failure and myocardial infarction and stroke. But lifelong prevention is even better, he added. “Doing things to prevent actually getting risk factors in the first place. So a healthy lifestyle including exercise, diet, hydration, sleep, relaxation, social contact, and a little sunlight might be the long-term keys and starting them at a young age, too.”
In an accompanying editorial, Jianhua Wu, PhD, a professor of biostatistics and health data science with the Wolfson Institute of Population Health at Queen Mary University of London, and a colleague, cited the study’s robust observational research and called the analysis noteworthy for its quantification of the long-term risks of post-AF sequelae. They cautioned, however, that its grouping into two 10-year periods (2000-2010 and 2011-2020) came at the cost of losing temporal resolution. They also called out the lack of reporting on the ethnic composition of the study population, a factor that influences lifetime AF risk, and the absence of subgroup analysis by socioeconomic status, which affects incidence and outcomes.
The editorialists noted that while interventions to prevent stroke dominated AF research and guidelines during the study time period, no evidence suggests these interventions can prevent incident heart failure. “Alignment of both randomised clinical trials and guidelines to better reflect the needs of the real-world population with atrial fibrillation is necessary because further improvements to patient prognosis are likely to require a broader perspective on atrial fibrillation management beyond prevention of stroke,” they wrote.
In the meantime this study “challenges research priorities and guideline design, and raises critical questions for the research and clinical communities about how the growing burden of atrial fibrillation can be stopped,” they wrote.
This work was supported by the Danish Cardiovascular Academy, which is funded by the Novo Nordisk Foundation, and The Danish Heart Foundation. Dr. Vinter has been an advisory board member and consultant for AstraZeneca and has an institutional research grant from BMS/Pfizer unrelated to the current study. He reported personal consulting fees from BMS and Pfizer. Other coauthors disclosed research support from and/or consulting work for private industry, as well as grants from not-for-profit research-funding organizations. Dr. Higgins had no competing interest to declare. The editorial writers had no relevant financial interests to declare. Dr. Wu is supported by Barts Charity.
Genetic Testing of Some Patients With Early-Onset AF Advised
Genetic testing may be considered in patients with early-onset atrial fibrillation (AF), particularly those with a positive family history and lack of conventional clinical risk factors, because specific genetic variants may underlie AF as well as “potentially more sinister cardiac conditions,” a new white paper from the Canadian Cardiovascular Society suggested.
“Given the resources and logistical challenges potentially imposed by genetic testing (that is, the majority of cardiology and arrhythmia clinics are not presently equipped to offer it), we have not recommended routine genetic testing for early-onset AF patients at this time,” lead author Jason D. Roberts, MD, associate professor of medicine at McMaster University in Hamilton, Ontario, Canada, told this news organization.
“We do, however, recommend that early-onset AF patients undergo clinical screening for potential coexistence of a ventricular arrhythmia or cardiomyopathy syndrome through careful history, including family history, and physical examination, along with standard clinical testing, including ECG, echocardiogram, and Holter monitoring,” he said.
The white paper was published online in the Canadian Journal of Cardiology.
Routine Testing Unwarranted
The Canadian Cardiovascular Society reviewed AF research in 2022 and concluded that a guideline update was not yet warranted. One area meriting consideration but lacking sufficient evidence for a formal guideline was the clinical application of AF genetics.
Therefore, the society formed a writing group to assess the evidence linking genetic factors to AF, discuss an approach to using genetic testing for early-onset patients with AF, and consider the potential value of genetic testing in the foreseeable future.
The resulting white paper reviews familial and epidemiologic evidence for a genetic contribution to AF. As an example, the authors pointed to work from the Framingham Heart Study showing a statistically significant risk for AF among first-degree relatives of patients with AF. The overall odds ratio (OR) for AF among first-degree relatives was 1.85. But for first-degree relatives of patients with AF onset at younger than age 75 years, the OR increased to 3.23.
Other evidence included the identification of two rare genetic variants: KCNQ1 in a Chinese family and NPPA in a family with Northern European ancestry. In case-control studies, a single gene, titin (TTN), was linked to an increased burden of loss-of-function variants in patients with AF compared with controls. The variant was associated with a 2.2-fold increased risk for AF.
For example, loss-of-function SCN5A variants are implicated in Brugada syndrome and cardiac conduction system disease, whereas gain-of-function variants cause long QT syndrome type 3 and multifocal ectopic Purkinje-related premature contractions. Each of these conditions was associated with an increased prevalence of AF.
Similarly, genes implicated in various other forms of ventricular channelopathies also have been implicated in AF, as have ion channels primarily expressed in the atria and not the ventricles, such as KCNA5 and GJA5.
Nevertheless, in most cases, AF is diagnosed in the context of older age and established cardiovascular risk factors, according to the authors. The contribution of genetic factors in this population is relatively low, highlighting the limited role for genetic testing when AF develops in the presence of multiple conventional clinical risk factors.
Cardiogenetic Expertise Required
“Although significant progress has been made, additional work is needed before [beginning] routine integration of clinical genetic testing for early-onset AF patients,” Dr. Roberts said. The ideal clinical genetic testing panel for AF is still unclear, and the inclusion of genes for which there is no strong evidence of involvement in AF “creates the potential for harm.”
Specifically, “a genetic variant could be incorrectly assigned as the cause of AF, which could create confusion for the patient and family members and lead to inappropriate clinical management,” said Dr. Roberts.
“Beyond cost, routine introduction of genetic testing for AF patients will require allocation of significant resources, given that interpretation of genetic testing results can be nuanced,” he noted. “This nuance is anticipated to be heightened in AF, given that many genetic variants have low-to-intermediate penetrance and can manifest with variable clinical phenotypes.”
“Traditionally, genetic testing has been performed and interpreted, and results communicated, by dedicated cardiogenetic clinics with specialized expertise,” he added. “Existing cardiogenetic clinics, however, are unlikely to be sufficient in number to accommodate the large volume of AF patients that may be eligible for testing.”
Careful Counseling
Jim W. Cheung, MD, chair of the American College of Cardiology Electrophysiology Council, told this news organization that the white paper is consistent with the latest European Heart Rhythm Association/Heart Rhythm Society/Asia Pacific Heart Rhythm Society/Latin American Heart Rhythm Society expert consensus statement published in 2022.
Overall, the approach suggested for genetic testing “is a sound one, but one that requires implementation by clinicians with access to cardiogenetic expertise,” said Cheung, who was not involved in the study. “Any patient undergoing genetic testing needs to be carefully counseled about the potential uncertainties associated with the actual test results and their implications on clinical management.”
Variants of uncertain significance that are detected with genetic testing “can be a source of stress for clinicians and patients,” he said. “Therefore, patient education prior to and after genetic testing is essential.”
Furthermore, he said, “in many patients with early-onset AF who harbor pathogenic variants, initial imaging studies may not detect any signs of cardiomyopathy. In these patients, regular follow-up to assess for development of cardiomyopathy in the future is necessary.”
