Cardiology

In 490 BC, Pheidippides (or possibly Philippides) ran from Athens to Sparta to ask for military aid against the invading Persian army, then back to Athens, then off to the battlefield of Marathon, then back to Athens to announce the army’s victory, after which he promptly died. The story, if it is to be believed (there is some doubt among historians), raises an interesting question: Are some forms of exercise dangerous?

Running a marathon is a lot of work. The “worst parade ever,” as one spectator described it, is not without its risks. As a runner myself, I know that it doesn’t take much to generate a bloody sock at the end of a long run. 

But when most people think about the risks of exercise, they mean the cardiovascular risks, such as sudden deaths during marathons, probably because of the aforementioned ancient Greek’s demise. The reality is more reassuring. An analysis of 10 years’ worth of data from US marathons and half-marathons found that out of 10.9 million runners, there were 59 cardiac arrests, an incidence rate of 0.54 per 100,000 participants. Others have found incidence rates in the same range. An analysis of the annual Marine Corps and Twin Cities marathons found a sudden death rate of 0.002%.

Marathon runners do sometimes require medical attention. In the Twin Cities cohort, 25 out of every 1000 finishers required medical attention, but 90% of their problems were mild. The majority included issues such as dehydration, vasovagal syncope, hyperthermia, and exhaustion. Musculoskeletal problems and skin abrasions made up the rest. Objectively, long distance running is fairly safe.
 

Running and Coronary Calcium

Then a study comes around suggesting that marathon runners have more coronary artery calcium (CAC). In 2008, German researchers compared 108 healthy male marathon runners over 50 years of age with Framingham risk–matched controls. The marathoners had a higher median CAC score (36 vs 12; P =.02), but scores across the board were quite low and not all studies were in agreement. The MESA study and another from Korea found an inverse relationship between physical activity and coronary calcium, but they compared sedentary people with vigorous exercisers, not specifically marathoners.

Two later studies, published in 2017, generally corroborated that endurance exercise was associated with higher calcium — with some caveats. A group from the Netherlands looked at lifelong exercise volume and compared men who accumulated > 2000 MET-min/week with those who exercised < 1000 MET-min/week. Again, the analysis was limited to men, and CAC scores, though statistically different, were still very low (9.4 vs 0; P =.02). Importantly, in men with coronary plaques, the more active group had less mixed plaque and more calcified plaque. 

A UK study of middle-aged masters-level athletes at low cardiovascular risk had similar findings. Most of the study population (70%) were men, and 77% were runners (not all were marathoners). Overall, the male athletes had not only more plaque but more calcified plaque than their sedentary peers, even though most male athletes (60%) had a CAC score of zero. 

The findings from these two studies were interpreted as reassuring. They confirmed that athletes are a generally low-risk group with low calcium scores, and although they might have more plaque and coronary calcium on average, it tends to be the more benign calcified type.
 

Masters at Heart

But the 2023 Master@Heart study challenged that assertion. It analyzed lifelong endurance athletes, late-onset endurance athletes (those who came to the game later in life), and healthy nonathletic controls. The median number of plaques and the average CAC score were the same across groups, but the plaque burden was higher in lifelong athletes compared with controls. The study also found more coronary stenoses in lifelong athletes, but the breakdown of calcified vs noncalcified vs mixed plaques was the same across groups, thus contradicting the idea that exercise exerted its protective effect by calcifying and therefore stabilizing said plaques. The silver lining was fewer vulnerable plaques in the lifelong athletes (defined via high-risk features) but these were generally rare across the entire population.

Whether Master@Heart is groundbreaking or an outlier depends on your point of view. In 2024, a study from Portugal suggested that the relationship between exercise and coronary calcification is more complicated. Among 105 male veteran athletes, a high volume of exercise was associated with more coronary atherosclerosis in those at higher cardiovascular risk, but it tended to be protective in those deemed lower risk. In fact, the high-volume exercise group had fewer individuals with a CAC score > 100 (16% vs 4%; P =.029), though again, the vast majority had low CAC scores.

A limitation of all these studies is that they had cross-sectional designs, measuring coronary calcium at a single point in time and relying on questionnaires and patient recall to determine lifelong exposure to exercise. Recall bias could have been a problem, and exercise patterns vary over time. It’s not unreasonable to wonder whether people at higher cardiovascular risk should start exercising to mitigate that risk. Granted, they might not start running marathons, but many of these studies looked only at physical activity levels. A study that measured the increase (or stability) of coronary calcium over time would be more helpful.

Prior research (in men again) showed that high levels of physical activity were associated with more coronary calcium, but not with all-cause or cardiovascular mortality. But it too looked only at a single time point. The most recent study added to the body of evidence included data on nearly 9000 men and women and found that higher exercise volume did not correlate with CAC progression over the mean follow-up of 7.8 years. The study measured physical activity of any variety and included physically taxing sports like golf (without a cart). So it was not an assessment of the dangers of endurance exercise.
 

Outstanding Questions and Bananas

Ultimately, many questions remain. Is the lack of risk seen in women a spurious finding because they are underrepresented in most studies, or might exercise affect men and women differently? Is it valid to combine studies on endurance exercise with those looking at physical activity more generally? How accurate are self-reports of exercise? Could endurance exercisers be using performance-enhancing drugs that are confounding the associations? Are people who engage in more physical activity healthier or just trying to mitigate a higher baseline cardiovascular risk? Why do they give out bananas at the end of marathons given that there are better sources of potassium? 

We have no randomized trials on the benefits and risks of endurance exercise. Even if you could get ethics approval, one imagines there would be few volunteers. In the end, we must make do with observational data and remember that coronary calcifications are a surrogate endpoint. 

When it comes to hard endpoints, an analysis of French Tour de France participants found a lower risk for both cardiovascular and cancer deaths compared with the general male population. So perhaps the most important take-home message is one that has been said many times: Beware of surrogate endpoints. And for those contemplating running a marathon, I am forced to agree with the person who wrote the sign I saw during my first race. It does seem like a lot of work for a free banana.
 

Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal, Quebec, Canada. He reported no relevant conflicts of interest.

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

In 490 BC, Pheidippides (or possibly Philippides) ran from Athens to Sparta to ask for military aid against the invading Persian army, then back to Athens, then off to the battlefield of Marathon, then back to Athens to announce the army’s victory, after which he promptly died. The story, if it is to be believed (there is some doubt among historians), raises an interesting question: Are some forms of exercise dangerous?

Running a marathon is a lot of work. The “worst parade ever,” as one spectator described it, is not without its risks. As a runner myself, I know that it doesn’t take much to generate a bloody sock at the end of a long run. 

But when most people think about the risks of exercise, they mean the cardiovascular risks, such as sudden deaths during marathons, probably because of the aforementioned ancient Greek’s demise. The reality is more reassuring. An analysis of 10 years’ worth of data from US marathons and half-marathons found that out of 10.9 million runners, there were 59 cardiac arrests, an incidence rate of 0.54 per 100,000 participants. Others have found incidence rates in the same range. An analysis of the annual Marine Corps and Twin Cities marathons found a sudden death rate of 0.002%.

Marathon runners do sometimes require medical attention. In the Twin Cities cohort, 25 out of every 1000 finishers required medical attention, but 90% of their problems were mild. The majority included issues such as dehydration, vasovagal syncope, hyperthermia, and exhaustion. Musculoskeletal problems and skin abrasions made up the rest. Objectively, long distance running is fairly safe.
 

Running and Coronary Calcium

Then a study comes around suggesting that marathon runners have more coronary artery calcium (CAC). In 2008, German researchers compared 108 healthy male marathon runners over 50 years of age with Framingham risk–matched controls. The marathoners had a higher median CAC score (36 vs 12; P =.02), but scores across the board were quite low and not all studies were in agreement. The MESA study and another from Korea found an inverse relationship between physical activity and coronary calcium, but they compared sedentary people with vigorous exercisers, not specifically marathoners.

Two later studies, published in 2017, generally corroborated that endurance exercise was associated with higher calcium — with some caveats. A group from the Netherlands looked at lifelong exercise volume and compared men who accumulated > 2000 MET-min/week with those who exercised < 1000 MET-min/week. Again, the analysis was limited to men, and CAC scores, though statistically different, were still very low (9.4 vs 0; P =.02). Importantly, in men with coronary plaques, the more active group had less mixed plaque and more calcified plaque. 

A UK study of middle-aged masters-level athletes at low cardiovascular risk had similar findings. Most of the study population (70%) were men, and 77% were runners (not all were marathoners). Overall, the male athletes had not only more plaque but more calcified plaque than their sedentary peers, even though most male athletes (60%) had a CAC score of zero. 

The findings from these two studies were interpreted as reassuring. They confirmed that athletes are a generally low-risk group with low calcium scores, and although they might have more plaque and coronary calcium on average, it tends to be the more benign calcified type.
 

Masters at Heart

But the 2023 Master@Heart study challenged that assertion. It analyzed lifelong endurance athletes, late-onset endurance athletes (those who came to the game later in life), and healthy nonathletic controls. The median number of plaques and the average CAC score were the same across groups, but the plaque burden was higher in lifelong athletes compared with controls. The study also found more coronary stenoses in lifelong athletes, but the breakdown of calcified vs noncalcified vs mixed plaques was the same across groups, thus contradicting the idea that exercise exerted its protective effect by calcifying and therefore stabilizing said plaques. The silver lining was fewer vulnerable plaques in the lifelong athletes (defined via high-risk features) but these were generally rare across the entire population.

Whether Master@Heart is groundbreaking or an outlier depends on your point of view. In 2024, a study from Portugal suggested that the relationship between exercise and coronary calcification is more complicated. Among 105 male veteran athletes, a high volume of exercise was associated with more coronary atherosclerosis in those at higher cardiovascular risk, but it tended to be protective in those deemed lower risk. In fact, the high-volume exercise group had fewer individuals with a CAC score > 100 (16% vs 4%; P =.029), though again, the vast majority had low CAC scores.

A limitation of all these studies is that they had cross-sectional designs, measuring coronary calcium at a single point in time and relying on questionnaires and patient recall to determine lifelong exposure to exercise. Recall bias could have been a problem, and exercise patterns vary over time. It’s not unreasonable to wonder whether people at higher cardiovascular risk should start exercising to mitigate that risk. Granted, they might not start running marathons, but many of these studies looked only at physical activity levels. A study that measured the increase (or stability) of coronary calcium over time would be more helpful.

Prior research (in men again) showed that high levels of physical activity were associated with more coronary calcium, but not with all-cause or cardiovascular mortality. But it too looked only at a single time point. The most recent study added to the body of evidence included data on nearly 9000 men and women and found that higher exercise volume did not correlate with CAC progression over the mean follow-up of 7.8 years. The study measured physical activity of any variety and included physically taxing sports like golf (without a cart). So it was not an assessment of the dangers of endurance exercise.
 

Outstanding Questions and Bananas

Ultimately, many questions remain. Is the lack of risk seen in women a spurious finding because they are underrepresented in most studies, or might exercise affect men and women differently? Is it valid to combine studies on endurance exercise with those looking at physical activity more generally? How accurate are self-reports of exercise? Could endurance exercisers be using performance-enhancing drugs that are confounding the associations? Are people who engage in more physical activity healthier or just trying to mitigate a higher baseline cardiovascular risk? Why do they give out bananas at the end of marathons given that there are better sources of potassium? 

We have no randomized trials on the benefits and risks of endurance exercise. Even if you could get ethics approval, one imagines there would be few volunteers. In the end, we must make do with observational data and remember that coronary calcifications are a surrogate endpoint. 

When it comes to hard endpoints, an analysis of French Tour de France participants found a lower risk for both cardiovascular and cancer deaths compared with the general male population. So perhaps the most important take-home message is one that has been said many times: Beware of surrogate endpoints. And for those contemplating running a marathon, I am forced to agree with the person who wrote the sign I saw during my first race. It does seem like a lot of work for a free banana.
 

Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal, Quebec, Canada. He reported no relevant conflicts of interest.

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

In 490 BC, Pheidippides (or possibly Philippides) ran from Athens to Sparta to ask for military aid against the invading Persian army, then back to Athens, then off to the battlefield of Marathon, then back to Athens to announce the army’s victory, after which he promptly died. The story, if it is to be believed (there is some doubt among historians), raises an interesting question: Are some forms of exercise dangerous?

Running a marathon is a lot of work. The “worst parade ever,” as one spectator described it, is not without its risks. As a runner myself, I know that it doesn’t take much to generate a bloody sock at the end of a long run. 

But when most people think about the risks of exercise, they mean the cardiovascular risks, such as sudden deaths during marathons, probably because of the aforementioned ancient Greek’s demise. The reality is more reassuring. An analysis of 10 years’ worth of data from US marathons and half-marathons found that out of 10.9 million runners, there were 59 cardiac arrests, an incidence rate of 0.54 per 100,000 participants. Others have found incidence rates in the same range. An analysis of the annual Marine Corps and Twin Cities marathons found a sudden death rate of 0.002%.

Marathon runners do sometimes require medical attention. In the Twin Cities cohort, 25 out of every 1000 finishers required medical attention, but 90% of their problems were mild. The majority included issues such as dehydration, vasovagal syncope, hyperthermia, and exhaustion. Musculoskeletal problems and skin abrasions made up the rest. Objectively, long distance running is fairly safe.
 

Running and Coronary Calcium

Then a study comes around suggesting that marathon runners have more coronary artery calcium (CAC). In 2008, German researchers compared 108 healthy male marathon runners over 50 years of age with Framingham risk–matched controls. The marathoners had a higher median CAC score (36 vs 12; P =.02), but scores across the board were quite low and not all studies were in agreement. The MESA study and another from Korea found an inverse relationship between physical activity and coronary calcium, but they compared sedentary people with vigorous exercisers, not specifically marathoners.

Two later studies, published in 2017, generally corroborated that endurance exercise was associated with higher calcium — with some caveats. A group from the Netherlands looked at lifelong exercise volume and compared men who accumulated > 2000 MET-min/week with those who exercised < 1000 MET-min/week. Again, the analysis was limited to men, and CAC scores, though statistically different, were still very low (9.4 vs 0; P =.02). Importantly, in men with coronary plaques, the more active group had less mixed plaque and more calcified plaque. 

A UK study of middle-aged masters-level athletes at low cardiovascular risk had similar findings. Most of the study population (70%) were men, and 77% were runners (not all were marathoners). Overall, the male athletes had not only more plaque but more calcified plaque than their sedentary peers, even though most male athletes (60%) had a CAC score of zero. 

The findings from these two studies were interpreted as reassuring. They confirmed that athletes are a generally low-risk group with low calcium scores, and although they might have more plaque and coronary calcium on average, it tends to be the more benign calcified type.
 

Masters at Heart

But the 2023 Master@Heart study challenged that assertion. It analyzed lifelong endurance athletes, late-onset endurance athletes (those who came to the game later in life), and healthy nonathletic controls. The median number of plaques and the average CAC score were the same across groups, but the plaque burden was higher in lifelong athletes compared with controls. The study also found more coronary stenoses in lifelong athletes, but the breakdown of calcified vs noncalcified vs mixed plaques was the same across groups, thus contradicting the idea that exercise exerted its protective effect by calcifying and therefore stabilizing said plaques. The silver lining was fewer vulnerable plaques in the lifelong athletes (defined via high-risk features) but these were generally rare across the entire population.

Whether Master@Heart is groundbreaking or an outlier depends on your point of view. In 2024, a study from Portugal suggested that the relationship between exercise and coronary calcification is more complicated. Among 105 male veteran athletes, a high volume of exercise was associated with more coronary atherosclerosis in those at higher cardiovascular risk, but it tended to be protective in those deemed lower risk. In fact, the high-volume exercise group had fewer individuals with a CAC score > 100 (16% vs 4%; P =.029), though again, the vast majority had low CAC scores.

A limitation of all these studies is that they had cross-sectional designs, measuring coronary calcium at a single point in time and relying on questionnaires and patient recall to determine lifelong exposure to exercise. Recall bias could have been a problem, and exercise patterns vary over time. It’s not unreasonable to wonder whether people at higher cardiovascular risk should start exercising to mitigate that risk. Granted, they might not start running marathons, but many of these studies looked only at physical activity levels. A study that measured the increase (or stability) of coronary calcium over time would be more helpful.

Prior research (in men again) showed that high levels of physical activity were associated with more coronary calcium, but not with all-cause or cardiovascular mortality. But it too looked only at a single time point. The most recent study added to the body of evidence included data on nearly 9000 men and women and found that higher exercise volume did not correlate with CAC progression over the mean follow-up of 7.8 years. The study measured physical activity of any variety and included physically taxing sports like golf (without a cart). So it was not an assessment of the dangers of endurance exercise.
 

Outstanding Questions and Bananas

Ultimately, many questions remain. Is the lack of risk seen in women a spurious finding because they are underrepresented in most studies, or might exercise affect men and women differently? Is it valid to combine studies on endurance exercise with those looking at physical activity more generally? How accurate are self-reports of exercise? Could endurance exercisers be using performance-enhancing drugs that are confounding the associations? Are people who engage in more physical activity healthier or just trying to mitigate a higher baseline cardiovascular risk? Why do they give out bananas at the end of marathons given that there are better sources of potassium? 

