Cardiology

Patient-reported symptoms and quality of life should guide treatment for the roughly 8.5 million people in the United States living with peripheral artery disease (PAD), the American Heart Association said in a new scientific statement released Oct. 13.

“The person living with PAD is the authority on the impact it has on their daily life. Our treatment must be grounded in their lived experiences and go beyond the clinical measures of how well blood flows through the arteries,” Kim G. Smolderen, PhD, lead author of the statement writing group, says in a release.

“We have spent years developing and validating standardized instruments to capture people’s experiences in a reliable and sensitive way. We are now at a point where we can start integrating this information into real-world care, through pilot programs that can develop quality benchmarks for different phenotypes of patients with PAD and the types of treatments they undergo, as seen from their perspective,” adds Dr. Smolderen, co-director of the Vascular Medicine Outcomes Research (VAMOS) lab at Yale University, New Haven, Conn.

The statement, “Advancing Peripheral Artery Disease Quality of Care and Outcomes Through Patient-Reported Health Status Assessment,” is published online in Circulation.

It comes on the heels of a 2021 AHA statement urging greater attention to PAD, which is underdiagnosed and undertreated in the United States despite its high prevalence.
 

Fragmented care

Dr. Smolderen said that the multidisciplinary writing group was united in one overarching goal: “How can we disrupt the fragmented care model for PAD and make PAD care more accountable, value-based, and patient-centered?”

“True disruption is needed in a clinical space where the treatment of lower-extremity disease lies in the hands of many different specialties and variability in care and outcomes is a major concern,” Dr. Smolderen said.

The statement calls for improving and individualizing PAD care by gathering feedback from their experience through treatment using systematic and validated patient-reported outcome measures (PROMs).

PROMs for PAD include the Walking Impairment Questionnaire (WIQ), the Vascular Quality of Life Questionnaire (VascuQoL), and Peripheral Artery Questionnaire (PAQ).
 

Accountability tied to reimbursement

Dr. Smolderen noted that PROMs are increasingly being integrated into definitions of what it means to deliver high-quality, patient-centered care, and PROMs scores may directly impact reimbursement.

“Using a template that has been implemented in other medical conditions, we propose a shift in metrics that will tell us whether high-quality PAD care has been delivered from a patients’ perspective,” Dr. Smolderen told this news organization.

That is, “have we been able to improve the health status of that person’s life? We may have removed the blockage in the arteries, but will the patient feel that this intervention has addressed their PAD-specific health status goals?”

To facilitate accountability in quality PAD care, the writing group calls for developing, testing, and implementing PAD-specific patient-reported outcomes performance measures – or PRO-PMs.

Pilot efforts demonstrating feasibility of PRO-PMs in various practice settings are needed, as is implementation research evaluating the integration of PRO-PMs and pragmatic clinical trial evidence to demonstrate efficacy of the use of PROs in real world care settings to improve overall PAD outcomes, the writing group says.

“Following that experience and data, we believe value-based models can be proposed integrating PRO information that will affect accountability in PAD care and may ultimately affect reimbursement,” Dr. Smolderen said.

“Adoption of this new paradigm will further improve the quality of care for PAD and will put the patient front and center, as an agent in their care,” she added.

This scientific statement was prepared by the volunteer writing group on behalf of the AHA Council on Peripheral Vascular Disease and the Council on Lifestyle and Cardiometabolic Health. The writing group includes a patient advocate and experts in clinical psychology, outcomes research, nursing, cardiology, vascular surgery, and vascular medicine.

This research had no commercial funding. Dr. Smolderen has disclosed relationships with Optum, Abbott, Cook Medical, Happify, and Tegus.

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

Patient-reported symptoms and quality of life should guide treatment for the roughly 8.5 million people in the United States living with peripheral artery disease (PAD), the American Heart Association said in a new scientific statement released Oct. 13.

“The person living with PAD is the authority on the impact it has on their daily life. Our treatment must be grounded in their lived experiences and go beyond the clinical measures of how well blood flows through the arteries,” Kim G. Smolderen, PhD, lead author of the statement writing group, says in a release.

“We have spent years developing and validating standardized instruments to capture people’s experiences in a reliable and sensitive way. We are now at a point where we can start integrating this information into real-world care, through pilot programs that can develop quality benchmarks for different phenotypes of patients with PAD and the types of treatments they undergo, as seen from their perspective,” adds Dr. Smolderen, co-director of the Vascular Medicine Outcomes Research (VAMOS) lab at Yale University, New Haven, Conn.

The statement, “Advancing Peripheral Artery Disease Quality of Care and Outcomes Through Patient-Reported Health Status Assessment,” is published online in Circulation.

It comes on the heels of a 2021 AHA statement urging greater attention to PAD, which is underdiagnosed and undertreated in the United States despite its high prevalence.
 

Fragmented care

Dr. Smolderen said that the multidisciplinary writing group was united in one overarching goal: “How can we disrupt the fragmented care model for PAD and make PAD care more accountable, value-based, and patient-centered?”

“True disruption is needed in a clinical space where the treatment of lower-extremity disease lies in the hands of many different specialties and variability in care and outcomes is a major concern,” Dr. Smolderen said.

The statement calls for improving and individualizing PAD care by gathering feedback from their experience through treatment using systematic and validated patient-reported outcome measures (PROMs).

PROMs for PAD include the Walking Impairment Questionnaire (WIQ), the Vascular Quality of Life Questionnaire (VascuQoL), and Peripheral Artery Questionnaire (PAQ).
 

Accountability tied to reimbursement

Dr. Smolderen noted that PROMs are increasingly being integrated into definitions of what it means to deliver high-quality, patient-centered care, and PROMs scores may directly impact reimbursement.

“Using a template that has been implemented in other medical conditions, we propose a shift in metrics that will tell us whether high-quality PAD care has been delivered from a patients’ perspective,” Dr. Smolderen told this news organization.

That is, “have we been able to improve the health status of that person’s life? We may have removed the blockage in the arteries, but will the patient feel that this intervention has addressed their PAD-specific health status goals?”

To facilitate accountability in quality PAD care, the writing group calls for developing, testing, and implementing PAD-specific patient-reported outcomes performance measures – or PRO-PMs.

Pilot efforts demonstrating feasibility of PRO-PMs in various practice settings are needed, as is implementation research evaluating the integration of PRO-PMs and pragmatic clinical trial evidence to demonstrate efficacy of the use of PROs in real world care settings to improve overall PAD outcomes, the writing group says.

“Following that experience and data, we believe value-based models can be proposed integrating PRO information that will affect accountability in PAD care and may ultimately affect reimbursement,” Dr. Smolderen said.

“Adoption of this new paradigm will further improve the quality of care for PAD and will put the patient front and center, as an agent in their care,” she added.

This scientific statement was prepared by the volunteer writing group on behalf of the AHA Council on Peripheral Vascular Disease and the Council on Lifestyle and Cardiometabolic Health. The writing group includes a patient advocate and experts in clinical psychology, outcomes research, nursing, cardiology, vascular surgery, and vascular medicine.

This research had no commercial funding. Dr. Smolderen has disclosed relationships with Optum, Abbott, Cook Medical, Happify, and Tegus.

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

Patient-reported symptoms and quality of life should guide treatment for the roughly 8.5 million people in the United States living with peripheral artery disease (PAD), the American Heart Association said in a new scientific statement released Oct. 13.

“The person living with PAD is the authority on the impact it has on their daily life. Our treatment must be grounded in their lived experiences and go beyond the clinical measures of how well blood flows through the arteries,” Kim G. Smolderen, PhD, lead author of the statement writing group, says in a release.

“We have spent years developing and validating standardized instruments to capture people’s experiences in a reliable and sensitive way. We are now at a point where we can start integrating this information into real-world care, through pilot programs that can develop quality benchmarks for different phenotypes of patients with PAD and the types of treatments they undergo, as seen from their perspective,” adds Dr. Smolderen, co-director of the Vascular Medicine Outcomes Research (VAMOS) lab at Yale University, New Haven, Conn.

The statement, “Advancing Peripheral Artery Disease Quality of Care and Outcomes Through Patient-Reported Health Status Assessment,” is published online in Circulation.

It comes on the heels of a 2021 AHA statement urging greater attention to PAD, which is underdiagnosed and undertreated in the United States despite its high prevalence.
 

Fragmented care

Dr. Smolderen said that the multidisciplinary writing group was united in one overarching goal: “How can we disrupt the fragmented care model for PAD and make PAD care more accountable, value-based, and patient-centered?”

“True disruption is needed in a clinical space where the treatment of lower-extremity disease lies in the hands of many different specialties and variability in care and outcomes is a major concern,” Dr. Smolderen said.

The statement calls for improving and individualizing PAD care by gathering feedback from their experience through treatment using systematic and validated patient-reported outcome measures (PROMs).

PROMs for PAD include the Walking Impairment Questionnaire (WIQ), the Vascular Quality of Life Questionnaire (VascuQoL), and Peripheral Artery Questionnaire (PAQ).
 

Accountability tied to reimbursement

Dr. Smolderen noted that PROMs are increasingly being integrated into definitions of what it means to deliver high-quality, patient-centered care, and PROMs scores may directly impact reimbursement.

“Using a template that has been implemented in other medical conditions, we propose a shift in metrics that will tell us whether high-quality PAD care has been delivered from a patients’ perspective,” Dr. Smolderen told this news organization.

That is, “have we been able to improve the health status of that person’s life? We may have removed the blockage in the arteries, but will the patient feel that this intervention has addressed their PAD-specific health status goals?”

To facilitate accountability in quality PAD care, the writing group calls for developing, testing, and implementing PAD-specific patient-reported outcomes performance measures – or PRO-PMs.

Pilot efforts demonstrating feasibility of PRO-PMs in various practice settings are needed, as is implementation research evaluating the integration of PRO-PMs and pragmatic clinical trial evidence to demonstrate efficacy of the use of PROs in real world care settings to improve overall PAD outcomes, the writing group says.

“Following that experience and data, we believe value-based models can be proposed integrating PRO information that will affect accountability in PAD care and may ultimately affect reimbursement,” Dr. Smolderen said.

“Adoption of this new paradigm will further improve the quality of care for PAD and will put the patient front and center, as an agent in their care,” she added.

This scientific statement was prepared by the volunteer writing group on behalf of the AHA Council on Peripheral Vascular Disease and the Council on Lifestyle and Cardiometabolic Health. The writing group includes a patient advocate and experts in clinical psychology, outcomes research, nursing, cardiology, vascular surgery, and vascular medicine.

This research had no commercial funding. Dr. Smolderen has disclosed relationships with Optum, Abbott, Cook Medical, Happify, and Tegus.

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

Athletes with mild hypertrophic cardiomyopathy (HCM) at low risk of sudden cardiac death (SCD) can safely continue to exercise at competitive levels, a retrospective study suggests.

During a mean follow-up of 4.5 years, athletes who continued to engage in high-intensity competitive sports after a mild HCM diagnosis were free of cardiac symptoms, and there were no deaths, incidents of sustained ventricular tachycardia or syncope, or changes in cardiac electrical, structural, or functional phenotypes.

Pavel1964/iStock/Getty Images

“This study supports emerging evidence that HCM individuals with a low-risk profile and mild hypertrophy may engage in vigorous exercise and competitive sport,” Sanjay Sharma, MD, of St. George’s University of London, said in an interview. Current guidelines from the European Society of Cardiology and the American College of Cardiology support a more liberal approach to exercise for these individuals.

That said, he added, “it is important to emphasize that our cohort consisted of a group of adult competitive athletes who had probably been competing for several years before the diagnosis was made and therefore represented a self-selected, low-risk cohort. It is difficult to extrapolate this data to adolescent athletes, who appear to be more vulnerable to exercise-related SCD from HCM.”

The study was published online in the Journal of the American College of Cardiology.
 

Vigorous exercise OK for some

Dr. Sharma and colleagues analyzed data from 53 athletes with HCM who continued to participate in competitive sports. The mean age was 39 years, 98% were men, and 72% were White. About half (53%) competed as professionals, and were most commonly engaged in cycling, football, running, and rugby.

Participants underwent 6-12 monthly assessments that included electrocardiograms, echocardiograms, cardiopulmonary exercise testing, Holter monitoring (≥ 24 hours), and cardiac magnetic resonance imaging. A majority (64.2%) were evaluated because of an abnormal electrocardiograms, and one presented with an incidental abnormal echocardiogram.

About a quarter (24.5%) were symptomatic and 5 (9.4%) were identified on family screening. Eight (15%) had a family history of HCM, and six (11.3%) of SCD.

At the baseline evaluation, all athletes had a “low” ESC 5-year SCD risk score for HCM (1.9% ± 0.9%). None had syncope. Mean peak VO₂ was 40.7 ± 6.8 mL/kg per minute.

The mean left ventricular wall thickness was 14.6 ± 2.3 mm; all had normal LV systolic and diastolic function and no LV outflow tract obstruction at rest or on provocation testing. In addition, none had an LV apical aneurysm.

Twenty-two (41%) showed late gadolinium enhancement on baseline cardiac magnetic resonance imaging.

A total of 19 participants underwent genotyping; 4 (21.1%) had a pathogenic/likely pathogenic sarcomeric variant. None took cardiovascular medication or had an implantable cardioverter defibrillator (ICD).

During a mean follow-up of 4.5 years, all participants continued to exercise at the same level as before their diagnosis; none underwent detraining. All stayed free of cardiac symptoms, and there were no deaths, sustained ventricular tachycardia episodes, or syncope.

Four demonstrated new, nonsustained ventricular tachycardia (NSVT) during follow-up, one of whom underwent ICD implantation because of an increased risk score and subsequently moderated exercise levels.

One participant had a 30-second atrial fibrillation (AFib) episode lasting longer than 30 seconds, started on a beta-blocker and oral anticoagulation, and also moderated exercise levels.

The event rate was 2.1% per year for asymptomatic arrhythmias (NSVT and AFib). No changes were observed in the cardiac electrical, structural, or functional phenotype during follow-up.

Dr. Sharma and colleagues stated: “Our sample size is small; however, it is nearly double the size of a previously studied Italian athletic cohort, and one-half were professional athletes. Furthermore, 17% of our cohort comprised Black athletes who are perceived to be at higher risk of SCD than White athletes.”

Daniele Massera, MD, assistant professor in the HCM program, department of medicine, Charney Division of Cardiology, New York University Langone Health, said in an interview: “Of note, these were athletes/patients at the very low end of phenotypic severity of HCM. ... It is also notable that diastolic function was normal in all of them, an uncommon finding in patients with HCM.”

Like Dr. Sharma, he said the findings are in line with recent guidelines, and cautioned: “This small study applies only to a very small subset of patients who are being evaluated at specialized HCM programs: asymptomatic male individuals who have mild, low-risk HCM and are on no medicines.

“The findings cannot be generalized to the population of symptomatic individuals with (or without) outflow obstruction, more severe hypertrophy, and who have ICDs and/or take medication for symptoms, nor to younger patients or adolescents, who may be at higher risk for adverse outcomes,” he concluded.
 

Individualized approach urged

Dr. Sharma was a coauthor of the recent article challenging the traditional restrictive approach to exercise for athletes diagnosed with HCM and other inherited cardiovascular diseases. The article suggested that individualized recommendations, taking risks into consideration, can help guide those who want to exercise or participate in competitive sports.

Dr. Sharma also is a coauthor of a 6-month follow-up to the SAFE-HCM study, which compared the effects of a supervised 12-week high-intensity exercise program to usual care in low-risk individuals with HCM (mean age, 45.7). 

In the 6-month follow-up study, published as an abstract in the European Journal of Preventive Cardiology 2021 supplement, “exercising individuals had improved functional capacity and atherosclerotic risk profile and there were no differences in the composite safety outcomes [cardiovascular death, cardiac arrest, device therapy, exercise-induced syncope, sustained VT, NSVT, or sustained atrial arrhythmias] between exercising individuals and usual care individuals,” Dr. Sharma said.

The full study will soon be ready to submit for publication, he added.

No commercial funding or relevant conflicts of interest were disclosed.

