CAD & Atherosclerosis

International experts have created recommendations on ways to improve adherence to statin therapy by offering doctors guidance on how to distinguish between true side effects of statins and those arising due to patients’ expectations of side effects.

A position paper from the International Lipid Expert Panel (ILEP), a group of over 70 experts worldwide, provides a step-by-step approach to diagnosing and managing symptoms, such as muscle aches, and encourages patients to continue the statin therapy they have been prescribed.

The authors described in their paper, published in the Journal of Cachexia, Sarcopenia, and Muscle, how statins are among the most commonly prescribed drugs globally, with “strong and unambiguous evidence” that statin treatment makes a significant difference in preventing cardiovascular disease and dying from it.

They said how, although a recent meta-analysis showed the prevalence of statin intolerance is less than 10%, “as many as 1 in 2 patients stop taking statins, reduce the dose, or take them irregularly because they believe they are responsible for side effects.”

In addition to misattribution of aches and pains, a substantial proportion of statin-associated muscle symptoms (SAMS) result from the action of taking medicines and the expectation that medicines cause side effects. A systematic review of trials estimated that between 38% and 78% of SAMS-related statin intolerance could be attributed to expectation alone.
 

Nocebo/drucebo effect

President of the ILEP, Professor Maciej Banach, of the Medical University of Lodz and the University of Zielona Góra, both in Poland, who originated these recommendations, said: “There is an enormous worldwide problem with diagnosing statin intolerance correctly. In addition, we know that most diagnosed statin side effects should not, in fact, be attributed to statin therapy.”

He highlighted how as much as 70% of statin side effect symptoms may be due to a psychological phenomenon called the “nocebo” or “drucebo” effect.

“The ‘nocebo/drucebo’ effect is when patients’ expectations that they will experience side effects from the statins result in them actually experiencing these symptoms,” Professor Banach explained. Knowledge gained from the internet, leaflets, friends and family, and other sources, for example, about the most common side effects – muscle pain and liver complaints – can “result in them discontinuing their therapy and, therefore, increasing their risk of heart problems, stroke, and death,” he cautioned.

First author of the paper, Dr. Peter Penson, a reader in Cardiovascular Pharmacology at Liverpool John Moores University, England, said “the benefits of statins are not seen immediately by patients, whilst the associated adverse effects are more tangible, and so many patients stop taking statins, thereby putting themselves at risk of serious illness or death.”
 

A practical evidence-based guide

The authors expressed hope that their recommendations would help doctors improve patient-centered care for those patients at risk of cardiovascular disease and help these patients understand the reason for their treatment, the benefits, including that statins may prolong their lives, and the potential harms, thus enabling the patient to “make a fully informed decision about commencing and continuing therapy.”

The recommendations include:

• That health care professionals should consider the nocebo/drucebo effect when they first prescribe statins and provide information to patients about the rationale and benefits of the therapy
• The Personalized Lipid Intervention Plan (PLIP) should be used to help this process. It estimates the patient’s 10-year risk of cardiovascular disease with and without statin therapy, as well as providing clear information on adverse side effects, including that muscle symptoms are common but rarely caused by statins
• How to effectively diagnose statin intolerance and exclude nocebo/drucebo effect
• Routine follow-up to check the safety and efficacy of the therapy is recommended, and strategies for managing patients with complete statin intolerance are provided, within the recommendations. Also offered is advice about improving adherence to statin therapy and suggestions for the identification and management of the “relatively small number of patients who have true statin intolerance.”

Dr. Penson emphasized how this was the first paper to deal explicitly with the nocebo/drucebo effect and offers “practical and evidence-based suggestions” to help support individuals who are at risk of cardiovascular disease but who experience adverse effects attributable to their medicines. He added how the PLIP summarizes important lifestyle advice to help patients reduce their risk of heart attacks and strokes and also discusses the evidence for non-statin drugs that can be used to lower cholesterol.

Dr. Penson pointed out how “the vast majority of patients can take statins safely and that the benefits greatly outweigh the potential risk of side effects” and, therefore, an individual’s risk of heart problems, stroke, and death, can be reduced.

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

International experts have created recommendations on ways to improve adherence to statin therapy by offering doctors guidance on how to distinguish between true side effects of statins and those arising due to patients’ expectations of side effects.

A position paper from the International Lipid Expert Panel (ILEP), a group of over 70 experts worldwide, provides a step-by-step approach to diagnosing and managing symptoms, such as muscle aches, and encourages patients to continue the statin therapy they have been prescribed.

The authors described in their paper, published in the Journal of Cachexia, Sarcopenia, and Muscle, how statins are among the most commonly prescribed drugs globally, with “strong and unambiguous evidence” that statin treatment makes a significant difference in preventing cardiovascular disease and dying from it.

They said how, although a recent meta-analysis showed the prevalence of statin intolerance is less than 10%, “as many as 1 in 2 patients stop taking statins, reduce the dose, or take them irregularly because they believe they are responsible for side effects.”

In addition to misattribution of aches and pains, a substantial proportion of statin-associated muscle symptoms (SAMS) result from the action of taking medicines and the expectation that medicines cause side effects. A systematic review of trials estimated that between 38% and 78% of SAMS-related statin intolerance could be attributed to expectation alone.
 

Nocebo/drucebo effect

President of the ILEP, Professor Maciej Banach, of the Medical University of Lodz and the University of Zielona Góra, both in Poland, who originated these recommendations, said: “There is an enormous worldwide problem with diagnosing statin intolerance correctly. In addition, we know that most diagnosed statin side effects should not, in fact, be attributed to statin therapy.”

He highlighted how as much as 70% of statin side effect symptoms may be due to a psychological phenomenon called the “nocebo” or “drucebo” effect.

“The ‘nocebo/drucebo’ effect is when patients’ expectations that they will experience side effects from the statins result in them actually experiencing these symptoms,” Professor Banach explained. Knowledge gained from the internet, leaflets, friends and family, and other sources, for example, about the most common side effects – muscle pain and liver complaints – can “result in them discontinuing their therapy and, therefore, increasing their risk of heart problems, stroke, and death,” he cautioned.

First author of the paper, Dr. Peter Penson, a reader in Cardiovascular Pharmacology at Liverpool John Moores University, England, said “the benefits of statins are not seen immediately by patients, whilst the associated adverse effects are more tangible, and so many patients stop taking statins, thereby putting themselves at risk of serious illness or death.”
 

A practical evidence-based guide

The authors expressed hope that their recommendations would help doctors improve patient-centered care for those patients at risk of cardiovascular disease and help these patients understand the reason for their treatment, the benefits, including that statins may prolong their lives, and the potential harms, thus enabling the patient to “make a fully informed decision about commencing and continuing therapy.”

The recommendations include:

• That health care professionals should consider the nocebo/drucebo effect when they first prescribe statins and provide information to patients about the rationale and benefits of the therapy
• The Personalized Lipid Intervention Plan (PLIP) should be used to help this process. It estimates the patient’s 10-year risk of cardiovascular disease with and without statin therapy, as well as providing clear information on adverse side effects, including that muscle symptoms are common but rarely caused by statins
• How to effectively diagnose statin intolerance and exclude nocebo/drucebo effect
• Routine follow-up to check the safety and efficacy of the therapy is recommended, and strategies for managing patients with complete statin intolerance are provided, within the recommendations. Also offered is advice about improving adherence to statin therapy and suggestions for the identification and management of the “relatively small number of patients who have true statin intolerance.”

Dr. Penson emphasized how this was the first paper to deal explicitly with the nocebo/drucebo effect and offers “practical and evidence-based suggestions” to help support individuals who are at risk of cardiovascular disease but who experience adverse effects attributable to their medicines. He added how the PLIP summarizes important lifestyle advice to help patients reduce their risk of heart attacks and strokes and also discusses the evidence for non-statin drugs that can be used to lower cholesterol.

Dr. Penson pointed out how “the vast majority of patients can take statins safely and that the benefits greatly outweigh the potential risk of side effects” and, therefore, an individual’s risk of heart problems, stroke, and death, can be reduced.

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

International experts have created recommendations on ways to improve adherence to statin therapy by offering doctors guidance on how to distinguish between true side effects of statins and those arising due to patients’ expectations of side effects.

A position paper from the International Lipid Expert Panel (ILEP), a group of over 70 experts worldwide, provides a step-by-step approach to diagnosing and managing symptoms, such as muscle aches, and encourages patients to continue the statin therapy they have been prescribed.

The authors described in their paper, published in the Journal of Cachexia, Sarcopenia, and Muscle, how statins are among the most commonly prescribed drugs globally, with “strong and unambiguous evidence” that statin treatment makes a significant difference in preventing cardiovascular disease and dying from it.

They said how, although a recent meta-analysis showed the prevalence of statin intolerance is less than 10%, “as many as 1 in 2 patients stop taking statins, reduce the dose, or take them irregularly because they believe they are responsible for side effects.”

In addition to misattribution of aches and pains, a substantial proportion of statin-associated muscle symptoms (SAMS) result from the action of taking medicines and the expectation that medicines cause side effects. A systematic review of trials estimated that between 38% and 78% of SAMS-related statin intolerance could be attributed to expectation alone.
 

Nocebo/drucebo effect

President of the ILEP, Professor Maciej Banach, of the Medical University of Lodz and the University of Zielona Góra, both in Poland, who originated these recommendations, said: “There is an enormous worldwide problem with diagnosing statin intolerance correctly. In addition, we know that most diagnosed statin side effects should not, in fact, be attributed to statin therapy.”

He highlighted how as much as 70% of statin side effect symptoms may be due to a psychological phenomenon called the “nocebo” or “drucebo” effect.

“The ‘nocebo/drucebo’ effect is when patients’ expectations that they will experience side effects from the statins result in them actually experiencing these symptoms,” Professor Banach explained. Knowledge gained from the internet, leaflets, friends and family, and other sources, for example, about the most common side effects – muscle pain and liver complaints – can “result in them discontinuing their therapy and, therefore, increasing their risk of heart problems, stroke, and death,” he cautioned.

First author of the paper, Dr. Peter Penson, a reader in Cardiovascular Pharmacology at Liverpool John Moores University, England, said “the benefits of statins are not seen immediately by patients, whilst the associated adverse effects are more tangible, and so many patients stop taking statins, thereby putting themselves at risk of serious illness or death.”
 

A practical evidence-based guide

The authors expressed hope that their recommendations would help doctors improve patient-centered care for those patients at risk of cardiovascular disease and help these patients understand the reason for their treatment, the benefits, including that statins may prolong their lives, and the potential harms, thus enabling the patient to “make a fully informed decision about commencing and continuing therapy.”

The recommendations include:

• That health care professionals should consider the nocebo/drucebo effect when they first prescribe statins and provide information to patients about the rationale and benefits of the therapy
• The Personalized Lipid Intervention Plan (PLIP) should be used to help this process. It estimates the patient’s 10-year risk of cardiovascular disease with and without statin therapy, as well as providing clear information on adverse side effects, including that muscle symptoms are common but rarely caused by statins
• How to effectively diagnose statin intolerance and exclude nocebo/drucebo effect
• Routine follow-up to check the safety and efficacy of the therapy is recommended, and strategies for managing patients with complete statin intolerance are provided, within the recommendations. Also offered is advice about improving adherence to statin therapy and suggestions for the identification and management of the “relatively small number of patients who have true statin intolerance.”

Dr. Penson emphasized how this was the first paper to deal explicitly with the nocebo/drucebo effect and offers “practical and evidence-based suggestions” to help support individuals who are at risk of cardiovascular disease but who experience adverse effects attributable to their medicines. He added how the PLIP summarizes important lifestyle advice to help patients reduce their risk of heart attacks and strokes and also discusses the evidence for non-statin drugs that can be used to lower cholesterol.

Dr. Penson pointed out how “the vast majority of patients can take statins safely and that the benefits greatly outweigh the potential risk of side effects” and, therefore, an individual’s risk of heart problems, stroke, and death, can be reduced.

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

A new report shows considerable gaps in the awareness, treatment, and control of hypertension in premenopausal women in the United States, with a key driver being regular access to health care.

In a nationally representative sample of women ages 35-54 with no prior cardiovascular disease, the prevalence of hypertension increased 8% from an estimated 15.2 million women between 2011 and 2014 to 16.4 million women between 2015 and 2018.

What’s more, the percentage of women with controlled hypertension dropped over the two time periods from 55% to 50%, which is well below the government’s Million Hearts target of 70%.

Missed opportunities for hypertension control in these premenopausal women were a lack of awareness of their hypertension in 23%, ineffective treatment in 34%, and a lack of health care access in 43%; increasing to 51% in non-Hispanic Black patients and 56% in Hispanic patients.

Notably, lack of health care access affected an estimated 3.1 million women (45%) in 2011-2014 and 3.5 million women (43%) in 2015-2018.

Equally stubborn over the two time periods was the lack of effective treatment, affecting 2.1 million (31%) versus 2.8 million (34%) women, and lack of awareness, affecting 1.6 million (24%) versus 1.9 million (23%) women.

“There’s been no improvement over the past decade, and there is evidence of race/ethnic disparities,” study author Susan Hennessy, PhD, said at the recent Epidemiology, Prevention/Lifestyle & Cardiometabolic Health (EPI|Lifestyle) 2022 conference sponsored by the American Heart Association.

The prevalence of uncontrolled hypertension among non-Hispanic Whites was less than that of the U.S. population, at 44%, and most of the missed opportunities were due to uncontrolled blood pressure (BP), noted Dr. Hennessy, a researcher with the University of California, San Francisco School of Medicine.

However, the uncontrolled prevalence was 54% in non-Hispanic Black women and 66% in Hispanic women. “In both of these subgroups, over half of the missed opportunities occur because these women have no regular access to health care,” she said.

In women who identified as “other,” which includes non-Hispanic Asian and mixed-race populations, the uncontrolled prevalence reached 70%, and the biggest missed opportunity was in those who were untreated.

