Cardiology

Amplified by the childhood obesity epidemic, primary hypertension is now the leading type of pediatric hypertension, especially in adolescence, yet the condition is “underrecognized,” the American Heart Association said in a new scientific statement.

“Children can have secondary hypertension that is caused by an underlying condition such as chronic kidney disease, endocrine disorders, cardiac anomalies, and some syndromes. However, primary hypertension is now recognized as the most common type of hypertension in childhood,” Bonita Falkner, MD, chair of the writing group and emeritus professor of medicine and pediatrics, Thomas Jefferson University, Philadelphia, said in an interview.

And hypertensive children are “highly likely” to become hypertensive adults and to have measurable target organ injury, particularly left ventricular hypertrophy and vascular stiffening, the writing group noted. 

The AHA statement on primary pediatric hypertension was published online in Hypertension.

Primary or essential hypertension occurs in up to 5% of children and adolescents in the United States and other countries.

The American Academy of Pediatrics (AAP), European Society of Hypertension and Hypertension Canada all define hypertension as repeated BP readings at or above the 95th percentile for children, but the thresholds differ by age.

The AAP adopts 130/80 mm Hg starting at age 13 years; the European Society of Hypertension adopts 140/90 mm Hg starting at age 16 years; and Hypertension Canada adopts 120/80 mm Hg for those aged 6-11 years and 130/85 mm Hg for those aged 12-17 years.

Adolescents entering adulthood with a BP < 120/80 mm Hg is an optimal goal, the writing group advised.

They recommend that health care professionals be trained on evidence-based methods to obtain accurate and reliable BP values with either auscultatory or oscillometric methods.

When the initial BP measurement is abnormal, repeat measurement by auscultation is recommended, within the same visit if possible, and then within weeks if the screening BP is hypertensive, or months if the screening BP is elevated.

Because BP levels are variable, even within a single visit, “best practice” is to obtain up to three BP measurements and to record the average of the latter two measurements unless the first measurement is normal, the writing group said. Further confirmation of diagnosis of hypertension can be obtained with 24-hour ambulatory BP monitoring (ABPM).

“Primary hypertension in youth is difficult to recognize in asymptomatic, otherwise healthy youth. There is now evidence that children and adolescents with primary hypertension may also have cardiac and vascular injury due to the hypertension,” Dr. Falkner told this news organization.

“If not identified and treated, the condition can progress to hypertension in young adulthood with heightened risk of premature cardiovascular events,” Dr. Falkner said.

The writing group said “primordial prevention” is an important public health goal because a population with lower BP will have fewer comorbidities related to hypertension and CVD.

Modifiable risk factors for primary hypertension in childhood include obesity, physical inactivity and poor diet/nutrition, disturbed sleep patterns, and environmental stress.

A healthy lifestyle in childhood – including eating healthy food, encouraging physical activity that leads to improved physical fitness and healthy sleep, and avoiding the development of obesity – may help mitigate the risk of hypertension in childhood, the writing group noted.  

Looking ahead, they said efforts to improve recognition and diagnosis of high BP in children, as well as clinical trials to evaluate medical treatment and recommend public health initiatives, are all vital to combat rising rates of primary hypertension in children.

This scientific statement was prepared by the volunteer writing group on behalf of the American Heart Association’s Council on Hypertension, the Council on Lifelong Congenital Heart Disease and Heart Health in the Young, the Council on Kidney in Cardiovascular Disease, the Council on Lifestyle and Cardiometabolic Health, and the Council on Cardiovascular and Stroke Nursing.
 

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

Amplified by the childhood obesity epidemic, primary hypertension is now the leading type of pediatric hypertension, especially in adolescence, yet the condition is “underrecognized,” the American Heart Association said in a new scientific statement.

“Children can have secondary hypertension that is caused by an underlying condition such as chronic kidney disease, endocrine disorders, cardiac anomalies, and some syndromes. However, primary hypertension is now recognized as the most common type of hypertension in childhood,” Bonita Falkner, MD, chair of the writing group and emeritus professor of medicine and pediatrics, Thomas Jefferson University, Philadelphia, said in an interview.

And hypertensive children are “highly likely” to become hypertensive adults and to have measurable target organ injury, particularly left ventricular hypertrophy and vascular stiffening, the writing group noted. 

The AHA statement on primary pediatric hypertension was published online in Hypertension.

Primary or essential hypertension occurs in up to 5% of children and adolescents in the United States and other countries.

The American Academy of Pediatrics (AAP), European Society of Hypertension and Hypertension Canada all define hypertension as repeated BP readings at or above the 95th percentile for children, but the thresholds differ by age.

The AAP adopts 130/80 mm Hg starting at age 13 years; the European Society of Hypertension adopts 140/90 mm Hg starting at age 16 years; and Hypertension Canada adopts 120/80 mm Hg for those aged 6-11 years and 130/85 mm Hg for those aged 12-17 years.

Adolescents entering adulthood with a BP < 120/80 mm Hg is an optimal goal, the writing group advised.

They recommend that health care professionals be trained on evidence-based methods to obtain accurate and reliable BP values with either auscultatory or oscillometric methods.

When the initial BP measurement is abnormal, repeat measurement by auscultation is recommended, within the same visit if possible, and then within weeks if the screening BP is hypertensive, or months if the screening BP is elevated.

Because BP levels are variable, even within a single visit, “best practice” is to obtain up to three BP measurements and to record the average of the latter two measurements unless the first measurement is normal, the writing group said. Further confirmation of diagnosis of hypertension can be obtained with 24-hour ambulatory BP monitoring (ABPM).

“Primary hypertension in youth is difficult to recognize in asymptomatic, otherwise healthy youth. There is now evidence that children and adolescents with primary hypertension may also have cardiac and vascular injury due to the hypertension,” Dr. Falkner told this news organization.

“If not identified and treated, the condition can progress to hypertension in young adulthood with heightened risk of premature cardiovascular events,” Dr. Falkner said.

The writing group said “primordial prevention” is an important public health goal because a population with lower BP will have fewer comorbidities related to hypertension and CVD.

Modifiable risk factors for primary hypertension in childhood include obesity, physical inactivity and poor diet/nutrition, disturbed sleep patterns, and environmental stress.

A healthy lifestyle in childhood – including eating healthy food, encouraging physical activity that leads to improved physical fitness and healthy sleep, and avoiding the development of obesity – may help mitigate the risk of hypertension in childhood, the writing group noted.  

Looking ahead, they said efforts to improve recognition and diagnosis of high BP in children, as well as clinical trials to evaluate medical treatment and recommend public health initiatives, are all vital to combat rising rates of primary hypertension in children.

This scientific statement was prepared by the volunteer writing group on behalf of the American Heart Association’s Council on Hypertension, the Council on Lifelong Congenital Heart Disease and Heart Health in the Young, the Council on Kidney in Cardiovascular Disease, the Council on Lifestyle and Cardiometabolic Health, and the Council on Cardiovascular and Stroke Nursing.
 

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

Amplified by the childhood obesity epidemic, primary hypertension is now the leading type of pediatric hypertension, especially in adolescence, yet the condition is “underrecognized,” the American Heart Association said in a new scientific statement.

“Children can have secondary hypertension that is caused by an underlying condition such as chronic kidney disease, endocrine disorders, cardiac anomalies, and some syndromes. However, primary hypertension is now recognized as the most common type of hypertension in childhood,” Bonita Falkner, MD, chair of the writing group and emeritus professor of medicine and pediatrics, Thomas Jefferson University, Philadelphia, said in an interview.

And hypertensive children are “highly likely” to become hypertensive adults and to have measurable target organ injury, particularly left ventricular hypertrophy and vascular stiffening, the writing group noted. 

The AHA statement on primary pediatric hypertension was published online in Hypertension.

Primary or essential hypertension occurs in up to 5% of children and adolescents in the United States and other countries.

The American Academy of Pediatrics (AAP), European Society of Hypertension and Hypertension Canada all define hypertension as repeated BP readings at or above the 95th percentile for children, but the thresholds differ by age.

The AAP adopts 130/80 mm Hg starting at age 13 years; the European Society of Hypertension adopts 140/90 mm Hg starting at age 16 years; and Hypertension Canada adopts 120/80 mm Hg for those aged 6-11 years and 130/85 mm Hg for those aged 12-17 years.

Adolescents entering adulthood with a BP < 120/80 mm Hg is an optimal goal, the writing group advised.

They recommend that health care professionals be trained on evidence-based methods to obtain accurate and reliable BP values with either auscultatory or oscillometric methods.

When the initial BP measurement is abnormal, repeat measurement by auscultation is recommended, within the same visit if possible, and then within weeks if the screening BP is hypertensive, or months if the screening BP is elevated.

Because BP levels are variable, even within a single visit, “best practice” is to obtain up to three BP measurements and to record the average of the latter two measurements unless the first measurement is normal, the writing group said. Further confirmation of diagnosis of hypertension can be obtained with 24-hour ambulatory BP monitoring (ABPM).

“Primary hypertension in youth is difficult to recognize in asymptomatic, otherwise healthy youth. There is now evidence that children and adolescents with primary hypertension may also have cardiac and vascular injury due to the hypertension,” Dr. Falkner told this news organization.

“If not identified and treated, the condition can progress to hypertension in young adulthood with heightened risk of premature cardiovascular events,” Dr. Falkner said.

The writing group said “primordial prevention” is an important public health goal because a population with lower BP will have fewer comorbidities related to hypertension and CVD.

Modifiable risk factors for primary hypertension in childhood include obesity, physical inactivity and poor diet/nutrition, disturbed sleep patterns, and environmental stress.

A healthy lifestyle in childhood – including eating healthy food, encouraging physical activity that leads to improved physical fitness and healthy sleep, and avoiding the development of obesity – may help mitigate the risk of hypertension in childhood, the writing group noted.  

Looking ahead, they said efforts to improve recognition and diagnosis of high BP in children, as well as clinical trials to evaluate medical treatment and recommend public health initiatives, are all vital to combat rising rates of primary hypertension in children.

This scientific statement was prepared by the volunteer writing group on behalf of the American Heart Association’s Council on Hypertension, the Council on Lifelong Congenital Heart Disease and Heart Health in the Young, the Council on Kidney in Cardiovascular Disease, the Council on Lifestyle and Cardiometabolic Health, and the Council on Cardiovascular and Stroke Nursing.
 

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

Researchers have identified specific regions of the brain that appear to be damaged by high blood pressure. The finding may explain the link between hypertension and cognitive impairment.

They used genetic information from genome-wide association studies (GWASs) and MRI scans of the brain to study the relationship between hypertension, changes in brain structures, and cognitive impairment. Using Mendelian randomization techniques, they identified nine brain structures related to cognitive impairment that are affected by blood pressure.

Dr Lorenzo Carnevale, IRCCS INM Neuromed, Pozzilli, Italy

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

Researchers have identified specific regions of the brain that appear to be damaged by high blood pressure. The finding may explain the link between hypertension and cognitive impairment.

They used genetic information from genome-wide association studies (GWASs) and MRI scans of the brain to study the relationship between hypertension, changes in brain structures, and cognitive impairment. Using Mendelian randomization techniques, they identified nine brain structures related to cognitive impairment that are affected by blood pressure.

Dr Lorenzo Carnevale, IRCCS INM Neuromed, Pozzilli, Italy

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

Researchers have identified specific regions of the brain that appear to be damaged by high blood pressure. The finding may explain the link between hypertension and cognitive impairment.

They used genetic information from genome-wide association studies (GWASs) and MRI scans of the brain to study the relationship between hypertension, changes in brain structures, and cognitive impairment. Using Mendelian randomization techniques, they identified nine brain structures related to cognitive impairment that are affected by blood pressure.

Dr Lorenzo Carnevale, IRCCS INM Neuromed, Pozzilli, Italy

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

A statement released by the American Heart Association and the American College of Cardiology advocates use of supervised exercise training in patients with heart failure with preserved ejection fraction (HFpEF), as well as coverage for these services by third-party payers.

The authors hope to boost the stature of supervised exercise training (SET) in HFpEF among practitioners and show Medicare and insurers that it deserves reimbursement. Currently, they noted, clinicians tend to recognize exercise as therapy more in HF with reduced ejection fraction (HFrEF). And Medicare covers exercise training within broader cardiac rehabilitation programs for patients with HFrEF but not HFpEF.

Yet exercise has been broadly effective in HFpEF clinical trials, as outlined in the document. And there are good mechanistic reasons to believe that patients with the disorder can gain as much or more from SET than those with HFrEF.