The white paper was drafted without outside funding. Dr. Roberts and Dr. Cheung reported no relevant financial relationships.
A version of this article appeared on Medscape.com.
Genetic testing may be considered in patients with early-onset atrial fibrillation (AF), particularly those with a positive family history and lack of conventional clinical risk factors, because specific genetic variants may underlie AF as well as “potentially more sinister cardiac conditions,” a new white paper from the Canadian Cardiovascular Society suggested.
“Given the resources and logistical challenges potentially imposed by genetic testing (that is, the majority of cardiology and arrhythmia clinics are not presently equipped to offer it), we have not recommended routine genetic testing for early-onset AF patients at this time,” lead author Jason D. Roberts, MD, associate professor of medicine at McMaster University in Hamilton, Ontario, Canada, told this news organization.
“We do, however, recommend that early-onset AF patients undergo clinical screening for potential coexistence of a ventricular arrhythmia or cardiomyopathy syndrome through careful history, including family history, and physical examination, along with standard clinical testing, including ECG, echocardiogram, and Holter monitoring,” he said.
The white paper was published online in the Canadian Journal of Cardiology.
Routine Testing Unwarranted
The Canadian Cardiovascular Society reviewed AF research in 2022 and concluded that a guideline update was not yet warranted. One area meriting consideration but lacking sufficient evidence for a formal guideline was the clinical application of AF genetics.
Therefore, the society formed a writing group to assess the evidence linking genetic factors to AF, discuss an approach to using genetic testing for early-onset patients with AF, and consider the potential value of genetic testing in the foreseeable future.
The resulting white paper reviews familial and epidemiologic evidence for a genetic contribution to AF. As an example, the authors pointed to work from the Framingham Heart Study showing a statistically significant risk for AF among first-degree relatives of patients with AF. The overall odds ratio (OR) for AF among first-degree relatives was 1.85. But for first-degree relatives of patients with AF onset at younger than age 75 years, the OR increased to 3.23.
Other evidence included the identification of two rare genetic variants: KCNQ1 in a Chinese family and NPPA in a family with Northern European ancestry. In case-control studies, a single gene, titin (TTN), was linked to an increased burden of loss-of-function variants in patients with AF compared with controls. The variant was associated with a 2.2-fold increased risk for AF.
For example, loss-of-function SCN5A variants are implicated in Brugada syndrome and cardiac conduction system disease, whereas gain-of-function variants cause long QT syndrome type 3 and multifocal ectopic Purkinje-related premature contractions. Each of these conditions was associated with an increased prevalence of AF.
Similarly, genes implicated in various other forms of ventricular channelopathies also have been implicated in AF, as have ion channels primarily expressed in the atria and not the ventricles, such as KCNA5 and GJA5.
Nevertheless, in most cases, AF is diagnosed in the context of older age and established cardiovascular risk factors, according to the authors. The contribution of genetic factors in this population is relatively low, highlighting the limited role for genetic testing when AF develops in the presence of multiple conventional clinical risk factors.
Cardiogenetic Expertise Required
“Although significant progress has been made, additional work is needed before [beginning] routine integration of clinical genetic testing for early-onset AF patients,” Dr. Roberts said. The ideal clinical genetic testing panel for AF is still unclear, and the inclusion of genes for which there is no strong evidence of involvement in AF “creates the potential for harm.”
Specifically, “a genetic variant could be incorrectly assigned as the cause of AF, which could create confusion for the patient and family members and lead to inappropriate clinical management,” said Dr. Roberts.
“Beyond cost, routine introduction of genetic testing for AF patients will require allocation of significant resources, given that interpretation of genetic testing results can be nuanced,” he noted. “This nuance is anticipated to be heightened in AF, given that many genetic variants have low-to-intermediate penetrance and can manifest with variable clinical phenotypes.”
“Traditionally, genetic testing has been performed and interpreted, and results communicated, by dedicated cardiogenetic clinics with specialized expertise,” he added. “Existing cardiogenetic clinics, however, are unlikely to be sufficient in number to accommodate the large volume of AF patients that may be eligible for testing.”
Careful Counseling
Jim W. Cheung, MD, chair of the American College of Cardiology Electrophysiology Council, told this news organization that the white paper is consistent with the latest European Heart Rhythm Association/Heart Rhythm Society/Asia Pacific Heart Rhythm Society/Latin American Heart Rhythm Society expert consensus statement published in 2022.
Overall, the approach suggested for genetic testing “is a sound one, but one that requires implementation by clinicians with access to cardiogenetic expertise,” said Cheung, who was not involved in the study. “Any patient undergoing genetic testing needs to be carefully counseled about the potential uncertainties associated with the actual test results and their implications on clinical management.”
Variants of uncertain significance that are detected with genetic testing “can be a source of stress for clinicians and patients,” he said. “Therefore, patient education prior to and after genetic testing is essential.”
Furthermore, he said, “in many patients with early-onset AF who harbor pathogenic variants, initial imaging studies may not detect any signs of cardiomyopathy. In these patients, regular follow-up to assess for development of cardiomyopathy in the future is necessary.”
The white paper was drafted without outside funding. Dr. Roberts and Dr. Cheung reported no relevant financial relationships.
A version of this article appeared on Medscape.com.
Genetic testing may be considered in patients with early-onset atrial fibrillation (AF), particularly those with a positive family history and lack of conventional clinical risk factors, because specific genetic variants may underlie AF as well as “potentially more sinister cardiac conditions,” a new white paper from the Canadian Cardiovascular Society suggested.
“Given the resources and logistical challenges potentially imposed by genetic testing (that is, the majority of cardiology and arrhythmia clinics are not presently equipped to offer it), we have not recommended routine genetic testing for early-onset AF patients at this time,” lead author Jason D. Roberts, MD, associate professor of medicine at McMaster University in Hamilton, Ontario, Canada, told this news organization.
“We do, however, recommend that early-onset AF patients undergo clinical screening for potential coexistence of a ventricular arrhythmia or cardiomyopathy syndrome through careful history, including family history, and physical examination, along with standard clinical testing, including ECG, echocardiogram, and Holter monitoring,” he said.
The white paper was published online in the Canadian Journal of Cardiology.
Routine Testing Unwarranted
The Canadian Cardiovascular Society reviewed AF research in 2022 and concluded that a guideline update was not yet warranted. One area meriting consideration but lacking sufficient evidence for a formal guideline was the clinical application of AF genetics.
Therefore, the society formed a writing group to assess the evidence linking genetic factors to AF, discuss an approach to using genetic testing for early-onset patients with AF, and consider the potential value of genetic testing in the foreseeable future.
The resulting white paper reviews familial and epidemiologic evidence for a genetic contribution to AF. As an example, the authors pointed to work from the Framingham Heart Study showing a statistically significant risk for AF among first-degree relatives of patients with AF. The overall odds ratio (OR) for AF among first-degree relatives was 1.85. But for first-degree relatives of patients with AF onset at younger than age 75 years, the OR increased to 3.23.