Raising awareness, empowering women, and delivery of guideline-concordant care will help premenopausal women gain control of their blood pressure, Dr. Hennessy said. “But underpinning all of this is ensuring equitable health care access, because if we fail to get women into the system, then we have no opportunity to help them lower their blood pressure.”

She reminded the audience that cardiovascular disease (CVD) is the number one killer of women in the United States and that CVD risk, mediated through hypertension, increases after menopause. Thus, managing hypertension prior to this life event is an important element of primary prevention of CVD and should be a priority.

Session moderator Sadiya S. Khan, MD, Northwestern University Feinberg School of Medicine, Chicago, told this news organization that the findings should raise “alarm and concern that hypertension is not just a disease of the old but very prevalent in younger women, particularly around the time of pregnancy. And this is a clear driver of maternal morbidity and mortality as well.”

“This idea that patients should ‘Know Your Numbers’ is really important, and we talk a lot about that for hypertension, but if you don’t have a doctor, if you don’t have someone to go to, it’s very hard to know or understand what your numbers mean,” she said. “I think that’s really the main message.”

Speaking to this news organization, Dr. Hennessy said there’s no simple solution to the problem, given that some women are not even in the system, whereas others are not being treated effectively, but that increasing opportunities to screen BP would be a start. That could be through community programs, similar to the Barbershop Hypertension trial, or by making BP devices available for home monitoring.

“Again, this is about empowering ourselves to take some level of control, but, as a system, we have to be able to make it equitable for everyone and make sure they have the right equipment, the right cuff size,” she said. “The disparities arise because of the social determinants of health, so if these women are struggling to put food on the table, they aren’t going to be able to afford a blood pressure cuff.”

During a discussion of the findings, audience members noted that the National Health and Nutrition Examination Survey (NHANES) data used for the analysis were somewhat dated. Dr. Hennessy also pointed out that NHANES blood pressure is measured up to three times during a single visit, which differs from clinical practice, and that responses were based on self-report and thus subject to recall bias.

The sample included 3,343 women aged 35-54 years with no prior cardiovascular disease, representing an estimated 31.6 million American women. Hypertension was defined by a systolic BP of at least 140 mm Hg or a diastolic BP of at least 90 mm Hg or current BP medication use.

The authors and Dr. Khan report no relevant financial relationships.

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

A new report shows considerable gaps in the awareness, treatment, and control of hypertension in premenopausal women in the United States, with a key driver being regular access to health care.

In a nationally representative sample of women ages 35-54 with no prior cardiovascular disease, the prevalence of hypertension increased 8% from an estimated 15.2 million women between 2011 and 2014 to 16.4 million women between 2015 and 2018.

What’s more, the percentage of women with controlled hypertension dropped over the two time periods from 55% to 50%, which is well below the government’s Million Hearts target of 70%.

Missed opportunities for hypertension control in these premenopausal women were a lack of awareness of their hypertension in 23%, ineffective treatment in 34%, and a lack of health care access in 43%; increasing to 51% in non-Hispanic Black patients and 56% in Hispanic patients.

Notably, lack of health care access affected an estimated 3.1 million women (45%) in 2011-2014 and 3.5 million women (43%) in 2015-2018.

Equally stubborn over the two time periods was the lack of effective treatment, affecting 2.1 million (31%) versus 2.8 million (34%) women, and lack of awareness, affecting 1.6 million (24%) versus 1.9 million (23%) women.

“There’s been no improvement over the past decade, and there is evidence of race/ethnic disparities,” study author Susan Hennessy, PhD, said at the recent Epidemiology, Prevention/Lifestyle & Cardiometabolic Health (EPI|Lifestyle) 2022 conference sponsored by the American Heart Association.

The prevalence of uncontrolled hypertension among non-Hispanic Whites was less than that of the U.S. population, at 44%, and most of the missed opportunities were due to uncontrolled blood pressure (BP), noted Dr. Hennessy, a researcher with the University of California, San Francisco School of Medicine.

However, the uncontrolled prevalence was 54% in non-Hispanic Black women and 66% in Hispanic women. “In both of these subgroups, over half of the missed opportunities occur because these women have no regular access to health care,” she said.

In women who identified as “other,” which includes non-Hispanic Asian and mixed-race populations, the uncontrolled prevalence reached 70%, and the biggest missed opportunity was in those who were untreated.

Raising awareness, empowering women, and delivery of guideline-concordant care will help premenopausal women gain control of their blood pressure, Dr. Hennessy said. “But underpinning all of this is ensuring equitable health care access, because if we fail to get women into the system, then we have no opportunity to help them lower their blood pressure.”

She reminded the audience that cardiovascular disease (CVD) is the number one killer of women in the United States and that CVD risk, mediated through hypertension, increases after menopause. Thus, managing hypertension prior to this life event is an important element of primary prevention of CVD and should be a priority.

Session moderator Sadiya S. Khan, MD, Northwestern University Feinberg School of Medicine, Chicago, told this news organization that the findings should raise “alarm and concern that hypertension is not just a disease of the old but very prevalent in younger women, particularly around the time of pregnancy. And this is a clear driver of maternal morbidity and mortality as well.”

“This idea that patients should ‘Know Your Numbers’ is really important, and we talk a lot about that for hypertension, but if you don’t have a doctor, if you don’t have someone to go to, it’s very hard to know or understand what your numbers mean,” she said. “I think that’s really the main message.”

Speaking to this news organization, Dr. Hennessy said there’s no simple solution to the problem, given that some women are not even in the system, whereas others are not being treated effectively, but that increasing opportunities to screen BP would be a start. That could be through community programs, similar to the Barbershop Hypertension trial, or by making BP devices available for home monitoring.

“Again, this is about empowering ourselves to take some level of control, but, as a system, we have to be able to make it equitable for everyone and make sure they have the right equipment, the right cuff size,” she said. “The disparities arise because of the social determinants of health, so if these women are struggling to put food on the table, they aren’t going to be able to afford a blood pressure cuff.”

During a discussion of the findings, audience members noted that the National Health and Nutrition Examination Survey (NHANES) data used for the analysis were somewhat dated. Dr. Hennessy also pointed out that NHANES blood pressure is measured up to three times during a single visit, which differs from clinical practice, and that responses were based on self-report and thus subject to recall bias.

The sample included 3,343 women aged 35-54 years with no prior cardiovascular disease, representing an estimated 31.6 million American women. Hypertension was defined by a systolic BP of at least 140 mm Hg or a diastolic BP of at least 90 mm Hg or current BP medication use.

The authors and Dr. Khan report no relevant financial relationships.

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

A new report shows considerable gaps in the awareness, treatment, and control of hypertension in premenopausal women in the United States, with a key driver being regular access to health care.

In a nationally representative sample of women ages 35-54 with no prior cardiovascular disease, the prevalence of hypertension increased 8% from an estimated 15.2 million women between 2011 and 2014 to 16.4 million women between 2015 and 2018.

What’s more, the percentage of women with controlled hypertension dropped over the two time periods from 55% to 50%, which is well below the government’s Million Hearts target of 70%.

Missed opportunities for hypertension control in these premenopausal women were a lack of awareness of their hypertension in 23%, ineffective treatment in 34%, and a lack of health care access in 43%; increasing to 51% in non-Hispanic Black patients and 56% in Hispanic patients.

Notably, lack of health care access affected an estimated 3.1 million women (45%) in 2011-2014 and 3.5 million women (43%) in 2015-2018.

Equally stubborn over the two time periods was the lack of effective treatment, affecting 2.1 million (31%) versus 2.8 million (34%) women, and lack of awareness, affecting 1.6 million (24%) versus 1.9 million (23%) women.

“There’s been no improvement over the past decade, and there is evidence of race/ethnic disparities,” study author Susan Hennessy, PhD, said at the recent Epidemiology, Prevention/Lifestyle & Cardiometabolic Health (EPI|Lifestyle) 2022 conference sponsored by the American Heart Association.

The prevalence of uncontrolled hypertension among non-Hispanic Whites was less than that of the U.S. population, at 44%, and most of the missed opportunities were due to uncontrolled blood pressure (BP), noted Dr. Hennessy, a researcher with the University of California, San Francisco School of Medicine.

However, the uncontrolled prevalence was 54% in non-Hispanic Black women and 66% in Hispanic women. “In both of these subgroups, over half of the missed opportunities occur because these women have no regular access to health care,” she said.

In women who identified as “other,” which includes non-Hispanic Asian and mixed-race populations, the uncontrolled prevalence reached 70%, and the biggest missed opportunity was in those who were untreated.

Raising awareness, empowering women, and delivery of guideline-concordant care will help premenopausal women gain control of their blood pressure, Dr. Hennessy said. “But underpinning all of this is ensuring equitable health care access, because if we fail to get women into the system, then we have no opportunity to help them lower their blood pressure.”

She reminded the audience that cardiovascular disease (CVD) is the number one killer of women in the United States and that CVD risk, mediated through hypertension, increases after menopause. Thus, managing hypertension prior to this life event is an important element of primary prevention of CVD and should be a priority.

Session moderator Sadiya S. Khan, MD, Northwestern University Feinberg School of Medicine, Chicago, told this news organization that the findings should raise “alarm and concern that hypertension is not just a disease of the old but very prevalent in younger women, particularly around the time of pregnancy. And this is a clear driver of maternal morbidity and mortality as well.”

“This idea that patients should ‘Know Your Numbers’ is really important, and we talk a lot about that for hypertension, but if you don’t have a doctor, if you don’t have someone to go to, it’s very hard to know or understand what your numbers mean,” she said. “I think that’s really the main message.”

Speaking to this news organization, Dr. Hennessy said there’s no simple solution to the problem, given that some women are not even in the system, whereas others are not being treated effectively, but that increasing opportunities to screen BP would be a start. That could be through community programs, similar to the Barbershop Hypertension trial, or by making BP devices available for home monitoring.

“Again, this is about empowering ourselves to take some level of control, but, as a system, we have to be able to make it equitable for everyone and make sure they have the right equipment, the right cuff size,” she said. “The disparities arise because of the social determinants of health, so if these women are struggling to put food on the table, they aren’t going to be able to afford a blood pressure cuff.”

During a discussion of the findings, audience members noted that the National Health and Nutrition Examination Survey (NHANES) data used for the analysis were somewhat dated. Dr. Hennessy also pointed out that NHANES blood pressure is measured up to three times during a single visit, which differs from clinical practice, and that responses were based on self-report and thus subject to recall bias.

The sample included 3,343 women aged 35-54 years with no prior cardiovascular disease, representing an estimated 31.6 million American women. Hypertension was defined by a systolic BP of at least 140 mm Hg or a diastolic BP of at least 90 mm Hg or current BP medication use.

The authors and Dr. Khan report no relevant financial relationships.

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

John Giacomini, MD, has pleaded guilty to one count of abusive sexual contact of a female physician he was supervising, the Department of Justice (DOJ) has announced.

Dr. Giacomini, 73, of Atherton, California, had practiced medicine and cardiology for more than 30 years and served as chief of the cardiology section at the VA Hospital in Palo Alto from 1985 to 2018.

According to the statement from DOJ, starting in the fall of 2017, Dr. Giacomini repeatedly subjected a subordinate doctor to unwanted and unwelcome sexual contact, which included hugging, kissing, and intimate touching while on VA premises.

The victim explicitly told Dr. Giacomini she was not interested in a romantic or sexual relationship with him and forcibly resisted his repeated attempts to kiss her, the statement notes.

The abuse continued, culminating in December 2017 with the incident of abusive sexual contact, the DOJ says.

Afterward, the victim resigned from her position at the VA, citing Dr. Giacomini’s behavior as her principal reason for leaving.

“As a federal employee for well over 30 years, [Dr.] Giacomini was trained throughout his career on the prevention of workplace sexual assault and sexual harassment,” the DOJ says.

“As a supervisor and manager, [Dr.] Giacomini had an obligation to the VA and to his subordinates to prevent workplace sexual harassment and disclose any harassing behavior of which he became aware. He failed to do this,” the DOJ says.

A federal grand jury indicted Dr. Giacomini in March 2020, charging him with one count of abusive sexual contact. Dr. Giacomini has now pleaded guilty to the charge, a felony.

Sentencing is scheduled for July 12. Dr. Giacomini faces a maximum sentence of 2 years in prison, a fine of $250,000, restitution, and supervised release.

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

John Giacomini, MD, has pleaded guilty to one count of abusive sexual contact of a female physician he was supervising, the Department of Justice (DOJ) has announced.

Dr. Giacomini, 73, of Atherton, California, had practiced medicine and cardiology for more than 30 years and served as chief of the cardiology section at the VA Hospital in Palo Alto from 1985 to 2018.

According to the statement from DOJ, starting in the fall of 2017, Dr. Giacomini repeatedly subjected a subordinate doctor to unwanted and unwelcome sexual contact, which included hugging, kissing, and intimate touching while on VA premises.

The victim explicitly told Dr. Giacomini she was not interested in a romantic or sexual relationship with him and forcibly resisted his repeated attempts to kiss her, the statement notes.

The abuse continued, culminating in December 2017 with the incident of abusive sexual contact, the DOJ says.

Afterward, the victim resigned from her position at the VA, citing Dr. Giacomini’s behavior as her principal reason for leaving.

“As a federal employee for well over 30 years, [Dr.] Giacomini was trained throughout his career on the prevention of workplace sexual assault and sexual harassment,” the DOJ says.

“As a supervisor and manager, [Dr.] Giacomini had an obligation to the VA and to his subordinates to prevent workplace sexual harassment and disclose any harassing behavior of which he became aware. He failed to do this,” the DOJ says.

A federal grand jury indicted Dr. Giacomini in March 2020, charging him with one count of abusive sexual contact. Dr. Giacomini has now pleaded guilty to the charge, a felony.

Sentencing is scheduled for July 12. Dr. Giacomini faces a maximum sentence of 2 years in prison, a fine of $250,000, restitution, and supervised release.

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

John Giacomini, MD, has pleaded guilty to one count of abusive sexual contact of a female physician he was supervising, the Department of Justice (DOJ) has announced.