“The signals for improvement from exercise training, in symptoms and objective measures of exercise capacity, are considerably larger for HFpEF than for HFrEF,” Dalane W. Kitzman, MD, Wake Forest University, Winston-Salem, N.C., said in an interview.

So, it’s a bit of a paradox that clinicians don’t prescribe it as often in HFpEF, probably because of the lack of reimbursement but also from less “awareness” and understanding of the disease itself, he proposed.

Dr. Kitzman is senior author on the statement sponsored by the AHA and the ACC. It was published in the societies’ flagship journals Circulation and the Journal of the American College of Cardiology. The statement was also endorsed by the Heart Failure Society of America, the American Association of Cardiovascular and Pulmonary Rehabilitation, and the American Association of Heart Failure Nurses.
 

Carefully chosen words

The statement makes its case in HFpEF specifically for SET rather than cardiac rehabilitation, the latter typically a comprehensive program that goes beyond exercise, Dr. Kitzman noted. And SET is closer to the exercise interventions used in the supportive HFpEF trials.

“Also, Medicare in recent years has approved something called ‘supervised exercise training’ for other disorders, such as peripheral artery disease.” So, the document specifies SET “to be fully aligned with the evidence base,” he said, as well as “align it with a type of treatment that Medicare has a precedent for approving for other disorders.”
 

Data and physiologic basis

Core features of the AHA/ACC statement is its review of HFpEF exercise physiology, survey of randomized trials supporting SET in the disease, and characterization of exercise as an especially suitable pleiotropic therapy.

Increasingly, “HFpEF is now accepted as a systemic disorder that affects and impacts all organs,” Dr. Kitzman observed. “With a systemic multiorgan disorder, it would make sense that a broad treatment like exercise might be just the right thing. We think that’s the reason that its benefits are really quite large in magnitude.”

The document notes that exercise seems “potentially well suited for the treatment of both the cardiac and, in particular, the extracardiac abnormalities that contribute to exercise intolerance in HFpEF.”

Its effects in the disorder are “anti-inflammatory, rheological, lipid lowering, antihypertensive, positive inotropic, positive lusitropic, negative chronotropic, vasodilation, diuretic, weight-reducing, hypoglycemic, hypnotic, and antidepressive,” the statement notes. It achieves them via multiple pathways involving the heart, lungs, vasculature and, notably, the skeletal muscles.

“It’s been widely overlooked that at least 50% of low exercise capacity and symptoms in HFpEF are due to skeletal muscle dysfunction,” said Dr. Kitzman, an authority on exercise physiology in heart failure.

“But we’ve spent about 95% of our attention trying to modify and understand the cardiac component.” Skeletal muscles, he said, “are not an innocent bystander. They’re part of the problem. And that’s why we should really spend more time focusing on them.”

Dr. Kitzman disclosed receiving consulting fees from Bayer, Medtronic, Corvia Medical, Boehringer Ingelheim, Keyto, Rivus, NovoNordisk, AstraZeneca, and Pfizer; holding stock in Gilead; and receiving grants to his institution from Bayer, Novo Nordisk, AstraZeneca, Rivus, and Pfizer.

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

A statement released by the American Heart Association and the American College of Cardiology advocates use of supervised exercise training in patients with heart failure with preserved ejection fraction (HFpEF), as well as coverage for these services by third-party payers.

The authors hope to boost the stature of supervised exercise training (SET) in HFpEF among practitioners and show Medicare and insurers that it deserves reimbursement. Currently, they noted, clinicians tend to recognize exercise as therapy more in HF with reduced ejection fraction (HFrEF). And Medicare covers exercise training within broader cardiac rehabilitation programs for patients with HFrEF but not HFpEF.

Yet exercise has been broadly effective in HFpEF clinical trials, as outlined in the document. And there are good mechanistic reasons to believe that patients with the disorder can gain as much or more from SET than those with HFrEF.

“The signals for improvement from exercise training, in symptoms and objective measures of exercise capacity, are considerably larger for HFpEF than for HFrEF,” Dalane W. Kitzman, MD, Wake Forest University, Winston-Salem, N.C., said in an interview.

So, it’s a bit of a paradox that clinicians don’t prescribe it as often in HFpEF, probably because of the lack of reimbursement but also from less “awareness” and understanding of the disease itself, he proposed.

Dr. Kitzman is senior author on the statement sponsored by the AHA and the ACC. It was published in the societies’ flagship journals Circulation and the Journal of the American College of Cardiology. The statement was also endorsed by the Heart Failure Society of America, the American Association of Cardiovascular and Pulmonary Rehabilitation, and the American Association of Heart Failure Nurses.
 

Carefully chosen words

The statement makes its case in HFpEF specifically for SET rather than cardiac rehabilitation, the latter typically a comprehensive program that goes beyond exercise, Dr. Kitzman noted. And SET is closer to the exercise interventions used in the supportive HFpEF trials.

“Also, Medicare in recent years has approved something called ‘supervised exercise training’ for other disorders, such as peripheral artery disease.” So, the document specifies SET “to be fully aligned with the evidence base,” he said, as well as “align it with a type of treatment that Medicare has a precedent for approving for other disorders.”
 

Data and physiologic basis

Core features of the AHA/ACC statement is its review of HFpEF exercise physiology, survey of randomized trials supporting SET in the disease, and characterization of exercise as an especially suitable pleiotropic therapy.

Increasingly, “HFpEF is now accepted as a systemic disorder that affects and impacts all organs,” Dr. Kitzman observed. “With a systemic multiorgan disorder, it would make sense that a broad treatment like exercise might be just the right thing. We think that’s the reason that its benefits are really quite large in magnitude.”

The document notes that exercise seems “potentially well suited for the treatment of both the cardiac and, in particular, the extracardiac abnormalities that contribute to exercise intolerance in HFpEF.”

Its effects in the disorder are “anti-inflammatory, rheological, lipid lowering, antihypertensive, positive inotropic, positive lusitropic, negative chronotropic, vasodilation, diuretic, weight-reducing, hypoglycemic, hypnotic, and antidepressive,” the statement notes. It achieves them via multiple pathways involving the heart, lungs, vasculature and, notably, the skeletal muscles.

“It’s been widely overlooked that at least 50% of low exercise capacity and symptoms in HFpEF are due to skeletal muscle dysfunction,” said Dr. Kitzman, an authority on exercise physiology in heart failure.

“But we’ve spent about 95% of our attention trying to modify and understand the cardiac component.” Skeletal muscles, he said, “are not an innocent bystander. They’re part of the problem. And that’s why we should really spend more time focusing on them.”

Dr. Kitzman disclosed receiving consulting fees from Bayer, Medtronic, Corvia Medical, Boehringer Ingelheim, Keyto, Rivus, NovoNordisk, AstraZeneca, and Pfizer; holding stock in Gilead; and receiving grants to his institution from Bayer, Novo Nordisk, AstraZeneca, Rivus, and Pfizer.

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

A statement released by the American Heart Association and the American College of Cardiology advocates use of supervised exercise training in patients with heart failure with preserved ejection fraction (HFpEF), as well as coverage for these services by third-party payers.

The authors hope to boost the stature of supervised exercise training (SET) in HFpEF among practitioners and show Medicare and insurers that it deserves reimbursement. Currently, they noted, clinicians tend to recognize exercise as therapy more in HF with reduced ejection fraction (HFrEF). And Medicare covers exercise training within broader cardiac rehabilitation programs for patients with HFrEF but not HFpEF.

Yet exercise has been broadly effective in HFpEF clinical trials, as outlined in the document. And there are good mechanistic reasons to believe that patients with the disorder can gain as much or more from SET than those with HFrEF.

“The signals for improvement from exercise training, in symptoms and objective measures of exercise capacity, are considerably larger for HFpEF than for HFrEF,” Dalane W. Kitzman, MD, Wake Forest University, Winston-Salem, N.C., said in an interview.

So, it’s a bit of a paradox that clinicians don’t prescribe it as often in HFpEF, probably because of the lack of reimbursement but also from less “awareness” and understanding of the disease itself, he proposed.

Dr. Kitzman is senior author on the statement sponsored by the AHA and the ACC. It was published in the societies’ flagship journals Circulation and the Journal of the American College of Cardiology. The statement was also endorsed by the Heart Failure Society of America, the American Association of Cardiovascular and Pulmonary Rehabilitation, and the American Association of Heart Failure Nurses.
 

Carefully chosen words

The statement makes its case in HFpEF specifically for SET rather than cardiac rehabilitation, the latter typically a comprehensive program that goes beyond exercise, Dr. Kitzman noted. And SET is closer to the exercise interventions used in the supportive HFpEF trials.

“Also, Medicare in recent years has approved something called ‘supervised exercise training’ for other disorders, such as peripheral artery disease.” So, the document specifies SET “to be fully aligned with the evidence base,” he said, as well as “align it with a type of treatment that Medicare has a precedent for approving for other disorders.”
 

Data and physiologic basis

Core features of the AHA/ACC statement is its review of HFpEF exercise physiology, survey of randomized trials supporting SET in the disease, and characterization of exercise as an especially suitable pleiotropic therapy.

Increasingly, “HFpEF is now accepted as a systemic disorder that affects and impacts all organs,” Dr. Kitzman observed. “With a systemic multiorgan disorder, it would make sense that a broad treatment like exercise might be just the right thing. We think that’s the reason that its benefits are really quite large in magnitude.”

The document notes that exercise seems “potentially well suited for the treatment of both the cardiac and, in particular, the extracardiac abnormalities that contribute to exercise intolerance in HFpEF.”

Its effects in the disorder are “anti-inflammatory, rheological, lipid lowering, antihypertensive, positive inotropic, positive lusitropic, negative chronotropic, vasodilation, diuretic, weight-reducing, hypoglycemic, hypnotic, and antidepressive,” the statement notes. It achieves them via multiple pathways involving the heart, lungs, vasculature and, notably, the skeletal muscles.

“It’s been widely overlooked that at least 50% of low exercise capacity and symptoms in HFpEF are due to skeletal muscle dysfunction,” said Dr. Kitzman, an authority on exercise physiology in heart failure.

“But we’ve spent about 95% of our attention trying to modify and understand the cardiac component.” Skeletal muscles, he said, “are not an innocent bystander. They’re part of the problem. And that’s why we should really spend more time focusing on them.”

Dr. Kitzman disclosed receiving consulting fees from Bayer, Medtronic, Corvia Medical, Boehringer Ingelheim, Keyto, Rivus, NovoNordisk, AstraZeneca, and Pfizer; holding stock in Gilead; and receiving grants to his institution from Bayer, Novo Nordisk, AstraZeneca, Rivus, and Pfizer.

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

Just 16% of psoriasis-related visits to dermatology providers in the United States involve screening for cardiovascular (CV) risk factors, with screening lowest in the region with the highest CV disease burden, according to an analysis of 10 years of national survey data.

From 2007 to 2016, national screening rates for four CV risk factors at 14.8 million psoriasis-related visits to dermatology providers were 11% (body-mass index), 7.4% (blood pressure), 2.9% (cholesterol), and 1.7% (glucose). Data from the National Ambulatory Medical Care Survey showed that at least one of the four factors was screened at 16% of dermatology visits, said William B. Song, BS, of the department of dermatology, University of Pennsylvania, Philadelphia, and associates.

The main focus of their study, however, was regional differences. “CV risk factor screening by dermatology providers for patients with psoriasis is low across all regions of the United States and lowest in the South, the region that experiences the highest CVD burden in the United States,” they wrote in a letter to the editor.

Compared with the South, the adjusted odds of any CV screening were 0.98 in the West, 1.25 in the Northeast, and 1.92 in the Midwest. Blood pressure screening was significantly higher in all three regions, compared with the South, while BMI screening was actually lower in the West (0.74), the investigators reported. Odds ratios were not available for cholesterol and glucose screening because of sample size limitations.

The regional variation in screening rates “is not explained by patient demographics or disease severity,” they noted, adding that 2.8 million visits with BP screening would have been added over the 10-year study period “if providers in the South screened patients with psoriasis for high blood pressure at the same rate as providers in the Northeast.”

Guidelines published in 2019 by the American Academy of Dermatology and the National Psoriasis Foundation – which were cowritten by Joel M. Gelfand, MD, senior author of the current study – noted that dermatologists “play an important role in evidence-based screening of CV risk factors in patients with psoriasis,” the investigators wrote. But the regional variations suggest “that some regions experience barriers to appropriate screening or challenges in adhering to guidelines for managing psoriasis and CV risk.”

While the lack of data from after 2016 is one of the study limitations, they added, “continued efforts to develop effective interventions to improve CV screening and care for people with psoriasis in all regions of the U.S. are needed to more effectively address the burden of CV disease experienced by people with psoriasis.”