We have no randomized trials on the benefits and risks of endurance exercise. Even if you could get ethics approval, one imagines there would be few volunteers. In the end, we must make do with observational data and remember that coronary calcifications are a surrogate endpoint. 

When it comes to hard endpoints, an analysis of French Tour de France participants found a lower risk for both cardiovascular and cancer deaths compared with the general male population. So perhaps the most important take-home message is one that has been said many times: Beware of surrogate endpoints. And for those contemplating running a marathon, I am forced to agree with the person who wrote the sign I saw during my first race. It does seem like a lot of work for a free banana.
 

Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal, Quebec, Canada. He reported no relevant conflicts of interest.

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

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

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

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

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

Class I Recommendation

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

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

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

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

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

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

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

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

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

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

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

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

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

Pathways Are Appropriate for All Patients

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

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

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

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

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

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

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

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

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

Class I Recommendation

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

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

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

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

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

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

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

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

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

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

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

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

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

Pathways Are Appropriate for All Patients

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

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

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

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

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

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

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

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

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

Class I Recommendation

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

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

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

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

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

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

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

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

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

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

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

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

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

Pathways Are Appropriate for All Patients

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

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

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

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

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

LONDON — Simplified and more aggressive targets are among the significant changes to the updated hypertension guidelines released by the European Society of Cardiology.

For most treated patients, the new systolic blood pressure goal is a target of 120 mm Hg to 129 mm Hg, which is a move away from the previous two-step recommendation.

Although the updated guidelines, presented here at the ESC Congress, continue to define hypertension as a systolic BP of at least 140 mm Hg and a diastolic BP of at least 90 mm Hg, there is a new category — elevated BP. This is defined as a systolic BP of 120 mm Hg to 139 mm Hg or a diastolic BP of 70 mm Hg to 89 mm Hg, and cardiovascular risk assessment is advised to guide treatment, particularly in patients with a BP of at least 130/80 mm Hg.

The guidelines also introduce new recommendations for lifestyle options to help lower BP, including changes to exercise advice and the addition of potassium supplementation. And for the first time, the ESC guidelines provide recommendations for the use of renal denervation to treat hypertension in certain circumstances.

The guidelines were produced by an international panel, led by Bill McEvoy, MB BCh, from the University of Galway, Ireland, and Rhian Touyz, MB BCh, PhD, from McGill University in Montreal.
 

Three Categories of Blood Pressure

There are now three categories for BP classification — non-elevated (< 120/70 mm Hg), elevated (120 mm Hg to139 mm Hg/70 mm Hg to 89 mm Hg), and hypertension (≥ 140/90 mm Hg) — Dr. McEvoy reported during a session on the new guidelines here at ESC.

The emphasis on out-of-office BP measurement is stronger than in previous guidelines, but office measurement will still be used, he said.

All patients in the hypertension category qualify for treatment, whereas those in the new elevated BP category will be subject to cardiovascular risk stratification before a treatment decision is made.

Patients in the elevated BP category who also have moderate or severe chronic kidney disease, established cardiovascular disease, diabetes, or familial hypercholesterolemia are among those considered at increased risk for cardiovascular disease, as are patients with an estimated 10-year cardiovascular risk of 10% or higher. In such patients with a confirmed BP of at least 130/80 mm Hg, after 3 months of lifestyle intervention, pharmacologic treatment is recommended.

“This new category of elevated blood pressure recognizes that people do not go from normal blood pressure to hypertensive overnight,” Dr. McEvoy said. “It is, in most cases, a steady gradient of change, and different subgroups of patients — for example, those at a higher risk of developing cardiovascular disease — could benefit from more intensive treatment before their blood pressure reaches the traditional threshold of hypertension.”
 

New Lower Target

The major change in target pressures in these guidelines is based on new clinical trial data that confirm that lower pressures lead to lower cardiovascular event rates, resulting in the new systolic BP target of 120 mm Hg to 129 mm Hg for most patients receiving antihypertensive medications.

This systolic target represents a major change from previous European guidelines, Dr. McEvoy said, which have generally recommended that patients be treated to a target of less than 140/90 mm Hg and, only after that has been reached, then treated to a target of less than 130/80 mm Hg (a two-step approach).

“This change is driven by new trial evidence confirming that more intensive blood pressure treatment targets reduce cardiovascular outcomes across a broad spectrum of eligible patients,” Dr. McEvoy said.

There are, however, several caveats to this recommendation, including the requirement that treatment to this target be well tolerated; more lenient targets can be considered in people with symptomatic orthostatic hypotension, those 85 years and older, and those with moderate to severe frailty or a limited life expectancy. For these patients, the guidelines recommend a target “that is as low as reasonably achievable.”
 

More in Line With US Guidelines

The new European guidelines are now more in line with the American guidelines, said Eugene Yang, MD, from the University of Washington in Seattle, who is chair of the Hypertension Writing Group at the American College of Cardiology.

“These new European guidelines have thoughtfully used the latest study data to simplify recommendations for a specific lower blood pressure target. This is a step forward. There is now a greater alignment of European and US guidelines. This is good to reduce confusion and build consensus across the world,” he said.

Both sets of guidelines now recommend a BP target of less than 130/80 mm Hg for most people. 

“I think the Europeans have now embraced this more aggressive target because there are many more studies now showing that these lower blood pressure levels do lead to a reduction in cardiovascular events,” Dr. Yang explained. “When the last European guidelines came out, there was only SPRINT. Now there are several more studies showing similar results.”
 

New Lifestyle Advice

The updated recommendation of 75 minutes of vigorous-intensity aerobic exercise per week has been added as an alternative to the previous recommendation of at least 2.5 hours per week of moderate-intensity aerobic exercise. This should be complemented with low- or moderate-intensity dynamic or isometric resistance training two to three times a week. 

It is also recommended that people with hypertension, but without moderate or advanced chronic kidney disease, increase potassium intake with salt substitutes or diets rich in fruits and vegetables.
 

Renal Denervation Included for First Time 

For the first time, the guidelines include the option of renal denervation for the treatment of hypertension — at medium- to high-volume centers — for patients with resistant hypertension that is uncontrolled despite a three-drug combination.

However, renal denervation is not recommended as a first-line treatment because of the lack of evidence of a benefit in cardiovascular outcomes. It is also not recommended for patients with highly impaired renal function or secondary causes of hypertension.

Dr. Yang said he approves of the inclusion of a frailty assessment in the new guidelines and less aggressive targets for people who are in poor health and older than age 85 years, but added that, “on the whole, they have less age-specific stratification than before, which is a significant change, and a good one in my view.” 

Again, this is like the American guidelines, which have no age cutoffs and a target of less than 130/80 mm Hg for all, with the caveat that clinical judgment may be needed for individuals who are institutionalized, he added.

Dr. Yang said he was not as keen on the requirement for a cardiovascular risk assessment to guide treatment decisions for people with a systolic BP in the 130 mm Hg to 139 mm Hg range, although this is also included in the current American guidelines.

“As a clinician, I think this complicates things a bit too much and, as such, will be a barrier to treatment. In my view, blood pressure treatment recommendations need to be as simple as possible, so I think we still have some work to do there,” he said.

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

LONDON — Simplified and more aggressive targets are among the significant changes to the updated hypertension guidelines released by the European Society of Cardiology.

For most treated patients, the new systolic blood pressure goal is a target of 120 mm Hg to 129 mm Hg, which is a move away from the previous two-step recommendation.

Although the updated guidelines, presented here at the ESC Congress, continue to define hypertension as a systolic BP of at least 140 mm Hg and a diastolic BP of at least 90 mm Hg, there is a new category — elevated BP. This is defined as a systolic BP of 120 mm Hg to 139 mm Hg or a diastolic BP of 70 mm Hg to 89 mm Hg, and cardiovascular risk assessment is advised to guide treatment, particularly in patients with a BP of at least 130/80 mm Hg.

The guidelines also introduce new recommendations for lifestyle options to help lower BP, including changes to exercise advice and the addition of potassium supplementation. And for the first time, the ESC guidelines provide recommendations for the use of renal denervation to treat hypertension in certain circumstances.

The guidelines were produced by an international panel, led by Bill McEvoy, MB BCh, from the University of Galway, Ireland, and Rhian Touyz, MB BCh, PhD, from McGill University in Montreal.
 

Three Categories of Blood Pressure

There are now three categories for BP classification — non-elevated (< 120/70 mm Hg), elevated (120 mm Hg to139 mm Hg/70 mm Hg to 89 mm Hg), and hypertension (≥ 140/90 mm Hg) — Dr. McEvoy reported during a session on the new guidelines here at ESC.

The emphasis on out-of-office BP measurement is stronger than in previous guidelines, but office measurement will still be used, he said.

All patients in the hypertension category qualify for treatment, whereas those in the new elevated BP category will be subject to cardiovascular risk stratification before a treatment decision is made.

Patients in the elevated BP category who also have moderate or severe chronic kidney disease, established cardiovascular disease, diabetes, or familial hypercholesterolemia are among those considered at increased risk for cardiovascular disease, as are patients with an estimated 10-year cardiovascular risk of 10% or higher. In such patients with a confirmed BP of at least 130/80 mm Hg, after 3 months of lifestyle intervention, pharmacologic treatment is recommended.

“This new category of elevated blood pressure recognizes that people do not go from normal blood pressure to hypertensive overnight,” Dr. McEvoy said. “It is, in most cases, a steady gradient of change, and different subgroups of patients — for example, those at a higher risk of developing cardiovascular disease — could benefit from more intensive treatment before their blood pressure reaches the traditional threshold of hypertension.”
 

New Lower Target

The major change in target pressures in these guidelines is based on new clinical trial data that confirm that lower pressures lead to lower cardiovascular event rates, resulting in the new systolic BP target of 120 mm Hg to 129 mm Hg for most patients receiving antihypertensive medications.

This systolic target represents a major change from previous European guidelines, Dr. McEvoy said, which have generally recommended that patients be treated to a target of less than 140/90 mm Hg and, only after that has been reached, then treated to a target of less than 130/80 mm Hg (a two-step approach).

“This change is driven by new trial evidence confirming that more intensive blood pressure treatment targets reduce cardiovascular outcomes across a broad spectrum of eligible patients,” Dr. McEvoy said.

There are, however, several caveats to this recommendation, including the requirement that treatment to this target be well tolerated; more lenient targets can be considered in people with symptomatic orthostatic hypotension, those 85 years and older, and those with moderate to severe frailty or a limited life expectancy. For these patients, the guidelines recommend a target “that is as low as reasonably achievable.”
 

More in Line With US Guidelines

The new European guidelines are now more in line with the American guidelines, said Eugene Yang, MD, from the University of Washington in Seattle, who is chair of the Hypertension Writing Group at the American College of Cardiology.

“These new European guidelines have thoughtfully used the latest study data to simplify recommendations for a specific lower blood pressure target. This is a step forward. There is now a greater alignment of European and US guidelines. This is good to reduce confusion and build consensus across the world,” he said.

Both sets of guidelines now recommend a BP target of less than 130/80 mm Hg for most people. 

“I think the Europeans have now embraced this more aggressive target because there are many more studies now showing that these lower blood pressure levels do lead to a reduction in cardiovascular events,” Dr. Yang explained. “When the last European guidelines came out, there was only SPRINT. Now there are several more studies showing similar results.”
 

New Lifestyle Advice

The updated recommendation of 75 minutes of vigorous-intensity aerobic exercise per week has been added as an alternative to the previous recommendation of at least 2.5 hours per week of moderate-intensity aerobic exercise. This should be complemented with low- or moderate-intensity dynamic or isometric resistance training two to three times a week. 

It is also recommended that people with hypertension, but without moderate or advanced chronic kidney disease, increase potassium intake with salt substitutes or diets rich in fruits and vegetables.
 

Renal Denervation Included for First Time 

For the first time, the guidelines include the option of renal denervation for the treatment of hypertension — at medium- to high-volume centers — for patients with resistant hypertension that is uncontrolled despite a three-drug combination.

However, renal denervation is not recommended as a first-line treatment because of the lack of evidence of a benefit in cardiovascular outcomes. It is also not recommended for patients with highly impaired renal function or secondary causes of hypertension.

Dr. Yang said he approves of the inclusion of a frailty assessment in the new guidelines and less aggressive targets for people who are in poor health and older than age 85 years, but added that, “on the whole, they have less age-specific stratification than before, which is a significant change, and a good one in my view.” 

Again, this is like the American guidelines, which have no age cutoffs and a target of less than 130/80 mm Hg for all, with the caveat that clinical judgment may be needed for individuals who are institutionalized, he added.

Dr. Yang said he was not as keen on the requirement for a cardiovascular risk assessment to guide treatment decisions for people with a systolic BP in the 130 mm Hg to 139 mm Hg range, although this is also included in the current American guidelines.

“As a clinician, I think this complicates things a bit too much and, as such, will be a barrier to treatment. In my view, blood pressure treatment recommendations need to be as simple as possible, so I think we still have some work to do there,” he said.

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

LONDON — Simplified and more aggressive targets are among the significant changes to the updated hypertension guidelines released by the European Society of Cardiology.

For most treated patients, the new systolic blood pressure goal is a target of 120 mm Hg to 129 mm Hg, which is a move away from the previous two-step recommendation.

Although the updated guidelines, presented here at the ESC Congress, continue to define hypertension as a systolic BP of at least 140 mm Hg and a diastolic BP of at least 90 mm Hg, there is a new category — elevated BP. This is defined as a systolic BP of 120 mm Hg to 139 mm Hg or a diastolic BP of 70 mm Hg to 89 mm Hg, and cardiovascular risk assessment is advised to guide treatment, particularly in patients with a BP of at least 130/80 mm Hg.

The guidelines also introduce new recommendations for lifestyle options to help lower BP, including changes to exercise advice and the addition of potassium supplementation. And for the first time, the ESC guidelines provide recommendations for the use of renal denervation to treat hypertension in certain circumstances.

The guidelines were produced by an international panel, led by Bill McEvoy, MB BCh, from the University of Galway, Ireland, and Rhian Touyz, MB BCh, PhD, from McGill University in Montreal.
 

Three Categories of Blood Pressure

There are now three categories for BP classification — non-elevated (< 120/70 mm Hg), elevated (120 mm Hg to139 mm Hg/70 mm Hg to 89 mm Hg), and hypertension (≥ 140/90 mm Hg) — Dr. McEvoy reported during a session on the new guidelines here at ESC.

The emphasis on out-of-office BP measurement is stronger than in previous guidelines, but office measurement will still be used, he said.

All patients in the hypertension category qualify for treatment, whereas those in the new elevated BP category will be subject to cardiovascular risk stratification before a treatment decision is made.

Patients in the elevated BP category who also have moderate or severe chronic kidney disease, established cardiovascular disease, diabetes, or familial hypercholesterolemia are among those considered at increased risk for cardiovascular disease, as are patients with an estimated 10-year cardiovascular risk of 10% or higher. In such patients with a confirmed BP of at least 130/80 mm Hg, after 3 months of lifestyle intervention, pharmacologic treatment is recommended.

“This new category of elevated blood pressure recognizes that people do not go from normal blood pressure to hypertensive overnight,” Dr. McEvoy said. “It is, in most cases, a steady gradient of change, and different subgroups of patients — for example, those at a higher risk of developing cardiovascular disease — could benefit from more intensive treatment before their blood pressure reaches the traditional threshold of hypertension.”
 

New Lower Target

The major change in target pressures in these guidelines is based on new clinical trial data that confirm that lower pressures lead to lower cardiovascular event rates, resulting in the new systolic BP target of 120 mm Hg to 129 mm Hg for most patients receiving antihypertensive medications.

This systolic target represents a major change from previous European guidelines, Dr. McEvoy said, which have generally recommended that patients be treated to a target of less than 140/90 mm Hg and, only after that has been reached, then treated to a target of less than 130/80 mm Hg (a two-step approach).

“This change is driven by new trial evidence confirming that more intensive blood pressure treatment targets reduce cardiovascular outcomes across a broad spectrum of eligible patients,” Dr. McEvoy said.

There are, however, several caveats to this recommendation, including the requirement that treatment to this target be well tolerated; more lenient targets can be considered in people with symptomatic orthostatic hypotension, those 85 years and older, and those with moderate to severe frailty or a limited life expectancy. For these patients, the guidelines recommend a target “that is as low as reasonably achievable.”
 

More in Line With US Guidelines

The new European guidelines are now more in line with the American guidelines, said Eugene Yang, MD, from the University of Washington in Seattle, who is chair of the Hypertension Writing Group at the American College of Cardiology.

“These new European guidelines have thoughtfully used the latest study data to simplify recommendations for a specific lower blood pressure target. This is a step forward. There is now a greater alignment of European and US guidelines. This is good to reduce confusion and build consensus across the world,” he said.

Both sets of guidelines now recommend a BP target of less than 130/80 mm Hg for most people. 

“I think the Europeans have now embraced this more aggressive target because there are many more studies now showing that these lower blood pressure levels do lead to a reduction in cardiovascular events,” Dr. Yang explained. “When the last European guidelines came out, there was only SPRINT. Now there are several more studies showing similar results.”
 

New Lifestyle Advice

The updated recommendation of 75 minutes of vigorous-intensity aerobic exercise per week has been added as an alternative to the previous recommendation of at least 2.5 hours per week of moderate-intensity aerobic exercise. This should be complemented with low- or moderate-intensity dynamic or isometric resistance training two to three times a week. 