Dr. Giacomini, 73, of Atherton, California, had practiced medicine and cardiology for more than 30 years and served as chief of the cardiology section at the VA Hospital in Palo Alto from 1985 to 2018.

According to the statement from DOJ, starting in the fall of 2017, Dr. Giacomini repeatedly subjected a subordinate doctor to unwanted and unwelcome sexual contact, which included hugging, kissing, and intimate touching while on VA premises.

The victim explicitly told Dr. Giacomini she was not interested in a romantic or sexual relationship with him and forcibly resisted his repeated attempts to kiss her, the statement notes.

The abuse continued, culminating in December 2017 with the incident of abusive sexual contact, the DOJ says.

Afterward, the victim resigned from her position at the VA, citing Dr. Giacomini’s behavior as her principal reason for leaving.

“As a federal employee for well over 30 years, [Dr.] Giacomini was trained throughout his career on the prevention of workplace sexual assault and sexual harassment,” the DOJ says.

“As a supervisor and manager, [Dr.] Giacomini had an obligation to the VA and to his subordinates to prevent workplace sexual harassment and disclose any harassing behavior of which he became aware. He failed to do this,” the DOJ says.

A federal grand jury indicted Dr. Giacomini in March 2020, charging him with one count of abusive sexual contact. Dr. Giacomini has now pleaded guilty to the charge, a felony.

Sentencing is scheduled for July 12. Dr. Giacomini faces a maximum sentence of 2 years in prison, a fine of $250,000, restitution, and supervised release.

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

The risk of cardiovascular (CV) events in patients with psoriatic disease rises with higher levels of two cardiac biomarkers in a manner independent of risk calculated by the Framingham Risk Score (FRS), a longitudinal cohort study has shown. But researchers who conducted the study note that neither of the two biomarkers identified in the study – cardiac troponin I (cTnI) and N-terminal pro-brain-type natriuretic peptide (NT-proBNP) – led to an improvement in predictive performance when combined with the FRS, despite their association with carotid plaque burden.

Psoriasis and psoriatic arthritis are both associated with greater risk of CV morbidity and mortality, partly because of systemic inflammation that leads to atherogenesis. Measures of CV risk such as the FRS rely on traditional measures of CV risk and thus are likely to underestimate the CV event risk of people with psoriatic disease, according to the authors of the new study, published online in Arthritis & Rheumatology. The effort was led by Keith Colaço, MSc; Lihi Eder, MD, PhD; and other researchers affiliated with the University of Toronto.

Alexander Raths/ThinkStock

“We are desperately in need of biomarker science advancement in psoriatic arthritis for a variety of places of guidance: How to choose a medication more accurately for the patient in front of us – that is, getting to be more like oncologists who use biomarkers to pick the best treatment or combination. That’s an important need. A second important need is how to guide clinicians regarding risk prediction for things like persistent, severe disease activity, progressive structural damage from disease, and, in this case, predicting a very common comorbidity that occurs in [psoriasis and] psoriatic arthritis patients,” Philip J. Mease, MD, told this news organization when asked to comment on the study.

Such biomarkers could assist with patient counseling, according to Dr. Mease, who is director of rheumatology research at Swedish Medical Center/Providence St. Joseph Health and is a clinical professor at the University of Washington, both in Seattle. Some patients may struggle with advice to lose weight or adopt lifestyle measures to limit CV risk, and more accurate predictions of risk may serve as further motivation. “It could well be that if you have a biomarker that accurately predicts a coming cataclysm, that it will lead you to redouble your efforts to do whatever it takes to reduce cardiovascular risk,” he said.

Both cTnI and NT-proBNP have been linked to increased CV risk in the general population, but little work has been done in the context of rheumatologic diseases.

The researchers analyzed data from 358 patients seen at the University of Toronto. The mean follow-up was 3.69 years. After adjustment for CV risk factors, lipid-lowering therapy, and creatinine levels, there was an association between cTnI levels and total carotid plaque area (adjusted beta coefficient, 0.21; 95% confidence interval, 0-0.41), but not for levels of NT-proBNP.

Atherosclerosis progressed in 89 participants overall, but multivariate adjustment revealed no significant relationship between progression and cTnI or NT-proBNP levels.

Separately, the researchers analyzed 1,000 individuals with psoriatic arthritis (n = 648) or with psoriasis and no arthritis (n = 352) whom they followed for a mean of 7.1 years after the patients underwent evaluation during 2002-2019. After adjustment for FRS, there was an association between the risk of a CV event and each 1–standard deviation increase in both cTnI (hazard ratio, 3.02; 95% CI, 1.12-8.16) and NT-proBNP (HR, 2.02; 95% CI, 1.28-3.18).

The combination of both biomarkers with the FRS predicted higher CV risk (HR, 1.91; 95% CI, 1.23-2.97). Neither biomarker made a statistically significant difference in changing CV risk prediction when added individually to FRS, although cTnI trended toward significance (HR, 2.60; 95% CI, 0.98-6.87).

Instead of the carotid plaque burden, Dr. Mease would have liked to have seen the authors evaluate calcium scores in coronary arteries as measured by CT. “I would have loved to have seen the researchers using that in addition to the carotid plaque assessment, to see what that would show us about these patients,” he said.

Only a small number of patients experienced CV events during the study period, which will likely make it necessary to conduct larger studies to identify a clear relationship. “You need a registry-type study with probably many hundreds if not thousands of patients in order to identify whether or not adding troponin could be useful to what we typically measure with patients when we’re trying to assess their risk,” Dr. Mease said.

The study was supported in part by the National Psoriasis Foundation and the Arthritis Society. Individual researchers have received support from a range of sources, including the Enid Walker Estate, the Women’s College Research Institute, the Arthritis Society, the National Psoriasis Foundation, the Edward Dunlop Foundation, the Ontario Ministry of Science and Innovation, and a Pfizer Chair Research Award. Some of the researchers have financial relationships with pharmaceutical companies that market drugs for psoriasis and psoriatic arthritis.

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

The risk of cardiovascular (CV) events in patients with psoriatic disease rises with higher levels of two cardiac biomarkers in a manner independent of risk calculated by the Framingham Risk Score (FRS), a longitudinal cohort study has shown. But researchers who conducted the study note that neither of the two biomarkers identified in the study – cardiac troponin I (cTnI) and N-terminal pro-brain-type natriuretic peptide (NT-proBNP) – led to an improvement in predictive performance when combined with the FRS, despite their association with carotid plaque burden.

Psoriasis and psoriatic arthritis are both associated with greater risk of CV morbidity and mortality, partly because of systemic inflammation that leads to atherogenesis. Measures of CV risk such as the FRS rely on traditional measures of CV risk and thus are likely to underestimate the CV event risk of people with psoriatic disease, according to the authors of the new study, published online in Arthritis & Rheumatology. The effort was led by Keith Colaço, MSc; Lihi Eder, MD, PhD; and other researchers affiliated with the University of Toronto.

Alexander Raths/ThinkStock

“We are desperately in need of biomarker science advancement in psoriatic arthritis for a variety of places of guidance: How to choose a medication more accurately for the patient in front of us – that is, getting to be more like oncologists who use biomarkers to pick the best treatment or combination. That’s an important need. A second important need is how to guide clinicians regarding risk prediction for things like persistent, severe disease activity, progressive structural damage from disease, and, in this case, predicting a very common comorbidity that occurs in [psoriasis and] psoriatic arthritis patients,” Philip J. Mease, MD, told this news organization when asked to comment on the study.

Such biomarkers could assist with patient counseling, according to Dr. Mease, who is director of rheumatology research at Swedish Medical Center/Providence St. Joseph Health and is a clinical professor at the University of Washington, both in Seattle. Some patients may struggle with advice to lose weight or adopt lifestyle measures to limit CV risk, and more accurate predictions of risk may serve as further motivation. “It could well be that if you have a biomarker that accurately predicts a coming cataclysm, that it will lead you to redouble your efforts to do whatever it takes to reduce cardiovascular risk,” he said.

Both cTnI and NT-proBNP have been linked to increased CV risk in the general population, but little work has been done in the context of rheumatologic diseases.

The researchers analyzed data from 358 patients seen at the University of Toronto. The mean follow-up was 3.69 years. After adjustment for CV risk factors, lipid-lowering therapy, and creatinine levels, there was an association between cTnI levels and total carotid plaque area (adjusted beta coefficient, 0.21; 95% confidence interval, 0-0.41), but not for levels of NT-proBNP.

Atherosclerosis progressed in 89 participants overall, but multivariate adjustment revealed no significant relationship between progression and cTnI or NT-proBNP levels.

Separately, the researchers analyzed 1,000 individuals with psoriatic arthritis (n = 648) or with psoriasis and no arthritis (n = 352) whom they followed for a mean of 7.1 years after the patients underwent evaluation during 2002-2019. After adjustment for FRS, there was an association between the risk of a CV event and each 1–standard deviation increase in both cTnI (hazard ratio, 3.02; 95% CI, 1.12-8.16) and NT-proBNP (HR, 2.02; 95% CI, 1.28-3.18).

The combination of both biomarkers with the FRS predicted higher CV risk (HR, 1.91; 95% CI, 1.23-2.97). Neither biomarker made a statistically significant difference in changing CV risk prediction when added individually to FRS, although cTnI trended toward significance (HR, 2.60; 95% CI, 0.98-6.87).

Instead of the carotid plaque burden, Dr. Mease would have liked to have seen the authors evaluate calcium scores in coronary arteries as measured by CT. “I would have loved to have seen the researchers using that in addition to the carotid plaque assessment, to see what that would show us about these patients,” he said.

Only a small number of patients experienced CV events during the study period, which will likely make it necessary to conduct larger studies to identify a clear relationship. “You need a registry-type study with probably many hundreds if not thousands of patients in order to identify whether or not adding troponin could be useful to what we typically measure with patients when we’re trying to assess their risk,” Dr. Mease said.

The study was supported in part by the National Psoriasis Foundation and the Arthritis Society. Individual researchers have received support from a range of sources, including the Enid Walker Estate, the Women’s College Research Institute, the Arthritis Society, the National Psoriasis Foundation, the Edward Dunlop Foundation, the Ontario Ministry of Science and Innovation, and a Pfizer Chair Research Award. Some of the researchers have financial relationships with pharmaceutical companies that market drugs for psoriasis and psoriatic arthritis.

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

The risk of cardiovascular (CV) events in patients with psoriatic disease rises with higher levels of two cardiac biomarkers in a manner independent of risk calculated by the Framingham Risk Score (FRS), a longitudinal cohort study has shown. But researchers who conducted the study note that neither of the two biomarkers identified in the study – cardiac troponin I (cTnI) and N-terminal pro-brain-type natriuretic peptide (NT-proBNP) – led to an improvement in predictive performance when combined with the FRS, despite their association with carotid plaque burden.

Psoriasis and psoriatic arthritis are both associated with greater risk of CV morbidity and mortality, partly because of systemic inflammation that leads to atherogenesis. Measures of CV risk such as the FRS rely on traditional measures of CV risk and thus are likely to underestimate the CV event risk of people with psoriatic disease, according to the authors of the new study, published online in Arthritis & Rheumatology. The effort was led by Keith Colaço, MSc; Lihi Eder, MD, PhD; and other researchers affiliated with the University of Toronto.

Alexander Raths/ThinkStock

“We are desperately in need of biomarker science advancement in psoriatic arthritis for a variety of places of guidance: How to choose a medication more accurately for the patient in front of us – that is, getting to be more like oncologists who use biomarkers to pick the best treatment or combination. That’s an important need. A second important need is how to guide clinicians regarding risk prediction for things like persistent, severe disease activity, progressive structural damage from disease, and, in this case, predicting a very common comorbidity that occurs in [psoriasis and] psoriatic arthritis patients,” Philip J. Mease, MD, told this news organization when asked to comment on the study.

Such biomarkers could assist with patient counseling, according to Dr. Mease, who is director of rheumatology research at Swedish Medical Center/Providence St. Joseph Health and is a clinical professor at the University of Washington, both in Seattle. Some patients may struggle with advice to lose weight or adopt lifestyle measures to limit CV risk, and more accurate predictions of risk may serve as further motivation. “It could well be that if you have a biomarker that accurately predicts a coming cataclysm, that it will lead you to redouble your efforts to do whatever it takes to reduce cardiovascular risk,” he said.

Both cTnI and NT-proBNP have been linked to increased CV risk in the general population, but little work has been done in the context of rheumatologic diseases.

The researchers analyzed data from 358 patients seen at the University of Toronto. The mean follow-up was 3.69 years. After adjustment for CV risk factors, lipid-lowering therapy, and creatinine levels, there was an association between cTnI levels and total carotid plaque area (adjusted beta coefficient, 0.21; 95% confidence interval, 0-0.41), but not for levels of NT-proBNP.

Atherosclerosis progressed in 89 participants overall, but multivariate adjustment revealed no significant relationship between progression and cTnI or NT-proBNP levels.

Separately, the researchers analyzed 1,000 individuals with psoriatic arthritis (n = 648) or with psoriasis and no arthritis (n = 352) whom they followed for a mean of 7.1 years after the patients underwent evaluation during 2002-2019. After adjustment for FRS, there was an association between the risk of a CV event and each 1–standard deviation increase in both cTnI (hazard ratio, 3.02; 95% CI, 1.12-8.16) and NT-proBNP (HR, 2.02; 95% CI, 1.28-3.18).

The combination of both biomarkers with the FRS predicted higher CV risk (HR, 1.91; 95% CI, 1.23-2.97). Neither biomarker made a statistically significant difference in changing CV risk prediction when added individually to FRS, although cTnI trended toward significance (HR, 2.60; 95% CI, 0.98-6.87).

Instead of the carotid plaque burden, Dr. Mease would have liked to have seen the authors evaluate calcium scores in coronary arteries as measured by CT. “I would have loved to have seen the researchers using that in addition to the carotid plaque assessment, to see what that would show us about these patients,” he said.

Only a small number of patients experienced CV events during the study period, which will likely make it necessary to conduct larger studies to identify a clear relationship. “You need a registry-type study with probably many hundreds if not thousands of patients in order to identify whether or not adding troponin could be useful to what we typically measure with patients when we’re trying to assess their risk,” Dr. Mease said.

