Acute Coronary Syndromes

TOPLINE:

Current use of hydroxychloroquine is associated with a lower risk for myocardial infarction (MI), stroke, and other thromboembolic events in patients with systemic lupus erythematosus (SLE). This protective effect diminishes after discontinuation of hydroxychloroquine treatment.

METHODOLOGY:

• Researchers used a nested case-control design to evaluate the association between exposure to hydroxychloroquine and the risk for cardiovascular events in patients with SLE.
• They included 52,883 adults with SLE (mean age, 44.23 years; 86.6% women) identified from the National System of Health Databases, which includes 99% of the French population.
• Among these, 1981 individuals with composite cardiovascular conditions were matched with 16,892 control individuals without cardiovascular conditions.
• Patients were categorized on the basis of hydroxychloroquine exposure into current users (last exposure within 90 days before a cardiovascular event), remote users (91-365 days before), and nonusers (no exposure within 365 days).
• The study outcomes included a composite of cardiovascular events, including MI, stroke (including transient ischemic attack), and other thromboembolic events such as phlebitis, thrombophlebitis, venous thrombosis, venous thromboembolism, and pulmonary embolism.

TAKEAWAY:

• Current hydroxychloroquine users had lower odds of experiencing a composite cardiovascular outcome than nonusers (adjusted odds ratio [aOR], 0.63; 95% CI, 0.57-0.70).
• The odds of MI (aOR, 0.72; 95% CI, 0.60-0.87), stroke (aOR, 0.71; 95% CI, 0.61-0.83), and other thromboembolic events (aOR, 0.58; 95% CI, 0.48-0.69) were also lower among current users than among nonusers.
• No significant association was found for remote hydroxychloroquine exposure and the risk for composite cardiovascular events, MI, stroke, and other thromboembolic events.

IN PRACTICE:

“These findings support the protective association of hydroxychloroquine against CV [cardiovascular] events and underscore the importance of continuous hydroxychloroquine therapy for patients diagnosed with SLE,” the authors wrote.

SOURCE:

The study was led by Lamiae Grimaldi-Bensouda, PharmD, PhD, Department of Pharmacology, Hospital Group Paris-Saclay, Assistance Publique-Hôpitaux de Paris, France. It was published online on August 30, 2024, in JAMA Network Open.

LIMITATIONS:

The observational nature of the study may have introduced confounding. Current hydroxychloroquine users were younger than nonusers, with an average age difference of almost 5 years. Current hydroxychloroquine users had a twofold longer duration of onset of SLE and had a higher prevalence of chronic kidney disease compared with nonusers.

DISCLOSURES:

This study was funded by the Banque pour l’Investissement, Deeptech. Some authors declared having financial ties with various institutions and companies outside of the current study.
 

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 appeared on Medscape.com.

TOPLINE:

Current use of hydroxychloroquine is associated with a lower risk for myocardial infarction (MI), stroke, and other thromboembolic events in patients with systemic lupus erythematosus (SLE). This protective effect diminishes after discontinuation of hydroxychloroquine treatment.

METHODOLOGY:

• Researchers used a nested case-control design to evaluate the association between exposure to hydroxychloroquine and the risk for cardiovascular events in patients with SLE.
• They included 52,883 adults with SLE (mean age, 44.23 years; 86.6% women) identified from the National System of Health Databases, which includes 99% of the French population.
• Among these, 1981 individuals with composite cardiovascular conditions were matched with 16,892 control individuals without cardiovascular conditions.
• Patients were categorized on the basis of hydroxychloroquine exposure into current users (last exposure within 90 days before a cardiovascular event), remote users (91-365 days before), and nonusers (no exposure within 365 days).
• The study outcomes included a composite of cardiovascular events, including MI, stroke (including transient ischemic attack), and other thromboembolic events such as phlebitis, thrombophlebitis, venous thrombosis, venous thromboembolism, and pulmonary embolism.

TAKEAWAY:

• Current hydroxychloroquine users had lower odds of experiencing a composite cardiovascular outcome than nonusers (adjusted odds ratio [aOR], 0.63; 95% CI, 0.57-0.70).
• The odds of MI (aOR, 0.72; 95% CI, 0.60-0.87), stroke (aOR, 0.71; 95% CI, 0.61-0.83), and other thromboembolic events (aOR, 0.58; 95% CI, 0.48-0.69) were also lower among current users than among nonusers.
• No significant association was found for remote hydroxychloroquine exposure and the risk for composite cardiovascular events, MI, stroke, and other thromboembolic events.

IN PRACTICE:

“These findings support the protective association of hydroxychloroquine against CV [cardiovascular] events and underscore the importance of continuous hydroxychloroquine therapy for patients diagnosed with SLE,” the authors wrote.

SOURCE:

The study was led by Lamiae Grimaldi-Bensouda, PharmD, PhD, Department of Pharmacology, Hospital Group Paris-Saclay, Assistance Publique-Hôpitaux de Paris, France. It was published online on August 30, 2024, in JAMA Network Open.

LIMITATIONS:

The observational nature of the study may have introduced confounding. Current hydroxychloroquine users were younger than nonusers, with an average age difference of almost 5 years. Current hydroxychloroquine users had a twofold longer duration of onset of SLE and had a higher prevalence of chronic kidney disease compared with nonusers.

DISCLOSURES:

This study was funded by the Banque pour l’Investissement, Deeptech. Some authors declared having financial ties with various institutions and companies outside of the current study.
 

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 appeared on Medscape.com.

TOPLINE:

Current use of hydroxychloroquine is associated with a lower risk for myocardial infarction (MI), stroke, and other thromboembolic events in patients with systemic lupus erythematosus (SLE). This protective effect diminishes after discontinuation of hydroxychloroquine treatment.

METHODOLOGY:

• Researchers used a nested case-control design to evaluate the association between exposure to hydroxychloroquine and the risk for cardiovascular events in patients with SLE.
• They included 52,883 adults with SLE (mean age, 44.23 years; 86.6% women) identified from the National System of Health Databases, which includes 99% of the French population.
• Among these, 1981 individuals with composite cardiovascular conditions were matched with 16,892 control individuals without cardiovascular conditions.
• Patients were categorized on the basis of hydroxychloroquine exposure into current users (last exposure within 90 days before a cardiovascular event), remote users (91-365 days before), and nonusers (no exposure within 365 days).
• The study outcomes included a composite of cardiovascular events, including MI, stroke (including transient ischemic attack), and other thromboembolic events such as phlebitis, thrombophlebitis, venous thrombosis, venous thromboembolism, and pulmonary embolism.

TAKEAWAY:

• Current hydroxychloroquine users had lower odds of experiencing a composite cardiovascular outcome than nonusers (adjusted odds ratio [aOR], 0.63; 95% CI, 0.57-0.70).
• The odds of MI (aOR, 0.72; 95% CI, 0.60-0.87), stroke (aOR, 0.71; 95% CI, 0.61-0.83), and other thromboembolic events (aOR, 0.58; 95% CI, 0.48-0.69) were also lower among current users than among nonusers.
• No significant association was found for remote hydroxychloroquine exposure and the risk for composite cardiovascular events, MI, stroke, and other thromboembolic events.

IN PRACTICE:

“These findings support the protective association of hydroxychloroquine against CV [cardiovascular] events and underscore the importance of continuous hydroxychloroquine therapy for patients diagnosed with SLE,” the authors wrote.

SOURCE:

The study was led by Lamiae Grimaldi-Bensouda, PharmD, PhD, Department of Pharmacology, Hospital Group Paris-Saclay, Assistance Publique-Hôpitaux de Paris, France. It was published online on August 30, 2024, in JAMA Network Open.

LIMITATIONS:

The observational nature of the study may have introduced confounding. Current hydroxychloroquine users were younger than nonusers, with an average age difference of almost 5 years. Current hydroxychloroquine users had a twofold longer duration of onset of SLE and had a higher prevalence of chronic kidney disease compared with nonusers.

DISCLOSURES:

This study was funded by the Banque pour l’Investissement, Deeptech. Some authors declared having financial ties with various institutions and companies outside of the current study.
 

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 appeared on Medscape.com.

Using a cell phone for at least one call per week is linked to a higher risk for cardiovascular disease (CVD), especially among smokers and patients with diabetes, according to a new UK Biobank analysis.

“We found that a poor sleep pattern, psychological distress, and neuroticism significantly mediated the positive association between weekly mobile phone usage time and the risk for incident CVD, with a mediating proportion of 5.11%, 11.50%, and 2.25%, respectively,” said principal investigator Xianhui Qin, MD, professor of nephrology at Southern Medical University, Guangzhou, China.

Poor sleep patterns and poor mental health could disrupt circadian rhythms and endocrine and metabolic functions, as well as increase inflammation, he explained.

In addition, chronic exposure to radiofrequency electromagnetic fields (RF-EMF) emitted from cell phones could lead to oxidative stress and an inflammatory response. Combined with smoking and diabetes, this exposure “may have a synergistic effect in increasing CVD risk,” Dr. Qin suggested.

The study was published online in the Canadian Journal of Cardiology.
 

Risk Underestimated?

The researchers aimed to examine the association of regular cell phone use with incident CVD and explore the mediating effects of sleep and mental health using linked hospital and mortality records.

Their analysis included 444,027 participants (mean age, 56 years; 44% men) without a history of CVD from the UK Biobank. A total of 378,161 participants were regular cell phone users.

Regular cell phone use was defined as at least one call per week. Weekly use was self-reported as the average time of calls per week during the previous 3 months.

The primary outcome was incident CVD. Secondary outcomes were each component of CVD (ie, coronary heart disease, stroke, atrial fibrillation, and heart failure) and increased carotid intima media thickness (CIMT).

Compared with nonregular cell phone users, regular users were younger, had higher proportions of current smokers and urban residents, and had lower proportions of history of hypertension and diabetes. They also had higher income, Townsend deprivation index, and body mass index, and lower education levels.

During a median follow-up of 12.3 years, 56,181 participants developed incident CVD. Compared with nonregular cell phone users, regular users had a significantly higher risk for incident CVD (hazard ratio, 1.04) and increased CIMT (odds ratio, 1.11).

Among regular cell phone users, the duration of cell phone use and hands-free device/speakerphone use during calls was not significantly associated with incident CVD. Yet a significant and positive dose-response relationship was seen between weekly cell phone usage time and the risk for CVD. The positive association was stronger in current vs noncurrent smokers and people with vs without diabetes.

To different extents, sleep patterns (5.11%), psychologic distress (11.5%), and neuroticism (2.25%) mediated the relationship between weekly cell phone usage time and the risk for incident CVD.

“Our study suggests that despite the advantages of mobile phone use, we should also pay attention to the potential harm of mobile phone use to cardiovascular health,” Dr. Qin said. “Future studies to assess the risk-benefit balance will help promote mobile phone use patterns that are conducive to cardiovascular health.”

Meanwhile, he added, “We encourage measures to reduce time spent on mobile phones to promote the primary prevention of CVD. On the other hand, improving sleep and mental health status may help reduce the higher risk of CVD associated with mobile phone use.”

There are several limitations to the study in addition to its observational nature, which cannot show cause and effect. The questionnaires on cell phone use were restricted to phone calls; other use patterns of cell phones (eg, messaging, watching videos, and browsing the web) were not considered. Although the researchers adjusted for many potential confounders, unmeasured confounding bias (eg, the type of cell phone used and other sources of RF-EMF) cannot be eliminated.
 

Weak Link?

In a comment, Nicholas Grubic, MSc, a PhD student in epidemiology at the University of Toronto, Ontario, Canada, and coauthor of a related editorial, said, “I found it interesting that there was a connection observed between mobile phone use and CVD. However, it is crucial to understand that this link appeared to be much weaker compared with other well-known cardiovascular risk factors, such as smoking, diabetes, and high blood pressure. For now, mobile phone use should not be a major concern for most people.”

Nevertheless, clinicians should encourage patients to practice healthy habits around their screen time, he advised. “This could include limiting mobile phone use before bedtime and taking regular breaks to engage in activities that promote heart health, such as exercising or spending time outdoors.

“For the time being, we probably won’t see mobile phone use included in standard assessments for cardiovascular risk or as a focal point of cardiovascular health promotion initiatives,” he added. Instead, clinicians should “focus on established risk factors that have a stronger impact on patients’ cardiovascular health.”

Nieca Goldberg, MD, a clinical associate professor of medicine at NYU Grossman School of Medicine in New York City and American Heart Association volunteer expert, had a similar message. “You don’t have to go back to using a landline,” she said. “Instead, patients should be more mindful of how much phone use is taking away from their physical activity, keeping them from sleeping, and causing them stress.” Clinicians should also remember to counsel smokers on smoking cessation.

“It would be important for future studies to look at time spent on the phone and the type of activities patients are doing on their phones, such as social media, calls, texts, movies, or streaming TV shows,” she said. “It would be important to see how phone use is leading to a sedentary lifestyle” and what that means for a larger, more diverse population.

The study was supported by the National Key R&D Program, the National Natural Science Foundation of China, and the Outstanding Youth Development Scheme of Nanfang Hospital, Southern Medical University. Dr. Qin, Dr. Grubic, and Dr. Goldberg reported having no relevant financial relationships.

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

Using a cell phone for at least one call per week is linked to a higher risk for cardiovascular disease (CVD), especially among smokers and patients with diabetes, according to a new UK Biobank analysis.

“We found that a poor sleep pattern, psychological distress, and neuroticism significantly mediated the positive association between weekly mobile phone usage time and the risk for incident CVD, with a mediating proportion of 5.11%, 11.50%, and 2.25%, respectively,” said principal investigator Xianhui Qin, MD, professor of nephrology at Southern Medical University, Guangzhou, China.

Poor sleep patterns and poor mental health could disrupt circadian rhythms and endocrine and metabolic functions, as well as increase inflammation, he explained.

In addition, chronic exposure to radiofrequency electromagnetic fields (RF-EMF) emitted from cell phones could lead to oxidative stress and an inflammatory response. Combined with smoking and diabetes, this exposure “may have a synergistic effect in increasing CVD risk,” Dr. Qin suggested.

The study was published online in the Canadian Journal of Cardiology.
 

Risk Underestimated?

The researchers aimed to examine the association of regular cell phone use with incident CVD and explore the mediating effects of sleep and mental health using linked hospital and mortality records.

Their analysis included 444,027 participants (mean age, 56 years; 44% men) without a history of CVD from the UK Biobank. A total of 378,161 participants were regular cell phone users.

Regular cell phone use was defined as at least one call per week. Weekly use was self-reported as the average time of calls per week during the previous 3 months.

The primary outcome was incident CVD. Secondary outcomes were each component of CVD (ie, coronary heart disease, stroke, atrial fibrillation, and heart failure) and increased carotid intima media thickness (CIMT).

Compared with nonregular cell phone users, regular users were younger, had higher proportions of current smokers and urban residents, and had lower proportions of history of hypertension and diabetes. They also had higher income, Townsend deprivation index, and body mass index, and lower education levels.

During a median follow-up of 12.3 years, 56,181 participants developed incident CVD. Compared with nonregular cell phone users, regular users had a significantly higher risk for incident CVD (hazard ratio, 1.04) and increased CIMT (odds ratio, 1.11).

Among regular cell phone users, the duration of cell phone use and hands-free device/speakerphone use during calls was not significantly associated with incident CVD. Yet a significant and positive dose-response relationship was seen between weekly cell phone usage time and the risk for CVD. The positive association was stronger in current vs noncurrent smokers and people with vs without diabetes.