Other evidence included the identification of two rare genetic variants: KCNQ1 in a Chinese family and NPPA in a family with Northern European ancestry. In case-control studies, a single gene, titin (TTN), was linked to an increased burden of loss-of-function variants in patients with AF compared with controls. The variant was associated with a 2.2-fold increased risk for AF.
For example, loss-of-function SCN5A variants are implicated in Brugada syndrome and cardiac conduction system disease, whereas gain-of-function variants cause long QT syndrome type 3 and multifocal ectopic Purkinje-related premature contractions. Each of these conditions was associated with an increased prevalence of AF.
Similarly, genes implicated in various other forms of ventricular channelopathies also have been implicated in AF, as have ion channels primarily expressed in the atria and not the ventricles, such as KCNA5 and GJA5.
Nevertheless, in most cases, AF is diagnosed in the context of older age and established cardiovascular risk factors, according to the authors. The contribution of genetic factors in this population is relatively low, highlighting the limited role for genetic testing when AF develops in the presence of multiple conventional clinical risk factors.
Cardiogenetic Expertise Required
“Although significant progress has been made, additional work is needed before [beginning] routine integration of clinical genetic testing for early-onset AF patients,” Dr. Roberts said. The ideal clinical genetic testing panel for AF is still unclear, and the inclusion of genes for which there is no strong evidence of involvement in AF “creates the potential for harm.”
Specifically, “a genetic variant could be incorrectly assigned as the cause of AF, which could create confusion for the patient and family members and lead to inappropriate clinical management,” said Dr. Roberts.
“Beyond cost, routine introduction of genetic testing for AF patients will require allocation of significant resources, given that interpretation of genetic testing results can be nuanced,” he noted. “This nuance is anticipated to be heightened in AF, given that many genetic variants have low-to-intermediate penetrance and can manifest with variable clinical phenotypes.”
“Traditionally, genetic testing has been performed and interpreted, and results communicated, by dedicated cardiogenetic clinics with specialized expertise,” he added. “Existing cardiogenetic clinics, however, are unlikely to be sufficient in number to accommodate the large volume of AF patients that may be eligible for testing.”
Careful Counseling
Jim W. Cheung, MD, chair of the American College of Cardiology Electrophysiology Council, told this news organization that the white paper is consistent with the latest European Heart Rhythm Association/Heart Rhythm Society/Asia Pacific Heart Rhythm Society/Latin American Heart Rhythm Society expert consensus statement published in 2022.
Overall, the approach suggested for genetic testing “is a sound one, but one that requires implementation by clinicians with access to cardiogenetic expertise,” said Cheung, who was not involved in the study. “Any patient undergoing genetic testing needs to be carefully counseled about the potential uncertainties associated with the actual test results and their implications on clinical management.”
Variants of uncertain significance that are detected with genetic testing “can be a source of stress for clinicians and patients,” he said. “Therefore, patient education prior to and after genetic testing is essential.”
Furthermore, he said, “in many patients with early-onset AF who harbor pathogenic variants, initial imaging studies may not detect any signs of cardiomyopathy. In these patients, regular follow-up to assess for development of cardiomyopathy in the future is necessary.”
The white paper was drafted without outside funding. Dr. Roberts and Dr. Cheung reported no relevant financial relationships.
A version of this article appeared on Medscape.com.
FROM THE CANADIAN JOURNAL OF CARDIOLOGY
Few Childhood Cancer Survivors Get Recommended Screenings
Among childhood cancer survivors in Ontario, Canada, who faced an elevated risk due to chemotherapy or radiation treatments, 53% followed screening recommendations for cardiomyopathy, 13% met colorectal cancer screening guidelines, and 6% adhered to breast cancer screening guidelines.
“Although over 80% of children newly diagnosed with cancer will become long-term survivors, as many as four out of five of these survivors will develop a serious or life-threatening late effect of their cancer therapy by age 45,” lead author Jennifer Shuldiner, PhD, MPH, a scientist at Women’s College Hospital Institute for Health Systems Solutions and Virtual Care in Toronto, told this news organization.
For instance, the risk for colorectal cancer in childhood cancer survivors is two to three times higher than it is among the general population, and the risk for breast cancer is similar between those who underwent chest radiation and those with a BRCA mutation. As many as 50% of those who received anthracycline chemotherapy or radiation involving the heart later develop cardiotoxicity.
The North American Children’s Oncology Group has published long-term follow-up guidelines for survivors of childhood cancer, yet many survivors don’t follow them because of lack of awareness or other barriers, said Dr. Shuldiner.
“Prior research has shown that many survivors do not complete these recommended tests,” she said. “With better knowledge of this at-risk population, we can design, test, and implement appropriate interventions and supports to tackle the issues.”
The study was published online on March 11 in CMAJ.
Changes in Adherence
The researchers conducted a retrospective population-based cohort study analyzing Ontario healthcare administrative data for adult survivors of childhood cancer diagnosed between 1986 and 2014 who faced an elevated risk for therapy-related colorectal cancer, breast cancer, or cardiomyopathy. The research team then assessed long-term adherence to the North American Children’s Oncology Group guidelines and predictors of adherence.
Among 3241 survivors, 3205 (99%) were at elevated risk for cardiomyopathy, 327 (10%) were at elevated risk for colorectal cancer, and 234 (7%) were at elevated risk for breast cancer. In addition, 2806 (87%) were at risk for one late effect, 345 (11%) were at risk for two late effects, and 90 (3%) were at risk for three late effects.
Overall, 53%, 13%, and 6% were adherent to their recommended surveillance for cardiomyopathy, colorectal cancer, and breast cancer, respectively. Over time, adherence increased for colorectal cancer and cardiomyopathy but decreased for breast cancer.
In addition, patients who were older at diagnosis were more likely to follow screening guidelines for colorectal and breast cancers, whereas those who were younger at diagnosis were more likely to follow screening guidelines for cardiomyopathy.
During a median follow-up of 7.8 years, the proportion of time spent adherent was 43% for cardiomyopathy, 14% for colorectal cancer, and 10% for breast cancer.
Survivors who attended a long-term follow-up clinic in the previous year had low adherence rates as well, though they were higher than in the rest of the cohort. In this group, the proportion of time that was spent adherent was 71% for cardiomyopathy, 27% for colorectal cancer, and 15% for breast cancer.
Shuldiner and colleagues are launching a research trial to determine whether a provincial support system can help childhood cancer survivors receive the recommended surveillance. The support system provides information about screening recommendations to survivors as well as reminders and sends key information to their family doctors.
“We now understand that childhood cancer survivors need help to complete the recommended tests,” said Dr. Shuldiner. “If the trial is successful, we hope it will be implemented in Ontario.”
