Cardiology News

TOPLINE:

An artificial intelligence–ECG risk estimation model designed to predict incident hypertension (AIRE-HTN) identifies cases and stratifies the risk for adverse outcomes in addition to traditional markers.

METHODOLOGY:

• Researchers conducted a development and external validation prognostic cohort study in a secondary care setting to identify individuals at risk for incident hypertension.
• They developed AIRE-HTN, which was trained on a derivation cohort from the Beth Israel Deaconess Medical Center in Boston, involving 1,163,401 ECGs from 189,539 patients (mean age, 57.7 years; 52.1% women; 64.5% White individuals).
• External validation was conducted on 65,610 ECGs from a UK-based volunteer cohort, drawn from an equal number of patients (mean age, 65.4 years; 51.5% women; 96.3% White individuals).
• Incident hypertension was evaluated in 19,423 individuals without hypertension from the medical center cohort and in 35,806 individuals without hypertension from the UK cohort.

TAKEAWAY:

• AIRE-HTN predicted incident hypertension with a C-index of 0.70 (95% CI, 0.69-0.71) in both the cohorts. Those in the quartile with the highest AIRE-HTN scores had a fourfold increased risk for incident hypertension (P < .001).
• The model’s predictive accuracy was maintained in individuals without left ventricular hypertrophy and those with normal ECGs and baseline blood pressure, indicating its robustness.
• The model was significantly additive to traditional clinical markers, with a continuous net reclassification index of 0.44 for the medical center cohort and 0.32 for the UK cohort.
• AIRE-HTN was an independent predictor of cardiovascular death (hazard ratio per 1-SD increase in score [HR], 2.24), heart failure (HR, 2.60), myocardial infarction (HR, 3.13), ischemic stroke (HR, 1.23), and chronic kidney disease (HR, 1.89) in outpatients from the medical center cohort (all P < .001), with largely consistent findings in the UK cohort.

IN PRACTICE:

“Results of exploratory and phenotypic analyses suggest the biological plausibility of these findings. Enhanced predictability could influence surveillance programs and primordial prevention,” the authors wrote.

SOURCE:

The study was led by Arunashis Sau, PhD, and Joseph Barker, MRes, National Heart and Lung Institute, Imperial College London, England. It was published online on January 2, 2025, in JAMA Cardiology.

LIMITATIONS:

In one cohort, hypertension was defined using International Classification of Diseases codes, which may lack granularity and not align with contemporary guidelines. The findings were not validated against ambulatory monitoring standards. The performance of the model in different populations and clinical settings remains to be explored.

DISCLOSURES:

The authors acknowledged receiving support from Imperial’s British Heart Foundation Centre for Excellence Award and disclosed receiving support from the British Heart Foundation, the National Institute for Health Research Imperial College Biomedical Research Centre, the EJP RD Research Mobility Fellowship, the Medical Research Council, and the Sir Jules Thorn Charitable Trust. Some authors reported receiving grants, personal fees, advisory fees, or laboratory work fees outside the submitted work.

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:

An artificial intelligence–ECG risk estimation model designed to predict incident hypertension (AIRE-HTN) identifies cases and stratifies the risk for adverse outcomes in addition to traditional markers.

METHODOLOGY:

• Researchers conducted a development and external validation prognostic cohort study in a secondary care setting to identify individuals at risk for incident hypertension.
• They developed AIRE-HTN, which was trained on a derivation cohort from the Beth Israel Deaconess Medical Center in Boston, involving 1,163,401 ECGs from 189,539 patients (mean age, 57.7 years; 52.1% women; 64.5% White individuals).
• External validation was conducted on 65,610 ECGs from a UK-based volunteer cohort, drawn from an equal number of patients (mean age, 65.4 years; 51.5% women; 96.3% White individuals).
• Incident hypertension was evaluated in 19,423 individuals without hypertension from the medical center cohort and in 35,806 individuals without hypertension from the UK cohort.

TAKEAWAY:

• AIRE-HTN predicted incident hypertension with a C-index of 0.70 (95% CI, 0.69-0.71) in both the cohorts. Those in the quartile with the highest AIRE-HTN scores had a fourfold increased risk for incident hypertension (P < .001).
• The model’s predictive accuracy was maintained in individuals without left ventricular hypertrophy and those with normal ECGs and baseline blood pressure, indicating its robustness.
• The model was significantly additive to traditional clinical markers, with a continuous net reclassification index of 0.44 for the medical center cohort and 0.32 for the UK cohort.
• AIRE-HTN was an independent predictor of cardiovascular death (hazard ratio per 1-SD increase in score [HR], 2.24), heart failure (HR, 2.60), myocardial infarction (HR, 3.13), ischemic stroke (HR, 1.23), and chronic kidney disease (HR, 1.89) in outpatients from the medical center cohort (all P < .001), with largely consistent findings in the UK cohort.