To different extents, sleep patterns (5.11%), psychologic distress (11.5%), and neuroticism (2.25%) mediated the relationship between weekly cell phone usage time and the risk for incident CVD.

“Our study suggests that despite the advantages of mobile phone use, we should also pay attention to the potential harm of mobile phone use to cardiovascular health,” Dr. Qin said. “Future studies to assess the risk-benefit balance will help promote mobile phone use patterns that are conducive to cardiovascular health.”

Meanwhile, he added, “We encourage measures to reduce time spent on mobile phones to promote the primary prevention of CVD. On the other hand, improving sleep and mental health status may help reduce the higher risk of CVD associated with mobile phone use.”

There are several limitations to the study in addition to its observational nature, which cannot show cause and effect. The questionnaires on cell phone use were restricted to phone calls; other use patterns of cell phones (eg, messaging, watching videos, and browsing the web) were not considered. Although the researchers adjusted for many potential confounders, unmeasured confounding bias (eg, the type of cell phone used and other sources of RF-EMF) cannot be eliminated.
 

Weak Link?

In a comment, Nicholas Grubic, MSc, a PhD student in epidemiology at the University of Toronto, Ontario, Canada, and coauthor of a related editorial, said, “I found it interesting that there was a connection observed between mobile phone use and CVD. However, it is crucial to understand that this link appeared to be much weaker compared with other well-known cardiovascular risk factors, such as smoking, diabetes, and high blood pressure. For now, mobile phone use should not be a major concern for most people.”

Nevertheless, clinicians should encourage patients to practice healthy habits around their screen time, he advised. “This could include limiting mobile phone use before bedtime and taking regular breaks to engage in activities that promote heart health, such as exercising or spending time outdoors.

“For the time being, we probably won’t see mobile phone use included in standard assessments for cardiovascular risk or as a focal point of cardiovascular health promotion initiatives,” he added. Instead, clinicians should “focus on established risk factors that have a stronger impact on patients’ cardiovascular health.”

Nieca Goldberg, MD, a clinical associate professor of medicine at NYU Grossman School of Medicine in New York City and American Heart Association volunteer expert, had a similar message. “You don’t have to go back to using a landline,” she said. “Instead, patients should be more mindful of how much phone use is taking away from their physical activity, keeping them from sleeping, and causing them stress.” Clinicians should also remember to counsel smokers on smoking cessation.

“It would be important for future studies to look at time spent on the phone and the type of activities patients are doing on their phones, such as social media, calls, texts, movies, or streaming TV shows,” she said. “It would be important to see how phone use is leading to a sedentary lifestyle” and what that means for a larger, more diverse population.

The study was supported by the National Key R&D Program, the National Natural Science Foundation of China, and the Outstanding Youth Development Scheme of Nanfang Hospital, Southern Medical University. Dr. Qin, Dr. Grubic, and Dr. Goldberg reported having no relevant financial relationships.

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

Using a cell phone for at least one call per week is linked to a higher risk for cardiovascular disease (CVD), especially among smokers and patients with diabetes, according to a new UK Biobank analysis.

“We found that a poor sleep pattern, psychological distress, and neuroticism significantly mediated the positive association between weekly mobile phone usage time and the risk for incident CVD, with a mediating proportion of 5.11%, 11.50%, and 2.25%, respectively,” said principal investigator Xianhui Qin, MD, professor of nephrology at Southern Medical University, Guangzhou, China.

Poor sleep patterns and poor mental health could disrupt circadian rhythms and endocrine and metabolic functions, as well as increase inflammation, he explained.

In addition, chronic exposure to radiofrequency electromagnetic fields (RF-EMF) emitted from cell phones could lead to oxidative stress and an inflammatory response. Combined with smoking and diabetes, this exposure “may have a synergistic effect in increasing CVD risk,” Dr. Qin suggested.

The study was published online in the Canadian Journal of Cardiology.
 

Risk Underestimated?

The researchers aimed to examine the association of regular cell phone use with incident CVD and explore the mediating effects of sleep and mental health using linked hospital and mortality records.

Their analysis included 444,027 participants (mean age, 56 years; 44% men) without a history of CVD from the UK Biobank. A total of 378,161 participants were regular cell phone users.

Regular cell phone use was defined as at least one call per week. Weekly use was self-reported as the average time of calls per week during the previous 3 months.

The primary outcome was incident CVD. Secondary outcomes were each component of CVD (ie, coronary heart disease, stroke, atrial fibrillation, and heart failure) and increased carotid intima media thickness (CIMT).

Compared with nonregular cell phone users, regular users were younger, had higher proportions of current smokers and urban residents, and had lower proportions of history of hypertension and diabetes. They also had higher income, Townsend deprivation index, and body mass index, and lower education levels.

During a median follow-up of 12.3 years, 56,181 participants developed incident CVD. Compared with nonregular cell phone users, regular users had a significantly higher risk for incident CVD (hazard ratio, 1.04) and increased CIMT (odds ratio, 1.11).

Among regular cell phone users, the duration of cell phone use and hands-free device/speakerphone use during calls was not significantly associated with incident CVD. Yet a significant and positive dose-response relationship was seen between weekly cell phone usage time and the risk for CVD. The positive association was stronger in current vs noncurrent smokers and people with vs without diabetes.

To different extents, sleep patterns (5.11%), psychologic distress (11.5%), and neuroticism (2.25%) mediated the relationship between weekly cell phone usage time and the risk for incident CVD.

“Our study suggests that despite the advantages of mobile phone use, we should also pay attention to the potential harm of mobile phone use to cardiovascular health,” Dr. Qin said. “Future studies to assess the risk-benefit balance will help promote mobile phone use patterns that are conducive to cardiovascular health.”

Meanwhile, he added, “We encourage measures to reduce time spent on mobile phones to promote the primary prevention of CVD. On the other hand, improving sleep and mental health status may help reduce the higher risk of CVD associated with mobile phone use.”

There are several limitations to the study in addition to its observational nature, which cannot show cause and effect. The questionnaires on cell phone use were restricted to phone calls; other use patterns of cell phones (eg, messaging, watching videos, and browsing the web) were not considered. Although the researchers adjusted for many potential confounders, unmeasured confounding bias (eg, the type of cell phone used and other sources of RF-EMF) cannot be eliminated.
 

Weak Link?

In a comment, Nicholas Grubic, MSc, a PhD student in epidemiology at the University of Toronto, Ontario, Canada, and coauthor of a related editorial, said, “I found it interesting that there was a connection observed between mobile phone use and CVD. However, it is crucial to understand that this link appeared to be much weaker compared with other well-known cardiovascular risk factors, such as smoking, diabetes, and high blood pressure. For now, mobile phone use should not be a major concern for most people.”

Nevertheless, clinicians should encourage patients to practice healthy habits around their screen time, he advised. “This could include limiting mobile phone use before bedtime and taking regular breaks to engage in activities that promote heart health, such as exercising or spending time outdoors.

“For the time being, we probably won’t see mobile phone use included in standard assessments for cardiovascular risk or as a focal point of cardiovascular health promotion initiatives,” he added. Instead, clinicians should “focus on established risk factors that have a stronger impact on patients’ cardiovascular health.”

Nieca Goldberg, MD, a clinical associate professor of medicine at NYU Grossman School of Medicine in New York City and American Heart Association volunteer expert, had a similar message. “You don’t have to go back to using a landline,” she said. “Instead, patients should be more mindful of how much phone use is taking away from their physical activity, keeping them from sleeping, and causing them stress.” Clinicians should also remember to counsel smokers on smoking cessation.

“It would be important for future studies to look at time spent on the phone and the type of activities patients are doing on their phones, such as social media, calls, texts, movies, or streaming TV shows,” she said. “It would be important to see how phone use is leading to a sedentary lifestyle” and what that means for a larger, more diverse population.

The study was supported by the National Key R&D Program, the National Natural Science Foundation of China, and the Outstanding Youth Development Scheme of Nanfang Hospital, Southern Medical University. Dr. Qin, Dr. Grubic, and Dr. Goldberg reported having no relevant financial relationships.

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

The ABYSS trial found that interruption of beta-blocker therapy in patients after myocardial infarction (MI) was not noninferior to continuing the drugs. 

I will argue why I think it is okay to stop beta-blockers after MI — despite this conclusion. The results of ABYSS are, in fact, similar to REDUCE-AMI, which compared beta-blocker use or nonuse immediately after MI, and found no difference in a composite endpoint of death or MI. 

Translation of the ABYSS trial results to patient care is a case where we must look past the paper’s abstract and conclusions. The key problem is the authors’ choice of primary endpoint, which obscures the correct clinical answer.
 

The ABYSS Trial

ABYSS investigators randomly assigned nearly 3700 patients who had MI and were prescribed a beta-blocker to either continue (control arm) or stop (active arm) the drug at 1 year. 

Patients had to have a left ventricular ejection fraction (LVEF) at least 40%; the median was 60%. 

The composite primary endpoint included death, MI, stroke, or hospitalization for any cardiovascular reason. ABYSS authors chose a noninferiority design. The assumption must have been that the interruption arm offered an easier option for patients — eg, fewer pills. 

Over 3 years, a primary endpoint occurred in 23.8% of the interruption group vs 21.1% in the continuation group. 

In ABYSS, the noninferiority margin was set at a 3% absolute risk increase. The 2.7% absolute risk increase had an upper bound of the 95% CI (worst case) of 5.5% leading to the not-noninferior conclusion (5.5% exceeds the noninferiority margins). 

More simply stated, the primary outcome event rate was higher in the interruption arm. 
 

Does This Mean we Should Continue Beta-Blockers in Post-MI Patients?

This led some to conclude that we should continue beta-blockers. I disagree. To properly interpret the ABYSS trial, you must consider trial procedures, components of the primary endpoint, and then compare ABYSS with REDUCE-AMI. 

It’s also reasonable to have extremely pessimistic prior beliefs about post-MI beta-blockade because the evidence establishing benefit comes from trials conducted before urgent revascularization became the standard therapy. 

ABYSS was a pragmatic open-label trial. The core problem with this design is that one of the components of the primary outcome (hospitalization for cardiovascular reasons) requires clinical judgment — and is therefore susceptible to bias, particularly in an open-label trial. 

This becomes apparent when we look at the components of the primary outcome in the two arms of the trial (interrupt vs continue): 

• For death, the rates were 4.1 and 4.0%
• For MI, the rates were 2.5 and 2.4%
• For stroke, the rates were 1.0% in both arms
• For CV hospitalization, the rates were 18.9% vs 16.6%

The higher rate CV hospitalization alone drove the results of ABYSS. Death, MI, and stroke rates were nearly identical. 

The most common reason for admission to the hospital in this category was for angiography. In fact, the rate of angiography was 2.3% higher in the interruption arm — identical to the rate increase in the CV hospitalization component of the primary endpoint. 

The results of ABYSS, therefore, were driven by higher rates of angiography in the interrupt arm. 

You need not imply malfeasance to speculate that patients who had their beta-blocker stopped might be treated differently regarding hospital admissions or angiography than those who stayed on beta-blockers. Researchers from Imperial College London called such a bias in unblinded trials “subtraction anxiety and faith healing.”

Had the ABYSS investigators chosen the simpler, less bias-prone endpoints of death, MI, or stroke, their results would have been the same as REDUCE-AMI. 
 

My Final Two Conclusions

I would conclude that interruption of beta-blockers at 1 year vs continuation in post-MI patients did not lead to an increase in death, MI, or stroke. 

ABYSS, therefore, is consistent with REDUCE-AMI. Taken together, along with the pessimistic priors, these are important findings because they allow us to stop a medicine and reduce the work of being a patient. 

My second conclusion concerns ways of knowing in medicine. I’ve long felt that randomized controlled trials (RCTs) are the best way to sort out causation. This idea led me to the believe that medicine should have more RCTs rather than follow expert opinion or therapeutic fashion. 

I’ve now modified my love of RCTs — a little. The ABYSS trial is yet another example of the need to be super careful with their design.

Something as seemingly simple as choosing what to measure can alter the way clinicians interpret and use the data. 

So, let’s have (slightly) more trials, but we should be really careful in their design. Slow and careful is the best way to practice medicine. And it’s surely the best way to do research as well.

Dr. Mandrola, clinical electrophysiologist, Baptist Medical Associates, Louisville, Kentucky, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

The ABYSS trial found that interruption of beta-blocker therapy in patients after myocardial infarction (MI) was not noninferior to continuing the drugs. 

I will argue why I think it is okay to stop beta-blockers after MI — despite this conclusion. The results of ABYSS are, in fact, similar to REDUCE-AMI, which compared beta-blocker use or nonuse immediately after MI, and found no difference in a composite endpoint of death or MI. 

Translation of the ABYSS trial results to patient care is a case where we must look past the paper’s abstract and conclusions. The key problem is the authors’ choice of primary endpoint, which obscures the correct clinical answer.
 

The ABYSS Trial

ABYSS investigators randomly assigned nearly 3700 patients who had MI and were prescribed a beta-blocker to either continue (control arm) or stop (active arm) the drug at 1 year. 

Patients had to have a left ventricular ejection fraction (LVEF) at least 40%; the median was 60%. 

The composite primary endpoint included death, MI, stroke, or hospitalization for any cardiovascular reason. ABYSS authors chose a noninferiority design. The assumption must have been that the interruption arm offered an easier option for patients — eg, fewer pills. 

Over 3 years, a primary endpoint occurred in 23.8% of the interruption group vs 21.1% in the continuation group. 

In ABYSS, the noninferiority margin was set at a 3% absolute risk increase. The 2.7% absolute risk increase had an upper bound of the 95% CI (worst case) of 5.5% leading to the not-noninferior conclusion (5.5% exceeds the noninferiority margins). 

More simply stated, the primary outcome event rate was higher in the interruption arm. 
 

Does This Mean we Should Continue Beta-Blockers in Post-MI Patients?

This led some to conclude that we should continue beta-blockers. I disagree. To properly interpret the ABYSS trial, you must consider trial procedures, components of the primary endpoint, and then compare ABYSS with REDUCE-AMI. 

It’s also reasonable to have extremely pessimistic prior beliefs about post-MI beta-blockade because the evidence establishing benefit comes from trials conducted before urgent revascularization became the standard therapy. 

ABYSS was a pragmatic open-label trial. The core problem with this design is that one of the components of the primary outcome (hospitalization for cardiovascular reasons) requires clinical judgment — and is therefore susceptible to bias, particularly in an open-label trial. 

This becomes apparent when we look at the components of the primary outcome in the two arms of the trial (interrupt vs continue): 

• For death, the rates were 4.1 and 4.0%
• For MI, the rates were 2.5 and 2.4%
• For stroke, the rates were 1.0% in both arms
• For CV hospitalization, the rates were 18.9% vs 16.6%

The higher rate CV hospitalization alone drove the results of ABYSS. Death, MI, and stroke rates were nearly identical. 

The most common reason for admission to the hospital in this category was for angiography. In fact, the rate of angiography was 2.3% higher in the interruption arm — identical to the rate increase in the CV hospitalization component of the primary endpoint. 

The results of ABYSS, therefore, were driven by higher rates of angiography in the interrupt arm. 