Survivorship Care Plans
Low screening rates may result from a lack of awareness about screening recommendations and the negative long-term effects of cancer treatments, the study authors wrote. Cancer survivors, caregivers, family physicians, specialists, and survivor support groups can share the responsibility of spreading awareness and adhering to guidelines, they noted. In some cases, a survivorship care plan (SCP) may help.
“SCPs are intended to improve adherence by providing follow-up information and facilitating the transition from cancer treatment to survivorship and from pediatric to adult care,” Adam Yan, MD, a staff oncologist and oncology informatics lead at the Hospital for Sick Children in Toronto, told this news organization.
Dr. Yan, who wasn’t involved with this study, has researched surveillance adherence for secondary cancers and cardiac dysfunction among childhood cancer survivors. He and his colleagues found that screening rates were typically low among survivors who faced high risks for cardiac dysfunction and breast, colorectal, or skin cancers.
However, having a survivorship care plan seemed to help, and survivors treated after 1990 were more likely to have an SCP.
“SCP possession by high-risk survivors was associated with increased breast, skin, and cardiac surveillance,” he said. “It is uncertain whether SCP possession leads to adherence or whether SCP possession is a marker of survivors who are focused on their health and thus likely to adhere to preventive health practices, including surveillance.”
The study was funded by the Canadian Institutes of Health Research and ICES, which receives support from the Ontario Ministry of Health and the Ministry of Long-Term Care. Dr. Shuldiner received a Canadian Institutes of Health Research Health System Impact Postdoctoral Fellowship in support of the work. Dr. Yan disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Among childhood cancer survivors in Ontario, Canada, who faced an elevated risk due to chemotherapy or radiation treatments, 53% followed screening recommendations for cardiomyopathy, 13% met colorectal cancer screening guidelines, and 6% adhered to breast cancer screening guidelines.
“Although over 80% of children newly diagnosed with cancer will become long-term survivors, as many as four out of five of these survivors will develop a serious or life-threatening late effect of their cancer therapy by age 45,” lead author Jennifer Shuldiner, PhD, MPH, a scientist at Women’s College Hospital Institute for Health Systems Solutions and Virtual Care in Toronto, told this news organization.
For instance, the risk for colorectal cancer in childhood cancer survivors is two to three times higher than it is among the general population, and the risk for breast cancer is similar between those who underwent chest radiation and those with a BRCA mutation. As many as 50% of those who received anthracycline chemotherapy or radiation involving the heart later develop cardiotoxicity.
The North American Children’s Oncology Group has published long-term follow-up guidelines for survivors of childhood cancer, yet many survivors don’t follow them because of lack of awareness or other barriers, said Dr. Shuldiner.
“Prior research has shown that many survivors do not complete these recommended tests,” she said. “With better knowledge of this at-risk population, we can design, test, and implement appropriate interventions and supports to tackle the issues.”
The study was published online on March 11 in CMAJ.
Changes in Adherence
The researchers conducted a retrospective population-based cohort study analyzing Ontario healthcare administrative data for adult survivors of childhood cancer diagnosed between 1986 and 2014 who faced an elevated risk for therapy-related colorectal cancer, breast cancer, or cardiomyopathy. The research team then assessed long-term adherence to the North American Children’s Oncology Group guidelines and predictors of adherence.
Among 3241 survivors, 3205 (99%) were at elevated risk for cardiomyopathy, 327 (10%) were at elevated risk for colorectal cancer, and 234 (7%) were at elevated risk for breast cancer. In addition, 2806 (87%) were at risk for one late effect, 345 (11%) were at risk for two late effects, and 90 (3%) were at risk for three late effects.
Overall, 53%, 13%, and 6% were adherent to their recommended surveillance for cardiomyopathy, colorectal cancer, and breast cancer, respectively. Over time, adherence increased for colorectal cancer and cardiomyopathy but decreased for breast cancer.
In addition, patients who were older at diagnosis were more likely to follow screening guidelines for colorectal and breast cancers, whereas those who were younger at diagnosis were more likely to follow screening guidelines for cardiomyopathy.
During a median follow-up of 7.8 years, the proportion of time spent adherent was 43% for cardiomyopathy, 14% for colorectal cancer, and 10% for breast cancer.
Survivors who attended a long-term follow-up clinic in the previous year had low adherence rates as well, though they were higher than in the rest of the cohort. In this group, the proportion of time that was spent adherent was 71% for cardiomyopathy, 27% for colorectal cancer, and 15% for breast cancer.
Shuldiner and colleagues are launching a research trial to determine whether a provincial support system can help childhood cancer survivors receive the recommended surveillance. The support system provides information about screening recommendations to survivors as well as reminders and sends key information to their family doctors.
“We now understand that childhood cancer survivors need help to complete the recommended tests,” said Dr. Shuldiner. “If the trial is successful, we hope it will be implemented in Ontario.”
Survivorship Care Plans
Low screening rates may result from a lack of awareness about screening recommendations and the negative long-term effects of cancer treatments, the study authors wrote. Cancer survivors, caregivers, family physicians, specialists, and survivor support groups can share the responsibility of spreading awareness and adhering to guidelines, they noted. In some cases, a survivorship care plan (SCP) may help.
“SCPs are intended to improve adherence by providing follow-up information and facilitating the transition from cancer treatment to survivorship and from pediatric to adult care,” Adam Yan, MD, a staff oncologist and oncology informatics lead at the Hospital for Sick Children in Toronto, told this news organization.
Dr. Yan, who wasn’t involved with this study, has researched surveillance adherence for secondary cancers and cardiac dysfunction among childhood cancer survivors. He and his colleagues found that screening rates were typically low among survivors who faced high risks for cardiac dysfunction and breast, colorectal, or skin cancers.
However, having a survivorship care plan seemed to help, and survivors treated after 1990 were more likely to have an SCP.
“SCP possession by high-risk survivors was associated with increased breast, skin, and cardiac surveillance,” he said. “It is uncertain whether SCP possession leads to adherence or whether SCP possession is a marker of survivors who are focused on their health and thus likely to adhere to preventive health practices, including surveillance.”
The study was funded by the Canadian Institutes of Health Research and ICES, which receives support from the Ontario Ministry of Health and the Ministry of Long-Term Care. Dr. Shuldiner received a Canadian Institutes of Health Research Health System Impact Postdoctoral Fellowship in support of the work. Dr. Yan disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Among childhood cancer survivors in Ontario, Canada, who faced an elevated risk due to chemotherapy or radiation treatments, 53% followed screening recommendations for cardiomyopathy, 13% met colorectal cancer screening guidelines, and 6% adhered to breast cancer screening guidelines.
“Although over 80% of children newly diagnosed with cancer will become long-term survivors, as many as four out of five of these survivors will develop a serious or life-threatening late effect of their cancer therapy by age 45,” lead author Jennifer Shuldiner, PhD, MPH, a scientist at Women’s College Hospital Institute for Health Systems Solutions and Virtual Care in Toronto, told this news organization.