It is also recommended that people with hypertension, but without moderate or advanced chronic kidney disease, increase potassium intake with salt substitutes or diets rich in fruits and vegetables.
 

Renal Denervation Included for First Time 

For the first time, the guidelines include the option of renal denervation for the treatment of hypertension — at medium- to high-volume centers — for patients with resistant hypertension that is uncontrolled despite a three-drug combination.

However, renal denervation is not recommended as a first-line treatment because of the lack of evidence of a benefit in cardiovascular outcomes. It is also not recommended for patients with highly impaired renal function or secondary causes of hypertension.

Dr. Yang said he approves of the inclusion of a frailty assessment in the new guidelines and less aggressive targets for people who are in poor health and older than age 85 years, but added that, “on the whole, they have less age-specific stratification than before, which is a significant change, and a good one in my view.” 

Again, this is like the American guidelines, which have no age cutoffs and a target of less than 130/80 mm Hg for all, with the caveat that clinical judgment may be needed for individuals who are institutionalized, he added.

Dr. Yang said he was not as keen on the requirement for a cardiovascular risk assessment to guide treatment decisions for people with a systolic BP in the 130 mm Hg to 139 mm Hg range, although this is also included in the current American guidelines.

“As a clinician, I think this complicates things a bit too much and, as such, will be a barrier to treatment. In my view, blood pressure treatment recommendations need to be as simple as possible, so I think we still have some work to do there,” he said.

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

A single night of sleep deprivation had a significant impact on human blood serum, based on new data from an analysis of nearly 500 proteins. Compromised sleep has demonstrated negative effects on cardiovascular, immune, and neuronal systems, and previous studies have shown human serum proteome changes after a simulation of night shift work, wrote Alvhild Alette Bjørkum, MD, of Western Norway University of Applied Sciences, Bergen, and colleagues.

In a pilot study published in Sleep Advances, the researchers recruited eight healthy adult women aged 22-57 years with no history of neurologic or psychiatric problems to participate in a study of the effect of compromised sleep on protein profiles, with implications for effects on cells, tissues, and organ systems. Each of the participants served as their own controls, and blood samples were taken after 6 hours of sleep at night, and again after 6 hours of sleep deprivation the following night.

The researchers identified analyzed 494 proteins using mass spectrometry. Of these, 66 were differentially expressed after 6 hours of sleep deprivation. The top enriched biologic processes of these significantly changed proteins were protein activation cascade, platelet degranulation, blood coagulation, and hemostasis.

Further analysis using gene ontology showed changes in response to sleep deprivation in biologic process, molecular function, and immune system process categories, including specific associations related to wound healing, cholesterol transport, high-density lipoprotein particle receptor binding, and granulocyte chemotaxis.

The findings were limited by several factors including the small sample size, inclusion only of adult females, and the use of data from only 1 night of sleep deprivation, the researchers noted. However, the results support previous studies showing a negative impact of sleep deprivation on biologic functions, they said.

“Our study was able to reveal another set of human serum proteins that were altered by sleep deprivation and could connect similar biological processes to sleep deprivation that have been identified before with slightly different methods,” the researchers concluded. The study findings add to the knowledge base for the protein profiling of sleep deprivation, which may inform the development of tools to manage lack of sleep and mistimed sleep, particularly in shift workers.
 

Too Soon for Clinical Implications

“The adverse impact of poor sleep across many organ systems is gaining recognition, but the mechanisms underlying sleep-related pathology are not well understood,” Evan L. Brittain, MD, of Vanderbilt University, Nashville, Tennessee, said in an interview. “Studies like this begin to shed light on the mechanisms by which poor or reduced sleep affects specific bodily functions,” added Dr. Brittain, who was not involved in the study.

“The effects of other acute physiologic stressor such as exercise on the circulating proteome are well described. In that regard, it is not surprising that a brief episode of sleep deprivation would lead to detectable changes in the circulation,” Dr. Brittain said.

However, the specific changes reported in this study are difficult to interpret because of methodological and analytical concerns, particularly the small sample size, lack of an external validation cohort, and absence of appropriate statistical adjustments in the results, Dr. Brittain noted. These limitations prevent consideration of clinical implications without further study.

The study received no outside funding. Neither the researchers nor Dr. Brittain disclosed any conflicts of interest.

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

A single night of sleep deprivation had a significant impact on human blood serum, based on new data from an analysis of nearly 500 proteins. Compromised sleep has demonstrated negative effects on cardiovascular, immune, and neuronal systems, and previous studies have shown human serum proteome changes after a simulation of night shift work, wrote Alvhild Alette Bjørkum, MD, of Western Norway University of Applied Sciences, Bergen, and colleagues.

In a pilot study published in Sleep Advances, the researchers recruited eight healthy adult women aged 22-57 years with no history of neurologic or psychiatric problems to participate in a study of the effect of compromised sleep on protein profiles, with implications for effects on cells, tissues, and organ systems. Each of the participants served as their own controls, and blood samples were taken after 6 hours of sleep at night, and again after 6 hours of sleep deprivation the following night.

The researchers identified analyzed 494 proteins using mass spectrometry. Of these, 66 were differentially expressed after 6 hours of sleep deprivation. The top enriched biologic processes of these significantly changed proteins were protein activation cascade, platelet degranulation, blood coagulation, and hemostasis.

Further analysis using gene ontology showed changes in response to sleep deprivation in biologic process, molecular function, and immune system process categories, including specific associations related to wound healing, cholesterol transport, high-density lipoprotein particle receptor binding, and granulocyte chemotaxis.

The findings were limited by several factors including the small sample size, inclusion only of adult females, and the use of data from only 1 night of sleep deprivation, the researchers noted. However, the results support previous studies showing a negative impact of sleep deprivation on biologic functions, they said.

“Our study was able to reveal another set of human serum proteins that were altered by sleep deprivation and could connect similar biological processes to sleep deprivation that have been identified before with slightly different methods,” the researchers concluded. The study findings add to the knowledge base for the protein profiling of sleep deprivation, which may inform the development of tools to manage lack of sleep and mistimed sleep, particularly in shift workers.
 

Too Soon for Clinical Implications

“The adverse impact of poor sleep across many organ systems is gaining recognition, but the mechanisms underlying sleep-related pathology are not well understood,” Evan L. Brittain, MD, of Vanderbilt University, Nashville, Tennessee, said in an interview. “Studies like this begin to shed light on the mechanisms by which poor or reduced sleep affects specific bodily functions,” added Dr. Brittain, who was not involved in the study.

“The effects of other acute physiologic stressor such as exercise on the circulating proteome are well described. In that regard, it is not surprising that a brief episode of sleep deprivation would lead to detectable changes in the circulation,” Dr. Brittain said.

However, the specific changes reported in this study are difficult to interpret because of methodological and analytical concerns, particularly the small sample size, lack of an external validation cohort, and absence of appropriate statistical adjustments in the results, Dr. Brittain noted. These limitations prevent consideration of clinical implications without further study.

The study received no outside funding. Neither the researchers nor Dr. Brittain disclosed any conflicts of interest.

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

A single night of sleep deprivation had a significant impact on human blood serum, based on new data from an analysis of nearly 500 proteins. Compromised sleep has demonstrated negative effects on cardiovascular, immune, and neuronal systems, and previous studies have shown human serum proteome changes after a simulation of night shift work, wrote Alvhild Alette Bjørkum, MD, of Western Norway University of Applied Sciences, Bergen, and colleagues.

In a pilot study published in Sleep Advances, the researchers recruited eight healthy adult women aged 22-57 years with no history of neurologic or psychiatric problems to participate in a study of the effect of compromised sleep on protein profiles, with implications for effects on cells, tissues, and organ systems. Each of the participants served as their own controls, and blood samples were taken after 6 hours of sleep at night, and again after 6 hours of sleep deprivation the following night.

The researchers identified analyzed 494 proteins using mass spectrometry. Of these, 66 were differentially expressed after 6 hours of sleep deprivation. The top enriched biologic processes of these significantly changed proteins were protein activation cascade, platelet degranulation, blood coagulation, and hemostasis.

Further analysis using gene ontology showed changes in response to sleep deprivation in biologic process, molecular function, and immune system process categories, including specific associations related to wound healing, cholesterol transport, high-density lipoprotein particle receptor binding, and granulocyte chemotaxis.

The findings were limited by several factors including the small sample size, inclusion only of adult females, and the use of data from only 1 night of sleep deprivation, the researchers noted. However, the results support previous studies showing a negative impact of sleep deprivation on biologic functions, they said.

“Our study was able to reveal another set of human serum proteins that were altered by sleep deprivation and could connect similar biological processes to sleep deprivation that have been identified before with slightly different methods,” the researchers concluded. The study findings add to the knowledge base for the protein profiling of sleep deprivation, which may inform the development of tools to manage lack of sleep and mistimed sleep, particularly in shift workers.
 

Too Soon for Clinical Implications

“The adverse impact of poor sleep across many organ systems is gaining recognition, but the mechanisms underlying sleep-related pathology are not well understood,” Evan L. Brittain, MD, of Vanderbilt University, Nashville, Tennessee, said in an interview. “Studies like this begin to shed light on the mechanisms by which poor or reduced sleep affects specific bodily functions,” added Dr. Brittain, who was not involved in the study.

“The effects of other acute physiologic stressor such as exercise on the circulating proteome are well described. In that regard, it is not surprising that a brief episode of sleep deprivation would lead to detectable changes in the circulation,” Dr. Brittain said.

However, the specific changes reported in this study are difficult to interpret because of methodological and analytical concerns, particularly the small sample size, lack of an external validation cohort, and absence of appropriate statistical adjustments in the results, Dr. Brittain noted. These limitations prevent consideration of clinical implications without further study.

The study received no outside funding. Neither the researchers nor Dr. Brittain disclosed any conflicts of interest.

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

We know exercise can be a powerful medical intervention. Now scientists are finally starting to understand why.

A recent study in rats found that exercise positively changes virtually every tissue in the body. The research was part of a large National Institutes of Health initiative called MoTrPAC (Molecular Transducers of Physical Activity Consortium) to understand how physical activity improves health and prevents disease. As part of the project, a large human study is also underway.

“What was mind-blowing to me was just how much every organ changed,” said cardiologist Euan A. Ashley, MD, professor of medicine at Stanford University, Stanford, California, and the study’s lead author. “You really are a different person on exercise.”

The study examined hundreds of previously sedentary rats that exercised on a treadmill for 8 weeks. Their tissues were compared with a control group of rats that stayed sedentary.

Your patients, unlike lab animals, can’t be randomly assigned to run on a treadmill until you switch the machine off.

So how do you persuade your patients to become more active?

We asked seven doctors what works for them. They shared 10 of their most effective persuasion tactics.
 

1. Focus on the First Step

“It’s easy to say you want to change behavior,” said Jordan Metzl, MD, a sports medicine specialist at the Hospital for Special Surgery in New York City who instructs medical students on how to prescribe exercise. “It’s much more difficult to do it.”

He compares it with moving a tractor tire from point A to point B. The hardest part is lifting the tire off the ground and starting to move it. “Once it’s rolling, it takes much less effort to keep it going in the same direction,” he said.

How much exercise a patient does is irrelevant until they’ve given that tire its first push.

“Any amount of exercise is better than nothing,” Dr. Ashley said. “Let’s just start with that. Making the move from sitting a lot to standing more has genuine health benefits.” 
 

2. Mind Your Language

Many patients have a deep-rooted aversion to words and phrases associated with physical activity.

“Exercise” is one. “Working out” is another.

“I often tell them they just have to start moving,” said Chris Raynor, MD, an orthopedic surgeon based in Ottawa, Ontario. “Don’t think about it as working out. Think about it as just moving. Start with something they already like doing and work from there.”
 

3. Make It Manageable

This also applies to patients who’re injured and either waiting for or recovering from surgery.

“Joints like motion,” said Rachel M. Frank, MD, an orthopedic surgeon at the University of Colorado Sports Medicine, Denver, Colorado. “The more mobile you can be, the easier your recovery’s going to be.”

That can be a challenge for a patient who wasn’t active before the injury, especially if he or she is fixed on the idea that exercise doesn’t matter unless they do it for 30-45 minutes at a time.

“I try to break it down into manageable bits they can do at home,” Dr. Frank said. “I say, ‘Look, you brush your teeth twice a day, right? Can you do these exercises for 5 or 10 minutes before or after you brush your teeth?’ ”
 

4. Connect Their Interests to Their Activity Level

Chad Waterbury, DPT, thought he knew how to motivate a postsurgical patient to become more active and improve her odds for a full recovery. He told her she’d feel better and have more energy — all the usual selling points.

None of it impressed her.

But one day she mentioned that she’d recently become a grandmother for the first time. Dr. Waterbury, a physical therapist based in Los Angeles, noticed how she lit up when she talked about her new granddaughter.

“So I started giving her scenarios, like taking her daughter to Disneyland when she’s 9 or 10. You have to be somewhat fit to do something like that.”

It worked, and Dr. Waterbury learned a fundamental lesson in motivation. “You have to connect the exercise to something that’s important in their life,” he said.
 

5. Don’t Let a Crisis Go to Waste

“There are very few things more motivating than having a heart attack,” Dr. Ashley said. “For the vast majority of people, that’s a very sobering moment where they reassess everything in their lives.”

There’ll never be a better time to persuade a patient to become more active. In his cardiology practice, Dr. Ashley has seen a lot of patients make that switch.

“They really do start to prioritize their health in a way they never did before,” he said.
 

6. Emphasize the Practical Over the Ideal

Not all patients attach negative feelings to working out. For some, it’s the goal.

Todd Ivan, MD, calls it the “ ’I need to get to the gym’ lament”: Something they’ve aspired to but rarely if ever done.

“I tell them I’d welcome a half-hour walk every day to get started,” said Dr. Ivan, a consultation-liaison psychiatrist at Summa Health in Akron, Ohio. “It’s a way to introduce the idea that fitness begins with small adjustments.”
 

7. Go Beneath the Surface

“Exercise doesn’t generally result in great weight loss,” said endocrinologist Karl Nadolsky, DO, an obesity specialist and co-host of the Docs Who Lift podcast.

But a lot of his patients struggle to break that connection. It’s understandable, given how many times they’ve been told they’d weigh less if they moved more.

Dr. Nadolsky tells them it’s what’s on the inside that counts. “I explain it as very literal, meaning their physical health, metabolic health, and mental health.”

By reframing physical activity with an internal rather than external focus — the plumbing and wiring vs the shutters and shingles — he gives them permission to approach exercise as a health upgrade rather than yet another part of their lifelong struggle to lose weight.

“A significant number of our patients respond well to that,” he said.
 

8. Appeal to Their Intellect

Some patients think like doctors: No matter how reluctant they may be to change their mind about something, they’ll respond to evidence.

Dr. Frank has learned to identify these scientifically inclined patients. “I’ll flood them with data,” she said. “I’ll say, ‘These studies show that if you do x, y, z, your outcome will be better.’ ”

Dr. Ashley takes a similar approach when his patients give him the most common reason for not exercising: “I don’t have time.”

He tells them that exercise doesn’t take time. It gives you time.

That’s according to a 2012 study of more than 650,000 adults that associated physical activity with an increased lifespan.

As one of the authors said in an interview, a middle-aged person who gets 150 minutes a week of moderate exercise will, on average, gain 7 more minutes of life for each minute of exercise, compared with someone who doesn’t get any exercise.

The strategy works because it brings patients out of their day-to-day lives and into the future, Dr. Ashley said.

“What about your entire life?” he asks them. “You’re actually in this world for 80-plus years, you hope. How are you going to spend that? You have to think about that when you’re in your 40s and 50s.”
 

9. Show Them the Money

Illness and injury, on top of everything else, can be really expensive.

Even with good insurance, a health problem that requires surgery and/or hospitalization might cost thousands of dollars out of pocket. With mediocre insurance, it might be tens of thousands.

Sometimes, Dr. Frank said, it helps to remind patients of the price they paid for their treatment. “I’ll say, ‘Let’s get moving so you don’t have to pay for this again.’ ”

Protecting their investment can be a powerful motivation.
 

10. Make It a Team Effort

While the doctors we interviewed have a wide range of specialties — cardiology, sports medicine, psychiatry, endocrinology, orthopedics, and physical therapy — their patients have one thing in common.

They don’t want to be in a doctor’s office. It means they have something, need something, or broke something.

It might be a treatable condition that’s merely inconvenient or a life-threatening event that’s flat-out terrifying.

Whatever it is, it pulls them out of their normal world. It can be a lonely, disorienting experience.

Sometimes the best thing a doctor can do is stay connected with the patient. “This is like a team sport,” Dr. Frank tells her patients. “I’m going to be your coach, but you’re the captain of the team.”

In some cases, she’ll ask the patient to message her on the portal after completing the daily or weekly exercises. That alone might motivate the patient — especially when she responds to their messages.

After all, nobody wants to let the coach down.
 

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

We know exercise can be a powerful medical intervention. Now scientists are finally starting to understand why.

A recent study in rats found that exercise positively changes virtually every tissue in the body. The research was part of a large National Institutes of Health initiative called MoTrPAC (Molecular Transducers of Physical Activity Consortium) to understand how physical activity improves health and prevents disease. As part of the project, a large human study is also underway.

