Cardiology

The link between influenza infection and a rise in short-term risk for acute myocardial infarction (MI) has been reaffirmed in a new study, which showed the risk appears to be particularly elevated in individuals with no prior diagnosis of coronary artery disease.

“Our study results confirm previous findings of an increased risk of MI during or immediately following acute severe flu infection and raises the idea of giving prophylactic anticoagulation to these patients,” reported Patricia Bruijning-Verhagen, MD, University Medical Center Utrecht, the Netherlands, who is the senior author of the study, which was published online in NEJM Evidence.

“Our results also change things — in that we now know the focus should be on people without a history of cardiovascular disease — and highlight the importance of flu vaccination, particularly for this group,” she pointed out.

The observational, self-controlled, case-series study linked laboratory records on respiratory virus polymerase chain reaction (PCR) testing from 16 laboratories in the Netherlands to national mortality, hospitalization, medication, and administrative registries. Investigators compared the incidence of acute MI during the risk period — days 1-7 after influenza infection — with that in the control period — 1 year before and 51 weeks after the risk period.

The researchers found 26,221 positive PCR tests for influenza, constituting 23,405 unique influenza illness episodes. Of the episodes of acute MI occurring in the year before or the year after confirmed influenza infection and included in the analysis, 25 cases of acute MI occurred on days 1-7 after influenza infection and 394 occurred during the control period.

The adjusted relative incidence of acute MI during the risk period compared with during the control period was 6.16 (95% CI, 4.11-9.24).

The relative incidence of acute MI in individuals with no previous hospitalization for coronary artery disease was 16.60 (95% CI, 10.45-26.37); for those with a previous hospital admission for coronary artery disease, the relative incidence was 1.43 (95% CI, 0.53-3.84).

A temporary increase in the risk for MI has been reported in several previous studies. A 2018 Canadian study by Kwong and colleagues showed a sixfold elevation in the risk for acute MI after influenza infection, which was subsequently confirmed in studies from the United States, Denmark, and Scotland.

In their study, Dr. Bruijning-Verhagen and colleagues aimed to further quantify the association between laboratory-confirmed influenza infection and acute MI and to look at specific subgroups that might have the potential to guide a more individualized approach to prevention.

They replicated the Canadian study using a self-controlled case-series design that corrects for time-invariant confounding and found very similar results: A sixfold increase in the risk for acute MI in the first week after laboratory-confirmed influenza infection.

“The fact that we found similar results to Kwong et al. strengthens the finding that acute flu infection is linked to increased MI risk. This is becoming more and more clear now. It also shows that this effect is generalizable to other countries,” Dr. Bruijning-Verhagen said.
 

People Without Cardiovascular Disease at Highest Risk 

The researchers moved the field ahead by also looking at whether there is a difference in risk between individuals with flu who already had cardiovascular disease and those who did not.

“Most previous studies of flu and MI didn’t stratify between individuals with and without existing cardiovascular disease. And the ones that did look at this weren’t able to show a difference with any confidence,” Dr. Bruijning-Verhagen explained. “There have been suggestions before of a higher risk of MI in individuals with acute flu infection who do not have existing known cardiovascular disease, but this was uncertain.” 

The current study showed a large difference between the two groups, with a much higher risk for MI linked to flu in individuals without any known cardiovascular disease.

“You would think patients with existing cardiovascular disease would be more at risk of MI with flu infection, so this was a surprising result,” reported Dr. Bruijning-Verhagen. “But I think the result is real. The difference between the two groups was too big for it not to be.”

Influenza can cause a hypercoagulable state, systemic inflammation, and vascular changes that can trigger MI, even in patients not thought to be at risk before, she pointed out. And this is on top of high cardiac demands because of the acute infection.

Patients who already have cardiovascular disease may be protected to some extent by the cardiovascular medications that they are taking, she added.

These results could justify the use of short-term anticoagulation in patients with severe flu infection to cover the high-risk period, Dr. Bruijning-Verhagen suggested. “We give short-term anticoagulation as prophylaxis to patients when they have surgery. This would not be that different. But obviously, this approach would have to be tested.”

Clinical studies looking at such a strategy are currently underway.
 

‘Get Your Flu Shot’

The results reinforce the need for anyone who is eligible to get the flu vaccine. “These results should give extra weight to the message to get your flu shot,” she said. “Even if you do not consider yourself someone at risk of cardiovascular disease, our study shows that you can still have an increased risk of MI as a result of severe flu infection.” 

In many countries, the flu vaccine is recommended for everyone older than 60 or 65 years and for younger people with a history of cardiovascular disease. Data on flu vaccination was not available in the current study, but the average age of patients infected with flu was 74 years, so most patients would have been eligible to receive vaccination, she said.

In the Netherlands where the research took place, flu vaccination is recommended for everyone older than 60 years, and uptake is about 60%.

“There will be some cases in younger people, but the number needed to vaccinate to show a benefit would be much larger in younger people, and that may not be cost-effective,” reported Dr. Bruijning-Verhagen.

Flu vaccination policies vary across the world, with many factors being taken into account; some countries already advocate for universal vaccination every year.
 

Extend Flu Vaccination to Prevent ACS 

This study “provides further impetus to policy makers to review and update guidelines on prevention of acute coronary syndromes,” Raina MacIntyre, MBBS, Zubair Akhtar, MPH, and Aye Moa, MPH, University of New South Wales, Sydney, Australia, wrote in an accompanying editorial.

“Although vaccination to prevent influenza is recommended and funded in many countries for people 65 years of age and older, the additional benefits of prevention of ACS [acute coronary syndromes] have not been adopted universally into policy and practice nor have recommendations considered prevention of ACS in people 50-64 years of age,” they added.

“Vaccination is low-hanging fruit for people at risk of acute myocardial infarction who have not yet had a first event. It is time that we viewed influenza vaccine as a routine preventive measure for ACS and for people with coronary artery disease risk factors, along with statins, blood pressure control, and smoking cessation,” she explained.

The question of whether the link found between elevated MI risk and severe flu infection might be the result of MI being more likely to be detected in patients hospitalized with severe flu infection, who would undergo a thorough workup, was raised in a second editorial by Lori E. Dodd, PhD, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.

“I think this would be very unlikely to account for the large effect we found,” responded Dr. Bruijning-Verhagen. “There may be the occasional silent MI that gets missed in patients who are not hospitalized, but, in general, acute MI is not something that goes undetected.”

A version of this article appeared on Medscape.com.

The link between influenza infection and a rise in short-term risk for acute myocardial infarction (MI) has been reaffirmed in a new study, which showed the risk appears to be particularly elevated in individuals with no prior diagnosis of coronary artery disease.

“Our study results confirm previous findings of an increased risk of MI during or immediately following acute severe flu infection and raises the idea of giving prophylactic anticoagulation to these patients,” reported Patricia Bruijning-Verhagen, MD, University Medical Center Utrecht, the Netherlands, who is the senior author of the study, which was published online in NEJM Evidence.

“Our results also change things — in that we now know the focus should be on people without a history of cardiovascular disease — and highlight the importance of flu vaccination, particularly for this group,” she pointed out.

The observational, self-controlled, case-series study linked laboratory records on respiratory virus polymerase chain reaction (PCR) testing from 16 laboratories in the Netherlands to national mortality, hospitalization, medication, and administrative registries. Investigators compared the incidence of acute MI during the risk period — days 1-7 after influenza infection — with that in the control period — 1 year before and 51 weeks after the risk period.

The researchers found 26,221 positive PCR tests for influenza, constituting 23,405 unique influenza illness episodes. Of the episodes of acute MI occurring in the year before or the year after confirmed influenza infection and included in the analysis, 25 cases of acute MI occurred on days 1-7 after influenza infection and 394 occurred during the control period.

The adjusted relative incidence of acute MI during the risk period compared with during the control period was 6.16 (95% CI, 4.11-9.24).

The relative incidence of acute MI in individuals with no previous hospitalization for coronary artery disease was 16.60 (95% CI, 10.45-26.37); for those with a previous hospital admission for coronary artery disease, the relative incidence was 1.43 (95% CI, 0.53-3.84).

A temporary increase in the risk for MI has been reported in several previous studies. A 2018 Canadian study by Kwong and colleagues showed a sixfold elevation in the risk for acute MI after influenza infection, which was subsequently confirmed in studies from the United States, Denmark, and Scotland.

In their study, Dr. Bruijning-Verhagen and colleagues aimed to further quantify the association between laboratory-confirmed influenza infection and acute MI and to look at specific subgroups that might have the potential to guide a more individualized approach to prevention.

They replicated the Canadian study using a self-controlled case-series design that corrects for time-invariant confounding and found very similar results: A sixfold increase in the risk for acute MI in the first week after laboratory-confirmed influenza infection.

“The fact that we found similar results to Kwong et al. strengthens the finding that acute flu infection is linked to increased MI risk. This is becoming more and more clear now. It also shows that this effect is generalizable to other countries,” Dr. Bruijning-Verhagen said.
 

People Without Cardiovascular Disease at Highest Risk 

The researchers moved the field ahead by also looking at whether there is a difference in risk between individuals with flu who already had cardiovascular disease and those who did not.

“Most previous studies of flu and MI didn’t stratify between individuals with and without existing cardiovascular disease. And the ones that did look at this weren’t able to show a difference with any confidence,” Dr. Bruijning-Verhagen explained. “There have been suggestions before of a higher risk of MI in individuals with acute flu infection who do not have existing known cardiovascular disease, but this was uncertain.” 

The current study showed a large difference between the two groups, with a much higher risk for MI linked to flu in individuals without any known cardiovascular disease.

“You would think patients with existing cardiovascular disease would be more at risk of MI with flu infection, so this was a surprising result,” reported Dr. Bruijning-Verhagen. “But I think the result is real. The difference between the two groups was too big for it not to be.”

Influenza can cause a hypercoagulable state, systemic inflammation, and vascular changes that can trigger MI, even in patients not thought to be at risk before, she pointed out. And this is on top of high cardiac demands because of the acute infection.

Patients who already have cardiovascular disease may be protected to some extent by the cardiovascular medications that they are taking, she added.

These results could justify the use of short-term anticoagulation in patients with severe flu infection to cover the high-risk period, Dr. Bruijning-Verhagen suggested. “We give short-term anticoagulation as prophylaxis to patients when they have surgery. This would not be that different. But obviously, this approach would have to be tested.”

Clinical studies looking at such a strategy are currently underway.
 

‘Get Your Flu Shot’

The results reinforce the need for anyone who is eligible to get the flu vaccine. “These results should give extra weight to the message to get your flu shot,” she said. “Even if you do not consider yourself someone at risk of cardiovascular disease, our study shows that you can still have an increased risk of MI as a result of severe flu infection.” 

In many countries, the flu vaccine is recommended for everyone older than 60 or 65 years and for younger people with a history of cardiovascular disease. Data on flu vaccination was not available in the current study, but the average age of patients infected with flu was 74 years, so most patients would have been eligible to receive vaccination, she said.

In the Netherlands where the research took place, flu vaccination is recommended for everyone older than 60 years, and uptake is about 60%.

“There will be some cases in younger people, but the number needed to vaccinate to show a benefit would be much larger in younger people, and that may not be cost-effective,” reported Dr. Bruijning-Verhagen.

Flu vaccination policies vary across the world, with many factors being taken into account; some countries already advocate for universal vaccination every year.
 

Extend Flu Vaccination to Prevent ACS 

This study “provides further impetus to policy makers to review and update guidelines on prevention of acute coronary syndromes,” Raina MacIntyre, MBBS, Zubair Akhtar, MPH, and Aye Moa, MPH, University of New South Wales, Sydney, Australia, wrote in an accompanying editorial.

“Although vaccination to prevent influenza is recommended and funded in many countries for people 65 years of age and older, the additional benefits of prevention of ACS [acute coronary syndromes] have not been adopted universally into policy and practice nor have recommendations considered prevention of ACS in people 50-64 years of age,” they added.

“Vaccination is low-hanging fruit for people at risk of acute myocardial infarction who have not yet had a first event. It is time that we viewed influenza vaccine as a routine preventive measure for ACS and for people with coronary artery disease risk factors, along with statins, blood pressure control, and smoking cessation,” she explained.

The question of whether the link found between elevated MI risk and severe flu infection might be the result of MI being more likely to be detected in patients hospitalized with severe flu infection, who would undergo a thorough workup, was raised in a second editorial by Lori E. Dodd, PhD, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.

“I think this would be very unlikely to account for the large effect we found,” responded Dr. Bruijning-Verhagen. “There may be the occasional silent MI that gets missed in patients who are not hospitalized, but, in general, acute MI is not something that goes undetected.”

A version of this article appeared on Medscape.com.

The link between influenza infection and a rise in short-term risk for acute myocardial infarction (MI) has been reaffirmed in a new study, which showed the risk appears to be particularly elevated in individuals with no prior diagnosis of coronary artery disease.

“Our study results confirm previous findings of an increased risk of MI during or immediately following acute severe flu infection and raises the idea of giving prophylactic anticoagulation to these patients,” reported Patricia Bruijning-Verhagen, MD, University Medical Center Utrecht, the Netherlands, who is the senior author of the study, which was published online in NEJM Evidence.

“Our results also change things — in that we now know the focus should be on people without a history of cardiovascular disease — and highlight the importance of flu vaccination, particularly for this group,” she pointed out.

The observational, self-controlled, case-series study linked laboratory records on respiratory virus polymerase chain reaction (PCR) testing from 16 laboratories in the Netherlands to national mortality, hospitalization, medication, and administrative registries. Investigators compared the incidence of acute MI during the risk period — days 1-7 after influenza infection — with that in the control period — 1 year before and 51 weeks after the risk period.

The researchers found 26,221 positive PCR tests for influenza, constituting 23,405 unique influenza illness episodes. Of the episodes of acute MI occurring in the year before or the year after confirmed influenza infection and included in the analysis, 25 cases of acute MI occurred on days 1-7 after influenza infection and 394 occurred during the control period.

The adjusted relative incidence of acute MI during the risk period compared with during the control period was 6.16 (95% CI, 4.11-9.24).

The relative incidence of acute MI in individuals with no previous hospitalization for coronary artery disease was 16.60 (95% CI, 10.45-26.37); for those with a previous hospital admission for coronary artery disease, the relative incidence was 1.43 (95% CI, 0.53-3.84).

A temporary increase in the risk for MI has been reported in several previous studies. A 2018 Canadian study by Kwong and colleagues showed a sixfold elevation in the risk for acute MI after influenza infection, which was subsequently confirmed in studies from the United States, Denmark, and Scotland.

In their study, Dr. Bruijning-Verhagen and colleagues aimed to further quantify the association between laboratory-confirmed influenza infection and acute MI and to look at specific subgroups that might have the potential to guide a more individualized approach to prevention.

They replicated the Canadian study using a self-controlled case-series design that corrects for time-invariant confounding and found very similar results: A sixfold increase in the risk for acute MI in the first week after laboratory-confirmed influenza infection.

“The fact that we found similar results to Kwong et al. strengthens the finding that acute flu infection is linked to increased MI risk. This is becoming more and more clear now. It also shows that this effect is generalizable to other countries,” Dr. Bruijning-Verhagen said.
 

People Without Cardiovascular Disease at Highest Risk 

The researchers moved the field ahead by also looking at whether there is a difference in risk between individuals with flu who already had cardiovascular disease and those who did not.