For instance, the risk for colorectal cancer in childhood cancer survivors is two to three times higher than it is among the general population, and the risk for breast cancer is similar between those who underwent chest radiation and those with a BRCA mutation. As many as 50% of those who received anthracycline chemotherapy or radiation involving the heart later develop cardiotoxicity.
The North American Children’s Oncology Group has published long-term follow-up guidelines for survivors of childhood cancer, yet many survivors don’t follow them because of lack of awareness or other barriers, said Dr. Shuldiner.
“Prior research has shown that many survivors do not complete these recommended tests,” she said. “With better knowledge of this at-risk population, we can design, test, and implement appropriate interventions and supports to tackle the issues.”
The study was published online on March 11 in CMAJ.
Changes in Adherence
The researchers conducted a retrospective population-based cohort study analyzing Ontario healthcare administrative data for adult survivors of childhood cancer diagnosed between 1986 and 2014 who faced an elevated risk for therapy-related colorectal cancer, breast cancer, or cardiomyopathy. The research team then assessed long-term adherence to the North American Children’s Oncology Group guidelines and predictors of adherence.
Among 3241 survivors, 3205 (99%) were at elevated risk for cardiomyopathy, 327 (10%) were at elevated risk for colorectal cancer, and 234 (7%) were at elevated risk for breast cancer. In addition, 2806 (87%) were at risk for one late effect, 345 (11%) were at risk for two late effects, and 90 (3%) were at risk for three late effects.
Overall, 53%, 13%, and 6% were adherent to their recommended surveillance for cardiomyopathy, colorectal cancer, and breast cancer, respectively. Over time, adherence increased for colorectal cancer and cardiomyopathy but decreased for breast cancer.
In addition, patients who were older at diagnosis were more likely to follow screening guidelines for colorectal and breast cancers, whereas those who were younger at diagnosis were more likely to follow screening guidelines for cardiomyopathy.
During a median follow-up of 7.8 years, the proportion of time spent adherent was 43% for cardiomyopathy, 14% for colorectal cancer, and 10% for breast cancer.
Survivors who attended a long-term follow-up clinic in the previous year had low adherence rates as well, though they were higher than in the rest of the cohort. In this group, the proportion of time that was spent adherent was 71% for cardiomyopathy, 27% for colorectal cancer, and 15% for breast cancer.
Shuldiner and colleagues are launching a research trial to determine whether a provincial support system can help childhood cancer survivors receive the recommended surveillance. The support system provides information about screening recommendations to survivors as well as reminders and sends key information to their family doctors.
“We now understand that childhood cancer survivors need help to complete the recommended tests,” said Dr. Shuldiner. “If the trial is successful, we hope it will be implemented in Ontario.”
Survivorship Care Plans
Low screening rates may result from a lack of awareness about screening recommendations and the negative long-term effects of cancer treatments, the study authors wrote. Cancer survivors, caregivers, family physicians, specialists, and survivor support groups can share the responsibility of spreading awareness and adhering to guidelines, they noted. In some cases, a survivorship care plan (SCP) may help.
“SCPs are intended to improve adherence by providing follow-up information and facilitating the transition from cancer treatment to survivorship and from pediatric to adult care,” Adam Yan, MD, a staff oncologist and oncology informatics lead at the Hospital for Sick Children in Toronto, told this news organization.
Dr. Yan, who wasn’t involved with this study, has researched surveillance adherence for secondary cancers and cardiac dysfunction among childhood cancer survivors. He and his colleagues found that screening rates were typically low among survivors who faced high risks for cardiac dysfunction and breast, colorectal, or skin cancers.
However, having a survivorship care plan seemed to help, and survivors treated after 1990 were more likely to have an SCP.
“SCP possession by high-risk survivors was associated with increased breast, skin, and cardiac surveillance,” he said. “It is uncertain whether SCP possession leads to adherence or whether SCP possession is a marker of survivors who are focused on their health and thus likely to adhere to preventive health practices, including surveillance.”
The study was funded by the Canadian Institutes of Health Research and ICES, which receives support from the Ontario Ministry of Health and the Ministry of Long-Term Care. Dr. Shuldiner received a Canadian Institutes of Health Research Health System Impact Postdoctoral Fellowship in support of the work. Dr. Yan disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
How Does Snoring Affect Cardiovascular Health?
Snoring is a common disorder that affects 20%-40% of the general population. The mechanism of snoring is the vibration of anatomical structures in the pharyngeal airways. The flutter of the soft palate explains the harsh aspect of the snoring sound, which occurs during natural sleep or drug-induced sleep. The presentation of snoring may vary throughout the night or between nights, with a subjective, and therefore inconsistent, assessment of its loudness.
Objective evaluation of snoring is important for clinical decision-making and predicting the effect of therapeutic interventions. It also provides information regarding the site and degree of upper airway obstruction. Snoring is one of the main features of sleep-disordered breathing, including hypopnea events, which reflect partial upper airway obstruction.
Obstructive sleep apnea (OSA) is characterized by episodes of complete (apnea) or partial (hypopnea) collapse of the upper airways with associated oxygen desaturation or awakening from sleep. Most patients with OSA snore loudly almost every night. However, in the Sleep Heart Health Study, one-third of participants with OSA reported no snoring, while one-third of snoring participants did not meet the criteria for OSA. Therefore, subjective assessments of snoring (self-reported) may not be sufficiently reliable to assess its potential impact on cardiovascular (CV) health outcomes.
CV Effects
OSA has been hypothesized as a modifiable risk factor for CV diseases (CVD), including hypertension, coronary artery disease (CAD), atrial fibrillation, heart failure, and stroke, primarily because of the results of traditional observational studies. Snoring is reported as a symptom of the early stage of OSA and has also been associated with a higher risk for CVD. However, establishing causality based on observational studies is difficult because of residual confounding from unknown or unmeasured factors and reverse causality (i.e., the scenario in which CVD increases the risk for OSA or snoring). A Mendelian randomization study, using the natural random allocation of genetic variants as instruments capable of producing results analogous to those of randomized controlled trials, suggested that OSA and snoring increase the risk for hypertension and CAD, with associations partly driven by body mass index (BMI). Conversely, no evidence was found that CVD causally influenced OSA or snoring.
Snoring has been associated with multiple subclinical markers of CV pathology, including high blood pressure, and loud snoring can interfere with restorative sleep and contribute to the risk for hypertension and other adverse outcomes in snorers. However, evidence on the associations between snoring and CV health outcomes remains limited and is primarily based on subjective assessments of snoring or small clinical samples with objective assessments of snoring for only 1 night.
Snoring and Hypertension
A study of 12,287 middle-aged patients (age, 50 years) who were predominantly males (88%) and generally overweight (BMI, 28 kg/m2) determined the prevalence of snoring and its association with the prevalence of hypertension using objective evaluation of snoring over multiple nights and multiple daytime blood pressure measurements. The findings included the following observations:
An increase in snoring duration was associated with a 3-mmHg increase in systolic (SBP) and a 4 mmHg increase in diastolic blood pressure (DBP) in patients with frequent and regular snoring, compared with those with infrequent snoring, regardless of age, BMI, sex, and estimated apnea/hypopnea index.