“What was mind-blowing to me was just how much every organ changed,” said cardiologist Euan A. Ashley, MD, professor of medicine at Stanford University, Stanford, California, and the study’s lead author. “You really are a different person on exercise.”

The study examined hundreds of previously sedentary rats that exercised on a treadmill for 8 weeks. Their tissues were compared with a control group of rats that stayed sedentary.

Your patients, unlike lab animals, can’t be randomly assigned to run on a treadmill until you switch the machine off.

So how do you persuade your patients to become more active?

We asked seven doctors what works for them. They shared 10 of their most effective persuasion tactics.
 

1. Focus on the First Step

“It’s easy to say you want to change behavior,” said Jordan Metzl, MD, a sports medicine specialist at the Hospital for Special Surgery in New York City who instructs medical students on how to prescribe exercise. “It’s much more difficult to do it.”

He compares it with moving a tractor tire from point A to point B. The hardest part is lifting the tire off the ground and starting to move it. “Once it’s rolling, it takes much less effort to keep it going in the same direction,” he said.

How much exercise a patient does is irrelevant until they’ve given that tire its first push.

“Any amount of exercise is better than nothing,” Dr. Ashley said. “Let’s just start with that. Making the move from sitting a lot to standing more has genuine health benefits.” 
 

2. Mind Your Language

Many patients have a deep-rooted aversion to words and phrases associated with physical activity.

“Exercise” is one. “Working out” is another.

“I often tell them they just have to start moving,” said Chris Raynor, MD, an orthopedic surgeon based in Ottawa, Ontario. “Don’t think about it as working out. Think about it as just moving. Start with something they already like doing and work from there.”
 

3. Make It Manageable

This also applies to patients who’re injured and either waiting for or recovering from surgery.

“Joints like motion,” said Rachel M. Frank, MD, an orthopedic surgeon at the University of Colorado Sports Medicine, Denver, Colorado. “The more mobile you can be, the easier your recovery’s going to be.”

That can be a challenge for a patient who wasn’t active before the injury, especially if he or she is fixed on the idea that exercise doesn’t matter unless they do it for 30-45 minutes at a time.

“I try to break it down into manageable bits they can do at home,” Dr. Frank said. “I say, ‘Look, you brush your teeth twice a day, right? Can you do these exercises for 5 or 10 minutes before or after you brush your teeth?’ ”
 

4. Connect Their Interests to Their Activity Level

Chad Waterbury, DPT, thought he knew how to motivate a postsurgical patient to become more active and improve her odds for a full recovery. He told her she’d feel better and have more energy — all the usual selling points.

None of it impressed her.

But one day she mentioned that she’d recently become a grandmother for the first time. Dr. Waterbury, a physical therapist based in Los Angeles, noticed how she lit up when she talked about her new granddaughter.

“So I started giving her scenarios, like taking her daughter to Disneyland when she’s 9 or 10. You have to be somewhat fit to do something like that.”

It worked, and Dr. Waterbury learned a fundamental lesson in motivation. “You have to connect the exercise to something that’s important in their life,” he said.
 

5. Don’t Let a Crisis Go to Waste

“There are very few things more motivating than having a heart attack,” Dr. Ashley said. “For the vast majority of people, that’s a very sobering moment where they reassess everything in their lives.”

There’ll never be a better time to persuade a patient to become more active. In his cardiology practice, Dr. Ashley has seen a lot of patients make that switch.

“They really do start to prioritize their health in a way they never did before,” he said.
 

6. Emphasize the Practical Over the Ideal

Not all patients attach negative feelings to working out. For some, it’s the goal.

Todd Ivan, MD, calls it the “ ’I need to get to the gym’ lament”: Something they’ve aspired to but rarely if ever done.

“I tell them I’d welcome a half-hour walk every day to get started,” said Dr. Ivan, a consultation-liaison psychiatrist at Summa Health in Akron, Ohio. “It’s a way to introduce the idea that fitness begins with small adjustments.”
 

7. Go Beneath the Surface

“Exercise doesn’t generally result in great weight loss,” said endocrinologist Karl Nadolsky, DO, an obesity specialist and co-host of the Docs Who Lift podcast.

But a lot of his patients struggle to break that connection. It’s understandable, given how many times they’ve been told they’d weigh less if they moved more.

Dr. Nadolsky tells them it’s what’s on the inside that counts. “I explain it as very literal, meaning their physical health, metabolic health, and mental health.”

By reframing physical activity with an internal rather than external focus — the plumbing and wiring vs the shutters and shingles — he gives them permission to approach exercise as a health upgrade rather than yet another part of their lifelong struggle to lose weight.

“A significant number of our patients respond well to that,” he said.
 

8. Appeal to Their Intellect

Some patients think like doctors: No matter how reluctant they may be to change their mind about something, they’ll respond to evidence.

Dr. Frank has learned to identify these scientifically inclined patients. “I’ll flood them with data,” she said. “I’ll say, ‘These studies show that if you do x, y, z, your outcome will be better.’ ”

Dr. Ashley takes a similar approach when his patients give him the most common reason for not exercising: “I don’t have time.”

He tells them that exercise doesn’t take time. It gives you time.

That’s according to a 2012 study of more than 650,000 adults that associated physical activity with an increased lifespan.

As one of the authors said in an interview, a middle-aged person who gets 150 minutes a week of moderate exercise will, on average, gain 7 more minutes of life for each minute of exercise, compared with someone who doesn’t get any exercise.

The strategy works because it brings patients out of their day-to-day lives and into the future, Dr. Ashley said.

“What about your entire life?” he asks them. “You’re actually in this world for 80-plus years, you hope. How are you going to spend that? You have to think about that when you’re in your 40s and 50s.”
 

9. Show Them the Money

Illness and injury, on top of everything else, can be really expensive.

Even with good insurance, a health problem that requires surgery and/or hospitalization might cost thousands of dollars out of pocket. With mediocre insurance, it might be tens of thousands.

Sometimes, Dr. Frank said, it helps to remind patients of the price they paid for their treatment. “I’ll say, ‘Let’s get moving so you don’t have to pay for this again.’ ”

Protecting their investment can be a powerful motivation.
 

10. Make It a Team Effort

While the doctors we interviewed have a wide range of specialties — cardiology, sports medicine, psychiatry, endocrinology, orthopedics, and physical therapy — their patients have one thing in common.

They don’t want to be in a doctor’s office. It means they have something, need something, or broke something.

It might be a treatable condition that’s merely inconvenient or a life-threatening event that’s flat-out terrifying.

Whatever it is, it pulls them out of their normal world. It can be a lonely, disorienting experience.

Sometimes the best thing a doctor can do is stay connected with the patient. “This is like a team sport,” Dr. Frank tells her patients. “I’m going to be your coach, but you’re the captain of the team.”

In some cases, she’ll ask the patient to message her on the portal after completing the daily or weekly exercises. That alone might motivate the patient — especially when she responds to their messages.

After all, nobody wants to let the coach down.
 

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

We know exercise can be a powerful medical intervention. Now scientists are finally starting to understand why.

A recent study in rats found that exercise positively changes virtually every tissue in the body. The research was part of a large National Institutes of Health initiative called MoTrPAC (Molecular Transducers of Physical Activity Consortium) to understand how physical activity improves health and prevents disease. As part of the project, a large human study is also underway.

“What was mind-blowing to me was just how much every organ changed,” said cardiologist Euan A. Ashley, MD, professor of medicine at Stanford University, Stanford, California, and the study’s lead author. “You really are a different person on exercise.”

The study examined hundreds of previously sedentary rats that exercised on a treadmill for 8 weeks. Their tissues were compared with a control group of rats that stayed sedentary.

Your patients, unlike lab animals, can’t be randomly assigned to run on a treadmill until you switch the machine off.

So how do you persuade your patients to become more active?

We asked seven doctors what works for them. They shared 10 of their most effective persuasion tactics.
 

1. Focus on the First Step

“It’s easy to say you want to change behavior,” said Jordan Metzl, MD, a sports medicine specialist at the Hospital for Special Surgery in New York City who instructs medical students on how to prescribe exercise. “It’s much more difficult to do it.”

He compares it with moving a tractor tire from point A to point B. The hardest part is lifting the tire off the ground and starting to move it. “Once it’s rolling, it takes much less effort to keep it going in the same direction,” he said.

How much exercise a patient does is irrelevant until they’ve given that tire its first push.

“Any amount of exercise is better than nothing,” Dr. Ashley said. “Let’s just start with that. Making the move from sitting a lot to standing more has genuine health benefits.” 
 

2. Mind Your Language

Many patients have a deep-rooted aversion to words and phrases associated with physical activity.

“Exercise” is one. “Working out” is another.

“I often tell them they just have to start moving,” said Chris Raynor, MD, an orthopedic surgeon based in Ottawa, Ontario. “Don’t think about it as working out. Think about it as just moving. Start with something they already like doing and work from there.”
 

3. Make It Manageable

This also applies to patients who’re injured and either waiting for or recovering from surgery.

“Joints like motion,” said Rachel M. Frank, MD, an orthopedic surgeon at the University of Colorado Sports Medicine, Denver, Colorado. “The more mobile you can be, the easier your recovery’s going to be.”

That can be a challenge for a patient who wasn’t active before the injury, especially if he or she is fixed on the idea that exercise doesn’t matter unless they do it for 30-45 minutes at a time.

“I try to break it down into manageable bits they can do at home,” Dr. Frank said. “I say, ‘Look, you brush your teeth twice a day, right? Can you do these exercises for 5 or 10 minutes before or after you brush your teeth?’ ”
 

4. Connect Their Interests to Their Activity Level

Chad Waterbury, DPT, thought he knew how to motivate a postsurgical patient to become more active and improve her odds for a full recovery. He told her she’d feel better and have more energy — all the usual selling points.

None of it impressed her.

But one day she mentioned that she’d recently become a grandmother for the first time. Dr. Waterbury, a physical therapist based in Los Angeles, noticed how she lit up when she talked about her new granddaughter.

“So I started giving her scenarios, like taking her daughter to Disneyland when she’s 9 or 10. You have to be somewhat fit to do something like that.”

It worked, and Dr. Waterbury learned a fundamental lesson in motivation. “You have to connect the exercise to something that’s important in their life,” he said.
 

5. Don’t Let a Crisis Go to Waste

“There are very few things more motivating than having a heart attack,” Dr. Ashley said. “For the vast majority of people, that’s a very sobering moment where they reassess everything in their lives.”

There’ll never be a better time to persuade a patient to become more active. In his cardiology practice, Dr. Ashley has seen a lot of patients make that switch.

“They really do start to prioritize their health in a way they never did before,” he said.
 

6. Emphasize the Practical Over the Ideal

Not all patients attach negative feelings to working out. For some, it’s the goal.

Todd Ivan, MD, calls it the “ ’I need to get to the gym’ lament”: Something they’ve aspired to but rarely if ever done.

“I tell them I’d welcome a half-hour walk every day to get started,” said Dr. Ivan, a consultation-liaison psychiatrist at Summa Health in Akron, Ohio. “It’s a way to introduce the idea that fitness begins with small adjustments.”
 

7. Go Beneath the Surface

“Exercise doesn’t generally result in great weight loss,” said endocrinologist Karl Nadolsky, DO, an obesity specialist and co-host of the Docs Who Lift podcast.

But a lot of his patients struggle to break that connection. It’s understandable, given how many times they’ve been told they’d weigh less if they moved more.

Dr. Nadolsky tells them it’s what’s on the inside that counts. “I explain it as very literal, meaning their physical health, metabolic health, and mental health.”

By reframing physical activity with an internal rather than external focus — the plumbing and wiring vs the shutters and shingles — he gives them permission to approach exercise as a health upgrade rather than yet another part of their lifelong struggle to lose weight.

“A significant number of our patients respond well to that,” he said.
 

8. Appeal to Their Intellect

Some patients think like doctors: No matter how reluctant they may be to change their mind about something, they’ll respond to evidence.

Dr. Frank has learned to identify these scientifically inclined patients. “I’ll flood them with data,” she said. “I’ll say, ‘These studies show that if you do x, y, z, your outcome will be better.’ ”

Dr. Ashley takes a similar approach when his patients give him the most common reason for not exercising: “I don’t have time.”

He tells them that exercise doesn’t take time. It gives you time.

That’s according to a 2012 study of more than 650,000 adults that associated physical activity with an increased lifespan.

As one of the authors said in an interview, a middle-aged person who gets 150 minutes a week of moderate exercise will, on average, gain 7 more minutes of life for each minute of exercise, compared with someone who doesn’t get any exercise.

The strategy works because it brings patients out of their day-to-day lives and into the future, Dr. Ashley said.

“What about your entire life?” he asks them. “You’re actually in this world for 80-plus years, you hope. How are you going to spend that? You have to think about that when you’re in your 40s and 50s.”
 

9. Show Them the Money

Illness and injury, on top of everything else, can be really expensive.

Even with good insurance, a health problem that requires surgery and/or hospitalization might cost thousands of dollars out of pocket. With mediocre insurance, it might be tens of thousands.

Sometimes, Dr. Frank said, it helps to remind patients of the price they paid for their treatment. “I’ll say, ‘Let’s get moving so you don’t have to pay for this again.’ ”

Protecting their investment can be a powerful motivation.
 

10. Make It a Team Effort

While the doctors we interviewed have a wide range of specialties — cardiology, sports medicine, psychiatry, endocrinology, orthopedics, and physical therapy — their patients have one thing in common.

They don’t want to be in a doctor’s office. It means they have something, need something, or broke something.

It might be a treatable condition that’s merely inconvenient or a life-threatening event that’s flat-out terrifying.

Whatever it is, it pulls them out of their normal world. It can be a lonely, disorienting experience.

Sometimes the best thing a doctor can do is stay connected with the patient. “This is like a team sport,” Dr. Frank tells her patients. “I’m going to be your coach, but you’re the captain of the team.”

In some cases, she’ll ask the patient to message her on the portal after completing the daily or weekly exercises. That alone might motivate the patient — especially when she responds to their messages.

After all, nobody wants to let the coach down.
 

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

TOPLINE:

Older adults with untreated hypertension have a 36% increased risk for Alzheimer’s disease (AD) compared with those without hypertension and a 42% increased risk for AD compared with those with treated hypertension.

METHODOLOGY:

• In this meta-analysis, researchers analyzed the data of 31,250 participants aged 60 years or older (mean age, 72.1 years; 41% men) from 14 community-based studies across 14 countries.
• Mean follow-up was 4.2 years, and blood pressure measurements, hypertension diagnosis, and antihypertensive medication use were recorded.
• Overall, 35.9% had no history of hypertension or antihypertensive medication use, 50.7% had a history of hypertension with antihypertensive medication use, and 9.4% had a history of hypertension without antihypertensive medication use.
• The main outcomes were AD and non-AD dementia.

TAKEAWAY:

• In total, 1415 participants developed AD, and 681 developed non-AD dementia.
• Participants with untreated hypertension had a 36% increased risk for AD compared with healthy controls (hazard ratio [HR], 1.36; P = .041) and a 42% increased risk for AD (HR, 1.42; P = .013) compared with those with treated hypertension.
• Compared with healthy controls, patients with treated hypertension did not show an elevated risk for AD (HR, 0.961; P = .6644).
• Patients with both treated (HR, 1.285; P = .027) and untreated (HR, 1.693; P = .003) hypertension had an increased risk for non-AD dementia compared with healthy controls. Patients with treated and untreated hypertension had a similar risk for non-AD dementia.

IN PRACTICE:

“These results suggest that treating high blood pressure as a person ages continues to be a crucial factor in reducing their risk of Alzheimer’s disease,” the lead author Matthew J. Lennon, MD, PhD, said in a press release.

SOURCE:

This study was led by Matthew J. Lennon, MD, PhD, School of Clinical Medicine, UNSW Sydney, Sydney, Australia. It was published online in Neurology.

LIMITATIONS: 

Varied definitions for hypertension across different locations might have led to discrepancies in diagnosis. Additionally, the study did not account for potential confounders such as stroke, transient ischemic attack, and heart disease, which may act as mediators rather than covariates. Furthermore, the study did not report mortality data, which may have affected the interpretation of dementia risk.

DISCLOSURES:

This research was supported by the National Institute on Aging of the National Institutes of Health. Some authors reported ties with several institutions and pharmaceutical companies outside this work. Full disclosures are available in the original article.

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:

Older adults with untreated hypertension have a 36% increased risk for Alzheimer’s disease (AD) compared with those without hypertension and a 42% increased risk for AD compared with those with treated hypertension.

METHODOLOGY:

• In this meta-analysis, researchers analyzed the data of 31,250 participants aged 60 years or older (mean age, 72.1 years; 41% men) from 14 community-based studies across 14 countries.
• Mean follow-up was 4.2 years, and blood pressure measurements, hypertension diagnosis, and antihypertensive medication use were recorded.
• Overall, 35.9% had no history of hypertension or antihypertensive medication use, 50.7% had a history of hypertension with antihypertensive medication use, and 9.4% had a history of hypertension without antihypertensive medication use.
• The main outcomes were AD and non-AD dementia.