“Most previous studies of flu and MI didn’t stratify between individuals with and without existing cardiovascular disease. And the ones that did look at this weren’t able to show a difference with any confidence,” Dr. Bruijning-Verhagen explained. “There have been suggestions before of a higher risk of MI in individuals with acute flu infection who do not have existing known cardiovascular disease, but this was uncertain.” 

The current study showed a large difference between the two groups, with a much higher risk for MI linked to flu in individuals without any known cardiovascular disease.

“You would think patients with existing cardiovascular disease would be more at risk of MI with flu infection, so this was a surprising result,” reported Dr. Bruijning-Verhagen. “But I think the result is real. The difference between the two groups was too big for it not to be.”

Influenza can cause a hypercoagulable state, systemic inflammation, and vascular changes that can trigger MI, even in patients not thought to be at risk before, she pointed out. And this is on top of high cardiac demands because of the acute infection.

Patients who already have cardiovascular disease may be protected to some extent by the cardiovascular medications that they are taking, she added.

These results could justify the use of short-term anticoagulation in patients with severe flu infection to cover the high-risk period, Dr. Bruijning-Verhagen suggested. “We give short-term anticoagulation as prophylaxis to patients when they have surgery. This would not be that different. But obviously, this approach would have to be tested.”

Clinical studies looking at such a strategy are currently underway.
 

‘Get Your Flu Shot’

The results reinforce the need for anyone who is eligible to get the flu vaccine. “These results should give extra weight to the message to get your flu shot,” she said. “Even if you do not consider yourself someone at risk of cardiovascular disease, our study shows that you can still have an increased risk of MI as a result of severe flu infection.” 

In many countries, the flu vaccine is recommended for everyone older than 60 or 65 years and for younger people with a history of cardiovascular disease. Data on flu vaccination was not available in the current study, but the average age of patients infected with flu was 74 years, so most patients would have been eligible to receive vaccination, she said.

In the Netherlands where the research took place, flu vaccination is recommended for everyone older than 60 years, and uptake is about 60%.

“There will be some cases in younger people, but the number needed to vaccinate to show a benefit would be much larger in younger people, and that may not be cost-effective,” reported Dr. Bruijning-Verhagen.

Flu vaccination policies vary across the world, with many factors being taken into account; some countries already advocate for universal vaccination every year.
 

Extend Flu Vaccination to Prevent ACS 

This study “provides further impetus to policy makers to review and update guidelines on prevention of acute coronary syndromes,” Raina MacIntyre, MBBS, Zubair Akhtar, MPH, and Aye Moa, MPH, University of New South Wales, Sydney, Australia, wrote in an accompanying editorial.

“Although vaccination to prevent influenza is recommended and funded in many countries for people 65 years of age and older, the additional benefits of prevention of ACS [acute coronary syndromes] have not been adopted universally into policy and practice nor have recommendations considered prevention of ACS in people 50-64 years of age,” they added.

“Vaccination is low-hanging fruit for people at risk of acute myocardial infarction who have not yet had a first event. It is time that we viewed influenza vaccine as a routine preventive measure for ACS and for people with coronary artery disease risk factors, along with statins, blood pressure control, and smoking cessation,” she explained.

The question of whether the link found between elevated MI risk and severe flu infection might be the result of MI being more likely to be detected in patients hospitalized with severe flu infection, who would undergo a thorough workup, was raised in a second editorial by Lori E. Dodd, PhD, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.

“I think this would be very unlikely to account for the large effect we found,” responded Dr. Bruijning-Verhagen. “There may be the occasional silent MI that gets missed in patients who are not hospitalized, but, in general, acute MI is not something that goes undetected.”

A version of this article appeared on Medscape.com.

TOPLINE:

Long-term gender-affirming hormone treatment with testosterone increases the risk for metabolic syndromes in transmasculine individuals, whereas transfeminine individuals receiving estradiol have a lower risk.

METHODOLOGY:

• Many transgender individuals receive exogenous sex hormone therapy to reduce gender dysphoria and improve quality of life. These treatments, however, may influence the development of metabolic syndrome.
• This retrospective, longitudinal cohort study investigated the association between gender-affirming hormone treatment and metabolic syndrome scores in transfeminine and transmasculine individuals compared with cisgender men and women not receiving the treatment.
• Overall, 645 transgender participants (mean age at index date, 41.3 years; 494 transfeminine and 151 transmasculine) were matched with 645 cisgender participants (280 women and 365 men) from the Veterans Health Administration.
• Metabolic syndrome scores were calculated based on blood pressure; body mass index (BMI); and levels of high-density lipoprotein (HDL) cholesterol, triglycerides, and blood glucose.
• Changes in metabolic syndrome scores before and after hormonal transition were compared among transgender and cisgender individuals for the corresponding dates.

TAKEAWAY:

• After hormonal transition, all measured metabolic syndrome components significantly worsened in the transmasculine group (P < .05 for all).
• In contrast, the systolic blood pressure and triglyceride levels decreased, HDL cholesterol levels increased, and BMI showed no significant change in the transfeminine group after hormonal transition.
• The increase in metabolic syndrome scores after vs before the date of hormonal transition was the highest for transmasculine individuals (298.0%; P < .001), followed by cisgender women (108.3%; P < .001), cisgender men (49.3%; P = .02), and transfeminine individuals (3.0%; P = .77).

IN PRACTICE:

“This is relevant for the management of metabolic syndrome risk factors in cisgender and transgender individuals and to potentially predict the risk of atherosclerotic cardiovascular disease, type 2 diabetes, systolic hypertension, insulin resistance, and nonalcoholic fatty liver disease,” the authors wrote.

SOURCE:

Leila Hashemi, MD, MS, of the Department of General Internal Medicine, David Geffen School of Medicine, University of California, Los Angeles, led this study, which was published online in JAMA Network Open.

LIMITATIONS:

Causal inferences could not be drawn because of the study’s observational nature. The transmasculine and cisgender female groups were limited in size, and military veterans have special circumstances not representative of the general population. Minority stress among the transgender veterans was also not considered, which may have affected the health and well-being outcomes.

DISCLOSURES:

This study was supported by the National Institutes of Health and Office of Research on Women’s Health grants. One author received grants from the National Institutes of Health.

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

TOPLINE:

Long-term gender-affirming hormone treatment with testosterone increases the risk for metabolic syndromes in transmasculine individuals, whereas transfeminine individuals receiving estradiol have a lower risk.

METHODOLOGY:

• Many transgender individuals receive exogenous sex hormone therapy to reduce gender dysphoria and improve quality of life. These treatments, however, may influence the development of metabolic syndrome.
• This retrospective, longitudinal cohort study investigated the association between gender-affirming hormone treatment and metabolic syndrome scores in transfeminine and transmasculine individuals compared with cisgender men and women not receiving the treatment.
• Overall, 645 transgender participants (mean age at index date, 41.3 years; 494 transfeminine and 151 transmasculine) were matched with 645 cisgender participants (280 women and 365 men) from the Veterans Health Administration.
• Metabolic syndrome scores were calculated based on blood pressure; body mass index (BMI); and levels of high-density lipoprotein (HDL) cholesterol, triglycerides, and blood glucose.
• Changes in metabolic syndrome scores before and after hormonal transition were compared among transgender and cisgender individuals for the corresponding dates.

TAKEAWAY:

• After hormonal transition, all measured metabolic syndrome components significantly worsened in the transmasculine group (P < .05 for all).
• In contrast, the systolic blood pressure and triglyceride levels decreased, HDL cholesterol levels increased, and BMI showed no significant change in the transfeminine group after hormonal transition.
• The increase in metabolic syndrome scores after vs before the date of hormonal transition was the highest for transmasculine individuals (298.0%; P < .001), followed by cisgender women (108.3%; P < .001), cisgender men (49.3%; P = .02), and transfeminine individuals (3.0%; P = .77).

IN PRACTICE:

“This is relevant for the management of metabolic syndrome risk factors in cisgender and transgender individuals and to potentially predict the risk of atherosclerotic cardiovascular disease, type 2 diabetes, systolic hypertension, insulin resistance, and nonalcoholic fatty liver disease,” the authors wrote.

SOURCE:

Leila Hashemi, MD, MS, of the Department of General Internal Medicine, David Geffen School of Medicine, University of California, Los Angeles, led this study, which was published online in JAMA Network Open.

LIMITATIONS:

Causal inferences could not be drawn because of the study’s observational nature. The transmasculine and cisgender female groups were limited in size, and military veterans have special circumstances not representative of the general population. Minority stress among the transgender veterans was also not considered, which may have affected the health and well-being outcomes.

DISCLOSURES:

This study was supported by the National Institutes of Health and Office of Research on Women’s Health grants. One author received grants from the National Institutes of Health.

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

TOPLINE:

Long-term gender-affirming hormone treatment with testosterone increases the risk for metabolic syndromes in transmasculine individuals, whereas transfeminine individuals receiving estradiol have a lower risk.

METHODOLOGY:

• Many transgender individuals receive exogenous sex hormone therapy to reduce gender dysphoria and improve quality of life. These treatments, however, may influence the development of metabolic syndrome.
• This retrospective, longitudinal cohort study investigated the association between gender-affirming hormone treatment and metabolic syndrome scores in transfeminine and transmasculine individuals compared with cisgender men and women not receiving the treatment.
• Overall, 645 transgender participants (mean age at index date, 41.3 years; 494 transfeminine and 151 transmasculine) were matched with 645 cisgender participants (280 women and 365 men) from the Veterans Health Administration.
• Metabolic syndrome scores were calculated based on blood pressure; body mass index (BMI); and levels of high-density lipoprotein (HDL) cholesterol, triglycerides, and blood glucose.
• Changes in metabolic syndrome scores before and after hormonal transition were compared among transgender and cisgender individuals for the corresponding dates.

TAKEAWAY:

• After hormonal transition, all measured metabolic syndrome components significantly worsened in the transmasculine group (P < .05 for all).
• In contrast, the systolic blood pressure and triglyceride levels decreased, HDL cholesterol levels increased, and BMI showed no significant change in the transfeminine group after hormonal transition.
• The increase in metabolic syndrome scores after vs before the date of hormonal transition was the highest for transmasculine individuals (298.0%; P < .001), followed by cisgender women (108.3%; P < .001), cisgender men (49.3%; P = .02), and transfeminine individuals (3.0%; P = .77).

IN PRACTICE:

“This is relevant for the management of metabolic syndrome risk factors in cisgender and transgender individuals and to potentially predict the risk of atherosclerotic cardiovascular disease, type 2 diabetes, systolic hypertension, insulin resistance, and nonalcoholic fatty liver disease,” the authors wrote.

SOURCE:

Leila Hashemi, MD, MS, of the Department of General Internal Medicine, David Geffen School of Medicine, University of California, Los Angeles, led this study, which was published online in JAMA Network Open.

LIMITATIONS:

Causal inferences could not be drawn because of the study’s observational nature. The transmasculine and cisgender female groups were limited in size, and military veterans have special circumstances not representative of the general population. Minority stress among the transgender veterans was also not considered, which may have affected the health and well-being outcomes.

DISCLOSURES:

This study was supported by the National Institutes of Health and Office of Research on Women’s Health grants. One author received grants from the National Institutes of Health.

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

TOPLINE:

Lowering the dose of edoxaban to 30 mg in patients 80 years of age and older with atrial fibrillation (AF) reduces major bleeding events without increasing ischemic events.

METHODOLOGY:

• Researchers conducted a parallel design, double-blind clinical trial of 21,105 patients with AF.
• Nearly 3000 patients aged 80 years and older were included in the secondary analysis, focusing on edoxaban, 60 mg vs 30 mg, and edoxaban 30 mg vs warfarin.
• The primary outcome was a composite of death, stroke or systemic embolism, and major bleeding, with secondary outcomes including ischemic stroke and all-cause death.
• People were excluded from the study if they had moderate or severe mitral stenosis, a mechanical heart valve, a high risk for bleeding, or were on antiplatelet drugs.

TAKEAWAY:

• Participants without dose-reduction criteria who received edoxaban 30 mg had lower rates of major bleeding than those who received 60 mg (hazard ratio [HR], 1.57; 95% CI, 1.04-2.38; P = .03).
• Rates of major gastrointestinal hemorrhage were higher with edoxaban 60 mg than with 30 mg (HR, 2.24; 95% CI, 1.29-3.90; P = .004).
• People who took edoxaban 30 mg had a 17% lower risk for all-cause death than those who received warfarin (HR, 0.83; 95% CI, 0.70-1.00; P = .046).
• In a little over 2400 participants with or without dose-reduction criteria, those receiving edoxaban 30 mg had the lower risk for major bleeding (HR, 0.59; 95% CI, 0.45-0.77; P < .001) and death (HR, 0.83; 95% CI, 0.70-1.00; P = .046); risk for stroke or systemic embolism was comparable between the two drugs.

IN PRACTICE:

“These data suggest that lower-dose anticoagulants, such as edoxaban, 30 mg once daily, may be considered in all patients 80 years and older with AF irrespective of dose-reduction criteria,” the study authors wrote.

SOURCE:

The study was led by André Zimerman, MD, PhD, of Brigham and Women’s Hospital and the Department of Medicine at Harvard Medical School in Boston. It was published online in JAMA Cardiology. The study was funded by Daiichi Sankyo for the TIMI Study Group.

LIMITATIONS:

The study did not adjust for multiple comparisons, increasing the risk for type I and type II errors. Additionally, the trial participants may represent a more compliant subset of the target population, which could influence the results.

DISCLOSURES:

Various authors reported receiving grants, consultant fees, and consulting fees from AstraZeneca, Merck, Novartis, Amgen, Boehringer Ingelheim/Lilly, and Cardurion Pharmaceuticals, among others.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Lowering the dose of edoxaban to 30 mg in patients 80 years of age and older with atrial fibrillation (AF) reduces major bleeding events without increasing ischemic events.

METHODOLOGY:

• Researchers conducted a parallel design, double-blind clinical trial of 21,105 patients with AF.
• Nearly 3000 patients aged 80 years and older were included in the secondary analysis, focusing on edoxaban, 60 mg vs 30 mg, and edoxaban 30 mg vs warfarin.
• The primary outcome was a composite of death, stroke or systemic embolism, and major bleeding, with secondary outcomes including ischemic stroke and all-cause death.
• People were excluded from the study if they had moderate or severe mitral stenosis, a mechanical heart valve, a high risk for bleeding, or were on antiplatelet drugs.

TAKEAWAY:

• Participants without dose-reduction criteria who received edoxaban 30 mg had lower rates of major bleeding than those who received 60 mg (hazard ratio [HR], 1.57; 95% CI, 1.04-2.38; P = .03).
• Rates of major gastrointestinal hemorrhage were higher with edoxaban 60 mg than with 30 mg (HR, 2.24; 95% CI, 1.29-3.90; P = .004).
• People who took edoxaban 30 mg had a 17% lower risk for all-cause death than those who received warfarin (HR, 0.83; 95% CI, 0.70-1.00; P = .046).
• In a little over 2400 participants with or without dose-reduction criteria, those receiving edoxaban 30 mg had the lower risk for major bleeding (HR, 0.59; 95% CI, 0.45-0.77; P < .001) and death (HR, 0.83; 95% CI, 0.70-1.00; P = .046); risk for stroke or systemic embolism was comparable between the two drugs.