You need not imply malfeasance to speculate that patients who had their beta-blocker stopped might be treated differently regarding hospital admissions or angiography than those who stayed on beta-blockers. Researchers from Imperial College London called such a bias in unblinded trials “subtraction anxiety and faith healing.”

Had the ABYSS investigators chosen the simpler, less bias-prone endpoints of death, MI, or stroke, their results would have been the same as REDUCE-AMI. 
 

My Final Two Conclusions

I would conclude that interruption of beta-blockers at 1 year vs continuation in post-MI patients did not lead to an increase in death, MI, or stroke. 

ABYSS, therefore, is consistent with REDUCE-AMI. Taken together, along with the pessimistic priors, these are important findings because they allow us to stop a medicine and reduce the work of being a patient. 

My second conclusion concerns ways of knowing in medicine. I’ve long felt that randomized controlled trials (RCTs) are the best way to sort out causation. This idea led me to the believe that medicine should have more RCTs rather than follow expert opinion or therapeutic fashion. 

I’ve now modified my love of RCTs — a little. The ABYSS trial is yet another example of the need to be super careful with their design.

Something as seemingly simple as choosing what to measure can alter the way clinicians interpret and use the data. 

So, let’s have (slightly) more trials, but we should be really careful in their design. Slow and careful is the best way to practice medicine. And it’s surely the best way to do research as well.

Dr. Mandrola, clinical electrophysiologist, Baptist Medical Associates, Louisville, Kentucky, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

The ABYSS trial found that interruption of beta-blocker therapy in patients after myocardial infarction (MI) was not noninferior to continuing the drugs. 

I will argue why I think it is okay to stop beta-blockers after MI — despite this conclusion. The results of ABYSS are, in fact, similar to REDUCE-AMI, which compared beta-blocker use or nonuse immediately after MI, and found no difference in a composite endpoint of death or MI. 

Translation of the ABYSS trial results to patient care is a case where we must look past the paper’s abstract and conclusions. The key problem is the authors’ choice of primary endpoint, which obscures the correct clinical answer.
 

The ABYSS Trial

ABYSS investigators randomly assigned nearly 3700 patients who had MI and were prescribed a beta-blocker to either continue (control arm) or stop (active arm) the drug at 1 year. 

Patients had to have a left ventricular ejection fraction (LVEF) at least 40%; the median was 60%. 

The composite primary endpoint included death, MI, stroke, or hospitalization for any cardiovascular reason. ABYSS authors chose a noninferiority design. The assumption must have been that the interruption arm offered an easier option for patients — eg, fewer pills. 

Over 3 years, a primary endpoint occurred in 23.8% of the interruption group vs 21.1% in the continuation group. 

In ABYSS, the noninferiority margin was set at a 3% absolute risk increase. The 2.7% absolute risk increase had an upper bound of the 95% CI (worst case) of 5.5% leading to the not-noninferior conclusion (5.5% exceeds the noninferiority margins). 

More simply stated, the primary outcome event rate was higher in the interruption arm. 
 

Does This Mean we Should Continue Beta-Blockers in Post-MI Patients?

This led some to conclude that we should continue beta-blockers. I disagree. To properly interpret the ABYSS trial, you must consider trial procedures, components of the primary endpoint, and then compare ABYSS with REDUCE-AMI. 

It’s also reasonable to have extremely pessimistic prior beliefs about post-MI beta-blockade because the evidence establishing benefit comes from trials conducted before urgent revascularization became the standard therapy. 

ABYSS was a pragmatic open-label trial. The core problem with this design is that one of the components of the primary outcome (hospitalization for cardiovascular reasons) requires clinical judgment — and is therefore susceptible to bias, particularly in an open-label trial. 

This becomes apparent when we look at the components of the primary outcome in the two arms of the trial (interrupt vs continue): 

• For death, the rates were 4.1 and 4.0%
• For MI, the rates were 2.5 and 2.4%
• For stroke, the rates were 1.0% in both arms
• For CV hospitalization, the rates were 18.9% vs 16.6%

The higher rate CV hospitalization alone drove the results of ABYSS. Death, MI, and stroke rates were nearly identical. 

The most common reason for admission to the hospital in this category was for angiography. In fact, the rate of angiography was 2.3% higher in the interruption arm — identical to the rate increase in the CV hospitalization component of the primary endpoint. 

The results of ABYSS, therefore, were driven by higher rates of angiography in the interrupt arm. 

You need not imply malfeasance to speculate that patients who had their beta-blocker stopped might be treated differently regarding hospital admissions or angiography than those who stayed on beta-blockers. Researchers from Imperial College London called such a bias in unblinded trials “subtraction anxiety and faith healing.”

Had the ABYSS investigators chosen the simpler, less bias-prone endpoints of death, MI, or stroke, their results would have been the same as REDUCE-AMI. 
 

My Final Two Conclusions

I would conclude that interruption of beta-blockers at 1 year vs continuation in post-MI patients did not lead to an increase in death, MI, or stroke. 

ABYSS, therefore, is consistent with REDUCE-AMI. Taken together, along with the pessimistic priors, these are important findings because they allow us to stop a medicine and reduce the work of being a patient. 

My second conclusion concerns ways of knowing in medicine. I’ve long felt that randomized controlled trials (RCTs) are the best way to sort out causation. This idea led me to the believe that medicine should have more RCTs rather than follow expert opinion or therapeutic fashion. 

I’ve now modified my love of RCTs — a little. The ABYSS trial is yet another example of the need to be super careful with their design.

Something as seemingly simple as choosing what to measure can alter the way clinicians interpret and use the data. 

So, let’s have (slightly) more trials, but we should be really careful in their design. Slow and careful is the best way to practice medicine. And it’s surely the best way to do research as well.

Dr. Mandrola, clinical electrophysiologist, Baptist Medical Associates, Louisville, Kentucky, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

LONDON — It may not be advisable for patients with a history of myocardial infarction and preserved left ventricular function to discontinue long-term beta-blocker therapy, warn investigators.

In the randomized ABYSS trial, although there was no difference in death, MI, or stroke between patients who discontinued and those who continued taking beta-blockers, those who stopped taking the drugs had a higher rate of cardiovascular hospitalization.

Discontinuation was also associated with an increase in blood pressure and heart rate, without any improvement in quality of life.

“We thought we would be able to withdraw beta-blockers safely and that this would result in improved quality of life, but our trial results suggest this is not the case,” said lead investigator Johanne Silvain, MD, PhD, from Pitié-Salpêtrière University Hospital in Paris, who presented the ABYSS findings here at the European Society of Cardiology (ESC) Congress. 

The results, which were simultaneously published online in The New England Journal of Medicine, call into question current guidelines, which suggest that beta-blockers may be discontinued after 1 year in certain patient groups.

Beta-blockers have long been considered the standard of care for patients after MI, but trials showing the benefit of these drugs were conducted before the modern era of myocardial reperfusion and pharmacotherapy, which have led to sharp decreases in the risk for heart failure and for death after MI, Dr. Silvain explained. 

This has led to questions about the add-on benefits of lifelong beta-blocker treatment for patients with MI and a preserved left ventricular ejection fraction and no other primary indication for beta-blocker therapy.
 

The ABYSS Trial

To explore this issue, the open-label, non-inferiority ABYSS trial randomly assigned 3698 patients with a history of MI to the discontinuation or continuation of beta-blocker treatment. All study participants had a left ventricular ejection fraction of at least 40%, were receiving long-term beta-blocker treatment, and had experienced no cardiovascular event in the previous 6 months. 

At a median follow-up of 3 years, the primary endpoint — a composite of death, MI, stroke, and hospitalization for cardiovascular reasons — occurred more often in the discontinuation group than in the continuation group (23.8% vs 21.1%; hazard ratio, 1.16; 95% CI, 1.01-1.33). This did not meet the criteria for non-inferiority of discontinuation, compared with continuation, of beta-blocker therapy (P for non-inferiority = .44).

The difference in event rates between the two groups was driven by cardiovascular hospitalizations, which occurred more often in the discontinuation group than in the continuation group (18.9% vs 16.6%).

Other key results showed that there was no difference in quality of life between the two groups.

However, 6 months after randomization, there were increases in blood pressure and heart rate in the discontinuation group. Systolic blood pressure increased by 3.7 mm Hg and diastolic blood pressure increased by 3.9 mm Hg. Resting heart rate increased by 9.8 beats per minute.

“We were not able to show the non-inferiority of stopping beta-blockers in terms of cardiovascular events, [but we] showed a safety signal with this strategy of an increase in blood pressure and heart rate, with no improvement in quality of life,” Dr. Sylvain said.

“While recent guidelines suggest it may be reasonable to stop beta-blockers in this population, after these results, I will not be stopping these drugs if they are being well tolerated,” he said.

Sylvain said he was surprised that there was not an improvement in quality of life in the group that discontinued beta-blockers. “We are always told that beta-blockers have many side effects, so we expected to see an improvement in quality of life in the patients who stopped these drugs.”

One possible reason for the lack of improvement in quality of life is that the trial participants had been taking beta-blockers for several years. “We may have, therefore, selected patients who tolerate these drugs quite well. Those who had tolerance issues had probably already stopped taking them,” he explained.

In addition, the patient population had relatively high quality-of-life scores at baseline. “They were well treated and the therapies they were taking were well tolerated, so maybe it is difficult to improve quality of life further,” he said.
 

The REDUCE-AMI Trial

The ABYSS results appear at first to differ from results from the recent REDUCE-AMI trial, which failed to show the superiority of beta-blocker therapy, compared with no beta-blocker therapy, in acute MI patients with preserved ejection fraction.

But the REDUCE-AMI primary endpoint was a composite of death from any cause or new myocardial infarction; it did not include cardiovascular hospitalization, which was the main driver of the difference in outcomes in the ABYSS study, Dr. Sylvain pointed out.

“We showed an increase in coronary cases of hospitalization with stopping beta-blockers, and you have to remember that beta-blockers were developed to reduce coronary disease,” he said.
 

‘Slightly Inconclusive’

Jane Armitage, MBBS, University of Oxford, England, the ABYSS discussant for the ESC HOTLINE session, pointed out some limitations of the study, which led her to report that the result was “slightly inconclusive.” 

The open-label design may have allowed some bias regarding the cardiovascular hospitalization endpoint, she said.

“The decision whether to admit a patient to [the] hospital is somewhat subjective and could be influenced by a physician’s knowledge of treatment allocation. That is why, ideally, we prefer blinded trials. I think there are questions there,” she explained.

She also questioned whether the non-inferiority margin could have been increased, given the higher-than-expected event rate.

More data on this issue will come from several trials that are currently ongoing, Dr. Armitage said.

The ABYSS and REDUCE-AMI trials together suggest that it is safe, with respect to serious cardiac events, to stop beta-blocker treatment in MI patients with preserved ejection fraction, writes Tomas Jernberg, MD, PhD, from the Karolinska Institute in Stockholm, Sweden, in an accompanying editorial.

However, “because of the anti-ischemic effects of beta-blockers, an interruption may increase the risk of recurrent angina and the need for rehospitalization,” he adds.

“It is prudent to wait for the results of additional ongoing trials of beta-blockers involving patients with MI and a preserved left ventricular ejection fraction before definitively updating guidelines,” Dr. Jernberg concludes.

The ABYSS trial was funded by the French Ministry of Health and the ACTION Study Group. Dr. Sylvain, Dr. Armitage, and Dr. Jernberg report no relevant financial relationships.

A version of this article appeared on Medscape.com.

LONDON — It may not be advisable for patients with a history of myocardial infarction and preserved left ventricular function to discontinue long-term beta-blocker therapy, warn investigators.

In the randomized ABYSS trial, although there was no difference in death, MI, or stroke between patients who discontinued and those who continued taking beta-blockers, those who stopped taking the drugs had a higher rate of cardiovascular hospitalization.

Discontinuation was also associated with an increase in blood pressure and heart rate, without any improvement in quality of life.

“We thought we would be able to withdraw beta-blockers safely and that this would result in improved quality of life, but our trial results suggest this is not the case,” said lead investigator Johanne Silvain, MD, PhD, from Pitié-Salpêtrière University Hospital in Paris, who presented the ABYSS findings here at the European Society of Cardiology (ESC) Congress. 

The results, which were simultaneously published online in The New England Journal of Medicine, call into question current guidelines, which suggest that beta-blockers may be discontinued after 1 year in certain patient groups.

Beta-blockers have long been considered the standard of care for patients after MI, but trials showing the benefit of these drugs were conducted before the modern era of myocardial reperfusion and pharmacotherapy, which have led to sharp decreases in the risk for heart failure and for death after MI, Dr. Silvain explained. 

This has led to questions about the add-on benefits of lifelong beta-blocker treatment for patients with MI and a preserved left ventricular ejection fraction and no other primary indication for beta-blocker therapy.
 

The ABYSS Trial

To explore this issue, the open-label, non-inferiority ABYSS trial randomly assigned 3698 patients with a history of MI to the discontinuation or continuation of beta-blocker treatment. All study participants had a left ventricular ejection fraction of at least 40%, were receiving long-term beta-blocker treatment, and had experienced no cardiovascular event in the previous 6 months. 

At a median follow-up of 3 years, the primary endpoint — a composite of death, MI, stroke, and hospitalization for cardiovascular reasons — occurred more often in the discontinuation group than in the continuation group (23.8% vs 21.1%; hazard ratio, 1.16; 95% CI, 1.01-1.33). This did not meet the criteria for non-inferiority of discontinuation, compared with continuation, of beta-blocker therapy (P for non-inferiority = .44).

The difference in event rates between the two groups was driven by cardiovascular hospitalizations, which occurred more often in the discontinuation group than in the continuation group (18.9% vs 16.6%).

Other key results showed that there was no difference in quality of life between the two groups.

However, 6 months after randomization, there were increases in blood pressure and heart rate in the discontinuation group. Systolic blood pressure increased by 3.7 mm Hg and diastolic blood pressure increased by 3.9 mm Hg. Resting heart rate increased by 9.8 beats per minute.

“We were not able to show the non-inferiority of stopping beta-blockers in terms of cardiovascular events, [but we] showed a safety signal with this strategy of an increase in blood pressure and heart rate, with no improvement in quality of life,” Dr. Sylvain said.

“While recent guidelines suggest it may be reasonable to stop beta-blockers in this population, after these results, I will not be stopping these drugs if they are being well tolerated,” he said.

Sylvain said he was surprised that there was not an improvement in quality of life in the group that discontinued beta-blockers. “We are always told that beta-blockers have many side effects, so we expected to see an improvement in quality of life in the patients who stopped these drugs.”

One possible reason for the lack of improvement in quality of life is that the trial participants had been taking beta-blockers for several years. “We may have, therefore, selected patients who tolerate these drugs quite well. Those who had tolerance issues had probably already stopped taking them,” he explained.

In addition, the patient population had relatively high quality-of-life scores at baseline. “They were well treated and the therapies they were taking were well tolerated, so maybe it is difficult to improve quality of life further,” he said.
 

The REDUCE-AMI Trial

The ABYSS results appear at first to differ from results from the recent REDUCE-AMI trial, which failed to show the superiority of beta-blocker therapy, compared with no beta-blocker therapy, in acute MI patients with preserved ejection fraction.

But the REDUCE-AMI primary endpoint was a composite of death from any cause or new myocardial infarction; it did not include cardiovascular hospitalization, which was the main driver of the difference in outcomes in the ABYSS study, Dr. Sylvain pointed out.