IN PRACTICE:

“Results of exploratory and phenotypic analyses suggest the biological plausibility of these findings. Enhanced predictability could influence surveillance programs and primordial prevention,” the authors wrote.

SOURCE:

The study was led by Arunashis Sau, PhD, and Joseph Barker, MRes, National Heart and Lung Institute, Imperial College London, England. It was published online on January 2, 2025, in JAMA Cardiology.

LIMITATIONS:

In one cohort, hypertension was defined using International Classification of Diseases codes, which may lack granularity and not align with contemporary guidelines. The findings were not validated against ambulatory monitoring standards. The performance of the model in different populations and clinical settings remains to be explored.

DISCLOSURES:

The authors acknowledged receiving support from Imperial’s British Heart Foundation Centre for Excellence Award and disclosed receiving support from the British Heart Foundation, the National Institute for Health Research Imperial College Biomedical Research Centre, the EJP RD Research Mobility Fellowship, the Medical Research Council, and the Sir Jules Thorn Charitable Trust. Some authors reported receiving grants, personal fees, advisory fees, or laboratory work fees outside the submitted work.

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:

An artificial intelligence–ECG risk estimation model designed to predict incident hypertension (AIRE-HTN) identifies cases and stratifies the risk for adverse outcomes in addition to traditional markers.

METHODOLOGY:

• Researchers conducted a development and external validation prognostic cohort study in a secondary care setting to identify individuals at risk for incident hypertension.
• They developed AIRE-HTN, which was trained on a derivation cohort from the Beth Israel Deaconess Medical Center in Boston, involving 1,163,401 ECGs from 189,539 patients (mean age, 57.7 years; 52.1% women; 64.5% White individuals).
• External validation was conducted on 65,610 ECGs from a UK-based volunteer cohort, drawn from an equal number of patients (mean age, 65.4 years; 51.5% women; 96.3% White individuals).
• Incident hypertension was evaluated in 19,423 individuals without hypertension from the medical center cohort and in 35,806 individuals without hypertension from the UK cohort.

TAKEAWAY:

• AIRE-HTN predicted incident hypertension with a C-index of 0.70 (95% CI, 0.69-0.71) in both the cohorts. Those in the quartile with the highest AIRE-HTN scores had a fourfold increased risk for incident hypertension (P < .001).
• The model’s predictive accuracy was maintained in individuals without left ventricular hypertrophy and those with normal ECGs and baseline blood pressure, indicating its robustness.
• The model was significantly additive to traditional clinical markers, with a continuous net reclassification index of 0.44 for the medical center cohort and 0.32 for the UK cohort.
• AIRE-HTN was an independent predictor of cardiovascular death (hazard ratio per 1-SD increase in score [HR], 2.24), heart failure (HR, 2.60), myocardial infarction (HR, 3.13), ischemic stroke (HR, 1.23), and chronic kidney disease (HR, 1.89) in outpatients from the medical center cohort (all P < .001), with largely consistent findings in the UK cohort.

IN PRACTICE:

“Results of exploratory and phenotypic analyses suggest the biological plausibility of these findings. Enhanced predictability could influence surveillance programs and primordial prevention,” the authors wrote.

SOURCE:

The study was led by Arunashis Sau, PhD, and Joseph Barker, MRes, National Heart and Lung Institute, Imperial College London, England. It was published online on January 2, 2025, in JAMA Cardiology.

LIMITATIONS:

In one cohort, hypertension was defined using International Classification of Diseases codes, which may lack granularity and not align with contemporary guidelines. The findings were not validated against ambulatory monitoring standards. The performance of the model in different populations and clinical settings remains to be explored.

DISCLOSURES:

The authors acknowledged receiving support from Imperial’s British Heart Foundation Centre for Excellence Award and disclosed receiving support from the British Heart Foundation, the National Institute for Health Research Imperial College Biomedical Research Centre, the EJP RD Research Mobility Fellowship, the Medical Research Council, and the Sir Jules Thorn Charitable Trust. Some authors reported receiving grants, personal fees, advisory fees, or laboratory work fees outside the submitted work.

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:

The cardiovascular benefits observed with intensive blood pressure (BP) control in patients with hypertension and elevated cardiovascular risk from the Systolic Blood Pressure Intervention Trial (SPRINT) can be largely replicated in real-world settings among patients with chronic kidney disease (CKD), highlighting the advantages of adopting intensive BP targets.
 