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

Athletes with mild hypertrophic cardiomyopathy (HCM) at low risk of sudden cardiac death (SCD) can safely continue to exercise at competitive levels, a retrospective study suggests.

During a mean follow-up of 4.5 years, athletes who continued to engage in high-intensity competitive sports after a mild HCM diagnosis were free of cardiac symptoms, and there were no deaths, incidents of sustained ventricular tachycardia or syncope, or changes in cardiac electrical, structural, or functional phenotypes.

Pavel1964/iStock/Getty Images

“This study supports emerging evidence that HCM individuals with a low-risk profile and mild hypertrophy may engage in vigorous exercise and competitive sport,” Sanjay Sharma, MD, of St. George’s University of London, said in an interview. Current guidelines from the European Society of Cardiology and the American College of Cardiology support a more liberal approach to exercise for these individuals.

That said, he added, “it is important to emphasize that our cohort consisted of a group of adult competitive athletes who had probably been competing for several years before the diagnosis was made and therefore represented a self-selected, low-risk cohort. It is difficult to extrapolate this data to adolescent athletes, who appear to be more vulnerable to exercise-related SCD from HCM.”

The study was published online in the Journal of the American College of Cardiology.
 

Vigorous exercise OK for some

Dr. Sharma and colleagues analyzed data from 53 athletes with HCM who continued to participate in competitive sports. The mean age was 39 years, 98% were men, and 72% were White. About half (53%) competed as professionals, and were most commonly engaged in cycling, football, running, and rugby.

Participants underwent 6-12 monthly assessments that included electrocardiograms, echocardiograms, cardiopulmonary exercise testing, Holter monitoring (≥ 24 hours), and cardiac magnetic resonance imaging. A majority (64.2%) were evaluated because of an abnormal electrocardiograms, and one presented with an incidental abnormal echocardiogram.

About a quarter (24.5%) were symptomatic and 5 (9.4%) were identified on family screening. Eight (15%) had a family history of HCM, and six (11.3%) of SCD.

At the baseline evaluation, all athletes had a “low” ESC 5-year SCD risk score for HCM (1.9% ± 0.9%). None had syncope. Mean peak VO₂ was 40.7 ± 6.8 mL/kg per minute.

The mean left ventricular wall thickness was 14.6 ± 2.3 mm; all had normal LV systolic and diastolic function and no LV outflow tract obstruction at rest or on provocation testing. In addition, none had an LV apical aneurysm.

Twenty-two (41%) showed late gadolinium enhancement on baseline cardiac magnetic resonance imaging.

A total of 19 participants underwent genotyping; 4 (21.1%) had a pathogenic/likely pathogenic sarcomeric variant. None took cardiovascular medication or had an implantable cardioverter defibrillator (ICD).

During a mean follow-up of 4.5 years, all participants continued to exercise at the same level as before their diagnosis; none underwent detraining. All stayed free of cardiac symptoms, and there were no deaths, sustained ventricular tachycardia episodes, or syncope.

Four demonstrated new, nonsustained ventricular tachycardia (NSVT) during follow-up, one of whom underwent ICD implantation because of an increased risk score and subsequently moderated exercise levels.

One participant had a 30-second atrial fibrillation (AFib) episode lasting longer than 30 seconds, started on a beta-blocker and oral anticoagulation, and also moderated exercise levels.

The event rate was 2.1% per year for asymptomatic arrhythmias (NSVT and AFib). No changes were observed in the cardiac electrical, structural, or functional phenotype during follow-up.

Dr. Sharma and colleagues stated: “Our sample size is small; however, it is nearly double the size of a previously studied Italian athletic cohort, and one-half were professional athletes. Furthermore, 17% of our cohort comprised Black athletes who are perceived to be at higher risk of SCD than White athletes.”

Daniele Massera, MD, assistant professor in the HCM program, department of medicine, Charney Division of Cardiology, New York University Langone Health, said in an interview: “Of note, these were athletes/patients at the very low end of phenotypic severity of HCM. ... It is also notable that diastolic function was normal in all of them, an uncommon finding in patients with HCM.”

Like Dr. Sharma, he said the findings are in line with recent guidelines, and cautioned: “This small study applies only to a very small subset of patients who are being evaluated at specialized HCM programs: asymptomatic male individuals who have mild, low-risk HCM and are on no medicines.

“The findings cannot be generalized to the population of symptomatic individuals with (or without) outflow obstruction, more severe hypertrophy, and who have ICDs and/or take medication for symptoms, nor to younger patients or adolescents, who may be at higher risk for adverse outcomes,” he concluded.
 

Individualized approach urged

Dr. Sharma was a coauthor of the recent article challenging the traditional restrictive approach to exercise for athletes diagnosed with HCM and other inherited cardiovascular diseases. The article suggested that individualized recommendations, taking risks into consideration, can help guide those who want to exercise or participate in competitive sports.

Dr. Sharma also is a coauthor of a 6-month follow-up to the SAFE-HCM study, which compared the effects of a supervised 12-week high-intensity exercise program to usual care in low-risk individuals with HCM (mean age, 45.7). 

In the 6-month follow-up study, published as an abstract in the European Journal of Preventive Cardiology 2021 supplement, “exercising individuals had improved functional capacity and atherosclerotic risk profile and there were no differences in the composite safety outcomes [cardiovascular death, cardiac arrest, device therapy, exercise-induced syncope, sustained VT, NSVT, or sustained atrial arrhythmias] between exercising individuals and usual care individuals,” Dr. Sharma said.

The full study will soon be ready to submit for publication, he added.

No commercial funding or relevant conflicts of interest were disclosed.

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

Athletes with mild hypertrophic cardiomyopathy (HCM) at low risk of sudden cardiac death (SCD) can safely continue to exercise at competitive levels, a retrospective study suggests.

During a mean follow-up of 4.5 years, athletes who continued to engage in high-intensity competitive sports after a mild HCM diagnosis were free of cardiac symptoms, and there were no deaths, incidents of sustained ventricular tachycardia or syncope, or changes in cardiac electrical, structural, or functional phenotypes.

Pavel1964/iStock/Getty Images

“This study supports emerging evidence that HCM individuals with a low-risk profile and mild hypertrophy may engage in vigorous exercise and competitive sport,” Sanjay Sharma, MD, of St. George’s University of London, said in an interview. Current guidelines from the European Society of Cardiology and the American College of Cardiology support a more liberal approach to exercise for these individuals.

That said, he added, “it is important to emphasize that our cohort consisted of a group of adult competitive athletes who had probably been competing for several years before the diagnosis was made and therefore represented a self-selected, low-risk cohort. It is difficult to extrapolate this data to adolescent athletes, who appear to be more vulnerable to exercise-related SCD from HCM.”

The study was published online in the Journal of the American College of Cardiology.
 

Vigorous exercise OK for some

Dr. Sharma and colleagues analyzed data from 53 athletes with HCM who continued to participate in competitive sports. The mean age was 39 years, 98% were men, and 72% were White. About half (53%) competed as professionals, and were most commonly engaged in cycling, football, running, and rugby.

Participants underwent 6-12 monthly assessments that included electrocardiograms, echocardiograms, cardiopulmonary exercise testing, Holter monitoring (≥ 24 hours), and cardiac magnetic resonance imaging. A majority (64.2%) were evaluated because of an abnormal electrocardiograms, and one presented with an incidental abnormal echocardiogram.

About a quarter (24.5%) were symptomatic and 5 (9.4%) were identified on family screening. Eight (15%) had a family history of HCM, and six (11.3%) of SCD.

At the baseline evaluation, all athletes had a “low” ESC 5-year SCD risk score for HCM (1.9% ± 0.9%). None had syncope. Mean peak VO₂ was 40.7 ± 6.8 mL/kg per minute.

The mean left ventricular wall thickness was 14.6 ± 2.3 mm; all had normal LV systolic and diastolic function and no LV outflow tract obstruction at rest or on provocation testing. In addition, none had an LV apical aneurysm.

Twenty-two (41%) showed late gadolinium enhancement on baseline cardiac magnetic resonance imaging.

A total of 19 participants underwent genotyping; 4 (21.1%) had a pathogenic/likely pathogenic sarcomeric variant. None took cardiovascular medication or had an implantable cardioverter defibrillator (ICD).

During a mean follow-up of 4.5 years, all participants continued to exercise at the same level as before their diagnosis; none underwent detraining. All stayed free of cardiac symptoms, and there were no deaths, sustained ventricular tachycardia episodes, or syncope.

Four demonstrated new, nonsustained ventricular tachycardia (NSVT) during follow-up, one of whom underwent ICD implantation because of an increased risk score and subsequently moderated exercise levels.

One participant had a 30-second atrial fibrillation (AFib) episode lasting longer than 30 seconds, started on a beta-blocker and oral anticoagulation, and also moderated exercise levels.

The event rate was 2.1% per year for asymptomatic arrhythmias (NSVT and AFib). No changes were observed in the cardiac electrical, structural, or functional phenotype during follow-up.

Dr. Sharma and colleagues stated: “Our sample size is small; however, it is nearly double the size of a previously studied Italian athletic cohort, and one-half were professional athletes. Furthermore, 17% of our cohort comprised Black athletes who are perceived to be at higher risk of SCD than White athletes.”

Daniele Massera, MD, assistant professor in the HCM program, department of medicine, Charney Division of Cardiology, New York University Langone Health, said in an interview: “Of note, these were athletes/patients at the very low end of phenotypic severity of HCM. ... It is also notable that diastolic function was normal in all of them, an uncommon finding in patients with HCM.”

Like Dr. Sharma, he said the findings are in line with recent guidelines, and cautioned: “This small study applies only to a very small subset of patients who are being evaluated at specialized HCM programs: asymptomatic male individuals who have mild, low-risk HCM and are on no medicines.

“The findings cannot be generalized to the population of symptomatic individuals with (or without) outflow obstruction, more severe hypertrophy, and who have ICDs and/or take medication for symptoms, nor to younger patients or adolescents, who may be at higher risk for adverse outcomes,” he concluded.
 

Individualized approach urged

Dr. Sharma was a coauthor of the recent article challenging the traditional restrictive approach to exercise for athletes diagnosed with HCM and other inherited cardiovascular diseases. The article suggested that individualized recommendations, taking risks into consideration, can help guide those who want to exercise or participate in competitive sports.

Dr. Sharma also is a coauthor of a 6-month follow-up to the SAFE-HCM study, which compared the effects of a supervised 12-week high-intensity exercise program to usual care in low-risk individuals with HCM (mean age, 45.7). 

In the 6-month follow-up study, published as an abstract in the European Journal of Preventive Cardiology 2021 supplement, “exercising individuals had improved functional capacity and atherosclerotic risk profile and there were no differences in the composite safety outcomes [cardiovascular death, cardiac arrest, device therapy, exercise-induced syncope, sustained VT, NSVT, or sustained atrial arrhythmias] between exercising individuals and usual care individuals,” Dr. Sharma said.

The full study will soon be ready to submit for publication, he added.

No commercial funding or relevant conflicts of interest were disclosed.

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

Individuals who experience out-of-hospital cardiac arrest (OHCA) with nonshockable presentations have a better chance of survival when first responders use a novel CPR approach that includes gradual head-up positioning combined with basic but effective circulation-enhancing adjuncts, as shown from data from more than 2,000 patients.

In a study presented at the annual meeting of the American College of Emergency Physicians, Paul Pepe, MD, medical director for Dallas County Emergency Medical Services, reviewed data from five EMS systems that had adopted the new approach. Data were collected prospectively over the past 2 years from a national registry of patients who had received what Dr. Pepe called a “neuroprotective CPR bundle” (NP-CPR).

The study compared 380 NP-CPR case patients to 1,852 control patients who had received conventional CPR. Control data came from high-performance EMS systems that had participated in well-monitored, published OHCA trials funded by the National Institutes of Health. The primary outcome that was used for comparison was successful survival to hospital discharge with neurologically intact status (SURV-NI).

Traditional CPR supine chest compression techniques, if performed early and properly, can be lifesaving, but they are suboptimal, Dr. Pepe said. “Current techniques create pressure waves that run up the arterial side, but they also create back-pressure on the venous side, increasing intracranial pressure (ICP), thus compromising optimal cerebral blood flow,” he told this news organization.

For that reason, a modified physiologic approach to CPR was designed. It involves an airway adjunct called an impedance threshold device (ITD) and active compression-decompression (ACD) with a device “resembling a toilet plunger,” Dr. Pepe said.

The devices draw more blood out of the brain and into the thorax in a complementary fashion. The combination of these two adjuncts had dramatically improved SURV-NI by 50% in a clinical trial, Dr. Pepe said.

The new technology uses automated gradual head-up/torso-up positioning (AHUP) after first “priming the pump” with ITD-ACD–enhanced circulation. It was found to markedly augment that effect even further. In the laboratory setting, this synergistic NP-CPR bundle has been shown to help normalize cerebral perfusion pressure, further promoting neuro-intact survival. Normalization of end-tidal CO2 is routinely observed, according to Dr. Pepe.

In contrast to patients who present with ventricular fibrillation (shockable cases), patients with nonshockable presentations always have had grim prognoses, Dr. Pepe said. Until now, lifesaving advances had not been found, despite the fact that nonshockable presentations (asystole or electrical activity with no pulse) constitute approximately 80% of OHCA cases, or about 250,000 to 300,00 cases a year in the United States, he said.

In the study, approximately 60% of both the NP-CPR patients and control patients had asystole (flatline) presentations. The NP-CPR group had a significant threefold improvement in SURV-NI, compared with patients treated with conventional CPR in the high-functioning systems (odds ratio, 3.09). In a propensity-scored analysis matching all variables known to affect outcome, the OR increased to nearly fourfold higher (OR, 3.87; 95% confidence interval, 1.27-11.78), Dr. Pepe said.

The researchers also found that the time from receipt of a 911 call to initiation of AHUP was associated with progressively higher chances of survival. The median time for application was 11 minutes; when the elapsed time was less than 11 minutes, the SURV-NI was nearly 11-fold higher for NP-CPR patients than for control patients (OR, 10.59), with survival chances of 6% versus 0.5%. ORs were even higher when the time to treatment was less than 16 minutes (OR, 13.58), with survival rates of 5% versus 0.4%.

The findings not only demonstrate proof of concept in these most futile cases but also that implementation is feasible for the majority of patients, considering that the median time to the start of any CPR by a first responder was 8 minutes for both NP-CPR patients and control patients, “let alone 11 minutes for the AHUP initiation,” Dr. Pepe said. “This finally gives some hope for these nonshockable cases,” he emphasized.

“All of these devices have now been cleared by the Food and Drug Administration and should be adopted by all first-in responders,” said Dr. Pepe. “But they should be implemented as a bundle and in the proper sequence and as soon as feasible.”

Training and implementation efforts continue to expand, and more lives can be saved as more firefighters and first-in response teams acquire equipment and training, which can cut the time to response, he said.

The registry will continue to monitor outcomes with NP-CPR – the term was suggested by a patient who survived through this new approach – and Dr. Pepe and colleagues expect the statistics to improve further with wider adoption and faster implementation with the fastest responders.

A recent study by Dr. Pepe’s team, published in Resuscitation, showed the effectiveness of the neuroprotective bundle in improving survival for OHCA patients overall. The current study confirmed its impact on neuro-intact survival for the subgroup of patients with nonshockable cases.

One other take-home message is that head-up CPR cannot yet be performed by lay bystanders. “Also, do not implement this unless you are going to do it right,” Dr. Pepe emphasized in an interview.

Advanced CPR Solutions provided some materials and research funding for an independent data collector. No other relevant financial relationships have been disclosed.

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

Individuals who experience out-of-hospital cardiac arrest (OHCA) with nonshockable presentations have a better chance of survival when first responders use a novel CPR approach that includes gradual head-up positioning combined with basic but effective circulation-enhancing adjuncts, as shown from data from more than 2,000 patients.

In a study presented at the annual meeting of the American College of Emergency Physicians, Paul Pepe, MD, medical director for Dallas County Emergency Medical Services, reviewed data from five EMS systems that had adopted the new approach. Data were collected prospectively over the past 2 years from a national registry of patients who had received what Dr. Pepe called a “neuroprotective CPR bundle” (NP-CPR).