The study was partly funded by the National Psoriasis Foundation. Three of the seven investigators disclosed earnings from private companies in the form of consultant fees, research support, and honoraria. Dr. Gelfand is a deputy editor for the Journal of Investigative Dermatology.

Just 16% of psoriasis-related visits to dermatology providers in the United States involve screening for cardiovascular (CV) risk factors, with screening lowest in the region with the highest CV disease burden, according to an analysis of 10 years of national survey data.

From 2007 to 2016, national screening rates for four CV risk factors at 14.8 million psoriasis-related visits to dermatology providers were 11% (body-mass index), 7.4% (blood pressure), 2.9% (cholesterol), and 1.7% (glucose). Data from the National Ambulatory Medical Care Survey showed that at least one of the four factors was screened at 16% of dermatology visits, said William B. Song, BS, of the department of dermatology, University of Pennsylvania, Philadelphia, and associates.

The main focus of their study, however, was regional differences. “CV risk factor screening by dermatology providers for patients with psoriasis is low across all regions of the United States and lowest in the South, the region that experiences the highest CVD burden in the United States,” they wrote in a letter to the editor.

Compared with the South, the adjusted odds of any CV screening were 0.98 in the West, 1.25 in the Northeast, and 1.92 in the Midwest. Blood pressure screening was significantly higher in all three regions, compared with the South, while BMI screening was actually lower in the West (0.74), the investigators reported. Odds ratios were not available for cholesterol and glucose screening because of sample size limitations.

The regional variation in screening rates “is not explained by patient demographics or disease severity,” they noted, adding that 2.8 million visits with BP screening would have been added over the 10-year study period “if providers in the South screened patients with psoriasis for high blood pressure at the same rate as providers in the Northeast.”

Guidelines published in 2019 by the American Academy of Dermatology and the National Psoriasis Foundation – which were cowritten by Joel M. Gelfand, MD, senior author of the current study – noted that dermatologists “play an important role in evidence-based screening of CV risk factors in patients with psoriasis,” the investigators wrote. But the regional variations suggest “that some regions experience barriers to appropriate screening or challenges in adhering to guidelines for managing psoriasis and CV risk.”

While the lack of data from after 2016 is one of the study limitations, they added, “continued efforts to develop effective interventions to improve CV screening and care for people with psoriasis in all regions of the U.S. are needed to more effectively address the burden of CV disease experienced by people with psoriasis.”

The study was partly funded by the National Psoriasis Foundation. Three of the seven investigators disclosed earnings from private companies in the form of consultant fees, research support, and honoraria. Dr. Gelfand is a deputy editor for the Journal of Investigative Dermatology.

Just 16% of psoriasis-related visits to dermatology providers in the United States involve screening for cardiovascular (CV) risk factors, with screening lowest in the region with the highest CV disease burden, according to an analysis of 10 years of national survey data.

From 2007 to 2016, national screening rates for four CV risk factors at 14.8 million psoriasis-related visits to dermatology providers were 11% (body-mass index), 7.4% (blood pressure), 2.9% (cholesterol), and 1.7% (glucose). Data from the National Ambulatory Medical Care Survey showed that at least one of the four factors was screened at 16% of dermatology visits, said William B. Song, BS, of the department of dermatology, University of Pennsylvania, Philadelphia, and associates.

The main focus of their study, however, was regional differences. “CV risk factor screening by dermatology providers for patients with psoriasis is low across all regions of the United States and lowest in the South, the region that experiences the highest CVD burden in the United States,” they wrote in a letter to the editor.

Compared with the South, the adjusted odds of any CV screening were 0.98 in the West, 1.25 in the Northeast, and 1.92 in the Midwest. Blood pressure screening was significantly higher in all three regions, compared with the South, while BMI screening was actually lower in the West (0.74), the investigators reported. Odds ratios were not available for cholesterol and glucose screening because of sample size limitations.

The regional variation in screening rates “is not explained by patient demographics or disease severity,” they noted, adding that 2.8 million visits with BP screening would have been added over the 10-year study period “if providers in the South screened patients with psoriasis for high blood pressure at the same rate as providers in the Northeast.”

Guidelines published in 2019 by the American Academy of Dermatology and the National Psoriasis Foundation – which were cowritten by Joel M. Gelfand, MD, senior author of the current study – noted that dermatologists “play an important role in evidence-based screening of CV risk factors in patients with psoriasis,” the investigators wrote. But the regional variations suggest “that some regions experience barriers to appropriate screening or challenges in adhering to guidelines for managing psoriasis and CV risk.”

While the lack of data from after 2016 is one of the study limitations, they added, “continued efforts to develop effective interventions to improve CV screening and care for people with psoriasis in all regions of the U.S. are needed to more effectively address the burden of CV disease experienced by people with psoriasis.”

The study was partly funded by the National Psoriasis Foundation. Three of the seven investigators disclosed earnings from private companies in the form of consultant fees, research support, and honoraria. Dr. Gelfand is a deputy editor for the Journal of Investigative Dermatology.

In an analysis of randomized trials, the Mediterranean diet and low-fat diets were linked to reduced risks of all-cause mortality and nonfatal MI over 3 years in adults at increased risk for cardiovascular disease (CVD), while the Mediterranean diet also showed lower risk of stroke.

Five other popular diets appeared to have little or no benefit with regard to these outcomes.

“These findings with data presentations are extremely important for patients who are skeptical about the desirability of diet change,” wrote the authors, led by Giorgio Karam, a medical student at the University of Manitoba, Winnipeg.

The results were published online in The BMJ.

Dietary guidelines recommend various diets along with physical activity or other cointerventions for adults at increased CVD risk, but they are often based on low-certainty evidence from nonrandomized studies and on surrogate outcomes.

Several meta-analyses of randomized controlled trials with mortality and major CV outcomes have reported benefits of some dietary programs, but those studies did not use network meta-analysis to give absolute estimates and certainty of estimates for adults at intermediate and high risk, the authors noted.

For this study, Mr. Karam and colleagues conducted a comprehensive systematic review and network meta-analysis in which they compared the effects of seven popular structured diets on mortality and CVD events for adults with CVD or CVD risk factors.

The seven diet plans were the Mediterranean, low fat, very low fat, modified fat, combined low fat and low sodium, Ornish, and Pritikin diets. Data for the analysis came from 40 randomized controlled trials that involved 35,548 participants who were followed for an average of 3 years.

There was evidence of “moderate” certainty that the Mediterranean diet was superior to minimal intervention for all-cause mortality (odds ratio [OR], 0.72), CV mortality (OR, 0.55), stroke (OR, 0.65), and nonfatal MI (OR, 0.48).

On an absolute basis (per 1,000 over 5 years), the Mediterranean diet let to 17 fewer deaths from any cause, 13 fewer CV deaths, seven fewer strokes, and 17 fewer nonfatal MIs.

There was evidence of moderate certainty that a low-fat diet was superior to minimal intervention for prevention of all-cause mortality (OR, 0.84; nine fewer deaths per 1,000) and nonfatal MI (OR, 0.77; seven fewer deaths per 1,000). The low-fat diet had little to no benefit with regard to stroke reduction.

The Mediterranean diet was not “convincingly” superior to a low-fat diet for mortality or nonfatal MI, the authors noted.

The absolute effects for the Mediterranean and low-fat diets were more pronounced in adults at high CVD risk. With the Mediterranean diet, there were 36 fewer all-cause deaths and 39 fewer CV deaths per 1,000 over 5 years.

The five other dietary programs generally had “little or no benefit” compared with minimal intervention. The evidence was of low to moderate certainty.

The studies did not provide enough data to gauge the impact of the diets on angina, heart failure, peripheral vascular events, and atrial fibrillation.

The researchers say that strengths of their analysis include a comprehensive review and thorough literature search and a rigorous assessment of study bias. In addition, the researchers adhered to recognized GRADE methods for assessing the certainty of estimates.

Limitations of their work include not being able to measure adherence to dietary programs and the possibility that some of the benefits may have been due to other factors, such as drug treatment and support for quitting smoking.

The study had no specific funding. The authors have disclosed no relevant financial relationships.

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

In an analysis of randomized trials, the Mediterranean diet and low-fat diets were linked to reduced risks of all-cause mortality and nonfatal MI over 3 years in adults at increased risk for cardiovascular disease (CVD), while the Mediterranean diet also showed lower risk of stroke.

Five other popular diets appeared to have little or no benefit with regard to these outcomes.

“These findings with data presentations are extremely important for patients who are skeptical about the desirability of diet change,” wrote the authors, led by Giorgio Karam, a medical student at the University of Manitoba, Winnipeg.

The results were published online in The BMJ.

Dietary guidelines recommend various diets along with physical activity or other cointerventions for adults at increased CVD risk, but they are often based on low-certainty evidence from nonrandomized studies and on surrogate outcomes.

Several meta-analyses of randomized controlled trials with mortality and major CV outcomes have reported benefits of some dietary programs, but those studies did not use network meta-analysis to give absolute estimates and certainty of estimates for adults at intermediate and high risk, the authors noted.

For this study, Mr. Karam and colleagues conducted a comprehensive systematic review and network meta-analysis in which they compared the effects of seven popular structured diets on mortality and CVD events for adults with CVD or CVD risk factors.

The seven diet plans were the Mediterranean, low fat, very low fat, modified fat, combined low fat and low sodium, Ornish, and Pritikin diets. Data for the analysis came from 40 randomized controlled trials that involved 35,548 participants who were followed for an average of 3 years.

There was evidence of “moderate” certainty that the Mediterranean diet was superior to minimal intervention for all-cause mortality (odds ratio [OR], 0.72), CV mortality (OR, 0.55), stroke (OR, 0.65), and nonfatal MI (OR, 0.48).

On an absolute basis (per 1,000 over 5 years), the Mediterranean diet let to 17 fewer deaths from any cause, 13 fewer CV deaths, seven fewer strokes, and 17 fewer nonfatal MIs.

There was evidence of moderate certainty that a low-fat diet was superior to minimal intervention for prevention of all-cause mortality (OR, 0.84; nine fewer deaths per 1,000) and nonfatal MI (OR, 0.77; seven fewer deaths per 1,000). The low-fat diet had little to no benefit with regard to stroke reduction.

The Mediterranean diet was not “convincingly” superior to a low-fat diet for mortality or nonfatal MI, the authors noted.

The absolute effects for the Mediterranean and low-fat diets were more pronounced in adults at high CVD risk. With the Mediterranean diet, there were 36 fewer all-cause deaths and 39 fewer CV deaths per 1,000 over 5 years.

The five other dietary programs generally had “little or no benefit” compared with minimal intervention. The evidence was of low to moderate certainty.

The studies did not provide enough data to gauge the impact of the diets on angina, heart failure, peripheral vascular events, and atrial fibrillation.

The researchers say that strengths of their analysis include a comprehensive review and thorough literature search and a rigorous assessment of study bias. In addition, the researchers adhered to recognized GRADE methods for assessing the certainty of estimates.

Limitations of their work include not being able to measure adherence to dietary programs and the possibility that some of the benefits may have been due to other factors, such as drug treatment and support for quitting smoking.

The study had no specific funding. The authors have disclosed no relevant financial relationships.

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

In an analysis of randomized trials, the Mediterranean diet and low-fat diets were linked to reduced risks of all-cause mortality and nonfatal MI over 3 years in adults at increased risk for cardiovascular disease (CVD), while the Mediterranean diet also showed lower risk of stroke.

Five other popular diets appeared to have little or no benefit with regard to these outcomes.

“These findings with data presentations are extremely important for patients who are skeptical about the desirability of diet change,” wrote the authors, led by Giorgio Karam, a medical student at the University of Manitoba, Winnipeg.

The results were published online in The BMJ.

Dietary guidelines recommend various diets along with physical activity or other cointerventions for adults at increased CVD risk, but they are often based on low-certainty evidence from nonrandomized studies and on surrogate outcomes.

Several meta-analyses of randomized controlled trials with mortality and major CV outcomes have reported benefits of some dietary programs, but those studies did not use network meta-analysis to give absolute estimates and certainty of estimates for adults at intermediate and high risk, the authors noted.

For this study, Mr. Karam and colleagues conducted a comprehensive systematic review and network meta-analysis in which they compared the effects of seven popular structured diets on mortality and CVD events for adults with CVD or CVD risk factors.

The seven diet plans were the Mediterranean, low fat, very low fat, modified fat, combined low fat and low sodium, Ornish, and Pritikin diets. Data for the analysis came from 40 randomized controlled trials that involved 35,548 participants who were followed for an average of 3 years.