The study was supported in part by the National Psoriasis Foundation and the Arthritis Society. Individual researchers have received support from a range of sources, including the Enid Walker Estate, the Women’s College Research Institute, the Arthritis Society, the National Psoriasis Foundation, the Edward Dunlop Foundation, the Ontario Ministry of Science and Innovation, and a Pfizer Chair Research Award. Some of the researchers have financial relationships with pharmaceutical companies that market drugs for psoriasis and psoriatic arthritis.

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

Patients with familial hypercholesterolemia (FH) who start lipid-lowering treatment earlier in life may reduce their cardiovascular risk, compared with those who don’t begin treatment early, according to results of a recent meta-analysis.

They showed a difference in the carotid intima-media thickness (IMT) between patients with and without FH that increased with age, but there was also a difference in IMT seen among patients with FH who started treatment early, compared with untreated patients with FH, Kika van Bergen en Henegouwen, of the departments of pediatrics and epidemiology and data science at Amsterdam University Medical Center, and colleagues wrote in their report, published in the Journal of Clinical Lipidology.

“The fact that the difference in IMT increases with age between FH patients and unaffected controls, and is more pronounced in studies with untreated FH patients than in studies with treated patients, suggests that starting treatment already at a young age in patients with FH is preferred,” the researchers wrote. “However, despite treatment, IMT in treated FH patients is still thicker in comparison to subjects without FH.”

The researchers identified 42 studies with among patients with FH and healthy control groups across the MEDLINE, EMBASE and Trials.gov databases up to a cutoff date of April 2020, with 39 studies specifically examining carotid IMT, 2 studies evaluating carotid and femoral IMT, and 1 study evaluating femoral IMT alone. Overall, the researchers examined IMT measurements in 3,796 patients with FH and 2,363 control group participants.

Although data on age and gender for FH and control groups were not available in 6 studies, the mean age ranged from 9 to 57 years for patients with FH and from 8 to 61 years in the control group. Men comprised just under half of both the FH and control groups.

The mean between-group difference in carotid IMT in 34 studies was 0.11 mm (95% confidence interval, 0.06-0.15 mm; P < .001) for patients with FH, compared with the control group, while the mean difference in femoral IMT in three studies was 0.47 mm (95% CI, 0.19-0.74 mm; P < .001) between FH and control groups.

In 13 studies in which data on differences between partly treated and untreated FH were available, there was a significant between-group difference in carotid IMT with partly treated patients with FH, compared with the control group (0.05 mm; 95% CI, 0.03-0.08 mm; P < .001), but a larger mean between-group difference in carotid IMT among untreated patients with FH, compared with a control group (0.12 mm; 95% CI, 0.03-0.21 mm; P = .009).

The researchers also analyzed how age impacts carotid IMT, and they found patients with FH had a mean increase of 0.0018 mm (95% CI, –0.0007 to 0.0042 mm) over a control group in 34 studies. For patients with partly treated FH, compared with patients with untreated FH, the mean between-group increase per year was smaller (0.0023 mm; 95% CI, 0.0021-0.0025 mm), compared with the control group (0.0104 mm; 95% CI, 0.0100-0.0108 mm).

“This sign of residual risk might suggest that more robust cholesterol-lowering treatment and achieving treatment targets, or earlier treatment initiation, is needed to reduce IMT progression to non-FH conditions,” the researchers said. “Therefore, we must find and diagnose these patients, and treat them according to current guidelines.”

Limitations of the authors’ meta-analyses include heterogeneity among studies, differences in IMT measurement protocols, and inclusion of studies with an open-label design. Although randomized clinical trials would be preferable to compare treatment effect, “since statin therapy is indicated in FH patients to reduce [cardiovascular disease], it would be unethical to have a placebo group,” they said.

The authors reported no relevant financial disclosures.

Patients with familial hypercholesterolemia (FH) who start lipid-lowering treatment earlier in life may reduce their cardiovascular risk, compared with those who don’t begin treatment early, according to results of a recent meta-analysis.

They showed a difference in the carotid intima-media thickness (IMT) between patients with and without FH that increased with age, but there was also a difference in IMT seen among patients with FH who started treatment early, compared with untreated patients with FH, Kika van Bergen en Henegouwen, of the departments of pediatrics and epidemiology and data science at Amsterdam University Medical Center, and colleagues wrote in their report, published in the Journal of Clinical Lipidology.

“The fact that the difference in IMT increases with age between FH patients and unaffected controls, and is more pronounced in studies with untreated FH patients than in studies with treated patients, suggests that starting treatment already at a young age in patients with FH is preferred,” the researchers wrote. “However, despite treatment, IMT in treated FH patients is still thicker in comparison to subjects without FH.”

The researchers identified 42 studies with among patients with FH and healthy control groups across the MEDLINE, EMBASE and Trials.gov databases up to a cutoff date of April 2020, with 39 studies specifically examining carotid IMT, 2 studies evaluating carotid and femoral IMT, and 1 study evaluating femoral IMT alone. Overall, the researchers examined IMT measurements in 3,796 patients with FH and 2,363 control group participants.

Although data on age and gender for FH and control groups were not available in 6 studies, the mean age ranged from 9 to 57 years for patients with FH and from 8 to 61 years in the control group. Men comprised just under half of both the FH and control groups.

The mean between-group difference in carotid IMT in 34 studies was 0.11 mm (95% confidence interval, 0.06-0.15 mm; P < .001) for patients with FH, compared with the control group, while the mean difference in femoral IMT in three studies was 0.47 mm (95% CI, 0.19-0.74 mm; P < .001) between FH and control groups.

In 13 studies in which data on differences between partly treated and untreated FH were available, there was a significant between-group difference in carotid IMT with partly treated patients with FH, compared with the control group (0.05 mm; 95% CI, 0.03-0.08 mm; P < .001), but a larger mean between-group difference in carotid IMT among untreated patients with FH, compared with a control group (0.12 mm; 95% CI, 0.03-0.21 mm; P = .009).

The researchers also analyzed how age impacts carotid IMT, and they found patients with FH had a mean increase of 0.0018 mm (95% CI, –0.0007 to 0.0042 mm) over a control group in 34 studies. For patients with partly treated FH, compared with patients with untreated FH, the mean between-group increase per year was smaller (0.0023 mm; 95% CI, 0.0021-0.0025 mm), compared with the control group (0.0104 mm; 95% CI, 0.0100-0.0108 mm).

“This sign of residual risk might suggest that more robust cholesterol-lowering treatment and achieving treatment targets, or earlier treatment initiation, is needed to reduce IMT progression to non-FH conditions,” the researchers said. “Therefore, we must find and diagnose these patients, and treat them according to current guidelines.”

Limitations of the authors’ meta-analyses include heterogeneity among studies, differences in IMT measurement protocols, and inclusion of studies with an open-label design. Although randomized clinical trials would be preferable to compare treatment effect, “since statin therapy is indicated in FH patients to reduce [cardiovascular disease], it would be unethical to have a placebo group,” they said.

The authors reported no relevant financial disclosures.

Patients with familial hypercholesterolemia (FH) who start lipid-lowering treatment earlier in life may reduce their cardiovascular risk, compared with those who don’t begin treatment early, according to results of a recent meta-analysis.

They showed a difference in the carotid intima-media thickness (IMT) between patients with and without FH that increased with age, but there was also a difference in IMT seen among patients with FH who started treatment early, compared with untreated patients with FH, Kika van Bergen en Henegouwen, of the departments of pediatrics and epidemiology and data science at Amsterdam University Medical Center, and colleagues wrote in their report, published in the Journal of Clinical Lipidology.

“The fact that the difference in IMT increases with age between FH patients and unaffected controls, and is more pronounced in studies with untreated FH patients than in studies with treated patients, suggests that starting treatment already at a young age in patients with FH is preferred,” the researchers wrote. “However, despite treatment, IMT in treated FH patients is still thicker in comparison to subjects without FH.”

The researchers identified 42 studies with among patients with FH and healthy control groups across the MEDLINE, EMBASE and Trials.gov databases up to a cutoff date of April 2020, with 39 studies specifically examining carotid IMT, 2 studies evaluating carotid and femoral IMT, and 1 study evaluating femoral IMT alone. Overall, the researchers examined IMT measurements in 3,796 patients with FH and 2,363 control group participants.

Although data on age and gender for FH and control groups were not available in 6 studies, the mean age ranged from 9 to 57 years for patients with FH and from 8 to 61 years in the control group. Men comprised just under half of both the FH and control groups.

The mean between-group difference in carotid IMT in 34 studies was 0.11 mm (95% confidence interval, 0.06-0.15 mm; P < .001) for patients with FH, compared with the control group, while the mean difference in femoral IMT in three studies was 0.47 mm (95% CI, 0.19-0.74 mm; P < .001) between FH and control groups.

In 13 studies in which data on differences between partly treated and untreated FH were available, there was a significant between-group difference in carotid IMT with partly treated patients with FH, compared with the control group (0.05 mm; 95% CI, 0.03-0.08 mm; P < .001), but a larger mean between-group difference in carotid IMT among untreated patients with FH, compared with a control group (0.12 mm; 95% CI, 0.03-0.21 mm; P = .009).

The researchers also analyzed how age impacts carotid IMT, and they found patients with FH had a mean increase of 0.0018 mm (95% CI, –0.0007 to 0.0042 mm) over a control group in 34 studies. For patients with partly treated FH, compared with patients with untreated FH, the mean between-group increase per year was smaller (0.0023 mm; 95% CI, 0.0021-0.0025 mm), compared with the control group (0.0104 mm; 95% CI, 0.0100-0.0108 mm).

“This sign of residual risk might suggest that more robust cholesterol-lowering treatment and achieving treatment targets, or earlier treatment initiation, is needed to reduce IMT progression to non-FH conditions,” the researchers said. “Therefore, we must find and diagnose these patients, and treat them according to current guidelines.”

Limitations of the authors’ meta-analyses include heterogeneity among studies, differences in IMT measurement protocols, and inclusion of studies with an open-label design. Although randomized clinical trials would be preferable to compare treatment effect, “since statin therapy is indicated in FH patients to reduce [cardiovascular disease], it would be unethical to have a placebo group,” they said.

The authors reported no relevant financial disclosures.

A look back at a pair of large cohort studies suggests a telling relation between two distinct predictors of atherosclerotic cardiovascular disease (ASCVD) risk and may offer guidance on how to interpret them together.

Elevated levels of lipoprotein(a), or Lp(a), and high coronary artery calcium (CAC) scores were both predictive of ASCVD risk over 10 years, but independent of each other and a host of more traditional cardiovascular risk factors, for example, in the analysis of data from the MESA (Multi-Ethnic Study of Atherosclerosis) and DHS (Dallas Heart Study) longitudinal cohorts.

Notably, the risk when both Lp(a) and CAC scores were high far exceeded that associated with either marker alone. But when CAC scores were less than 100 Agatston units, predicted ASCVD risk wasn’t influenced by levels of Lp(a). Indeed, a CAC score of 0 predicted the lowest levels of ASCVD risk, even with elevated Lp(a).

That is, the findings suggest, the addition of Lp(a) makes a difference to the risk assessment only when CAC scores are high, at least 100 units, and elevated Lp(a) doesn’t mean increased ASCVD risk in the absence of coronary calcium.

“Our novel findings indicate that elevated Lp(a) drives ASCVD risk independent of the subclinical coronary atherosclerosis burden captured by CAC score,” concluded a report on the analysis, published in the Journal of the American College of Cardiology, with lead author Anurag Mehta, MD, Emory University, Atlanta.

There are no formal recommendations on how to interpret Lp(a) and CAC scores together, but the current findings “provide impetus for measuring Lp(a) in more individuals as part of the shared decision-making process,” the authors contended.

“Really, the calcium score carries the majority of the information in terms of risk, except in the highest CAC score group. That is, if you have a high Lp(a) and a high burden of calcium, your risk is significantly higher than if you just have the high calcium score and the normal Lp(a),” senior author Parag H. Joshi, MD, MHS, said in an interview.

“We thought we would see that the group with higher Lp(a) would have more events over 10 years, even among those who didn’t have coronary calcium,” said Dr. Joshi, of the University of Texas Southwestern Medical Center, Dallas. “But we really don’t see that, at least in a statistically significant way.”

A CAC score of 0 would at least support a more conservative approach in a patient with elevated Lp(a) “who is hesitant to be on a statin or to be more aggressive managing their risk,” Dr. Joshi said.

“This study should be very reassuring for a patient like that,” Ron Blankstein, MD, director of cardiac computed tomography at Brigham and Women’s Hospital, Boston, said in an interview.

“If you have a high Lp(a) and you’re concerned, I think this study really supports the role of calcium scoring for further risk assessment,” said Dr. Blankstein, who is not associated with the new report. “We often check Lp(a) in individuals who perhaps have a family history or who come to see us in a preventive cardiology clinic. If it is high and there is concern, a calcium score can be very helpful. If it’s zero, that really means a very low risk of events. And if it’s elevated, I think we’re going to be more concerned about that patient.”

The current analysis suggests “that, when a patient without clinical cardiovascular disease is identified with either CAC ≥100 or Lp(a) >50 mg/dL, the next step in the risk evaluation should be to measure either Lp(a) or CAC, respectively – if not already performed – to identify the patients at highest risk,” Sotirios Tsimikas, MD, director of vascular medicine at University of California, San Diego, wrote in an accompanying editorial.

“Both Lp(a) and CAC should be more broadly applied in clinical care settings in patients without prior ASCVD to identify those that most likely will benefit from more aggressive therapy and, in the future, from Lp(a)-lowering therapies,” he wrote.

The analyses were conducted separately on data from 4,512 initially asymptomatic patients in MESA and 2,078 from the DHS cohort, who were followed for ASCVD events an average of 13 years and 11 years, respectively. Such events included coronary heart disease–related death, nonfatal MI, and fatal or nonfatal stroke.