The study compared 380 NP-CPR case patients to 1,852 control patients who had received conventional CPR. Control data came from high-performance EMS systems that had participated in well-monitored, published OHCA trials funded by the National Institutes of Health. The primary outcome that was used for comparison was successful survival to hospital discharge with neurologically intact status (SURV-NI).

Traditional CPR supine chest compression techniques, if performed early and properly, can be lifesaving, but they are suboptimal, Dr. Pepe said. “Current techniques create pressure waves that run up the arterial side, but they also create back-pressure on the venous side, increasing intracranial pressure (ICP), thus compromising optimal cerebral blood flow,” he told this news organization.

For that reason, a modified physiologic approach to CPR was designed. It involves an airway adjunct called an impedance threshold device (ITD) and active compression-decompression (ACD) with a device “resembling a toilet plunger,” Dr. Pepe said.

The devices draw more blood out of the brain and into the thorax in a complementary fashion. The combination of these two adjuncts had dramatically improved SURV-NI by 50% in a clinical trial, Dr. Pepe said.

The new technology uses automated gradual head-up/torso-up positioning (AHUP) after first “priming the pump” with ITD-ACD–enhanced circulation. It was found to markedly augment that effect even further. In the laboratory setting, this synergistic NP-CPR bundle has been shown to help normalize cerebral perfusion pressure, further promoting neuro-intact survival. Normalization of end-tidal CO2 is routinely observed, according to Dr. Pepe.

In contrast to patients who present with ventricular fibrillation (shockable cases), patients with nonshockable presentations always have had grim prognoses, Dr. Pepe said. Until now, lifesaving advances had not been found, despite the fact that nonshockable presentations (asystole or electrical activity with no pulse) constitute approximately 80% of OHCA cases, or about 250,000 to 300,00 cases a year in the United States, he said.

In the study, approximately 60% of both the NP-CPR patients and control patients had asystole (flatline) presentations. The NP-CPR group had a significant threefold improvement in SURV-NI, compared with patients treated with conventional CPR in the high-functioning systems (odds ratio, 3.09). In a propensity-scored analysis matching all variables known to affect outcome, the OR increased to nearly fourfold higher (OR, 3.87; 95% confidence interval, 1.27-11.78), Dr. Pepe said.

The researchers also found that the time from receipt of a 911 call to initiation of AHUP was associated with progressively higher chances of survival. The median time for application was 11 minutes; when the elapsed time was less than 11 minutes, the SURV-NI was nearly 11-fold higher for NP-CPR patients than for control patients (OR, 10.59), with survival chances of 6% versus 0.5%. ORs were even higher when the time to treatment was less than 16 minutes (OR, 13.58), with survival rates of 5% versus 0.4%.

The findings not only demonstrate proof of concept in these most futile cases but also that implementation is feasible for the majority of patients, considering that the median time to the start of any CPR by a first responder was 8 minutes for both NP-CPR patients and control patients, “let alone 11 minutes for the AHUP initiation,” Dr. Pepe said. “This finally gives some hope for these nonshockable cases,” he emphasized.

“All of these devices have now been cleared by the Food and Drug Administration and should be adopted by all first-in responders,” said Dr. Pepe. “But they should be implemented as a bundle and in the proper sequence and as soon as feasible.”

Training and implementation efforts continue to expand, and more lives can be saved as more firefighters and first-in response teams acquire equipment and training, which can cut the time to response, he said.

The registry will continue to monitor outcomes with NP-CPR – the term was suggested by a patient who survived through this new approach – and Dr. Pepe and colleagues expect the statistics to improve further with wider adoption and faster implementation with the fastest responders.

A recent study by Dr. Pepe’s team, published in Resuscitation, showed the effectiveness of the neuroprotective bundle in improving survival for OHCA patients overall. The current study confirmed its impact on neuro-intact survival for the subgroup of patients with nonshockable cases.

One other take-home message is that head-up CPR cannot yet be performed by lay bystanders. “Also, do not implement this unless you are going to do it right,” Dr. Pepe emphasized in an interview.

Advanced CPR Solutions provided some materials and research funding for an independent data collector. No other relevant financial relationships have been disclosed.

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

Individuals who experience out-of-hospital cardiac arrest (OHCA) with nonshockable presentations have a better chance of survival when first responders use a novel CPR approach that includes gradual head-up positioning combined with basic but effective circulation-enhancing adjuncts, as shown from data from more than 2,000 patients.

In a study presented at the annual meeting of the American College of Emergency Physicians, Paul Pepe, MD, medical director for Dallas County Emergency Medical Services, reviewed data from five EMS systems that had adopted the new approach. Data were collected prospectively over the past 2 years from a national registry of patients who had received what Dr. Pepe called a “neuroprotective CPR bundle” (NP-CPR).

The study compared 380 NP-CPR case patients to 1,852 control patients who had received conventional CPR. Control data came from high-performance EMS systems that had participated in well-monitored, published OHCA trials funded by the National Institutes of Health. The primary outcome that was used for comparison was successful survival to hospital discharge with neurologically intact status (SURV-NI).

Traditional CPR supine chest compression techniques, if performed early and properly, can be lifesaving, but they are suboptimal, Dr. Pepe said. “Current techniques create pressure waves that run up the arterial side, but they also create back-pressure on the venous side, increasing intracranial pressure (ICP), thus compromising optimal cerebral blood flow,” he told this news organization.

For that reason, a modified physiologic approach to CPR was designed. It involves an airway adjunct called an impedance threshold device (ITD) and active compression-decompression (ACD) with a device “resembling a toilet plunger,” Dr. Pepe said.

The devices draw more blood out of the brain and into the thorax in a complementary fashion. The combination of these two adjuncts had dramatically improved SURV-NI by 50% in a clinical trial, Dr. Pepe said.

The new technology uses automated gradual head-up/torso-up positioning (AHUP) after first “priming the pump” with ITD-ACD–enhanced circulation. It was found to markedly augment that effect even further. In the laboratory setting, this synergistic NP-CPR bundle has been shown to help normalize cerebral perfusion pressure, further promoting neuro-intact survival. Normalization of end-tidal CO2 is routinely observed, according to Dr. Pepe.

In contrast to patients who present with ventricular fibrillation (shockable cases), patients with nonshockable presentations always have had grim prognoses, Dr. Pepe said. Until now, lifesaving advances had not been found, despite the fact that nonshockable presentations (asystole or electrical activity with no pulse) constitute approximately 80% of OHCA cases, or about 250,000 to 300,00 cases a year in the United States, he said.

In the study, approximately 60% of both the NP-CPR patients and control patients had asystole (flatline) presentations. The NP-CPR group had a significant threefold improvement in SURV-NI, compared with patients treated with conventional CPR in the high-functioning systems (odds ratio, 3.09). In a propensity-scored analysis matching all variables known to affect outcome, the OR increased to nearly fourfold higher (OR, 3.87; 95% confidence interval, 1.27-11.78), Dr. Pepe said.

The researchers also found that the time from receipt of a 911 call to initiation of AHUP was associated with progressively higher chances of survival. The median time for application was 11 minutes; when the elapsed time was less than 11 minutes, the SURV-NI was nearly 11-fold higher for NP-CPR patients than for control patients (OR, 10.59), with survival chances of 6% versus 0.5%. ORs were even higher when the time to treatment was less than 16 minutes (OR, 13.58), with survival rates of 5% versus 0.4%.

The findings not only demonstrate proof of concept in these most futile cases but also that implementation is feasible for the majority of patients, considering that the median time to the start of any CPR by a first responder was 8 minutes for both NP-CPR patients and control patients, “let alone 11 minutes for the AHUP initiation,” Dr. Pepe said. “This finally gives some hope for these nonshockable cases,” he emphasized.

“All of these devices have now been cleared by the Food and Drug Administration and should be adopted by all first-in responders,” said Dr. Pepe. “But they should be implemented as a bundle and in the proper sequence and as soon as feasible.”

Training and implementation efforts continue to expand, and more lives can be saved as more firefighters and first-in response teams acquire equipment and training, which can cut the time to response, he said.

The registry will continue to monitor outcomes with NP-CPR – the term was suggested by a patient who survived through this new approach – and Dr. Pepe and colleagues expect the statistics to improve further with wider adoption and faster implementation with the fastest responders.

A recent study by Dr. Pepe’s team, published in Resuscitation, showed the effectiveness of the neuroprotective bundle in improving survival for OHCA patients overall. The current study confirmed its impact on neuro-intact survival for the subgroup of patients with nonshockable cases.

One other take-home message is that head-up CPR cannot yet be performed by lay bystanders. “Also, do not implement this unless you are going to do it right,” Dr. Pepe emphasized in an interview.

Advanced CPR Solutions provided some materials and research funding for an independent data collector. No other relevant financial relationships have been disclosed.

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

The Food and Drug Administration has approved a furosemide preparation (Furoscix, scPharmaceuticals) intended for subcutaneous self-administration by outpatients with chronic heart failure and volume overload, the company has announced.

The product is indicated for use with a SmartDose On-Body Infuser (West Pharmaceutical Services) single-use subcutaneous administration device, which affixes to the abdomen.

Olivier Le Moal/Getty Images

The infuser is loaded by the patient or caregiver with a prefilled cartridge and is programmed to deliver Furoscix 30 mg over 1 hour followed by a 4-hour infusion at 12.5 mg/h, for a total fixed dose of 80 mg, scPharmaceuticals said in a press release on the drug approval.

Furosemide, a loop diuretic and one of the world’s most frequently used drugs, is conventionally given intravenously in the hospital or orally on an outpatient basis.

The company describes its furosemide preparation, used with the infuser, as “the first and only FDA-approved subcutaneous loop diuretic that delivers [intravenous]-equivalent diuresis at home.” It has been shown to “produce similar diuresis and natriuresis compared to intravenous furosemide.”

“This marks a tremendous opportunity to improve the at-home management of worsening congestion in patients with heart failure who display reduced responsiveness to oral diuretics and require administration of [intravenous] diuretics, which typically requires admission to the hospital,” William T. Abraham, MD, said in the press release.

The FDA approval “is significant and will allow patients to be treated outside of the hospital setting,” said Dr. Abraham, of Ohio State University, Columbus, and an scPharmaceuticals board member.

The Furoscix indication doesn’t cover emergent use or use in acute pulmonary edema, nor is it meant to be used chronically “and should be replaced with oral diuretics as soon as practical,” the company states.

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

The Food and Drug Administration has approved a furosemide preparation (Furoscix, scPharmaceuticals) intended for subcutaneous self-administration by outpatients with chronic heart failure and volume overload, the company has announced.

The product is indicated for use with a SmartDose On-Body Infuser (West Pharmaceutical Services) single-use subcutaneous administration device, which affixes to the abdomen.

Olivier Le Moal/Getty Images

The infuser is loaded by the patient or caregiver with a prefilled cartridge and is programmed to deliver Furoscix 30 mg over 1 hour followed by a 4-hour infusion at 12.5 mg/h, for a total fixed dose of 80 mg, scPharmaceuticals said in a press release on the drug approval.

Furosemide, a loop diuretic and one of the world’s most frequently used drugs, is conventionally given intravenously in the hospital or orally on an outpatient basis.

The company describes its furosemide preparation, used with the infuser, as “the first and only FDA-approved subcutaneous loop diuretic that delivers [intravenous]-equivalent diuresis at home.” It has been shown to “produce similar diuresis and natriuresis compared to intravenous furosemide.”

“This marks a tremendous opportunity to improve the at-home management of worsening congestion in patients with heart failure who display reduced responsiveness to oral diuretics and require administration of [intravenous] diuretics, which typically requires admission to the hospital,” William T. Abraham, MD, said in the press release.

The FDA approval “is significant and will allow patients to be treated outside of the hospital setting,” said Dr. Abraham, of Ohio State University, Columbus, and an scPharmaceuticals board member.

The Furoscix indication doesn’t cover emergent use or use in acute pulmonary edema, nor is it meant to be used chronically “and should be replaced with oral diuretics as soon as practical,” the company states.

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

The Food and Drug Administration has approved a furosemide preparation (Furoscix, scPharmaceuticals) intended for subcutaneous self-administration by outpatients with chronic heart failure and volume overload, the company has announced.

The product is indicated for use with a SmartDose On-Body Infuser (West Pharmaceutical Services) single-use subcutaneous administration device, which affixes to the abdomen.

Olivier Le Moal/Getty Images

The infuser is loaded by the patient or caregiver with a prefilled cartridge and is programmed to deliver Furoscix 30 mg over 1 hour followed by a 4-hour infusion at 12.5 mg/h, for a total fixed dose of 80 mg, scPharmaceuticals said in a press release on the drug approval.

Furosemide, a loop diuretic and one of the world’s most frequently used drugs, is conventionally given intravenously in the hospital or orally on an outpatient basis.

The company describes its furosemide preparation, used with the infuser, as “the first and only FDA-approved subcutaneous loop diuretic that delivers [intravenous]-equivalent diuresis at home.” It has been shown to “produce similar diuresis and natriuresis compared to intravenous furosemide.”

“This marks a tremendous opportunity to improve the at-home management of worsening congestion in patients with heart failure who display reduced responsiveness to oral diuretics and require administration of [intravenous] diuretics, which typically requires admission to the hospital,” William T. Abraham, MD, said in the press release.

The FDA approval “is significant and will allow patients to be treated outside of the hospital setting,” said Dr. Abraham, of Ohio State University, Columbus, and an scPharmaceuticals board member.

The Furoscix indication doesn’t cover emergent use or use in acute pulmonary edema, nor is it meant to be used chronically “and should be replaced with oral diuretics as soon as practical,” the company states.

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

STOCKHOLM – New insights into the benefits of treatment with the “twincretin” tirzepatide for people with overweight or obesity – with or without diabetes – come from new findings reported at the annual meeting of the European Association for the Study of Diabetes.

Additional results from the SURMOUNT-1 trial, which matched tirzepatide against placebo in people with overweight or obesity, provide further details on the favorable changes produced by 72 weeks of tirzepatide treatment on outcomes that included fat and lean mass, insulin sensitivity, and patient-reported outcomes related to functional health and well being, reported Ania M. Jastreboff, MD, PhD.

Mitchel L. Zoler/MDedge News

And results from a meta-analysis of six trials that compared tirzepatide (Mounjaro) against several different comparators in patients with type 2 diabetes further confirm the drug’s ability to reliably produce positive changes in blood lipids, especially by significantly lowering levels of triglycerides, LDL cholesterol, and very LDL (VLDL) cholesterol, said Thomas Karagiannis, MD, PhD, in a separate report at the meeting.

Tirzepatide works as an agonist on receptors for both the glucagonlike peptide–1 (GLP-1), and for the glucose-dependent insulinotropic polypeptide, and received Food and Drug Administration approval for treating people with type 2 diabetes in May 2022. On the basis of results from SURMOUNT-1, the FDA on Oct. 6 granted tirzepatide fast-track designation for a proposed labeling of the agent for treating people with overweight or obesity. This FDA decision will likely remain pending at least until results from a second trial in people with overweight or obesity but without diabetes, SURMOUNT-2, become available in 2023.

SURMOUNT-1 randomized 2,539 people with obesity or overweight and at least one weight-related complication to a weekly injection of tirzepatide or placebo for 72 weeks. The study’s primary efficacy endpoints were the average reduction in weight from baseline, and the percentage of people in each treatment arm achieving weight loss of at least 5% from baseline.

For both endpoints, the outcomes with tirzepatide significantly surpassed placebo effects. Average weight loss ranged from 15%-21% from baseline, depending on dose, compared with 3% on placebo. The rate of participants with at least a 5% weight loss ranged from 85% to 91%, compared with 35% with placebo, as reported in July 2022 in the New England Journal of Medicine.

Cutting fat mass, boosting lean mass

New results from the trial reported by Dr. Jastreboff included a cut in fat mass from 46.2% of total body mass at baseline to 38.5% after 72 weeks, compared with a change from 46.8% at baseline to 44.7% after 72 weeks in the placebo group. Concurrently, lean mass increased with tirzepatide treatment from 51.0% at baseline to 58.1% after 72 weeks.