There was evidence of “moderate” certainty that the Mediterranean diet was superior to minimal intervention for all-cause mortality (odds ratio [OR], 0.72), CV mortality (OR, 0.55), stroke (OR, 0.65), and nonfatal MI (OR, 0.48).

On an absolute basis (per 1,000 over 5 years), the Mediterranean diet let to 17 fewer deaths from any cause, 13 fewer CV deaths, seven fewer strokes, and 17 fewer nonfatal MIs.

There was evidence of moderate certainty that a low-fat diet was superior to minimal intervention for prevention of all-cause mortality (OR, 0.84; nine fewer deaths per 1,000) and nonfatal MI (OR, 0.77; seven fewer deaths per 1,000). The low-fat diet had little to no benefit with regard to stroke reduction.

The Mediterranean diet was not “convincingly” superior to a low-fat diet for mortality or nonfatal MI, the authors noted.

The absolute effects for the Mediterranean and low-fat diets were more pronounced in adults at high CVD risk. With the Mediterranean diet, there were 36 fewer all-cause deaths and 39 fewer CV deaths per 1,000 over 5 years.

The five other dietary programs generally had “little or no benefit” compared with minimal intervention. The evidence was of low to moderate certainty.

The studies did not provide enough data to gauge the impact of the diets on angina, heart failure, peripheral vascular events, and atrial fibrillation.

The researchers say that strengths of their analysis include a comprehensive review and thorough literature search and a rigorous assessment of study bias. In addition, the researchers adhered to recognized GRADE methods for assessing the certainty of estimates.

Limitations of their work include not being able to measure adherence to dietary programs and the possibility that some of the benefits may have been due to other factors, such as drug treatment and support for quitting smoking.

The study had no specific funding. The authors have disclosed no relevant financial relationships.

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

About half of middle-aged adults in the community without cardiovascular (CV) symptoms have coronary atherosclerosis by CT angiography (CTA) that puts them at substantial risk for myocardial infarction (MI), suggests a prospective cohort study.

The 10% of participants who had subclinical disease considered obstructive at CTA showed a ninefold increased risk for MI over several years. Obstructive disease seemed to elevate risk more than subclinical disease that wasn’t obstructive but still considered extensive within the coronary arteries.

The findings, based on a Copenhagen General Population Study cohort, are new for CTA but consistent with research based on coronary artery calcium (CAC) scores and other ways to assess CV risk, say researchers.

Although all participants underwent CTA, such imaging isn’t used in the general population for atherosclerosis screening. But the findings may have implications for “opportunistic screening” for subclinical coronary disease at CTA conducted for other reasons, notes the study’s report, published online in the Annals of Internal Medicine.

“Identification of luminal obstructive or extensive subclinical coronary atherosclerosis” could potentially provide “clinically relevant, incremental risk assessment” in nonischemic patients who undergo cardiac CT or electrocardiogram-gated chest CT before procedures such as arrhythmia ablation or valve repair, it states.

Such patients found with subclinical coronary atherosclerosis might potentially “benefit from referral to intensified cardiovascular primary prevention therapy,” write the authors, led by Andreas Fuchs, MD, PhD, Copenhagen University Hospital-Rigshospitalet.

The group acknowledges the findings may not entirely apply to a non-Danish population.


 

A screening role for CTA?

Whether CTA has a role to play in adults without symptoms “is a big, open question in the field right now,” observed Ron Blankstein, MD, not associated with the current analysis, for this news organization.

Brigham and Women&#039;s Hospital

Most population studies of CV risk prediction, such as MESA, have looked at CAC scores, not CTA, and have shown that “the more plaque individuals have, the higher the risk.” The current findings are similar but novel in coming from coronary CTA in a large asymptomatic community population, said Dr. Blankstein, who is director of cardiac CT at Brigham and Women’s Hospital, Boston.

“It’s possible that patients who have obstructive plaque in general tend to have a larger amount of plaque as well,” he said. So, while the study suggests that “the more plaque individuals have, the worse their overall risk,” it also shows that the risk “is enhanced even more if they have obstructive disease.”

The Danish cohort analysis “provides a unique opportunity to study the contemporary natural history of coronary artery disease in the absence of intervention,” notes an accompanying editorial.

For example, both patients and clinicians were blinded to CTA results, and CV preventive therapies weren’t common, observe Michael McDermott, MBChB, and David E. Newby, DM, PhD, of the BHF Centre for Cardiovascular Science, University of Edinburgh.

The analysis suggests that subclinical coronary disease that is obstructive predicts MI risk more strongly than extensive coronary disease, they note, and may be present in two-thirds of MI patients. “This contrasts with symptomatic populations, where nonobstructive disease accounts for most future myocardial infarctions, presumably from plaque rupture.”

It also points to “strong associations between nonobstructive extensive disease and adverse plaque characteristics,” write Dr. McDermott and Dr. Newby. “This underscores the major importance of plaque burden” for the prediction of coronary events.
 

Graded risk

The analysis included 9,533 persons aged 40 and older without known ischemic heart disease or symptoms with available CTA assessments.

Obstructive disease, defined as presence of a luminal stenosis of at least 50%, was seen in 10% and nonobstructive disease in 36% of the total cohort, the report states.

Disease occupying more than one-third of the coronary tree was considered extensive and less than one-third of the coronaries nonextensive, occurring in 10.5% and 35.8% of the cohort, respectively.

There were 71 MIs and 193 deaths over a median of 3.5 years. The adjusted relative risk for MI, compared with those without coronary atherosclerosis, was:

• 7.65 (95% confidence interval, 3.53-16.57) overall in patients with extensive disease.
• 8.28 (95% CI, 3.75-18.32) in those with obstructive but nonextensive disease.
• 9.19 (95% CI, 4.49-18.82) overall in those with obstructive disease.
• 12.48 (95% CI, 5.50-28.12) in those with or obstructive and extensive disease.

The adjusted RR for the composite of death or MI was also elevated in persons with extensive disease:

• 2.70 (95% CI, 1.72-4.25) in those with extensive but nonobstructive disease.
• 3.15 (95% CI, 2.05-4.83) in those with extensive and obstructive disease.

“It’s one thing to show that the more plaque, the higher the risk,” Dr. Blankstein said. But “does the information ultimately lead to better outcomes? Do patients have fewer MIs or fewer deaths?” Several ongoing randomized trials are exploring these questions.

They include DANE-HEART (Computed Tomography Coronary Angiography for Primary Prevention), projected to enroll about 6,000 participants from the Copenhagen General Population Study cohort who have at least one CV risk factor, and SCOT-HEART 2 (second Computed Tomography Coronary Angiography for the Prevention of Myocardial Infarction), enrolling a similar cohort in Scotland.

The study was supported by grants from AP Møller og Hustru Chastine Mc-Kinney Møllers Fond, the Research Council of Rigshospitalet, and Danish Heart Foundation. Dr. Fuchs reports no relevant financial relationships. Disclosures for the other authors can be found here. Dr. Blankstein recently disclosed serving as a consultant to Amgen, Caristo Diagnostics, Novartis, and Silence Therapeutics. Disclosures for Dr. McDermott and Dr. Newby, who are SCOT-HEART 2 investigators, can be found here.

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

About half of middle-aged adults in the community without cardiovascular (CV) symptoms have coronary atherosclerosis by CT angiography (CTA) that puts them at substantial risk for myocardial infarction (MI), suggests a prospective cohort study.

The 10% of participants who had subclinical disease considered obstructive at CTA showed a ninefold increased risk for MI over several years. Obstructive disease seemed to elevate risk more than subclinical disease that wasn’t obstructive but still considered extensive within the coronary arteries.

The findings, based on a Copenhagen General Population Study cohort, are new for CTA but consistent with research based on coronary artery calcium (CAC) scores and other ways to assess CV risk, say researchers.

Although all participants underwent CTA, such imaging isn’t used in the general population for atherosclerosis screening. But the findings may have implications for “opportunistic screening” for subclinical coronary disease at CTA conducted for other reasons, notes the study’s report, published online in the Annals of Internal Medicine.

“Identification of luminal obstructive or extensive subclinical coronary atherosclerosis” could potentially provide “clinically relevant, incremental risk assessment” in nonischemic patients who undergo cardiac CT or electrocardiogram-gated chest CT before procedures such as arrhythmia ablation or valve repair, it states.

Such patients found with subclinical coronary atherosclerosis might potentially “benefit from referral to intensified cardiovascular primary prevention therapy,” write the authors, led by Andreas Fuchs, MD, PhD, Copenhagen University Hospital-Rigshospitalet.

The group acknowledges the findings may not entirely apply to a non-Danish population.


 

A screening role for CTA?

Whether CTA has a role to play in adults without symptoms “is a big, open question in the field right now,” observed Ron Blankstein, MD, not associated with the current analysis, for this news organization.

Brigham and Women&#039;s Hospital

Most population studies of CV risk prediction, such as MESA, have looked at CAC scores, not CTA, and have shown that “the more plaque individuals have, the higher the risk.” The current findings are similar but novel in coming from coronary CTA in a large asymptomatic community population, said Dr. Blankstein, who is director of cardiac CT at Brigham and Women’s Hospital, Boston.

“It’s possible that patients who have obstructive plaque in general tend to have a larger amount of plaque as well,” he said. So, while the study suggests that “the more plaque individuals have, the worse their overall risk,” it also shows that the risk “is enhanced even more if they have obstructive disease.”

The Danish cohort analysis “provides a unique opportunity to study the contemporary natural history of coronary artery disease in the absence of intervention,” notes an accompanying editorial.

For example, both patients and clinicians were blinded to CTA results, and CV preventive therapies weren’t common, observe Michael McDermott, MBChB, and David E. Newby, DM, PhD, of the BHF Centre for Cardiovascular Science, University of Edinburgh.

The analysis suggests that subclinical coronary disease that is obstructive predicts MI risk more strongly than extensive coronary disease, they note, and may be present in two-thirds of MI patients. “This contrasts with symptomatic populations, where nonobstructive disease accounts for most future myocardial infarctions, presumably from plaque rupture.”

It also points to “strong associations between nonobstructive extensive disease and adverse plaque characteristics,” write Dr. McDermott and Dr. Newby. “This underscores the major importance of plaque burden” for the prediction of coronary events.
 

Graded risk

The analysis included 9,533 persons aged 40 and older without known ischemic heart disease or symptoms with available CTA assessments.

Obstructive disease, defined as presence of a luminal stenosis of at least 50%, was seen in 10% and nonobstructive disease in 36% of the total cohort, the report states.

Disease occupying more than one-third of the coronary tree was considered extensive and less than one-third of the coronaries nonextensive, occurring in 10.5% and 35.8% of the cohort, respectively.

There were 71 MIs and 193 deaths over a median of 3.5 years. The adjusted relative risk for MI, compared with those without coronary atherosclerosis, was:

• 7.65 (95% confidence interval, 3.53-16.57) overall in patients with extensive disease.
• 8.28 (95% CI, 3.75-18.32) in those with obstructive but nonextensive disease.
• 9.19 (95% CI, 4.49-18.82) overall in those with obstructive disease.
• 12.48 (95% CI, 5.50-28.12) in those with or obstructive and extensive disease.

The adjusted RR for the composite of death or MI was also elevated in persons with extensive disease:

• 2.70 (95% CI, 1.72-4.25) in those with extensive but nonobstructive disease.
• 3.15 (95% CI, 2.05-4.83) in those with extensive and obstructive disease.

“It’s one thing to show that the more plaque, the higher the risk,” Dr. Blankstein said. But “does the information ultimately lead to better outcomes? Do patients have fewer MIs or fewer deaths?” Several ongoing randomized trials are exploring these questions.

They include DANE-HEART (Computed Tomography Coronary Angiography for Primary Prevention), projected to enroll about 6,000 participants from the Copenhagen General Population Study cohort who have at least one CV risk factor, and SCOT-HEART 2 (second Computed Tomography Coronary Angiography for the Prevention of Myocardial Infarction), enrolling a similar cohort in Scotland.

The study was supported by grants from AP Møller og Hustru Chastine Mc-Kinney Møllers Fond, the Research Council of Rigshospitalet, and Danish Heart Foundation. Dr. Fuchs reports no relevant financial relationships. Disclosures for the other authors can be found here. Dr. Blankstein recently disclosed serving as a consultant to Amgen, Caristo Diagnostics, Novartis, and Silence Therapeutics. Disclosures for Dr. McDermott and Dr. Newby, who are SCOT-HEART 2 investigators, can be found here.

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

About half of middle-aged adults in the community without cardiovascular (CV) symptoms have coronary atherosclerosis by CT angiography (CTA) that puts them at substantial risk for myocardial infarction (MI), suggests a prospective cohort study.