IN PRACTICE:

“These data suggest that lower-dose anticoagulants, such as edoxaban, 30 mg once daily, may be considered in all patients 80 years and older with AF irrespective of dose-reduction criteria,” the study authors wrote.

SOURCE:

The study was led by André Zimerman, MD, PhD, of Brigham and Women’s Hospital and the Department of Medicine at Harvard Medical School in Boston. It was published online in JAMA Cardiology. The study was funded by Daiichi Sankyo for the TIMI Study Group.

LIMITATIONS:

The study did not adjust for multiple comparisons, increasing the risk for type I and type II errors. Additionally, the trial participants may represent a more compliant subset of the target population, which could influence the results.

DISCLOSURES:

Various authors reported receiving grants, consultant fees, and consulting fees from AstraZeneca, Merck, Novartis, Amgen, Boehringer Ingelheim/Lilly, and Cardurion Pharmaceuticals, among others.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Lowering the dose of edoxaban to 30 mg in patients 80 years of age and older with atrial fibrillation (AF) reduces major bleeding events without increasing ischemic events.

METHODOLOGY:

• Researchers conducted a parallel design, double-blind clinical trial of 21,105 patients with AF.
• Nearly 3000 patients aged 80 years and older were included in the secondary analysis, focusing on edoxaban, 60 mg vs 30 mg, and edoxaban 30 mg vs warfarin.
• The primary outcome was a composite of death, stroke or systemic embolism, and major bleeding, with secondary outcomes including ischemic stroke and all-cause death.
• People were excluded from the study if they had moderate or severe mitral stenosis, a mechanical heart valve, a high risk for bleeding, or were on antiplatelet drugs.

TAKEAWAY:

• Participants without dose-reduction criteria who received edoxaban 30 mg had lower rates of major bleeding than those who received 60 mg (hazard ratio [HR], 1.57; 95% CI, 1.04-2.38; P = .03).
• Rates of major gastrointestinal hemorrhage were higher with edoxaban 60 mg than with 30 mg (HR, 2.24; 95% CI, 1.29-3.90; P = .004).
• People who took edoxaban 30 mg had a 17% lower risk for all-cause death than those who received warfarin (HR, 0.83; 95% CI, 0.70-1.00; P = .046).
• In a little over 2400 participants with or without dose-reduction criteria, those receiving edoxaban 30 mg had the lower risk for major bleeding (HR, 0.59; 95% CI, 0.45-0.77; P < .001) and death (HR, 0.83; 95% CI, 0.70-1.00; P = .046); risk for stroke or systemic embolism was comparable between the two drugs.

IN PRACTICE:

“These data suggest that lower-dose anticoagulants, such as edoxaban, 30 mg once daily, may be considered in all patients 80 years and older with AF irrespective of dose-reduction criteria,” the study authors wrote.

SOURCE:

The study was led by André Zimerman, MD, PhD, of Brigham and Women’s Hospital and the Department of Medicine at Harvard Medical School in Boston. It was published online in JAMA Cardiology. The study was funded by Daiichi Sankyo for the TIMI Study Group.

LIMITATIONS:

The study did not adjust for multiple comparisons, increasing the risk for type I and type II errors. Additionally, the trial participants may represent a more compliant subset of the target population, which could influence the results.

DISCLOSURES:

Various authors reported receiving grants, consultant fees, and consulting fees from AstraZeneca, Merck, Novartis, Amgen, Boehringer Ingelheim/Lilly, and Cardurion Pharmaceuticals, among others.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

New-onset atrial fibrillation (AF) is associated with a substantially higher risk for all-cause dementia in patients with type 2 diabetes (T2D).

METHODOLOGY:

• Studies suggest a potential link between AF and dementia in the broader population, but evidence is scarce in people with diabetes, who are at increased risk for both conditions.
• This longitudinal observational study assessed the association between new-onset AF and dementia in 22,989 patients with T2D (median age at enrollment, 61.0 years; 62.3% men; 86.3% White individuals).
• New-onset AF was identified through hospital admission records using the International Classification of Diseases – 9th Revision (ICD-9) and ICD-10 codes, and dementia cases were identified using an algorithm developed by the UK Biobank.
• Time-varying Cox proportional hazard regression models were used to determine the association between incident dementia and new-onset AF.

TAKEAWAY:

• Over a median follow-up duration of about 12 years, 844 patients developed all-cause dementia, 342 were diagnosed with Alzheimer’s disease, and 246 had vascular dementia.
• Patients with incident AF had a higher risk of developing all-cause dementia (hazard ratio [HR], 2.15; 95% CI, 1.80-2.57), Alzheimer’s disease (HR, 1.44; 95% CI, 1.06-1.96), and vascular dementia (HR, 3.11; 95% CI, 2.32-4.17) than those without incident AF.
• The results are independent of common dementia risk factors, such as sociodemographic characteristics and lifestyle factors.
• The mean time intervals from the onset of AF to all-cause dementia, Alzheimer’s disease and vascular dementia were 2.95, 2.81, and 3.37 years, respectively.

IN PRACTICE:

“AF is a significant risk factor for dementia in patients with type 2 diabetes, suggesting the importance of timely and effective treatment of AF, such as early rhythm control strategies and anticoagulant use, in preventing dementia among this demographic,” the authors wrote.
 

SOURCE:

The study, led by Ying Zhou, PhD, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China, was published online in Diabetes, Obesity and Metabolism.

LIMITATIONS:

The study could not explore the link between different AF subtypes and dementia owing to its small sample size. The effects of AF treatment on the risk for dementia in patients with type 2 diabetes were not considered because of lack of information. The mostly White study population limits the generalizability of the findings to other races and ethnicities.

DISCLOSURES:

The study was supported by the National Social Science Fund of China. The authors declared no conflicts of interest.

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

TOPLINE:

New-onset atrial fibrillation (AF) is associated with a substantially higher risk for all-cause dementia in patients with type 2 diabetes (T2D).

METHODOLOGY:

• Studies suggest a potential link between AF and dementia in the broader population, but evidence is scarce in people with diabetes, who are at increased risk for both conditions.
• This longitudinal observational study assessed the association between new-onset AF and dementia in 22,989 patients with T2D (median age at enrollment, 61.0 years; 62.3% men; 86.3% White individuals).
• New-onset AF was identified through hospital admission records using the International Classification of Diseases – 9th Revision (ICD-9) and ICD-10 codes, and dementia cases were identified using an algorithm developed by the UK Biobank.
• Time-varying Cox proportional hazard regression models were used to determine the association between incident dementia and new-onset AF.

TAKEAWAY:

• Over a median follow-up duration of about 12 years, 844 patients developed all-cause dementia, 342 were diagnosed with Alzheimer’s disease, and 246 had vascular dementia.
• Patients with incident AF had a higher risk of developing all-cause dementia (hazard ratio [HR], 2.15; 95% CI, 1.80-2.57), Alzheimer’s disease (HR, 1.44; 95% CI, 1.06-1.96), and vascular dementia (HR, 3.11; 95% CI, 2.32-4.17) than those without incident AF.
• The results are independent of common dementia risk factors, such as sociodemographic characteristics and lifestyle factors.
• The mean time intervals from the onset of AF to all-cause dementia, Alzheimer’s disease and vascular dementia were 2.95, 2.81, and 3.37 years, respectively.

IN PRACTICE:

“AF is a significant risk factor for dementia in patients with type 2 diabetes, suggesting the importance of timely and effective treatment of AF, such as early rhythm control strategies and anticoagulant use, in preventing dementia among this demographic,” the authors wrote.
 

SOURCE:

The study, led by Ying Zhou, PhD, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China, was published online in Diabetes, Obesity and Metabolism.

LIMITATIONS:

The study could not explore the link between different AF subtypes and dementia owing to its small sample size. The effects of AF treatment on the risk for dementia in patients with type 2 diabetes were not considered because of lack of information. The mostly White study population limits the generalizability of the findings to other races and ethnicities.

DISCLOSURES:

The study was supported by the National Social Science Fund of China. The authors declared no conflicts of interest.

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

TOPLINE:

New-onset atrial fibrillation (AF) is associated with a substantially higher risk for all-cause dementia in patients with type 2 diabetes (T2D).

METHODOLOGY:

• Studies suggest a potential link between AF and dementia in the broader population, but evidence is scarce in people with diabetes, who are at increased risk for both conditions.
• This longitudinal observational study assessed the association between new-onset AF and dementia in 22,989 patients with T2D (median age at enrollment, 61.0 years; 62.3% men; 86.3% White individuals).
• New-onset AF was identified through hospital admission records using the International Classification of Diseases – 9th Revision (ICD-9) and ICD-10 codes, and dementia cases were identified using an algorithm developed by the UK Biobank.
• Time-varying Cox proportional hazard regression models were used to determine the association between incident dementia and new-onset AF.

TAKEAWAY:

• Over a median follow-up duration of about 12 years, 844 patients developed all-cause dementia, 342 were diagnosed with Alzheimer’s disease, and 246 had vascular dementia.
• Patients with incident AF had a higher risk of developing all-cause dementia (hazard ratio [HR], 2.15; 95% CI, 1.80-2.57), Alzheimer’s disease (HR, 1.44; 95% CI, 1.06-1.96), and vascular dementia (HR, 3.11; 95% CI, 2.32-4.17) than those without incident AF.
• The results are independent of common dementia risk factors, such as sociodemographic characteristics and lifestyle factors.
• The mean time intervals from the onset of AF to all-cause dementia, Alzheimer’s disease and vascular dementia were 2.95, 2.81, and 3.37 years, respectively.

IN PRACTICE:

“AF is a significant risk factor for dementia in patients with type 2 diabetes, suggesting the importance of timely and effective treatment of AF, such as early rhythm control strategies and anticoagulant use, in preventing dementia among this demographic,” the authors wrote.
 

SOURCE:

The study, led by Ying Zhou, PhD, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China, was published online in Diabetes, Obesity and Metabolism.

LIMITATIONS:

The study could not explore the link between different AF subtypes and dementia owing to its small sample size. The effects of AF treatment on the risk for dementia in patients with type 2 diabetes were not considered because of lack of information. The mostly White study population limits the generalizability of the findings to other races and ethnicities.

DISCLOSURES:

The study was supported by the National Social Science Fund of China. The authors declared no conflicts of interest.

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

An international trial of the Impella heart pump in patients with ST elevation myocardial infarction (STEMI) and cardiogenic shock has been stopped by the sponsor, Abiomed Inc. The termination followed news that another international trial, DanGer Shock, found that the pump improved survival in these patients.

Abiomed Inc., which manufactures the Impella microaxial flow pump, said in a statement that the trial’s Data and Safety Monitoring Board recommended stopping RECOVER IV.

“I was convinced that the study could not continue,” one of the principal investigators William O’Neill, MD, an interventional cardiologist with the Henry Ford Health in Detroit, said in an interview. After 3.5 years of work and thousands of person-hours, he added, “It’s not a decision that people took lightly.”

The trial already had three sites in Europe and one in the United States up and running, with two more US sites slated to join the trial. It had started enrolling patients, although few to date.

DanGer Shock trial results were expected to have a serious effect on how RECOVER IV would unfold. It was previously uncertain whether the Impella heart pump would save lives vs existing approaches, said O’Neill and co-principal investigator Navin Kapur, MD, an interventional cardiologist at Tufts Medical Center in Boston. Once the DanGer Shock trial showed the benefits of using the heart pump, that equipoise vanished.
 

Loss of Clinical Equipoise

“The clinicians were challenged in getting consent from patients where they had to say, ‘If you are randomized to the control arm, we are not able to use an Impella,’ ” said Dr. Kapur. He pointed out that patients would be unlikely to agree to participate in a trial where they might not get the treatment already shown to improve survival.

Dr. Kapur and Dr. O’Neill said the clinicians participating in the trial expressed discomfort at continuing. The RECOVER IV trial was expected to take many years to enroll the targeted number of patients. To participate, hospitals had to have the equipment and expertise to use the Impella heart pump, as well as the control treatments — balloon-pump support and extracorporeal membrane oxygenation (ECMO), Dr. Kapur explained. He said most patients with STEMI and cardiogenic shock would present to their nearest community hospitals, many of which would not have these treatments and would be unable to participate in the study.

Patients with STEMI and cardiogenic shock are uncommon. About 80,000 patients in the United States each year present with cardiogenic shock, of whom about 40% are not experiencing a STEMI, said Dr. O’Neill.

But those who do fit into the population of both STEMI and cardiogenic shock are at very high risk, said Dr. Kapur. “One in three or one in two patients with STEMI and cardiogenic shock will die in hospital.”
 

Getting Hearts Pumping

The Impella heart pump was originally developed by Impella Cardiosystems in Aachen, Germany, which was acquired by Abiomed in 2005, according to the Abiomed website. And Abiomed was acquired by Johnson & Johnson MedTech in 2022. The company has developed a series of models over the years and said that Impella CP — the model used in DanGer Shock and RECOVER IV trials — is the world’s smallest heart pump.

“Impella is the only heart pump that can be introduced percutaneously through the leg,” said Dr. O’Neill, whereas other pumps available are used only in open-heart surgery. While Impella is the first pump to be used this way, he said it won’t be the last. Other, more powerful pumps are being developed.
 

DanGer Shock: A Leap Forward

Despite leading to the halt of another trial, the DanGer Shock results are a good news story, said the RECOVER IV investigators.

“The DanGer trial is a huge advance,” said Dr. O’Neill. “It’s the first study this century that shows something that improves survival in cardiogenic shock. You treat eight patients, and you save one life.” Dr. O’Neill said this is one of the best outcomes he has seen during his long career.

Dr. Kapur said the DanGer trial is also a leap forward in designing trials for cardiogenic shock. He said previous trials of mechanical support in cardiogenic shock had neutral results, probably due to broad inclusion criteria for patients.

“The DanGer trial was selective in its inclusion and exclusion criteria. That made it more difficult to enroll the population, so it took a lot longer. But it used the right device at the right time in the right patient, and it was successful,” he said.

“The DanGer investigators need to be applauded,” he added. “The lesson is, we have to design the right trials.”
 

New Cardiogenic Shock Trials

Dr. O’Neill and Dr. Kapur said the groundwork they laid for RECOVER IV can be used for new trials.

“We have 50 sites in the US, Germany, and Denmark. They’re interested, and they’re waiting,” said Dr. O’Neill. The researchers are poised to begin new trials once protocols are developed.

What will the next trials investigate?

DanGer Shock results showed higher rates of adverse events following Impella use than after standard care. “We need to come up with strategies to decrease bleeding problems and renal failure,” said Dr. O’Neill, and these could be tested in trials.

Other questions he would like to see investigated are using the Impella heart pump before or after angioplasty, and multi-vessel vs culprit-vessel percutaneous coronary intervention in cardiogenic shock with Impella support.

Dr. Kapur mentioned studying patients excluded from the DanGer Shock trial — such as those needing right ventricular support — because DanGer Shock covered only left ventricular support and those suffering cardiac arrest outside hospital. He said trials could compare differences between models of Impella and investigate the role of ECMO.

“I’m optimistic that we can design more randomized controlled trials with the right patient population and right treatment algorithm,” Dr. Kapur said. This is a critical step toward better outcomes for patients, he added. Another step is optimizing the design of heart pumps, which should decrease the rates of adverse events, he said. “I have a lot of optimism for the future of device design.”