Participants who received tirzepatide, compared with those who received placebo, had “proportionately greater decrease in fat mass and proportionately greater increase in lean mass” compared with those who received placebo, said Dr. Jastreboff, an endocrinologist and obesity medicine specialist with Yale Medicine in New Haven, Conn. “I was impressed by the amount of visceral fat lost.”

These effects translated into a significant reduction in fat mass-to-lean mass ratio among the people treated with tirzepatide, with the greatest reduction in those who lost at least 15% of their starting weight. In that subgroup the fat-to-lean mass ratio dropped from 0.94 at baseline to 0.64 after 72 weeks of treatment, she said.
 

Focus on diet quality

People treated with tirzepatide “eat so little food that we need to improve the quality of what they eat to protect their muscle,” commented Carel le Roux, MBChB, PhD, a professor in the Diabetes Complications Research Centre of University College Dublin. “You no longer need a dietitian to help people lose weight, because the drug does that. You need dietitians to look after the nutritional health of patients while they lose weight,” Dr. le Roux said in a separate session at the meeting.

Mitchel L. Zoler/MDedge News

Additional tests showed that blood glucose and insulin levels were all significantly lower among trial participants on all three doses of tirzepatide compared with those on placebo, and the tirzepatide-treated subjects also had significant, roughly twofold elevations in their insulin sensitivity measured by the Matsuda Index.

The impact of tirzepatide on glucose and insulin levels and on insulin sensitivity was similar regardless of whether study participants had normoglycemia or prediabetes at entry. By design, no study participants had diabetes.

The trial assessed patient-reported quality-of-life outcomes using the 36-Item Short Form Survey (SF-36). Participants had significant increases in all eight domains within the SF-36 at all three tirzepatide doses, compared with placebo, at 72 weeks, Dr. Jastreboff reported. Improvements in the physical function domain increased most notably among study participants on tirzepatide who had functional limitations at baseline. Heart rate rose among participants who received either of the two highest tirzepatide doses by 2.3-2.5 beats/min, comparable with the effect of other injected incretin-based treatments.

Lipids improve in those with type 2 diabetes

Tirzepatide treatment also results in a “secondary effect” of improving levels of several lipids in people with type 2 diabetes, according to a meta-analysis of findings from six randomized trials. The meta-analysis collectively involved 4,502 participants treated for numerous weeks with one of three doses of tirzepatide and 2,144 people in comparator groups, reported Dr. Karagiannis, a diabetes researcher at Aristotle University of Thessaloniki (Greece).

Among the significant lipid changes linked with tirzepatide treatment, compared with placebo, were an average 13 mg/dL decrease in LDL cholesterol, an average 6 mg/dL decrease in VLDL cholesterol, and an average 50 mg/dL decrease in triglycerides. In comparison to a GLP-1 receptor agonist, an average 25 mg/dL decrease in triglycerides and an average 4 mg/dL reduction in VLDL cholesterol were seen. And trials comparing tirzepatide with basal insulin saw average reductions of 7% in LDL cholesterol, 15% in VLDL cholesterol, 15% in triglycerides, and an 8% increase in HDL cholesterol.

Dr. Karagiannis highlighted that the clinical impact of these effects is unclear, although he noted that the average reduction in LDL cholesterol relative to placebo is of a magnitude that could have a modest effect on long-term outcomes.

These lipid effects of tirzepatide “should be considered alongside” tirzepatide’s “key metabolic effects” on weight and hemoglobin A1c as well as the drug’s safety, concluded Dr. Karagiannis.

The tirzepatide trials were all funded by Eli Lilly, which markets tirzepatide (Mounjaro). Dr. Jastreboff has been an adviser and consultant to Eli Lilly, as well as to Intellihealth, Novo Nordisk, Pfizer, Rhythm Scholars, Roche, and Weight Watchers, and she has received research funding from Eli Lilly and Novo Nordisk. Dr. Karagiannis had no disclosures. Dr. le Roux has had financial relationships with Eli Lilly, as well as with Boehringer Ingelheim, Consilient Health, Covidion, Fractyl, GL Dynamics, Herbalife, Johnson & Johnson, Keyron, and Novo Nordisk.

STOCKHOLM – New insights into the benefits of treatment with the “twincretin” tirzepatide for people with overweight or obesity – with or without diabetes – come from new findings reported at the annual meeting of the European Association for the Study of Diabetes.

Additional results from the SURMOUNT-1 trial, which matched tirzepatide against placebo in people with overweight or obesity, provide further details on the favorable changes produced by 72 weeks of tirzepatide treatment on outcomes that included fat and lean mass, insulin sensitivity, and patient-reported outcomes related to functional health and well being, reported Ania M. Jastreboff, MD, PhD.

Mitchel L. Zoler/MDedge News

And results from a meta-analysis of six trials that compared tirzepatide (Mounjaro) against several different comparators in patients with type 2 diabetes further confirm the drug’s ability to reliably produce positive changes in blood lipids, especially by significantly lowering levels of triglycerides, LDL cholesterol, and very LDL (VLDL) cholesterol, said Thomas Karagiannis, MD, PhD, in a separate report at the meeting.

Tirzepatide works as an agonist on receptors for both the glucagonlike peptide–1 (GLP-1), and for the glucose-dependent insulinotropic polypeptide, and received Food and Drug Administration approval for treating people with type 2 diabetes in May 2022. On the basis of results from SURMOUNT-1, the FDA on Oct. 6 granted tirzepatide fast-track designation for a proposed labeling of the agent for treating people with overweight or obesity. This FDA decision will likely remain pending at least until results from a second trial in people with overweight or obesity but without diabetes, SURMOUNT-2, become available in 2023.

SURMOUNT-1 randomized 2,539 people with obesity or overweight and at least one weight-related complication to a weekly injection of tirzepatide or placebo for 72 weeks. The study’s primary efficacy endpoints were the average reduction in weight from baseline, and the percentage of people in each treatment arm achieving weight loss of at least 5% from baseline.

For both endpoints, the outcomes with tirzepatide significantly surpassed placebo effects. Average weight loss ranged from 15%-21% from baseline, depending on dose, compared with 3% on placebo. The rate of participants with at least a 5% weight loss ranged from 85% to 91%, compared with 35% with placebo, as reported in July 2022 in the New England Journal of Medicine.

Cutting fat mass, boosting lean mass

New results from the trial reported by Dr. Jastreboff included a cut in fat mass from 46.2% of total body mass at baseline to 38.5% after 72 weeks, compared with a change from 46.8% at baseline to 44.7% after 72 weeks in the placebo group. Concurrently, lean mass increased with tirzepatide treatment from 51.0% at baseline to 58.1% after 72 weeks.

Participants who received tirzepatide, compared with those who received placebo, had “proportionately greater decrease in fat mass and proportionately greater increase in lean mass” compared with those who received placebo, said Dr. Jastreboff, an endocrinologist and obesity medicine specialist with Yale Medicine in New Haven, Conn. “I was impressed by the amount of visceral fat lost.”

These effects translated into a significant reduction in fat mass-to-lean mass ratio among the people treated with tirzepatide, with the greatest reduction in those who lost at least 15% of their starting weight. In that subgroup the fat-to-lean mass ratio dropped from 0.94 at baseline to 0.64 after 72 weeks of treatment, she said.
 

Focus on diet quality

People treated with tirzepatide “eat so little food that we need to improve the quality of what they eat to protect their muscle,” commented Carel le Roux, MBChB, PhD, a professor in the Diabetes Complications Research Centre of University College Dublin. “You no longer need a dietitian to help people lose weight, because the drug does that. You need dietitians to look after the nutritional health of patients while they lose weight,” Dr. le Roux said in a separate session at the meeting.

Mitchel L. Zoler/MDedge News

Additional tests showed that blood glucose and insulin levels were all significantly lower among trial participants on all three doses of tirzepatide compared with those on placebo, and the tirzepatide-treated subjects also had significant, roughly twofold elevations in their insulin sensitivity measured by the Matsuda Index.

The impact of tirzepatide on glucose and insulin levels and on insulin sensitivity was similar regardless of whether study participants had normoglycemia or prediabetes at entry. By design, no study participants had diabetes.

The trial assessed patient-reported quality-of-life outcomes using the 36-Item Short Form Survey (SF-36). Participants had significant increases in all eight domains within the SF-36 at all three tirzepatide doses, compared with placebo, at 72 weeks, Dr. Jastreboff reported. Improvements in the physical function domain increased most notably among study participants on tirzepatide who had functional limitations at baseline. Heart rate rose among participants who received either of the two highest tirzepatide doses by 2.3-2.5 beats/min, comparable with the effect of other injected incretin-based treatments.

Lipids improve in those with type 2 diabetes

Tirzepatide treatment also results in a “secondary effect” of improving levels of several lipids in people with type 2 diabetes, according to a meta-analysis of findings from six randomized trials. The meta-analysis collectively involved 4,502 participants treated for numerous weeks with one of three doses of tirzepatide and 2,144 people in comparator groups, reported Dr. Karagiannis, a diabetes researcher at Aristotle University of Thessaloniki (Greece).

Among the significant lipid changes linked with tirzepatide treatment, compared with placebo, were an average 13 mg/dL decrease in LDL cholesterol, an average 6 mg/dL decrease in VLDL cholesterol, and an average 50 mg/dL decrease in triglycerides. In comparison to a GLP-1 receptor agonist, an average 25 mg/dL decrease in triglycerides and an average 4 mg/dL reduction in VLDL cholesterol were seen. And trials comparing tirzepatide with basal insulin saw average reductions of 7% in LDL cholesterol, 15% in VLDL cholesterol, 15% in triglycerides, and an 8% increase in HDL cholesterol.

Dr. Karagiannis highlighted that the clinical impact of these effects is unclear, although he noted that the average reduction in LDL cholesterol relative to placebo is of a magnitude that could have a modest effect on long-term outcomes.

These lipid effects of tirzepatide “should be considered alongside” tirzepatide’s “key metabolic effects” on weight and hemoglobin A1c as well as the drug’s safety, concluded Dr. Karagiannis.

The tirzepatide trials were all funded by Eli Lilly, which markets tirzepatide (Mounjaro). Dr. Jastreboff has been an adviser and consultant to Eli Lilly, as well as to Intellihealth, Novo Nordisk, Pfizer, Rhythm Scholars, Roche, and Weight Watchers, and she has received research funding from Eli Lilly and Novo Nordisk. Dr. Karagiannis had no disclosures. Dr. le Roux has had financial relationships with Eli Lilly, as well as with Boehringer Ingelheim, Consilient Health, Covidion, Fractyl, GL Dynamics, Herbalife, Johnson & Johnson, Keyron, and Novo Nordisk.

STOCKHOLM – New insights into the benefits of treatment with the “twincretin” tirzepatide for people with overweight or obesity – with or without diabetes – come from new findings reported at the annual meeting of the European Association for the Study of Diabetes.

Additional results from the SURMOUNT-1 trial, which matched tirzepatide against placebo in people with overweight or obesity, provide further details on the favorable changes produced by 72 weeks of tirzepatide treatment on outcomes that included fat and lean mass, insulin sensitivity, and patient-reported outcomes related to functional health and well being, reported Ania M. Jastreboff, MD, PhD.

Mitchel L. Zoler/MDedge News

And results from a meta-analysis of six trials that compared tirzepatide (Mounjaro) against several different comparators in patients with type 2 diabetes further confirm the drug’s ability to reliably produce positive changes in blood lipids, especially by significantly lowering levels of triglycerides, LDL cholesterol, and very LDL (VLDL) cholesterol, said Thomas Karagiannis, MD, PhD, in a separate report at the meeting.

Tirzepatide works as an agonist on receptors for both the glucagonlike peptide–1 (GLP-1), and for the glucose-dependent insulinotropic polypeptide, and received Food and Drug Administration approval for treating people with type 2 diabetes in May 2022. On the basis of results from SURMOUNT-1, the FDA on Oct. 6 granted tirzepatide fast-track designation for a proposed labeling of the agent for treating people with overweight or obesity. This FDA decision will likely remain pending at least until results from a second trial in people with overweight or obesity but without diabetes, SURMOUNT-2, become available in 2023.

SURMOUNT-1 randomized 2,539 people with obesity or overweight and at least one weight-related complication to a weekly injection of tirzepatide or placebo for 72 weeks. The study’s primary efficacy endpoints were the average reduction in weight from baseline, and the percentage of people in each treatment arm achieving weight loss of at least 5% from baseline.

For both endpoints, the outcomes with tirzepatide significantly surpassed placebo effects. Average weight loss ranged from 15%-21% from baseline, depending on dose, compared with 3% on placebo. The rate of participants with at least a 5% weight loss ranged from 85% to 91%, compared with 35% with placebo, as reported in July 2022 in the New England Journal of Medicine.

Cutting fat mass, boosting lean mass

New results from the trial reported by Dr. Jastreboff included a cut in fat mass from 46.2% of total body mass at baseline to 38.5% after 72 weeks, compared with a change from 46.8% at baseline to 44.7% after 72 weeks in the placebo group. Concurrently, lean mass increased with tirzepatide treatment from 51.0% at baseline to 58.1% after 72 weeks.

Participants who received tirzepatide, compared with those who received placebo, had “proportionately greater decrease in fat mass and proportionately greater increase in lean mass” compared with those who received placebo, said Dr. Jastreboff, an endocrinologist and obesity medicine specialist with Yale Medicine in New Haven, Conn. “I was impressed by the amount of visceral fat lost.”

These effects translated into a significant reduction in fat mass-to-lean mass ratio among the people treated with tirzepatide, with the greatest reduction in those who lost at least 15% of their starting weight. In that subgroup the fat-to-lean mass ratio dropped from 0.94 at baseline to 0.64 after 72 weeks of treatment, she said.
 

Focus on diet quality

People treated with tirzepatide “eat so little food that we need to improve the quality of what they eat to protect their muscle,” commented Carel le Roux, MBChB, PhD, a professor in the Diabetes Complications Research Centre of University College Dublin. “You no longer need a dietitian to help people lose weight, because the drug does that. You need dietitians to look after the nutritional health of patients while they lose weight,” Dr. le Roux said in a separate session at the meeting.

Mitchel L. Zoler/MDedge News

Additional tests showed that blood glucose and insulin levels were all significantly lower among trial participants on all three doses of tirzepatide compared with those on placebo, and the tirzepatide-treated subjects also had significant, roughly twofold elevations in their insulin sensitivity measured by the Matsuda Index.

The impact of tirzepatide on glucose and insulin levels and on insulin sensitivity was similar regardless of whether study participants had normoglycemia or prediabetes at entry. By design, no study participants had diabetes.

The trial assessed patient-reported quality-of-life outcomes using the 36-Item Short Form Survey (SF-36). Participants had significant increases in all eight domains within the SF-36 at all three tirzepatide doses, compared with placebo, at 72 weeks, Dr. Jastreboff reported. Improvements in the physical function domain increased most notably among study participants on tirzepatide who had functional limitations at baseline. Heart rate rose among participants who received either of the two highest tirzepatide doses by 2.3-2.5 beats/min, comparable with the effect of other injected incretin-based treatments.

Lipids improve in those with type 2 diabetes

Tirzepatide treatment also results in a “secondary effect” of improving levels of several lipids in people with type 2 diabetes, according to a meta-analysis of findings from six randomized trials. The meta-analysis collectively involved 4,502 participants treated for numerous weeks with one of three doses of tirzepatide and 2,144 people in comparator groups, reported Dr. Karagiannis, a diabetes researcher at Aristotle University of Thessaloniki (Greece).

Among the significant lipid changes linked with tirzepatide treatment, compared with placebo, were an average 13 mg/dL decrease in LDL cholesterol, an average 6 mg/dL decrease in VLDL cholesterol, and an average 50 mg/dL decrease in triglycerides. In comparison to a GLP-1 receptor agonist, an average 25 mg/dL decrease in triglycerides and an average 4 mg/dL reduction in VLDL cholesterol were seen. And trials comparing tirzepatide with basal insulin saw average reductions of 7% in LDL cholesterol, 15% in VLDL cholesterol, 15% in triglycerides, and an 8% increase in HDL cholesterol.