The association between severe OSA alone and blood pressure had an effect size similar to that of the association between snoring alone and blood pressure. In a model where OSA severity was classified and snoring duration was stratified into quartiles, severe OSA without snoring was associated with 3.6 mmHg higher SBP and 3.5 mmHg higher DBP, compared with the absence of snoring or OSA. Participants without OSA but with intense snoring (4th quartile) had 3.8 mmHg higher SBP and 4.5 mmHg higher DBP compared with participants without nighttime apnea or snoring.
Snoring was significantly associated with uncontrolled hypertension. There was a 20% increase in the probability of uncontrolled hypertension in subjects aged > 50 years with obesity and a 98% increase in subjects aged ≤ 50 years with normal BMI.
Duration of snoring was associated with an 87% increase in the likelihood of uncontrolled hypertension.
Implications for Practice
This study indicates that 15% of a predominantly overweight male population snore for > 20% of the night and about 10% of these subjects without nighttime apnea snore for > 12% of the night.
Regular nighttime snoring is associated with elevated blood pressure and uncontrolled hypertension, regardless of the presence or severity of OSA.
Physicians must be aware of the potential consequences of snoring on the risk for hypertension, and these results highlight the need to consider snoring in clinical care and in the management of sleep problems, especially in the context of managing arterial hypertension.
This story was translated from Univadis Italy, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Snoring is a common disorder that affects 20%-40% of the general population. The mechanism of snoring is the vibration of anatomical structures in the pharyngeal airways. The flutter of the soft palate explains the harsh aspect of the snoring sound, which occurs during natural sleep or drug-induced sleep. The presentation of snoring may vary throughout the night or between nights, with a subjective, and therefore inconsistent, assessment of its loudness.
Objective evaluation of snoring is important for clinical decision-making and predicting the effect of therapeutic interventions. It also provides information regarding the site and degree of upper airway obstruction. Snoring is one of the main features of sleep-disordered breathing, including hypopnea events, which reflect partial upper airway obstruction.
Obstructive sleep apnea (OSA) is characterized by episodes of complete (apnea) or partial (hypopnea) collapse of the upper airways with associated oxygen desaturation or awakening from sleep. Most patients with OSA snore loudly almost every night. However, in the Sleep Heart Health Study, one-third of participants with OSA reported no snoring, while one-third of snoring participants did not meet the criteria for OSA. Therefore, subjective assessments of snoring (self-reported) may not be sufficiently reliable to assess its potential impact on cardiovascular (CV) health outcomes.
CV Effects
OSA has been hypothesized as a modifiable risk factor for CV diseases (CVD), including hypertension, coronary artery disease (CAD), atrial fibrillation, heart failure, and stroke, primarily because of the results of traditional observational studies. Snoring is reported as a symptom of the early stage of OSA and has also been associated with a higher risk for CVD. However, establishing causality based on observational studies is difficult because of residual confounding from unknown or unmeasured factors and reverse causality (i.e., the scenario in which CVD increases the risk for OSA or snoring). A Mendelian randomization study, using the natural random allocation of genetic variants as instruments capable of producing results analogous to those of randomized controlled trials, suggested that OSA and snoring increase the risk for hypertension and CAD, with associations partly driven by body mass index (BMI). Conversely, no evidence was found that CVD causally influenced OSA or snoring.
Snoring has been associated with multiple subclinical markers of CV pathology, including high blood pressure, and loud snoring can interfere with restorative sleep and contribute to the risk for hypertension and other adverse outcomes in snorers. However, evidence on the associations between snoring and CV health outcomes remains limited and is primarily based on subjective assessments of snoring or small clinical samples with objective assessments of snoring for only 1 night.
Snoring and Hypertension
A study of 12,287 middle-aged patients (age, 50 years) who were predominantly males (88%) and generally overweight (BMI, 28 kg/m2) determined the prevalence of snoring and its association with the prevalence of hypertension using objective evaluation of snoring over multiple nights and multiple daytime blood pressure measurements. The findings included the following observations:
An increase in snoring duration was associated with a 3-mmHg increase in systolic (SBP) and a 4 mmHg increase in diastolic blood pressure (DBP) in patients with frequent and regular snoring, compared with those with infrequent snoring, regardless of age, BMI, sex, and estimated apnea/hypopnea index.
The association between severe OSA alone and blood pressure had an effect size similar to that of the association between snoring alone and blood pressure. In a model where OSA severity was classified and snoring duration was stratified into quartiles, severe OSA without snoring was associated with 3.6 mmHg higher SBP and 3.5 mmHg higher DBP, compared with the absence of snoring or OSA. Participants without OSA but with intense snoring (4th quartile) had 3.8 mmHg higher SBP and 4.5 mmHg higher DBP compared with participants without nighttime apnea or snoring.
Snoring was significantly associated with uncontrolled hypertension. There was a 20% increase in the probability of uncontrolled hypertension in subjects aged > 50 years with obesity and a 98% increase in subjects aged ≤ 50 years with normal BMI.
Duration of snoring was associated with an 87% increase in the likelihood of uncontrolled hypertension.
Implications for Practice
This study indicates that 15% of a predominantly overweight male population snore for > 20% of the night and about 10% of these subjects without nighttime apnea snore for > 12% of the night.
Regular nighttime snoring is associated with elevated blood pressure and uncontrolled hypertension, regardless of the presence or severity of OSA.
Physicians must be aware of the potential consequences of snoring on the risk for hypertension, and these results highlight the need to consider snoring in clinical care and in the management of sleep problems, especially in the context of managing arterial hypertension.
This story was translated from Univadis Italy, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Snoring is a common disorder that affects 20%-40% of the general population. The mechanism of snoring is the vibration of anatomical structures in the pharyngeal airways. The flutter of the soft palate explains the harsh aspect of the snoring sound, which occurs during natural sleep or drug-induced sleep. The presentation of snoring may vary throughout the night or between nights, with a subjective, and therefore inconsistent, assessment of its loudness.
Objective evaluation of snoring is important for clinical decision-making and predicting the effect of therapeutic interventions. It also provides information regarding the site and degree of upper airway obstruction. Snoring is one of the main features of sleep-disordered breathing, including hypopnea events, which reflect partial upper airway obstruction.
Obstructive sleep apnea (OSA) is characterized by episodes of complete (apnea) or partial (hypopnea) collapse of the upper airways with associated oxygen desaturation or awakening from sleep. Most patients with OSA snore loudly almost every night. However, in the Sleep Heart Health Study, one-third of participants with OSA reported no snoring, while one-third of snoring participants did not meet the criteria for OSA. Therefore, subjective assessments of snoring (self-reported) may not be sufficiently reliable to assess its potential impact on cardiovascular (CV) health outcomes.