“We showed an increase in coronary cases of hospitalization with stopping beta-blockers, and you have to remember that beta-blockers were developed to reduce coronary disease,” he said.
 

‘Slightly Inconclusive’

Jane Armitage, MBBS, University of Oxford, England, the ABYSS discussant for the ESC HOTLINE session, pointed out some limitations of the study, which led her to report that the result was “slightly inconclusive.” 

The open-label design may have allowed some bias regarding the cardiovascular hospitalization endpoint, she said.

“The decision whether to admit a patient to [the] hospital is somewhat subjective and could be influenced by a physician’s knowledge of treatment allocation. That is why, ideally, we prefer blinded trials. I think there are questions there,” she explained.

She also questioned whether the non-inferiority margin could have been increased, given the higher-than-expected event rate.

More data on this issue will come from several trials that are currently ongoing, Dr. Armitage said.

The ABYSS and REDUCE-AMI trials together suggest that it is safe, with respect to serious cardiac events, to stop beta-blocker treatment in MI patients with preserved ejection fraction, writes Tomas Jernberg, MD, PhD, from the Karolinska Institute in Stockholm, Sweden, in an accompanying editorial.

However, “because of the anti-ischemic effects of beta-blockers, an interruption may increase the risk of recurrent angina and the need for rehospitalization,” he adds.

“It is prudent to wait for the results of additional ongoing trials of beta-blockers involving patients with MI and a preserved left ventricular ejection fraction before definitively updating guidelines,” Dr. Jernberg concludes.

The ABYSS trial was funded by the French Ministry of Health and the ACTION Study Group. Dr. Sylvain, Dr. Armitage, and Dr. Jernberg report no relevant financial relationships.

A version of this article appeared on Medscape.com.

LONDON — It may not be advisable for patients with a history of myocardial infarction and preserved left ventricular function to discontinue long-term beta-blocker therapy, warn investigators.

In the randomized ABYSS trial, although there was no difference in death, MI, or stroke between patients who discontinued and those who continued taking beta-blockers, those who stopped taking the drugs had a higher rate of cardiovascular hospitalization.

Discontinuation was also associated with an increase in blood pressure and heart rate, without any improvement in quality of life.

“We thought we would be able to withdraw beta-blockers safely and that this would result in improved quality of life, but our trial results suggest this is not the case,” said lead investigator Johanne Silvain, MD, PhD, from Pitié-Salpêtrière University Hospital in Paris, who presented the ABYSS findings here at the European Society of Cardiology (ESC) Congress. 

The results, which were simultaneously published online in The New England Journal of Medicine, call into question current guidelines, which suggest that beta-blockers may be discontinued after 1 year in certain patient groups.

Beta-blockers have long been considered the standard of care for patients after MI, but trials showing the benefit of these drugs were conducted before the modern era of myocardial reperfusion and pharmacotherapy, which have led to sharp decreases in the risk for heart failure and for death after MI, Dr. Silvain explained. 

This has led to questions about the add-on benefits of lifelong beta-blocker treatment for patients with MI and a preserved left ventricular ejection fraction and no other primary indication for beta-blocker therapy.
 

The ABYSS Trial

To explore this issue, the open-label, non-inferiority ABYSS trial randomly assigned 3698 patients with a history of MI to the discontinuation or continuation of beta-blocker treatment. All study participants had a left ventricular ejection fraction of at least 40%, were receiving long-term beta-blocker treatment, and had experienced no cardiovascular event in the previous 6 months. 

At a median follow-up of 3 years, the primary endpoint — a composite of death, MI, stroke, and hospitalization for cardiovascular reasons — occurred more often in the discontinuation group than in the continuation group (23.8% vs 21.1%; hazard ratio, 1.16; 95% CI, 1.01-1.33). This did not meet the criteria for non-inferiority of discontinuation, compared with continuation, of beta-blocker therapy (P for non-inferiority = .44).

The difference in event rates between the two groups was driven by cardiovascular hospitalizations, which occurred more often in the discontinuation group than in the continuation group (18.9% vs 16.6%).

Other key results showed that there was no difference in quality of life between the two groups.

However, 6 months after randomization, there were increases in blood pressure and heart rate in the discontinuation group. Systolic blood pressure increased by 3.7 mm Hg and diastolic blood pressure increased by 3.9 mm Hg. Resting heart rate increased by 9.8 beats per minute.

“We were not able to show the non-inferiority of stopping beta-blockers in terms of cardiovascular events, [but we] showed a safety signal with this strategy of an increase in blood pressure and heart rate, with no improvement in quality of life,” Dr. Sylvain said.

“While recent guidelines suggest it may be reasonable to stop beta-blockers in this population, after these results, I will not be stopping these drugs if they are being well tolerated,” he said.

Sylvain said he was surprised that there was not an improvement in quality of life in the group that discontinued beta-blockers. “We are always told that beta-blockers have many side effects, so we expected to see an improvement in quality of life in the patients who stopped these drugs.”

One possible reason for the lack of improvement in quality of life is that the trial participants had been taking beta-blockers for several years. “We may have, therefore, selected patients who tolerate these drugs quite well. Those who had tolerance issues had probably already stopped taking them,” he explained.

In addition, the patient population had relatively high quality-of-life scores at baseline. “They were well treated and the therapies they were taking were well tolerated, so maybe it is difficult to improve quality of life further,” he said.
 

The REDUCE-AMI Trial

The ABYSS results appear at first to differ from results from the recent REDUCE-AMI trial, which failed to show the superiority of beta-blocker therapy, compared with no beta-blocker therapy, in acute MI patients with preserved ejection fraction.

But the REDUCE-AMI primary endpoint was a composite of death from any cause or new myocardial infarction; it did not include cardiovascular hospitalization, which was the main driver of the difference in outcomes in the ABYSS study, Dr. Sylvain pointed out.

“We showed an increase in coronary cases of hospitalization with stopping beta-blockers, and you have to remember that beta-blockers were developed to reduce coronary disease,” he said.
 

‘Slightly Inconclusive’

Jane Armitage, MBBS, University of Oxford, England, the ABYSS discussant for the ESC HOTLINE session, pointed out some limitations of the study, which led her to report that the result was “slightly inconclusive.” 

The open-label design may have allowed some bias regarding the cardiovascular hospitalization endpoint, she said.

“The decision whether to admit a patient to [the] hospital is somewhat subjective and could be influenced by a physician’s knowledge of treatment allocation. That is why, ideally, we prefer blinded trials. I think there are questions there,” she explained.

She also questioned whether the non-inferiority margin could have been increased, given the higher-than-expected event rate.

More data on this issue will come from several trials that are currently ongoing, Dr. Armitage said.

The ABYSS and REDUCE-AMI trials together suggest that it is safe, with respect to serious cardiac events, to stop beta-blocker treatment in MI patients with preserved ejection fraction, writes Tomas Jernberg, MD, PhD, from the Karolinska Institute in Stockholm, Sweden, in an accompanying editorial.

However, “because of the anti-ischemic effects of beta-blockers, an interruption may increase the risk of recurrent angina and the need for rehospitalization,” he adds.

“It is prudent to wait for the results of additional ongoing trials of beta-blockers involving patients with MI and a preserved left ventricular ejection fraction before definitively updating guidelines,” Dr. Jernberg concludes.

The ABYSS trial was funded by the French Ministry of Health and the ACTION Study Group. Dr. Sylvain, Dr. Armitage, and Dr. Jernberg report no relevant financial relationships.

A version of this article appeared on Medscape.com.

TOPLINE:

A higher resting heart rate, even within the normal range, is linked to an increased risk for mortality and cardiovascular events in patients with non–dialysis-dependent chronic kidney disease (CKD).

METHODOLOGY:

• An elevated resting heart rate is an independent risk factor for all-cause mortality and cardiovascular events in the general population; however, the correlation between heart rate and mortality in patients with CKD is unclear.
• Researchers analyzed the longitudinal data of patients with non–dialysis-dependent CKD enrolled in the Fukushima CKD Cohort Study to investigate the association between resting heart rate and adverse clinical outcomes.
• The patient cohort was stratified into four groups on the basis of resting heart rates: < 70, 70-79, 80-89, and ≥ 90 beats/min.
• The primary and secondary outcomes were all-cause mortality and cardiovascular events, respectively, the latter category including myocardial infarction, angina pectoris, and heart failure.

TAKEAWAY:

• Researchers enrolled 1353 patients with non–dialysis-dependent CKD (median age, 65 years; 56.7% men; median estimated glomerular filtration rate, 52.2 mL/min/1.73 m²) who had a median heart rate of 76 beats/min.
• During the median observation period of 4.9 years, 123 patients died and 163 developed cardiovascular events.
• Compared with patients with a resting heart rate < 70 beats/min, those with a resting heart rate of 80-89 and ≥ 90 beats/min had an adjusted hazard ratio of 1.74 and 2.61 for all-cause mortality, respectively.
• Similarly, the risk for cardiovascular events was higher in patients with a heart rate of 80-89 beats/min than in those with a heart rate < 70 beats/min (adjusted hazard ratio, 1.70).

IN PRACTICE:

“The present study supported the idea that reducing heart rate might be effective for CKD patients with a heart rate ≥ 70/min, since the lowest risk of mortality was seen in patients with heart rate < 70/min,” the authors concluded. 

SOURCE:

This study was led by Hirotaka Saito, Department of Nephrology and Hypertension, Fukushima Medical University, Fukushima City, Japan. It was published online in Scientific Reports.

LIMITATIONS:

Heart rate was measured using a standard sphygmomanometer or an automated device, rather than an electrocardiograph, which may have introduced measurement variability. The observational nature of the study precluded the establishment of cause-and-effect relationships between heart rate and clinical outcomes. Additionally, variables such as lifestyle factors, underlying health conditions, and socioeconomic factors were not measured, which could have affected the results. 

DISCLOSURES:

Some authors received research funding from Chugai Pharmaceutical, Kowa Pharmaceutical, Ono Pharmaceutical, and other sources. They declared having no competing interests.

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:

A higher resting heart rate, even within the normal range, is linked to an increased risk for mortality and cardiovascular events in patients with non–dialysis-dependent chronic kidney disease (CKD).

METHODOLOGY:

• An elevated resting heart rate is an independent risk factor for all-cause mortality and cardiovascular events in the general population; however, the correlation between heart rate and mortality in patients with CKD is unclear.
• Researchers analyzed the longitudinal data of patients with non–dialysis-dependent CKD enrolled in the Fukushima CKD Cohort Study to investigate the association between resting heart rate and adverse clinical outcomes.
• The patient cohort was stratified into four groups on the basis of resting heart rates: < 70, 70-79, 80-89, and ≥ 90 beats/min.
• The primary and secondary outcomes were all-cause mortality and cardiovascular events, respectively, the latter category including myocardial infarction, angina pectoris, and heart failure.

TAKEAWAY:

• Researchers enrolled 1353 patients with non–dialysis-dependent CKD (median age, 65 years; 56.7% men; median estimated glomerular filtration rate, 52.2 mL/min/1.73 m²) who had a median heart rate of 76 beats/min.
• During the median observation period of 4.9 years, 123 patients died and 163 developed cardiovascular events.
• Compared with patients with a resting heart rate < 70 beats/min, those with a resting heart rate of 80-89 and ≥ 90 beats/min had an adjusted hazard ratio of 1.74 and 2.61 for all-cause mortality, respectively.
• Similarly, the risk for cardiovascular events was higher in patients with a heart rate of 80-89 beats/min than in those with a heart rate < 70 beats/min (adjusted hazard ratio, 1.70).

IN PRACTICE:

“The present study supported the idea that reducing heart rate might be effective for CKD patients with a heart rate ≥ 70/min, since the lowest risk of mortality was seen in patients with heart rate < 70/min,” the authors concluded. 

SOURCE:

This study was led by Hirotaka Saito, Department of Nephrology and Hypertension, Fukushima Medical University, Fukushima City, Japan. It was published online in Scientific Reports.

LIMITATIONS:

Heart rate was measured using a standard sphygmomanometer or an automated device, rather than an electrocardiograph, which may have introduced measurement variability. The observational nature of the study precluded the establishment of cause-and-effect relationships between heart rate and clinical outcomes. Additionally, variables such as lifestyle factors, underlying health conditions, and socioeconomic factors were not measured, which could have affected the results. 

DISCLOSURES:

Some authors received research funding from Chugai Pharmaceutical, Kowa Pharmaceutical, Ono Pharmaceutical, and other sources. They declared having no competing interests.

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:

A higher resting heart rate, even within the normal range, is linked to an increased risk for mortality and cardiovascular events in patients with non–dialysis-dependent chronic kidney disease (CKD).

METHODOLOGY:

• An elevated resting heart rate is an independent risk factor for all-cause mortality and cardiovascular events in the general population; however, the correlation between heart rate and mortality in patients with CKD is unclear.
• Researchers analyzed the longitudinal data of patients with non–dialysis-dependent CKD enrolled in the Fukushima CKD Cohort Study to investigate the association between resting heart rate and adverse clinical outcomes.
• The patient cohort was stratified into four groups on the basis of resting heart rates: < 70, 70-79, 80-89, and ≥ 90 beats/min.
• The primary and secondary outcomes were all-cause mortality and cardiovascular events, respectively, the latter category including myocardial infarction, angina pectoris, and heart failure.

TAKEAWAY:

• Researchers enrolled 1353 patients with non–dialysis-dependent CKD (median age, 65 years; 56.7% men; median estimated glomerular filtration rate, 52.2 mL/min/1.73 m²) who had a median heart rate of 76 beats/min.
• During the median observation period of 4.9 years, 123 patients died and 163 developed cardiovascular events.
• Compared with patients with a resting heart rate < 70 beats/min, those with a resting heart rate of 80-89 and ≥ 90 beats/min had an adjusted hazard ratio of 1.74 and 2.61 for all-cause mortality, respectively.
• Similarly, the risk for cardiovascular events was higher in patients with a heart rate of 80-89 beats/min than in those with a heart rate < 70 beats/min (adjusted hazard ratio, 1.70).

IN PRACTICE:

“The present study supported the idea that reducing heart rate might be effective for CKD patients with a heart rate ≥ 70/min, since the lowest risk of mortality was seen in patients with heart rate < 70/min,” the authors concluded. 

SOURCE:

This study was led by Hirotaka Saito, Department of Nephrology and Hypertension, Fukushima Medical University, Fukushima City, Japan. It was published online in Scientific Reports.

LIMITATIONS:

Heart rate was measured using a standard sphygmomanometer or an automated device, rather than an electrocardiograph, which may have introduced measurement variability. The observational nature of the study precluded the establishment of cause-and-effect relationships between heart rate and clinical outcomes. Additionally, variables such as lifestyle factors, underlying health conditions, and socioeconomic factors were not measured, which could have affected the results. 

DISCLOSURES:

Some authors received research funding from Chugai Pharmaceutical, Kowa Pharmaceutical, Ono Pharmaceutical, and other sources. They declared having no competing interests.

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:

Xanthelasma palpebrarum, characterized by yellowish plaques on the eyelids, is not associated with increased rates of dyslipidemia or cardiovascular disease.

METHODOLOGY:

• Researchers conducted a case-control study at a single tertiary care center in Israel and analyzed data from 35,452 individuals (mean age, 52.2 years; 69% men) who underwent medical screening from 2001 to 2020.
• They compared 203 patients with xanthelasma palpebrarum with 2030 individuals without the disease (control).
• Primary outcomes were prevalence of dyslipidemia and cardiovascular disease between the two groups.