Dr. Karagiannis highlighted that the clinical impact of these effects is unclear, although he noted that the average reduction in LDL cholesterol relative to placebo is of a magnitude that could have a modest effect on long-term outcomes.

These lipid effects of tirzepatide “should be considered alongside” tirzepatide’s “key metabolic effects” on weight and hemoglobin A1c as well as the drug’s safety, concluded Dr. Karagiannis.

The tirzepatide trials were all funded by Eli Lilly, which markets tirzepatide (Mounjaro). Dr. Jastreboff has been an adviser and consultant to Eli Lilly, as well as to Intellihealth, Novo Nordisk, Pfizer, Rhythm Scholars, Roche, and Weight Watchers, and she has received research funding from Eli Lilly and Novo Nordisk. Dr. Karagiannis had no disclosures. Dr. le Roux has had financial relationships with Eli Lilly, as well as with Boehringer Ingelheim, Consilient Health, Covidion, Fractyl, GL Dynamics, Herbalife, Johnson & Johnson, Keyron, and Novo Nordisk.

The American College of Cardiology has released an Expert Consensus Decision Pathway on the evaluation and disposition of acute chest pain in the emergency department.

Chest pain accounts for more than 7 million ED visits annually. A major challenge is to quickly identify the small number of patients with acute coronary syndrome (ACS) among the large number of patients who have noncardiac conditions.

The new document is intended to provide guidance on how to “practically apply” recommendations from the 2021 American Heart Association/American College of Cardiology Guideline for the Evaluation and Diagnosis of Chest Pain, focusing specifically on patients who present to the ED, the writing group explains.

“A systematic approach – both at the level of the institution and the individual patient – is essential to achieve optimal outcomes for patients presenting with chest pain to the ED,” say writing group chair Michael Kontos, MD, Virginia Commonwealth University, Richmond, and colleagues.

At the institution level, this decision pathway recommends high-sensitivity cardiac troponin (hs-cTn) assays coupled with a clinical decision pathway (CDP) to reduce ED “dwell” times and increase the number of patients with chest pain who can safely be discharged without additional testing. This will decrease ED crowding and limit unnecessary testing, they point out. 

At the individual patient level, this document aims to provide structure for the ED evaluation of chest pain, accelerating the evaluation process and matching the intensity of testing and treatment to patient risk.

The 36-page document was published online in the Journal of the American College of Cardiology.

Key summary points in the document include the following:

• Electrocardiogram remains the best initial test for evaluation of chest pain in the ED and should be performed and interpreted within 10 minutes of ED arrival.
• In patients who arrive via ambulance, the prehospital ECG should be reviewed, because ischemic changes may have resolved before ED arrival.
• When the ECG shows evidence of acute infarction or ischemia, subsequent care should follow current guidelines for management of acute ST-segment elevation myocardial infarction (STEMI) and non–ST-segment elevation ACS (NSTE-ACS).
• Patients with a nonischemic ECG can enter an accelerated CDP designed to provide rapid risk assessment and exclusion of ACS.
• Patients who are hemodynamically unstable, have significant arrhythmias, or evidence of significant heart failure should be evaluated and treated appropriately and are not candidates for an accelerated CDP.
• High-sensitivity cardiac troponin T (hs-cTnT) and high-sensitivity cardiac troponin I (hs-cTnI) are the preferred biomarkers for evaluation of possible ACS.
• Patients classified as low risk (rule out) using the current hs-cTn-based CDPs can generally be discharged directly from the ED without additional testing, although outpatient testing may be considered in selected cases.
• Patients with substantially elevated initial hs-cTn values or those with significant dynamic changes over 1-3 hours are assigned to the abnormal/high-risk category and should be further classified according to the universal definition of myocardial infarction type 1 or 2 or acute or chronic nonischemic cardiac injury.
• High-risk patients should usually be admitted to an inpatient setting for further evaluation and treatment.
• Patients determined to be intermediate risk with the CDP should undergo additional observation with repeat hs-cTn measurements at 3-6 hours and risk assessment using either the modified HEART (history, ECG, age, risk factors, and troponin) score or the ED assessment of chest pain score (EDACS).
• Noninvasive testing should be considered for the intermediate-risk group unless low-risk features are identified using risk scores or noninvasive testing has been performed recently with normal or low-risk findings.

The writing group notes that “safe and efficient” management of chest pain in the ED requires appropriate follow-up after discharge. Timing of follow-up and referral for outpatient noninvasive testing should be influenced by patient risk and results of cardiac testing.

Disclosures for members of the writing group are available with the original article.

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

The American College of Cardiology has released an Expert Consensus Decision Pathway on the evaluation and disposition of acute chest pain in the emergency department.

Chest pain accounts for more than 7 million ED visits annually. A major challenge is to quickly identify the small number of patients with acute coronary syndrome (ACS) among the large number of patients who have noncardiac conditions.

The new document is intended to provide guidance on how to “practically apply” recommendations from the 2021 American Heart Association/American College of Cardiology Guideline for the Evaluation and Diagnosis of Chest Pain, focusing specifically on patients who present to the ED, the writing group explains.

“A systematic approach – both at the level of the institution and the individual patient – is essential to achieve optimal outcomes for patients presenting with chest pain to the ED,” say writing group chair Michael Kontos, MD, Virginia Commonwealth University, Richmond, and colleagues.

At the institution level, this decision pathway recommends high-sensitivity cardiac troponin (hs-cTn) assays coupled with a clinical decision pathway (CDP) to reduce ED “dwell” times and increase the number of patients with chest pain who can safely be discharged without additional testing. This will decrease ED crowding and limit unnecessary testing, they point out. 

At the individual patient level, this document aims to provide structure for the ED evaluation of chest pain, accelerating the evaluation process and matching the intensity of testing and treatment to patient risk.

The 36-page document was published online in the Journal of the American College of Cardiology.

Key summary points in the document include the following:

• Electrocardiogram remains the best initial test for evaluation of chest pain in the ED and should be performed and interpreted within 10 minutes of ED arrival.
• In patients who arrive via ambulance, the prehospital ECG should be reviewed, because ischemic changes may have resolved before ED arrival.
• When the ECG shows evidence of acute infarction or ischemia, subsequent care should follow current guidelines for management of acute ST-segment elevation myocardial infarction (STEMI) and non–ST-segment elevation ACS (NSTE-ACS).
• Patients with a nonischemic ECG can enter an accelerated CDP designed to provide rapid risk assessment and exclusion of ACS.
• Patients who are hemodynamically unstable, have significant arrhythmias, or evidence of significant heart failure should be evaluated and treated appropriately and are not candidates for an accelerated CDP.
• High-sensitivity cardiac troponin T (hs-cTnT) and high-sensitivity cardiac troponin I (hs-cTnI) are the preferred biomarkers for evaluation of possible ACS.
• Patients classified as low risk (rule out) using the current hs-cTn-based CDPs can generally be discharged directly from the ED without additional testing, although outpatient testing may be considered in selected cases.
• Patients with substantially elevated initial hs-cTn values or those with significant dynamic changes over 1-3 hours are assigned to the abnormal/high-risk category and should be further classified according to the universal definition of myocardial infarction type 1 or 2 or acute or chronic nonischemic cardiac injury.
• High-risk patients should usually be admitted to an inpatient setting for further evaluation and treatment.
• Patients determined to be intermediate risk with the CDP should undergo additional observation with repeat hs-cTn measurements at 3-6 hours and risk assessment using either the modified HEART (history, ECG, age, risk factors, and troponin) score or the ED assessment of chest pain score (EDACS).
• Noninvasive testing should be considered for the intermediate-risk group unless low-risk features are identified using risk scores or noninvasive testing has been performed recently with normal or low-risk findings.

The writing group notes that “safe and efficient” management of chest pain in the ED requires appropriate follow-up after discharge. Timing of follow-up and referral for outpatient noninvasive testing should be influenced by patient risk and results of cardiac testing.

Disclosures for members of the writing group are available with the original article.

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

The American College of Cardiology has released an Expert Consensus Decision Pathway on the evaluation and disposition of acute chest pain in the emergency department.

Chest pain accounts for more than 7 million ED visits annually. A major challenge is to quickly identify the small number of patients with acute coronary syndrome (ACS) among the large number of patients who have noncardiac conditions.

The new document is intended to provide guidance on how to “practically apply” recommendations from the 2021 American Heart Association/American College of Cardiology Guideline for the Evaluation and Diagnosis of Chest Pain, focusing specifically on patients who present to the ED, the writing group explains.

“A systematic approach – both at the level of the institution and the individual patient – is essential to achieve optimal outcomes for patients presenting with chest pain to the ED,” say writing group chair Michael Kontos, MD, Virginia Commonwealth University, Richmond, and colleagues.

At the institution level, this decision pathway recommends high-sensitivity cardiac troponin (hs-cTn) assays coupled with a clinical decision pathway (CDP) to reduce ED “dwell” times and increase the number of patients with chest pain who can safely be discharged without additional testing. This will decrease ED crowding and limit unnecessary testing, they point out. 

At the individual patient level, this document aims to provide structure for the ED evaluation of chest pain, accelerating the evaluation process and matching the intensity of testing and treatment to patient risk.

The 36-page document was published online in the Journal of the American College of Cardiology.

Key summary points in the document include the following:

• Electrocardiogram remains the best initial test for evaluation of chest pain in the ED and should be performed and interpreted within 10 minutes of ED arrival.
• In patients who arrive via ambulance, the prehospital ECG should be reviewed, because ischemic changes may have resolved before ED arrival.
• When the ECG shows evidence of acute infarction or ischemia, subsequent care should follow current guidelines for management of acute ST-segment elevation myocardial infarction (STEMI) and non–ST-segment elevation ACS (NSTE-ACS).
• Patients with a nonischemic ECG can enter an accelerated CDP designed to provide rapid risk assessment and exclusion of ACS.
• Patients who are hemodynamically unstable, have significant arrhythmias, or evidence of significant heart failure should be evaluated and treated appropriately and are not candidates for an accelerated CDP.
• High-sensitivity cardiac troponin T (hs-cTnT) and high-sensitivity cardiac troponin I (hs-cTnI) are the preferred biomarkers for evaluation of possible ACS.
• Patients classified as low risk (rule out) using the current hs-cTn-based CDPs can generally be discharged directly from the ED without additional testing, although outpatient testing may be considered in selected cases.
• Patients with substantially elevated initial hs-cTn values or those with significant dynamic changes over 1-3 hours are assigned to the abnormal/high-risk category and should be further classified according to the universal definition of myocardial infarction type 1 or 2 or acute or chronic nonischemic cardiac injury.
• High-risk patients should usually be admitted to an inpatient setting for further evaluation and treatment.
• Patients determined to be intermediate risk with the CDP should undergo additional observation with repeat hs-cTn measurements at 3-6 hours and risk assessment using either the modified HEART (history, ECG, age, risk factors, and troponin) score or the ED assessment of chest pain score (EDACS).
• Noninvasive testing should be considered for the intermediate-risk group unless low-risk features are identified using risk scores or noninvasive testing has been performed recently with normal or low-risk findings.

The writing group notes that “safe and efficient” management of chest pain in the ED requires appropriate follow-up after discharge. Timing of follow-up and referral for outpatient noninvasive testing should be influenced by patient risk and results of cardiac testing.

Disclosures for members of the writing group are available with the original article.

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

A recent medical meeting I attended included multiple sessions on the use of artificial intelligence (AI), a mere preview, I suspect, of what is to come for both patients and physicians.

I vow not to be a contrarian, but I have concerns. If we’d known how cell phones would permeate nearly every waking moment of our lives, would we have built in more protections from the onset?

Although anyone can see the enormous potential of AI in medicine, harnessing the wonders of it without guarding against the dangers could be paramount to texting and driving. 

A palpable disruption in the common work-a-day human interaction is a given. CEOs who mind the bottom line will seek every opportunity to cut personnel whenever machine learning can deliver. As our dependence on algorithms increases, our need to understand electrocardiogram interpretation and echocardiographic calculations will wane. Subtle case information will go undetected. Nuanced subconscious alerts regarding the patient condition will go unnoticed.

These realities are never reflected in the pronouncements of companies who promote and develop AI.
 

The 2-minute echo

In September 2020, Carolyn Lam, MBBS, PhD, and James Hare, MBA, founders of the AI tech company US2.AI, told Healthcare Transformers that AI advances in echocardiology will turn “a manual process of 30 minutes, 250 clicks, with up to 21% variability among fully trained sonographers analyzing the same exam, into an AI-automated process taking 2 minutes, 1 click, with 0% variability.”

Let’s contrast this 2-minute human-machine interaction with the standard 20- to 30-minute human-to-human echocardiography procedure.

Take Mrs. Smith, for instance. She is referred for echocardiography for shortness of breath. She’s shown to a room and instructed to lie down on a table, where she undergoes a brief AI-directed acquisition of images and then a cheery dismissal from the imaging lab. Medical corporate chief financial officers will salivate at the efficiency, the decrease in cost for personnel, and the sharp increase in put-through for the echo lab schedule.

But what if Mrs. Smith gets a standard 30-minute sonographer-directed exam and the astute echocardiographer notes a left ventricular ejection fraction of 38%. A conversation with the patient reveals that she lost her son a few weeks ago. Upon completion of the study, the patient stands up and then adds, “I hope I can sleep in my bed tonight.” Thinking there may be more to the patient’s insomnia than grief-driven anxiety, the sonographer asks her to explain. “I had to sleep in a chair last night because I couldn’t breathe,” Mrs. Smith replies.

The sonographer reasons correctly that Mrs. Smith is likely a few weeks past an acute coronary syndrome for which she didn’t seek attention and is now in heart failure. The consulting cardiologist is alerted. Mrs. Smith is worked into the office schedule a week earlier than planned, and a costly in-patient stay for acute heart failure or worse is avoided.

Here’s a true-life example (some details have been changed to protect the patient’s identity): Mr. Rodriquez was referred for echocardiography because of dizziness. The sonographer notes significant mitral regurgitation and a decline in left ventricular ejection fraction from moderately impaired to severely reduced. When the sonographer inquires about a fresh bruise over Mr. Rodriguez’s left eye, he replies that he “must have fallen, but can’t remember.” The sonographer also notes runs of nonsustained ventricular tachycardia on the echo telemetry, and after a phone call from the echo lab to the ordering physician, Mr. Rodriquez is admitted. Instead of chancing a sudden death at home while awaiting follow-up, he undergoes catheterization and gets an implantable cardioverter defibrillator.

These scenarios illustrate that a 2-minute visit for AI-directed acquisition of echocardiogram images will never garner the protections of a conversation with a human. Any attempts at downplaying the importance of these human interactions are misguided.

Sometimes we embrace the latest advances in medicine while failing to tend to the most rudimentary necessities of data analysis and reporting. Catherine M. Otto, MD, director of the heart valve clinic and a professor of cardiology at the University of Washington Medical Center, Seattle, is a fan of the basics.

At the recent annual congress of the European Society of Cardiology, she commented on the AI-ENHANCED trial, which used an AI decision support algorithm to identify patients with moderate to severe aortic stenosis, which is associated with poor survival if left untreated. She correctly highlighted that while we are discussing the merits of AI-driven assessment of aortic stenosis, we are doing so in an era when many echo interpreters exclude critical information. The vital findings of aortic valve area, Vmax, and ejection fraction are often nowhere to be seen on reports. We should attend to our basic flaws in interpretation and reporting before we shift our focus to AI.
 

Flawed algorithms

Incorrect AI algorithms that are broadly adopted could negatively affect the health of millions.

Perhaps the most unsettling claim is made by causaLens: “Causal AI is the only technology that can reason and make choices like humans do,” the website states. A tantalizing tag line that is categorically untrue.

Our mysterious and complex neurophysiological function of reasoning still eludes understanding, but one thing is certain: medical reasoning originates with listening, seeing, and touching.