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

An international trial of the Impella heart pump in patients with ST elevation myocardial infarction (STEMI) and cardiogenic shock has been stopped by the sponsor, Abiomed Inc. The termination followed news that another international trial, DanGer Shock, found that the pump improved survival in these patients.

Abiomed Inc., which manufactures the Impella microaxial flow pump, said in a statement that the trial’s Data and Safety Monitoring Board recommended stopping RECOVER IV.

“I was convinced that the study could not continue,” one of the principal investigators William O’Neill, MD, an interventional cardiologist with the Henry Ford Health in Detroit, said in an interview. After 3.5 years of work and thousands of person-hours, he added, “It’s not a decision that people took lightly.”

The trial already had three sites in Europe and one in the United States up and running, with two more US sites slated to join the trial. It had started enrolling patients, although few to date.

DanGer Shock trial results were expected to have a serious effect on how RECOVER IV would unfold. It was previously uncertain whether the Impella heart pump would save lives vs existing approaches, said O’Neill and co-principal investigator Navin Kapur, MD, an interventional cardiologist at Tufts Medical Center in Boston. Once the DanGer Shock trial showed the benefits of using the heart pump, that equipoise vanished.
 

Loss of Clinical Equipoise

“The clinicians were challenged in getting consent from patients where they had to say, ‘If you are randomized to the control arm, we are not able to use an Impella,’ ” said Dr. Kapur. He pointed out that patients would be unlikely to agree to participate in a trial where they might not get the treatment already shown to improve survival.

Dr. Kapur and Dr. O’Neill said the clinicians participating in the trial expressed discomfort at continuing. The RECOVER IV trial was expected to take many years to enroll the targeted number of patients. To participate, hospitals had to have the equipment and expertise to use the Impella heart pump, as well as the control treatments — balloon-pump support and extracorporeal membrane oxygenation (ECMO), Dr. Kapur explained. He said most patients with STEMI and cardiogenic shock would present to their nearest community hospitals, many of which would not have these treatments and would be unable to participate in the study.

Patients with STEMI and cardiogenic shock are uncommon. About 80,000 patients in the United States each year present with cardiogenic shock, of whom about 40% are not experiencing a STEMI, said Dr. O’Neill.

But those who do fit into the population of both STEMI and cardiogenic shock are at very high risk, said Dr. Kapur. “One in three or one in two patients with STEMI and cardiogenic shock will die in hospital.”
 

Getting Hearts Pumping

The Impella heart pump was originally developed by Impella Cardiosystems in Aachen, Germany, which was acquired by Abiomed in 2005, according to the Abiomed website. And Abiomed was acquired by Johnson & Johnson MedTech in 2022. The company has developed a series of models over the years and said that Impella CP — the model used in DanGer Shock and RECOVER IV trials — is the world’s smallest heart pump.

“Impella is the only heart pump that can be introduced percutaneously through the leg,” said Dr. O’Neill, whereas other pumps available are used only in open-heart surgery. While Impella is the first pump to be used this way, he said it won’t be the last. Other, more powerful pumps are being developed.
 

DanGer Shock: A Leap Forward

Despite leading to the halt of another trial, the DanGer Shock results are a good news story, said the RECOVER IV investigators.

“The DanGer trial is a huge advance,” said Dr. O’Neill. “It’s the first study this century that shows something that improves survival in cardiogenic shock. You treat eight patients, and you save one life.” Dr. O’Neill said this is one of the best outcomes he has seen during his long career.

Dr. Kapur said the DanGer trial is also a leap forward in designing trials for cardiogenic shock. He said previous trials of mechanical support in cardiogenic shock had neutral results, probably due to broad inclusion criteria for patients.

“The DanGer trial was selective in its inclusion and exclusion criteria. That made it more difficult to enroll the population, so it took a lot longer. But it used the right device at the right time in the right patient, and it was successful,” he said.

“The DanGer investigators need to be applauded,” he added. “The lesson is, we have to design the right trials.”
 

New Cardiogenic Shock Trials

Dr. O’Neill and Dr. Kapur said the groundwork they laid for RECOVER IV can be used for new trials.

“We have 50 sites in the US, Germany, and Denmark. They’re interested, and they’re waiting,” said Dr. O’Neill. The researchers are poised to begin new trials once protocols are developed.

What will the next trials investigate?

DanGer Shock results showed higher rates of adverse events following Impella use than after standard care. “We need to come up with strategies to decrease bleeding problems and renal failure,” said Dr. O’Neill, and these could be tested in trials.

Other questions he would like to see investigated are using the Impella heart pump before or after angioplasty, and multi-vessel vs culprit-vessel percutaneous coronary intervention in cardiogenic shock with Impella support.

Dr. Kapur mentioned studying patients excluded from the DanGer Shock trial — such as those needing right ventricular support — because DanGer Shock covered only left ventricular support and those suffering cardiac arrest outside hospital. He said trials could compare differences between models of Impella and investigate the role of ECMO.

“I’m optimistic that we can design more randomized controlled trials with the right patient population and right treatment algorithm,” Dr. Kapur said. This is a critical step toward better outcomes for patients, he added. Another step is optimizing the design of heart pumps, which should decrease the rates of adverse events, he said. “I have a lot of optimism for the future of device design.”

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

An international trial of the Impella heart pump in patients with ST elevation myocardial infarction (STEMI) and cardiogenic shock has been stopped by the sponsor, Abiomed Inc. The termination followed news that another international trial, DanGer Shock, found that the pump improved survival in these patients.

Abiomed Inc., which manufactures the Impella microaxial flow pump, said in a statement that the trial’s Data and Safety Monitoring Board recommended stopping RECOVER IV.

“I was convinced that the study could not continue,” one of the principal investigators William O’Neill, MD, an interventional cardiologist with the Henry Ford Health in Detroit, said in an interview. After 3.5 years of work and thousands of person-hours, he added, “It’s not a decision that people took lightly.”

The trial already had three sites in Europe and one in the United States up and running, with two more US sites slated to join the trial. It had started enrolling patients, although few to date.

DanGer Shock trial results were expected to have a serious effect on how RECOVER IV would unfold. It was previously uncertain whether the Impella heart pump would save lives vs existing approaches, said O’Neill and co-principal investigator Navin Kapur, MD, an interventional cardiologist at Tufts Medical Center in Boston. Once the DanGer Shock trial showed the benefits of using the heart pump, that equipoise vanished.
 

Loss of Clinical Equipoise

“The clinicians were challenged in getting consent from patients where they had to say, ‘If you are randomized to the control arm, we are not able to use an Impella,’ ” said Dr. Kapur. He pointed out that patients would be unlikely to agree to participate in a trial where they might not get the treatment already shown to improve survival.

Dr. Kapur and Dr. O’Neill said the clinicians participating in the trial expressed discomfort at continuing. The RECOVER IV trial was expected to take many years to enroll the targeted number of patients. To participate, hospitals had to have the equipment and expertise to use the Impella heart pump, as well as the control treatments — balloon-pump support and extracorporeal membrane oxygenation (ECMO), Dr. Kapur explained. He said most patients with STEMI and cardiogenic shock would present to their nearest community hospitals, many of which would not have these treatments and would be unable to participate in the study.

Patients with STEMI and cardiogenic shock are uncommon. About 80,000 patients in the United States each year present with cardiogenic shock, of whom about 40% are not experiencing a STEMI, said Dr. O’Neill.

But those who do fit into the population of both STEMI and cardiogenic shock are at very high risk, said Dr. Kapur. “One in three or one in two patients with STEMI and cardiogenic shock will die in hospital.”
 

Getting Hearts Pumping

The Impella heart pump was originally developed by Impella Cardiosystems in Aachen, Germany, which was acquired by Abiomed in 2005, according to the Abiomed website. And Abiomed was acquired by Johnson & Johnson MedTech in 2022. The company has developed a series of models over the years and said that Impella CP — the model used in DanGer Shock and RECOVER IV trials — is the world’s smallest heart pump.

“Impella is the only heart pump that can be introduced percutaneously through the leg,” said Dr. O’Neill, whereas other pumps available are used only in open-heart surgery. While Impella is the first pump to be used this way, he said it won’t be the last. Other, more powerful pumps are being developed.
 

DanGer Shock: A Leap Forward

Despite leading to the halt of another trial, the DanGer Shock results are a good news story, said the RECOVER IV investigators.

“The DanGer trial is a huge advance,” said Dr. O’Neill. “It’s the first study this century that shows something that improves survival in cardiogenic shock. You treat eight patients, and you save one life.” Dr. O’Neill said this is one of the best outcomes he has seen during his long career.

Dr. Kapur said the DanGer trial is also a leap forward in designing trials for cardiogenic shock. He said previous trials of mechanical support in cardiogenic shock had neutral results, probably due to broad inclusion criteria for patients.

“The DanGer trial was selective in its inclusion and exclusion criteria. That made it more difficult to enroll the population, so it took a lot longer. But it used the right device at the right time in the right patient, and it was successful,” he said.

“The DanGer investigators need to be applauded,” he added. “The lesson is, we have to design the right trials.”
 

New Cardiogenic Shock Trials

Dr. O’Neill and Dr. Kapur said the groundwork they laid for RECOVER IV can be used for new trials.

“We have 50 sites in the US, Germany, and Denmark. They’re interested, and they’re waiting,” said Dr. O’Neill. The researchers are poised to begin new trials once protocols are developed.

What will the next trials investigate?

DanGer Shock results showed higher rates of adverse events following Impella use than after standard care. “We need to come up with strategies to decrease bleeding problems and renal failure,” said Dr. O’Neill, and these could be tested in trials.

Other questions he would like to see investigated are using the Impella heart pump before or after angioplasty, and multi-vessel vs culprit-vessel percutaneous coronary intervention in cardiogenic shock with Impella support.

Dr. Kapur mentioned studying patients excluded from the DanGer Shock trial — such as those needing right ventricular support — because DanGer Shock covered only left ventricular support and those suffering cardiac arrest outside hospital. He said trials could compare differences between models of Impella and investigate the role of ECMO.

“I’m optimistic that we can design more randomized controlled trials with the right patient population and right treatment algorithm,” Dr. Kapur said. This is a critical step toward better outcomes for patients, he added. Another step is optimizing the design of heart pumps, which should decrease the rates of adverse events, he said. “I have a lot of optimism for the future of device design.”

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

It is a great day when a patient shows up at clinical appointment already motivated to make lifestyle behavior changes. Often, they have been inspired by health information they consumed elsewhere, such as from a book, movie, documentary, TV show, a friend, or something out in the community.

Currently, one of the more public representations of health and longevity promotion is Blue Zones. The organization, named for specific areas of the world — the so-called blue zones, where people experience less disease and live longer lives — has created considerable public awareness for healthy living. Today, there are more than 75 Blue Zones Project communities across the United States, where community leaders, businesses, organizations, and citizens collaborate to make healthier choices the easier choices. A recent Netflix special, Live to 100: Secrets of the Blue Zones, further propelled blue zones into the public consciousness.

For clinicians trained in lifestyle medicine, Blue Zones’ consumer awareness is an opportunity. There is considerable crossover between the lifestyle habits advocated by Blue Zones, known as the Power9, and the six pillars of lifestyle medicine. The Blue Zones emphasis on “plant-slant” diet, natural movement, purpose and contribution, downshifting, and family and community intersect with the lifestyle medicine pillars of whole-food, plant-predominant eating patterns, regular physical activity, stress management, restorative sleep, and positive social connections. Both Blue Zones and lifestyle medicine share a goal of creating healthier and stronger individuals and communities.

For those reasons, it made perfect sense that Blue Zones and the American College of Lifestyle Medicine (ACLM) recently announced a partnership to synergize both organizations’ strengths and resources. Among other things, the collaboration will establish a new certification status of Blue Zones–Certified Physician or Blue Zones–Certified Healthcare Professional, available in 2025 exclusively to clinicians who already are or become certified in lifestyle medicine.

Because of Blue Zones’ considerable consumer awareness, physicians and other health professionals who earn the certification will stand out to potential patients as clinicians with the training and knowledge to help them make sustainable lifestyle behavior changes. A challenging part of any clinician’s job is educating and convincing patients on the proven health benefits of lifestyle behavior change within the time restraints of a routine clinical visit. Patients familiar with Blue Zones are more likely to arrive already interested in changing lifestyle behavior, and clinicians should have the skills to help them achieve their goals.

In addition, community infrastructure developed through Blue Zones that supports healthful lifestyle choices is significant for patients. Lack of resources in their home, work, and community environments is a common obstacle that patients cite when discussing lifestyle change with a clinician. Bicycle lanes for commuting, parks with exercise equipment, accessible healthy food options, and community events to facilitate positive social connections enhance lifestyle-medicine prescriptions. Workplaces, restaurants, places of worship, and grocery stores are examples of community stakeholders that collaborate in Blue Zones communities to promote healthy lifestyle decisions. Although lifestyle medicine clinicians can and do identify creative ways to support patients in communities without strong healthy choice infrastructure, the Blue Zones road map is a welcome companion.

The timing is right for this synthesis of Blue Zones and lifestyle medicine. As consumer interest in Blue Zones has risen, so has clinician interest in evidence-based lifestyle medicine. Since certification in lifestyle medicine began in 2017, almost 6700 physicians and other health professionals have become certified worldwide. More than 43,000 health care professionals have registered for ACLM’s complimentary lifestyle and food-as-medicine courses highlighted by the White House Conference on Hunger, Nutrition, and Health. 

What if more patients came to us motivated to make lifestyle changes because of awareness infused in their work and supported in their surrounding community? Matching lifestyle medicine certification with Blue Zone communities equips clinicians to help these patients achieve what they really want: to live longer and better.

Dr. Collings is Director of Lifestyle Medicine, Silicon Valley Medical Development, and Past President, American College of Lifestyle Medicine, Mountain View, California. She has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

It is a great day when a patient shows up at clinical appointment already motivated to make lifestyle behavior changes. Often, they have been inspired by health information they consumed elsewhere, such as from a book, movie, documentary, TV show, a friend, or something out in the community.

Currently, one of the more public representations of health and longevity promotion is Blue Zones. The organization, named for specific areas of the world — the so-called blue zones, where people experience less disease and live longer lives — has created considerable public awareness for healthy living. Today, there are more than 75 Blue Zones Project communities across the United States, where community leaders, businesses, organizations, and citizens collaborate to make healthier choices the easier choices. A recent Netflix special, Live to 100: Secrets of the Blue Zones, further propelled blue zones into the public consciousness.

For clinicians trained in lifestyle medicine, Blue Zones’ consumer awareness is an opportunity. There is considerable crossover between the lifestyle habits advocated by Blue Zones, known as the Power9, and the six pillars of lifestyle medicine. The Blue Zones emphasis on “plant-slant” diet, natural movement, purpose and contribution, downshifting, and family and community intersect with the lifestyle medicine pillars of whole-food, plant-predominant eating patterns, regular physical activity, stress management, restorative sleep, and positive social connections. Both Blue Zones and lifestyle medicine share a goal of creating healthier and stronger individuals and communities.