The 10% of participants who had subclinical disease considered obstructive at CTA showed a ninefold increased risk for MI over several years. Obstructive disease seemed to elevate risk more than subclinical disease that wasn’t obstructive but still considered extensive within the coronary arteries.

The findings, based on a Copenhagen General Population Study cohort, are new for CTA but consistent with research based on coronary artery calcium (CAC) scores and other ways to assess CV risk, say researchers.

Although all participants underwent CTA, such imaging isn’t used in the general population for atherosclerosis screening. But the findings may have implications for “opportunistic screening” for subclinical coronary disease at CTA conducted for other reasons, notes the study’s report, published online in the Annals of Internal Medicine.

“Identification of luminal obstructive or extensive subclinical coronary atherosclerosis” could potentially provide “clinically relevant, incremental risk assessment” in nonischemic patients who undergo cardiac CT or electrocardiogram-gated chest CT before procedures such as arrhythmia ablation or valve repair, it states.

Such patients found with subclinical coronary atherosclerosis might potentially “benefit from referral to intensified cardiovascular primary prevention therapy,” write the authors, led by Andreas Fuchs, MD, PhD, Copenhagen University Hospital-Rigshospitalet.

The group acknowledges the findings may not entirely apply to a non-Danish population.


 

A screening role for CTA?

Whether CTA has a role to play in adults without symptoms “is a big, open question in the field right now,” observed Ron Blankstein, MD, not associated with the current analysis, for this news organization.

Brigham and Women&#039;s Hospital

Most population studies of CV risk prediction, such as MESA, have looked at CAC scores, not CTA, and have shown that “the more plaque individuals have, the higher the risk.” The current findings are similar but novel in coming from coronary CTA in a large asymptomatic community population, said Dr. Blankstein, who is director of cardiac CT at Brigham and Women’s Hospital, Boston.

“It’s possible that patients who have obstructive plaque in general tend to have a larger amount of plaque as well,” he said. So, while the study suggests that “the more plaque individuals have, the worse their overall risk,” it also shows that the risk “is enhanced even more if they have obstructive disease.”

The Danish cohort analysis “provides a unique opportunity to study the contemporary natural history of coronary artery disease in the absence of intervention,” notes an accompanying editorial.

For example, both patients and clinicians were blinded to CTA results, and CV preventive therapies weren’t common, observe Michael McDermott, MBChB, and David E. Newby, DM, PhD, of the BHF Centre for Cardiovascular Science, University of Edinburgh.

The analysis suggests that subclinical coronary disease that is obstructive predicts MI risk more strongly than extensive coronary disease, they note, and may be present in two-thirds of MI patients. “This contrasts with symptomatic populations, where nonobstructive disease accounts for most future myocardial infarctions, presumably from plaque rupture.”

It also points to “strong associations between nonobstructive extensive disease and adverse plaque characteristics,” write Dr. McDermott and Dr. Newby. “This underscores the major importance of plaque burden” for the prediction of coronary events.
 

Graded risk

The analysis included 9,533 persons aged 40 and older without known ischemic heart disease or symptoms with available CTA assessments.

Obstructive disease, defined as presence of a luminal stenosis of at least 50%, was seen in 10% and nonobstructive disease in 36% of the total cohort, the report states.

Disease occupying more than one-third of the coronary tree was considered extensive and less than one-third of the coronaries nonextensive, occurring in 10.5% and 35.8% of the cohort, respectively.

There were 71 MIs and 193 deaths over a median of 3.5 years. The adjusted relative risk for MI, compared with those without coronary atherosclerosis, was:

• 7.65 (95% confidence interval, 3.53-16.57) overall in patients with extensive disease.
• 8.28 (95% CI, 3.75-18.32) in those with obstructive but nonextensive disease.
• 9.19 (95% CI, 4.49-18.82) overall in those with obstructive disease.
• 12.48 (95% CI, 5.50-28.12) in those with or obstructive and extensive disease.

The adjusted RR for the composite of death or MI was also elevated in persons with extensive disease:

• 2.70 (95% CI, 1.72-4.25) in those with extensive but nonobstructive disease.
• 3.15 (95% CI, 2.05-4.83) in those with extensive and obstructive disease.

“It’s one thing to show that the more plaque, the higher the risk,” Dr. Blankstein said. But “does the information ultimately lead to better outcomes? Do patients have fewer MIs or fewer deaths?” Several ongoing randomized trials are exploring these questions.

They include DANE-HEART (Computed Tomography Coronary Angiography for Primary Prevention), projected to enroll about 6,000 participants from the Copenhagen General Population Study cohort who have at least one CV risk factor, and SCOT-HEART 2 (second Computed Tomography Coronary Angiography for the Prevention of Myocardial Infarction), enrolling a similar cohort in Scotland.

The study was supported by grants from AP Møller og Hustru Chastine Mc-Kinney Møllers Fond, the Research Council of Rigshospitalet, and Danish Heart Foundation. Dr. Fuchs reports no relevant financial relationships. Disclosures for the other authors can be found here. Dr. Blankstein recently disclosed serving as a consultant to Amgen, Caristo Diagnostics, Novartis, and Silence Therapeutics. Disclosures for Dr. McDermott and Dr. Newby, who are SCOT-HEART 2 investigators, can be found here.

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

Recent trial evidence has failed to show a cardiovascular benefit to treating high triglycerides. The publication of the PROMINENT trial, where pemafibrate successfully lowered high levels but was not associated with a lower risk for cardiovascular events, reinforced the point. Is it time to stop measuring and treating high triglycerides?

There may be noncardiovascular reasons to treat hypertriglyceridemia. Pancreatitis is the most cited one, given that the risk for pancreatitis increases with increasing triglyceride levels, especially in patients with a prior episode.

There may also be practical reasons to lower trigs. Because most cholesterol panels use the Friedewald equation to calculate low-density lipoprotein cholesterol (LDL-C) rather than measuring it directly, very high triglyceride levels can invalidate the calculation and return error messages on lab reports.

But we now have alternatives to measuring LDL-C, including non–high-density lipoprotein cholesterol (HDL-C) and apolipoprotein B (apoB), that better predict risk and are usable even in the setting of nonfasting samples when triglycerides are elevated.
 

Independent cardiovascular risk factor?

If we are going to measure and treat high triglycerides for cardiovascular reasons, the relevant question is, are high triglycerides an independent risk factor for cardiovascular disease?

Proponents have a broad swath of supportive literature to point at. Multiple studies have shown an association between triglyceride levels and cardiovascular risk. The evidence even extends beyond traditional epidemiologic analyses, to genetic studies that should be free from some of the problems seen in observational cohorts.

But it is difficult to be certain whether these associations are causal or merely confounding. An unhealthy diet will increase triglycerides, as will alcohol. Patients with diabetes or metabolic syndrome have high triglycerides. So do patients with nephrotic syndrome or hypothyroidism, or hypertensive patients taking thiazide diuretics. Adjusting for these baseline factors is possible but imperfect, and residual confounding is always an issue. An analysis of the Reykjavik and the EPIC-Norfolk studies found an association between triglyceride levels and cardiovascular risk. That risk was attenuated, but not eliminated, when adjusted for traditional risk factors such as age, smoking, blood pressure, diabetes, and cholesterol.

Randomized trials of triglyceride-lowering therapies would help resolve the question of whether hypertriglyceridemia contributes to coronary disease or simply identifies high-risk patients. Early trials seemed to support the idea of a causal link. The Helsinki Heart Study randomized patients to gemfibrozil or placebo and found a 34% relative risk reduction in coronary artery disease with the fibrate. But gemfibrozil didn’t only reduce triglycerides. It also increased HDL-C and lowered LDL-C relative to placebo, which may explain the observed benefit.

Gemfibrozil is rarely used today because we can achieve much greater LDL-C reductions with statins, as well as ezetimibe and PCSK9 inhibitors. The success of these drugs may not leave any room for triglyceride-lowering medications.
 

The pre- vs. post-statin era

In the 2005 FIELD study, participants were randomized to receive fenofibrate or placebo. Although patients weren’t taking statin at study entry, 17% of the placebo group started taking one during the trial. Fenofibrate wasn’t associated with a reduction in the primary endpoint, a combination of coronary heart disease death or nonfatal myocardial infarction (MI). Among the many secondary endpoints, nonfatal MI was lower but cardiovascular mortality was not in the fibrate-treated patients. In the same vein, the 2010 ACCORD study randomized patients to receive simvastatin plus fenofibrate or simvastatin alone. The composite primary outcome of MI, stroke, and cardiovascular mortality was not lowered nor were any secondary outcomes with the combination therapy. In the statin era, triglyceride-lowering therapies have not shown much benefit.

The final nail in the coffin may very well be the aforementioned PROMINENT trial. The new agent, pemafibrate, fared no better than its predecessor fenofibrate. Pemafibrate had no impact on the study’s primary composite outcome of nonfatal MI, stroke, coronary revascularization, or cardiovascular death despite being very effective at lowering triglycerides (by more than 25%). Patients treated with pemafibrate had increased LDL-C and apoB compared with the placebo group. When you realize that, the results of the study are not very surprising.

Some point to the results of REDUCE-IT as proof that triglycerides are still a valid target for pharmacotherapy. The debate on whether REDUCE-IT tested a good drug or a bad placebo is one for another day. The salient point for today is that the benefits of eicosapentaenoic acid (EPA) were seen regardless of either baseline or final triglyceride level. EPA may lower cardiac risk, but there is no widespread consensus that it does so by lowering triglycerides. There may be other mechanisms at work.

You could still argue that high triglycerides have value as a risk prediction tool even if their role as a target for drug therapy is questionable. There was a time when medications to lower triglycerides had a benefit. But this is the post-statin era, and that time has passed.

If you see patients with high triglycerides, treating them with triglyceride-lowering medication probably isn’t going to reduce their cardiovascular risk. Dietary interventions, encouraging exercise, and reducing alcohol consumption are better options. Not only will they lead to lower cholesterol levels, but they’ll lower cardiovascular risk, too.

Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal, with a degree in epidemiology. He has disclosed no relevant financial relationships. He spends most of his time doing things that he doesn’t get paid for, like research, teaching, and podcasting. Occasionally he finds time to practice cardiology to pay the rent. He realizes that half of his research findings will be disproved in 5 years; he just doesn’t know which half. He is a regular contributor to the Montreal Gazette, CJAD radio, and CTV television in Montreal and is host of the award-winning podcast The Body of Evidence. The Body of Evidence.

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

Recent trial evidence has failed to show a cardiovascular benefit to treating high triglycerides. The publication of the PROMINENT trial, where pemafibrate successfully lowered high levels but was not associated with a lower risk for cardiovascular events, reinforced the point. Is it time to stop measuring and treating high triglycerides?

There may be noncardiovascular reasons to treat hypertriglyceridemia. Pancreatitis is the most cited one, given that the risk for pancreatitis increases with increasing triglyceride levels, especially in patients with a prior episode.

There may also be practical reasons to lower trigs. Because most cholesterol panels use the Friedewald equation to calculate low-density lipoprotein cholesterol (LDL-C) rather than measuring it directly, very high triglyceride levels can invalidate the calculation and return error messages on lab reports.

But we now have alternatives to measuring LDL-C, including non–high-density lipoprotein cholesterol (HDL-C) and apolipoprotein B (apoB), that better predict risk and are usable even in the setting of nonfasting samples when triglycerides are elevated.
 

Independent cardiovascular risk factor?

If we are going to measure and treat high triglycerides for cardiovascular reasons, the relevant question is, are high triglycerides an independent risk factor for cardiovascular disease?

Proponents have a broad swath of supportive literature to point at. Multiple studies have shown an association between triglyceride levels and cardiovascular risk. The evidence even extends beyond traditional epidemiologic analyses, to genetic studies that should be free from some of the problems seen in observational cohorts.

But it is difficult to be certain whether these associations are causal or merely confounding. An unhealthy diet will increase triglycerides, as will alcohol. Patients with diabetes or metabolic syndrome have high triglycerides. So do patients with nephrotic syndrome or hypothyroidism, or hypertensive patients taking thiazide diuretics. Adjusting for these baseline factors is possible but imperfect, and residual confounding is always an issue. An analysis of the Reykjavik and the EPIC-Norfolk studies found an association between triglyceride levels and cardiovascular risk. That risk was attenuated, but not eliminated, when adjusted for traditional risk factors such as age, smoking, blood pressure, diabetes, and cholesterol.