TAKEAWAY:

• Lipid profiles were similar between the two groups, with no difference in total cholesterol, high- and low-density lipoprotein, and triglyceride levels (all P > .05).
• The prevalence of dyslipidemia was similar for patients with xanthelasma palpebrarum and controls (46% vs 42%, respectively; P = .29), as was the incidence of cardiovascular disease (8.9% vs 10%, respectively; P = .56).
• The incidence of diabetes (P = .13), cerebrovascular accidents (P > .99), ischemic heart disease (P = .73), and hypertension (P = .56) were not significantly different between the two groups.

IN PRACTICE:

“Our study conducted on a large population of individuals undergoing comprehensive ophthalmic and systemic screening tests did not find a significant association between xanthelasma palpebrarum and an increased prevalence of lipid abnormalities or cardiovascular disease,” the authors wrote.

SOURCE:

The study was led by Yael Lustig, MD, of the Goldschleger Eye Institute at Sheba Medical Center, in Ramat Gan, Israel. It was published online on August 5, 2024, in Ophthalmology.

LIMITATIONS:

The retrospective nature of the study and the single-center design may have limited the generalizability of the findings. The study population was self-selected, potentially introducing selection bias. Lack of histopathologic examination could have affected the accuracy of the diagnosis.

DISCLOSURES:

No funding sources were disclosed for this study. The authors declared no conflicts of interest.

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:

Xanthelasma palpebrarum, characterized by yellowish plaques on the eyelids, is not associated with increased rates of dyslipidemia or cardiovascular disease.

METHODOLOGY:

• Researchers conducted a case-control study at a single tertiary care center in Israel and analyzed data from 35,452 individuals (mean age, 52.2 years; 69% men) who underwent medical screening from 2001 to 2020.
• They compared 203 patients with xanthelasma palpebrarum with 2030 individuals without the disease (control).
• Primary outcomes were prevalence of dyslipidemia and cardiovascular disease between the two groups.

TAKEAWAY:

• Lipid profiles were similar between the two groups, with no difference in total cholesterol, high- and low-density lipoprotein, and triglyceride levels (all P > .05).
• The prevalence of dyslipidemia was similar for patients with xanthelasma palpebrarum and controls (46% vs 42%, respectively; P = .29), as was the incidence of cardiovascular disease (8.9% vs 10%, respectively; P = .56).
• The incidence of diabetes (P = .13), cerebrovascular accidents (P > .99), ischemic heart disease (P = .73), and hypertension (P = .56) were not significantly different between the two groups.

IN PRACTICE:

“Our study conducted on a large population of individuals undergoing comprehensive ophthalmic and systemic screening tests did not find a significant association between xanthelasma palpebrarum and an increased prevalence of lipid abnormalities or cardiovascular disease,” the authors wrote.

SOURCE:

The study was led by Yael Lustig, MD, of the Goldschleger Eye Institute at Sheba Medical Center, in Ramat Gan, Israel. It was published online on August 5, 2024, in Ophthalmology.

LIMITATIONS:

The retrospective nature of the study and the single-center design may have limited the generalizability of the findings. The study population was self-selected, potentially introducing selection bias. Lack of histopathologic examination could have affected the accuracy of the diagnosis.

DISCLOSURES:

No funding sources were disclosed for this study. The authors declared no conflicts of interest.

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:

Xanthelasma palpebrarum, characterized by yellowish plaques on the eyelids, is not associated with increased rates of dyslipidemia or cardiovascular disease.

METHODOLOGY:

• Researchers conducted a case-control study at a single tertiary care center in Israel and analyzed data from 35,452 individuals (mean age, 52.2 years; 69% men) who underwent medical screening from 2001 to 2020.
• They compared 203 patients with xanthelasma palpebrarum with 2030 individuals without the disease (control).
• Primary outcomes were prevalence of dyslipidemia and cardiovascular disease between the two groups.

TAKEAWAY:

• Lipid profiles were similar between the two groups, with no difference in total cholesterol, high- and low-density lipoprotein, and triglyceride levels (all P > .05).
• The prevalence of dyslipidemia was similar for patients with xanthelasma palpebrarum and controls (46% vs 42%, respectively; P = .29), as was the incidence of cardiovascular disease (8.9% vs 10%, respectively; P = .56).
• The incidence of diabetes (P = .13), cerebrovascular accidents (P > .99), ischemic heart disease (P = .73), and hypertension (P = .56) were not significantly different between the two groups.

IN PRACTICE:

“Our study conducted on a large population of individuals undergoing comprehensive ophthalmic and systemic screening tests did not find a significant association between xanthelasma palpebrarum and an increased prevalence of lipid abnormalities or cardiovascular disease,” the authors wrote.

SOURCE:

The study was led by Yael Lustig, MD, of the Goldschleger Eye Institute at Sheba Medical Center, in Ramat Gan, Israel. It was published online on August 5, 2024, in Ophthalmology.

LIMITATIONS:

The retrospective nature of the study and the single-center design may have limited the generalizability of the findings. The study population was self-selected, potentially introducing selection bias. Lack of histopathologic examination could have affected the accuracy of the diagnosis.

DISCLOSURES:

No funding sources were disclosed for this study. The authors declared no conflicts of interest.

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.

The new American Heart Association Predicting Risk of cardiovascular disease EVENTs (PREVENT) equation outperforms the standard pooled cohort equation (PCE). But there is a problem. A big one, actually. 

The new score incorporates kidney function and social situation, and it eliminates race from the estimate. It was derived from larger, more modern datasets and can be applied to younger adults. 

Two luminaries in preventive cardiology recently called the PREVENT calculator a “substantial improvement over the PCE in terms of accuracy and precision of risk estimates over the entire population and within demographic subgroups.”
 

Now to the Problem of PREVENT vs PCE

A recent study comparing PREVENT and PCE found that the PREVENT equation would assign lower 10-year risks to millions of US adults. 

The authors estimated that the more accurate calculator would result in an estimated 14 million adults no longer reaching the statin eligibility risk threshold of 7.5% over 10 years. Nearly 3 million adults would also not reach the threshold for blood pressure therapy. 

Because statins and blood pressure drugs reduce cardiac events, the authors further estimated that more than 100,000 excess myocardial infarctions (MIs) would occur if the PREVENT equation was used along with the current risk thresholds for statin eligibility.

The change in eligibility induced by PREVENT would affect more men than women and a greater proportion of Black adults than White adults. 
 

The Tension of Arbitrary Thresholds

Modern cardiac therapeutics are amazing, but it’s still better to prevent an event than to treat it. 

Statin drugs reduce cardiac risk by about 20%-25% at all absolute risks. American experts chose a 10-year risk of 7.5% as the threshold where statin benefit exceed risk. The USPSTF chose 10%. But the thresholds are arbitrary and derived only by opinion. 

If your frame is population health, the more patients who take statins, the fewer cardiac events there will be. Anything that reduces statin use increases cardiac events. 

The tension occurs because a more accurate equation decreases the number of people who meet eligibility for primary prevention therapy and therefore increases the number of cardiac events. 

I write from the perspective of both a clinician and a possible patient. As a clinician, patients often ask me whether they should take a statin. (Sadly, most have not had a risk-based discussion with their clinician. But that is another column.) 

The incidence of MI or stroke in a population has no effect on either of these scenarios. I see three broad categories of patients: minimizers, maximizers, and those in between. 

I am a minimizer. I don’t worry much about heart disease. First, I won’t ignore symptoms, and I know that we have great treatments. Second, my wife, Staci, practiced hospice and palliative care medicine, and this taught me that worrying about one specific disease is folly. In the next decade, I, like anyone my age, could have many other bad things happen: cancer, trauma, infection, etc. Given these competing risks for serious disease, a PREVENT-calculated risk of 4% or a PCE-calculated risk of 8% makes no difference. I don’t like pills, and, with risks in this range, I decline statin drugs. 

Then there are the maximizers. This person wants to avoid heart disease. Maybe they have family or friends who had terrible cardiac events. This person will maximize everything to avoid heart disease. The calculated 10-year risk makes little difference to a maximizer. Whether it is 4% or 8% matters not. They will take a statin or blood pressure drugs to reduce risk to as low as possible. 

There are people between minimizers and maximizers. I am not sure that there are that many truly undecided people, but I challenge you to translate a difference of a few percent over a decade to them. I feel comfortable with numbers but struggle to sort out these small absolute differences over such a long time frame. 
 

Other Issues With Risk-Based Decisions 

Venk Murthy, MD, PhD, from the University of Michigan, wrote on X about two other issues with a risk-based decision. One is that it does not consider life-years lost. If a 50-year-old person has a fatal MI, that counts as one event. But in life-years lost, that one event is much worse than a fatal MI in a 79-year-old. Cardiac prevention, therefore, may have a greater effect in lower-risk younger people. 

Another point Dr. Murthy made is that risk and benefit are driven by many different preferences and rare events. Minimizers and maximizers come to the decision with widely disparate preferences. Risk-based decisions treat patients as if they were automatons who make decisions based simply on calculated probabilities. Clinicians know how untrue that is. 
 

Conclusion

If you carry forward the logic of being disturbed by the estimate of more MIs using the PREVENT score, then you could justify putting statins in the water — because that would reduce population estimates of MIs. 

I am not disturbed by the PREVENT score. Clinicians treat individuals, not populations. Individuals want a more accurate score. They don’t need expert-based thresholds. Clinician and patient can discuss the evidence and come up with an agreeable decision, one that is concordant with a person’s goals. The next patient may have a different decision despite seeing the same evidence. 

The tension created by this comparative study exposes the gap between population health and basic clinical care. I don’t think clinicians need to worry about populations. 
 

Dr. Mandrola, a clinical electrophysiologist at Baptist Medical Associates, Louisville, Kentucky, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

The new American Heart Association Predicting Risk of cardiovascular disease EVENTs (PREVENT) equation outperforms the standard pooled cohort equation (PCE). But there is a problem. A big one, actually. 

The new score incorporates kidney function and social situation, and it eliminates race from the estimate. It was derived from larger, more modern datasets and can be applied to younger adults. 

Two luminaries in preventive cardiology recently called the PREVENT calculator a “substantial improvement over the PCE in terms of accuracy and precision of risk estimates over the entire population and within demographic subgroups.”
 

Now to the Problem of PREVENT vs PCE

A recent study comparing PREVENT and PCE found that the PREVENT equation would assign lower 10-year risks to millions of US adults. 

The authors estimated that the more accurate calculator would result in an estimated 14 million adults no longer reaching the statin eligibility risk threshold of 7.5% over 10 years. Nearly 3 million adults would also not reach the threshold for blood pressure therapy. 

Because statins and blood pressure drugs reduce cardiac events, the authors further estimated that more than 100,000 excess myocardial infarctions (MIs) would occur if the PREVENT equation was used along with the current risk thresholds for statin eligibility.

The change in eligibility induced by PREVENT would affect more men than women and a greater proportion of Black adults than White adults. 
 

The Tension of Arbitrary Thresholds

Modern cardiac therapeutics are amazing, but it’s still better to prevent an event than to treat it. 

Statin drugs reduce cardiac risk by about 20%-25% at all absolute risks. American experts chose a 10-year risk of 7.5% as the threshold where statin benefit exceed risk. The USPSTF chose 10%. But the thresholds are arbitrary and derived only by opinion. 

If your frame is population health, the more patients who take statins, the fewer cardiac events there will be. Anything that reduces statin use increases cardiac events. 

The tension occurs because a more accurate equation decreases the number of people who meet eligibility for primary prevention therapy and therefore increases the number of cardiac events. 

I write from the perspective of both a clinician and a possible patient. As a clinician, patients often ask me whether they should take a statin. (Sadly, most have not had a risk-based discussion with their clinician. But that is another column.) 

The incidence of MI or stroke in a population has no effect on either of these scenarios. I see three broad categories of patients: minimizers, maximizers, and those in between. 

I am a minimizer. I don’t worry much about heart disease. First, I won’t ignore symptoms, and I know that we have great treatments. Second, my wife, Staci, practiced hospice and palliative care medicine, and this taught me that worrying about one specific disease is folly. In the next decade, I, like anyone my age, could have many other bad things happen: cancer, trauma, infection, etc. Given these competing risks for serious disease, a PREVENT-calculated risk of 4% or a PCE-calculated risk of 8% makes no difference. I don’t like pills, and, with risks in this range, I decline statin drugs. 

Then there are the maximizers. This person wants to avoid heart disease. Maybe they have family or friends who had terrible cardiac events. This person will maximize everything to avoid heart disease. The calculated 10-year risk makes little difference to a maximizer. Whether it is 4% or 8% matters not. They will take a statin or blood pressure drugs to reduce risk to as low as possible. 

There are people between minimizers and maximizers. I am not sure that there are that many truly undecided people, but I challenge you to translate a difference of a few percent over a decade to them. I feel comfortable with numbers but struggle to sort out these small absolute differences over such a long time frame. 
 

Other Issues With Risk-Based Decisions 

Venk Murthy, MD, PhD, from the University of Michigan, wrote on X about two other issues with a risk-based decision. One is that it does not consider life-years lost. If a 50-year-old person has a fatal MI, that counts as one event. But in life-years lost, that one event is much worse than a fatal MI in a 79-year-old. Cardiac prevention, therefore, may have a greater effect in lower-risk younger people. 

Another point Dr. Murthy made is that risk and benefit are driven by many different preferences and rare events. Minimizers and maximizers come to the decision with widely disparate preferences. Risk-based decisions treat patients as if they were automatons who make decisions based simply on calculated probabilities. Clinicians know how untrue that is. 
 

Conclusion

If you carry forward the logic of being disturbed by the estimate of more MIs using the PREVENT score, then you could justify putting statins in the water — because that would reduce population estimates of MIs. 

I am not disturbed by the PREVENT score. Clinicians treat individuals, not populations. Individuals want a more accurate score. They don’t need expert-based thresholds. Clinician and patient can discuss the evidence and come up with an agreeable decision, one that is concordant with a person’s goals. The next patient may have a different decision despite seeing the same evidence. 

The tension created by this comparative study exposes the gap between population health and basic clinical care. I don’t think clinicians need to worry about populations. 
 

Dr. Mandrola, a clinical electrophysiologist at Baptist Medical Associates, Louisville, Kentucky, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

The new American Heart Association Predicting Risk of cardiovascular disease EVENTs (PREVENT) equation outperforms the standard pooled cohort equation (PCE). But there is a problem. A big one, actually. 

The new score incorporates kidney function and social situation, and it eliminates race from the estimate. It was derived from larger, more modern datasets and can be applied to younger adults. 

Two luminaries in preventive cardiology recently called the PREVENT calculator a “substantial improvement over the PCE in terms of accuracy and precision of risk estimates over the entire population and within demographic subgroups.”
 

Now to the Problem of PREVENT vs PCE

A recent study comparing PREVENT and PCE found that the PREVENT equation would assign lower 10-year risks to millions of US adults. 

The authors estimated that the more accurate calculator would result in an estimated 14 million adults no longer reaching the statin eligibility risk threshold of 7.5% over 10 years. Nearly 3 million adults would also not reach the threshold for blood pressure therapy. 

Because statins and blood pressure drugs reduce cardiac events, the authors further estimated that more than 100,000 excess myocardial infarctions (MIs) would occur if the PREVENT equation was used along with the current risk thresholds for statin eligibility.