As AI infiltrates mainstream medicine, opportunities for hearing, observing, and palpating will be greatly reduced.

Folkert Asselbergs from University Medical Center Utrecht, the Netherlands, who has cautioned against overhyping AI, was the discussant for an ESC study on the use of causal AI to improve  cardiovascular risk estimation.

He flashed a slide of a 2019 Science article on racial bias in an algorithm that U.S. health care systems use.  Remedying that bias “would increase the percentage of Black people receiving additional help from 17.7% to 46.5%,” according to the authors.  

Successful integration of AI-driven technology will come only if we build human interaction into every patient encounter.

I hope I don’t live to see the rise of the physician cyborg.

Artificial intelligence could be the greatest boon since the invention of the stethoscope, but it will be our downfall if we stop administering a healthy dose of humanity to every patient encounter.

Melissa Walton-Shirley, MD, is a clinical cardiologist in Nashville, Tenn., who has retired from full-time invasive cardiology. She disclosed no relevant conflicts of interest.
 

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

A recent medical meeting I attended included multiple sessions on the use of artificial intelligence (AI), a mere preview, I suspect, of what is to come for both patients and physicians.

I vow not to be a contrarian, but I have concerns. If we’d known how cell phones would permeate nearly every waking moment of our lives, would we have built in more protections from the onset?

Although anyone can see the enormous potential of AI in medicine, harnessing the wonders of it without guarding against the dangers could be paramount to texting and driving. 

A palpable disruption in the common work-a-day human interaction is a given. CEOs who mind the bottom line will seek every opportunity to cut personnel whenever machine learning can deliver. As our dependence on algorithms increases, our need to understand electrocardiogram interpretation and echocardiographic calculations will wane. Subtle case information will go undetected. Nuanced subconscious alerts regarding the patient condition will go unnoticed.

These realities are never reflected in the pronouncements of companies who promote and develop AI.
 

The 2-minute echo

In September 2020, Carolyn Lam, MBBS, PhD, and James Hare, MBA, founders of the AI tech company US2.AI, told Healthcare Transformers that AI advances in echocardiology will turn “a manual process of 30 minutes, 250 clicks, with up to 21% variability among fully trained sonographers analyzing the same exam, into an AI-automated process taking 2 minutes, 1 click, with 0% variability.”

Let’s contrast this 2-minute human-machine interaction with the standard 20- to 30-minute human-to-human echocardiography procedure.

Take Mrs. Smith, for instance. She is referred for echocardiography for shortness of breath. She’s shown to a room and instructed to lie down on a table, where she undergoes a brief AI-directed acquisition of images and then a cheery dismissal from the imaging lab. Medical corporate chief financial officers will salivate at the efficiency, the decrease in cost for personnel, and the sharp increase in put-through for the echo lab schedule.

But what if Mrs. Smith gets a standard 30-minute sonographer-directed exam and the astute echocardiographer notes a left ventricular ejection fraction of 38%. A conversation with the patient reveals that she lost her son a few weeks ago. Upon completion of the study, the patient stands up and then adds, “I hope I can sleep in my bed tonight.” Thinking there may be more to the patient’s insomnia than grief-driven anxiety, the sonographer asks her to explain. “I had to sleep in a chair last night because I couldn’t breathe,” Mrs. Smith replies.

The sonographer reasons correctly that Mrs. Smith is likely a few weeks past an acute coronary syndrome for which she didn’t seek attention and is now in heart failure. The consulting cardiologist is alerted. Mrs. Smith is worked into the office schedule a week earlier than planned, and a costly in-patient stay for acute heart failure or worse is avoided.

Here’s a true-life example (some details have been changed to protect the patient’s identity): Mr. Rodriquez was referred for echocardiography because of dizziness. The sonographer notes significant mitral regurgitation and a decline in left ventricular ejection fraction from moderately impaired to severely reduced. When the sonographer inquires about a fresh bruise over Mr. Rodriguez’s left eye, he replies that he “must have fallen, but can’t remember.” The sonographer also notes runs of nonsustained ventricular tachycardia on the echo telemetry, and after a phone call from the echo lab to the ordering physician, Mr. Rodriquez is admitted. Instead of chancing a sudden death at home while awaiting follow-up, he undergoes catheterization and gets an implantable cardioverter defibrillator.

These scenarios illustrate that a 2-minute visit for AI-directed acquisition of echocardiogram images will never garner the protections of a conversation with a human. Any attempts at downplaying the importance of these human interactions are misguided.

Sometimes we embrace the latest advances in medicine while failing to tend to the most rudimentary necessities of data analysis and reporting. Catherine M. Otto, MD, director of the heart valve clinic and a professor of cardiology at the University of Washington Medical Center, Seattle, is a fan of the basics.

At the recent annual congress of the European Society of Cardiology, she commented on the AI-ENHANCED trial, which used an AI decision support algorithm to identify patients with moderate to severe aortic stenosis, which is associated with poor survival if left untreated. She correctly highlighted that while we are discussing the merits of AI-driven assessment of aortic stenosis, we are doing so in an era when many echo interpreters exclude critical information. The vital findings of aortic valve area, Vmax, and ejection fraction are often nowhere to be seen on reports. We should attend to our basic flaws in interpretation and reporting before we shift our focus to AI.
 

Flawed algorithms

Incorrect AI algorithms that are broadly adopted could negatively affect the health of millions.

Perhaps the most unsettling claim is made by causaLens: “Causal AI is the only technology that can reason and make choices like humans do,” the website states. A tantalizing tag line that is categorically untrue.

Our mysterious and complex neurophysiological function of reasoning still eludes understanding, but one thing is certain: medical reasoning originates with listening, seeing, and touching.

As AI infiltrates mainstream medicine, opportunities for hearing, observing, and palpating will be greatly reduced.

Folkert Asselbergs from University Medical Center Utrecht, the Netherlands, who has cautioned against overhyping AI, was the discussant for an ESC study on the use of causal AI to improve  cardiovascular risk estimation.

He flashed a slide of a 2019 Science article on racial bias in an algorithm that U.S. health care systems use.  Remedying that bias “would increase the percentage of Black people receiving additional help from 17.7% to 46.5%,” according to the authors.  

Successful integration of AI-driven technology will come only if we build human interaction into every patient encounter.

I hope I don’t live to see the rise of the physician cyborg.

Artificial intelligence could be the greatest boon since the invention of the stethoscope, but it will be our downfall if we stop administering a healthy dose of humanity to every patient encounter.

Melissa Walton-Shirley, MD, is a clinical cardiologist in Nashville, Tenn., who has retired from full-time invasive cardiology. She disclosed no relevant conflicts of interest.
 

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

A recent medical meeting I attended included multiple sessions on the use of artificial intelligence (AI), a mere preview, I suspect, of what is to come for both patients and physicians.

I vow not to be a contrarian, but I have concerns. If we’d known how cell phones would permeate nearly every waking moment of our lives, would we have built in more protections from the onset?

Although anyone can see the enormous potential of AI in medicine, harnessing the wonders of it without guarding against the dangers could be paramount to texting and driving. 

A palpable disruption in the common work-a-day human interaction is a given. CEOs who mind the bottom line will seek every opportunity to cut personnel whenever machine learning can deliver. As our dependence on algorithms increases, our need to understand electrocardiogram interpretation and echocardiographic calculations will wane. Subtle case information will go undetected. Nuanced subconscious alerts regarding the patient condition will go unnoticed.

These realities are never reflected in the pronouncements of companies who promote and develop AI.
 

The 2-minute echo

In September 2020, Carolyn Lam, MBBS, PhD, and James Hare, MBA, founders of the AI tech company US2.AI, told Healthcare Transformers that AI advances in echocardiology will turn “a manual process of 30 minutes, 250 clicks, with up to 21% variability among fully trained sonographers analyzing the same exam, into an AI-automated process taking 2 minutes, 1 click, with 0% variability.”

Let’s contrast this 2-minute human-machine interaction with the standard 20- to 30-minute human-to-human echocardiography procedure.

Take Mrs. Smith, for instance. She is referred for echocardiography for shortness of breath. She’s shown to a room and instructed to lie down on a table, where she undergoes a brief AI-directed acquisition of images and then a cheery dismissal from the imaging lab. Medical corporate chief financial officers will salivate at the efficiency, the decrease in cost for personnel, and the sharp increase in put-through for the echo lab schedule.

But what if Mrs. Smith gets a standard 30-minute sonographer-directed exam and the astute echocardiographer notes a left ventricular ejection fraction of 38%. A conversation with the patient reveals that she lost her son a few weeks ago. Upon completion of the study, the patient stands up and then adds, “I hope I can sleep in my bed tonight.” Thinking there may be more to the patient’s insomnia than grief-driven anxiety, the sonographer asks her to explain. “I had to sleep in a chair last night because I couldn’t breathe,” Mrs. Smith replies.

The sonographer reasons correctly that Mrs. Smith is likely a few weeks past an acute coronary syndrome for which she didn’t seek attention and is now in heart failure. The consulting cardiologist is alerted. Mrs. Smith is worked into the office schedule a week earlier than planned, and a costly in-patient stay for acute heart failure or worse is avoided.

Here’s a true-life example (some details have been changed to protect the patient’s identity): Mr. Rodriquez was referred for echocardiography because of dizziness. The sonographer notes significant mitral regurgitation and a decline in left ventricular ejection fraction from moderately impaired to severely reduced. When the sonographer inquires about a fresh bruise over Mr. Rodriguez’s left eye, he replies that he “must have fallen, but can’t remember.” The sonographer also notes runs of nonsustained ventricular tachycardia on the echo telemetry, and after a phone call from the echo lab to the ordering physician, Mr. Rodriquez is admitted. Instead of chancing a sudden death at home while awaiting follow-up, he undergoes catheterization and gets an implantable cardioverter defibrillator.

These scenarios illustrate that a 2-minute visit for AI-directed acquisition of echocardiogram images will never garner the protections of a conversation with a human. Any attempts at downplaying the importance of these human interactions are misguided.

Sometimes we embrace the latest advances in medicine while failing to tend to the most rudimentary necessities of data analysis and reporting. Catherine M. Otto, MD, director of the heart valve clinic and a professor of cardiology at the University of Washington Medical Center, Seattle, is a fan of the basics.

At the recent annual congress of the European Society of Cardiology, she commented on the AI-ENHANCED trial, which used an AI decision support algorithm to identify patients with moderate to severe aortic stenosis, which is associated with poor survival if left untreated. She correctly highlighted that while we are discussing the merits of AI-driven assessment of aortic stenosis, we are doing so in an era when many echo interpreters exclude critical information. The vital findings of aortic valve area, Vmax, and ejection fraction are often nowhere to be seen on reports. We should attend to our basic flaws in interpretation and reporting before we shift our focus to AI.
 

Flawed algorithms

Incorrect AI algorithms that are broadly adopted could negatively affect the health of millions.

Perhaps the most unsettling claim is made by causaLens: “Causal AI is the only technology that can reason and make choices like humans do,” the website states. A tantalizing tag line that is categorically untrue.

Our mysterious and complex neurophysiological function of reasoning still eludes understanding, but one thing is certain: medical reasoning originates with listening, seeing, and touching.

As AI infiltrates mainstream medicine, opportunities for hearing, observing, and palpating will be greatly reduced.

Folkert Asselbergs from University Medical Center Utrecht, the Netherlands, who has cautioned against overhyping AI, was the discussant for an ESC study on the use of causal AI to improve  cardiovascular risk estimation.

He flashed a slide of a 2019 Science article on racial bias in an algorithm that U.S. health care systems use.  Remedying that bias “would increase the percentage of Black people receiving additional help from 17.7% to 46.5%,” according to the authors.  

Successful integration of AI-driven technology will come only if we build human interaction into every patient encounter.

I hope I don’t live to see the rise of the physician cyborg.

Artificial intelligence could be the greatest boon since the invention of the stethoscope, but it will be our downfall if we stop administering a healthy dose of humanity to every patient encounter.

Melissa Walton-Shirley, MD, is a clinical cardiologist in Nashville, Tenn., who has retired from full-time invasive cardiology. She disclosed no relevant conflicts of interest.
 

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

Whatever the mechanism of benefit from dapagliflozin (Farxiga) in patients with heart failure (HF) – and potentially also other sodium-glucose cotransporter 2 (SGLT2) inhibitors – its blood pressure lowering effects aren’t likely to contribute much.

Indeed, at least in patients with HF and non-reduced ejection fractions, dapagliflozin has only a modest BP-lowering effect and cuts cardiovascular (CV) risk regardless of baseline pressure or change in systolic BP, suggests a secondary analysis from the large placebo-controlled DELIVER trial.

Systolic BP fell over 1 month by just under 2 mmHg, on average, in trial patients with either mildly reduced or preserved ejection fraction (HFmrEF or HFpEF, respectively) assigned to take dapagliflozin versus placebo.

The effect was achieved without increasing the risk for adverse events from dapagliflozin, even among patients with the lowest baseline systolic pressures. Adverse outcomes overall, however, were more common at the lowest systolic BP level than at higher pressures, researchers reported.

They say the findings should help alleviate long-standing concerns that initiating SGLT2 inhibitors, with their recognized diuretic effects, might present a hazard in patients with HF and low systolic BP.

“It is a consistent theme in heart failure trials that the blood pressure–lowering effect of SGLT2 inhibitors is more modest than it is in non–heart-failure populations,” Senthil Selvaraj, MD, Duke University, Durham, N.C., told this news organization.

Changes to antihypertensive drug therapy throughout the trial, which presumably enhanced BP responses and “might occur more frequently in the placebo group,” Dr. Selvaraj said, “might explain why the blood pressure effect is a little bit more modest in this population.”

Dr. Selvaraj presented the analysis at the Annual Scientific Meeting of the Heart Failure Society of America, held in National Harbor, Md., and is lead author on its same-day publication in JACC: Heart Failure.

The findings “reinforce the clinical benefits of SGLT2 inhibitors in patients with heart failure across the full spectrum of ejection fractions and large range of systolic blood pressures,” said Gregg C. Fonarow, MD, University of California, Los Angeles Medical Center, who was not part of the DELIVER analysis.

The study’s greater adjusted risks for CV and all-cause mortality risks at the lowest baseline systolic pressures “parallels a series of observational analyses from registries, including OPTIMIZE-HF,” Dr. Fonarow observed.

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

Whatever the mechanism of benefit from dapagliflozin (Farxiga) in patients with heart failure (HF) – and potentially also other sodium-glucose cotransporter 2 (SGLT2) inhibitors – its blood pressure lowering effects aren’t likely to contribute much.

Indeed, at least in patients with HF and non-reduced ejection fractions, dapagliflozin has only a modest BP-lowering effect and cuts cardiovascular (CV) risk regardless of baseline pressure or change in systolic BP, suggests a secondary analysis from the large placebo-controlled DELIVER trial.

Systolic BP fell over 1 month by just under 2 mmHg, on average, in trial patients with either mildly reduced or preserved ejection fraction (HFmrEF or HFpEF, respectively) assigned to take dapagliflozin versus placebo.

The effect was achieved without increasing the risk for adverse events from dapagliflozin, even among patients with the lowest baseline systolic pressures. Adverse outcomes overall, however, were more common at the lowest systolic BP level than at higher pressures, researchers reported.

They say the findings should help alleviate long-standing concerns that initiating SGLT2 inhibitors, with their recognized diuretic effects, might present a hazard in patients with HF and low systolic BP.

“It is a consistent theme in heart failure trials that the blood pressure–lowering effect of SGLT2 inhibitors is more modest than it is in non–heart-failure populations,” Senthil Selvaraj, MD, Duke University, Durham, N.C., told this news organization.

Changes to antihypertensive drug therapy throughout the trial, which presumably enhanced BP responses and “might occur more frequently in the placebo group,” Dr. Selvaraj said, “might explain why the blood pressure effect is a little bit more modest in this population.”

Dr. Selvaraj presented the analysis at the Annual Scientific Meeting of the Heart Failure Society of America, held in National Harbor, Md., and is lead author on its same-day publication in JACC: Heart Failure.