For those reasons, it made perfect sense that Blue Zones and the American College of Lifestyle Medicine (ACLM) recently announced a partnership to synergize both organizations’ strengths and resources. Among other things, the collaboration will establish a new certification status of Blue Zones–Certified Physician or Blue Zones–Certified Healthcare Professional, available in 2025 exclusively to clinicians who already are or become certified in lifestyle medicine.

Because of Blue Zones’ considerable consumer awareness, physicians and other health professionals who earn the certification will stand out to potential patients as clinicians with the training and knowledge to help them make sustainable lifestyle behavior changes. A challenging part of any clinician’s job is educating and convincing patients on the proven health benefits of lifestyle behavior change within the time restraints of a routine clinical visit. Patients familiar with Blue Zones are more likely to arrive already interested in changing lifestyle behavior, and clinicians should have the skills to help them achieve their goals.

In addition, community infrastructure developed through Blue Zones that supports healthful lifestyle choices is significant for patients. Lack of resources in their home, work, and community environments is a common obstacle that patients cite when discussing lifestyle change with a clinician. Bicycle lanes for commuting, parks with exercise equipment, accessible healthy food options, and community events to facilitate positive social connections enhance lifestyle-medicine prescriptions. Workplaces, restaurants, places of worship, and grocery stores are examples of community stakeholders that collaborate in Blue Zones communities to promote healthy lifestyle decisions. Although lifestyle medicine clinicians can and do identify creative ways to support patients in communities without strong healthy choice infrastructure, the Blue Zones road map is a welcome companion.

The timing is right for this synthesis of Blue Zones and lifestyle medicine. As consumer interest in Blue Zones has risen, so has clinician interest in evidence-based lifestyle medicine. Since certification in lifestyle medicine began in 2017, almost 6700 physicians and other health professionals have become certified worldwide. More than 43,000 health care professionals have registered for ACLM’s complimentary lifestyle and food-as-medicine courses highlighted by the White House Conference on Hunger, Nutrition, and Health. 

What if more patients came to us motivated to make lifestyle changes because of awareness infused in their work and supported in their surrounding community? Matching lifestyle medicine certification with Blue Zone communities equips clinicians to help these patients achieve what they really want: to live longer and better.

Dr. Collings is Director of Lifestyle Medicine, Silicon Valley Medical Development, and Past President, American College of Lifestyle Medicine, Mountain View, California. She has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

It is a great day when a patient shows up at clinical appointment already motivated to make lifestyle behavior changes. Often, they have been inspired by health information they consumed elsewhere, such as from a book, movie, documentary, TV show, a friend, or something out in the community.

Currently, one of the more public representations of health and longevity promotion is Blue Zones. The organization, named for specific areas of the world — the so-called blue zones, where people experience less disease and live longer lives — has created considerable public awareness for healthy living. Today, there are more than 75 Blue Zones Project communities across the United States, where community leaders, businesses, organizations, and citizens collaborate to make healthier choices the easier choices. A recent Netflix special, Live to 100: Secrets of the Blue Zones, further propelled blue zones into the public consciousness.

For clinicians trained in lifestyle medicine, Blue Zones’ consumer awareness is an opportunity. There is considerable crossover between the lifestyle habits advocated by Blue Zones, known as the Power9, and the six pillars of lifestyle medicine. The Blue Zones emphasis on “plant-slant” diet, natural movement, purpose and contribution, downshifting, and family and community intersect with the lifestyle medicine pillars of whole-food, plant-predominant eating patterns, regular physical activity, stress management, restorative sleep, and positive social connections. Both Blue Zones and lifestyle medicine share a goal of creating healthier and stronger individuals and communities.

For those reasons, it made perfect sense that Blue Zones and the American College of Lifestyle Medicine (ACLM) recently announced a partnership to synergize both organizations’ strengths and resources. Among other things, the collaboration will establish a new certification status of Blue Zones–Certified Physician or Blue Zones–Certified Healthcare Professional, available in 2025 exclusively to clinicians who already are or become certified in lifestyle medicine.

Because of Blue Zones’ considerable consumer awareness, physicians and other health professionals who earn the certification will stand out to potential patients as clinicians with the training and knowledge to help them make sustainable lifestyle behavior changes. A challenging part of any clinician’s job is educating and convincing patients on the proven health benefits of lifestyle behavior change within the time restraints of a routine clinical visit. Patients familiar with Blue Zones are more likely to arrive already interested in changing lifestyle behavior, and clinicians should have the skills to help them achieve their goals.

In addition, community infrastructure developed through Blue Zones that supports healthful lifestyle choices is significant for patients. Lack of resources in their home, work, and community environments is a common obstacle that patients cite when discussing lifestyle change with a clinician. Bicycle lanes for commuting, parks with exercise equipment, accessible healthy food options, and community events to facilitate positive social connections enhance lifestyle-medicine prescriptions. Workplaces, restaurants, places of worship, and grocery stores are examples of community stakeholders that collaborate in Blue Zones communities to promote healthy lifestyle decisions. Although lifestyle medicine clinicians can and do identify creative ways to support patients in communities without strong healthy choice infrastructure, the Blue Zones road map is a welcome companion.

The timing is right for this synthesis of Blue Zones and lifestyle medicine. As consumer interest in Blue Zones has risen, so has clinician interest in evidence-based lifestyle medicine. Since certification in lifestyle medicine began in 2017, almost 6700 physicians and other health professionals have become certified worldwide. More than 43,000 health care professionals have registered for ACLM’s complimentary lifestyle and food-as-medicine courses highlighted by the White House Conference on Hunger, Nutrition, and Health. 

What if more patients came to us motivated to make lifestyle changes because of awareness infused in their work and supported in their surrounding community? Matching lifestyle medicine certification with Blue Zone communities equips clinicians to help these patients achieve what they really want: to live longer and better.

Dr. Collings is Director of Lifestyle Medicine, Silicon Valley Medical Development, and Past President, American College of Lifestyle Medicine, Mountain View, California. She has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Strict sodium intake — with or without restrictions on fluid intake — is unlikely to confer clinical benefits on patients with heart failure, reported investigators.

Their review of studies showed sodium should only be moderately restricted because “patients are more likely to follow instructions that are not too draconian, and there is no evidence that severe sodium restriction saves lives or delays hospital admissions.”

In fact, moderate daily intake of sodium (3.0-4.5 g) may improve the quality of life and functional status of these patients, even if it will not improve life expectancy or the hospitalization rate, Paolo Raggi, MD, from the University of Alberta, Edmonton, Alberta, Canada, explained in his narrative review published online in the European Journal of Clinical Investigation.

“It is always a little hard to give up long-held beliefs, and you try to find fault in the new evidence before your eyes,” he said.

Dr. Raggi, who is also coeditor of Atherosclerosis, explained this work was prompted in part by the large, multicenter SODIUM-HF study, which showed that sodium restriction did not reduce the composite outcome of all-cause mortality, cardiovascular hospitalization, and cardiovascular-related emergency department visits, although it did improve quality of life and New York Heart Association class.

And “excessive fluid restriction — typically we were taught to restrict fluid intake to 1 L/d or, at the most, 1.5 L — does not reduce mortality or hospitalization rates and inflicts unnecessary strain and pain on patients,” he said. “Clinicians need to get on board with this novel information.”
 

Examining the Evidence

For the narrative review, the researchers conducted a literature search for the terms heart failure, salt, sodium, and fluid intake to identify relevant reports.

Most randomized trials were small and examined widely heterogeneous interventions. The identified trials published from 2000 to 2021 had populations that ranged from 12 to 203 participants, had inpatients and outpatients, and included people with reduced and preserved ejection fraction. Sodium interventions varied from extreme reductions (< 800 mg/d) to more moderate approaches (2-3 g/d). No study, regardless of the level of restriction, showed a reduction in mortality or hospitalization rates.

Notably, SODIUM-HF — the randomized clinical trial of sodium restriction to a target of 1.5 g/d — was stopped early after an interim analysis demonstrated the futility of the intervention, and the COVID pandemic made it difficult to continue the trial.

Although a moderate sodium intake of 3-4.5 g/d “seems prudent” for patients with recurrent hospital admissions and fluid overload, an intake of 2-3 g/d may be a more acceptable level. “A more aggressive sodium restriction may be necessary in the presence of chronic kidney disease, where the handling of sodium by the kidneys is hampered,” Dr. Raggi reported.

“The debate on tight sodium restriction in heart failure continues to appear in major medical journals, yet it would seem that after many years of controversy, the time has come to close it,” he said.
 

‘One Approach Does Not Fit All’

Sodium restriction is difficult to quantify in a large cohort of patients because many studies are based on recall questionnaires and qualitative measurements, said Johanna Contreras, MD, an advanced heart failure and transplant cardiologist at the Mount Sinai Fuster Heart Hospital in New York City.

“Many patients are not aware that processed and precooked foods are very high in sodium and don’t count them as sodium-rich foods,” she said.

Nevertheless, heart failure has many etiologies and stages, so “one approach does not fit all,” she said. For example, patients with stage C heart failure “will clearly get more decompensated when they consume sodium-rich diets, which will increase water absorption.” And patients with heart failure secondary to hypertension are “particularly susceptible” and are likely to become more symptomatic and acutely congestive on diets high in sodium and water, which can increase both morbidity and mortality.

“It is important to understand the kinds of patients we are referring to, how advanced they are, and what comorbidities the patients have,” she said. “We also know that there are race, ethnicity, and gender differences in sensitivity to sodium.”

We should aim for a moderate sodium intake, she said, but patients with high sensitivity, multiple comorbidities, kidney disease, and certain demographic characteristics “need to be more careful.”

Overall, “patients should aim to consume fresh fruits and vegetables and [be aware of] processed foods and adding salt at the table when they are eating,” Dr. Contreras said.

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

Strict sodium intake — with or without restrictions on fluid intake — is unlikely to confer clinical benefits on patients with heart failure, reported investigators.

Their review of studies showed sodium should only be moderately restricted because “patients are more likely to follow instructions that are not too draconian, and there is no evidence that severe sodium restriction saves lives or delays hospital admissions.”

In fact, moderate daily intake of sodium (3.0-4.5 g) may improve the quality of life and functional status of these patients, even if it will not improve life expectancy or the hospitalization rate, Paolo Raggi, MD, from the University of Alberta, Edmonton, Alberta, Canada, explained in his narrative review published online in the European Journal of Clinical Investigation.

“It is always a little hard to give up long-held beliefs, and you try to find fault in the new evidence before your eyes,” he said.

Dr. Raggi, who is also coeditor of Atherosclerosis, explained this work was prompted in part by the large, multicenter SODIUM-HF study, which showed that sodium restriction did not reduce the composite outcome of all-cause mortality, cardiovascular hospitalization, and cardiovascular-related emergency department visits, although it did improve quality of life and New York Heart Association class.

And “excessive fluid restriction — typically we were taught to restrict fluid intake to 1 L/d or, at the most, 1.5 L — does not reduce mortality or hospitalization rates and inflicts unnecessary strain and pain on patients,” he said. “Clinicians need to get on board with this novel information.”
 

Examining the Evidence

For the narrative review, the researchers conducted a literature search for the terms heart failure, salt, sodium, and fluid intake to identify relevant reports.

Most randomized trials were small and examined widely heterogeneous interventions. The identified trials published from 2000 to 2021 had populations that ranged from 12 to 203 participants, had inpatients and outpatients, and included people with reduced and preserved ejection fraction. Sodium interventions varied from extreme reductions (< 800 mg/d) to more moderate approaches (2-3 g/d). No study, regardless of the level of restriction, showed a reduction in mortality or hospitalization rates.

Notably, SODIUM-HF — the randomized clinical trial of sodium restriction to a target of 1.5 g/d — was stopped early after an interim analysis demonstrated the futility of the intervention, and the COVID pandemic made it difficult to continue the trial.

Although a moderate sodium intake of 3-4.5 g/d “seems prudent” for patients with recurrent hospital admissions and fluid overload, an intake of 2-3 g/d may be a more acceptable level. “A more aggressive sodium restriction may be necessary in the presence of chronic kidney disease, where the handling of sodium by the kidneys is hampered,” Dr. Raggi reported.

“The debate on tight sodium restriction in heart failure continues to appear in major medical journals, yet it would seem that after many years of controversy, the time has come to close it,” he said.
 

‘One Approach Does Not Fit All’

Sodium restriction is difficult to quantify in a large cohort of patients because many studies are based on recall questionnaires and qualitative measurements, said Johanna Contreras, MD, an advanced heart failure and transplant cardiologist at the Mount Sinai Fuster Heart Hospital in New York City.

“Many patients are not aware that processed and precooked foods are very high in sodium and don’t count them as sodium-rich foods,” she said.

Nevertheless, heart failure has many etiologies and stages, so “one approach does not fit all,” she said. For example, patients with stage C heart failure “will clearly get more decompensated when they consume sodium-rich diets, which will increase water absorption.” And patients with heart failure secondary to hypertension are “particularly susceptible” and are likely to become more symptomatic and acutely congestive on diets high in sodium and water, which can increase both morbidity and mortality.

“It is important to understand the kinds of patients we are referring to, how advanced they are, and what comorbidities the patients have,” she said. “We also know that there are race, ethnicity, and gender differences in sensitivity to sodium.”

We should aim for a moderate sodium intake, she said, but patients with high sensitivity, multiple comorbidities, kidney disease, and certain demographic characteristics “need to be more careful.”

Overall, “patients should aim to consume fresh fruits and vegetables and [be aware of] processed foods and adding salt at the table when they are eating,” Dr. Contreras said.

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

Strict sodium intake — with or without restrictions on fluid intake — is unlikely to confer clinical benefits on patients with heart failure, reported investigators.

Their review of studies showed sodium should only be moderately restricted because “patients are more likely to follow instructions that are not too draconian, and there is no evidence that severe sodium restriction saves lives or delays hospital admissions.”

In fact, moderate daily intake of sodium (3.0-4.5 g) may improve the quality of life and functional status of these patients, even if it will not improve life expectancy or the hospitalization rate, Paolo Raggi, MD, from the University of Alberta, Edmonton, Alberta, Canada, explained in his narrative review published online in the European Journal of Clinical Investigation.

“It is always a little hard to give up long-held beliefs, and you try to find fault in the new evidence before your eyes,” he said.

Dr. Raggi, who is also coeditor of Atherosclerosis, explained this work was prompted in part by the large, multicenter SODIUM-HF study, which showed that sodium restriction did not reduce the composite outcome of all-cause mortality, cardiovascular hospitalization, and cardiovascular-related emergency department visits, although it did improve quality of life and New York Heart Association class.

And “excessive fluid restriction — typically we were taught to restrict fluid intake to 1 L/d or, at the most, 1.5 L — does not reduce mortality or hospitalization rates and inflicts unnecessary strain and pain on patients,” he said. “Clinicians need to get on board with this novel information.”
 

Examining the Evidence

For the narrative review, the researchers conducted a literature search for the terms heart failure, salt, sodium, and fluid intake to identify relevant reports.

Most randomized trials were small and examined widely heterogeneous interventions. The identified trials published from 2000 to 2021 had populations that ranged from 12 to 203 participants, had inpatients and outpatients, and included people with reduced and preserved ejection fraction. Sodium interventions varied from extreme reductions (< 800 mg/d) to more moderate approaches (2-3 g/d). No study, regardless of the level of restriction, showed a reduction in mortality or hospitalization rates.