The change in eligibility induced by PREVENT would affect more men than women and a greater proportion of Black adults than White adults. 
 

The Tension of Arbitrary Thresholds

Modern cardiac therapeutics are amazing, but it’s still better to prevent an event than to treat it. 

Statin drugs reduce cardiac risk by about 20%-25% at all absolute risks. American experts chose a 10-year risk of 7.5% as the threshold where statin benefit exceed risk. The USPSTF chose 10%. But the thresholds are arbitrary and derived only by opinion. 

If your frame is population health, the more patients who take statins, the fewer cardiac events there will be. Anything that reduces statin use increases cardiac events. 

The tension occurs because a more accurate equation decreases the number of people who meet eligibility for primary prevention therapy and therefore increases the number of cardiac events. 

I write from the perspective of both a clinician and a possible patient. As a clinician, patients often ask me whether they should take a statin. (Sadly, most have not had a risk-based discussion with their clinician. But that is another column.) 

The incidence of MI or stroke in a population has no effect on either of these scenarios. I see three broad categories of patients: minimizers, maximizers, and those in between. 

I am a minimizer. I don’t worry much about heart disease. First, I won’t ignore symptoms, and I know that we have great treatments. Second, my wife, Staci, practiced hospice and palliative care medicine, and this taught me that worrying about one specific disease is folly. In the next decade, I, like anyone my age, could have many other bad things happen: cancer, trauma, infection, etc. Given these competing risks for serious disease, a PREVENT-calculated risk of 4% or a PCE-calculated risk of 8% makes no difference. I don’t like pills, and, with risks in this range, I decline statin drugs. 

Then there are the maximizers. This person wants to avoid heart disease. Maybe they have family or friends who had terrible cardiac events. This person will maximize everything to avoid heart disease. The calculated 10-year risk makes little difference to a maximizer. Whether it is 4% or 8% matters not. They will take a statin or blood pressure drugs to reduce risk to as low as possible. 

There are people between minimizers and maximizers. I am not sure that there are that many truly undecided people, but I challenge you to translate a difference of a few percent over a decade to them. I feel comfortable with numbers but struggle to sort out these small absolute differences over such a long time frame. 
 

Other Issues With Risk-Based Decisions 

Venk Murthy, MD, PhD, from the University of Michigan, wrote on X about two other issues with a risk-based decision. One is that it does not consider life-years lost. If a 50-year-old person has a fatal MI, that counts as one event. But in life-years lost, that one event is much worse than a fatal MI in a 79-year-old. Cardiac prevention, therefore, may have a greater effect in lower-risk younger people. 

Another point Dr. Murthy made is that risk and benefit are driven by many different preferences and rare events. Minimizers and maximizers come to the decision with widely disparate preferences. Risk-based decisions treat patients as if they were automatons who make decisions based simply on calculated probabilities. Clinicians know how untrue that is. 
 

Conclusion

If you carry forward the logic of being disturbed by the estimate of more MIs using the PREVENT score, then you could justify putting statins in the water — because that would reduce population estimates of MIs. 

I am not disturbed by the PREVENT score. Clinicians treat individuals, not populations. Individuals want a more accurate score. They don’t need expert-based thresholds. Clinician and patient can discuss the evidence and come up with an agreeable decision, one that is concordant with a person’s goals. The next patient may have a different decision despite seeing the same evidence. 

The tension created by this comparative study exposes the gap between population health and basic clinical care. I don’t think clinicians need to worry about populations. 
 

Dr. Mandrola, a clinical electrophysiologist at Baptist Medical Associates, Louisville, Kentucky, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Giving patients a beta-blocker after a myocardial infarction is standard of care. It’s in the guidelines. It’s one of the performance measures used by the American College of Cardiology (ACC) and the American Heart Association (AHA). If you aren’t putting your post–acute coronary syndrome (ACS) patients on a beta-blocker, the ACC and the AHA both think you suck. 

They are very disappointed in you, just like your mother was when you told her you didn’t want to become a surgeon because you don’t like waking up early, your hands shake when you get nervous, it’s not your fault, there’s nothing you can do about it, so just leave me alone!

The data on beta-blockers are decades old. In the time before stents, statins, angiotensin-converting enzyme inhibitors, and dual antiplatelet therapy, when patients either died or got better on their own, beta-blockers showed major benefits. Studies like the Norwegian Multicenter Study Group, the BHAT trial, and the ISIS-1 trial proved the benefits of beta blockade. These studies date back to the 1980s, when you could call a study ISIS without controversy. 

It was a simpler time, when all you had to worry about was the Cold War, apartheid, and the global AIDS pandemic. It was a time when doctors smoked in their offices, and patients had bigger infarcts that caused large scars and systolic dysfunction. That world is no longer our world, except for the war, the global pandemic, and the out-of-control gas prices. 

The reality is that, before troponins, we probably missed most small heart attacks. Now, most infarcts are small, and most patients walk away from their heart attacks with essentially normal hearts. Do beta-blockers still matter? If you’re a fan of Cochrane reviews, the answer is yes. 

In 2021, Cochrane published a review of beta-blockers in patients without heart failure after myocardial infarction (MI). The authors of that analysis concluded, after the usual caveats about heterogeneity, potential bias, and the whims of a random universe, that, yes, beta-blockers do reduce mortality. The risk ratio for max all-cause mortality was 0.81. 

What does that mean practically? The absolute risk was reduced from 10.9% to 8.7%, a 2.2–percentage point absolute decrease and about a 20% relative drop. A little math gives us a third number: 46. That’s the number needed to treat. If you think about how many patients you admit during a typical week of critical care unit with an MI, a number needed to treat of 46 is a pretty good trade-off for a fairly inexpensive medication with fairly minimal side effects. 

Of course, these are the same people who claim that masks don’t stop the spread of COVID-19. Sure, were they the only people who thought that handwashing was the best way to stop a respiratory virus? No. We all believed that fantasy for far longer than we should have. Not everybody can bat a thousand, if by batting a thousand, you mean reflecting on how your words will impact on a broader population primed to believe misinformation because of the increasingly toxic social media environment and worsening politicization and radicalization of our politics. 

By the way, if any of you want to come to Canada, you can stay with me. Things are incrementally better here. In this day and age, incrementally better is the best we can hope for. 

Here’s the wrinkle with the Cochrane beta-blocker review: Many of the studies took place before early revascularization became the norm and before our current armamentarium of drugs became standard of care. 

Back in the day, bed rest and the power of positive thinking were the mainstays of cardiac treatment. Also, many of these studies mixed together ST-segment MI (STEMI) and non-STEMI patients, so you’re obviously going to see more benefits in STEMI patients who are at higher risk. Some of them used intravenous (IV) beta-blockers right away, whereas some were looking only at oral beta-blockers started days after the infarct. 

We don’t use IV beta-blockers that much anymore because of the risk for shock. 

Also, some studies had short-term follow-up where the benefits were less pronounced, and some studies used doses and types of beta-blockers rarely used today. Some of the studies had a mix of coronary and heart failure patients, which muddies the water because the heart failure patients would clearly benefit from being on a beta-blocker. 

Basically, the data are not definitive because they are old and don’t reflect our current standard of care. The data contain a heterogeneous mix of patients that aren’t really relevant to the question that we’re asking. The question we’re asking is, should you put all your post-MI patients on a beta-blocker routinely, even if they don’t have heart failure? 

The REDUCE-AMI trial is the first of a few trials testing, or to be more accurate, retesting, whether beta-blockers are useful after an MI. BETAMI, REBOOT, DANBLOCK— you’ll be hearing these names in the next few years, either because the studies get published or because they’re the Twitter handles of people harassing you online. Either/or. (By the way, I’ll be cold in my grave before I call it X.) 

For now, REDUCE-AMI is the first across the finish line, and at least in cardiology, finishing first is a good thing. This study enrolled patients with ACS, both STEMI and non-STEMI, with a post-MI ejection fraction ≥ 50%, and the result was nothing. The risk ratio for all-cause mortality was 0.94 and was not statistically significant. 

In absolute terms, that’s a reduction from 4.1% to 3.9%, or a 0.2–percentage point decrease; this translates into a number needed to treat of 500, which is 10 times higher than what the Cochrane review found. That’s if you assume that there is, in fact, a small benefit amidst all the statistical noise, which there probably isn’t. 

Now, studies like this can never rule out small effects, either positive or negative, so maybe there is a small benefit from using beta-blockers. If it’s there, it’s really small. Do beta-blockers work? Well, yes, obviously, for heart failure and atrial fibrillation — which, let’s face it, are not exactly rare and often coexist in patients with heart disease. They probably aren’t that great as blood pressure pills, but that’s a story for another day and another video. 

Yes, beta-blockers are useful pills, and they are standard of care, just maybe not for post-MI patients with normal ejection fractions because they probably don’t really need them. They worked in the pre-stent, pre-aspirin, pre-anything era. 

That’s not our world anymore. Things change. It’s not the 1980s. That’s why I don’t have a mullet, and that’s why you need to update your kitchen. 
 

Dr. Labos, a cardiologist at Kirkland Medical Center, Montreal, Quebec, Canada, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Giving patients a beta-blocker after a myocardial infarction is standard of care. It’s in the guidelines. It’s one of the performance measures used by the American College of Cardiology (ACC) and the American Heart Association (AHA). If you aren’t putting your post–acute coronary syndrome (ACS) patients on a beta-blocker, the ACC and the AHA both think you suck. 

They are very disappointed in you, just like your mother was when you told her you didn’t want to become a surgeon because you don’t like waking up early, your hands shake when you get nervous, it’s not your fault, there’s nothing you can do about it, so just leave me alone!

The data on beta-blockers are decades old. In the time before stents, statins, angiotensin-converting enzyme inhibitors, and dual antiplatelet therapy, when patients either died or got better on their own, beta-blockers showed major benefits. Studies like the Norwegian Multicenter Study Group, the BHAT trial, and the ISIS-1 trial proved the benefits of beta blockade. These studies date back to the 1980s, when you could call a study ISIS without controversy. 

It was a simpler time, when all you had to worry about was the Cold War, apartheid, and the global AIDS pandemic. It was a time when doctors smoked in their offices, and patients had bigger infarcts that caused large scars and systolic dysfunction. That world is no longer our world, except for the war, the global pandemic, and the out-of-control gas prices. 

The reality is that, before troponins, we probably missed most small heart attacks. Now, most infarcts are small, and most patients walk away from their heart attacks with essentially normal hearts. Do beta-blockers still matter? If you’re a fan of Cochrane reviews, the answer is yes. 

In 2021, Cochrane published a review of beta-blockers in patients without heart failure after myocardial infarction (MI). The authors of that analysis concluded, after the usual caveats about heterogeneity, potential bias, and the whims of a random universe, that, yes, beta-blockers do reduce mortality. The risk ratio for max all-cause mortality was 0.81. 

What does that mean practically? The absolute risk was reduced from 10.9% to 8.7%, a 2.2–percentage point absolute decrease and about a 20% relative drop. A little math gives us a third number: 46. That’s the number needed to treat. If you think about how many patients you admit during a typical week of critical care unit with an MI, a number needed to treat of 46 is a pretty good trade-off for a fairly inexpensive medication with fairly minimal side effects. 

Of course, these are the same people who claim that masks don’t stop the spread of COVID-19. Sure, were they the only people who thought that handwashing was the best way to stop a respiratory virus? No. We all believed that fantasy for far longer than we should have. Not everybody can bat a thousand, if by batting a thousand, you mean reflecting on how your words will impact on a broader population primed to believe misinformation because of the increasingly toxic social media environment and worsening politicization and radicalization of our politics. 

By the way, if any of you want to come to Canada, you can stay with me. Things are incrementally better here. In this day and age, incrementally better is the best we can hope for. 

Here’s the wrinkle with the Cochrane beta-blocker review: Many of the studies took place before early revascularization became the norm and before our current armamentarium of drugs became standard of care. 

Back in the day, bed rest and the power of positive thinking were the mainstays of cardiac treatment. Also, many of these studies mixed together ST-segment MI (STEMI) and non-STEMI patients, so you’re obviously going to see more benefits in STEMI patients who are at higher risk. Some of them used intravenous (IV) beta-blockers right away, whereas some were looking only at oral beta-blockers started days after the infarct. 

We don’t use IV beta-blockers that much anymore because of the risk for shock. 

Also, some studies had short-term follow-up where the benefits were less pronounced, and some studies used doses and types of beta-blockers rarely used today. Some of the studies had a mix of coronary and heart failure patients, which muddies the water because the heart failure patients would clearly benefit from being on a beta-blocker. 

Basically, the data are not definitive because they are old and don’t reflect our current standard of care. The data contain a heterogeneous mix of patients that aren’t really relevant to the question that we’re asking. The question we’re asking is, should you put all your post-MI patients on a beta-blocker routinely, even if they don’t have heart failure? 

The REDUCE-AMI trial is the first of a few trials testing, or to be more accurate, retesting, whether beta-blockers are useful after an MI. BETAMI, REBOOT, DANBLOCK— you’ll be hearing these names in the next few years, either because the studies get published or because they’re the Twitter handles of people harassing you online. Either/or. (By the way, I’ll be cold in my grave before I call it X.) 

For now, REDUCE-AMI is the first across the finish line, and at least in cardiology, finishing first is a good thing. This study enrolled patients with ACS, both STEMI and non-STEMI, with a post-MI ejection fraction ≥ 50%, and the result was nothing. The risk ratio for all-cause mortality was 0.94 and was not statistically significant. 

In absolute terms, that’s a reduction from 4.1% to 3.9%, or a 0.2–percentage point decrease; this translates into a number needed to treat of 500, which is 10 times higher than what the Cochrane review found. That’s if you assume that there is, in fact, a small benefit amidst all the statistical noise, which there probably isn’t. 

Now, studies like this can never rule out small effects, either positive or negative, so maybe there is a small benefit from using beta-blockers. If it’s there, it’s really small. Do beta-blockers work? Well, yes, obviously, for heart failure and atrial fibrillation — which, let’s face it, are not exactly rare and often coexist in patients with heart disease. They probably aren’t that great as blood pressure pills, but that’s a story for another day and another video. 

Yes, beta-blockers are useful pills, and they are standard of care, just maybe not for post-MI patients with normal ejection fractions because they probably don’t really need them. They worked in the pre-stent, pre-aspirin, pre-anything era. 

That’s not our world anymore. Things change. It’s not the 1980s. That’s why I don’t have a mullet, and that’s why you need to update your kitchen. 
 

Dr. Labos, a cardiologist at Kirkland Medical Center, Montreal, Quebec, Canada, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Giving patients a beta-blocker after a myocardial infarction is standard of care. It’s in the guidelines. It’s one of the performance measures used by the American College of Cardiology (ACC) and the American Heart Association (AHA). If you aren’t putting your post–acute coronary syndrome (ACS) patients on a beta-blocker, the ACC and the AHA both think you suck. 

They are very disappointed in you, just like your mother was when you told her you didn’t want to become a surgeon because you don’t like waking up early, your hands shake when you get nervous, it’s not your fault, there’s nothing you can do about it, so just leave me alone!

The data on beta-blockers are decades old. In the time before stents, statins, angiotensin-converting enzyme inhibitors, and dual antiplatelet therapy, when patients either died or got better on their own, beta-blockers showed major benefits. Studies like the Norwegian Multicenter Study Group, the BHAT trial, and the ISIS-1 trial proved the benefits of beta blockade. These studies date back to the 1980s, when you could call a study ISIS without controversy. 