In the MESA cohort – 52% women, 36.8% White, 29.3% Black, 22.2% Hispanic, and 11.7% Chinese – elevated Lp(a) (quintile 5 vs. quintiles 1-4) and CAC scores of 1-99 and above 100 (both compared with 0) were each independently associated with increased risk for ASCVD events. The hazard ratio was 1.29 (P = .02) for elevated Lp(a), 1.68 (P < .01) for a CAC score of 1-99, and 2.66 (P < .01) for a CAC score of at least 100.

The corresponding HRs in the DHS cohort were 1.54 (P = .07) for Lp(a), 3.32 (P < .01) for a CAC score of 1-99, and 5.21 (P < .01) for a CAC score of at least 100.

Of note, the authors wrote, ASCVD risk among MESA participants with a CAC score of 0 was not significantly different in those with normal and elevated Lp(a).

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

A look back at a pair of large cohort studies suggests a telling relation between two distinct predictors of atherosclerotic cardiovascular disease (ASCVD) risk and may offer guidance on how to interpret them together.

Elevated levels of lipoprotein(a), or Lp(a), and high coronary artery calcium (CAC) scores were both predictive of ASCVD risk over 10 years, but independent of each other and a host of more traditional cardiovascular risk factors, for example, in the analysis of data from the MESA (Multi-Ethnic Study of Atherosclerosis) and DHS (Dallas Heart Study) longitudinal cohorts.

Notably, the risk when both Lp(a) and CAC scores were high far exceeded that associated with either marker alone. But when CAC scores were less than 100 Agatston units, predicted ASCVD risk wasn’t influenced by levels of Lp(a). Indeed, a CAC score of 0 predicted the lowest levels of ASCVD risk, even with elevated Lp(a).

That is, the findings suggest, the addition of Lp(a) makes a difference to the risk assessment only when CAC scores are high, at least 100 units, and elevated Lp(a) doesn’t mean increased ASCVD risk in the absence of coronary calcium.

“Our novel findings indicate that elevated Lp(a) drives ASCVD risk independent of the subclinical coronary atherosclerosis burden captured by CAC score,” concluded a report on the analysis, published in the Journal of the American College of Cardiology, with lead author Anurag Mehta, MD, Emory University, Atlanta.

There are no formal recommendations on how to interpret Lp(a) and CAC scores together, but the current findings “provide impetus for measuring Lp(a) in more individuals as part of the shared decision-making process,” the authors contended.

“Really, the calcium score carries the majority of the information in terms of risk, except in the highest CAC score group. That is, if you have a high Lp(a) and a high burden of calcium, your risk is significantly higher than if you just have the high calcium score and the normal Lp(a),” senior author Parag H. Joshi, MD, MHS, said in an interview.

“We thought we would see that the group with higher Lp(a) would have more events over 10 years, even among those who didn’t have coronary calcium,” said Dr. Joshi, of the University of Texas Southwestern Medical Center, Dallas. “But we really don’t see that, at least in a statistically significant way.”

A CAC score of 0 would at least support a more conservative approach in a patient with elevated Lp(a) “who is hesitant to be on a statin or to be more aggressive managing their risk,” Dr. Joshi said.

“This study should be very reassuring for a patient like that,” Ron Blankstein, MD, director of cardiac computed tomography at Brigham and Women’s Hospital, Boston, said in an interview.

“If you have a high Lp(a) and you’re concerned, I think this study really supports the role of calcium scoring for further risk assessment,” said Dr. Blankstein, who is not associated with the new report. “We often check Lp(a) in individuals who perhaps have a family history or who come to see us in a preventive cardiology clinic. If it is high and there is concern, a calcium score can be very helpful. If it’s zero, that really means a very low risk of events. And if it’s elevated, I think we’re going to be more concerned about that patient.”

The current analysis suggests “that, when a patient without clinical cardiovascular disease is identified with either CAC ≥100 or Lp(a) >50 mg/dL, the next step in the risk evaluation should be to measure either Lp(a) or CAC, respectively – if not already performed – to identify the patients at highest risk,” Sotirios Tsimikas, MD, director of vascular medicine at University of California, San Diego, wrote in an accompanying editorial.

“Both Lp(a) and CAC should be more broadly applied in clinical care settings in patients without prior ASCVD to identify those that most likely will benefit from more aggressive therapy and, in the future, from Lp(a)-lowering therapies,” he wrote.

The analyses were conducted separately on data from 4,512 initially asymptomatic patients in MESA and 2,078 from the DHS cohort, who were followed for ASCVD events an average of 13 years and 11 years, respectively. Such events included coronary heart disease–related death, nonfatal MI, and fatal or nonfatal stroke.

In the MESA cohort – 52% women, 36.8% White, 29.3% Black, 22.2% Hispanic, and 11.7% Chinese – elevated Lp(a) (quintile 5 vs. quintiles 1-4) and CAC scores of 1-99 and above 100 (both compared with 0) were each independently associated with increased risk for ASCVD events. The hazard ratio was 1.29 (P = .02) for elevated Lp(a), 1.68 (P < .01) for a CAC score of 1-99, and 2.66 (P < .01) for a CAC score of at least 100.

The corresponding HRs in the DHS cohort were 1.54 (P = .07) for Lp(a), 3.32 (P < .01) for a CAC score of 1-99, and 5.21 (P < .01) for a CAC score of at least 100.

Of note, the authors wrote, ASCVD risk among MESA participants with a CAC score of 0 was not significantly different in those with normal and elevated Lp(a).

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

A look back at a pair of large cohort studies suggests a telling relation between two distinct predictors of atherosclerotic cardiovascular disease (ASCVD) risk and may offer guidance on how to interpret them together.

Elevated levels of lipoprotein(a), or Lp(a), and high coronary artery calcium (CAC) scores were both predictive of ASCVD risk over 10 years, but independent of each other and a host of more traditional cardiovascular risk factors, for example, in the analysis of data from the MESA (Multi-Ethnic Study of Atherosclerosis) and DHS (Dallas Heart Study) longitudinal cohorts.

Notably, the risk when both Lp(a) and CAC scores were high far exceeded that associated with either marker alone. But when CAC scores were less than 100 Agatston units, predicted ASCVD risk wasn’t influenced by levels of Lp(a). Indeed, a CAC score of 0 predicted the lowest levels of ASCVD risk, even with elevated Lp(a).

That is, the findings suggest, the addition of Lp(a) makes a difference to the risk assessment only when CAC scores are high, at least 100 units, and elevated Lp(a) doesn’t mean increased ASCVD risk in the absence of coronary calcium.

“Our novel findings indicate that elevated Lp(a) drives ASCVD risk independent of the subclinical coronary atherosclerosis burden captured by CAC score,” concluded a report on the analysis, published in the Journal of the American College of Cardiology, with lead author Anurag Mehta, MD, Emory University, Atlanta.

There are no formal recommendations on how to interpret Lp(a) and CAC scores together, but the current findings “provide impetus for measuring Lp(a) in more individuals as part of the shared decision-making process,” the authors contended.

“Really, the calcium score carries the majority of the information in terms of risk, except in the highest CAC score group. That is, if you have a high Lp(a) and a high burden of calcium, your risk is significantly higher than if you just have the high calcium score and the normal Lp(a),” senior author Parag H. Joshi, MD, MHS, said in an interview.

“We thought we would see that the group with higher Lp(a) would have more events over 10 years, even among those who didn’t have coronary calcium,” said Dr. Joshi, of the University of Texas Southwestern Medical Center, Dallas. “But we really don’t see that, at least in a statistically significant way.”

A CAC score of 0 would at least support a more conservative approach in a patient with elevated Lp(a) “who is hesitant to be on a statin or to be more aggressive managing their risk,” Dr. Joshi said.

“This study should be very reassuring for a patient like that,” Ron Blankstein, MD, director of cardiac computed tomography at Brigham and Women’s Hospital, Boston, said in an interview.

“If you have a high Lp(a) and you’re concerned, I think this study really supports the role of calcium scoring for further risk assessment,” said Dr. Blankstein, who is not associated with the new report. “We often check Lp(a) in individuals who perhaps have a family history or who come to see us in a preventive cardiology clinic. If it is high and there is concern, a calcium score can be very helpful. If it’s zero, that really means a very low risk of events. And if it’s elevated, I think we’re going to be more concerned about that patient.”

The current analysis suggests “that, when a patient without clinical cardiovascular disease is identified with either CAC ≥100 or Lp(a) >50 mg/dL, the next step in the risk evaluation should be to measure either Lp(a) or CAC, respectively – if not already performed – to identify the patients at highest risk,” Sotirios Tsimikas, MD, director of vascular medicine at University of California, San Diego, wrote in an accompanying editorial.

“Both Lp(a) and CAC should be more broadly applied in clinical care settings in patients without prior ASCVD to identify those that most likely will benefit from more aggressive therapy and, in the future, from Lp(a)-lowering therapies,” he wrote.

The analyses were conducted separately on data from 4,512 initially asymptomatic patients in MESA and 2,078 from the DHS cohort, who were followed for ASCVD events an average of 13 years and 11 years, respectively. Such events included coronary heart disease–related death, nonfatal MI, and fatal or nonfatal stroke.

In the MESA cohort – 52% women, 36.8% White, 29.3% Black, 22.2% Hispanic, and 11.7% Chinese – elevated Lp(a) (quintile 5 vs. quintiles 1-4) and CAC scores of 1-99 and above 100 (both compared with 0) were each independently associated with increased risk for ASCVD events. The hazard ratio was 1.29 (P = .02) for elevated Lp(a), 1.68 (P < .01) for a CAC score of 1-99, and 2.66 (P < .01) for a CAC score of at least 100.

The corresponding HRs in the DHS cohort were 1.54 (P = .07) for Lp(a), 3.32 (P < .01) for a CAC score of 1-99, and 5.21 (P < .01) for a CAC score of at least 100.

Of note, the authors wrote, ASCVD risk among MESA participants with a CAC score of 0 was not significantly different in those with normal and elevated Lp(a).

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

Building on several previous reports that the newest models of mobile telephones and other electronics that use magnets pose a threat to the function of defibrillators and other implantable cardiovascular devices, a new study implicates any device that emits a 10-gauss (G) magnetic field more than a couple of inches.

“Beside the devices described in our manuscript, this can be any portable consumer product [with magnets] like electric cigarettes or smart watches,” explained study author Sven Knecht, DSc, a research electrophysiologist associated with the department of cardiology, University Hospital Basel (Switzerland).

In the newly published article, the investigators evaluated earphones, earphone charging cases, and two electronic pens used to draw on electronic tablets. These particular devices are of interest because, like mobile phones, they are of a size and shape to fit in a breast pocket adjacent to where many cardiovascular devices are implanted.

The study joins several previous studies that have shown the same risk, but this study used three-dimensional (3D) mapping of the magnetic field rather than a one-axis sensor, which is a standard adopted by the U.S. Food and Drug Administration, according to the investigators.
 

3D mapping assessment used

Because of the 3D nature of magnetic fields, 3D mapping serves as a better tool to assess the risk of the magnetic force as the intensity gradient diminishes with distance from the source, the authors contended. The 3D maps used in this study have a resolution to 2 mm.

The ex vivo measurements of the magnetic field, which could be displayed in a configurable 3D volume in relation to the electronic products were performed on five different explanted cardioverter defibrillators from two manufacturers.

In the ex vivo setting, the ability of the earphones, earphone charging cases, and electronic pens to interfere with defibrillator function was compared to that of the Apple iPhone 12 Max, which was the subject of a small in vivo study published in 2021. When the iPhone 12 Max was placed on the skin over a cardiac implantable device in that study, clinically identifiable interference could be detected in all 3 patients evaluated.

Based on previous work, the International Organization for Standardization has established that a minimal field strength of 10 G is needed to interfere with an implantable device, but the actual risk from any specific device is determined by the distance at which this strength of magnetic field is projected.

In the 3D analysis, the 10-G intensity was found to project 20 mm from the surface of the ear phones, ear phone charging case, and one of the electronic pens and to project 29 mm from the other electronic pen. When tested against the five defibrillators, magnetic reversion mode was triggered by the portable electronics at distances ranging from 8 to 18 mm.

In an interview, Dr. Knecht explained that this study adds more devices to the list of those associated with potential for interfering with implantable cardiovascular devices, but added that the more important point is that any device that contains magnets emitting a force of 10 G or greater for more than a few inches can be expected to be associated with clinically meaningful interference. The devices tested in this study were produced by Apple and Microsoft, but a focus on specific devices obscures the main message.

“All portable electronics with an embedded permanent magnet creating a 10-G magnetic field have a theoretical capability of triggering implantable devices,” he said.

For pacemakers, the interference is likely to trigger constant pacing, which would not be expected to pose a significant health threat if detected with a reasonable period, according to Dr. Knecht. Interference is potentially more serious for defibrillators, which might fail during magnetic interference to provide the shock needed to terminate a serious arrhythmia.

The combination of events – interference at the time of an arrhythmia – make this risk “very low,” but Dr. Knecht said it is sufficient to mean that patients receiving an implantable cardiovascular device should be made aware of the risk and the need to avoid placing portable electronic products near the implanted device.

When in vivo evidence of a disturbance with the iPhone 12 was reported in 2021, it amplified existing concern. The American Heart Association maintains a list of electronic products with the potential to interfere with implantable devices on its website. But, again, understanding the potential for risk and the need to keep electronic products with magnets at a safe distance from cardiovascular implantable devices is more important than trying to memorize the ever-growing list of devices with this capability.

“Prudent education of patients receiving an implantable device is important,” said N.A. Mark Estes III, MD, professor of medicine in the division of cardiology at the University of Pittsburgh. However, in an interview, he warned that the growing list of implicated devices makes a complete survey impractical, and, even if achievable, likely to leave patients “feeling overwhelmed.”
 

In Dr. Estes’s practice, he does provide printed information about the risks of electronics to interfere with implantable devices as well as a list of dos and don’ts. He agreed that the absolute risk of interference from a device causing significant clinical complications is low, but the goal is to “bring it as close to zero as possible.”