METHODOLOGY:

• The SPRINT showed that an intensive systolic BP goal < 120 mm Hg reduced mortality, cardiovascular events, and mild cognitive impairment in patients with hypertension and elevated cardiovascular risk, including in patients with CKD.
• Researchers conducted a comparative effectiveness study to determine if the beneficial and adverse effects of intensive vs standard BP control observed in SPRINT were replicable in patients with CKD and hypertension in clinical practice.
• They identified 85,938 patients (mean age, 75.7 years; 95.0% men) and 13,983 patients (mean age, 77.4 years; 38.4% men) from the Veterans Health Administration (VHA) and Kaiser Permanente of Southern California (KPSC) databases, respectively.
• The treatment effect was estimated by combining baseline covariate, treatment, and outcome data of participants from the SPRINT with covariate data from the VHA and KPSC databases.
• The primary outcomes included major cardiovascular events, all-cause death, cognitive impairment, CKD progression, and adverse events at 4 years.

TAKEAWAY:

• Compared with SPRINT participants, those in the VHA and KPSC databases were older, had less prevalent cardiovascular disease, higher albuminuria, and used more statins.
• The benefits of intensive vs standard BP control on major cardiovascular events, all-cause mortality, and certain adverse events (hypotension, syncope, bradycardia, acute kidney injury, and electrolyte abnormality) were transferable from the trial to the VHA and KPSC populations.
• The treatment effect of intensive BP management on CKD progression was transportable to the KPSC population but not to the VHA population. However, the trial’s impact on cognitive outcomes, such as dementia, was not transportable to either the VHA or KPSC populations.
• On the absolute scale, intensive vs standard BP treatment showed greater cardiovascular benefits and fewer safety concerns in the VHA and KPSC populations than in the SPRINT.

IN PRACTICE:

“This example highlights the potential for transportability methods to provide insights that can bridge evidence gaps and inform the application of novel therapies to patients with CKD who are treated in everyday practice,” the authors wrote.
 

SOURCE:

This study was led by Manjula Kurella Tamura, MD, MPH, Division of Nephrology, Department of Medicine, Stanford University School of Medicine, Palo Alto, California. It was published online on January 7, 2025, in JAMA Network Open.
 

LIMITATIONS:

Transportability analyses could not account for characteristics that were not well-documented in electronic health records, such as limited life expectancy. The study was conducted before the widespread use of sodium-glucose cotransporter 2 inhibitors, glucagon-like peptide 1 receptor agonists, and nonsteroidal mineralocorticoid receptor antagonists, making it unclear whether intensive BP treatment would result in similar benefits with current pharmacotherapy regimens. Eligibility for this study was based on BP measurements in routine practice, which tend to be more variable than those collected in research settings.
 

DISCLOSURES:

This study was supported by grants from the National Institutes of Health. Some authors disclosed serving as a consultant and receiving grants, personal fees, and consulting fees from pharmaceutical companies and other sources.
 

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:

The cardiovascular benefits observed with intensive blood pressure (BP) control in patients with hypertension and elevated cardiovascular risk from the Systolic Blood Pressure Intervention Trial (SPRINT) can be largely replicated in real-world settings among patients with chronic kidney disease (CKD), highlighting the advantages of adopting intensive BP targets.
 

METHODOLOGY:

• The SPRINT showed that an intensive systolic BP goal < 120 mm Hg reduced mortality, cardiovascular events, and mild cognitive impairment in patients with hypertension and elevated cardiovascular risk, including in patients with CKD.
• Researchers conducted a comparative effectiveness study to determine if the beneficial and adverse effects of intensive vs standard BP control observed in SPRINT were replicable in patients with CKD and hypertension in clinical practice.
• They identified 85,938 patients (mean age, 75.7 years; 95.0% men) and 13,983 patients (mean age, 77.4 years; 38.4% men) from the Veterans Health Administration (VHA) and Kaiser Permanente of Southern California (KPSC) databases, respectively.
• The treatment effect was estimated by combining baseline covariate, treatment, and outcome data of participants from the SPRINT with covariate data from the VHA and KPSC databases.
• The primary outcomes included major cardiovascular events, all-cause death, cognitive impairment, CKD progression, and adverse events at 4 years.

TAKEAWAY:

• Compared with SPRINT participants, those in the VHA and KPSC databases were older, had less prevalent cardiovascular disease, higher albuminuria, and used more statins.
• The benefits of intensive vs standard BP control on major cardiovascular events, all-cause mortality, and certain adverse events (hypotension, syncope, bradycardia, acute kidney injury, and electrolyte abnormality) were transferable from the trial to the VHA and KPSC populations.
• The treatment effect of intensive BP management on CKD progression was transportable to the KPSC population but not to the VHA population. However, the trial’s impact on cognitive outcomes, such as dementia, was not transportable to either the VHA or KPSC populations.
• On the absolute scale, intensive vs standard BP treatment showed greater cardiovascular benefits and fewer safety concerns in the VHA and KPSC populations than in the SPRINT.