It was a simpler time, when all you had to worry about was the Cold War, apartheid, and the global AIDS pandemic. It was a time when doctors smoked in their offices, and patients had bigger infarcts that caused large scars and systolic dysfunction. That world is no longer our world, except for the war, the global pandemic, and the out-of-control gas prices. 

The reality is that, before troponins, we probably missed most small heart attacks. Now, most infarcts are small, and most patients walk away from their heart attacks with essentially normal hearts. Do beta-blockers still matter? If you’re a fan of Cochrane reviews, the answer is yes. 

In 2021, Cochrane published a review of beta-blockers in patients without heart failure after myocardial infarction (MI). The authors of that analysis concluded, after the usual caveats about heterogeneity, potential bias, and the whims of a random universe, that, yes, beta-blockers do reduce mortality. The risk ratio for max all-cause mortality was 0.81. 

What does that mean practically? The absolute risk was reduced from 10.9% to 8.7%, a 2.2–percentage point absolute decrease and about a 20% relative drop. A little math gives us a third number: 46. That’s the number needed to treat. If you think about how many patients you admit during a typical week of critical care unit with an MI, a number needed to treat of 46 is a pretty good trade-off for a fairly inexpensive medication with fairly minimal side effects. 

Of course, these are the same people who claim that masks don’t stop the spread of COVID-19. Sure, were they the only people who thought that handwashing was the best way to stop a respiratory virus? No. We all believed that fantasy for far longer than we should have. Not everybody can bat a thousand, if by batting a thousand, you mean reflecting on how your words will impact on a broader population primed to believe misinformation because of the increasingly toxic social media environment and worsening politicization and radicalization of our politics. 

By the way, if any of you want to come to Canada, you can stay with me. Things are incrementally better here. In this day and age, incrementally better is the best we can hope for. 

Here’s the wrinkle with the Cochrane beta-blocker review: Many of the studies took place before early revascularization became the norm and before our current armamentarium of drugs became standard of care. 

Back in the day, bed rest and the power of positive thinking were the mainstays of cardiac treatment. Also, many of these studies mixed together ST-segment MI (STEMI) and non-STEMI patients, so you’re obviously going to see more benefits in STEMI patients who are at higher risk. Some of them used intravenous (IV) beta-blockers right away, whereas some were looking only at oral beta-blockers started days after the infarct. 

We don’t use IV beta-blockers that much anymore because of the risk for shock. 

Also, some studies had short-term follow-up where the benefits were less pronounced, and some studies used doses and types of beta-blockers rarely used today. Some of the studies had a mix of coronary and heart failure patients, which muddies the water because the heart failure patients would clearly benefit from being on a beta-blocker. 

Basically, the data are not definitive because they are old and don’t reflect our current standard of care. The data contain a heterogeneous mix of patients that aren’t really relevant to the question that we’re asking. The question we’re asking is, should you put all your post-MI patients on a beta-blocker routinely, even if they don’t have heart failure? 

The REDUCE-AMI trial is the first of a few trials testing, or to be more accurate, retesting, whether beta-blockers are useful after an MI. BETAMI, REBOOT, DANBLOCK— you’ll be hearing these names in the next few years, either because the studies get published or because they’re the Twitter handles of people harassing you online. Either/or. (By the way, I’ll be cold in my grave before I call it X.) 

For now, REDUCE-AMI is the first across the finish line, and at least in cardiology, finishing first is a good thing. This study enrolled patients with ACS, both STEMI and non-STEMI, with a post-MI ejection fraction ≥ 50%, and the result was nothing. The risk ratio for all-cause mortality was 0.94 and was not statistically significant. 

In absolute terms, that’s a reduction from 4.1% to 3.9%, or a 0.2–percentage point decrease; this translates into a number needed to treat of 500, which is 10 times higher than what the Cochrane review found. That’s if you assume that there is, in fact, a small benefit amidst all the statistical noise, which there probably isn’t. 

Now, studies like this can never rule out small effects, either positive or negative, so maybe there is a small benefit from using beta-blockers. If it’s there, it’s really small. Do beta-blockers work? Well, yes, obviously, for heart failure and atrial fibrillation — which, let’s face it, are not exactly rare and often coexist in patients with heart disease. They probably aren’t that great as blood pressure pills, but that’s a story for another day and another video. 

Yes, beta-blockers are useful pills, and they are standard of care, just maybe not for post-MI patients with normal ejection fractions because they probably don’t really need them. They worked in the pre-stent, pre-aspirin, pre-anything era. 

That’s not our world anymore. Things change. It’s not the 1980s. That’s why I don’t have a mullet, and that’s why you need to update your kitchen. 
 

Dr. Labos, a cardiologist at Kirkland Medical Center, Montreal, Quebec, Canada, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Progression of chronic kidney disease (CKD) and cardiovascular disease risk in hypertensive adults was significantly slower among those who consumed more fruits and vegetables or oral sodium bicarbonate, compared with controls who received usual care.

A primary focus on pharmacologic strategies has failed to reduced hypertension-related CKD and cardiovascular disease mortality, Nimrit Goraya, MD, of Texas A&M Health Sciences Center College of Medicine, Temple, and colleagues wrote. High-acid diets (those with greater amounts of animal-sourced foods) have been associated with increased incidence and progression of CKD and with increased risk of cardiovascular disease.

Diets high in fruits and vegetables are associated with reduced CKD and cardiovascular disease but are not routinely used as part of hypertension treatment. The researchers hypothesized that dietary acid reduction could slow kidney disease progression and reduce cardiovascular disease risk.

In a study published in The American Journal of Medicine, the researchers randomized 153 adults aged 18-70 years with hypertension and CKD to fruits and vegetables, oral sodium bicarbonate (NaHCO₃), or usual care; 51 to each group. The fruit and vegetable group received 2-4 cups daily of base-producing food items including apples, apricots, oranges, peaches, pears, raisins, strawberries, carrots, cauliflower, eggplant, lettuce, potatoes, spinach, tomatoes, and zucchini. Participants were not instructed how to incorporate these foods into their diets. The sodium bicarbonate group received an average of four to five NaHCO₃ tablets daily (650 mg), divided into two doses.

The mean age of the participants was 48.8 years, 51% were female, and 47% were African American. The primary outcome was CKD progression and cardiovascular disease risk over 5 years. All participants met criteria at baseline for macroalbuminuria (a urine albumin to creatinine ratio of at least 200 mg/g) and were considered at increased risk for CKD progression.

Over the 5-year follow-up, CKD progression was significantly slower in the groups receiving fruits and vegetables and oral sodium bicarbonate, compared with usual care, based on trajectories showing a lower decline of estimated glomerular filtration rates (mean declines of 1.08 and 1.17 for fruits/vegetables and NaHCO₃, respectively, vs 19.4 for usual care, P < .001 for both).

However, systolic blood pressure and subsequent cardiovascular disease risk indicators were lower only in the fruit and vegetable group, compared with both the NaHCO₃ or usual-care groups over the long term. “Specifically, with fruits and vegetables, systolic blood pressure, plasma LDL and Lp(a) cholesterol, and body mass index decreased from baseline, consistent with better cardiovascular disease protection,” the researchers wrote. The protection against cardiovascular disease in the fruits and vegetables group occurred with lower doses of antihypertensive and statin medications and was not affected by baseline differences in medication doses.

The findings were limited by several factors, including the lack of data on compliance with the NaHCO₃ supplements, although urine net acid excretion in this group suggested increased alkali intake similar to that provided by fruits and vegetables, the researchers noted. Other limitations included the focus only on individuals with very high albuminuria.

More basic science studies are needed to explore how the potential vascular injury suggested by albuminuria affects CKD progression and cardiovascular disease, and clinical studies are needed to assess the impact of dietary acid reduction on patients with lower levels of albuminuria that the current study, the researchers said.

However, the results suggest that consuming fruits and vegetables, rather than NaHCO₃, is the preferred strategy for dietary acid reduction for patients with primary hypertension and CKD, they concluded. The findings also support routine measurement of urine albumin-to-creatinine ratios in hypertensive patients to identify CKD and assess risk for progression and subsequent cardiovascular disease.

The study was supported by the Larry and Jane Woirhaye Memorial Endowment in Renal Research at the Texas Tech University Health Sciences Center, the University Medical Center (both in Lubbock, Texas), the Endowment, Academic Operations Division of Baylor Scott & White Health, and the Episcopal Health Foundation. The researchers had no financial conflicts to disclose.

Progression of chronic kidney disease (CKD) and cardiovascular disease risk in hypertensive adults was significantly slower among those who consumed more fruits and vegetables or oral sodium bicarbonate, compared with controls who received usual care.

A primary focus on pharmacologic strategies has failed to reduced hypertension-related CKD and cardiovascular disease mortality, Nimrit Goraya, MD, of Texas A&M Health Sciences Center College of Medicine, Temple, and colleagues wrote. High-acid diets (those with greater amounts of animal-sourced foods) have been associated with increased incidence and progression of CKD and with increased risk of cardiovascular disease.

Diets high in fruits and vegetables are associated with reduced CKD and cardiovascular disease but are not routinely used as part of hypertension treatment. The researchers hypothesized that dietary acid reduction could slow kidney disease progression and reduce cardiovascular disease risk.

In a study published in The American Journal of Medicine, the researchers randomized 153 adults aged 18-70 years with hypertension and CKD to fruits and vegetables, oral sodium bicarbonate (NaHCO₃), or usual care; 51 to each group. The fruit and vegetable group received 2-4 cups daily of base-producing food items including apples, apricots, oranges, peaches, pears, raisins, strawberries, carrots, cauliflower, eggplant, lettuce, potatoes, spinach, tomatoes, and zucchini. Participants were not instructed how to incorporate these foods into their diets. The sodium bicarbonate group received an average of four to five NaHCO₃ tablets daily (650 mg), divided into two doses.

The mean age of the participants was 48.8 years, 51% were female, and 47% were African American. The primary outcome was CKD progression and cardiovascular disease risk over 5 years. All participants met criteria at baseline for macroalbuminuria (a urine albumin to creatinine ratio of at least 200 mg/g) and were considered at increased risk for CKD progression.

Over the 5-year follow-up, CKD progression was significantly slower in the groups receiving fruits and vegetables and oral sodium bicarbonate, compared with usual care, based on trajectories showing a lower decline of estimated glomerular filtration rates (mean declines of 1.08 and 1.17 for fruits/vegetables and NaHCO₃, respectively, vs 19.4 for usual care, P < .001 for both).

However, systolic blood pressure and subsequent cardiovascular disease risk indicators were lower only in the fruit and vegetable group, compared with both the NaHCO₃ or usual-care groups over the long term. “Specifically, with fruits and vegetables, systolic blood pressure, plasma LDL and Lp(a) cholesterol, and body mass index decreased from baseline, consistent with better cardiovascular disease protection,” the researchers wrote. The protection against cardiovascular disease in the fruits and vegetables group occurred with lower doses of antihypertensive and statin medications and was not affected by baseline differences in medication doses.

The findings were limited by several factors, including the lack of data on compliance with the NaHCO₃ supplements, although urine net acid excretion in this group suggested increased alkali intake similar to that provided by fruits and vegetables, the researchers noted. Other limitations included the focus only on individuals with very high albuminuria.

More basic science studies are needed to explore how the potential vascular injury suggested by albuminuria affects CKD progression and cardiovascular disease, and clinical studies are needed to assess the impact of dietary acid reduction on patients with lower levels of albuminuria that the current study, the researchers said.

However, the results suggest that consuming fruits and vegetables, rather than NaHCO₃, is the preferred strategy for dietary acid reduction for patients with primary hypertension and CKD, they concluded. The findings also support routine measurement of urine albumin-to-creatinine ratios in hypertensive patients to identify CKD and assess risk for progression and subsequent cardiovascular disease.

The study was supported by the Larry and Jane Woirhaye Memorial Endowment in Renal Research at the Texas Tech University Health Sciences Center, the University Medical Center (both in Lubbock, Texas), the Endowment, Academic Operations Division of Baylor Scott & White Health, and the Episcopal Health Foundation. The researchers had no financial conflicts to disclose.

Progression of chronic kidney disease (CKD) and cardiovascular disease risk in hypertensive adults was significantly slower among those who consumed more fruits and vegetables or oral sodium bicarbonate, compared with controls who received usual care.

A primary focus on pharmacologic strategies has failed to reduced hypertension-related CKD and cardiovascular disease mortality, Nimrit Goraya, MD, of Texas A&M Health Sciences Center College of Medicine, Temple, and colleagues wrote. High-acid diets (those with greater amounts of animal-sourced foods) have been associated with increased incidence and progression of CKD and with increased risk of cardiovascular disease.

Diets high in fruits and vegetables are associated with reduced CKD and cardiovascular disease but are not routinely used as part of hypertension treatment. The researchers hypothesized that dietary acid reduction could slow kidney disease progression and reduce cardiovascular disease risk.

In a study published in The American Journal of Medicine, the researchers randomized 153 adults aged 18-70 years with hypertension and CKD to fruits and vegetables, oral sodium bicarbonate (NaHCO₃), or usual care; 51 to each group. The fruit and vegetable group received 2-4 cups daily of base-producing food items including apples, apricots, oranges, peaches, pears, raisins, strawberries, carrots, cauliflower, eggplant, lettuce, potatoes, spinach, tomatoes, and zucchini. Participants were not instructed how to incorporate these foods into their diets. The sodium bicarbonate group received an average of four to five NaHCO₃ tablets daily (650 mg), divided into two doses.

The mean age of the participants was 48.8 years, 51% were female, and 47% were African American. The primary outcome was CKD progression and cardiovascular disease risk over 5 years. All participants met criteria at baseline for macroalbuminuria (a urine albumin to creatinine ratio of at least 200 mg/g) and were considered at increased risk for CKD progression.

Over the 5-year follow-up, CKD progression was significantly slower in the groups receiving fruits and vegetables and oral sodium bicarbonate, compared with usual care, based on trajectories showing a lower decline of estimated glomerular filtration rates (mean declines of 1.08 and 1.17 for fruits/vegetables and NaHCO₃, respectively, vs 19.4 for usual care, P < .001 for both).

However, systolic blood pressure and subsequent cardiovascular disease risk indicators were lower only in the fruit and vegetable group, compared with both the NaHCO₃ or usual-care groups over the long term. “Specifically, with fruits and vegetables, systolic blood pressure, plasma LDL and Lp(a) cholesterol, and body mass index decreased from baseline, consistent with better cardiovascular disease protection,” the researchers wrote. The protection against cardiovascular disease in the fruits and vegetables group occurred with lower doses of antihypertensive and statin medications and was not affected by baseline differences in medication doses.

The findings were limited by several factors, including the lack of data on compliance with the NaHCO₃ supplements, although urine net acid excretion in this group suggested increased alkali intake similar to that provided by fruits and vegetables, the researchers noted. Other limitations included the focus only on individuals with very high albuminuria.

More basic science studies are needed to explore how the potential vascular injury suggested by albuminuria affects CKD progression and cardiovascular disease, and clinical studies are needed to assess the impact of dietary acid reduction on patients with lower levels of albuminuria that the current study, the researchers said.