CV Effects
OSA has been hypothesized as a modifiable risk factor for CV diseases (CVD), including hypertension, coronary artery disease (CAD), atrial fibrillation, heart failure, and stroke, primarily because of the results of traditional observational studies. Snoring is reported as a symptom of the early stage of OSA and has also been associated with a higher risk for CVD. However, establishing causality based on observational studies is difficult because of residual confounding from unknown or unmeasured factors and reverse causality (i.e., the scenario in which CVD increases the risk for OSA or snoring). A Mendelian randomization study, using the natural random allocation of genetic variants as instruments capable of producing results analogous to those of randomized controlled trials, suggested that OSA and snoring increase the risk for hypertension and CAD, with associations partly driven by body mass index (BMI). Conversely, no evidence was found that CVD causally influenced OSA or snoring.
Snoring has been associated with multiple subclinical markers of CV pathology, including high blood pressure, and loud snoring can interfere with restorative sleep and contribute to the risk for hypertension and other adverse outcomes in snorers. However, evidence on the associations between snoring and CV health outcomes remains limited and is primarily based on subjective assessments of snoring or small clinical samples with objective assessments of snoring for only 1 night.
Snoring and Hypertension
A study of 12,287 middle-aged patients (age, 50 years) who were predominantly males (88%) and generally overweight (BMI, 28 kg/m2) determined the prevalence of snoring and its association with the prevalence of hypertension using objective evaluation of snoring over multiple nights and multiple daytime blood pressure measurements. The findings included the following observations:
An increase in snoring duration was associated with a 3-mmHg increase in systolic (SBP) and a 4 mmHg increase in diastolic blood pressure (DBP) in patients with frequent and regular snoring, compared with those with infrequent snoring, regardless of age, BMI, sex, and estimated apnea/hypopnea index.
The association between severe OSA alone and blood pressure had an effect size similar to that of the association between snoring alone and blood pressure. In a model where OSA severity was classified and snoring duration was stratified into quartiles, severe OSA without snoring was associated with 3.6 mmHg higher SBP and 3.5 mmHg higher DBP, compared with the absence of snoring or OSA. Participants without OSA but with intense snoring (4th quartile) had 3.8 mmHg higher SBP and 4.5 mmHg higher DBP compared with participants without nighttime apnea or snoring.
Snoring was significantly associated with uncontrolled hypertension. There was a 20% increase in the probability of uncontrolled hypertension in subjects aged > 50 years with obesity and a 98% increase in subjects aged ≤ 50 years with normal BMI.
Duration of snoring was associated with an 87% increase in the likelihood of uncontrolled hypertension.
Implications for Practice
This study indicates that 15% of a predominantly overweight male population snore for > 20% of the night and about 10% of these subjects without nighttime apnea snore for > 12% of the night.
Regular nighttime snoring is associated with elevated blood pressure and uncontrolled hypertension, regardless of the presence or severity of OSA.
Physicians must be aware of the potential consequences of snoring on the risk for hypertension, and these results highlight the need to consider snoring in clinical care and in the management of sleep problems, especially in the context of managing arterial hypertension.
This story was translated from Univadis Italy, which is part of the Medscape professional network, using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.
Artificially Sweetened Drinks Linked to Increased AF Risk
TOPLINE:
(AF) in a new observational study.
METHODOLOGY:
- The population-based cohort study looked at the associations of sugar-sweetened beverages, artificial sweetened beverages, and pure fruit juice consumption with the risk for incident AF and evaluated whether genetic susceptibility modifies these associations.
- The authors analyzed data from the UK Biobank on 201,856 participants who were free of baseline AF, had genetic data available, and completed a 24-hour diet questionnaire. The diagnosis of AF was obtained by linkage from primary care, hospital inpatient, and death register records.
- The results were adjusted for a wide range of potential confounders including age, sex, ethnicity, education level, socioeconomic status, smoking, alcohol consumption, physical activity level, sleep duration, body mass index, blood pressure, kidney function, sleep apnea, coronary heart disease, diabetes, and the use of lipid-lowering or antihypertensive medication.
TAKEAWAY:
- During a median follow-up of 9.9 years, 9362 incident AF cases were documented.
- Compared with nonconsumers, individuals who consumed more than 2 L per week of artificially sweetened beverages had a 20% increased risk of developing AF (hazard ratio [HR], 1.20; 95% CI, 1.10-1.31).
- Those who drank more than 2 L per week of sugar-sweetened beverages had a 10% increased risk for AF (HR, 1.10; 95% CI, 1.01-1.20).
- Consumption of 1 L or less per week of pure fruit juice was associated with an 8% lower risk of developing AF (HR, 0.92; 95% CI, 0.87-0.97).
- The associations persisted after adjustment for genetic susceptibility for AF.
IN PRACTICE:
The study authors concluded that this study does not demonstrate that consumption of sugar-sweetened or artificially sweetened beverages alters AF risk but rather that the consumption of these drinks may predict AF risk beyond traditional risk factors. They added that intervention studies and basic research are warranted to confirm whether the observed associations are causal. Commenting on the study, Duane Mellor, MD, registered dietitian at Aston University, Birmingham, England, said it is unclear if the observations in this study are a chance finding as there is a lack of a clear biological link. Naveed Sattar, MD, professor of metabolic medicine at the University of Glasgow, Glasgow, Scotland, added that although the authors tried to adjust for many factors, there is a strong chance that other behavioral aspects linked to beverage choice could be more relevant as a cause of AF rather than the drinks themselves. Tom Sanders, MD, professor emeritus of nutrition and dietetics, King’s College London, London, England, pointed out that as this is the first study that has reported such an effect with artificially sweetened drinks, the finding needs replication before any conclusions can be drawn. “It remains good dietary advice to recommend the consumption of low-calorie artificially sweetened drink in place of sugar-sweetened drinks and alcohol,” he added.
SOURCE:
The study, led by Ying Sun, MD, Shanghai Jiao Tong University School of Medicine, Shanghai, China, was published online in Circulation: Arrhythmia and Electrophysiology.
LIMITATIONS:
The consumption of beverages was self-reported and based on only five separate single-day food intake recalls which were taken over the first 3 years of the study, which was extrapolated to estimate weekly intake. The researchers could not tell whether the sugar-sweetened and artificially sweetened drinks were caffeinated and could not rule out residual confounding by other unmeasured or unknown factors.
DISCLOSURES:
This study was supported by the National Natural Science Foundation of China, Shanghai Municipal Health Commission, Shanghai Municipal Human Resources and Social Security Bureau, Clinical Research Plan of Shanghai Hospital Development Center, Postdoctoral Scientific Research Foundation of Shanghai Ninth People’s Hospital, and Shanghai Jiao Tong University School of Medicine.
A version of this article appeared on Medscape.com.
TOPLINE:
(AF) in a new observational study.
METHODOLOGY:
- The population-based cohort study looked at the associations of sugar-sweetened beverages, artificial sweetened beverages, and pure fruit juice consumption with the risk for incident AF and evaluated whether genetic susceptibility modifies these associations.