TAKEAWAY:

• In total, 1415 participants developed AD, and 681 developed non-AD dementia.
• Participants with untreated hypertension had a 36% increased risk for AD compared with healthy controls (hazard ratio [HR], 1.36; P = .041) and a 42% increased risk for AD (HR, 1.42; P = .013) compared with those with treated hypertension.
• Compared with healthy controls, patients with treated hypertension did not show an elevated risk for AD (HR, 0.961; P = .6644).
• Patients with both treated (HR, 1.285; P = .027) and untreated (HR, 1.693; P = .003) hypertension had an increased risk for non-AD dementia compared with healthy controls. Patients with treated and untreated hypertension had a similar risk for non-AD dementia.

IN PRACTICE:

“These results suggest that treating high blood pressure as a person ages continues to be a crucial factor in reducing their risk of Alzheimer’s disease,” the lead author Matthew J. Lennon, MD, PhD, said in a press release.

SOURCE:

This study was led by Matthew J. Lennon, MD, PhD, School of Clinical Medicine, UNSW Sydney, Sydney, Australia. It was published online in Neurology.

LIMITATIONS: 

Varied definitions for hypertension across different locations might have led to discrepancies in diagnosis. Additionally, the study did not account for potential confounders such as stroke, transient ischemic attack, and heart disease, which may act as mediators rather than covariates. Furthermore, the study did not report mortality data, which may have affected the interpretation of dementia risk.

DISCLOSURES:

This research was supported by the National Institute on Aging of the National Institutes of Health. Some authors reported ties with several institutions and pharmaceutical companies outside this work. Full disclosures are available in the original article.

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:

Older adults with untreated hypertension have a 36% increased risk for Alzheimer’s disease (AD) compared with those without hypertension and a 42% increased risk for AD compared with those with treated hypertension.

METHODOLOGY:

• In this meta-analysis, researchers analyzed the data of 31,250 participants aged 60 years or older (mean age, 72.1 years; 41% men) from 14 community-based studies across 14 countries.
• Mean follow-up was 4.2 years, and blood pressure measurements, hypertension diagnosis, and antihypertensive medication use were recorded.
• Overall, 35.9% had no history of hypertension or antihypertensive medication use, 50.7% had a history of hypertension with antihypertensive medication use, and 9.4% had a history of hypertension without antihypertensive medication use.
• The main outcomes were AD and non-AD dementia.

TAKEAWAY:

• In total, 1415 participants developed AD, and 681 developed non-AD dementia.
• Participants with untreated hypertension had a 36% increased risk for AD compared with healthy controls (hazard ratio [HR], 1.36; P = .041) and a 42% increased risk for AD (HR, 1.42; P = .013) compared with those with treated hypertension.
• Compared with healthy controls, patients with treated hypertension did not show an elevated risk for AD (HR, 0.961; P = .6644).
• Patients with both treated (HR, 1.285; P = .027) and untreated (HR, 1.693; P = .003) hypertension had an increased risk for non-AD dementia compared with healthy controls. Patients with treated and untreated hypertension had a similar risk for non-AD dementia.

IN PRACTICE:

“These results suggest that treating high blood pressure as a person ages continues to be a crucial factor in reducing their risk of Alzheimer’s disease,” the lead author Matthew J. Lennon, MD, PhD, said in a press release.

SOURCE:

This study was led by Matthew J. Lennon, MD, PhD, School of Clinical Medicine, UNSW Sydney, Sydney, Australia. It was published online in Neurology.

LIMITATIONS: 

Varied definitions for hypertension across different locations might have led to discrepancies in diagnosis. Additionally, the study did not account for potential confounders such as stroke, transient ischemic attack, and heart disease, which may act as mediators rather than covariates. Furthermore, the study did not report mortality data, which may have affected the interpretation of dementia risk.

DISCLOSURES:

This research was supported by the National Institute on Aging of the National Institutes of Health. Some authors reported ties with several institutions and pharmaceutical companies outside this work. Full disclosures are available in the original article.

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:

Compared with dipeptidyl peptidase 4 (DPP-4) inhibitors, glucagon-like peptide 1 receptor agonists (GLP-1 RAs) are associated with a lower risk for all-cause mortality and major adverse cardiovascular events (MACE) in patients with immune-mediated inflammatory diseases (IMIDs) and type 2 diabetes (T2D).

METHODOLOGY:

• GLP-1 RAs reduce the risk for all-cause mortality, cardiovascular mortality, and stroke in patients with diabetes. However, previous trials have excluded those with IMIDs, leaving a gap in understanding the cardioprotective effects of GLP-1 RAs in this population.
• Researchers conducted a population-based cohort study to assess if patients with an IMID derive greater benefits from GLP-1 RAs than DPP-4 inhibitors.
• They used administrative health data from British Columbia, Canada, to include 10,855 patients with IMIDs (rheumatoid arthritis, psoriatic disease, ankylosing spondylitis, inflammatory bowel disease, or systemic autoimmune rheumatic disease) and T2D who initiated either GLP-1 RA (n = 3570) or DPP-4 inhibitor (n = 7285).
• The mean follow-up was 1.46 and 1.88 years in the GLP-1 RA and DPP-4 inhibitor cohorts, respectively.
• The primary outcome was all-cause mortality, and the secondary outcome was MACE, including cardiovascular death, myocardial infarction, and ischemic stroke.

TAKEAWAY:

• The risk for all-cause mortality was 52% lower in patients who initiated GLP-1 RAs than in those who initiated DPP-4 inhibitors (weighted hazard ratio [HR], 0.48; 95% CI, 0.31-0.75).
• Additionally, patients initiating DPP-4 inhibitors.
• In the subgroup of patients with GLP-1 RAs had a significantly lower risk for MACE (weighted HR, 0.66; 95% CI, 0.50-0.88), particularly myocardial infarction (weighted HR, 0.62; 95% CI, 0.40-0.96), than those initiating rheumatoid arthritis and T2D, those who initiated GLP-1 RAs had a 55% lower risk for all-cause mortality and 61% lower risk for MACE than those who initiated DPP-4 inhibitors.

IN PRACTICE:

“This corresponds to nine fewer deaths and 11 fewer MACE per 1000 person-years, respectively, supporting the hypothesis that these agents have a cardioprotective effect in this high-risk population,” the authors wrote.

SOURCE:

This study was led by Derin Karacabeyli, MD, Division of Rheumatology, Department of Medicine, University of British Columbia, Vancouver, Canada, and was published online on August 8, 2024, in PLOS ONE.

LIMITATIONS:

The study’s dependence on administrative health data might have resulted in incomplete capture of comorbidities, particularly obesity. The mean follow-up period was relatively short, which might have limited the long-term applicability of these findings. The accuracy of the case definitions for IMIDs and T2D, according to International Classification of Diseases codes, could not be fully ascertained.

DISCLOSURES:

The study was supported by grants from the Canadian Institutes of Health Research. Two authors declared receiving research support, consulting fees, or participating in advisory boards outside the submitted work.

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:

Compared with dipeptidyl peptidase 4 (DPP-4) inhibitors, glucagon-like peptide 1 receptor agonists (GLP-1 RAs) are associated with a lower risk for all-cause mortality and major adverse cardiovascular events (MACE) in patients with immune-mediated inflammatory diseases (IMIDs) and type 2 diabetes (T2D).

METHODOLOGY:

• GLP-1 RAs reduce the risk for all-cause mortality, cardiovascular mortality, and stroke in patients with diabetes. However, previous trials have excluded those with IMIDs, leaving a gap in understanding the cardioprotective effects of GLP-1 RAs in this population.
• Researchers conducted a population-based cohort study to assess if patients with an IMID derive greater benefits from GLP-1 RAs than DPP-4 inhibitors.
• They used administrative health data from British Columbia, Canada, to include 10,855 patients with IMIDs (rheumatoid arthritis, psoriatic disease, ankylosing spondylitis, inflammatory bowel disease, or systemic autoimmune rheumatic disease) and T2D who initiated either GLP-1 RA (n = 3570) or DPP-4 inhibitor (n = 7285).
• The mean follow-up was 1.46 and 1.88 years in the GLP-1 RA and DPP-4 inhibitor cohorts, respectively.
• The primary outcome was all-cause mortality, and the secondary outcome was MACE, including cardiovascular death, myocardial infarction, and ischemic stroke.

TAKEAWAY:

• The risk for all-cause mortality was 52% lower in patients who initiated GLP-1 RAs than in those who initiated DPP-4 inhibitors (weighted hazard ratio [HR], 0.48; 95% CI, 0.31-0.75).
• Additionally, patients initiating DPP-4 inhibitors.
• In the subgroup of patients with GLP-1 RAs had a significantly lower risk for MACE (weighted HR, 0.66; 95% CI, 0.50-0.88), particularly myocardial infarction (weighted HR, 0.62; 95% CI, 0.40-0.96), than those initiating rheumatoid arthritis and T2D, those who initiated GLP-1 RAs had a 55% lower risk for all-cause mortality and 61% lower risk for MACE than those who initiated DPP-4 inhibitors.

IN PRACTICE:

“This corresponds to nine fewer deaths and 11 fewer MACE per 1000 person-years, respectively, supporting the hypothesis that these agents have a cardioprotective effect in this high-risk population,” the authors wrote.

SOURCE:

This study was led by Derin Karacabeyli, MD, Division of Rheumatology, Department of Medicine, University of British Columbia, Vancouver, Canada, and was published online on August 8, 2024, in PLOS ONE.

LIMITATIONS:

The study’s dependence on administrative health data might have resulted in incomplete capture of comorbidities, particularly obesity. The mean follow-up period was relatively short, which might have limited the long-term applicability of these findings. The accuracy of the case definitions for IMIDs and T2D, according to International Classification of Diseases codes, could not be fully ascertained.

DISCLOSURES:

The study was supported by grants from the Canadian Institutes of Health Research. Two authors declared receiving research support, consulting fees, or participating in advisory boards outside the submitted work.

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:

Compared with dipeptidyl peptidase 4 (DPP-4) inhibitors, glucagon-like peptide 1 receptor agonists (GLP-1 RAs) are associated with a lower risk for all-cause mortality and major adverse cardiovascular events (MACE) in patients with immune-mediated inflammatory diseases (IMIDs) and type 2 diabetes (T2D).

METHODOLOGY:

• GLP-1 RAs reduce the risk for all-cause mortality, cardiovascular mortality, and stroke in patients with diabetes. However, previous trials have excluded those with IMIDs, leaving a gap in understanding the cardioprotective effects of GLP-1 RAs in this population.
• Researchers conducted a population-based cohort study to assess if patients with an IMID derive greater benefits from GLP-1 RAs than DPP-4 inhibitors.
• They used administrative health data from British Columbia, Canada, to include 10,855 patients with IMIDs (rheumatoid arthritis, psoriatic disease, ankylosing spondylitis, inflammatory bowel disease, or systemic autoimmune rheumatic disease) and T2D who initiated either GLP-1 RA (n = 3570) or DPP-4 inhibitor (n = 7285).
• The mean follow-up was 1.46 and 1.88 years in the GLP-1 RA and DPP-4 inhibitor cohorts, respectively.
• The primary outcome was all-cause mortality, and the secondary outcome was MACE, including cardiovascular death, myocardial infarction, and ischemic stroke.

TAKEAWAY:

• The risk for all-cause mortality was 52% lower in patients who initiated GLP-1 RAs than in those who initiated DPP-4 inhibitors (weighted hazard ratio [HR], 0.48; 95% CI, 0.31-0.75).
• Additionally, patients initiating DPP-4 inhibitors.
• In the subgroup of patients with GLP-1 RAs had a significantly lower risk for MACE (weighted HR, 0.66; 95% CI, 0.50-0.88), particularly myocardial infarction (weighted HR, 0.62; 95% CI, 0.40-0.96), than those initiating rheumatoid arthritis and T2D, those who initiated GLP-1 RAs had a 55% lower risk for all-cause mortality and 61% lower risk for MACE than those who initiated DPP-4 inhibitors.

IN PRACTICE:

“This corresponds to nine fewer deaths and 11 fewer MACE per 1000 person-years, respectively, supporting the hypothesis that these agents have a cardioprotective effect in this high-risk population,” the authors wrote.

SOURCE:

This study was led by Derin Karacabeyli, MD, Division of Rheumatology, Department of Medicine, University of British Columbia, Vancouver, Canada, and was published online on August 8, 2024, in PLOS ONE.

LIMITATIONS:

The study’s dependence on administrative health data might have resulted in incomplete capture of comorbidities, particularly obesity. The mean follow-up period was relatively short, which might have limited the long-term applicability of these findings. The accuracy of the case definitions for IMIDs and T2D, according to International Classification of Diseases codes, could not be fully ascertained.

DISCLOSURES:

The study was supported by grants from the Canadian Institutes of Health Research. Two authors declared receiving research support, consulting fees, or participating in advisory boards outside the submitted work.

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.

Take a look at any of the evidence-based US obesity treatment guidelines. The key criteria for diagnosing overweight and obesity is based on the body mass index (BMI). 

The guidelines also use BMI to stratify care options to decrease cardiovascular risk. For example, persons with BMI ≥30 are classified as having obesity, and antiobesity medications are recommended. Those with BMI ≥ 40 are classified as having severe obesity, and metabolic bariatric surgery may be appropriate. 

But where did these cutoff points for more and less aggressive treatments come from? These BMI cutoffs are based primarily on mortality data collected from large non-Hispanic White populations, without data on potential differences by gender and ethnicity. In fact, by itself, BMI is an incomplete measure of cardiometabolic risk, especially in a multiethnic clinic with all genders represented.

For example, it is certainly true that those with BMI ≥ 30 have more cardiovascular risk factors than those with BMI < 30. But Asian American individuals have more risk factors at lower BMIs than do White or African American individuals likely because of more visceral fat accumulation at lower BMIs.

Besides the variation in gender and ethnicity, BMI does not take the type and location of body fat into consideration. Adipose tissue in visceral or ectopic areas have much higher risks for disease than subcutaneous adipose tissue because of the associated inflammation. Measures such as waist circumference, waist-to-hip ratio, and skinfold measurements aim to capture this aspect but often fall short because of variation in techniques.

BMI does not account for muscle mass either, so fit athletes and bodybuilders can be classified as having obesity by BMI alone. More accurate body fat percent measures, such as dual-energy X-ray absorptiometry or MRI specifically for ectopic fat, are labor intensive, expensive, and not feasible to perform in a busy primary care or endocrinology clinic.
 

Assessing Risks From Obesity Beyond BMI

Clearly, better risk measures than BMI are needed, but until they are available, supplemental clinical tools can aid diagnosis and treatment decisions at obesity medicine specialty centers, endocrinology and diabetes centers, and those centers that focus on the treatment of obesity.

For example, a seca scale can measure percent body fat by bioelectric impedance analysis. This technique also has its limitations, but for persons who are well hydrated, it can be used as a baseline to determine efficacy of behavioral interventions, such as resistance-exercise training and a high-protein diet to protect muscle mass as the patient loses weight.

A lot also can be gleaned from diet and exercise history, social history, family history, and physical exam as well as laboratory analyses. For example, an Asian American patient with a BMI of 26 who has been gaining weight mostly in the abdominal region after age 35 years is likely to have cardiometabolic risk, and a family history can solidify that. An exam can show signs of acanthosis nigricans or an enlarged liver and generous abdominal adipose tissue. This would be the patient in whom you would want to obtain a hemoglobin A1c measurement in the chance that it is elevated at > 5.7 mg/dL, suggesting high risk for type 2 diabetes. 

A Fibrosis-4 score can assess the risk for liver disease from aspartate transaminase and alanine aminotransferase and platelet count and age, providing clues to cardiometabolic disease risk.

In the next 10, years there may be a better measure for cardiometabolic risk that is more accurate than BMI is. It could be the sagittal abdominal diameter, which has been purported to more accurately measure visceral abdominal fat. But this has not made it to be one of the vital signs in a busy primary care clinic, however. 
 

Will New Body Fat Tools Change Practice?

In the next 10 years, there may be an affordable gadget to scan the body to determine visceral vs subcutaneous deposition of fat — like radiography for tissue. Now, three-dimensional (3D) total-body scanners can obtain body composition, but they are extremely expensive. The more important clinical question is: How will the use of these imaging modalities change your practice protocol for a particular patient? 

Think about the FibroScan, a type of ultrasound used to determine fatty liver disease and fibrosis. We order the test for those patients in whom we already have a strong suspicion for liver disease and, in obesity practices, for fatty liver and metabolic-associated fatty liver disease or metabolic associated steatohepatitis.

The test results do much to educate the patient and help the patient understand the need for aggressive treatment for their obesity. But it doesn’t necessarily change the clinician’s practice protocols and decisions. We would still recommend weight management and medications or surgery to patients regardless of the findings. 

A FibroScan is an expense, and not all primary care or endocrine practitioners may feel it necessary to purchase one for the added benefit of patient education. And I would argue that a 3D body scanner is a great tool but more for educational purposes than to really determine practice decision-making or outcomes. 

In the meantime, an old-fashioned physical examination, along with a thorough medical, social, and family history should give even the busiest primary care provider enough information to decide whether their patient is a candidate for preventive measures to reduce body fat with diet, exercise, and medication as well as whether the patient is a candidate for metabolic bariatric surgery. Higher suspicion of cardiovascular risk at lower BMI ranges for various ethnicities can help primary care providers pick up on the patients with low BMI but who are at higher risk for type 2 diabetes or prediabetes and cardiovascular disease. 