“No clinical case of a meaningful interaction of an electronic product and dysfunction of an implantable device has ever been documented,” he said. Given the widespread use of the new generation of cellphones that contain magnets powerful enough to induce dysfunction in an implantable device, “this speaks to the fact that the risk continues to be very low.”

Dr. Knecht and coinvestigators, along with Dr. Estes, reported no potential conflicts of interest.

Building on several previous reports that the newest models of mobile telephones and other electronics that use magnets pose a threat to the function of defibrillators and other implantable cardiovascular devices, a new study implicates any device that emits a 10-gauss (G) magnetic field more than a couple of inches.

“Beside the devices described in our manuscript, this can be any portable consumer product [with magnets] like electric cigarettes or smart watches,” explained study author Sven Knecht, DSc, a research electrophysiologist associated with the department of cardiology, University Hospital Basel (Switzerland).

In the newly published article, the investigators evaluated earphones, earphone charging cases, and two electronic pens used to draw on electronic tablets. These particular devices are of interest because, like mobile phones, they are of a size and shape to fit in a breast pocket adjacent to where many cardiovascular devices are implanted.

The study joins several previous studies that have shown the same risk, but this study used three-dimensional (3D) mapping of the magnetic field rather than a one-axis sensor, which is a standard adopted by the U.S. Food and Drug Administration, according to the investigators.
 

3D mapping assessment used

Because of the 3D nature of magnetic fields, 3D mapping serves as a better tool to assess the risk of the magnetic force as the intensity gradient diminishes with distance from the source, the authors contended. The 3D maps used in this study have a resolution to 2 mm.

The ex vivo measurements of the magnetic field, which could be displayed in a configurable 3D volume in relation to the electronic products were performed on five different explanted cardioverter defibrillators from two manufacturers.

In the ex vivo setting, the ability of the earphones, earphone charging cases, and electronic pens to interfere with defibrillator function was compared to that of the Apple iPhone 12 Max, which was the subject of a small in vivo study published in 2021. When the iPhone 12 Max was placed on the skin over a cardiac implantable device in that study, clinically identifiable interference could be detected in all 3 patients evaluated.

Based on previous work, the International Organization for Standardization has established that a minimal field strength of 10 G is needed to interfere with an implantable device, but the actual risk from any specific device is determined by the distance at which this strength of magnetic field is projected.

In the 3D analysis, the 10-G intensity was found to project 20 mm from the surface of the ear phones, ear phone charging case, and one of the electronic pens and to project 29 mm from the other electronic pen. When tested against the five defibrillators, magnetic reversion mode was triggered by the portable electronics at distances ranging from 8 to 18 mm.

In an interview, Dr. Knecht explained that this study adds more devices to the list of those associated with potential for interfering with implantable cardiovascular devices, but added that the more important point is that any device that contains magnets emitting a force of 10 G or greater for more than a few inches can be expected to be associated with clinically meaningful interference. The devices tested in this study were produced by Apple and Microsoft, but a focus on specific devices obscures the main message.

“All portable electronics with an embedded permanent magnet creating a 10-G magnetic field have a theoretical capability of triggering implantable devices,” he said.

For pacemakers, the interference is likely to trigger constant pacing, which would not be expected to pose a significant health threat if detected with a reasonable period, according to Dr. Knecht. Interference is potentially more serious for defibrillators, which might fail during magnetic interference to provide the shock needed to terminate a serious arrhythmia.

The combination of events – interference at the time of an arrhythmia – make this risk “very low,” but Dr. Knecht said it is sufficient to mean that patients receiving an implantable cardiovascular device should be made aware of the risk and the need to avoid placing portable electronic products near the implanted device.

When in vivo evidence of a disturbance with the iPhone 12 was reported in 2021, it amplified existing concern. The American Heart Association maintains a list of electronic products with the potential to interfere with implantable devices on its website. But, again, understanding the potential for risk and the need to keep electronic products with magnets at a safe distance from cardiovascular implantable devices is more important than trying to memorize the ever-growing list of devices with this capability.

“Prudent education of patients receiving an implantable device is important,” said N.A. Mark Estes III, MD, professor of medicine in the division of cardiology at the University of Pittsburgh. However, in an interview, he warned that the growing list of implicated devices makes a complete survey impractical, and, even if achievable, likely to leave patients “feeling overwhelmed.”
 

In Dr. Estes’s practice, he does provide printed information about the risks of electronics to interfere with implantable devices as well as a list of dos and don’ts. He agreed that the absolute risk of interference from a device causing significant clinical complications is low, but the goal is to “bring it as close to zero as possible.”

“No clinical case of a meaningful interaction of an electronic product and dysfunction of an implantable device has ever been documented,” he said. Given the widespread use of the new generation of cellphones that contain magnets powerful enough to induce dysfunction in an implantable device, “this speaks to the fact that the risk continues to be very low.”

Dr. Knecht and coinvestigators, along with Dr. Estes, reported no potential conflicts of interest.

Building on several previous reports that the newest models of mobile telephones and other electronics that use magnets pose a threat to the function of defibrillators and other implantable cardiovascular devices, a new study implicates any device that emits a 10-gauss (G) magnetic field more than a couple of inches.

“Beside the devices described in our manuscript, this can be any portable consumer product [with magnets] like electric cigarettes or smart watches,” explained study author Sven Knecht, DSc, a research electrophysiologist associated with the department of cardiology, University Hospital Basel (Switzerland).

In the newly published article, the investigators evaluated earphones, earphone charging cases, and two electronic pens used to draw on electronic tablets. These particular devices are of interest because, like mobile phones, they are of a size and shape to fit in a breast pocket adjacent to where many cardiovascular devices are implanted.

The study joins several previous studies that have shown the same risk, but this study used three-dimensional (3D) mapping of the magnetic field rather than a one-axis sensor, which is a standard adopted by the U.S. Food and Drug Administration, according to the investigators.
 

3D mapping assessment used

Because of the 3D nature of magnetic fields, 3D mapping serves as a better tool to assess the risk of the magnetic force as the intensity gradient diminishes with distance from the source, the authors contended. The 3D maps used in this study have a resolution to 2 mm.

The ex vivo measurements of the magnetic field, which could be displayed in a configurable 3D volume in relation to the electronic products were performed on five different explanted cardioverter defibrillators from two manufacturers.

In the ex vivo setting, the ability of the earphones, earphone charging cases, and electronic pens to interfere with defibrillator function was compared to that of the Apple iPhone 12 Max, which was the subject of a small in vivo study published in 2021. When the iPhone 12 Max was placed on the skin over a cardiac implantable device in that study, clinically identifiable interference could be detected in all 3 patients evaluated.

Based on previous work, the International Organization for Standardization has established that a minimal field strength of 10 G is needed to interfere with an implantable device, but the actual risk from any specific device is determined by the distance at which this strength of magnetic field is projected.

In the 3D analysis, the 10-G intensity was found to project 20 mm from the surface of the ear phones, ear phone charging case, and one of the electronic pens and to project 29 mm from the other electronic pen. When tested against the five defibrillators, magnetic reversion mode was triggered by the portable electronics at distances ranging from 8 to 18 mm.

In an interview, Dr. Knecht explained that this study adds more devices to the list of those associated with potential for interfering with implantable cardiovascular devices, but added that the more important point is that any device that contains magnets emitting a force of 10 G or greater for more than a few inches can be expected to be associated with clinically meaningful interference. The devices tested in this study were produced by Apple and Microsoft, but a focus on specific devices obscures the main message.

“All portable electronics with an embedded permanent magnet creating a 10-G magnetic field have a theoretical capability of triggering implantable devices,” he said.

For pacemakers, the interference is likely to trigger constant pacing, which would not be expected to pose a significant health threat if detected with a reasonable period, according to Dr. Knecht. Interference is potentially more serious for defibrillators, which might fail during magnetic interference to provide the shock needed to terminate a serious arrhythmia.

The combination of events – interference at the time of an arrhythmia – make this risk “very low,” but Dr. Knecht said it is sufficient to mean that patients receiving an implantable cardiovascular device should be made aware of the risk and the need to avoid placing portable electronic products near the implanted device.

When in vivo evidence of a disturbance with the iPhone 12 was reported in 2021, it amplified existing concern. The American Heart Association maintains a list of electronic products with the potential to interfere with implantable devices on its website. But, again, understanding the potential for risk and the need to keep electronic products with magnets at a safe distance from cardiovascular implantable devices is more important than trying to memorize the ever-growing list of devices with this capability.

“Prudent education of patients receiving an implantable device is important,” said N.A. Mark Estes III, MD, professor of medicine in the division of cardiology at the University of Pittsburgh. However, in an interview, he warned that the growing list of implicated devices makes a complete survey impractical, and, even if achievable, likely to leave patients “feeling overwhelmed.”
 

In Dr. Estes’s practice, he does provide printed information about the risks of electronics to interfere with implantable devices as well as a list of dos and don’ts. He agreed that the absolute risk of interference from a device causing significant clinical complications is low, but the goal is to “bring it as close to zero as possible.”

“No clinical case of a meaningful interaction of an electronic product and dysfunction of an implantable device has ever been documented,” he said. Given the widespread use of the new generation of cellphones that contain magnets powerful enough to induce dysfunction in an implantable device, “this speaks to the fact that the risk continues to be very low.”

Dr. Knecht and coinvestigators, along with Dr. Estes, reported no potential conflicts of interest.

Less than half of women in the United States enter pregnancy in favorable cardiovascular health, new research suggests.

In 2019, among women aged 20 to 44 years with live births in the United States, only 40.2% were in favorable cardiovascular health prior to pregnancy, defined as normal weight, no diabetes, and no hypertension.

Although all regions and states showed a decline in prepregnancy favorable cardiometabolic health, there were significant differences among geographic regions in the country, the authors report. “These data reveal critical deficiencies and geographic disparities in prepregnancy cardiometabolic health,” they conclude.

“One of the things that we know in the U.S. is that the maternal mortality rate has been increasing, and there are significant differences at the state level in both adverse maternal outcomes, such as maternal mortality, as well as adverse pregnancy outcomes,” corresponding author Sadiya S. Khan, MD, MS, FACC, Northwestern University Feinberg School of Medicine, Chicago, told this news organization.

“These outcomes are often related to health factors that predate pregnancy,” Dr. Khan explained, “and the processes that begin at the very, very beginning of conception are informed by health factors prior to pregnancy, in particular cardiometabolic factors like body mass index or obesity, high blood pressure, and diabetes.”

The results were published online on Feb. 14 in a special “Go Red for Women” spotlight issue of Circulation.
 

Cardiometabolic health factors

Using maternal birth records from live births in the Centers for Disease Control and Prevention Natality Database between 2016 and 2019, the authors analyzed data on 14,174,625 women with live births aged 20 to 44 years. The majority (81.4%) were 20 to 34 years of age, 22.7% were Hispanic or Latina, and 52.7% were non-Hispanic White.

Favorable cardiometabolic health was defined as a BMI of 18 to 24.9 kg/m2, absence of diabetes, and absence of hypertension.

Although all regions and states experienced a decline in favorable cardiometabolic health during the study period of 2016 to 2019, with a drop overall of 3.2% – from 43.5 to 40.2 per 100 live births – it was especially true of the South and Midwest regions.

In 2019, favorable prepregnancy cardiometabolic health was lowest in the South (38.1%) and Midwest (38.8%) and highest in the West (42.2%) and Northeast (43.6%).

State by state, the lowest prevalence of favorable cardiometabolic health was found in Mississippi, at 31.2%, and highest in Utah, at 47.2%.

They also found a correlation between favorable cardiometabolic health and state-level percentages of high-school education or less and enrollment in Medicaid in 2019.

Similar to what has been seen with cardiovascular disease, “we observe that the states with the lowest prevalence of favorable cardiometabolic health were in the Southeast United States,” said Dr. Khan, “and similar geographic variation was observed with some more patterns in education and Medicaid coverage for birth, and these were used as proxies for socioeconomic status in those areas.”

Although Dr. Khan notes that the relationships cannot be determined to be causal from this analysis, she said that “it does suggest that upstream social determinants of health are important determinants of cardiometabolic health.”
 

Socioeconomic intervention

Dr. Khan noted that policies at the federal and state level can identify ways to “ensure that individuals who are thinking about pregnancy have access to health care and have access to resources, too, from a broad range of health determinants, including housing stability, food security, as well as access to health care be optimized prior to pregnancy.”

The authors note that this analysis may actually overestimate the prevalence of favorable cardiometabolic health, and data on cholesterol, diet, a distinction between type 1 and type 2 diabetes, and physical activity were not available.

Only individuals with live births were included, which could result in the elimination of a potentially high-risk group; however, late pregnancy losses represent less than 0.3% of all pregnancies, they say.

The authors conclude that “future research is needed to equitably improve health prior to pregnancy and quantify the potential benefits in cardiovascular disease outcomes for birthing individuals and their offspring.”

This work was supported by grants from the National Heart, Lung, and Blood Institute and American Heart Association Transformational Project Award awarded to Sadiya S. Khan.

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

Less than half of women in the United States enter pregnancy in favorable cardiovascular health, new research suggests.

In 2019, among women aged 20 to 44 years with live births in the United States, only 40.2% were in favorable cardiovascular health prior to pregnancy, defined as normal weight, no diabetes, and no hypertension.

Although all regions and states showed a decline in prepregnancy favorable cardiometabolic health, there were significant differences among geographic regions in the country, the authors report. “These data reveal critical deficiencies and geographic disparities in prepregnancy cardiometabolic health,” they conclude.

“One of the things that we know in the U.S. is that the maternal mortality rate has been increasing, and there are significant differences at the state level in both adverse maternal outcomes, such as maternal mortality, as well as adverse pregnancy outcomes,” corresponding author Sadiya S. Khan, MD, MS, FACC, Northwestern University Feinberg School of Medicine, Chicago, told this news organization.

“These outcomes are often related to health factors that predate pregnancy,” Dr. Khan explained, “and the processes that begin at the very, very beginning of conception are informed by health factors prior to pregnancy, in particular cardiometabolic factors like body mass index or obesity, high blood pressure, and diabetes.”