Notably, SODIUM-HF — the randomized clinical trial of sodium restriction to a target of 1.5 g/d — was stopped early after an interim analysis demonstrated the futility of the intervention, and the COVID pandemic made it difficult to continue the trial.

Although a moderate sodium intake of 3-4.5 g/d “seems prudent” for patients with recurrent hospital admissions and fluid overload, an intake of 2-3 g/d may be a more acceptable level. “A more aggressive sodium restriction may be necessary in the presence of chronic kidney disease, where the handling of sodium by the kidneys is hampered,” Dr. Raggi reported.

“The debate on tight sodium restriction in heart failure continues to appear in major medical journals, yet it would seem that after many years of controversy, the time has come to close it,” he said.
 

‘One Approach Does Not Fit All’

Sodium restriction is difficult to quantify in a large cohort of patients because many studies are based on recall questionnaires and qualitative measurements, said Johanna Contreras, MD, an advanced heart failure and transplant cardiologist at the Mount Sinai Fuster Heart Hospital in New York City.

“Many patients are not aware that processed and precooked foods are very high in sodium and don’t count them as sodium-rich foods,” she said.

Nevertheless, heart failure has many etiologies and stages, so “one approach does not fit all,” she said. For example, patients with stage C heart failure “will clearly get more decompensated when they consume sodium-rich diets, which will increase water absorption.” And patients with heart failure secondary to hypertension are “particularly susceptible” and are likely to become more symptomatic and acutely congestive on diets high in sodium and water, which can increase both morbidity and mortality.

“It is important to understand the kinds of patients we are referring to, how advanced they are, and what comorbidities the patients have,” she said. “We also know that there are race, ethnicity, and gender differences in sensitivity to sodium.”

We should aim for a moderate sodium intake, she said, but patients with high sensitivity, multiple comorbidities, kidney disease, and certain demographic characteristics “need to be more careful.”

Overall, “patients should aim to consume fresh fruits and vegetables and [be aware of] processed foods and adding salt at the table when they are eating,” Dr. Contreras said.

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

Replacing meat with plant-based meat alternatives (PBMAs) can improve cardiovascular disease risk factors, including low-density lipoprotein cholesterol (LDL-C), a review of randomized controlled trials suggested.

Long-term randomized controlled trials and prospective cohort studies that evaluate cardiovascular disease events such as myocardial infarction and stroke are needed to draw definitive conclusions, according to the authors.

“Our take-home is that plant-based meats are a healthy alternative to animal meat, based on intermediate cardiovascular endpoints such as lipids, triglycerides, blood pressure, and other cardiovascular disease risk factors,” said senior author Ehud Ur, MB, professor of medicine at the University of British Columbia, Vancouver, in Canada, and an endocrinologist at St. Paul’s Hospital in Vancouver.

“However, we also found that there’s a lack of clinical outcome trials that would determine definitively whether plant-based meats are healthy. But certainly, everything points in the direction of cardiovascular benefit,” said Dr. Ur.

The review was published on June 25 in the Canadian Journal of Cardiology.
 

Ultraprocessed Foods

PBMAs are foods that mimic meats and contain ingredients such as protein derivatives from soy, pea, wheat, and fungi. A growing number of Canadians are limiting meat or excluding it from their diets. Some are opting to eat PBMAs instead.

But most PBMAs are classified as ultraprocessed foods. Such foods are produced primarily from substances extracted from whole food sources, such as sugar, salt, oil, and protein. Alternatively, they may be created in a laboratory using flavor enhancers and food coloring. This classification has caused the public and health professionals to question the potential health implications of PBMAs, said Dr. Ur.

“One of the concerns is that these products are highly processed, and things that are highly processed are considered bad. And so, are you swapping one set of risks for another?” he said.

To shed more light on this question, Dr. Ur’s team, which was led by Matthew Nagra, ND, of the Vancouver Naturopathic Clinic, assessed the literature on PBMAs and their impact on health.

“While the plant-based meat market has experienced significant growth in recent years and more and more Canadians are enjoying plant-based burgers, surprisingly little is known about how these meat alternatives may impact health and, in particular, cardiovascular disease risk,” Dr. Nagra said in a statement. “Thus, we sought to review the available literature on the topic to identify what is currently known and to provide direction for future research.”
 

Less Saturated Fat, Cholesterol

The researchers assessed the literature that was published from 1970 to 2023 on PBMAs, their contents, nutritional profiles, and impact on cardiovascular disease risk factors, such as cholesterol levels and blood pressure.

They found that, compared with meat, PBMAs had less saturated fat, less cholesterol, more fiber, more carbohydrates, fewer calories, less monounsaturated fat, more polyunsaturated fat, and more sodium.

In addition, several randomized controlled trials showed that PBMAs reduced total cholesterol and LDL-C, as well as apolipoprotein B-100, body weight, and waist circumference. PBMAs were not shown to raise blood pressure, despite some products’ high sodium content.

“No currently available evidence suggests that the concerning aspects of PBMAs (eg, food processing and high sodium content) negate the potential cardiovascular benefits,” wrote the researchers.

Unfortunately, no long-term research has evaluated how these alternatives may affect the risk of developing a myocardial infarction or stroke. Similarly, there is little research on the healthfulness of some common components of PBMAs, such as vital wheat gluten.

To shed light on these important issues would require large clinical trials, involving many patients, and great expense, said Dr. Ur. “Drug companies can afford to do large clinical trials, even if they are expensive to do, because they must do them to get approval for their drug. But these plant-based meats are produced by companies that most likely are not able to do clinical outcome trials. Such trials would have to be done by the National Institutes of Health in the United States, or in Canada, the National Research Council,” he said.

There are many reasons to avoid meat, Dr. Ur added. “There are ethical reasons against killing animals. Then there is the issue of global warming. Meat is a very expensive source of food energy. As an individual, the biggest impact you can make on global warming is to not eat meat. Then there is the argument about personal health, which is where our study comes in. For those people who like the taste of meat and who struggle with giving it up, the PBMAs allow them to have a reasonably diverse diet,” he said.
 

Are Eggs Healthy?

Meat substitutes are helpful for people who want to reduce their cardiovascular disease risk, J. David Spence, MD, professor emeritus of neurology and clinical pharmacology at the University of Western Ontario in London, Canada, wrote in an accompanying editorial.

“Eating too much meat and egg yolk increases cardiovascular risk, and it’s a challenge for patients to learn to eat less meat and cut out egg yolks. If we can find good substitutes that are tasty and enjoyable, that’s a good thing,” Dr. Spence told this news organization.

“Besides plant-based meat substitutes, there is great potential for reduction of cardiovascular risk with the use of egg substitutes,” he said.

Dr. Spence pointed out that two large egg yolks contain 474 mg of cholesterol, almost twice the amount contained in a Hardee’s Monster Thickburger (265 mg).

Cholesterol elevates plasma levels of toxic metabolites of the intestinal microbiome, such as trimethylamine N-oxide (TMAO). Plasma levels of TMAO increase in a linear fashion with egg consumption, and TMAO is bad for the arteries, said Dr. Spence.

“Eggs are terrible and should not be eaten by people at risk for cardiovascular disease. But people don’t understand that because the egg marketing propaganda has been so effective. The yolk is terrible. The egg marketing board is extremely effective in persuading people that eggs are healthy, and they’re not.”

Dr. Spence recommends using egg substitutes, such as Egg Beaters or Better’n Eggs, instead of whole eggs, and says it’s never too late to switch. “That’s the mistake people make, but the arteries can actually improve,” he said.

No funding source for the study was reported. Dr. Ur and Dr. Spence reported having no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

Replacing meat with plant-based meat alternatives (PBMAs) can improve cardiovascular disease risk factors, including low-density lipoprotein cholesterol (LDL-C), a review of randomized controlled trials suggested.

Long-term randomized controlled trials and prospective cohort studies that evaluate cardiovascular disease events such as myocardial infarction and stroke are needed to draw definitive conclusions, according to the authors.

“Our take-home is that plant-based meats are a healthy alternative to animal meat, based on intermediate cardiovascular endpoints such as lipids, triglycerides, blood pressure, and other cardiovascular disease risk factors,” said senior author Ehud Ur, MB, professor of medicine at the University of British Columbia, Vancouver, in Canada, and an endocrinologist at St. Paul’s Hospital in Vancouver.

“However, we also found that there’s a lack of clinical outcome trials that would determine definitively whether plant-based meats are healthy. But certainly, everything points in the direction of cardiovascular benefit,” said Dr. Ur.

The review was published on June 25 in the Canadian Journal of Cardiology.
 

Ultraprocessed Foods

PBMAs are foods that mimic meats and contain ingredients such as protein derivatives from soy, pea, wheat, and fungi. A growing number of Canadians are limiting meat or excluding it from their diets. Some are opting to eat PBMAs instead.

But most PBMAs are classified as ultraprocessed foods. Such foods are produced primarily from substances extracted from whole food sources, such as sugar, salt, oil, and protein. Alternatively, they may be created in a laboratory using flavor enhancers and food coloring. This classification has caused the public and health professionals to question the potential health implications of PBMAs, said Dr. Ur.

“One of the concerns is that these products are highly processed, and things that are highly processed are considered bad. And so, are you swapping one set of risks for another?” he said.

To shed more light on this question, Dr. Ur’s team, which was led by Matthew Nagra, ND, of the Vancouver Naturopathic Clinic, assessed the literature on PBMAs and their impact on health.

“While the plant-based meat market has experienced significant growth in recent years and more and more Canadians are enjoying plant-based burgers, surprisingly little is known about how these meat alternatives may impact health and, in particular, cardiovascular disease risk,” Dr. Nagra said in a statement. “Thus, we sought to review the available literature on the topic to identify what is currently known and to provide direction for future research.”
 

Less Saturated Fat, Cholesterol

The researchers assessed the literature that was published from 1970 to 2023 on PBMAs, their contents, nutritional profiles, and impact on cardiovascular disease risk factors, such as cholesterol levels and blood pressure.

They found that, compared with meat, PBMAs had less saturated fat, less cholesterol, more fiber, more carbohydrates, fewer calories, less monounsaturated fat, more polyunsaturated fat, and more sodium.

In addition, several randomized controlled trials showed that PBMAs reduced total cholesterol and LDL-C, as well as apolipoprotein B-100, body weight, and waist circumference. PBMAs were not shown to raise blood pressure, despite some products’ high sodium content.

“No currently available evidence suggests that the concerning aspects of PBMAs (eg, food processing and high sodium content) negate the potential cardiovascular benefits,” wrote the researchers.

Unfortunately, no long-term research has evaluated how these alternatives may affect the risk of developing a myocardial infarction or stroke. Similarly, there is little research on the healthfulness of some common components of PBMAs, such as vital wheat gluten.

To shed light on these important issues would require large clinical trials, involving many patients, and great expense, said Dr. Ur. “Drug companies can afford to do large clinical trials, even if they are expensive to do, because they must do them to get approval for their drug. But these plant-based meats are produced by companies that most likely are not able to do clinical outcome trials. Such trials would have to be done by the National Institutes of Health in the United States, or in Canada, the National Research Council,” he said.

There are many reasons to avoid meat, Dr. Ur added. “There are ethical reasons against killing animals. Then there is the issue of global warming. Meat is a very expensive source of food energy. As an individual, the biggest impact you can make on global warming is to not eat meat. Then there is the argument about personal health, which is where our study comes in. For those people who like the taste of meat and who struggle with giving it up, the PBMAs allow them to have a reasonably diverse diet,” he said.
 

Are Eggs Healthy?

Meat substitutes are helpful for people who want to reduce their cardiovascular disease risk, J. David Spence, MD, professor emeritus of neurology and clinical pharmacology at the University of Western Ontario in London, Canada, wrote in an accompanying editorial.

“Eating too much meat and egg yolk increases cardiovascular risk, and it’s a challenge for patients to learn to eat less meat and cut out egg yolks. If we can find good substitutes that are tasty and enjoyable, that’s a good thing,” Dr. Spence told this news organization.

“Besides plant-based meat substitutes, there is great potential for reduction of cardiovascular risk with the use of egg substitutes,” he said.

Dr. Spence pointed out that two large egg yolks contain 474 mg of cholesterol, almost twice the amount contained in a Hardee’s Monster Thickburger (265 mg).

Cholesterol elevates plasma levels of toxic metabolites of the intestinal microbiome, such as trimethylamine N-oxide (TMAO). Plasma levels of TMAO increase in a linear fashion with egg consumption, and TMAO is bad for the arteries, said Dr. Spence.

“Eggs are terrible and should not be eaten by people at risk for cardiovascular disease. But people don’t understand that because the egg marketing propaganda has been so effective. The yolk is terrible. The egg marketing board is extremely effective in persuading people that eggs are healthy, and they’re not.”

Dr. Spence recommends using egg substitutes, such as Egg Beaters or Better’n Eggs, instead of whole eggs, and says it’s never too late to switch. “That’s the mistake people make, but the arteries can actually improve,” he said.

No funding source for the study was reported. Dr. Ur and Dr. Spence reported having no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

Replacing meat with plant-based meat alternatives (PBMAs) can improve cardiovascular disease risk factors, including low-density lipoprotein cholesterol (LDL-C), a review of randomized controlled trials suggested.

Long-term randomized controlled trials and prospective cohort studies that evaluate cardiovascular disease events such as myocardial infarction and stroke are needed to draw definitive conclusions, according to the authors.

“Our take-home is that plant-based meats are a healthy alternative to animal meat, based on intermediate cardiovascular endpoints such as lipids, triglycerides, blood pressure, and other cardiovascular disease risk factors,” said senior author Ehud Ur, MB, professor of medicine at the University of British Columbia, Vancouver, in Canada, and an endocrinologist at St. Paul’s Hospital in Vancouver.

“However, we also found that there’s a lack of clinical outcome trials that would determine definitively whether plant-based meats are healthy. But certainly, everything points in the direction of cardiovascular benefit,” said Dr. Ur.

The review was published on June 25 in the Canadian Journal of Cardiology.
 

Ultraprocessed Foods

PBMAs are foods that mimic meats and contain ingredients such as protein derivatives from soy, pea, wheat, and fungi. A growing number of Canadians are limiting meat or excluding it from their diets. Some are opting to eat PBMAs instead.

But most PBMAs are classified as ultraprocessed foods. Such foods are produced primarily from substances extracted from whole food sources, such as sugar, salt, oil, and protein. Alternatively, they may be created in a laboratory using flavor enhancers and food coloring. This classification has caused the public and health professionals to question the potential health implications of PBMAs, said Dr. Ur.

“One of the concerns is that these products are highly processed, and things that are highly processed are considered bad. And so, are you swapping one set of risks for another?” he said.

To shed more light on this question, Dr. Ur’s team, which was led by Matthew Nagra, ND, of the Vancouver Naturopathic Clinic, assessed the literature on PBMAs and their impact on health.

“While the plant-based meat market has experienced significant growth in recent years and more and more Canadians are enjoying plant-based burgers, surprisingly little is known about how these meat alternatives may impact health and, in particular, cardiovascular disease risk,” Dr. Nagra said in a statement. “Thus, we sought to review the available literature on the topic to identify what is currently known and to provide direction for future research.”
 