- The authors analyzed data from the UK Biobank on 201,856 participants who were free of baseline AF, had genetic data available, and completed a 24-hour diet questionnaire. The diagnosis of AF was obtained by linkage from primary care, hospital inpatient, and death register records.
- The results were adjusted for a wide range of potential confounders including age, sex, ethnicity, education level, socioeconomic status, smoking, alcohol consumption, physical activity level, sleep duration, body mass index, blood pressure, kidney function, sleep apnea, coronary heart disease, diabetes, and the use of lipid-lowering or antihypertensive medication.
TAKEAWAY:
- During a median follow-up of 9.9 years, 9362 incident AF cases were documented.
- Compared with nonconsumers, individuals who consumed more than 2 L per week of artificially sweetened beverages had a 20% increased risk of developing AF (hazard ratio [HR], 1.20; 95% CI, 1.10-1.31).
- Those who drank more than 2 L per week of sugar-sweetened beverages had a 10% increased risk for AF (HR, 1.10; 95% CI, 1.01-1.20).
- Consumption of 1 L or less per week of pure fruit juice was associated with an 8% lower risk of developing AF (HR, 0.92; 95% CI, 0.87-0.97).
- The associations persisted after adjustment for genetic susceptibility for AF.
IN PRACTICE:
The study authors concluded that this study does not demonstrate that consumption of sugar-sweetened or artificially sweetened beverages alters AF risk but rather that the consumption of these drinks may predict AF risk beyond traditional risk factors. They added that intervention studies and basic research are warranted to confirm whether the observed associations are causal. Commenting on the study, Duane Mellor, MD, registered dietitian at Aston University, Birmingham, England, said it is unclear if the observations in this study are a chance finding as there is a lack of a clear biological link. Naveed Sattar, MD, professor of metabolic medicine at the University of Glasgow, Glasgow, Scotland, added that although the authors tried to adjust for many factors, there is a strong chance that other behavioral aspects linked to beverage choice could be more relevant as a cause of AF rather than the drinks themselves. Tom Sanders, MD, professor emeritus of nutrition and dietetics, King’s College London, London, England, pointed out that as this is the first study that has reported such an effect with artificially sweetened drinks, the finding needs replication before any conclusions can be drawn. “It remains good dietary advice to recommend the consumption of low-calorie artificially sweetened drink in place of sugar-sweetened drinks and alcohol,” he added.
SOURCE:
The study, led by Ying Sun, MD, Shanghai Jiao Tong University School of Medicine, Shanghai, China, was published online in Circulation: Arrhythmia and Electrophysiology.
LIMITATIONS:
The consumption of beverages was self-reported and based on only five separate single-day food intake recalls which were taken over the first 3 years of the study, which was extrapolated to estimate weekly intake. The researchers could not tell whether the sugar-sweetened and artificially sweetened drinks were caffeinated and could not rule out residual confounding by other unmeasured or unknown factors.
DISCLOSURES:
This study was supported by the National Natural Science Foundation of China, Shanghai Municipal Health Commission, Shanghai Municipal Human Resources and Social Security Bureau, Clinical Research Plan of Shanghai Hospital Development Center, Postdoctoral Scientific Research Foundation of Shanghai Ninth People’s Hospital, and Shanghai Jiao Tong University School of Medicine.
A version of this article appeared on Medscape.com.
TOPLINE:
(AF) in a new observational study.
METHODOLOGY:
- The population-based cohort study looked at the associations of sugar-sweetened beverages, artificial sweetened beverages, and pure fruit juice consumption with the risk for incident AF and evaluated whether genetic susceptibility modifies these associations.
- The authors analyzed data from the UK Biobank on 201,856 participants who were free of baseline AF, had genetic data available, and completed a 24-hour diet questionnaire. The diagnosis of AF was obtained by linkage from primary care, hospital inpatient, and death register records.
- The results were adjusted for a wide range of potential confounders including age, sex, ethnicity, education level, socioeconomic status, smoking, alcohol consumption, physical activity level, sleep duration, body mass index, blood pressure, kidney function, sleep apnea, coronary heart disease, diabetes, and the use of lipid-lowering or antihypertensive medication.
TAKEAWAY:
- During a median follow-up of 9.9 years, 9362 incident AF cases were documented.
- Compared with nonconsumers, individuals who consumed more than 2 L per week of artificially sweetened beverages had a 20% increased risk of developing AF (hazard ratio [HR], 1.20; 95% CI, 1.10-1.31).
- Those who drank more than 2 L per week of sugar-sweetened beverages had a 10% increased risk for AF (HR, 1.10; 95% CI, 1.01-1.20).
- Consumption of 1 L or less per week of pure fruit juice was associated with an 8% lower risk of developing AF (HR, 0.92; 95% CI, 0.87-0.97).
- The associations persisted after adjustment for genetic susceptibility for AF.
IN PRACTICE:
The study authors concluded that this study does not demonstrate that consumption of sugar-sweetened or artificially sweetened beverages alters AF risk but rather that the consumption of these drinks may predict AF risk beyond traditional risk factors. They added that intervention studies and basic research are warranted to confirm whether the observed associations are causal. Commenting on the study, Duane Mellor, MD, registered dietitian at Aston University, Birmingham, England, said it is unclear if the observations in this study are a chance finding as there is a lack of a clear biological link. Naveed Sattar, MD, professor of metabolic medicine at the University of Glasgow, Glasgow, Scotland, added that although the authors tried to adjust for many factors, there is a strong chance that other behavioral aspects linked to beverage choice could be more relevant as a cause of AF rather than the drinks themselves. Tom Sanders, MD, professor emeritus of nutrition and dietetics, King’s College London, London, England, pointed out that as this is the first study that has reported such an effect with artificially sweetened drinks, the finding needs replication before any conclusions can be drawn. “It remains good dietary advice to recommend the consumption of low-calorie artificially sweetened drink in place of sugar-sweetened drinks and alcohol,” he added.
SOURCE:
The study, led by Ying Sun, MD, Shanghai Jiao Tong University School of Medicine, Shanghai, China, was published online in Circulation: Arrhythmia and Electrophysiology.
LIMITATIONS:
The consumption of beverages was self-reported and based on only five separate single-day food intake recalls which were taken over the first 3 years of the study, which was extrapolated to estimate weekly intake. The researchers could not tell whether the sugar-sweetened and artificially sweetened drinks were caffeinated and could not rule out residual confounding by other unmeasured or unknown factors.
DISCLOSURES:
This study was supported by the National Natural Science Foundation of China, Shanghai Municipal Health Commission, Shanghai Municipal Human Resources and Social Security Bureau, Clinical Research Plan of Shanghai Hospital Development Center, Postdoctoral Scientific Research Foundation of Shanghai Ninth People’s Hospital, and Shanghai Jiao Tong University School of Medicine.
A version of this article appeared on Medscape.com.