Randomized trials of triglyceride-lowering therapies would help resolve the question of whether hypertriglyceridemia contributes to coronary disease or simply identifies high-risk patients. Early trials seemed to support the idea of a causal link. The Helsinki Heart Study randomized patients to gemfibrozil or placebo and found a 34% relative risk reduction in coronary artery disease with the fibrate. But gemfibrozil didn’t only reduce triglycerides. It also increased HDL-C and lowered LDL-C relative to placebo, which may explain the observed benefit.

Gemfibrozil is rarely used today because we can achieve much greater LDL-C reductions with statins, as well as ezetimibe and PCSK9 inhibitors. The success of these drugs may not leave any room for triglyceride-lowering medications.
 

The pre- vs. post-statin era

In the 2005 FIELD study, participants were randomized to receive fenofibrate or placebo. Although patients weren’t taking statin at study entry, 17% of the placebo group started taking one during the trial. Fenofibrate wasn’t associated with a reduction in the primary endpoint, a combination of coronary heart disease death or nonfatal myocardial infarction (MI). Among the many secondary endpoints, nonfatal MI was lower but cardiovascular mortality was not in the fibrate-treated patients. In the same vein, the 2010 ACCORD study randomized patients to receive simvastatin plus fenofibrate or simvastatin alone. The composite primary outcome of MI, stroke, and cardiovascular mortality was not lowered nor were any secondary outcomes with the combination therapy. In the statin era, triglyceride-lowering therapies have not shown much benefit.

The final nail in the coffin may very well be the aforementioned PROMINENT trial. The new agent, pemafibrate, fared no better than its predecessor fenofibrate. Pemafibrate had no impact on the study’s primary composite outcome of nonfatal MI, stroke, coronary revascularization, or cardiovascular death despite being very effective at lowering triglycerides (by more than 25%). Patients treated with pemafibrate had increased LDL-C and apoB compared with the placebo group. When you realize that, the results of the study are not very surprising.

Some point to the results of REDUCE-IT as proof that triglycerides are still a valid target for pharmacotherapy. The debate on whether REDUCE-IT tested a good drug or a bad placebo is one for another day. The salient point for today is that the benefits of eicosapentaenoic acid (EPA) were seen regardless of either baseline or final triglyceride level. EPA may lower cardiac risk, but there is no widespread consensus that it does so by lowering triglycerides. There may be other mechanisms at work.

You could still argue that high triglycerides have value as a risk prediction tool even if their role as a target for drug therapy is questionable. There was a time when medications to lower triglycerides had a benefit. But this is the post-statin era, and that time has passed.

If you see patients with high triglycerides, treating them with triglyceride-lowering medication probably isn’t going to reduce their cardiovascular risk. Dietary interventions, encouraging exercise, and reducing alcohol consumption are better options. Not only will they lead to lower cholesterol levels, but they’ll lower cardiovascular risk, too.

Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal, with a degree in epidemiology. He has disclosed no relevant financial relationships. He spends most of his time doing things that he doesn’t get paid for, like research, teaching, and podcasting. Occasionally he finds time to practice cardiology to pay the rent. He realizes that half of his research findings will be disproved in 5 years; he just doesn’t know which half. He is a regular contributor to the Montreal Gazette, CJAD radio, and CTV television in Montreal and is host of the award-winning podcast The Body of Evidence. The Body of Evidence.

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

Recent trial evidence has failed to show a cardiovascular benefit to treating high triglycerides. The publication of the PROMINENT trial, where pemafibrate successfully lowered high levels but was not associated with a lower risk for cardiovascular events, reinforced the point. Is it time to stop measuring and treating high triglycerides?

There may be noncardiovascular reasons to treat hypertriglyceridemia. Pancreatitis is the most cited one, given that the risk for pancreatitis increases with increasing triglyceride levels, especially in patients with a prior episode.

There may also be practical reasons to lower trigs. Because most cholesterol panels use the Friedewald equation to calculate low-density lipoprotein cholesterol (LDL-C) rather than measuring it directly, very high triglyceride levels can invalidate the calculation and return error messages on lab reports.

But we now have alternatives to measuring LDL-C, including non–high-density lipoprotein cholesterol (HDL-C) and apolipoprotein B (apoB), that better predict risk and are usable even in the setting of nonfasting samples when triglycerides are elevated.
 

Independent cardiovascular risk factor?

If we are going to measure and treat high triglycerides for cardiovascular reasons, the relevant question is, are high triglycerides an independent risk factor for cardiovascular disease?

Proponents have a broad swath of supportive literature to point at. Multiple studies have shown an association between triglyceride levels and cardiovascular risk. The evidence even extends beyond traditional epidemiologic analyses, to genetic studies that should be free from some of the problems seen in observational cohorts.

But it is difficult to be certain whether these associations are causal or merely confounding. An unhealthy diet will increase triglycerides, as will alcohol. Patients with diabetes or metabolic syndrome have high triglycerides. So do patients with nephrotic syndrome or hypothyroidism, or hypertensive patients taking thiazide diuretics. Adjusting for these baseline factors is possible but imperfect, and residual confounding is always an issue. An analysis of the Reykjavik and the EPIC-Norfolk studies found an association between triglyceride levels and cardiovascular risk. That risk was attenuated, but not eliminated, when adjusted for traditional risk factors such as age, smoking, blood pressure, diabetes, and cholesterol.

Randomized trials of triglyceride-lowering therapies would help resolve the question of whether hypertriglyceridemia contributes to coronary disease or simply identifies high-risk patients. Early trials seemed to support the idea of a causal link. The Helsinki Heart Study randomized patients to gemfibrozil or placebo and found a 34% relative risk reduction in coronary artery disease with the fibrate. But gemfibrozil didn’t only reduce triglycerides. It also increased HDL-C and lowered LDL-C relative to placebo, which may explain the observed benefit.

Gemfibrozil is rarely used today because we can achieve much greater LDL-C reductions with statins, as well as ezetimibe and PCSK9 inhibitors. The success of these drugs may not leave any room for triglyceride-lowering medications.
 

The pre- vs. post-statin era

In the 2005 FIELD study, participants were randomized to receive fenofibrate or placebo. Although patients weren’t taking statin at study entry, 17% of the placebo group started taking one during the trial. Fenofibrate wasn’t associated with a reduction in the primary endpoint, a combination of coronary heart disease death or nonfatal myocardial infarction (MI). Among the many secondary endpoints, nonfatal MI was lower but cardiovascular mortality was not in the fibrate-treated patients. In the same vein, the 2010 ACCORD study randomized patients to receive simvastatin plus fenofibrate or simvastatin alone. The composite primary outcome of MI, stroke, and cardiovascular mortality was not lowered nor were any secondary outcomes with the combination therapy. In the statin era, triglyceride-lowering therapies have not shown much benefit.

The final nail in the coffin may very well be the aforementioned PROMINENT trial. The new agent, pemafibrate, fared no better than its predecessor fenofibrate. Pemafibrate had no impact on the study’s primary composite outcome of nonfatal MI, stroke, coronary revascularization, or cardiovascular death despite being very effective at lowering triglycerides (by more than 25%). Patients treated with pemafibrate had increased LDL-C and apoB compared with the placebo group. When you realize that, the results of the study are not very surprising.

Some point to the results of REDUCE-IT as proof that triglycerides are still a valid target for pharmacotherapy. The debate on whether REDUCE-IT tested a good drug or a bad placebo is one for another day. The salient point for today is that the benefits of eicosapentaenoic acid (EPA) were seen regardless of either baseline or final triglyceride level. EPA may lower cardiac risk, but there is no widespread consensus that it does so by lowering triglycerides. There may be other mechanisms at work.

You could still argue that high triglycerides have value as a risk prediction tool even if their role as a target for drug therapy is questionable. There was a time when medications to lower triglycerides had a benefit. But this is the post-statin era, and that time has passed.

If you see patients with high triglycerides, treating them with triglyceride-lowering medication probably isn’t going to reduce their cardiovascular risk. Dietary interventions, encouraging exercise, and reducing alcohol consumption are better options. Not only will they lead to lower cholesterol levels, but they’ll lower cardiovascular risk, too.

Dr. Labos is a cardiologist at Hôpital Notre-Dame, Montreal, with a degree in epidemiology. He has disclosed no relevant financial relationships. He spends most of his time doing things that he doesn’t get paid for, like research, teaching, and podcasting. Occasionally he finds time to practice cardiology to pay the rent. He realizes that half of his research findings will be disproved in 5 years; he just doesn’t know which half. He is a regular contributor to the Montreal Gazette, CJAD radio, and CTV television in Montreal and is host of the award-winning podcast The Body of Evidence. The Body of Evidence.

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

Sudden cardiac arrest (SCA) due to commotio cordis occurs more frequently in non–sport-related settings than is commonly thought, resulting in lower rates of resuscitation and increased mortality, especially among young women, a new review suggests.

The condition is rare, caused by an often fatal arrhythmia secondary to a blunt, nonpenetrating impact over the precordium, without direct structural damage to the heart itself. Common causes in nonsport settings include assault, motor vehicle accidents (MVAs), and daily activities such as occupational accidents.

“We found a stark difference in mortality outcomes between non–sport-related commotio cordis compared to sport-related events,” at 88% vs. 66%, Han S. Lim, MBBS, PhD, of the University of Melbourne, and Austin Health, Heidelberg, Australia, told this news organization. “Rates of cardiopulmonary resuscitation (CPR) (27% vs. 97%) and defibrillation (17% vs. 81%) were considerably lower in the non–sport-related events.”

“Although still being male-predominant, of concern, we saw a higher proportion of females in non–sport-related commotio cordis due to assault, MVAs, and other activities,” he noted. Such events may occur “in secluded domestic settings, may not be witnessed, or may occur as intentional harm, whereby the witness could also be the perpetrator, reducing the likelihood of prompt diagnosis, CPR, and defibrillation administration.”

The study was published online in JACC: Clinical Electrophysiology.
 

Young women affected

Dr. Lim and colleagues searched the literature through 2021 for all cases of commotio cordis. Three hundred and thirty-four cases from among 53 citations were included in the analysis; of those, 121 (36%) occurred in non–sport-related settings, including assault (76%), MVAs (7%), and daily activities (16%). “Daily activities” comprised activities that were expected in a person’s day-to-day routine such as falls, play fighting (in children), and occupational accidents.

Non–sport-related cases primarily involved nonprojectile etiologies (95%), including bodily contact (79%), such as impacts from fists, feet, and knees; impacts with handlebars or steering wheels; and solid stick-like weapons and flat surfaces.

Sport-related cases involved a significantly higher proportion of projectiles (94% vs. 5%) and occurred across a range of sports, mostly at the competitive level (66%).

Both sport-related and non–sport-related commotio cordis affected a similar younger demographic (mean age, 19; mostly males). No statistically significant differences between the two groups were seen with regard to previous cardiac history or family history of cardiac disease, or in arrhythmias on electrocardiogram, biomarkers, or imaging findings.

However, in non–sport-related events, the proportion of females affected was significantly higher (13% vs. 2%), as was mortality (88% vs. 66%). Rates were lower for CPR (27% vs. 97%) and defibrillation use (17% vs. 81%), and resuscitation was more commonly delayed beyond 3 minutes (80% vs. 5%).

The finding that more than a third of reported cases were non–sport-related “is higher than previously reported, and included data from 15 different countries,” the authors noted.

Study limitations included the use of data only from published studies, inclusion of a case series limited to fatal cases, small sample sizes, and lack of consistent reporting of demographic data, mechanisms, investigation results, management, and outcomes.
 

Increased awareness ‘essential’

Dr. Lim and colleagues concluded that increased awareness of non–sport-related commotio cordis is “essential” for early recognition, resuscitation, and mortality reduction. 

Jim Cheung, MD, chair of the American College of Cardiology’s electrophysiology section, “completely agrees.” Greater awareness among the general population could reduce barriers to CPR and automated external defibrillator (AED) use, he said, which in turn, can lead to improved survival.

Furthermore, Dr. Cheung added, “This study underscores the importance of ensuring that non–cardiology-trained physicians such as emergency medicine physicians and trauma surgeons who might encounter patients with non–sports-related commotio cordis recognize the entity during the course of treatment.”

Because the review relied only on published cases, “it may not represent the true breadth of cases that are occurring in the real world,” he noted. “I suspect that cases that occur outside of sports-related activities, such as MVAs and assault, are more likely to be underreported and that the true proportion of non–sports-related commotio cordis may be significantly higher than 36%.” Increased reporting of cases as part of an international commotio cordis registry would help provide additional insights, he suggested.

“There is a common misperception that SCA only occurs among older patients and patients with known coronary artery disease or heart failure,” he said. “For us to move the needle on improving SCA survival, we will need to tackle the problem from multiple angles including increasing public awareness, training the public on CPR and AED use, and improving access to AEDs by addressing structural barriers.”