Less Saturated Fat, Cholesterol

The researchers assessed the literature that was published from 1970 to 2023 on PBMAs, their contents, nutritional profiles, and impact on cardiovascular disease risk factors, such as cholesterol levels and blood pressure.

They found that, compared with meat, PBMAs had less saturated fat, less cholesterol, more fiber, more carbohydrates, fewer calories, less monounsaturated fat, more polyunsaturated fat, and more sodium.

In addition, several randomized controlled trials showed that PBMAs reduced total cholesterol and LDL-C, as well as apolipoprotein B-100, body weight, and waist circumference. PBMAs were not shown to raise blood pressure, despite some products’ high sodium content.

“No currently available evidence suggests that the concerning aspects of PBMAs (eg, food processing and high sodium content) negate the potential cardiovascular benefits,” wrote the researchers.

Unfortunately, no long-term research has evaluated how these alternatives may affect the risk of developing a myocardial infarction or stroke. Similarly, there is little research on the healthfulness of some common components of PBMAs, such as vital wheat gluten.

To shed light on these important issues would require large clinical trials, involving many patients, and great expense, said Dr. Ur. “Drug companies can afford to do large clinical trials, even if they are expensive to do, because they must do them to get approval for their drug. But these plant-based meats are produced by companies that most likely are not able to do clinical outcome trials. Such trials would have to be done by the National Institutes of Health in the United States, or in Canada, the National Research Council,” he said.

There are many reasons to avoid meat, Dr. Ur added. “There are ethical reasons against killing animals. Then there is the issue of global warming. Meat is a very expensive source of food energy. As an individual, the biggest impact you can make on global warming is to not eat meat. Then there is the argument about personal health, which is where our study comes in. For those people who like the taste of meat and who struggle with giving it up, the PBMAs allow them to have a reasonably diverse diet,” he said.
 

Are Eggs Healthy?

Meat substitutes are helpful for people who want to reduce their cardiovascular disease risk, J. David Spence, MD, professor emeritus of neurology and clinical pharmacology at the University of Western Ontario in London, Canada, wrote in an accompanying editorial.

“Eating too much meat and egg yolk increases cardiovascular risk, and it’s a challenge for patients to learn to eat less meat and cut out egg yolks. If we can find good substitutes that are tasty and enjoyable, that’s a good thing,” Dr. Spence told this news organization.

“Besides plant-based meat substitutes, there is great potential for reduction of cardiovascular risk with the use of egg substitutes,” he said.

Dr. Spence pointed out that two large egg yolks contain 474 mg of cholesterol, almost twice the amount contained in a Hardee’s Monster Thickburger (265 mg).

Cholesterol elevates plasma levels of toxic metabolites of the intestinal microbiome, such as trimethylamine N-oxide (TMAO). Plasma levels of TMAO increase in a linear fashion with egg consumption, and TMAO is bad for the arteries, said Dr. Spence.

“Eggs are terrible and should not be eaten by people at risk for cardiovascular disease. But people don’t understand that because the egg marketing propaganda has been so effective. The yolk is terrible. The egg marketing board is extremely effective in persuading people that eggs are healthy, and they’re not.”

Dr. Spence recommends using egg substitutes, such as Egg Beaters or Better’n Eggs, instead of whole eggs, and says it’s never too late to switch. “That’s the mistake people make, but the arteries can actually improve,” he said.

No funding source for the study was reported. Dr. Ur and Dr. Spence reported having no relevant financial relationships.
 

A version of this article appeared on Medscape.com.

Should a patient with high lipoprotein (a), or Lp(a), be started on low-dose aspirin?

This is the conundrum facing many physicians and patients, but even getting to that point will require more availability and coverage of tests and a greater appreciation of the risk associated with Lp(a), said cardiologists.
 

Lp(a): The Silent Risk

On Lp(a) Awareness Day, C. Michael Gibson, MD, MA, CEO of the Baim Institute for Clinical Research, Boston, Massachusetts, and PERFUSE took the opportunity to talk about his experiences with testing on X.

The professor of medicine at Harvard Medical School, also in Boston, said he was surprised to find that he had a very high calcium score, despite a low-density lipoprotein (LDL) cholesterol level of just 70 mg/dL. Eventually, he found out that he had a “very, very high Lp(a),” which was particularly concerning because his grandfather died of a heart attack at 45 years of age.

But how much risk does that represent?

A 2022 consensus statement from the European Atherosclerosis Society (EAS) highlighted that epidemiologic and genetic studies “strongly support a causal and continuous association between Lp(a) concentration and cardiovascular outcomes,” even at very low LDL cholesterol levels.

This is because Lp(a) has proinflammatory and proatherosclerotic properties, and high levels are associated with both micro- and macrocalcification of the aortic valve. Findings from a US registry study also suggest the threshold related to increased cardiovascular risk may differ for primary and secondary prevention populations (J Am Coll Cardiol. 2024 Mar 5;83[9]:873-886).

Lp(a) is, however, genetically determined, and there are no drugs available that directly lower levels, although some are on the horizon. In the meantime, the experts behind the consensus statement recommend that all adults be tested at least once in their lifetime.
 

Testing Cost and Availability

This recommendation has been translated into guidelines in “many, many” countries, said lead author Florian Kronenberg, MD, MAE, Institute of Genetic Epidemiology, Medical University of Innsbruck, Innsbruck, Austria, but “we are far away from reaching that goal.”

“We’ve got a real problem,” added Stephen Nicholls, MD, PhD, director of the Victorian Heart Institute and a professor of cardiology at Monash University, Melbourne, Australia, as there is “not a country in the world where there’s good access to Lp(a) testing.”

Dr. Kronenberg said that the consensus statement “created a kind of momentum” toward universal testing.

Ulrich Laufs, MD, PhD, professor and chair, Department of Cardiology, University Hospital Leipzig, Leipzig, Germany, agreed, saying that, overall, Lp(a) testing has “increased dramatically,” albeit from “extremely low levels.”

Dr. Kronenberg believes that “we have to be really patient.” He cited a lack of knowledge among physicians as one of the biggest barriers to greater uptake of testing.

“There is still no appreciation of the role of Lp(a),” agreed Alberico L. Catapano, MD, PhD, director of Cardiovascular Research and of the Lipoproteins and Atherosclerosis Laboratory of IRCCS Multimedica, Milan, Italy, and past president of the EAS.

“That’s why it’s not mentioned” to patients, he said. “What is really needed is to inform physician colleagues that Lp(a) is not only a risk factor but is the cause” of atherosclerotic cardiovascular disease (ASCVD).

Dr. Kronenberg said that the pressure for testing can often come from the patient themselves.

Physicians then question why the patient wants to be tested when there are no medications to treat it, he added. “We really tried very hard when we did the consensus paper to say that we should perform the test and give people advice on what to do.”

Dr. Catapano believes that another major obstacle is the cost of the test, which remains high “because very few people do it,” and there is some debate over which test to use.

Taken together, these issues have meant that “payers are really struggling with the idea of funding Lp(a),” said Dr. Nicholls, adding that “there seems to be this fixation on: ‘Well, if you can’t lower Lp(a), why measure it?’ ”

Rather than blame the payers, he says there is a need to educate about the science behind testing and underline that Lp(a) is an “important risk enhancer” for cardiovascular disease.

“Because if we’re going to make people pay out of pocket, then you’re creating a massive equity issue in that only those who can afford the test have it.”
 

High Lp(a) Now What?

But once the test has been performed, there then comes the question as to what to do about the result.

“Before we get anywhere near an agent that effectively lowers Lp(a) and get it into the clinic, there are lots of things that we can do today,” said Dr. Nicholls.

If someone has an intermediate or high background cardiovascular risk and they have got a high Lp(a) level, they “should be treated more intensively, as we know that high Lp(a) patients do better if their LDL cholesterol and their blood pressure is lower.”

For Dr. Catapano, this means having the “same mindset as you do with [a patient with] high blood pressure, high LDL cholesterol, and so on, because it’s exactly the same thing: It’s interacting with your other risk factors to increase your overall risk.”

Dr. Gibson agreed. Through a range of measures, including weight loss and statin therapy, he was able to reduce his overall cardiovascular risk, and his LDL cholesterol level dropped to just 20 mg/dL.
 

A Role for Aspirin?

However, one debate that has been rolling on in recent months is whether to start patients with elevated Lp(a) on low-dose aspirin.

It gained added momentum when Pablo Corral, MD, a lipidologist and a professor in the School of Medicine, Pharmacology Department, FASTA University, Mar del Plata, Buenos Aires, Argentina, highlighted the issue on X.

He pointed to a recent study, which showed that regular aspirin use was associated with a significantly lower rate of ASCVD mortality in adults without clinical ASCVD but who had elevated Lp(a).

Dr. Nicholls said that, when you “peel away the layers” of the current evidence, there is some suggestion that Lp(a)may be prothrombotic. “So in theory, perhaps aspirin might be maybe more intuitively useful there.”

He noted that the ASPREE primary prevention study found that low-dose aspirin in older adults resulted in a significantly higher risk for major hemorrhage over placebo and did not significantly reduce the risk for cardiovascular disease.

But an analysis he and his colleagues did suggest that aspirin may indeed benefit older individuals if they have elevated Lp(a) genotypes.
 

An Individual Decision

For Dr. Kronenberg and Dr. Laufs, there is currently a lack of appropriate data to make a recommendation either way, particularly for primary prevention.

They warned that the risk for thrombosis in patients with mildly elevated Lp(a) cannot be discounted, and in most cases either “the existing risk of bleeding exceeds the beneficial effects [of aspirin], or it’s not indicated,” said Dr. Laufs.

“When we make a recommendation, we should have evidence-based data,” Dr. Kronenberg said, but, at the moment, people “somehow put their finger in the air and see” which way the wind is blowing.

Dr. Catapano urged patients to talk to their physician, as even low-dose aspirin is “very potent” at inhibiting platelets.

Dr. Gibson agreed, saying that he is in two minds, as the potential benefit has to be weighed against the bleeding risk.

He personally takes low-dose aspirin because “I know I have a low bleeding risk,” but it is a decision “that has to be taken individually between a patient and their physician.”

Dr. Gibson, Dr. Kronenberg, Dr. Nicholls, and Dr. Catapano all reported conflicts of interest with numerous pharmaceutical companies and organizations.

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

Should a patient with high lipoprotein (a), or Lp(a), be started on low-dose aspirin?

This is the conundrum facing many physicians and patients, but even getting to that point will require more availability and coverage of tests and a greater appreciation of the risk associated with Lp(a), said cardiologists.
 

Lp(a): The Silent Risk

On Lp(a) Awareness Day, C. Michael Gibson, MD, MA, CEO of the Baim Institute for Clinical Research, Boston, Massachusetts, and PERFUSE took the opportunity to talk about his experiences with testing on X.

The professor of medicine at Harvard Medical School, also in Boston, said he was surprised to find that he had a very high calcium score, despite a low-density lipoprotein (LDL) cholesterol level of just 70 mg/dL. Eventually, he found out that he had a “very, very high Lp(a),” which was particularly concerning because his grandfather died of a heart attack at 45 years of age.

But how much risk does that represent?

A 2022 consensus statement from the European Atherosclerosis Society (EAS) highlighted that epidemiologic and genetic studies “strongly support a causal and continuous association between Lp(a) concentration and cardiovascular outcomes,” even at very low LDL cholesterol levels.

This is because Lp(a) has proinflammatory and proatherosclerotic properties, and high levels are associated with both micro- and macrocalcification of the aortic valve. Findings from a US registry study also suggest the threshold related to increased cardiovascular risk may differ for primary and secondary prevention populations (J Am Coll Cardiol. 2024 Mar 5;83[9]:873-886).

Lp(a) is, however, genetically determined, and there are no drugs available that directly lower levels, although some are on the horizon. In the meantime, the experts behind the consensus statement recommend that all adults be tested at least once in their lifetime.
 

Testing Cost and Availability

This recommendation has been translated into guidelines in “many, many” countries, said lead author Florian Kronenberg, MD, MAE, Institute of Genetic Epidemiology, Medical University of Innsbruck, Innsbruck, Austria, but “we are far away from reaching that goal.”

“We’ve got a real problem,” added Stephen Nicholls, MD, PhD, director of the Victorian Heart Institute and a professor of cardiology at Monash University, Melbourne, Australia, as there is “not a country in the world where there’s good access to Lp(a) testing.”

Dr. Kronenberg said that the consensus statement “created a kind of momentum” toward universal testing.

Ulrich Laufs, MD, PhD, professor and chair, Department of Cardiology, University Hospital Leipzig, Leipzig, Germany, agreed, saying that, overall, Lp(a) testing has “increased dramatically,” albeit from “extremely low levels.”

Dr. Kronenberg believes that “we have to be really patient.” He cited a lack of knowledge among physicians as one of the biggest barriers to greater uptake of testing.

“There is still no appreciation of the role of Lp(a),” agreed Alberico L. Catapano, MD, PhD, director of Cardiovascular Research and of the Lipoproteins and Atherosclerosis Laboratory of IRCCS Multimedica, Milan, Italy, and past president of the EAS.

“That’s why it’s not mentioned” to patients, he said. “What is really needed is to inform physician colleagues that Lp(a) is not only a risk factor but is the cause” of atherosclerotic cardiovascular disease (ASCVD).

Dr. Kronenberg said that the pressure for testing can often come from the patient themselves.

Physicians then question why the patient wants to be tested when there are no medications to treat it, he added. “We really tried very hard when we did the consensus paper to say that we should perform the test and give people advice on what to do.”

Dr. Catapano believes that another major obstacle is the cost of the test, which remains high “because very few people do it,” and there is some debate over which test to use.

Taken together, these issues have meant that “payers are really struggling with the idea of funding Lp(a),” said Dr. Nicholls, adding that “there seems to be this fixation on: ‘Well, if you can’t lower Lp(a), why measure it?’ ”

Rather than blame the payers, he says there is a need to educate about the science behind testing and underline that Lp(a) is an “important risk enhancer” for cardiovascular disease.

“Because if we’re going to make people pay out of pocket, then you’re creating a massive equity issue in that only those who can afford the test have it.”
 

High Lp(a) Now What?

But once the test has been performed, there then comes the question as to what to do about the result.

“Before we get anywhere near an agent that effectively lowers Lp(a) and get it into the clinic, there are lots of things that we can do today,” said Dr. Nicholls.

If someone has an intermediate or high background cardiovascular risk and they have got a high Lp(a) level, they “should be treated more intensively, as we know that high Lp(a) patients do better if their LDL cholesterol and their blood pressure is lower.”

For Dr. Catapano, this means having the “same mindset as you do with [a patient with] high blood pressure, high LDL cholesterol, and so on, because it’s exactly the same thing: It’s interacting with your other risk factors to increase your overall risk.”

Dr. Gibson agreed. Through a range of measures, including weight loss and statin therapy, he was able to reduce his overall cardiovascular risk, and his LDL cholesterol level dropped to just 20 mg/dL.
 

A Role for Aspirin?

However, one debate that has been rolling on in recent months is whether to start patients with elevated Lp(a) on low-dose aspirin.

It gained added momentum when Pablo Corral, MD, a lipidologist and a professor in the School of Medicine, Pharmacology Department, FASTA University, Mar del Plata, Buenos Aires, Argentina, highlighted the issue on X.

He pointed to a recent study, which showed that regular aspirin use was associated with a significantly lower rate of ASCVD mortality in adults without clinical ASCVD but who had elevated Lp(a).