The findings “reinforce the clinical benefits of SGLT2 inhibitors in patients with heart failure across the full spectrum of ejection fractions and large range of systolic blood pressures,” said Gregg C. Fonarow, MD, University of California, Los Angeles Medical Center, who was not part of the DELIVER analysis.

The study’s greater adjusted risks for CV and all-cause mortality risks at the lowest baseline systolic pressures “parallels a series of observational analyses from registries, including OPTIMIZE-HF,” Dr. Fonarow observed.

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

Whatever the mechanism of benefit from dapagliflozin (Farxiga) in patients with heart failure (HF) – and potentially also other sodium-glucose cotransporter 2 (SGLT2) inhibitors – its blood pressure lowering effects aren’t likely to contribute much.

Indeed, at least in patients with HF and non-reduced ejection fractions, dapagliflozin has only a modest BP-lowering effect and cuts cardiovascular (CV) risk regardless of baseline pressure or change in systolic BP, suggests a secondary analysis from the large placebo-controlled DELIVER trial.

Systolic BP fell over 1 month by just under 2 mmHg, on average, in trial patients with either mildly reduced or preserved ejection fraction (HFmrEF or HFpEF, respectively) assigned to take dapagliflozin versus placebo.

The effect was achieved without increasing the risk for adverse events from dapagliflozin, even among patients with the lowest baseline systolic pressures. Adverse outcomes overall, however, were more common at the lowest systolic BP level than at higher pressures, researchers reported.

They say the findings should help alleviate long-standing concerns that initiating SGLT2 inhibitors, with their recognized diuretic effects, might present a hazard in patients with HF and low systolic BP.

“It is a consistent theme in heart failure trials that the blood pressure–lowering effect of SGLT2 inhibitors is more modest than it is in non–heart-failure populations,” Senthil Selvaraj, MD, Duke University, Durham, N.C., told this news organization.

Changes to antihypertensive drug therapy throughout the trial, which presumably enhanced BP responses and “might occur more frequently in the placebo group,” Dr. Selvaraj said, “might explain why the blood pressure effect is a little bit more modest in this population.”

Dr. Selvaraj presented the analysis at the Annual Scientific Meeting of the Heart Failure Society of America, held in National Harbor, Md., and is lead author on its same-day publication in JACC: Heart Failure.

The findings “reinforce the clinical benefits of SGLT2 inhibitors in patients with heart failure across the full spectrum of ejection fractions and large range of systolic blood pressures,” said Gregg C. Fonarow, MD, University of California, Los Angeles Medical Center, who was not part of the DELIVER analysis.

The study’s greater adjusted risks for CV and all-cause mortality risks at the lowest baseline systolic pressures “parallels a series of observational analyses from registries, including OPTIMIZE-HF,” Dr. Fonarow observed.

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

Weight loss after bariatric surgery was linked with visceral fat reduction as well as reduced blood pressure, fasting glucose, and left ventricular remodeling, based an imaging study in 213 patients.

“We found that ventricular function measured by strain imaging improved in both the left and right sides of the heart, but function measured in the traditional method using endocardial motion [in other words, ejection fraction] actually worsened,” senior investigator Barry A. Borlaug, MD, said in an interview.

Although previous studies have shown positive effects of weight loss on the heart after bariatric surgery, most have been short term and have not specifically examined the effects of visceral fat reduction, wrote the investigators.

“We are in the middle of an increasing epidemic of obesity worldwide, but particularly in the United States, where it is currently projected that one in two adults will be obese by 2030,” added Dr. Borlaug of Mayo Clinic, Rochester, Minn. “Heart failure with preserved ejection fraction (HFpEF) is growing in tandem, and numerous recent studies have shown that obesity is one of the strongest risk factors for developing HFpEF, and that the severity of HFpEF is intimately linked to excess body fat. This suggests that therapies to reduce body fat could improve the cardiac abnormalities that cause HFpEF, which was our focus in this study,” he explained.

In the study, published in the Journal of the American College of Cardiology, the researchers reviewed echocardiography data from 213 obese patients before and more than 180 days after bariatric surgery. They also measured abdominal visceral adipose tissue (VAT) of 52 patients via computed tomography. The average age of the patients was 54 years, the average body mass index was 45 kg/m², and 67% were women. Comorbidities included hypertension, diabetes, dyslipidemia, and obstructive sleep apnea.

The primary outcome was changes in cardiac structure and function.

After a median follow-up of 5.3 years, patients overall averaged a 23% reduction in body weight and a 22% reduction in BMI. In the 52 patients with abdominal scans, the VAT area decreased by 30% overall. Changes in left ventricular mass were significantly correlated to changes in the VAT.

Epicardial adipose thickness decreased by 14% overall. Left and right ventricular longitudinal strains improved at follow-up, but left atrial strain deteriorated, the researchers noted.

Although the mechanism of action remains unclear, the results suggest that left ventricular remodeling was associated with visceral adiposity rather than subcutaneous fat, the researchers wrote.

They also found that right ventricular strain was negatively correlated with VAT, but not with body weight or BMI.

“These findings suggest that weight loss, particularly reduction in visceral adiposity, benefits [right ventricular] structure and function in a manner akin to that observed in the [left ventricle],” the researchers noted.

Some surprises and limitations

Dr. Borlaug said he found some, but not all, of the results surprising. “Earlier studies had shown evidence for benefit from weight loss on cardiac structure and function, but had been limited by smaller sample sizes, shorter durations of evaluation, and variable methods used,” he said in an interview.

The findings that strain imaging showed both left and right ventricular function improved while EF declined “shows some of the problems with using EF, as it is affected by chamber size and geometry. We have previously shown that patients with HFpEF display an increase in fat around the heart, and this affects cardiac function and interaction between the left and right sides of the heart, so we expected to see that this fat depot would be reduced, and this was indeed the case,” Dr. Borlaug added.

In the current study, “visceral fat was most strongly tied to the heart remodeling in obesity, and changes in visceral fat were most strongly tied to improvements in cardiac structure following weight loss,” Dr. Borlaug told this news organization. “This further supports this concept that excess visceral fat plays a key role in HFpEF, especially in the abdomen and around the heart,” he said.

However, “The biggest surprise was the discordant effects in the left atrium,” Dr. Borlaug said. “Left atrial remodeling and dysfunction play a crucial role in HFpEF as well, and we expected that this would improve following weight loss, but in fact we observed that left atrial function deteriorated, and other indicators of atrial myopathy worsened, including higher estimates of left atrial pressures and increased prevalence of atrial fibrillation,” he said.

This difference emphasizes that weight loss may not address all abnormalities that lead to HFpEF, although a key limitation of the current study was the lack of a control group of patients with the same degree of obesity and no weight-loss intervention, and the deterioration in left atrial function might have been even greater in the absence of weight loss, Dr. Borlaug added.
 

Larger numbers support effects

Previous research shows that structural heart changes associated with obesity can be reversed through weight loss, but the current study fills a gap by providing long-term data in a larger sample than previously studied, wrote Paul Heidenreich, MD, of Stanford (Calif.) University in an accompanying editorial).

“There has been uncertainty regarding the prolonged effect of weight loss on cardiac function; this study was larger than many prior studies and provided a longer follow-up,” Dr. Heidenreich said in an interview.

“One unusual finding was that, while weight loss led to left ventricle reverse remodeling (reduction in wall thickness), the same effect was not seen for the left atrium; the left atrial size continued to increase,” he said. “I would have expected the left atrial changes to mirror the changes in the left ventricle,” he noted.

The findings support the greater cardiac risk of visceral vs. subcutaneous adipose tissue, and although body mass index will retain prognostic value, measures of central obesity are more likely predictors of cardiac structural changes and events and should be reported in clinical studies, Dr. Heidenreich wrote.

However, “We need a better understanding of the factors that influence left atrial remodeling and reverse remodeling,” Dr. Heidenreich told this news organization. “While left ventricular compliance and pressure play a role, there are other factors that need to be elucidated,” he said.

 

Studies in progress may inform practice

The current data call for further study to test novel treatments to facilitate weight loss in patients with HFpEF and those at risk for HFpEF, and some of these studies with medicines are underway, Dr. Borlaug said in the interview.

“Until such studies are completed, we will not truly understand the effects of weight loss on the heart, but the present data certainly provide strong support that patients who have obesity and HFpEF or are at risk for HFpEF should try to lose weight through lifestyle interventions,” he said. 

Whether the cardiac changes seen in the current study would be different with nonsurgical weight loss remains a key question because many obese patients are reluctant to undergo bariatric surgery, Dr. Borlaug said. “We cannot assess whether the effects would differ with nonsurgical weight loss, and this requires further study,” he added.

As for additional research, “Randomized, controlled trials of weight-loss interventions, with appropriate controls and comprehensive assessments of cardiac structure, function, and hemodynamics will be most informative,” said Dr. Borlaug. “Larger trials powered to evaluate cardiovascular outcomes such as heart failure hospitalization or cardiovascular death also are critically important to better understand the role of weight loss to treat and prevent HFpEF, the ultimate form of obesity-related heart disease,” he emphasized.

The study was supported in part by grants to lead author Dr. Hidemi Sorimachi of the Mayo Clinic from the Uehara Memorial Foundation, Japan, and to corresponding author Dr. Borlaug from the National Institutes of Health. Dr. Borlaug also disclosed previous grants from National Institutes of Health/National Heart, Lung, and Blood Institute, AstraZeneca, Corvia, Medtronic, GlaxoSmithKline, Mesoblast, Novartis, and Tenax Therapeutics; and consulting fees from Actelion, Amgen, Aria, Axon Therapies, Boehringer Ingelheim, Edwards Lifesciences, Eli Lilly, Imbria, Janssen, Merck, Novo Nordisk, and VADovations. Dr. Heidenreich had no financial disclosures.

Weight loss after bariatric surgery was linked with visceral fat reduction as well as reduced blood pressure, fasting glucose, and left ventricular remodeling, based an imaging study in 213 patients.

“We found that ventricular function measured by strain imaging improved in both the left and right sides of the heart, but function measured in the traditional method using endocardial motion [in other words, ejection fraction] actually worsened,” senior investigator Barry A. Borlaug, MD, said in an interview.

Although previous studies have shown positive effects of weight loss on the heart after bariatric surgery, most have been short term and have not specifically examined the effects of visceral fat reduction, wrote the investigators.

“We are in the middle of an increasing epidemic of obesity worldwide, but particularly in the United States, where it is currently projected that one in two adults will be obese by 2030,” added Dr. Borlaug of Mayo Clinic, Rochester, Minn. “Heart failure with preserved ejection fraction (HFpEF) is growing in tandem, and numerous recent studies have shown that obesity is one of the strongest risk factors for developing HFpEF, and that the severity of HFpEF is intimately linked to excess body fat. This suggests that therapies to reduce body fat could improve the cardiac abnormalities that cause HFpEF, which was our focus in this study,” he explained.

In the study, published in the Journal of the American College of Cardiology, the researchers reviewed echocardiography data from 213 obese patients before and more than 180 days after bariatric surgery. They also measured abdominal visceral adipose tissue (VAT) of 52 patients via computed tomography. The average age of the patients was 54 years, the average body mass index was 45 kg/m², and 67% were women. Comorbidities included hypertension, diabetes, dyslipidemia, and obstructive sleep apnea.

The primary outcome was changes in cardiac structure and function.

After a median follow-up of 5.3 years, patients overall averaged a 23% reduction in body weight and a 22% reduction in BMI. In the 52 patients with abdominal scans, the VAT area decreased by 30% overall. Changes in left ventricular mass were significantly correlated to changes in the VAT.

Epicardial adipose thickness decreased by 14% overall. Left and right ventricular longitudinal strains improved at follow-up, but left atrial strain deteriorated, the researchers noted.

Although the mechanism of action remains unclear, the results suggest that left ventricular remodeling was associated with visceral adiposity rather than subcutaneous fat, the researchers wrote.

They also found that right ventricular strain was negatively correlated with VAT, but not with body weight or BMI.

“These findings suggest that weight loss, particularly reduction in visceral adiposity, benefits [right ventricular] structure and function in a manner akin to that observed in the [left ventricle],” the researchers noted.

Some surprises and limitations

Dr. Borlaug said he found some, but not all, of the results surprising. “Earlier studies had shown evidence for benefit from weight loss on cardiac structure and function, but had been limited by smaller sample sizes, shorter durations of evaluation, and variable methods used,” he said in an interview.

The findings that strain imaging showed both left and right ventricular function improved while EF declined “shows some of the problems with using EF, as it is affected by chamber size and geometry. We have previously shown that patients with HFpEF display an increase in fat around the heart, and this affects cardiac function and interaction between the left and right sides of the heart, so we expected to see that this fat depot would be reduced, and this was indeed the case,” Dr. Borlaug added.

In the current study, “visceral fat was most strongly tied to the heart remodeling in obesity, and changes in visceral fat were most strongly tied to improvements in cardiac structure following weight loss,” Dr. Borlaug told this news organization. “This further supports this concept that excess visceral fat plays a key role in HFpEF, especially in the abdomen and around the heart,” he said.

However, “The biggest surprise was the discordant effects in the left atrium,” Dr. Borlaug said. “Left atrial remodeling and dysfunction play a crucial role in HFpEF as well, and we expected that this would improve following weight loss, but in fact we observed that left atrial function deteriorated, and other indicators of atrial myopathy worsened, including higher estimates of left atrial pressures and increased prevalence of atrial fibrillation,” he said.

This difference emphasizes that weight loss may not address all abnormalities that lead to HFpEF, although a key limitation of the current study was the lack of a control group of patients with the same degree of obesity and no weight-loss intervention, and the deterioration in left atrial function might have been even greater in the absence of weight loss, Dr. Borlaug added.
 

Larger numbers support effects

Previous research shows that structural heart changes associated with obesity can be reversed through weight loss, but the current study fills a gap by providing long-term data in a larger sample than previously studied, wrote Paul Heidenreich, MD, of Stanford (Calif.) University in an accompanying editorial).

“There has been uncertainty regarding the prolonged effect of weight loss on cardiac function; this study was larger than many prior studies and provided a longer follow-up,” Dr. Heidenreich said in an interview.

“One unusual finding was that, while weight loss led to left ventricle reverse remodeling (reduction in wall thickness), the same effect was not seen for the left atrium; the left atrial size continued to increase,” he said. “I would have expected the left atrial changes to mirror the changes in the left ventricle,” he noted.

The findings support the greater cardiac risk of visceral vs. subcutaneous adipose tissue, and although body mass index will retain prognostic value, measures of central obesity are more likely predictors of cardiac structural changes and events and should be reported in clinical studies, Dr. Heidenreich wrote.

However, “We need a better understanding of the factors that influence left atrial remodeling and reverse remodeling,” Dr. Heidenreich told this news organization. “While left ventricular compliance and pressure play a role, there are other factors that need to be elucidated,” he said.

 

Studies in progress may inform practice

The current data call for further study to test novel treatments to facilitate weight loss in patients with HFpEF and those at risk for HFpEF, and some of these studies with medicines are underway, Dr. Borlaug said in the interview.

“Until such studies are completed, we will not truly understand the effects of weight loss on the heart, but the present data certainly provide strong support that patients who have obesity and HFpEF or are at risk for HFpEF should try to lose weight through lifestyle interventions,” he said. 

Whether the cardiac changes seen in the current study would be different with nonsurgical weight loss remains a key question because many obese patients are reluctant to undergo bariatric surgery, Dr. Borlaug said. “We cannot assess whether the effects would differ with nonsurgical weight loss, and this requires further study,” he added.

As for additional research, “Randomized, controlled trials of weight-loss interventions, with appropriate controls and comprehensive assessments of cardiac structure, function, and hemodynamics will be most informative,” said Dr. Borlaug. “Larger trials powered to evaluate cardiovascular outcomes such as heart failure hospitalization or cardiovascular death also are critically important to better understand the role of weight loss to treat and prevent HFpEF, the ultimate form of obesity-related heart disease,” he emphasized.