The results were published online on Feb. 14 in a special “Go Red for Women” spotlight issue of Circulation.
 

Cardiometabolic health factors

Using maternal birth records from live births in the Centers for Disease Control and Prevention Natality Database between 2016 and 2019, the authors analyzed data on 14,174,625 women with live births aged 20 to 44 years. The majority (81.4%) were 20 to 34 years of age, 22.7% were Hispanic or Latina, and 52.7% were non-Hispanic White.

Favorable cardiometabolic health was defined as a BMI of 18 to 24.9 kg/m2, absence of diabetes, and absence of hypertension.

Although all regions and states experienced a decline in favorable cardiometabolic health during the study period of 2016 to 2019, with a drop overall of 3.2% – from 43.5 to 40.2 per 100 live births – it was especially true of the South and Midwest regions.

In 2019, favorable prepregnancy cardiometabolic health was lowest in the South (38.1%) and Midwest (38.8%) and highest in the West (42.2%) and Northeast (43.6%).

State by state, the lowest prevalence of favorable cardiometabolic health was found in Mississippi, at 31.2%, and highest in Utah, at 47.2%.

They also found a correlation between favorable cardiometabolic health and state-level percentages of high-school education or less and enrollment in Medicaid in 2019.

Similar to what has been seen with cardiovascular disease, “we observe that the states with the lowest prevalence of favorable cardiometabolic health were in the Southeast United States,” said Dr. Khan, “and similar geographic variation was observed with some more patterns in education and Medicaid coverage for birth, and these were used as proxies for socioeconomic status in those areas.”

Although Dr. Khan notes that the relationships cannot be determined to be causal from this analysis, she said that “it does suggest that upstream social determinants of health are important determinants of cardiometabolic health.”
 

Socioeconomic intervention

Dr. Khan noted that policies at the federal and state level can identify ways to “ensure that individuals who are thinking about pregnancy have access to health care and have access to resources, too, from a broad range of health determinants, including housing stability, food security, as well as access to health care be optimized prior to pregnancy.”

The authors note that this analysis may actually overestimate the prevalence of favorable cardiometabolic health, and data on cholesterol, diet, a distinction between type 1 and type 2 diabetes, and physical activity were not available.

Only individuals with live births were included, which could result in the elimination of a potentially high-risk group; however, late pregnancy losses represent less than 0.3% of all pregnancies, they say.

The authors conclude that “future research is needed to equitably improve health prior to pregnancy and quantify the potential benefits in cardiovascular disease outcomes for birthing individuals and their offspring.”

This work was supported by grants from the National Heart, Lung, and Blood Institute and American Heart Association Transformational Project Award awarded to Sadiya S. Khan.

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

Less than half of women in the United States enter pregnancy in favorable cardiovascular health, new research suggests.

In 2019, among women aged 20 to 44 years with live births in the United States, only 40.2% were in favorable cardiovascular health prior to pregnancy, defined as normal weight, no diabetes, and no hypertension.

Although all regions and states showed a decline in prepregnancy favorable cardiometabolic health, there were significant differences among geographic regions in the country, the authors report. “These data reveal critical deficiencies and geographic disparities in prepregnancy cardiometabolic health,” they conclude.

“One of the things that we know in the U.S. is that the maternal mortality rate has been increasing, and there are significant differences at the state level in both adverse maternal outcomes, such as maternal mortality, as well as adverse pregnancy outcomes,” corresponding author Sadiya S. Khan, MD, MS, FACC, Northwestern University Feinberg School of Medicine, Chicago, told this news organization.

“These outcomes are often related to health factors that predate pregnancy,” Dr. Khan explained, “and the processes that begin at the very, very beginning of conception are informed by health factors prior to pregnancy, in particular cardiometabolic factors like body mass index or obesity, high blood pressure, and diabetes.”

The results were published online on Feb. 14 in a special “Go Red for Women” spotlight issue of Circulation.
 

Cardiometabolic health factors

Using maternal birth records from live births in the Centers for Disease Control and Prevention Natality Database between 2016 and 2019, the authors analyzed data on 14,174,625 women with live births aged 20 to 44 years. The majority (81.4%) were 20 to 34 years of age, 22.7% were Hispanic or Latina, and 52.7% were non-Hispanic White.

Favorable cardiometabolic health was defined as a BMI of 18 to 24.9 kg/m2, absence of diabetes, and absence of hypertension.

Although all regions and states experienced a decline in favorable cardiometabolic health during the study period of 2016 to 2019, with a drop overall of 3.2% – from 43.5 to 40.2 per 100 live births – it was especially true of the South and Midwest regions.

In 2019, favorable prepregnancy cardiometabolic health was lowest in the South (38.1%) and Midwest (38.8%) and highest in the West (42.2%) and Northeast (43.6%).

State by state, the lowest prevalence of favorable cardiometabolic health was found in Mississippi, at 31.2%, and highest in Utah, at 47.2%.

They also found a correlation between favorable cardiometabolic health and state-level percentages of high-school education or less and enrollment in Medicaid in 2019.

Similar to what has been seen with cardiovascular disease, “we observe that the states with the lowest prevalence of favorable cardiometabolic health were in the Southeast United States,” said Dr. Khan, “and similar geographic variation was observed with some more patterns in education and Medicaid coverage for birth, and these were used as proxies for socioeconomic status in those areas.”

Although Dr. Khan notes that the relationships cannot be determined to be causal from this analysis, she said that “it does suggest that upstream social determinants of health are important determinants of cardiometabolic health.”
 

Socioeconomic intervention

Dr. Khan noted that policies at the federal and state level can identify ways to “ensure that individuals who are thinking about pregnancy have access to health care and have access to resources, too, from a broad range of health determinants, including housing stability, food security, as well as access to health care be optimized prior to pregnancy.”

The authors note that this analysis may actually overestimate the prevalence of favorable cardiometabolic health, and data on cholesterol, diet, a distinction between type 1 and type 2 diabetes, and physical activity were not available.

Only individuals with live births were included, which could result in the elimination of a potentially high-risk group; however, late pregnancy losses represent less than 0.3% of all pregnancies, they say.

The authors conclude that “future research is needed to equitably improve health prior to pregnancy and quantify the potential benefits in cardiovascular disease outcomes for birthing individuals and their offspring.”

This work was supported by grants from the National Heart, Lung, and Blood Institute and American Heart Association Transformational Project Award awarded to Sadiya S. Khan.

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

Regular use of acetaminophen, also known as paracetamol, in effervescent or soluble formulations that contain sodium increases the risk of cardiovascular disease (CVD) and death in people with or without hypertension, a large observational study of more than 300,000 adults suggests.

“Numerous studies have reported that high sodium intake is associated with increased risks of cardiovascular disease,” Yuqing Zhang, DSc, with Massachusetts General Hospital and Harvard Medical School, Boston, told this news organization. “Given that the pain relief effect of non–sodium-containing acetaminophen is similar to that of sodium-containing acetaminophen, clinicians may prescribe non–sodium-containing acetaminophen to their patients to minimize the risk of CVD and mortality,” Dr. Zhang said.

The study was published online Feb. 24 in the European Heart Journal.
 

‘Compelling results’

Dr. Zhang and colleagues note that the effervescent and soluble formulations of 0.5 g acetaminophen contain 0.44 and 0.39 g of sodium, respectively.

Therefore, the intake of maximum daily dose (4 g/day) of sodium-containing acetaminophen corresponds to the ingestion of more than 3 g of sodium, a dose that alone exceeds the recommended total daily sodium intake allowance of the World Health Organization (2 g/day).

“This hidden extra sodium intake is often overlooked,” Dr. Zhang told this news organization.

Using data from the Health Improvement Network, a U.K. primary care database, the researchers examined 4,532 patients with hypertension taking sodium-containing acetaminophen and compared them with 146,866 patients with hypertension taking non–sodium-containing acetaminophen (tablet, capsule, or oral suspension formulations).

After 1 year, the risk of incident CVD (myocardial infarction, stroke, and heart failure) was 5.6% in those taking sodium-containing acetaminophen, compared with 4.6% in those taking non–sodium-containing acetaminophen (average weighted hazard ratio, 1.59; 95% confidence interval, 1.32-1.92).

A separate analysis of normotensive patients taking sodium-containing acetaminophen (n = 5,351) or non–sodium-containing acetaminophen (n = 141,948) gave similar results.

The 1-year risk of incident CVD was 4.4% in those taking sodium-containing acetaminophen vs. 3.7% among those taking non–sodium-containing acetaminophen (average weighted HR, 1.45; 95% CI, 1.18-1.79).

There was also evidence of a dose-response relationship.

In those with hypertension, CVD risk increased by roughly one-quarter (odds ratio, 1.26) for those with one prescription of sodium-containing acetaminophen and by nearly one half (OR, 1.45) for those with five or more prescriptions of sodium-containing acetaminophen. Similar findings were observed among adults without hypertension.

Mortality at 1 year was also higher in those taking sodium-containing acetaminophen than non–sodium-containing acetaminophen, in patients with hypertension (7.6% vs. 6.1%) and without hypertension (7.3% vs. 5.9%).

“The results are compelling,” write the authors of an editorial published with the study.

“The direct message from this study is clear – there are likely to be millions of people worldwide taking paracetamol on a daily basis in a ‘fast-acting’ effervescent or soluble formulation who are increasing their risks of cardiovascular disease and premature death,” say Aletta Schutte, PhD, and Bruce Neal, MBChB, PhD, of the George Institute for Global Health, Sydney.

“The weight of the evidence makes ongoing inaction on sodium-containing medications untenable. The widespread use of effervescent medication in the general population, and the enormous doses of sodium that can be consumed inadvertently by unsuspecting consumers requires urgent action,” Dr. Schutte and Dr. Neal say.

The study was supported by the National Natural Science Foundation of China, the National Key Research and Development Project, the Project Program of National Clinical Research Center for Geriatric Disorders, the Key Research and Development Program of Hunan Province, and the Science and Technology Program of Hunan Province. Dr. Zhang, Dr. Schutte, and Dr. Neal have disclosed no relevant financial relationships.

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

Regular use of acetaminophen, also known as paracetamol, in effervescent or soluble formulations that contain sodium increases the risk of cardiovascular disease (CVD) and death in people with or without hypertension, a large observational study of more than 300,000 adults suggests.

“Numerous studies have reported that high sodium intake is associated with increased risks of cardiovascular disease,” Yuqing Zhang, DSc, with Massachusetts General Hospital and Harvard Medical School, Boston, told this news organization. “Given that the pain relief effect of non–sodium-containing acetaminophen is similar to that of sodium-containing acetaminophen, clinicians may prescribe non–sodium-containing acetaminophen to their patients to minimize the risk of CVD and mortality,” Dr. Zhang said.

The study was published online Feb. 24 in the European Heart Journal.
 

‘Compelling results’

Dr. Zhang and colleagues note that the effervescent and soluble formulations of 0.5 g acetaminophen contain 0.44 and 0.39 g of sodium, respectively.

Therefore, the intake of maximum daily dose (4 g/day) of sodium-containing acetaminophen corresponds to the ingestion of more than 3 g of sodium, a dose that alone exceeds the recommended total daily sodium intake allowance of the World Health Organization (2 g/day).

“This hidden extra sodium intake is often overlooked,” Dr. Zhang told this news organization.

Using data from the Health Improvement Network, a U.K. primary care database, the researchers examined 4,532 patients with hypertension taking sodium-containing acetaminophen and compared them with 146,866 patients with hypertension taking non–sodium-containing acetaminophen (tablet, capsule, or oral suspension formulations).

After 1 year, the risk of incident CVD (myocardial infarction, stroke, and heart failure) was 5.6% in those taking sodium-containing acetaminophen, compared with 4.6% in those taking non–sodium-containing acetaminophen (average weighted hazard ratio, 1.59; 95% confidence interval, 1.32-1.92).

A separate analysis of normotensive patients taking sodium-containing acetaminophen (n = 5,351) or non–sodium-containing acetaminophen (n = 141,948) gave similar results.

The 1-year risk of incident CVD was 4.4% in those taking sodium-containing acetaminophen vs. 3.7% among those taking non–sodium-containing acetaminophen (average weighted HR, 1.45; 95% CI, 1.18-1.79).

There was also evidence of a dose-response relationship.

In those with hypertension, CVD risk increased by roughly one-quarter (odds ratio, 1.26) for those with one prescription of sodium-containing acetaminophen and by nearly one half (OR, 1.45) for those with five or more prescriptions of sodium-containing acetaminophen. Similar findings were observed among adults without hypertension.

Mortality at 1 year was also higher in those taking sodium-containing acetaminophen than non–sodium-containing acetaminophen, in patients with hypertension (7.6% vs. 6.1%) and without hypertension (7.3% vs. 5.9%).

“The results are compelling,” write the authors of an editorial published with the study.

“The direct message from this study is clear – there are likely to be millions of people worldwide taking paracetamol on a daily basis in a ‘fast-acting’ effervescent or soluble formulation who are increasing their risks of cardiovascular disease and premature death,” say Aletta Schutte, PhD, and Bruce Neal, MBChB, PhD, of the George Institute for Global Health, Sydney.

“The weight of the evidence makes ongoing inaction on sodium-containing medications untenable. The widespread use of effervescent medication in the general population, and the enormous doses of sodium that can be consumed inadvertently by unsuspecting consumers requires urgent action,” Dr. Schutte and Dr. Neal say.

The study was supported by the National Natural Science Foundation of China, the National Key Research and Development Project, the Project Program of National Clinical Research Center for Geriatric Disorders, the Key Research and Development Program of Hunan Province, and the Science and Technology Program of Hunan Province. Dr. Zhang, Dr. Schutte, and Dr. Neal have disclosed no relevant financial relationships.

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

Regular use of acetaminophen, also known as paracetamol, in effervescent or soluble formulations that contain sodium increases the risk of cardiovascular disease (CVD) and death in people with or without hypertension, a large observational study of more than 300,000 adults suggests.