Dr. Nicholls said that, when you “peel away the layers” of the current evidence, there is some suggestion that Lp(a)may be prothrombotic. “So in theory, perhaps aspirin might be maybe more intuitively useful there.”

He noted that the ASPREE primary prevention study found that low-dose aspirin in older adults resulted in a significantly higher risk for major hemorrhage over placebo and did not significantly reduce the risk for cardiovascular disease.

But an analysis he and his colleagues did suggest that aspirin may indeed benefit older individuals if they have elevated Lp(a) genotypes.
 

An Individual Decision

For Dr. Kronenberg and Dr. Laufs, there is currently a lack of appropriate data to make a recommendation either way, particularly for primary prevention.

They warned that the risk for thrombosis in patients with mildly elevated Lp(a) cannot be discounted, and in most cases either “the existing risk of bleeding exceeds the beneficial effects [of aspirin], or it’s not indicated,” said Dr. Laufs.

“When we make a recommendation, we should have evidence-based data,” Dr. Kronenberg said, but, at the moment, people “somehow put their finger in the air and see” which way the wind is blowing.

Dr. Catapano urged patients to talk to their physician, as even low-dose aspirin is “very potent” at inhibiting platelets.

Dr. Gibson agreed, saying that he is in two minds, as the potential benefit has to be weighed against the bleeding risk.

He personally takes low-dose aspirin because “I know I have a low bleeding risk,” but it is a decision “that has to be taken individually between a patient and their physician.”

Dr. Gibson, Dr. Kronenberg, Dr. Nicholls, and Dr. Catapano all reported conflicts of interest with numerous pharmaceutical companies and organizations.

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

Should a patient with high lipoprotein (a), or Lp(a), be started on low-dose aspirin?

This is the conundrum facing many physicians and patients, but even getting to that point will require more availability and coverage of tests and a greater appreciation of the risk associated with Lp(a), said cardiologists.
 

Lp(a): The Silent Risk

On Lp(a) Awareness Day, C. Michael Gibson, MD, MA, CEO of the Baim Institute for Clinical Research, Boston, Massachusetts, and PERFUSE took the opportunity to talk about his experiences with testing on X.

The professor of medicine at Harvard Medical School, also in Boston, said he was surprised to find that he had a very high calcium score, despite a low-density lipoprotein (LDL) cholesterol level of just 70 mg/dL. Eventually, he found out that he had a “very, very high Lp(a),” which was particularly concerning because his grandfather died of a heart attack at 45 years of age.

But how much risk does that represent?

A 2022 consensus statement from the European Atherosclerosis Society (EAS) highlighted that epidemiologic and genetic studies “strongly support a causal and continuous association between Lp(a) concentration and cardiovascular outcomes,” even at very low LDL cholesterol levels.

This is because Lp(a) has proinflammatory and proatherosclerotic properties, and high levels are associated with both micro- and macrocalcification of the aortic valve. Findings from a US registry study also suggest the threshold related to increased cardiovascular risk may differ for primary and secondary prevention populations (J Am Coll Cardiol. 2024 Mar 5;83[9]:873-886).

Lp(a) is, however, genetically determined, and there are no drugs available that directly lower levels, although some are on the horizon. In the meantime, the experts behind the consensus statement recommend that all adults be tested at least once in their lifetime.
 

Testing Cost and Availability

This recommendation has been translated into guidelines in “many, many” countries, said lead author Florian Kronenberg, MD, MAE, Institute of Genetic Epidemiology, Medical University of Innsbruck, Innsbruck, Austria, but “we are far away from reaching that goal.”

“We’ve got a real problem,” added Stephen Nicholls, MD, PhD, director of the Victorian Heart Institute and a professor of cardiology at Monash University, Melbourne, Australia, as there is “not a country in the world where there’s good access to Lp(a) testing.”

Dr. Kronenberg said that the consensus statement “created a kind of momentum” toward universal testing.

Ulrich Laufs, MD, PhD, professor and chair, Department of Cardiology, University Hospital Leipzig, Leipzig, Germany, agreed, saying that, overall, Lp(a) testing has “increased dramatically,” albeit from “extremely low levels.”

Dr. Kronenberg believes that “we have to be really patient.” He cited a lack of knowledge among physicians as one of the biggest barriers to greater uptake of testing.

“There is still no appreciation of the role of Lp(a),” agreed Alberico L. Catapano, MD, PhD, director of Cardiovascular Research and of the Lipoproteins and Atherosclerosis Laboratory of IRCCS Multimedica, Milan, Italy, and past president of the EAS.

“That’s why it’s not mentioned” to patients, he said. “What is really needed is to inform physician colleagues that Lp(a) is not only a risk factor but is the cause” of atherosclerotic cardiovascular disease (ASCVD).

Dr. Kronenberg said that the pressure for testing can often come from the patient themselves.

Physicians then question why the patient wants to be tested when there are no medications to treat it, he added. “We really tried very hard when we did the consensus paper to say that we should perform the test and give people advice on what to do.”

Dr. Catapano believes that another major obstacle is the cost of the test, which remains high “because very few people do it,” and there is some debate over which test to use.

Taken together, these issues have meant that “payers are really struggling with the idea of funding Lp(a),” said Dr. Nicholls, adding that “there seems to be this fixation on: ‘Well, if you can’t lower Lp(a), why measure it?’ ”

Rather than blame the payers, he says there is a need to educate about the science behind testing and underline that Lp(a) is an “important risk enhancer” for cardiovascular disease.

“Because if we’re going to make people pay out of pocket, then you’re creating a massive equity issue in that only those who can afford the test have it.”
 

High Lp(a) Now What?

But once the test has been performed, there then comes the question as to what to do about the result.

“Before we get anywhere near an agent that effectively lowers Lp(a) and get it into the clinic, there are lots of things that we can do today,” said Dr. Nicholls.

If someone has an intermediate or high background cardiovascular risk and they have got a high Lp(a) level, they “should be treated more intensively, as we know that high Lp(a) patients do better if their LDL cholesterol and their blood pressure is lower.”

For Dr. Catapano, this means having the “same mindset as you do with [a patient with] high blood pressure, high LDL cholesterol, and so on, because it’s exactly the same thing: It’s interacting with your other risk factors to increase your overall risk.”

Dr. Gibson agreed. Through a range of measures, including weight loss and statin therapy, he was able to reduce his overall cardiovascular risk, and his LDL cholesterol level dropped to just 20 mg/dL.
 

A Role for Aspirin?

However, one debate that has been rolling on in recent months is whether to start patients with elevated Lp(a) on low-dose aspirin.

It gained added momentum when Pablo Corral, MD, a lipidologist and a professor in the School of Medicine, Pharmacology Department, FASTA University, Mar del Plata, Buenos Aires, Argentina, highlighted the issue on X.

He pointed to a recent study, which showed that regular aspirin use was associated with a significantly lower rate of ASCVD mortality in adults without clinical ASCVD but who had elevated Lp(a).

Dr. Nicholls said that, when you “peel away the layers” of the current evidence, there is some suggestion that Lp(a)may be prothrombotic. “So in theory, perhaps aspirin might be maybe more intuitively useful there.”

He noted that the ASPREE primary prevention study found that low-dose aspirin in older adults resulted in a significantly higher risk for major hemorrhage over placebo and did not significantly reduce the risk for cardiovascular disease.

But an analysis he and his colleagues did suggest that aspirin may indeed benefit older individuals if they have elevated Lp(a) genotypes.
 

An Individual Decision

For Dr. Kronenberg and Dr. Laufs, there is currently a lack of appropriate data to make a recommendation either way, particularly for primary prevention.

They warned that the risk for thrombosis in patients with mildly elevated Lp(a) cannot be discounted, and in most cases either “the existing risk of bleeding exceeds the beneficial effects [of aspirin], or it’s not indicated,” said Dr. Laufs.

“When we make a recommendation, we should have evidence-based data,” Dr. Kronenberg said, but, at the moment, people “somehow put their finger in the air and see” which way the wind is blowing.

Dr. Catapano urged patients to talk to their physician, as even low-dose aspirin is “very potent” at inhibiting platelets.

Dr. Gibson agreed, saying that he is in two minds, as the potential benefit has to be weighed against the bleeding risk.

He personally takes low-dose aspirin because “I know I have a low bleeding risk,” but it is a decision “that has to be taken individually between a patient and their physician.”

Dr. Gibson, Dr. Kronenberg, Dr. Nicholls, and Dr. Catapano all reported conflicts of interest with numerous pharmaceutical companies and organizations.

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

This transcript has been edited for clarity. 

My oldest daughter is at sleepaway camp for a couple of weeks, and the camp has a photographer who goes around all day taking pictures of the kids, which get uploaded to a private Facebook group. In the past, I would go online every day (or, okay, several times a day) and scroll through all those pictures looking for one that features my kid. 

I don’t have to do that anymore. This year, I simply uploaded a picture of my daughter to an app and artificial intelligence (AI) takes care of the rest, recognizing her face amidst the sea of smiling children, and flagging just those photos for me to peruse. It’s amazing, really. And a bit scary.

The fact that facial recognition has penetrated the summer camp market should tell you that the tech is truly ubiquitous. But today we’re going to think a bit more about what AI can do with a picture of your face, because the power of facial recognition is not just skin deep.

What’s got me hot and bothered about facial images is this paper, appearing in Cell Metabolism, which adds a new layer to the standard facial-analysis playbook: facial temperature.

To understand this paper, you need to understand a whole field of research that is developing various different “clocks” for age. 

It turns out that age really is just a number. Our cells, our proteins, our biochemistry can be analyzed to give different numbers. These “clocks,” as distinct from the calendar we usually use to measure our age, might have more predictive power than the number itself. 

There are numerous molecular clocks, such as telomere length, that not only correlate with calendar age but are superior to calendar age in predicting age-related complications. Testing telomere length typically requires a blood sample — and remains costly. But we can use other sources to estimate age; how about a photo?

I mean, we do this all the time when we meet someone new or, as a physician, when we meet a new patient. I have often written that a patient “appears younger than their stated age,” and we’ve all had the experience of hearing how old someone is and being shocked. I mean, have you seen Sharon Stone recently? She’s 66 years old. Okay — to be fair, there might be some outside help there. But you get the point.

Back to the Cell Metabolism paper. Researchers report on multiple algorithms to obtain an “age” from a picture of an individual’s face. 

The first algorithm is pretty straightforward. Researchers collected 2811 images, all of Han Chinese individuals ranging in age from 20 to 90 years, and reconstructed a 3D facial map from those. 

Cell Metabolism

Cell Metabolism

Dr. Wilson

Cell Metabolism

Cell Metabolism

Cell Metabolism

Cell Metabolism

Cell Metabolism

Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.

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

This transcript has been edited for clarity. 

My oldest daughter is at sleepaway camp for a couple of weeks, and the camp has a photographer who goes around all day taking pictures of the kids, which get uploaded to a private Facebook group. In the past, I would go online every day (or, okay, several times a day) and scroll through all those pictures looking for one that features my kid. 

I don’t have to do that anymore. This year, I simply uploaded a picture of my daughter to an app and artificial intelligence (AI) takes care of the rest, recognizing her face amidst the sea of smiling children, and flagging just those photos for me to peruse. It’s amazing, really. And a bit scary.

The fact that facial recognition has penetrated the summer camp market should tell you that the tech is truly ubiquitous. But today we’re going to think a bit more about what AI can do with a picture of your face, because the power of facial recognition is not just skin deep.

What’s got me hot and bothered about facial images is this paper, appearing in Cell Metabolism, which adds a new layer to the standard facial-analysis playbook: facial temperature.

To understand this paper, you need to understand a whole field of research that is developing various different “clocks” for age. 

It turns out that age really is just a number. Our cells, our proteins, our biochemistry can be analyzed to give different numbers. These “clocks,” as distinct from the calendar we usually use to measure our age, might have more predictive power than the number itself. 

There are numerous molecular clocks, such as telomere length, that not only correlate with calendar age but are superior to calendar age in predicting age-related complications. Testing telomere length typically requires a blood sample — and remains costly. But we can use other sources to estimate age; how about a photo?

I mean, we do this all the time when we meet someone new or, as a physician, when we meet a new patient. I have often written that a patient “appears younger than their stated age,” and we’ve all had the experience of hearing how old someone is and being shocked. I mean, have you seen Sharon Stone recently? She’s 66 years old. Okay — to be fair, there might be some outside help there. But you get the point.

Back to the Cell Metabolism paper. Researchers report on multiple algorithms to obtain an “age” from a picture of an individual’s face. 

The first algorithm is pretty straightforward. Researchers collected 2811 images, all of Han Chinese individuals ranging in age from 20 to 90 years, and reconstructed a 3D facial map from those. 

Cell Metabolism

Cell Metabolism

Dr. Wilson

Cell Metabolism

Cell Metabolism

Cell Metabolism

Cell Metabolism

Cell Metabolism

Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.

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

This transcript has been edited for clarity. 

My oldest daughter is at sleepaway camp for a couple of weeks, and the camp has a photographer who goes around all day taking pictures of the kids, which get uploaded to a private Facebook group. In the past, I would go online every day (or, okay, several times a day) and scroll through all those pictures looking for one that features my kid. 

I don’t have to do that anymore. This year, I simply uploaded a picture of my daughter to an app and artificial intelligence (AI) takes care of the rest, recognizing her face amidst the sea of smiling children, and flagging just those photos for me to peruse. It’s amazing, really. And a bit scary.

The fact that facial recognition has penetrated the summer camp market should tell you that the tech is truly ubiquitous. But today we’re going to think a bit more about what AI can do with a picture of your face, because the power of facial recognition is not just skin deep.

What’s got me hot and bothered about facial images is this paper, appearing in Cell Metabolism, which adds a new layer to the standard facial-analysis playbook: facial temperature.

To understand this paper, you need to understand a whole field of research that is developing various different “clocks” for age. 

It turns out that age really is just a number. Our cells, our proteins, our biochemistry can be analyzed to give different numbers. These “clocks,” as distinct from the calendar we usually use to measure our age, might have more predictive power than the number itself. 

There are numerous molecular clocks, such as telomere length, that not only correlate with calendar age but are superior to calendar age in predicting age-related complications. Testing telomere length typically requires a blood sample — and remains costly. But we can use other sources to estimate age; how about a photo?

I mean, we do this all the time when we meet someone new or, as a physician, when we meet a new patient. I have often written that a patient “appears younger than their stated age,” and we’ve all had the experience of hearing how old someone is and being shocked. I mean, have you seen Sharon Stone recently? She’s 66 years old. Okay — to be fair, there might be some outside help there. But you get the point.

Back to the Cell Metabolism paper. Researchers report on multiple algorithms to obtain an “age” from a picture of an individual’s face. 

The first algorithm is pretty straightforward. Researchers collected 2811 images, all of Han Chinese individuals ranging in age from 20 to 90 years, and reconstructed a 3D facial map from those. 

Cell Metabolism

Cell Metabolism

Dr. Wilson

Cell Metabolism

Cell Metabolism

Cell Metabolism

Cell Metabolism

Cell Metabolism

Dr. Wilson is associate professor of medicine and public health and director of the Clinical and Translational Research Accelerator at Yale University, New Haven, Conn. He has disclosed no relevant financial relationships.

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