The study was supported in part by grants to lead author Dr. Hidemi Sorimachi of the Mayo Clinic from the Uehara Memorial Foundation, Japan, and to corresponding author Dr. Borlaug from the National Institutes of Health. Dr. Borlaug also disclosed previous grants from National Institutes of Health/National Heart, Lung, and Blood Institute, AstraZeneca, Corvia, Medtronic, GlaxoSmithKline, Mesoblast, Novartis, and Tenax Therapeutics; and consulting fees from Actelion, Amgen, Aria, Axon Therapies, Boehringer Ingelheim, Edwards Lifesciences, Eli Lilly, Imbria, Janssen, Merck, Novo Nordisk, and VADovations. Dr. Heidenreich had no financial disclosures.

Weight loss after bariatric surgery was linked with visceral fat reduction as well as reduced blood pressure, fasting glucose, and left ventricular remodeling, based an imaging study in 213 patients.

“We found that ventricular function measured by strain imaging improved in both the left and right sides of the heart, but function measured in the traditional method using endocardial motion [in other words, ejection fraction] actually worsened,” senior investigator Barry A. Borlaug, MD, said in an interview.

Although previous studies have shown positive effects of weight loss on the heart after bariatric surgery, most have been short term and have not specifically examined the effects of visceral fat reduction, wrote the investigators.

“We are in the middle of an increasing epidemic of obesity worldwide, but particularly in the United States, where it is currently projected that one in two adults will be obese by 2030,” added Dr. Borlaug of Mayo Clinic, Rochester, Minn. “Heart failure with preserved ejection fraction (HFpEF) is growing in tandem, and numerous recent studies have shown that obesity is one of the strongest risk factors for developing HFpEF, and that the severity of HFpEF is intimately linked to excess body fat. This suggests that therapies to reduce body fat could improve the cardiac abnormalities that cause HFpEF, which was our focus in this study,” he explained.

In the study, published in the Journal of the American College of Cardiology, the researchers reviewed echocardiography data from 213 obese patients before and more than 180 days after bariatric surgery. They also measured abdominal visceral adipose tissue (VAT) of 52 patients via computed tomography. The average age of the patients was 54 years, the average body mass index was 45 kg/m², and 67% were women. Comorbidities included hypertension, diabetes, dyslipidemia, and obstructive sleep apnea.

The primary outcome was changes in cardiac structure and function.

After a median follow-up of 5.3 years, patients overall averaged a 23% reduction in body weight and a 22% reduction in BMI. In the 52 patients with abdominal scans, the VAT area decreased by 30% overall. Changes in left ventricular mass were significantly correlated to changes in the VAT.

Epicardial adipose thickness decreased by 14% overall. Left and right ventricular longitudinal strains improved at follow-up, but left atrial strain deteriorated, the researchers noted.

Although the mechanism of action remains unclear, the results suggest that left ventricular remodeling was associated with visceral adiposity rather than subcutaneous fat, the researchers wrote.

They also found that right ventricular strain was negatively correlated with VAT, but not with body weight or BMI.

“These findings suggest that weight loss, particularly reduction in visceral adiposity, benefits [right ventricular] structure and function in a manner akin to that observed in the [left ventricle],” the researchers noted.

Some surprises and limitations

Dr. Borlaug said he found some, but not all, of the results surprising. “Earlier studies had shown evidence for benefit from weight loss on cardiac structure and function, but had been limited by smaller sample sizes, shorter durations of evaluation, and variable methods used,” he said in an interview.

The findings that strain imaging showed both left and right ventricular function improved while EF declined “shows some of the problems with using EF, as it is affected by chamber size and geometry. We have previously shown that patients with HFpEF display an increase in fat around the heart, and this affects cardiac function and interaction between the left and right sides of the heart, so we expected to see that this fat depot would be reduced, and this was indeed the case,” Dr. Borlaug added.

In the current study, “visceral fat was most strongly tied to the heart remodeling in obesity, and changes in visceral fat were most strongly tied to improvements in cardiac structure following weight loss,” Dr. Borlaug told this news organization. “This further supports this concept that excess visceral fat plays a key role in HFpEF, especially in the abdomen and around the heart,” he said.

However, “The biggest surprise was the discordant effects in the left atrium,” Dr. Borlaug said. “Left atrial remodeling and dysfunction play a crucial role in HFpEF as well, and we expected that this would improve following weight loss, but in fact we observed that left atrial function deteriorated, and other indicators of atrial myopathy worsened, including higher estimates of left atrial pressures and increased prevalence of atrial fibrillation,” he said.

This difference emphasizes that weight loss may not address all abnormalities that lead to HFpEF, although a key limitation of the current study was the lack of a control group of patients with the same degree of obesity and no weight-loss intervention, and the deterioration in left atrial function might have been even greater in the absence of weight loss, Dr. Borlaug added.
 

Larger numbers support effects

Previous research shows that structural heart changes associated with obesity can be reversed through weight loss, but the current study fills a gap by providing long-term data in a larger sample than previously studied, wrote Paul Heidenreich, MD, of Stanford (Calif.) University in an accompanying editorial).

“There has been uncertainty regarding the prolonged effect of weight loss on cardiac function; this study was larger than many prior studies and provided a longer follow-up,” Dr. Heidenreich said in an interview.

“One unusual finding was that, while weight loss led to left ventricle reverse remodeling (reduction in wall thickness), the same effect was not seen for the left atrium; the left atrial size continued to increase,” he said. “I would have expected the left atrial changes to mirror the changes in the left ventricle,” he noted.

The findings support the greater cardiac risk of visceral vs. subcutaneous adipose tissue, and although body mass index will retain prognostic value, measures of central obesity are more likely predictors of cardiac structural changes and events and should be reported in clinical studies, Dr. Heidenreich wrote.

However, “We need a better understanding of the factors that influence left atrial remodeling and reverse remodeling,” Dr. Heidenreich told this news organization. “While left ventricular compliance and pressure play a role, there are other factors that need to be elucidated,” he said.

 

Studies in progress may inform practice

The current data call for further study to test novel treatments to facilitate weight loss in patients with HFpEF and those at risk for HFpEF, and some of these studies with medicines are underway, Dr. Borlaug said in the interview.

“Until such studies are completed, we will not truly understand the effects of weight loss on the heart, but the present data certainly provide strong support that patients who have obesity and HFpEF or are at risk for HFpEF should try to lose weight through lifestyle interventions,” he said. 

Whether the cardiac changes seen in the current study would be different with nonsurgical weight loss remains a key question because many obese patients are reluctant to undergo bariatric surgery, Dr. Borlaug said. “We cannot assess whether the effects would differ with nonsurgical weight loss, and this requires further study,” he added.

As for additional research, “Randomized, controlled trials of weight-loss interventions, with appropriate controls and comprehensive assessments of cardiac structure, function, and hemodynamics will be most informative,” said Dr. Borlaug. “Larger trials powered to evaluate cardiovascular outcomes such as heart failure hospitalization or cardiovascular death also are critically important to better understand the role of weight loss to treat and prevent HFpEF, the ultimate form of obesity-related heart disease,” he emphasized.

The study was supported in part by grants to lead author Dr. Hidemi Sorimachi of the Mayo Clinic from the Uehara Memorial Foundation, Japan, and to corresponding author Dr. Borlaug from the National Institutes of Health. Dr. Borlaug also disclosed previous grants from National Institutes of Health/National Heart, Lung, and Blood Institute, AstraZeneca, Corvia, Medtronic, GlaxoSmithKline, Mesoblast, Novartis, and Tenax Therapeutics; and consulting fees from Actelion, Amgen, Aria, Axon Therapies, Boehringer Ingelheim, Edwards Lifesciences, Eli Lilly, Imbria, Janssen, Merck, Novo Nordisk, and VADovations. Dr. Heidenreich had no financial disclosures.

Exposure to air pollution not only raises stroke risk, but it is also tied to poor post-stroke outcomes, including death. Results of a UK biobank study show high levels of air pollution were associated with an increased risk of transition from health to a first stroke and subsequent progression to cardiovascular (CV) events and death.

“These results indicate that understanding and reducing the effects of air pollutants on different transition stages in stroke will be beneficial in managing people’s health and preventing the occurrence and progression of stroke,” study investigator Hualiang Lin, PhD, of Sun Yat-sen University School of Public Health, Guangzhou, China, said in a news release.

The study was published online  in the journal Neurology.
 

A way to stop stroke progression?

The researchers assessed air pollution exposure in 318,752 people (mean age, 56) from the UK biobank database. None had a history of stroke or heart disease at the start of the study. Annual concentrations of air pollution near where people lived were estimated through land-use regressions.

During an average follow-up of 12 years, 5,967 people had a stroke, 2,985 developed post-stroke CVD, and 1,020 died.

After adjusting for confounding factors, every 5 µg/m³ increase in exposure to fine particulate matter (PM_2.5) was associated with a 24% increase in transition from healthy to first stroke (hazard ratio, 1.24; 95% confidence interval, 1.10-1.40) and a 30% increase in transition from being healthy to dying (HR, 1.30; 95% CI, 1.21-1.40).

PM_2.5 is less than 2.5 microns in diameter and includes fly ash from coal combustion. The World Health Organization recommends that annual PM_2.5 exposure should not exceed 5 µg/m³.

Those who had a stroke during the study had an average exposure of 10.03 µg/m³ of PM_2.5, compared with 9.97 µg/m³ for those who did not have a stroke.

The air pollutants nitrogen oxide and nitrogen dioxide were also associated with an increased risk of stroke and death, but the associations were weaker.

“More research is needed, but it’s possible that decreasing exposure to heavy levels of air pollution could play a role in reducing the progression of stroke,” Dr. Lin said.

“People can reduce their exposure by staying indoors on heavy pollution days, reducing their outdoor exercise, wearing masks to filter out particulate matter, and using air purifiers,” Dr. Lin added.

Public policy implications

Reached for comment, Steffen E. Petersen, MD, MPH, professor of cardiovascular medicine, Barts Health NHS Trust, London, said the study “elegantly confirms the increased risk of stroke due to air pollution in the UK Biobank population study but interestingly suggests that the impact of air pollution may continue to adversely impact cardiovascular health even after the stroke occurred.”

“This is further evidence to inform policymakers to tackle air pollution and get levels below the recommended levels,” Dr. Petersen said.

“On a personal level, everyone, including stroke patients, may wish to consider personal measures to reduce exposure to air pollution, such as avoiding walking along polluted streets and rather take a less polluted route away from the main roads,” Dr. Petersen added.

The study had no targeted funding. Dr. Lin and Dr. Petersen report no relevant financial relationships.

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

Exposure to air pollution not only raises stroke risk, but it is also tied to poor post-stroke outcomes, including death. Results of a UK biobank study show high levels of air pollution were associated with an increased risk of transition from health to a first stroke and subsequent progression to cardiovascular (CV) events and death.

“These results indicate that understanding and reducing the effects of air pollutants on different transition stages in stroke will be beneficial in managing people’s health and preventing the occurrence and progression of stroke,” study investigator Hualiang Lin, PhD, of Sun Yat-sen University School of Public Health, Guangzhou, China, said in a news release.

The study was published online  in the journal Neurology.
 

A way to stop stroke progression?

The researchers assessed air pollution exposure in 318,752 people (mean age, 56) from the UK biobank database. None had a history of stroke or heart disease at the start of the study. Annual concentrations of air pollution near where people lived were estimated through land-use regressions.

During an average follow-up of 12 years, 5,967 people had a stroke, 2,985 developed post-stroke CVD, and 1,020 died.

After adjusting for confounding factors, every 5 µg/m³ increase in exposure to fine particulate matter (PM_2.5) was associated with a 24% increase in transition from healthy to first stroke (hazard ratio, 1.24; 95% confidence interval, 1.10-1.40) and a 30% increase in transition from being healthy to dying (HR, 1.30; 95% CI, 1.21-1.40).

PM_2.5 is less than 2.5 microns in diameter and includes fly ash from coal combustion. The World Health Organization recommends that annual PM_2.5 exposure should not exceed 5 µg/m³.

Those who had a stroke during the study had an average exposure of 10.03 µg/m³ of PM_2.5, compared with 9.97 µg/m³ for those who did not have a stroke.

The air pollutants nitrogen oxide and nitrogen dioxide were also associated with an increased risk of stroke and death, but the associations were weaker.

“More research is needed, but it’s possible that decreasing exposure to heavy levels of air pollution could play a role in reducing the progression of stroke,” Dr. Lin said.

“People can reduce their exposure by staying indoors on heavy pollution days, reducing their outdoor exercise, wearing masks to filter out particulate matter, and using air purifiers,” Dr. Lin added.

Public policy implications

Reached for comment, Steffen E. Petersen, MD, MPH, professor of cardiovascular medicine, Barts Health NHS Trust, London, said the study “elegantly confirms the increased risk of stroke due to air pollution in the UK Biobank population study but interestingly suggests that the impact of air pollution may continue to adversely impact cardiovascular health even after the stroke occurred.”

“This is further evidence to inform policymakers to tackle air pollution and get levels below the recommended levels,” Dr. Petersen said.

“On a personal level, everyone, including stroke patients, may wish to consider personal measures to reduce exposure to air pollution, such as avoiding walking along polluted streets and rather take a less polluted route away from the main roads,” Dr. Petersen added.

The study had no targeted funding. Dr. Lin and Dr. Petersen report no relevant financial relationships.

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

Exposure to air pollution not only raises stroke risk, but it is also tied to poor post-stroke outcomes, including death. Results of a UK biobank study show high levels of air pollution were associated with an increased risk of transition from health to a first stroke and subsequent progression to cardiovascular (CV) events and death.

“These results indicate that understanding and reducing the effects of air pollutants on different transition stages in stroke will be beneficial in managing people’s health and preventing the occurrence and progression of stroke,” study investigator Hualiang Lin, PhD, of Sun Yat-sen University School of Public Health, Guangzhou, China, said in a news release.

The study was published online  in the journal Neurology.
 

A way to stop stroke progression?

The researchers assessed air pollution exposure in 318,752 people (mean age, 56) from the UK biobank database. None had a history of stroke or heart disease at the start of the study. Annual concentrations of air pollution near where people lived were estimated through land-use regressions.

During an average follow-up of 12 years, 5,967 people had a stroke, 2,985 developed post-stroke CVD, and 1,020 died.

After adjusting for confounding factors, every 5 µg/m³ increase in exposure to fine particulate matter (PM_2.5) was associated with a 24% increase in transition from healthy to first stroke (hazard ratio, 1.24; 95% confidence interval, 1.10-1.40) and a 30% increase in transition from being healthy to dying (HR, 1.30; 95% CI, 1.21-1.40).

PM_2.5 is less than 2.5 microns in diameter and includes fly ash from coal combustion. The World Health Organization recommends that annual PM_2.5 exposure should not exceed 5 µg/m³.

Those who had a stroke during the study had an average exposure of 10.03 µg/m³ of PM_2.5, compared with 9.97 µg/m³ for those who did not have a stroke.

The air pollutants nitrogen oxide and nitrogen dioxide were also associated with an increased risk of stroke and death, but the associations were weaker.

“More research is needed, but it’s possible that decreasing exposure to heavy levels of air pollution could play a role in reducing the progression of stroke,” Dr. Lin said.

“People can reduce their exposure by staying indoors on heavy pollution days, reducing their outdoor exercise, wearing masks to filter out particulate matter, and using air purifiers,” Dr. Lin added.

Public policy implications

Reached for comment, Steffen E. Petersen, MD, MPH, professor of cardiovascular medicine, Barts Health NHS Trust, London, said the study “elegantly confirms the increased risk of stroke due to air pollution in the UK Biobank population study but interestingly suggests that the impact of air pollution may continue to adversely impact cardiovascular health even after the stroke occurred.”

“This is further evidence to inform policymakers to tackle air pollution and get levels below the recommended levels,” Dr. Petersen said.

“On a personal level, everyone, including stroke patients, may wish to consider personal measures to reduce exposure to air pollution, such as avoiding walking along polluted streets and rather take a less polluted route away from the main roads,” Dr. Petersen added.

The study had no targeted funding. Dr. Lin and Dr. Petersen report no relevant financial relationships.

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