“Numerous studies have reported that high sodium intake is associated with increased risks of cardiovascular disease,” Yuqing Zhang, DSc, with Massachusetts General Hospital and Harvard Medical School, Boston, told this news organization. “Given that the pain relief effect of non–sodium-containing acetaminophen is similar to that of sodium-containing acetaminophen, clinicians may prescribe non–sodium-containing acetaminophen to their patients to minimize the risk of CVD and mortality,” Dr. Zhang said.

The study was published online Feb. 24 in the European Heart Journal.
 

‘Compelling results’

Dr. Zhang and colleagues note that the effervescent and soluble formulations of 0.5 g acetaminophen contain 0.44 and 0.39 g of sodium, respectively.

Therefore, the intake of maximum daily dose (4 g/day) of sodium-containing acetaminophen corresponds to the ingestion of more than 3 g of sodium, a dose that alone exceeds the recommended total daily sodium intake allowance of the World Health Organization (2 g/day).

“This hidden extra sodium intake is often overlooked,” Dr. Zhang told this news organization.

Using data from the Health Improvement Network, a U.K. primary care database, the researchers examined 4,532 patients with hypertension taking sodium-containing acetaminophen and compared them with 146,866 patients with hypertension taking non–sodium-containing acetaminophen (tablet, capsule, or oral suspension formulations).

After 1 year, the risk of incident CVD (myocardial infarction, stroke, and heart failure) was 5.6% in those taking sodium-containing acetaminophen, compared with 4.6% in those taking non–sodium-containing acetaminophen (average weighted hazard ratio, 1.59; 95% confidence interval, 1.32-1.92).

A separate analysis of normotensive patients taking sodium-containing acetaminophen (n = 5,351) or non–sodium-containing acetaminophen (n = 141,948) gave similar results.

The 1-year risk of incident CVD was 4.4% in those taking sodium-containing acetaminophen vs. 3.7% among those taking non–sodium-containing acetaminophen (average weighted HR, 1.45; 95% CI, 1.18-1.79).

There was also evidence of a dose-response relationship.

In those with hypertension, CVD risk increased by roughly one-quarter (odds ratio, 1.26) for those with one prescription of sodium-containing acetaminophen and by nearly one half (OR, 1.45) for those with five or more prescriptions of sodium-containing acetaminophen. Similar findings were observed among adults without hypertension.

Mortality at 1 year was also higher in those taking sodium-containing acetaminophen than non–sodium-containing acetaminophen, in patients with hypertension (7.6% vs. 6.1%) and without hypertension (7.3% vs. 5.9%).

“The results are compelling,” write the authors of an editorial published with the study.

“The direct message from this study is clear – there are likely to be millions of people worldwide taking paracetamol on a daily basis in a ‘fast-acting’ effervescent or soluble formulation who are increasing their risks of cardiovascular disease and premature death,” say Aletta Schutte, PhD, and Bruce Neal, MBChB, PhD, of the George Institute for Global Health, Sydney.

“The weight of the evidence makes ongoing inaction on sodium-containing medications untenable. The widespread use of effervescent medication in the general population, and the enormous doses of sodium that can be consumed inadvertently by unsuspecting consumers requires urgent action,” Dr. Schutte and Dr. Neal say.

The study was supported by the National Natural Science Foundation of China, the National Key Research and Development Project, the Project Program of National Clinical Research Center for Geriatric Disorders, the Key Research and Development Program of Hunan Province, and the Science and Technology Program of Hunan Province. Dr. Zhang, Dr. Schutte, and Dr. Neal have disclosed no relevant financial relationships.

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

Low-value health care services that provide little or no benefit to patients are “common, potentially harmful, and costly,” and there is a critical need to reduce this kind of care, the American Heart Association said in a newly released scientific statement.

Each year, nearly half of patients in the United States will receive at least one low-value test or procedure, with the attendant risk of avoidable complications from cascades of care and excess costs to individuals and society, the authors noted. Reducing low-value care is particularly important in cardiology, given the high prevalence and costs of cardiovascular disease in the United States.

The statement was published online Feb. 22, 2022, in Circulation: Cardiovascular Quality and Outcomes.
 

High burden with uncertain benefit

“Cardiovascular disease is common and can present suddenly, such as a heart attack or abnormal heart rhythm,” Vinay Kini, MD, chair of the statement writing group and assistant professor of medicine at Weill Cornell Medicine, New York, said in a news release.

“Our desire to be vigilant about treating and preventing cardiovascular disease may sometimes lead to use of tests and procedures where the benefits to patients may be uncertain,” Dr. Kini said. “This may impose burdens on patients, in the form of increased risk of physical harm from the low-value procedure or potential complications, as well as follow-up care and out-of-pocket financial costs.”

For example, studies have shown that up to one in five echocardiograms and up to half of all stress tests performed in the United States may be rated as rarely appropriate, based on established guidelines for their use.

In addition, up to 15% of percutaneous coronary interventions (PCIs) are classified as rarely appropriate, the writing group said.

Annually, among Medicare fee-for-service beneficiaries, low-value stress testing in patients with stable coronary artery disease is estimated to cost between $212 million and $2.1 billion, while costs of PCI for stable CAD range from $212 million to $2.8 billion, the writing group noted.

“At best, spending on low-value care potentially diverts resources from higher-value services that would benefit patients more effectively at the same or reduced cost. At worst, low-value care results in physical harm in the form of preventable morbidity and mortality,” they said.

“Thus, reducing low-value care is one of the few patient-centered solutions that directly address both the need to control health care spending and the societal imperative to devote its limited resources to beneficial health care services that improve health,” they added.

The group outlines several ways to reduce low-value cardiovascular care targeting patients, providers, and payers/policymakers.

For patients, education and shared decision-making may help reduce low-value care and dispel misconceptions about the intended purpose of test or treatment, they suggested.

For clinicians, a “layered” approach to reducing low-value care may be most effective, such as through education, audit and feedback, and behavioral science tools (“nudges”) to shift behaviors and practices, they said.

For payers and policy leaders, interventions to reduce low-value care include national insurance coverage determinations; prior authorization; alternative payment models that reward lower costs and higher-quality health care; value-based insurance designs that financially penalize low-value care; and medical liability reform to reduce defensive medical practices.

Low-value cardiovascular care is a complex problem, the writing group acknowledged, and achieving meaningful reductions in low-value cardiovascular care will require a multidisciplinary approach that includes continuous research, implementation, evaluation, and adjustment while ensuring equitable access to care.

“Each approach has benefits and drawbacks,” Dr. Kini said. “For example, prior authorization imposes a large burden on health care professionals to obtain insurance approval for tests and treatments. Prior authorization and some value-based payment models may unintentionally worsen existing racial and ethnic health care disparities.

“A one-size-fits-all approach to reducing low-value care is unlikely to succeed; rather, acting through multiple perspectives and frequently measuring impacts and potential unintended consequences is critical,” he concluded.

The scientific statement was prepared by the volunteer writing group on behalf of the AHA’s Council on Quality of Care and Outcomes Research.

The research had no commercial funding. Dr. Kini disclosed no relevant financial relationships.

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

Low-value health care services that provide little or no benefit to patients are “common, potentially harmful, and costly,” and there is a critical need to reduce this kind of care, the American Heart Association said in a newly released scientific statement.

Each year, nearly half of patients in the United States will receive at least one low-value test or procedure, with the attendant risk of avoidable complications from cascades of care and excess costs to individuals and society, the authors noted. Reducing low-value care is particularly important in cardiology, given the high prevalence and costs of cardiovascular disease in the United States.

The statement was published online Feb. 22, 2022, in Circulation: Cardiovascular Quality and Outcomes.
 

High burden with uncertain benefit

“Cardiovascular disease is common and can present suddenly, such as a heart attack or abnormal heart rhythm,” Vinay Kini, MD, chair of the statement writing group and assistant professor of medicine at Weill Cornell Medicine, New York, said in a news release.

“Our desire to be vigilant about treating and preventing cardiovascular disease may sometimes lead to use of tests and procedures where the benefits to patients may be uncertain,” Dr. Kini said. “This may impose burdens on patients, in the form of increased risk of physical harm from the low-value procedure or potential complications, as well as follow-up care and out-of-pocket financial costs.”

For example, studies have shown that up to one in five echocardiograms and up to half of all stress tests performed in the United States may be rated as rarely appropriate, based on established guidelines for their use.

In addition, up to 15% of percutaneous coronary interventions (PCIs) are classified as rarely appropriate, the writing group said.

Annually, among Medicare fee-for-service beneficiaries, low-value stress testing in patients with stable coronary artery disease is estimated to cost between $212 million and $2.1 billion, while costs of PCI for stable CAD range from $212 million to $2.8 billion, the writing group noted.

“At best, spending on low-value care potentially diverts resources from higher-value services that would benefit patients more effectively at the same or reduced cost. At worst, low-value care results in physical harm in the form of preventable morbidity and mortality,” they said.

“Thus, reducing low-value care is one of the few patient-centered solutions that directly address both the need to control health care spending and the societal imperative to devote its limited resources to beneficial health care services that improve health,” they added.

The group outlines several ways to reduce low-value cardiovascular care targeting patients, providers, and payers/policymakers.

For patients, education and shared decision-making may help reduce low-value care and dispel misconceptions about the intended purpose of test or treatment, they suggested.

For clinicians, a “layered” approach to reducing low-value care may be most effective, such as through education, audit and feedback, and behavioral science tools (“nudges”) to shift behaviors and practices, they said.

For payers and policy leaders, interventions to reduce low-value care include national insurance coverage determinations; prior authorization; alternative payment models that reward lower costs and higher-quality health care; value-based insurance designs that financially penalize low-value care; and medical liability reform to reduce defensive medical practices.

Low-value cardiovascular care is a complex problem, the writing group acknowledged, and achieving meaningful reductions in low-value cardiovascular care will require a multidisciplinary approach that includes continuous research, implementation, evaluation, and adjustment while ensuring equitable access to care.

“Each approach has benefits and drawbacks,” Dr. Kini said. “For example, prior authorization imposes a large burden on health care professionals to obtain insurance approval for tests and treatments. Prior authorization and some value-based payment models may unintentionally worsen existing racial and ethnic health care disparities.

“A one-size-fits-all approach to reducing low-value care is unlikely to succeed; rather, acting through multiple perspectives and frequently measuring impacts and potential unintended consequences is critical,” he concluded.

The scientific statement was prepared by the volunteer writing group on behalf of the AHA’s Council on Quality of Care and Outcomes Research.

The research had no commercial funding. Dr. Kini disclosed no relevant financial relationships.

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

Low-value health care services that provide little or no benefit to patients are “common, potentially harmful, and costly,” and there is a critical need to reduce this kind of care, the American Heart Association said in a newly released scientific statement.

Each year, nearly half of patients in the United States will receive at least one low-value test or procedure, with the attendant risk of avoidable complications from cascades of care and excess costs to individuals and society, the authors noted. Reducing low-value care is particularly important in cardiology, given the high prevalence and costs of cardiovascular disease in the United States.

The statement was published online Feb. 22, 2022, in Circulation: Cardiovascular Quality and Outcomes.
 

High burden with uncertain benefit

“Cardiovascular disease is common and can present suddenly, such as a heart attack or abnormal heart rhythm,” Vinay Kini, MD, chair of the statement writing group and assistant professor of medicine at Weill Cornell Medicine, New York, said in a news release.

“Our desire to be vigilant about treating and preventing cardiovascular disease may sometimes lead to use of tests and procedures where the benefits to patients may be uncertain,” Dr. Kini said. “This may impose burdens on patients, in the form of increased risk of physical harm from the low-value procedure or potential complications, as well as follow-up care and out-of-pocket financial costs.”

For example, studies have shown that up to one in five echocardiograms and up to half of all stress tests performed in the United States may be rated as rarely appropriate, based on established guidelines for their use.

In addition, up to 15% of percutaneous coronary interventions (PCIs) are classified as rarely appropriate, the writing group said.

Annually, among Medicare fee-for-service beneficiaries, low-value stress testing in patients with stable coronary artery disease is estimated to cost between $212 million and $2.1 billion, while costs of PCI for stable CAD range from $212 million to $2.8 billion, the writing group noted.

“At best, spending on low-value care potentially diverts resources from higher-value services that would benefit patients more effectively at the same or reduced cost. At worst, low-value care results in physical harm in the form of preventable morbidity and mortality,” they said.

“Thus, reducing low-value care is one of the few patient-centered solutions that directly address both the need to control health care spending and the societal imperative to devote its limited resources to beneficial health care services that improve health,” they added.

The group outlines several ways to reduce low-value cardiovascular care targeting patients, providers, and payers/policymakers.

For patients, education and shared decision-making may help reduce low-value care and dispel misconceptions about the intended purpose of test or treatment, they suggested.

For clinicians, a “layered” approach to reducing low-value care may be most effective, such as through education, audit and feedback, and behavioral science tools (“nudges”) to shift behaviors and practices, they said.

For payers and policy leaders, interventions to reduce low-value care include national insurance coverage determinations; prior authorization; alternative payment models that reward lower costs and higher-quality health care; value-based insurance designs that financially penalize low-value care; and medical liability reform to reduce defensive medical practices.

Low-value cardiovascular care is a complex problem, the writing group acknowledged, and achieving meaningful reductions in low-value cardiovascular care will require a multidisciplinary approach that includes continuous research, implementation, evaluation, and adjustment while ensuring equitable access to care.

“Each approach has benefits and drawbacks,” Dr. Kini said. “For example, prior authorization imposes a large burden on health care professionals to obtain insurance approval for tests and treatments. Prior authorization and some value-based payment models may unintentionally worsen existing racial and ethnic health care disparities.

“A one-size-fits-all approach to reducing low-value care is unlikely to succeed; rather, acting through multiple perspectives and frequently measuring impacts and potential unintended consequences is critical,” he concluded.

The scientific statement was prepared by the volunteer writing group on behalf of the AHA’s Council on Quality of Care and Outcomes Research.

The research had no commercial funding. Dr. Kini disclosed no relevant financial relationships.

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