So the answer to whether we need a better measure than the BMI: Yes, we do. We need a physical examination on all patients.

Dr. Apovian, professor of medicine, Harvard Medical School, and codirector, Center for Weight Management and Wellness, Brigham and Women’s Hospital, both in Boston, Massachusetts, disclosed ties with Altimmune, CinFina Pharma, Cowen and Company, EPG Communication Holdings, Form Health, Gelesis, L-Nutra, NeuroBo Pharm, Novo, OptumRx, Pain Script, Palatin, Pursuit by You, Roman Health, Xeno, and Riverview School.

A version of this article appeared on Medscape.com.

Take a look at any of the evidence-based US obesity treatment guidelines. The key criteria for diagnosing overweight and obesity is based on the body mass index (BMI). 

The guidelines also use BMI to stratify care options to decrease cardiovascular risk. For example, persons with BMI ≥30 are classified as having obesity, and antiobesity medications are recommended. Those with BMI ≥ 40 are classified as having severe obesity, and metabolic bariatric surgery may be appropriate. 

But where did these cutoff points for more and less aggressive treatments come from? These BMI cutoffs are based primarily on mortality data collected from large non-Hispanic White populations, without data on potential differences by gender and ethnicity. In fact, by itself, BMI is an incomplete measure of cardiometabolic risk, especially in a multiethnic clinic with all genders represented.

For example, it is certainly true that those with BMI ≥ 30 have more cardiovascular risk factors than those with BMI < 30. But Asian American individuals have more risk factors at lower BMIs than do White or African American individuals likely because of more visceral fat accumulation at lower BMIs.

Besides the variation in gender and ethnicity, BMI does not take the type and location of body fat into consideration. Adipose tissue in visceral or ectopic areas have much higher risks for disease than subcutaneous adipose tissue because of the associated inflammation. Measures such as waist circumference, waist-to-hip ratio, and skinfold measurements aim to capture this aspect but often fall short because of variation in techniques.

BMI does not account for muscle mass either, so fit athletes and bodybuilders can be classified as having obesity by BMI alone. More accurate body fat percent measures, such as dual-energy X-ray absorptiometry or MRI specifically for ectopic fat, are labor intensive, expensive, and not feasible to perform in a busy primary care or endocrinology clinic.
 

Assessing Risks From Obesity Beyond BMI

Clearly, better risk measures than BMI are needed, but until they are available, supplemental clinical tools can aid diagnosis and treatment decisions at obesity medicine specialty centers, endocrinology and diabetes centers, and those centers that focus on the treatment of obesity.

For example, a seca scale can measure percent body fat by bioelectric impedance analysis. This technique also has its limitations, but for persons who are well hydrated, it can be used as a baseline to determine efficacy of behavioral interventions, such as resistance-exercise training and a high-protein diet to protect muscle mass as the patient loses weight.

A lot also can be gleaned from diet and exercise history, social history, family history, and physical exam as well as laboratory analyses. For example, an Asian American patient with a BMI of 26 who has been gaining weight mostly in the abdominal region after age 35 years is likely to have cardiometabolic risk, and a family history can solidify that. An exam can show signs of acanthosis nigricans or an enlarged liver and generous abdominal adipose tissue. This would be the patient in whom you would want to obtain a hemoglobin A1c measurement in the chance that it is elevated at > 5.7 mg/dL, suggesting high risk for type 2 diabetes. 

A Fibrosis-4 score can assess the risk for liver disease from aspartate transaminase and alanine aminotransferase and platelet count and age, providing clues to cardiometabolic disease risk.

In the next 10, years there may be a better measure for cardiometabolic risk that is more accurate than BMI is. It could be the sagittal abdominal diameter, which has been purported to more accurately measure visceral abdominal fat. But this has not made it to be one of the vital signs in a busy primary care clinic, however. 
 

Will New Body Fat Tools Change Practice?

In the next 10 years, there may be an affordable gadget to scan the body to determine visceral vs subcutaneous deposition of fat — like radiography for tissue. Now, three-dimensional (3D) total-body scanners can obtain body composition, but they are extremely expensive. The more important clinical question is: How will the use of these imaging modalities change your practice protocol for a particular patient? 

Think about the FibroScan, a type of ultrasound used to determine fatty liver disease and fibrosis. We order the test for those patients in whom we already have a strong suspicion for liver disease and, in obesity practices, for fatty liver and metabolic-associated fatty liver disease or metabolic associated steatohepatitis.

The test results do much to educate the patient and help the patient understand the need for aggressive treatment for their obesity. But it doesn’t necessarily change the clinician’s practice protocols and decisions. We would still recommend weight management and medications or surgery to patients regardless of the findings. 

A FibroScan is an expense, and not all primary care or endocrine practitioners may feel it necessary to purchase one for the added benefit of patient education. And I would argue that a 3D body scanner is a great tool but more for educational purposes than to really determine practice decision-making or outcomes. 

In the meantime, an old-fashioned physical examination, along with a thorough medical, social, and family history should give even the busiest primary care provider enough information to decide whether their patient is a candidate for preventive measures to reduce body fat with diet, exercise, and medication as well as whether the patient is a candidate for metabolic bariatric surgery. Higher suspicion of cardiovascular risk at lower BMI ranges for various ethnicities can help primary care providers pick up on the patients with low BMI but who are at higher risk for type 2 diabetes or prediabetes and cardiovascular disease. 

So the answer to whether we need a better measure than the BMI: Yes, we do. We need a physical examination on all patients.

Dr. Apovian, professor of medicine, Harvard Medical School, and codirector, Center for Weight Management and Wellness, Brigham and Women’s Hospital, both in Boston, Massachusetts, disclosed ties with Altimmune, CinFina Pharma, Cowen and Company, EPG Communication Holdings, Form Health, Gelesis, L-Nutra, NeuroBo Pharm, Novo, OptumRx, Pain Script, Palatin, Pursuit by You, Roman Health, Xeno, and Riverview School.

A version of this article appeared on Medscape.com.

Take a look at any of the evidence-based US obesity treatment guidelines. The key criteria for diagnosing overweight and obesity is based on the body mass index (BMI). 

The guidelines also use BMI to stratify care options to decrease cardiovascular risk. For example, persons with BMI ≥30 are classified as having obesity, and antiobesity medications are recommended. Those with BMI ≥ 40 are classified as having severe obesity, and metabolic bariatric surgery may be appropriate. 

But where did these cutoff points for more and less aggressive treatments come from? These BMI cutoffs are based primarily on mortality data collected from large non-Hispanic White populations, without data on potential differences by gender and ethnicity. In fact, by itself, BMI is an incomplete measure of cardiometabolic risk, especially in a multiethnic clinic with all genders represented.

For example, it is certainly true that those with BMI ≥ 30 have more cardiovascular risk factors than those with BMI < 30. But Asian American individuals have more risk factors at lower BMIs than do White or African American individuals likely because of more visceral fat accumulation at lower BMIs.

Besides the variation in gender and ethnicity, BMI does not take the type and location of body fat into consideration. Adipose tissue in visceral or ectopic areas have much higher risks for disease than subcutaneous adipose tissue because of the associated inflammation. Measures such as waist circumference, waist-to-hip ratio, and skinfold measurements aim to capture this aspect but often fall short because of variation in techniques.

BMI does not account for muscle mass either, so fit athletes and bodybuilders can be classified as having obesity by BMI alone. More accurate body fat percent measures, such as dual-energy X-ray absorptiometry or MRI specifically for ectopic fat, are labor intensive, expensive, and not feasible to perform in a busy primary care or endocrinology clinic.
 

Assessing Risks From Obesity Beyond BMI

Clearly, better risk measures than BMI are needed, but until they are available, supplemental clinical tools can aid diagnosis and treatment decisions at obesity medicine specialty centers, endocrinology and diabetes centers, and those centers that focus on the treatment of obesity.

For example, a seca scale can measure percent body fat by bioelectric impedance analysis. This technique also has its limitations, but for persons who are well hydrated, it can be used as a baseline to determine efficacy of behavioral interventions, such as resistance-exercise training and a high-protein diet to protect muscle mass as the patient loses weight.

A lot also can be gleaned from diet and exercise history, social history, family history, and physical exam as well as laboratory analyses. For example, an Asian American patient with a BMI of 26 who has been gaining weight mostly in the abdominal region after age 35 years is likely to have cardiometabolic risk, and a family history can solidify that. An exam can show signs of acanthosis nigricans or an enlarged liver and generous abdominal adipose tissue. This would be the patient in whom you would want to obtain a hemoglobin A1c measurement in the chance that it is elevated at > 5.7 mg/dL, suggesting high risk for type 2 diabetes. 

A Fibrosis-4 score can assess the risk for liver disease from aspartate transaminase and alanine aminotransferase and platelet count and age, providing clues to cardiometabolic disease risk.

In the next 10, years there may be a better measure for cardiometabolic risk that is more accurate than BMI is. It could be the sagittal abdominal diameter, which has been purported to more accurately measure visceral abdominal fat. But this has not made it to be one of the vital signs in a busy primary care clinic, however. 
 

Will New Body Fat Tools Change Practice?

In the next 10 years, there may be an affordable gadget to scan the body to determine visceral vs subcutaneous deposition of fat — like radiography for tissue. Now, three-dimensional (3D) total-body scanners can obtain body composition, but they are extremely expensive. The more important clinical question is: How will the use of these imaging modalities change your practice protocol for a particular patient? 

Think about the FibroScan, a type of ultrasound used to determine fatty liver disease and fibrosis. We order the test for those patients in whom we already have a strong suspicion for liver disease and, in obesity practices, for fatty liver and metabolic-associated fatty liver disease or metabolic associated steatohepatitis.

The test results do much to educate the patient and help the patient understand the need for aggressive treatment for their obesity. But it doesn’t necessarily change the clinician’s practice protocols and decisions. We would still recommend weight management and medications or surgery to patients regardless of the findings. 

A FibroScan is an expense, and not all primary care or endocrine practitioners may feel it necessary to purchase one for the added benefit of patient education. And I would argue that a 3D body scanner is a great tool but more for educational purposes than to really determine practice decision-making or outcomes. 

In the meantime, an old-fashioned physical examination, along with a thorough medical, social, and family history should give even the busiest primary care provider enough information to decide whether their patient is a candidate for preventive measures to reduce body fat with diet, exercise, and medication as well as whether the patient is a candidate for metabolic bariatric surgery. Higher suspicion of cardiovascular risk at lower BMI ranges for various ethnicities can help primary care providers pick up on the patients with low BMI but who are at higher risk for type 2 diabetes or prediabetes and cardiovascular disease. 

So the answer to whether we need a better measure than the BMI: Yes, we do. We need a physical examination on all patients.

Dr. Apovian, professor of medicine, Harvard Medical School, and codirector, Center for Weight Management and Wellness, Brigham and Women’s Hospital, both in Boston, Massachusetts, disclosed ties with Altimmune, CinFina Pharma, Cowen and Company, EPG Communication Holdings, Form Health, Gelesis, L-Nutra, NeuroBo Pharm, Novo, OptumRx, Pain Script, Palatin, Pursuit by You, Roman Health, Xeno, and Riverview School.

A version of this article appeared on Medscape.com.

An estimated 450,000 US deaths are expected this year from conditions attributed to cigarette smoking. Although the percentage of adults who smoke declined from 21% in 2005 to 11% in 2022, the annual death toll has been stable since 2005 and isn’t expected to decline until 2030, owing to an aging population of current and former smokers.

In 2022, based on a national survey, two thirds of the 28.8 million US adult smokers wanted to quit, and more than half tried quitting on their own or with the help of clinicians, but less than 9% succeeded in kicking the habit. The health benefits of quitting, summarized in a patient education handout from the American Cancer Society, include a lower risk for cancer, diabetes, and cardiovascular disease. Furthermore, the handout states, “quitting smoking can add as much as 10 years to your life, compared to if you continued to smoke.”

For my patients older than age 50 who are lifelong smokers, the qualifier “as much as” can be a sticking point. Although most recognize that continuing to smoke exposes them to greater health risks and are willing to undergo lung cancer screening and receive pneumococcal vaccines, a kind of fatalism frequently sets in. I’ve heard more times than I can recall some version of the declaration, “It’s too late for quitting to make much difference for me.” Many smokers think that once they reach middle age, gains in life expectancy will be too small to be worth the intense effort and multiple failed attempts that are typically required to quit permanently. Until recently, there were few data I could call on to persuade them they were wrong.

In February 2024, Dr. Eo Rin Cho and colleagues pooled data from four national cohort studies (United States, United Kingdom, Norway, and Canada) to calculate mortality differences among current, former, and never smokers aged 20-79 years. Compared with never smokers, lifelong smokers died an average of 12-13 years earlier. However, quitting before age 50 nearly eliminated the excess mortality associated with smoking, and in the 50- to 59-year-old age group, cessation eventually reduced excess mortality by 92%-95%. Better yet, more than half of the benefits occurred within the first 3 years after cessation.

At first glance, these estimates may seem too good to be true. A few months later, though, a different research group, using data from a large cancer prevention study and 2018 US population census and mortality rates, largely confirmed their findings. Dr. Thuy Le and colleagues found that quitting at age 35, 45, 55, 65, or 75 years resulted in average life gains of 8, 5.6, 3.5, 1.7, and 0.7 years, respectively, relative to continuing to smoke. Because no patient is average, the analysis also presented some helpful probabilities. For example, a smoker who quits at age 65 has about a 1 in 4 chance of gaining at least 1 full year of life and a 1 in 6 chance of gaining at least 4 years. In other words, from a life expectancy perspective alone, it’s almost never too late to quit smoking.

Dr. Lin is a family physician and Associate Director, Family Medicine Residency Program, Lancaster General Hospital, Lancaster, Pennsylvania. He blogs at Common Sense Family Doctor. He has disclosed no relevant financial relationships.

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

An estimated 450,000 US deaths are expected this year from conditions attributed to cigarette smoking. Although the percentage of adults who smoke declined from 21% in 2005 to 11% in 2022, the annual death toll has been stable since 2005 and isn’t expected to decline until 2030, owing to an aging population of current and former smokers.

In 2022, based on a national survey, two thirds of the 28.8 million US adult smokers wanted to quit, and more than half tried quitting on their own or with the help of clinicians, but less than 9% succeeded in kicking the habit. The health benefits of quitting, summarized in a patient education handout from the American Cancer Society, include a lower risk for cancer, diabetes, and cardiovascular disease. Furthermore, the handout states, “quitting smoking can add as much as 10 years to your life, compared to if you continued to smoke.”

For my patients older than age 50 who are lifelong smokers, the qualifier “as much as” can be a sticking point. Although most recognize that continuing to smoke exposes them to greater health risks and are willing to undergo lung cancer screening and receive pneumococcal vaccines, a kind of fatalism frequently sets in. I’ve heard more times than I can recall some version of the declaration, “It’s too late for quitting to make much difference for me.” Many smokers think that once they reach middle age, gains in life expectancy will be too small to be worth the intense effort and multiple failed attempts that are typically required to quit permanently. Until recently, there were few data I could call on to persuade them they were wrong.

In February 2024, Dr. Eo Rin Cho and colleagues pooled data from four national cohort studies (United States, United Kingdom, Norway, and Canada) to calculate mortality differences among current, former, and never smokers aged 20-79 years. Compared with never smokers, lifelong smokers died an average of 12-13 years earlier. However, quitting before age 50 nearly eliminated the excess mortality associated with smoking, and in the 50- to 59-year-old age group, cessation eventually reduced excess mortality by 92%-95%. Better yet, more than half of the benefits occurred within the first 3 years after cessation.

At first glance, these estimates may seem too good to be true. A few months later, though, a different research group, using data from a large cancer prevention study and 2018 US population census and mortality rates, largely confirmed their findings. Dr. Thuy Le and colleagues found that quitting at age 35, 45, 55, 65, or 75 years resulted in average life gains of 8, 5.6, 3.5, 1.7, and 0.7 years, respectively, relative to continuing to smoke. Because no patient is average, the analysis also presented some helpful probabilities. For example, a smoker who quits at age 65 has about a 1 in 4 chance of gaining at least 1 full year of life and a 1 in 6 chance of gaining at least 4 years. In other words, from a life expectancy perspective alone, it’s almost never too late to quit smoking.

Dr. Lin is a family physician and Associate Director, Family Medicine Residency Program, Lancaster General Hospital, Lancaster, Pennsylvania. He blogs at Common Sense Family Doctor. He has disclosed no relevant financial relationships.

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

An estimated 450,000 US deaths are expected this year from conditions attributed to cigarette smoking. Although the percentage of adults who smoke declined from 21% in 2005 to 11% in 2022, the annual death toll has been stable since 2005 and isn’t expected to decline until 2030, owing to an aging population of current and former smokers.

In 2022, based on a national survey, two thirds of the 28.8 million US adult smokers wanted to quit, and more than half tried quitting on their own or with the help of clinicians, but less than 9% succeeded in kicking the habit. The health benefits of quitting, summarized in a patient education handout from the American Cancer Society, include a lower risk for cancer, diabetes, and cardiovascular disease. Furthermore, the handout states, “quitting smoking can add as much as 10 years to your life, compared to if you continued to smoke.”