Dr. Cheung pointed to ongoing efforts by nonprofit, patient-driven organizations such as the SADS Foundation and Omar Carter Foundation, and professional societies such as the American College of Cardiology, the American Heart Association, and Heart Rhythm Society, to direct public awareness campaigns and legislative proposals to address this problem.

Similar efforts are underway among cardiac societies and SCA awareness groups in Australia, Dr. Lim said.

No funding or relevant financial relationships were disclosed.
 

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

Sudden cardiac arrest (SCA) due to commotio cordis occurs more frequently in non–sport-related settings than is commonly thought, resulting in lower rates of resuscitation and increased mortality, especially among young women, a new review suggests.

The condition is rare, caused by an often fatal arrhythmia secondary to a blunt, nonpenetrating impact over the precordium, without direct structural damage to the heart itself. Common causes in nonsport settings include assault, motor vehicle accidents (MVAs), and daily activities such as occupational accidents.

“We found a stark difference in mortality outcomes between non–sport-related commotio cordis compared to sport-related events,” at 88% vs. 66%, Han S. Lim, MBBS, PhD, of the University of Melbourne, and Austin Health, Heidelberg, Australia, told this news organization. “Rates of cardiopulmonary resuscitation (CPR) (27% vs. 97%) and defibrillation (17% vs. 81%) were considerably lower in the non–sport-related events.”

“Although still being male-predominant, of concern, we saw a higher proportion of females in non–sport-related commotio cordis due to assault, MVAs, and other activities,” he noted. Such events may occur “in secluded domestic settings, may not be witnessed, or may occur as intentional harm, whereby the witness could also be the perpetrator, reducing the likelihood of prompt diagnosis, CPR, and defibrillation administration.”

The study was published online in JACC: Clinical Electrophysiology.
 

Young women affected

Dr. Lim and colleagues searched the literature through 2021 for all cases of commotio cordis. Three hundred and thirty-four cases from among 53 citations were included in the analysis; of those, 121 (36%) occurred in non–sport-related settings, including assault (76%), MVAs (7%), and daily activities (16%). “Daily activities” comprised activities that were expected in a person’s day-to-day routine such as falls, play fighting (in children), and occupational accidents.

Non–sport-related cases primarily involved nonprojectile etiologies (95%), including bodily contact (79%), such as impacts from fists, feet, and knees; impacts with handlebars or steering wheels; and solid stick-like weapons and flat surfaces.

Sport-related cases involved a significantly higher proportion of projectiles (94% vs. 5%) and occurred across a range of sports, mostly at the competitive level (66%).

Both sport-related and non–sport-related commotio cordis affected a similar younger demographic (mean age, 19; mostly males). No statistically significant differences between the two groups were seen with regard to previous cardiac history or family history of cardiac disease, or in arrhythmias on electrocardiogram, biomarkers, or imaging findings.

However, in non–sport-related events, the proportion of females affected was significantly higher (13% vs. 2%), as was mortality (88% vs. 66%). Rates were lower for CPR (27% vs. 97%) and defibrillation use (17% vs. 81%), and resuscitation was more commonly delayed beyond 3 minutes (80% vs. 5%).

The finding that more than a third of reported cases were non–sport-related “is higher than previously reported, and included data from 15 different countries,” the authors noted.

Study limitations included the use of data only from published studies, inclusion of a case series limited to fatal cases, small sample sizes, and lack of consistent reporting of demographic data, mechanisms, investigation results, management, and outcomes.
 

Increased awareness ‘essential’

Dr. Lim and colleagues concluded that increased awareness of non–sport-related commotio cordis is “essential” for early recognition, resuscitation, and mortality reduction. 

Jim Cheung, MD, chair of the American College of Cardiology’s electrophysiology section, “completely agrees.” Greater awareness among the general population could reduce barriers to CPR and automated external defibrillator (AED) use, he said, which in turn, can lead to improved survival.

Furthermore, Dr. Cheung added, “This study underscores the importance of ensuring that non–cardiology-trained physicians such as emergency medicine physicians and trauma surgeons who might encounter patients with non–sports-related commotio cordis recognize the entity during the course of treatment.”

Because the review relied only on published cases, “it may not represent the true breadth of cases that are occurring in the real world,” he noted. “I suspect that cases that occur outside of sports-related activities, such as MVAs and assault, are more likely to be underreported and that the true proportion of non–sports-related commotio cordis may be significantly higher than 36%.” Increased reporting of cases as part of an international commotio cordis registry would help provide additional insights, he suggested.

“There is a common misperception that SCA only occurs among older patients and patients with known coronary artery disease or heart failure,” he said. “For us to move the needle on improving SCA survival, we will need to tackle the problem from multiple angles including increasing public awareness, training the public on CPR and AED use, and improving access to AEDs by addressing structural barriers.”

Dr. Cheung pointed to ongoing efforts by nonprofit, patient-driven organizations such as the SADS Foundation and Omar Carter Foundation, and professional societies such as the American College of Cardiology, the American Heart Association, and Heart Rhythm Society, to direct public awareness campaigns and legislative proposals to address this problem.

Similar efforts are underway among cardiac societies and SCA awareness groups in Australia, Dr. Lim said.

No funding or relevant financial relationships were disclosed.
 

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

Sudden cardiac arrest (SCA) due to commotio cordis occurs more frequently in non–sport-related settings than is commonly thought, resulting in lower rates of resuscitation and increased mortality, especially among young women, a new review suggests.

The condition is rare, caused by an often fatal arrhythmia secondary to a blunt, nonpenetrating impact over the precordium, without direct structural damage to the heart itself. Common causes in nonsport settings include assault, motor vehicle accidents (MVAs), and daily activities such as occupational accidents.

“We found a stark difference in mortality outcomes between non–sport-related commotio cordis compared to sport-related events,” at 88% vs. 66%, Han S. Lim, MBBS, PhD, of the University of Melbourne, and Austin Health, Heidelberg, Australia, told this news organization. “Rates of cardiopulmonary resuscitation (CPR) (27% vs. 97%) and defibrillation (17% vs. 81%) were considerably lower in the non–sport-related events.”

“Although still being male-predominant, of concern, we saw a higher proportion of females in non–sport-related commotio cordis due to assault, MVAs, and other activities,” he noted. Such events may occur “in secluded domestic settings, may not be witnessed, or may occur as intentional harm, whereby the witness could also be the perpetrator, reducing the likelihood of prompt diagnosis, CPR, and defibrillation administration.”

The study was published online in JACC: Clinical Electrophysiology.
 

Young women affected

Dr. Lim and colleagues searched the literature through 2021 for all cases of commotio cordis. Three hundred and thirty-four cases from among 53 citations were included in the analysis; of those, 121 (36%) occurred in non–sport-related settings, including assault (76%), MVAs (7%), and daily activities (16%). “Daily activities” comprised activities that were expected in a person’s day-to-day routine such as falls, play fighting (in children), and occupational accidents.

Non–sport-related cases primarily involved nonprojectile etiologies (95%), including bodily contact (79%), such as impacts from fists, feet, and knees; impacts with handlebars or steering wheels; and solid stick-like weapons and flat surfaces.

Sport-related cases involved a significantly higher proportion of projectiles (94% vs. 5%) and occurred across a range of sports, mostly at the competitive level (66%).

Both sport-related and non–sport-related commotio cordis affected a similar younger demographic (mean age, 19; mostly males). No statistically significant differences between the two groups were seen with regard to previous cardiac history or family history of cardiac disease, or in arrhythmias on electrocardiogram, biomarkers, or imaging findings.

However, in non–sport-related events, the proportion of females affected was significantly higher (13% vs. 2%), as was mortality (88% vs. 66%). Rates were lower for CPR (27% vs. 97%) and defibrillation use (17% vs. 81%), and resuscitation was more commonly delayed beyond 3 minutes (80% vs. 5%).

The finding that more than a third of reported cases were non–sport-related “is higher than previously reported, and included data from 15 different countries,” the authors noted.

Study limitations included the use of data only from published studies, inclusion of a case series limited to fatal cases, small sample sizes, and lack of consistent reporting of demographic data, mechanisms, investigation results, management, and outcomes.
 

Increased awareness ‘essential’

Dr. Lim and colleagues concluded that increased awareness of non–sport-related commotio cordis is “essential” for early recognition, resuscitation, and mortality reduction. 

Jim Cheung, MD, chair of the American College of Cardiology’s electrophysiology section, “completely agrees.” Greater awareness among the general population could reduce barriers to CPR and automated external defibrillator (AED) use, he said, which in turn, can lead to improved survival.

Furthermore, Dr. Cheung added, “This study underscores the importance of ensuring that non–cardiology-trained physicians such as emergency medicine physicians and trauma surgeons who might encounter patients with non–sports-related commotio cordis recognize the entity during the course of treatment.”

Because the review relied only on published cases, “it may not represent the true breadth of cases that are occurring in the real world,” he noted. “I suspect that cases that occur outside of sports-related activities, such as MVAs and assault, are more likely to be underreported and that the true proportion of non–sports-related commotio cordis may be significantly higher than 36%.” Increased reporting of cases as part of an international commotio cordis registry would help provide additional insights, he suggested.

“There is a common misperception that SCA only occurs among older patients and patients with known coronary artery disease or heart failure,” he said. “For us to move the needle on improving SCA survival, we will need to tackle the problem from multiple angles including increasing public awareness, training the public on CPR and AED use, and improving access to AEDs by addressing structural barriers.”

Dr. Cheung pointed to ongoing efforts by nonprofit, patient-driven organizations such as the SADS Foundation and Omar Carter Foundation, and professional societies such as the American College of Cardiology, the American Heart Association, and Heart Rhythm Society, to direct public awareness campaigns and legislative proposals to address this problem.

Similar efforts are underway among cardiac societies and SCA awareness groups in Australia, Dr. Lim said.

No funding or relevant financial relationships were disclosed.
 

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

Taking 8,000 steps or more for just 1 or 2 days a week was linked to a significant reduction in all-cause and cardiovascular mortality, according to a study of about 3,000 adults.

Previous research has shown lower mortality rates among individuals who walk consistently, especially those who log at least 8,000 steps daily, but the benefit of intense walking just once or twice a week on long-term health outcomes has not been examined, wrote Kosuke Inoue, MD, of Kyoto University, Japan, and colleagues.

iStock/thinkstockphotos

In a study published in JAMA Network Open, the researchers reviewed 10-year follow-up data for 3,101 adults aged 20 years and older who were part of the 2005 and 2006 National Health and Nutrition Examination Survey (NHANES).

The participants were asked to wear accelerometers to track their steps for 7 consecutive days. The researchers assessed the dose-response relationship between days of taking 8,000 steps or more (about 4 miles) during 1 week, and the primary outcome of all-cause mortality risk after 10 years. Cardiovascular mortality risk after 10 years was a secondary outcome.

The mean age of the participants was 50.5 years and 51% were women. The breakdown by ethnicity was 51% White, 21% Black, 24% Hispanic, and 4% other races/ethnicities. A total of 632 individuals took 8,000 steps or more 0 days a week, 532 took at least 8,000 steps 1-2 days per week, and 1,937 took at least 8,000 steps 3-7 days a week.

During the 10-year follow-up period, overall all-cause mortality was 14.2% and cardiovascular mortality was 5.3% across all step groups.

In an adjusted analysis, individuals who took at least 8,000 steps 1-2 days a week had a 14.9% lower all-cause mortality risk compared with those who never reached 8,000 daily steps. This difference was similar to the 16.5% reduced mortality risk for those who took at least 8,000 steps 3-7 days a week.

Similarly, compared with the group with no days of at least 8,000 steps, cardiovascular mortality risk was 8.1% lower for those who took 8,000 steps 1-2 days per week and 8.4% lower for those who took at least 8,000 steps 3-7 days per week. The decreased mortality risk plateaued at 3-4 days.

These patterns in reduced all-cause mortality risk persisted in a stratified analysis by age (younger than 65 years and 65 years and older) and sex. Similar patterns in reduced mortality also emerged when the researchers used different thresholds of daily steps, such as a minimum of 10,000 steps instead of 8,000. The adjusted all-cause mortality for groups who took at least 10,000 steps 1-2 days a week, 3-7 days a week, and no days a week were 8.1%, 7.3%, and 16.7%, respectively, with corresponding cardiovascular mortality risks of 2.4%, 2.3%, and 7.0%, respectively.

“Given the simplicity and ease of counting daily steps, our findings indicate that the recommended number of steps taken on as few as 1 to 2 days per week may be a feasible option for individuals who are striving to achieve some health benefits through adhering to a recommended daily step count but are unable to accomplish this on a daily basis,” the researchers wrote in their discussion.