However, the results suggest that consuming fruits and vegetables, rather than NaHCO₃, is the preferred strategy for dietary acid reduction for patients with primary hypertension and CKD, they concluded. The findings also support routine measurement of urine albumin-to-creatinine ratios in hypertensive patients to identify CKD and assess risk for progression and subsequent cardiovascular disease.

The study was supported by the Larry and Jane Woirhaye Memorial Endowment in Renal Research at the Texas Tech University Health Sciences Center, the University Medical Center (both in Lubbock, Texas), the Endowment, Academic Operations Division of Baylor Scott & White Health, and the Episcopal Health Foundation. The researchers had no financial conflicts to disclose.

Hyperkalemia tends to cause panic in healthcare professionals, and rightfully so. On a good day, it causes weakness in the legs; on a bad day, it causes cardiac arrest.

It makes sense that a high potassium level causes clinicians to feel a bit jumpy. This anxiety tends to result in treating the issue by overly restricting potassium in the diet. The problem with this method is that it should be temporary but often isn’t. There are only a few concerns that justify long-term potassium restriction.

As a dietitian, I have seen numerous patients with varying disease states who are terrified of potassium because they were never properly educated on the situation that required restriction or were never notified that their potassium was corrected. 

I’ve seen patients whose potassium level hasn’t been elevated in years refuse banana bread because they were told that they could never eat a banana again. I’ve worked with patients who continued to needlessly restrict, which eventually led to hypokalemia.

Not only does this indicate ineffective education — banana bread is actually a low-potassium food at about 80 mg per slice — but also poor follow-up. 

Potassium has been designated by the United States Department of Agriculture as a nutrient of public health concern due to its underconsumption in the general population. Although there is concern in the public health community that the current guidelines for potassium intake (3500-4700 mg/d) are unattainable, with some professionals arguing for lowering the standard, there remains significant deficiency in the general population. This deficiency has also been connected to increasing rates of hypertension and cardiovascular disease. 
 

Nondietary Causes of Hyperkalemia 

There are many causes of hyperkalemia, of which excessive potassium intake is only one, and an uncommon one at that. A high potassium level should resolve during the course of treatment for metabolic acidosis, hyperglycemia, and dehydration. We may also see resolution with medication changes. But the question remains: Are we relaying this information to patients?

Renal insufficiency is a common cause of hyperkalemia, but it is also a common cause of chronic constipation that can cause hyperkalemia as well. Are we addressing bowel movements with these patients? I often work with patients who aren’t having their bowel movements addressed until the patient themselves voices discomfort. 

Depending upon the urgency of treatment, potassium restriction may be the most effective and efficient way to address an acutely elevated value. However, long-term potassium restriction may not be an appropriate intervention for all patients, even those with kidney conditions.

As a dietitian, I have seen many patients who overly restrict dietary potassium because they had one elevated value. These patients tend to view potassium as the enemy because they were never educated on the actual cause of their hyperkalemia. They were simply given a list of high-potassium foods and told to avoid them. A lack of follow-up education may cause them to avoid those foods forever. 
 

Benefits of Potassium

The problem with this perpetual avoidance of high potassium foods is that a potassium-rich diet has been shown to be exceptionally beneficial. 

Potassium exists in many forms in the Western diet: as a preservative and additive, a salt substitute, and naturally occurring in both animal and plant products. My concern regarding blanket potassium restriction is that potassium-rich plant and animal products can actually be beneficial, even to those with kidney and heart conditions who are most often advised to restrict its intake. 

Adequate potassium intake can: 

• Decrease blood pressure by increasing urinary excretion of sodium
• Improve nephrolithiasis by decreasing urinary excretion of calcium
• Decrease incidence of metabolic acidosis by providing precursors to bicarbonate that facilitate excretion of potassium
• Increase bone density in postmenopausal women
• Decrease risk for stroke and cardiovascular disease in the general population

One study found that metabolic acidosis can be corrected in patients with stage 4 chronic kidney disease, without hyperkalemia, by increasing fruit and vegetable intake when compared with those treated with bicarbonate alone, thus preserving kidney function.

Do I suggest encouraging a patient with acute hyperkalemia to eat a banana? Of course not. But I would suggest finding ways to work with patients who have chronic hyperkalemia to increase intake of potassium-rich plant foods to maintain homeostasis while liberalizing diet and preventing progression of chronic kidney disease. 
 

When to Refer to a Dietitian

In patients for whom a potassium-restricted diet is a necessary long-term treatment of hyperkalemia, education with a registered dietitian can be beneficial. A registered dietitian has the time and expertise to address the areas in the diet where excessive potassium exists without forfeiting other nutritional benefits that come from whole foods like fruits, vegetables, lean protein, legumes, nuts, and seeds in a way that is both realistic and helpful. A dietitian can work with patients to reduce intake of potassium-containing salt substitutes, preservatives, and other additives while still encouraging a whole-food diet rich in antioxidants, fiber, and healthy fats.

Dietitians also provide education on serving size and methods to reduce potassium content of food.

For example, tomatoes are a high-potassium food at 300+ mg per medium-sized tomato. But how often does a patient eat a whole tomato? A slice of tomato on a sandwich or a handful of cherry tomatoes in a salad are actually low in potassium per serving and can provide additional nutrients like vitamin C, beta-carotene, and antioxidants like lycopene, which is linked to a decreased incidence of prostate cancer.

By incorporating the assistance of a registered dietitian into the treatment of chronic hyperkalemia, we can develop individualized restrictions that are realistic for the patient and tailored to their nutritional needs to promote optimal health and thus encourage continued compliance. 

Ms. Winfree is a renal dietitian in private practice in Mary Esther, Florida. She disclosed no relevant conflicts of interest.

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

Hyperkalemia tends to cause panic in healthcare professionals, and rightfully so. On a good day, it causes weakness in the legs; on a bad day, it causes cardiac arrest.

It makes sense that a high potassium level causes clinicians to feel a bit jumpy. This anxiety tends to result in treating the issue by overly restricting potassium in the diet. The problem with this method is that it should be temporary but often isn’t. There are only a few concerns that justify long-term potassium restriction.

As a dietitian, I have seen numerous patients with varying disease states who are terrified of potassium because they were never properly educated on the situation that required restriction or were never notified that their potassium was corrected. 

I’ve seen patients whose potassium level hasn’t been elevated in years refuse banana bread because they were told that they could never eat a banana again. I’ve worked with patients who continued to needlessly restrict, which eventually led to hypokalemia.

Not only does this indicate ineffective education — banana bread is actually a low-potassium food at about 80 mg per slice — but also poor follow-up. 

Potassium has been designated by the United States Department of Agriculture as a nutrient of public health concern due to its underconsumption in the general population. Although there is concern in the public health community that the current guidelines for potassium intake (3500-4700 mg/d) are unattainable, with some professionals arguing for lowering the standard, there remains significant deficiency in the general population. This deficiency has also been connected to increasing rates of hypertension and cardiovascular disease. 
 

Nondietary Causes of Hyperkalemia 

There are many causes of hyperkalemia, of which excessive potassium intake is only one, and an uncommon one at that. A high potassium level should resolve during the course of treatment for metabolic acidosis, hyperglycemia, and dehydration. We may also see resolution with medication changes. But the question remains: Are we relaying this information to patients?

Renal insufficiency is a common cause of hyperkalemia, but it is also a common cause of chronic constipation that can cause hyperkalemia as well. Are we addressing bowel movements with these patients? I often work with patients who aren’t having their bowel movements addressed until the patient themselves voices discomfort. 

Depending upon the urgency of treatment, potassium restriction may be the most effective and efficient way to address an acutely elevated value. However, long-term potassium restriction may not be an appropriate intervention for all patients, even those with kidney conditions.

As a dietitian, I have seen many patients who overly restrict dietary potassium because they had one elevated value. These patients tend to view potassium as the enemy because they were never educated on the actual cause of their hyperkalemia. They were simply given a list of high-potassium foods and told to avoid them. A lack of follow-up education may cause them to avoid those foods forever. 
 

Benefits of Potassium

The problem with this perpetual avoidance of high potassium foods is that a potassium-rich diet has been shown to be exceptionally beneficial. 

Potassium exists in many forms in the Western diet: as a preservative and additive, a salt substitute, and naturally occurring in both animal and plant products. My concern regarding blanket potassium restriction is that potassium-rich plant and animal products can actually be beneficial, even to those with kidney and heart conditions who are most often advised to restrict its intake. 

Adequate potassium intake can: 

• Decrease blood pressure by increasing urinary excretion of sodium
• Improve nephrolithiasis by decreasing urinary excretion of calcium
• Decrease incidence of metabolic acidosis by providing precursors to bicarbonate that facilitate excretion of potassium
• Increase bone density in postmenopausal women
• Decrease risk for stroke and cardiovascular disease in the general population

One study found that metabolic acidosis can be corrected in patients with stage 4 chronic kidney disease, without hyperkalemia, by increasing fruit and vegetable intake when compared with those treated with bicarbonate alone, thus preserving kidney function.

Do I suggest encouraging a patient with acute hyperkalemia to eat a banana? Of course not. But I would suggest finding ways to work with patients who have chronic hyperkalemia to increase intake of potassium-rich plant foods to maintain homeostasis while liberalizing diet and preventing progression of chronic kidney disease. 
 

When to Refer to a Dietitian

In patients for whom a potassium-restricted diet is a necessary long-term treatment of hyperkalemia, education with a registered dietitian can be beneficial. A registered dietitian has the time and expertise to address the areas in the diet where excessive potassium exists without forfeiting other nutritional benefits that come from whole foods like fruits, vegetables, lean protein, legumes, nuts, and seeds in a way that is both realistic and helpful. A dietitian can work with patients to reduce intake of potassium-containing salt substitutes, preservatives, and other additives while still encouraging a whole-food diet rich in antioxidants, fiber, and healthy fats.

Dietitians also provide education on serving size and methods to reduce potassium content of food.

For example, tomatoes are a high-potassium food at 300+ mg per medium-sized tomato. But how often does a patient eat a whole tomato? A slice of tomato on a sandwich or a handful of cherry tomatoes in a salad are actually low in potassium per serving and can provide additional nutrients like vitamin C, beta-carotene, and antioxidants like lycopene, which is linked to a decreased incidence of prostate cancer.

By incorporating the assistance of a registered dietitian into the treatment of chronic hyperkalemia, we can develop individualized restrictions that are realistic for the patient and tailored to their nutritional needs to promote optimal health and thus encourage continued compliance. 

Ms. Winfree is a renal dietitian in private practice in Mary Esther, Florida. She disclosed no relevant conflicts of interest.

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

Hyperkalemia tends to cause panic in healthcare professionals, and rightfully so. On a good day, it causes weakness in the legs; on a bad day, it causes cardiac arrest.

It makes sense that a high potassium level causes clinicians to feel a bit jumpy. This anxiety tends to result in treating the issue by overly restricting potassium in the diet. The problem with this method is that it should be temporary but often isn’t. There are only a few concerns that justify long-term potassium restriction.

As a dietitian, I have seen numerous patients with varying disease states who are terrified of potassium because they were never properly educated on the situation that required restriction or were never notified that their potassium was corrected. 

I’ve seen patients whose potassium level hasn’t been elevated in years refuse banana bread because they were told that they could never eat a banana again. I’ve worked with patients who continued to needlessly restrict, which eventually led to hypokalemia.

Not only does this indicate ineffective education — banana bread is actually a low-potassium food at about 80 mg per slice — but also poor follow-up. 

Potassium has been designated by the United States Department of Agriculture as a nutrient of public health concern due to its underconsumption in the general population. Although there is concern in the public health community that the current guidelines for potassium intake (3500-4700 mg/d) are unattainable, with some professionals arguing for lowering the standard, there remains significant deficiency in the general population. This deficiency has also been connected to increasing rates of hypertension and cardiovascular disease. 
 

Nondietary Causes of Hyperkalemia 

There are many causes of hyperkalemia, of which excessive potassium intake is only one, and an uncommon one at that. A high potassium level should resolve during the course of treatment for metabolic acidosis, hyperglycemia, and dehydration. We may also see resolution with medication changes. But the question remains: Are we relaying this information to patients?

Renal insufficiency is a common cause of hyperkalemia, but it is also a common cause of chronic constipation that can cause hyperkalemia as well. Are we addressing bowel movements with these patients? I often work with patients who aren’t having their bowel movements addressed until the patient themselves voices discomfort. 

Depending upon the urgency of treatment, potassium restriction may be the most effective and efficient way to address an acutely elevated value. However, long-term potassium restriction may not be an appropriate intervention for all patients, even those with kidney conditions.

As a dietitian, I have seen many patients who overly restrict dietary potassium because they had one elevated value. These patients tend to view potassium as the enemy because they were never educated on the actual cause of their hyperkalemia. They were simply given a list of high-potassium foods and told to avoid them. A lack of follow-up education may cause them to avoid those foods forever. 
 

Benefits of Potassium

The problem with this perpetual avoidance of high potassium foods is that a potassium-rich diet has been shown to be exceptionally beneficial. 

Potassium exists in many forms in the Western diet: as a preservative and additive, a salt substitute, and naturally occurring in both animal and plant products. My concern regarding blanket potassium restriction is that potassium-rich plant and animal products can actually be beneficial, even to those with kidney and heart conditions who are most often advised to restrict its intake. 

Adequate potassium intake can: 

• Decrease blood pressure by increasing urinary excretion of sodium
• Improve nephrolithiasis by decreasing urinary excretion of calcium
• Decrease incidence of metabolic acidosis by providing precursors to bicarbonate that facilitate excretion of potassium
• Increase bone density in postmenopausal women
• Decrease risk for stroke and cardiovascular disease in the general population

One study found that metabolic acidosis can be corrected in patients with stage 4 chronic kidney disease, without hyperkalemia, by increasing fruit and vegetable intake when compared with those treated with bicarbonate alone, thus preserving kidney function.

Do I suggest encouraging a patient with acute hyperkalemia to eat a banana? Of course not. But I would suggest finding ways to work with patients who have chronic hyperkalemia to increase intake of potassium-rich plant foods to maintain homeostasis while liberalizing diet and preventing progression of chronic kidney disease. 
 

When to Refer to a Dietitian

In patients for whom a potassium-restricted diet is a necessary long-term treatment of hyperkalemia, education with a registered dietitian can be beneficial. A registered dietitian has the time and expertise to address the areas in the diet where excessive potassium exists without forfeiting other nutritional benefits that come from whole foods like fruits, vegetables, lean protein, legumes, nuts, and seeds in a way that is both realistic and helpful. A dietitian can work with patients to reduce intake of potassium-containing salt substitutes, preservatives, and other additives while still encouraging a whole-food diet rich in antioxidants, fiber, and healthy fats.

Dietitians also provide education on serving size and methods to reduce potassium content of food.

For example, tomatoes are a high-potassium food at 300+ mg per medium-sized tomato. But how often does a patient eat a whole tomato? A slice of tomato on a sandwich or a handful of cherry tomatoes in a salad are actually low in potassium per serving and can provide additional nutrients like vitamin C, beta-carotene, and antioxidants like lycopene, which is linked to a decreased incidence of prostate cancer.

By incorporating the assistance of a registered dietitian into the treatment of chronic hyperkalemia, we can develop individualized restrictions that are realistic for the patient and tailored to their nutritional needs to promote optimal health and thus encourage continued compliance. 

Ms. Winfree is a renal dietitian in private practice in Mary Esther, Florida. She disclosed no relevant conflicts of interest.

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