For my patients older than age 50 who are lifelong smokers, the qualifier “as much as” can be a sticking point. Although most recognize that continuing to smoke exposes them to greater health risks and are willing to undergo lung cancer screening and receive pneumococcal vaccines, a kind of fatalism frequently sets in. I’ve heard more times than I can recall some version of the declaration, “It’s too late for quitting to make much difference for me.” Many smokers think that once they reach middle age, gains in life expectancy will be too small to be worth the intense effort and multiple failed attempts that are typically required to quit permanently. Until recently, there were few data I could call on to persuade them they were wrong.

In February 2024, Dr. Eo Rin Cho and colleagues pooled data from four national cohort studies (United States, United Kingdom, Norway, and Canada) to calculate mortality differences among current, former, and never smokers aged 20-79 years. Compared with never smokers, lifelong smokers died an average of 12-13 years earlier. However, quitting before age 50 nearly eliminated the excess mortality associated with smoking, and in the 50- to 59-year-old age group, cessation eventually reduced excess mortality by 92%-95%. Better yet, more than half of the benefits occurred within the first 3 years after cessation.

At first glance, these estimates may seem too good to be true. A few months later, though, a different research group, using data from a large cancer prevention study and 2018 US population census and mortality rates, largely confirmed their findings. Dr. Thuy Le and colleagues found that quitting at age 35, 45, 55, 65, or 75 years resulted in average life gains of 8, 5.6, 3.5, 1.7, and 0.7 years, respectively, relative to continuing to smoke. Because no patient is average, the analysis also presented some helpful probabilities. For example, a smoker who quits at age 65 has about a 1 in 4 chance of gaining at least 1 full year of life and a 1 in 6 chance of gaining at least 4 years. In other words, from a life expectancy perspective alone, it’s almost never too late to quit smoking.

Dr. Lin is a family physician and Associate Director, Family Medicine Residency Program, Lancaster General Hospital, Lancaster, Pennsylvania. He blogs at Common Sense Family Doctor. He has disclosed no relevant financial relationships.

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

In 2016, medical device giant Abbott issued a recall for its MitraClip cardiac device — “a Class I recall, the most serious type,” the FDA said.

“Use of this device may cause serious injuries or death,” an FDA notice about the recall said.

But neither the manufacturer nor the FDA actually recalled the device or suspended its use. They allowed doctors to continue implanting the clips in leaky heart valves in what has become a common procedure.

In a notice, the manufacturer explained, “Abbott is not removing product from commercial distribution.” Rather, Abbott revised instructions for use and required doctors who implant the clips to undergo training.

When it comes to medical devices, recalls can include not only “removals,” in which the device is removed from where it is used or sold, but also “corrections,” which address the problem in the field — for instance, by repairing, adjusting, relabeling, or inspecting a device.

“It’s very oxymoronic,” said Rita Redberg, a cardiologist at the University of California-San Francisco and former editor-in-chief of the journal JAMA Internal Medicine. “A recall makes it sound like it’s recalled. But that is not actually what it means.”

Though the FDA and federal regulations call these actions recalls, they might be described more aptly as “non-recalls.” And they have happened repeatedly in recent years. For instance, in addition to other Abbott devices, products made by Medtronic, Abiomed, and Getinge have had recalls that left them in use.
 

Safeguarding the Public

Recalls that leave what the FDA identifies as potentially dangerous products in the marketplace can raise the question: Do they do enough to protect the public?

There are other ways to handle recalls. In announcements about products as varied as crib bumpers, pool drain covers, bicycle helmets, and coffee mugs, the Consumer Product Safety Commission routinely alerts consumers to stop using recalled products and contact the manufacturers for refunds, repairs, or replacements. The National Highway Traffic Safety Administration regularly advises consumers to bring recalled cars back to the dealer to have them fixed. When the U.S. Department of Agriculture and the FDA announce food recalls, they routinely tell consumers to return or discard the food.

In some cases, a medical device that is the subject of a recall can be kept on the market safely because there is a simple fix, said Sanket Dhruva, a cardiologist and an associate professor at UCSF who has studied FDA oversight of devices. In other cases, recalls that don’t remove devices from the market can provide unwarranted reassurance and leave the public at risk, Dhruva said.

From 2019 through 2023, there were 338 Class I medical device recalls, 164 of which were corrections and 174 of which were removals, FDA spokesperson Amanda Hils said.

Some products undergo recall after recall while they remain on the market. Products in the MitraClip line have been the subject of three rounds of recalls, none of which removed devices from use.

“When deciding whether a recall warrants device removal from the field, the FDA considers the frequency and severity of adverse events, effectiveness of the corrective actions that have been executed, and the benefits and risks of preserving patient access to the device,” FDA spokesperson Audra Harrison said.

Where recalled devices have already been implanted, “removal” doesn’t necessarily mean removing them from patients’ bodies. “When an implanted device has the potential to fail unexpectedly, companies often tell doctors to contact their patients to discuss the risk of removing the device compared to the risk of leaving it in place,” the FDA website says.

The FDA allowed the recalled MitraClip devices to remain in use “because the agency believed that the overall benefits of the device continued to outweigh the risks and the firm’s recall strategy was appropriate and adequate,” Harrison said.

The FDA reviews the recall strategies that manufacturers propose and often provides input to ensure the public will be protected, Hils said. The agency also monitors the effectiveness of recalls and, before terminating them, makes sure the strategy was carried out, Hils said.

Abbott, the maker of MitraClip, said the device has been proven safe and effective “based on more than 20 years of clinical evidence and has profoundly improved the lives of people living with mitral regurgitation,” a condition in which blood flows backward through the heart’s mitral valve. The condition can lead to heart failure and death.

“With MitraClip, we’re addressing the needs of people with MR who often have no other options,” company spokesperson Brent Tippen said.

Speaking of the MitraClip recalls, Redberg said, “So hard to imagine these are effective actions in protecting patients.”

In 2021, for Medtronic’s StealthStation S7 cranial software, the company and the FDA sent a different message.

StealthStation is an elaborate system of screens and other equipment that guides neurosurgeons using instruments in the brain — for instance, to biopsy or cut out tumors. Drawing from CT scans, MRIs, and other imaging, it’s meant to show the location of the surgical instruments.

In connection with a Class I November 2021 recall, the FDA website said potential inaccuracies in a biopsy depth gauge could result in “life-threatening injury (such as hemorrhage, unintended tissue damage, or permanent neurological injury), which could lead to death.”

The FDA website explained what Medtronic was doing about it.

“The recalling firm will provide a warning and instructional placard to be applied to impacted systems,” the website said. “Until a software update is available, ensure you are following the instructions below to prevent the issue from occurring,” it advised doctors.

In a statement to KFF Health News, Medtronic spokesperson Erika Winkels said the safety and well-being of patients is the company’s primary concern, and certain issues “can be safely and effectively remedied with a correction on site.”

Richard Everson, a neurosurgeon and an assistant professor at UCLA, noted that the 2021 recall allowed doctors to continue using unaffected StealthStation features, a benefit for patients and facilities depending on them.

“But, I mean, then you could ask, ‘Well, why don’t they just disable the view [of the brain] that’s bugged?’” Everson said. “Why would they give you the option of looking at an inaccurate one?”

“That’s kind of a strange solution,” he said.

The FDA lists the 2021 recall as still open, explaining “not all products have been corrected or removed.”

That recall was not the last word on problems with StealthStation. Since then, the manufacturer has submitted adverse event reports to the FDA describing trouble in cases involving various versions of StealthStation.

In a September 2022 case, guidance provided by a StealthStation device was allegedly off the mark, a procedure was aborted, and, when the patient awoke, they “had almost no speech for two days,” according to a Medtronic report. In the report, Medtronic said there was “insufficient information to determine the relationship of the software to the reported issue.”

In a February 2024 case, after brain surgery, an MRI found that the operation “missed the tumor” and that other tissue was removed instead, according to a report Medtronic submitted to the FDA. In the report, Medtronic said that when a company representative tested the system, it performed as intended.

In March 2024, Medtronic recalled versions of StealthStation S8 without removing them from hospitals. The company said at the time that it would provide a software update.

“Software updates are available to correct the anomalies identified in the 2021 S7 and 2024 S8 recalls and are actively being deployed,” Medtronic’s Winkels told KFF Health News in a July email. “While the software updates for the 2021 S7 recall are complete in the US, they remain ongoing in some international regions.”

In June 2023, Abiomed issued an urgent medical device correction for its Impella 2.5 intravascular micro axial blood pump, which supports the heart. In patients with a certain type of replacement heart valve, there was a risk of “destruction of the impeller blades,” which could cause “low flow” and “embolization of the fractured impeller material,” an entry on the FDA website said.

“Clinicians are cautioned to position the Impella system carefully in patients,” the FDA website said, among other instructions.

The updated instructions “provide technical guidance to mitigate the risk of rare complications,” Abiomed spokesperson Ryan Carbain said. There were no product removals and no reports of adverse events “related to product design or manufacturing,” Carbain said.

Another set of medical devices, Cardiosave Hybrid and Rescue Intra-Aortic Balloon Pumps made by Getinge of Sweden, have failed persistently, according to FDA records.

The devices — which are placed in the aorta, a major artery, to assist the heart — were the subject of eight Class I recalls from December 2022 to July 2023. All were corrections rather than removals, a KFF Health News analysis found.

In a May 2024 letter to health care providers, the FDA said that, in the previous 12 months, it had received almost 3,000 adverse event reports related to the balloon pumps. It was referring to reports of malfunctions and cases in which the products might have caused or contributed to a death or injury. Of those, 15 reportedly involved serious injury or death, the FDA said.

During the summer of 2023, the FDA noted that “alternative treatments are limited” and said the devices could continue to be used.

But, in May, the FDA changed its stance. The agency advised health care facilities to “transition away from these devices and seek alternatives, if possible.”

“These recommendations are based on our continued concerns” that the manufacturer “has not sufficiently addressed the problems and risks with these recalled devices.”

Getinge sent KFF Health News written answers from Elin Frostehav, the company’s president of Acute Care Therapies.

“There is no question that we would have liked to have solved these issues in full much earlier,” she said.

As a result of the FDA’s May action, the company “immediately paused proactive marketing” of the balloon pumps in the United States, and it is selling them only to customers who have no alternatives, Frostehav said.

“We are working with the agency to finalize remediation and product update solutions,” Frostehav said.
 

‘Known Possible Complications’

Abbott’s MitraClip system includes tiny clips implanted in the heart’s mitral valve and the equipment used to implant them. The apparatus features a steering mechanism with hand controls and a catheter that is threaded through a major vein, typically from an incision in the groin, to place one or more clips in the heart.

Worldwide, more than 200,000 people have been treated with MitraClip, according to an Abbott website.

The 2016 MitraClip recall described cases in which “the user was unable to separate the implantable Clip from the delivery system.”

In a news release at the time, Abbott said it had “received a small number of reports” in which that happened.

Those cases “resulted in surgical interventions to remove the delivery system or replace the mitral valve, and it is expected that any future similar incidents would also require surgery to correct the problem,” the FDA said in a 2016 notice. “There was one patient death in these cases as a result of severe comorbidities following surgery.”

Years later, something similar happened.

In February 2021, a clip was implanted in an 81-year-old patient but the doctor couldn’t separate the clip from the delivery system, according to a report Abbott filed with the FDA. The patient was transferred to surgery, where the delivery system “had to be cut down in order to detach the clip.”

The patient then underwent an operation to replace the mitral valve, and, hours later, the patient was brought back to surgery to address bleeding, the report said.

The patient “coded” the next day and died from an aortic bleed, the report said.

In the report to the FDA, the manufacturer blamed “case-specific circumstances.”

“Cardiac arrest, hemorrhage and death are listed” in the device instructions “as known possible complications associated with mitraclip procedures,” the company said. “There is no indication of a product issue with respect to manufacture, design or labeling.”

The third MitraClip recall, initiated in September 2022, cited an “increase in clip locking malfunctions.”

Most of the reported malfunctions were not associated with adverse outcomes, the FDA said then. Treatment with MitraClip “remains within the anticipated risk levels,” the company told customers.

As with the two earlier recalls, the third advised doctors to follow the device’s instructions. But the 2022 recall identified a contributing factor: the way the device was made.

“Abbott has identified a contributing cause … as a change in the material properties of one of the Clip locking components,” the company said in a 2022 letter to customers.

“Abbott is working on producing new lots with updated manufacturing processing and raw material,” the company wrote. In the same letter, Abbott told doctors that, in the meantime, they could use the devices they had in stock.

Six days later, a clip opened while locked and a patient died, according to a report the manufacturer submitted to the FDA.

“There is no evidence that death was related to the device but it was likely related to the procedure,” Abbott wrote.

Now, almost two years later, the 2022 recall remains open, according to the FDA website, and “not all products have been corrected or removed.”

KFF Health News data editor Holly K. Hacker contributed to this report.
 

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF — the independent source for health policy research, polling, and journalism.

In 2016, medical device giant Abbott issued a recall for its MitraClip cardiac device — “a Class I recall, the most serious type,” the FDA said.

“Use of this device may cause serious injuries or death,” an FDA notice about the recall said.

But neither the manufacturer nor the FDA actually recalled the device or suspended its use. They allowed doctors to continue implanting the clips in leaky heart valves in what has become a common procedure.

In a notice, the manufacturer explained, “Abbott is not removing product from commercial distribution.” Rather, Abbott revised instructions for use and required doctors who implant the clips to undergo training.

When it comes to medical devices, recalls can include not only “removals,” in which the device is removed from where it is used or sold, but also “corrections,” which address the problem in the field — for instance, by repairing, adjusting, relabeling, or inspecting a device.

“It’s very oxymoronic,” said Rita Redberg, a cardiologist at the University of California-San Francisco and former editor-in-chief of the journal JAMA Internal Medicine. “A recall makes it sound like it’s recalled. But that is not actually what it means.”

Though the FDA and federal regulations call these actions recalls, they might be described more aptly as “non-recalls.” And they have happened repeatedly in recent years. For instance, in addition to other Abbott devices, products made by Medtronic, Abiomed, and Getinge have had recalls that left them in use.
 

Safeguarding the Public

Recalls that leave what the FDA identifies as potentially dangerous products in the marketplace can raise the question: Do they do enough to protect the public?

There are other ways to handle recalls. In announcements about products as varied as crib bumpers, pool drain covers, bicycle helmets, and coffee mugs, the Consumer Product Safety Commission routinely alerts consumers to stop using recalled products and contact the manufacturers for refunds, repairs, or replacements. The National Highway Traffic Safety Administration regularly advises consumers to bring recalled cars back to the dealer to have them fixed. When the U.S. Department of Agriculture and the FDA announce food recalls, they routinely tell consumers to return or discard the food.

In some cases, a medical device that is the subject of a recall can be kept on the market safely because there is a simple fix, said Sanket Dhruva, a cardiologist and an associate professor at UCSF who has studied FDA oversight of devices. In other cases, recalls that don’t remove devices from the market can provide unwarranted reassurance and leave the public at risk, Dhruva said.

From 2019 through 2023, there were 338 Class I medical device recalls, 164 of which were corrections and 174 of which were removals, FDA spokesperson Amanda Hils said.

Some products undergo recall after recall while they remain on the market. Products in the MitraClip line have been the subject of three rounds of recalls, none of which removed devices from use.

“When deciding whether a recall warrants device removal from the field, the FDA considers the frequency and severity of adverse events, effectiveness of the corrective actions that have been executed, and the benefits and risks of preserving patient access to the device,” FDA spokesperson Audra Harrison said.

Where recalled devices have already been implanted, “removal” doesn’t necessarily mean removing them from patients’ bodies. “When an implanted device has the potential to fail unexpectedly, companies often tell doctors to contact their patients to discuss the risk of removing the device compared to the risk of leaving it in place,” the FDA website says.

The FDA allowed the recalled MitraClip devices to remain in use “because the agency believed that the overall benefits of the device continued to outweigh the risks and the firm’s recall strategy was appropriate and adequate,” Harrison said.

The FDA reviews the recall strategies that manufacturers propose and often provides input to ensure the public will be protected, Hils said. The agency also monitors the effectiveness of recalls and, before terminating them, makes sure the strategy was carried out, Hils said.

Abbott, the maker of MitraClip, said the device has been proven safe and effective “based on more than 20 years of clinical evidence and has profoundly improved the lives of people living with mitral regurgitation,” a condition in which blood flows backward through the heart’s mitral valve. The condition can lead to heart failure and death.

“With MitraClip, we’re addressing the needs of people with MR who often have no other options,” company spokesperson Brent Tippen said.

Speaking of the MitraClip recalls, Redberg said, “So hard to imagine these are effective actions in protecting patients.”

In 2021, for Medtronic’s StealthStation S7 cranial software, the company and the FDA sent a different message.

StealthStation is an elaborate system of screens and other equipment that guides neurosurgeons using instruments in the brain — for instance, to biopsy or cut out tumors. Drawing from CT scans, MRIs, and other imaging, it’s meant to show the location of the surgical instruments.

In connection with a Class I November 2021 recall, the FDA website said potential inaccuracies in a biopsy depth gauge could result in “life-threatening injury (such as hemorrhage, unintended tissue damage, or permanent neurological injury), which could lead to death.”

The FDA website explained what Medtronic was doing about it.

“The recalling firm will provide a warning and instructional placard to be applied to impacted systems,” the website said. “Until a software update is available, ensure you are following the instructions below to prevent the issue from occurring,” it advised doctors.