The findings were limited by several factors including the use daily step measures for 1 week only at baseline, with no data on how physical activity changes might impact mortality risk, the researchers noted. Other limitations included possible accelerometer error and misclassification of activity, possible selection bias, and lack of data on cause-specific mortality outside of cardiovascular death, they said.

However, the results were strengthened by the use of accelerometers as objective measures of activity and by the availability of 10-year follow-up data for nearly 100% of the participants, they said.

“Although our findings might suffer from residual confounding that should be addressed in future research, they suggest that people may receive substantial health benefits even if a sufficient number of steps are taken on only a couple days of the week,” they concluded.
 

Proceed with caution

The current study findings should be interpreted cautiously in light of the potential unmeasured confounding factors and selection bias that often occur in studies of physical activity, James Sawalla Guseh, MD, of Massachusetts General Hospital, and Jose F. Figueroa, MD, of Harvard T.H. Chan School of Public Health, Boston, wrote in an accompanying editorial.

The results support previous studies showing some longevity benefits with “weekend warrior” patterns of intense physical activity for only a couple of days; however, “the body of evidence for sporadic activity is not as robust as the evidence for sustained and regular aerobic activity,” the authors emphasized.

The editorial authors also highlighted the limitations of the current study, including the observational design and significant differences in demographics and comorbidities between the 1- to 2-days of 8,000 steps exercise group and the 0-day group, as well as the reliance on only a week’s worth of data to infer 10 years’ mortality.

Although the data are consistent with previous observations that increased exercise volume reduces mortality, more research is needed, as the current study findings may not reflect other dimensions of health, including neurological health, they said.

Despite the need for cautious interpretation of the results, the current study “supports the emerging and popular idea that step counting, which does not require consideration of exercise duration or intensity, can offer guidance toward robust and favorable health outcomes,” and may inform step-based activity goals to improve public health, the editorialists wrote.

The study was supported by the Japan Agency for Medical Research and Development, the Japan Society for the Promotion of Science, the Japan Endocrine Society, and the Meiji Yasuda Life Foundation of Health and Welfare. Dr. Inoue also was supported by the Program for the Development of Next-Generation Leading Scientists With Global Insight sponsored by the Ministry of Education, Culture, Sports, Science and Technology, Japan. The other researchers had no relevant financial conflicts to disclose. The editorial authors had no financial conflicts to disclose.

Taking 8,000 steps or more for just 1 or 2 days a week was linked to a significant reduction in all-cause and cardiovascular mortality, according to a study of about 3,000 adults.

Previous research has shown lower mortality rates among individuals who walk consistently, especially those who log at least 8,000 steps daily, but the benefit of intense walking just once or twice a week on long-term health outcomes has not been examined, wrote Kosuke Inoue, MD, of Kyoto University, Japan, and colleagues.

iStock/thinkstockphotos

In a study published in JAMA Network Open, the researchers reviewed 10-year follow-up data for 3,101 adults aged 20 years and older who were part of the 2005 and 2006 National Health and Nutrition Examination Survey (NHANES).

The participants were asked to wear accelerometers to track their steps for 7 consecutive days. The researchers assessed the dose-response relationship between days of taking 8,000 steps or more (about 4 miles) during 1 week, and the primary outcome of all-cause mortality risk after 10 years. Cardiovascular mortality risk after 10 years was a secondary outcome.

The mean age of the participants was 50.5 years and 51% were women. The breakdown by ethnicity was 51% White, 21% Black, 24% Hispanic, and 4% other races/ethnicities. A total of 632 individuals took 8,000 steps or more 0 days a week, 532 took at least 8,000 steps 1-2 days per week, and 1,937 took at least 8,000 steps 3-7 days a week.

During the 10-year follow-up period, overall all-cause mortality was 14.2% and cardiovascular mortality was 5.3% across all step groups.

In an adjusted analysis, individuals who took at least 8,000 steps 1-2 days a week had a 14.9% lower all-cause mortality risk compared with those who never reached 8,000 daily steps. This difference was similar to the 16.5% reduced mortality risk for those who took at least 8,000 steps 3-7 days a week.

Similarly, compared with the group with no days of at least 8,000 steps, cardiovascular mortality risk was 8.1% lower for those who took 8,000 steps 1-2 days per week and 8.4% lower for those who took at least 8,000 steps 3-7 days per week. The decreased mortality risk plateaued at 3-4 days.

These patterns in reduced all-cause mortality risk persisted in a stratified analysis by age (younger than 65 years and 65 years and older) and sex. Similar patterns in reduced mortality also emerged when the researchers used different thresholds of daily steps, such as a minimum of 10,000 steps instead of 8,000. The adjusted all-cause mortality for groups who took at least 10,000 steps 1-2 days a week, 3-7 days a week, and no days a week were 8.1%, 7.3%, and 16.7%, respectively, with corresponding cardiovascular mortality risks of 2.4%, 2.3%, and 7.0%, respectively.

“Given the simplicity and ease of counting daily steps, our findings indicate that the recommended number of steps taken on as few as 1 to 2 days per week may be a feasible option for individuals who are striving to achieve some health benefits through adhering to a recommended daily step count but are unable to accomplish this on a daily basis,” the researchers wrote in their discussion.

The findings were limited by several factors including the use daily step measures for 1 week only at baseline, with no data on how physical activity changes might impact mortality risk, the researchers noted. Other limitations included possible accelerometer error and misclassification of activity, possible selection bias, and lack of data on cause-specific mortality outside of cardiovascular death, they said.

However, the results were strengthened by the use of accelerometers as objective measures of activity and by the availability of 10-year follow-up data for nearly 100% of the participants, they said.

“Although our findings might suffer from residual confounding that should be addressed in future research, they suggest that people may receive substantial health benefits even if a sufficient number of steps are taken on only a couple days of the week,” they concluded.
 

Proceed with caution

The current study findings should be interpreted cautiously in light of the potential unmeasured confounding factors and selection bias that often occur in studies of physical activity, James Sawalla Guseh, MD, of Massachusetts General Hospital, and Jose F. Figueroa, MD, of Harvard T.H. Chan School of Public Health, Boston, wrote in an accompanying editorial.

The results support previous studies showing some longevity benefits with “weekend warrior” patterns of intense physical activity for only a couple of days; however, “the body of evidence for sporadic activity is not as robust as the evidence for sustained and regular aerobic activity,” the authors emphasized.

The editorial authors also highlighted the limitations of the current study, including the observational design and significant differences in demographics and comorbidities between the 1- to 2-days of 8,000 steps exercise group and the 0-day group, as well as the reliance on only a week’s worth of data to infer 10 years’ mortality.

Although the data are consistent with previous observations that increased exercise volume reduces mortality, more research is needed, as the current study findings may not reflect other dimensions of health, including neurological health, they said.

Despite the need for cautious interpretation of the results, the current study “supports the emerging and popular idea that step counting, which does not require consideration of exercise duration or intensity, can offer guidance toward robust and favorable health outcomes,” and may inform step-based activity goals to improve public health, the editorialists wrote.

The study was supported by the Japan Agency for Medical Research and Development, the Japan Society for the Promotion of Science, the Japan Endocrine Society, and the Meiji Yasuda Life Foundation of Health and Welfare. Dr. Inoue also was supported by the Program for the Development of Next-Generation Leading Scientists With Global Insight sponsored by the Ministry of Education, Culture, Sports, Science and Technology, Japan. The other researchers had no relevant financial conflicts to disclose. The editorial authors had no financial conflicts to disclose.

Taking 8,000 steps or more for just 1 or 2 days a week was linked to a significant reduction in all-cause and cardiovascular mortality, according to a study of about 3,000 adults.

Previous research has shown lower mortality rates among individuals who walk consistently, especially those who log at least 8,000 steps daily, but the benefit of intense walking just once or twice a week on long-term health outcomes has not been examined, wrote Kosuke Inoue, MD, of Kyoto University, Japan, and colleagues.

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In a study published in JAMA Network Open, the researchers reviewed 10-year follow-up data for 3,101 adults aged 20 years and older who were part of the 2005 and 2006 National Health and Nutrition Examination Survey (NHANES).

The participants were asked to wear accelerometers to track their steps for 7 consecutive days. The researchers assessed the dose-response relationship between days of taking 8,000 steps or more (about 4 miles) during 1 week, and the primary outcome of all-cause mortality risk after 10 years. Cardiovascular mortality risk after 10 years was a secondary outcome.

The mean age of the participants was 50.5 years and 51% were women. The breakdown by ethnicity was 51% White, 21% Black, 24% Hispanic, and 4% other races/ethnicities. A total of 632 individuals took 8,000 steps or more 0 days a week, 532 took at least 8,000 steps 1-2 days per week, and 1,937 took at least 8,000 steps 3-7 days a week.

During the 10-year follow-up period, overall all-cause mortality was 14.2% and cardiovascular mortality was 5.3% across all step groups.

In an adjusted analysis, individuals who took at least 8,000 steps 1-2 days a week had a 14.9% lower all-cause mortality risk compared with those who never reached 8,000 daily steps. This difference was similar to the 16.5% reduced mortality risk for those who took at least 8,000 steps 3-7 days a week.

Similarly, compared with the group with no days of at least 8,000 steps, cardiovascular mortality risk was 8.1% lower for those who took 8,000 steps 1-2 days per week and 8.4% lower for those who took at least 8,000 steps 3-7 days per week. The decreased mortality risk plateaued at 3-4 days.

These patterns in reduced all-cause mortality risk persisted in a stratified analysis by age (younger than 65 years and 65 years and older) and sex. Similar patterns in reduced mortality also emerged when the researchers used different thresholds of daily steps, such as a minimum of 10,000 steps instead of 8,000. The adjusted all-cause mortality for groups who took at least 10,000 steps 1-2 days a week, 3-7 days a week, and no days a week were 8.1%, 7.3%, and 16.7%, respectively, with corresponding cardiovascular mortality risks of 2.4%, 2.3%, and 7.0%, respectively.

“Given the simplicity and ease of counting daily steps, our findings indicate that the recommended number of steps taken on as few as 1 to 2 days per week may be a feasible option for individuals who are striving to achieve some health benefits through adhering to a recommended daily step count but are unable to accomplish this on a daily basis,” the researchers wrote in their discussion.

The findings were limited by several factors including the use daily step measures for 1 week only at baseline, with no data on how physical activity changes might impact mortality risk, the researchers noted. Other limitations included possible accelerometer error and misclassification of activity, possible selection bias, and lack of data on cause-specific mortality outside of cardiovascular death, they said.

However, the results were strengthened by the use of accelerometers as objective measures of activity and by the availability of 10-year follow-up data for nearly 100% of the participants, they said.

“Although our findings might suffer from residual confounding that should be addressed in future research, they suggest that people may receive substantial health benefits even if a sufficient number of steps are taken on only a couple days of the week,” they concluded.
 

Proceed with caution

The current study findings should be interpreted cautiously in light of the potential unmeasured confounding factors and selection bias that often occur in studies of physical activity, James Sawalla Guseh, MD, of Massachusetts General Hospital, and Jose F. Figueroa, MD, of Harvard T.H. Chan School of Public Health, Boston, wrote in an accompanying editorial.

The results support previous studies showing some longevity benefits with “weekend warrior” patterns of intense physical activity for only a couple of days; however, “the body of evidence for sporadic activity is not as robust as the evidence for sustained and regular aerobic activity,” the authors emphasized.

The editorial authors also highlighted the limitations of the current study, including the observational design and significant differences in demographics and comorbidities between the 1- to 2-days of 8,000 steps exercise group and the 0-day group, as well as the reliance on only a week’s worth of data to infer 10 years’ mortality.

Although the data are consistent with previous observations that increased exercise volume reduces mortality, more research is needed, as the current study findings may not reflect other dimensions of health, including neurological health, they said.

Despite the need for cautious interpretation of the results, the current study “supports the emerging and popular idea that step counting, which does not require consideration of exercise duration or intensity, can offer guidance toward robust and favorable health outcomes,” and may inform step-based activity goals to improve public health, the editorialists wrote.

The study was supported by the Japan Agency for Medical Research and Development, the Japan Society for the Promotion of Science, the Japan Endocrine Society, and the Meiji Yasuda Life Foundation of Health and Welfare. Dr. Inoue also was supported by the Program for the Development of Next-Generation Leading Scientists With Global Insight sponsored by the Ministry of Education, Culture, Sports, Science and Technology, Japan. The other researchers had no relevant financial conflicts to disclose. The editorial authors had no financial conflicts to disclose.