In a statement to KFF Health News, Medtronic spokesperson Erika Winkels said the safety and well-being of patients is the company’s primary concern, and certain issues “can be safely and effectively remedied with a correction on site.”

Richard Everson, a neurosurgeon and an assistant professor at UCLA, noted that the 2021 recall allowed doctors to continue using unaffected StealthStation features, a benefit for patients and facilities depending on them.

“But, I mean, then you could ask, ‘Well, why don’t they just disable the view [of the brain] that’s bugged?’” Everson said. “Why would they give you the option of looking at an inaccurate one?”

“That’s kind of a strange solution,” he said.

The FDA lists the 2021 recall as still open, explaining “not all products have been corrected or removed.”

That recall was not the last word on problems with StealthStation. Since then, the manufacturer has submitted adverse event reports to the FDA describing trouble in cases involving various versions of StealthStation.

In a September 2022 case, guidance provided by a StealthStation device was allegedly off the mark, a procedure was aborted, and, when the patient awoke, they “had almost no speech for two days,” according to a Medtronic report. In the report, Medtronic said there was “insufficient information to determine the relationship of the software to the reported issue.”

In a February 2024 case, after brain surgery, an MRI found that the operation “missed the tumor” and that other tissue was removed instead, according to a report Medtronic submitted to the FDA. In the report, Medtronic said that when a company representative tested the system, it performed as intended.

In March 2024, Medtronic recalled versions of StealthStation S8 without removing them from hospitals. The company said at the time that it would provide a software update.

“Software updates are available to correct the anomalies identified in the 2021 S7 and 2024 S8 recalls and are actively being deployed,” Medtronic’s Winkels told KFF Health News in a July email. “While the software updates for the 2021 S7 recall are complete in the US, they remain ongoing in some international regions.”

In June 2023, Abiomed issued an urgent medical device correction for its Impella 2.5 intravascular micro axial blood pump, which supports the heart. In patients with a certain type of replacement heart valve, there was a risk of “destruction of the impeller blades,” which could cause “low flow” and “embolization of the fractured impeller material,” an entry on the FDA website said.

“Clinicians are cautioned to position the Impella system carefully in patients,” the FDA website said, among other instructions.

The updated instructions “provide technical guidance to mitigate the risk of rare complications,” Abiomed spokesperson Ryan Carbain said. There were no product removals and no reports of adverse events “related to product design or manufacturing,” Carbain said.

Another set of medical devices, Cardiosave Hybrid and Rescue Intra-Aortic Balloon Pumps made by Getinge of Sweden, have failed persistently, according to FDA records.

The devices — which are placed in the aorta, a major artery, to assist the heart — were the subject of eight Class I recalls from December 2022 to July 2023. All were corrections rather than removals, a KFF Health News analysis found.

In a May 2024 letter to health care providers, the FDA said that, in the previous 12 months, it had received almost 3,000 adverse event reports related to the balloon pumps. It was referring to reports of malfunctions and cases in which the products might have caused or contributed to a death or injury. Of those, 15 reportedly involved serious injury or death, the FDA said.

During the summer of 2023, the FDA noted that “alternative treatments are limited” and said the devices could continue to be used.

But, in May, the FDA changed its stance. The agency advised health care facilities to “transition away from these devices and seek alternatives, if possible.”

“These recommendations are based on our continued concerns” that the manufacturer “has not sufficiently addressed the problems and risks with these recalled devices.”

Getinge sent KFF Health News written answers from Elin Frostehav, the company’s president of Acute Care Therapies.

“There is no question that we would have liked to have solved these issues in full much earlier,” she said.

As a result of the FDA’s May action, the company “immediately paused proactive marketing” of the balloon pumps in the United States, and it is selling them only to customers who have no alternatives, Frostehav said.

“We are working with the agency to finalize remediation and product update solutions,” Frostehav said.
 

‘Known Possible Complications’

Abbott’s MitraClip system includes tiny clips implanted in the heart’s mitral valve and the equipment used to implant them. The apparatus features a steering mechanism with hand controls and a catheter that is threaded through a major vein, typically from an incision in the groin, to place one or more clips in the heart.

Worldwide, more than 200,000 people have been treated with MitraClip, according to an Abbott website.

The 2016 MitraClip recall described cases in which “the user was unable to separate the implantable Clip from the delivery system.”

In a news release at the time, Abbott said it had “received a small number of reports” in which that happened.

Those cases “resulted in surgical interventions to remove the delivery system or replace the mitral valve, and it is expected that any future similar incidents would also require surgery to correct the problem,” the FDA said in a 2016 notice. “There was one patient death in these cases as a result of severe comorbidities following surgery.”

Years later, something similar happened.

In February 2021, a clip was implanted in an 81-year-old patient but the doctor couldn’t separate the clip from the delivery system, according to a report Abbott filed with the FDA. The patient was transferred to surgery, where the delivery system “had to be cut down in order to detach the clip.”

The patient then underwent an operation to replace the mitral valve, and, hours later, the patient was brought back to surgery to address bleeding, the report said.

The patient “coded” the next day and died from an aortic bleed, the report said.

In the report to the FDA, the manufacturer blamed “case-specific circumstances.”

“Cardiac arrest, hemorrhage and death are listed” in the device instructions “as known possible complications associated with mitraclip procedures,” the company said. “There is no indication of a product issue with respect to manufacture, design or labeling.”

The third MitraClip recall, initiated in September 2022, cited an “increase in clip locking malfunctions.”

Most of the reported malfunctions were not associated with adverse outcomes, the FDA said then. Treatment with MitraClip “remains within the anticipated risk levels,” the company told customers.

As with the two earlier recalls, the third advised doctors to follow the device’s instructions. But the 2022 recall identified a contributing factor: the way the device was made.

“Abbott has identified a contributing cause … as a change in the material properties of one of the Clip locking components,” the company said in a 2022 letter to customers.

“Abbott is working on producing new lots with updated manufacturing processing and raw material,” the company wrote. In the same letter, Abbott told doctors that, in the meantime, they could use the devices they had in stock.

Six days later, a clip opened while locked and a patient died, according to a report the manufacturer submitted to the FDA.

“There is no evidence that death was related to the device but it was likely related to the procedure,” Abbott wrote.

Now, almost two years later, the 2022 recall remains open, according to the FDA website, and “not all products have been corrected or removed.”

KFF Health News data editor Holly K. Hacker contributed to this report.
 

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF — the independent source for health policy research, polling, and journalism.

In 2016, medical device giant Abbott issued a recall for its MitraClip cardiac device — “a Class I recall, the most serious type,” the FDA said.

“Use of this device may cause serious injuries or death,” an FDA notice about the recall said.

But neither the manufacturer nor the FDA actually recalled the device or suspended its use. They allowed doctors to continue implanting the clips in leaky heart valves in what has become a common procedure.

In a notice, the manufacturer explained, “Abbott is not removing product from commercial distribution.” Rather, Abbott revised instructions for use and required doctors who implant the clips to undergo training.

When it comes to medical devices, recalls can include not only “removals,” in which the device is removed from where it is used or sold, but also “corrections,” which address the problem in the field — for instance, by repairing, adjusting, relabeling, or inspecting a device.

“It’s very oxymoronic,” said Rita Redberg, a cardiologist at the University of California-San Francisco and former editor-in-chief of the journal JAMA Internal Medicine. “A recall makes it sound like it’s recalled. But that is not actually what it means.”

Though the FDA and federal regulations call these actions recalls, they might be described more aptly as “non-recalls.” And they have happened repeatedly in recent years. For instance, in addition to other Abbott devices, products made by Medtronic, Abiomed, and Getinge have had recalls that left them in use.
 

Safeguarding the Public

Recalls that leave what the FDA identifies as potentially dangerous products in the marketplace can raise the question: Do they do enough to protect the public?

There are other ways to handle recalls. In announcements about products as varied as crib bumpers, pool drain covers, bicycle helmets, and coffee mugs, the Consumer Product Safety Commission routinely alerts consumers to stop using recalled products and contact the manufacturers for refunds, repairs, or replacements. The National Highway Traffic Safety Administration regularly advises consumers to bring recalled cars back to the dealer to have them fixed. When the U.S. Department of Agriculture and the FDA announce food recalls, they routinely tell consumers to return or discard the food.

In some cases, a medical device that is the subject of a recall can be kept on the market safely because there is a simple fix, said Sanket Dhruva, a cardiologist and an associate professor at UCSF who has studied FDA oversight of devices. In other cases, recalls that don’t remove devices from the market can provide unwarranted reassurance and leave the public at risk, Dhruva said.

From 2019 through 2023, there were 338 Class I medical device recalls, 164 of which were corrections and 174 of which were removals, FDA spokesperson Amanda Hils said.

Some products undergo recall after recall while they remain on the market. Products in the MitraClip line have been the subject of three rounds of recalls, none of which removed devices from use.

“When deciding whether a recall warrants device removal from the field, the FDA considers the frequency and severity of adverse events, effectiveness of the corrective actions that have been executed, and the benefits and risks of preserving patient access to the device,” FDA spokesperson Audra Harrison said.

Where recalled devices have already been implanted, “removal” doesn’t necessarily mean removing them from patients’ bodies. “When an implanted device has the potential to fail unexpectedly, companies often tell doctors to contact their patients to discuss the risk of removing the device compared to the risk of leaving it in place,” the FDA website says.

The FDA allowed the recalled MitraClip devices to remain in use “because the agency believed that the overall benefits of the device continued to outweigh the risks and the firm’s recall strategy was appropriate and adequate,” Harrison said.

The FDA reviews the recall strategies that manufacturers propose and often provides input to ensure the public will be protected, Hils said. The agency also monitors the effectiveness of recalls and, before terminating them, makes sure the strategy was carried out, Hils said.

Abbott, the maker of MitraClip, said the device has been proven safe and effective “based on more than 20 years of clinical evidence and has profoundly improved the lives of people living with mitral regurgitation,” a condition in which blood flows backward through the heart’s mitral valve. The condition can lead to heart failure and death.

“With MitraClip, we’re addressing the needs of people with MR who often have no other options,” company spokesperson Brent Tippen said.

Speaking of the MitraClip recalls, Redberg said, “So hard to imagine these are effective actions in protecting patients.”

In 2021, for Medtronic’s StealthStation S7 cranial software, the company and the FDA sent a different message.

StealthStation is an elaborate system of screens and other equipment that guides neurosurgeons using instruments in the brain — for instance, to biopsy or cut out tumors. Drawing from CT scans, MRIs, and other imaging, it’s meant to show the location of the surgical instruments.

In connection with a Class I November 2021 recall, the FDA website said potential inaccuracies in a biopsy depth gauge could result in “life-threatening injury (such as hemorrhage, unintended tissue damage, or permanent neurological injury), which could lead to death.”

The FDA website explained what Medtronic was doing about it.

“The recalling firm will provide a warning and instructional placard to be applied to impacted systems,” the website said. “Until a software update is available, ensure you are following the instructions below to prevent the issue from occurring,” it advised doctors.

In a statement to KFF Health News, Medtronic spokesperson Erika Winkels said the safety and well-being of patients is the company’s primary concern, and certain issues “can be safely and effectively remedied with a correction on site.”

Richard Everson, a neurosurgeon and an assistant professor at UCLA, noted that the 2021 recall allowed doctors to continue using unaffected StealthStation features, a benefit for patients and facilities depending on them.

“But, I mean, then you could ask, ‘Well, why don’t they just disable the view [of the brain] that’s bugged?’” Everson said. “Why would they give you the option of looking at an inaccurate one?”

“That’s kind of a strange solution,” he said.

The FDA lists the 2021 recall as still open, explaining “not all products have been corrected or removed.”

That recall was not the last word on problems with StealthStation. Since then, the manufacturer has submitted adverse event reports to the FDA describing trouble in cases involving various versions of StealthStation.

In a September 2022 case, guidance provided by a StealthStation device was allegedly off the mark, a procedure was aborted, and, when the patient awoke, they “had almost no speech for two days,” according to a Medtronic report. In the report, Medtronic said there was “insufficient information to determine the relationship of the software to the reported issue.”

In a February 2024 case, after brain surgery, an MRI found that the operation “missed the tumor” and that other tissue was removed instead, according to a report Medtronic submitted to the FDA. In the report, Medtronic said that when a company representative tested the system, it performed as intended.

In March 2024, Medtronic recalled versions of StealthStation S8 without removing them from hospitals. The company said at the time that it would provide a software update.

“Software updates are available to correct the anomalies identified in the 2021 S7 and 2024 S8 recalls and are actively being deployed,” Medtronic’s Winkels told KFF Health News in a July email. “While the software updates for the 2021 S7 recall are complete in the US, they remain ongoing in some international regions.”

In June 2023, Abiomed issued an urgent medical device correction for its Impella 2.5 intravascular micro axial blood pump, which supports the heart. In patients with a certain type of replacement heart valve, there was a risk of “destruction of the impeller blades,” which could cause “low flow” and “embolization of the fractured impeller material,” an entry on the FDA website said.

“Clinicians are cautioned to position the Impella system carefully in patients,” the FDA website said, among other instructions.

The updated instructions “provide technical guidance to mitigate the risk of rare complications,” Abiomed spokesperson Ryan Carbain said. There were no product removals and no reports of adverse events “related to product design or manufacturing,” Carbain said.

Another set of medical devices, Cardiosave Hybrid and Rescue Intra-Aortic Balloon Pumps made by Getinge of Sweden, have failed persistently, according to FDA records.

The devices — which are placed in the aorta, a major artery, to assist the heart — were the subject of eight Class I recalls from December 2022 to July 2023. All were corrections rather than removals, a KFF Health News analysis found.

In a May 2024 letter to health care providers, the FDA said that, in the previous 12 months, it had received almost 3,000 adverse event reports related to the balloon pumps. It was referring to reports of malfunctions and cases in which the products might have caused or contributed to a death or injury. Of those, 15 reportedly involved serious injury or death, the FDA said.

During the summer of 2023, the FDA noted that “alternative treatments are limited” and said the devices could continue to be used.

But, in May, the FDA changed its stance. The agency advised health care facilities to “transition away from these devices and seek alternatives, if possible.”

“These recommendations are based on our continued concerns” that the manufacturer “has not sufficiently addressed the problems and risks with these recalled devices.”

Getinge sent KFF Health News written answers from Elin Frostehav, the company’s president of Acute Care Therapies.

“There is no question that we would have liked to have solved these issues in full much earlier,” she said.

As a result of the FDA’s May action, the company “immediately paused proactive marketing” of the balloon pumps in the United States, and it is selling them only to customers who have no alternatives, Frostehav said.

“We are working with the agency to finalize remediation and product update solutions,” Frostehav said.
 

‘Known Possible Complications’

Abbott’s MitraClip system includes tiny clips implanted in the heart’s mitral valve and the equipment used to implant them. The apparatus features a steering mechanism with hand controls and a catheter that is threaded through a major vein, typically from an incision in the groin, to place one or more clips in the heart.

Worldwide, more than 200,000 people have been treated with MitraClip, according to an Abbott website.

The 2016 MitraClip recall described cases in which “the user was unable to separate the implantable Clip from the delivery system.”

In a news release at the time, Abbott said it had “received a small number of reports” in which that happened.

Those cases “resulted in surgical interventions to remove the delivery system or replace the mitral valve, and it is expected that any future similar incidents would also require surgery to correct the problem,” the FDA said in a 2016 notice. “There was one patient death in these cases as a result of severe comorbidities following surgery.”

Years later, something similar happened.

In February 2021, a clip was implanted in an 81-year-old patient but the doctor couldn’t separate the clip from the delivery system, according to a report Abbott filed with the FDA. The patient was transferred to surgery, where the delivery system “had to be cut down in order to detach the clip.”

The patient then underwent an operation to replace the mitral valve, and, hours later, the patient was brought back to surgery to address bleeding, the report said.

The patient “coded” the next day and died from an aortic bleed, the report said.

In the report to the FDA, the manufacturer blamed “case-specific circumstances.”

“Cardiac arrest, hemorrhage and death are listed” in the device instructions “as known possible complications associated with mitraclip procedures,” the company said. “There is no indication of a product issue with respect to manufacture, design or labeling.”

The third MitraClip recall, initiated in September 2022, cited an “increase in clip locking malfunctions.”

Most of the reported malfunctions were not associated with adverse outcomes, the FDA said then. Treatment with MitraClip “remains within the anticipated risk levels,” the company told customers.

As with the two earlier recalls, the third advised doctors to follow the device’s instructions. But the 2022 recall identified a contributing factor: the way the device was made.

“Abbott has identified a contributing cause … as a change in the material properties of one of the Clip locking components,” the company said in a 2022 letter to customers.

“Abbott is working on producing new lots with updated manufacturing processing and raw material,” the company wrote. In the same letter, Abbott told doctors that, in the meantime, they could use the devices they had in stock.

Six days later, a clip opened while locked and a patient died, according to a report the manufacturer submitted to the FDA.

“There is no evidence that death was related to the device but it was likely related to the procedure,” Abbott wrote.

Now, almost two years later, the 2022 recall remains open, according to the FDA website, and “not all products have been corrected or removed.”

KFF Health News data editor Holly K. Hacker contributed to this report.
 

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF — the independent source for health policy research, polling, and journalism.