IN PRACTICE:

“This example highlights the potential for transportability methods to provide insights that can bridge evidence gaps and inform the application of novel therapies to patients with CKD who are treated in everyday practice,” the authors wrote.
 

SOURCE:

This study was led by Manjula Kurella Tamura, MD, MPH, Division of Nephrology, Department of Medicine, Stanford University School of Medicine, Palo Alto, California. It was published online on January 7, 2025, in JAMA Network Open.
 

LIMITATIONS:

Transportability analyses could not account for characteristics that were not well-documented in electronic health records, such as limited life expectancy. The study was conducted before the widespread use of sodium-glucose cotransporter 2 inhibitors, glucagon-like peptide 1 receptor agonists, and nonsteroidal mineralocorticoid receptor antagonists, making it unclear whether intensive BP treatment would result in similar benefits with current pharmacotherapy regimens. Eligibility for this study was based on BP measurements in routine practice, which tend to be more variable than those collected in research settings.
 

DISCLOSURES:

This study was supported by grants from the National Institutes of Health. Some authors disclosed serving as a consultant and receiving grants, personal fees, and consulting fees from pharmaceutical companies and other sources.
 

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:

The cardiovascular benefits observed with intensive blood pressure (BP) control in patients with hypertension and elevated cardiovascular risk from the Systolic Blood Pressure Intervention Trial (SPRINT) can be largely replicated in real-world settings among patients with chronic kidney disease (CKD), highlighting the advantages of adopting intensive BP targets.
 

METHODOLOGY:

• The SPRINT showed that an intensive systolic BP goal < 120 mm Hg reduced mortality, cardiovascular events, and mild cognitive impairment in patients with hypertension and elevated cardiovascular risk, including in patients with CKD.
• Researchers conducted a comparative effectiveness study to determine if the beneficial and adverse effects of intensive vs standard BP control observed in SPRINT were replicable in patients with CKD and hypertension in clinical practice.
• They identified 85,938 patients (mean age, 75.7 years; 95.0% men) and 13,983 patients (mean age, 77.4 years; 38.4% men) from the Veterans Health Administration (VHA) and Kaiser Permanente of Southern California (KPSC) databases, respectively.
• The treatment effect was estimated by combining baseline covariate, treatment, and outcome data of participants from the SPRINT with covariate data from the VHA and KPSC databases.
• The primary outcomes included major cardiovascular events, all-cause death, cognitive impairment, CKD progression, and adverse events at 4 years.

TAKEAWAY:

• Compared with SPRINT participants, those in the VHA and KPSC databases were older, had less prevalent cardiovascular disease, higher albuminuria, and used more statins.
• The benefits of intensive vs standard BP control on major cardiovascular events, all-cause mortality, and certain adverse events (hypotension, syncope, bradycardia, acute kidney injury, and electrolyte abnormality) were transferable from the trial to the VHA and KPSC populations.
• The treatment effect of intensive BP management on CKD progression was transportable to the KPSC population but not to the VHA population. However, the trial’s impact on cognitive outcomes, such as dementia, was not transportable to either the VHA or KPSC populations.
• On the absolute scale, intensive vs standard BP treatment showed greater cardiovascular benefits and fewer safety concerns in the VHA and KPSC populations than in the SPRINT.

IN PRACTICE:

“This example highlights the potential for transportability methods to provide insights that can bridge evidence gaps and inform the application of novel therapies to patients with CKD who are treated in everyday practice,” the authors wrote.
 

SOURCE:

This study was led by Manjula Kurella Tamura, MD, MPH, Division of Nephrology, Department of Medicine, Stanford University School of Medicine, Palo Alto, California. It was published online on January 7, 2025, in JAMA Network Open.
 

LIMITATIONS:

Transportability analyses could not account for characteristics that were not well-documented in electronic health records, such as limited life expectancy. The study was conducted before the widespread use of sodium-glucose cotransporter 2 inhibitors, glucagon-like peptide 1 receptor agonists, and nonsteroidal mineralocorticoid receptor antagonists, making it unclear whether intensive BP treatment would result in similar benefits with current pharmacotherapy regimens. Eligibility for this study was based on BP measurements in routine practice, which tend to be more variable than those collected in research settings.
 

DISCLOSURES:

This study was supported by grants from the National Institutes of Health. Some authors disclosed serving as a consultant and receiving grants, personal fees, and consulting fees from pharmaceutical companies and other sources.
 

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.

For millennia in medicine, alcohol, particularly red wine, carried a health halo; in small doses, it has historically been thought to have cardioprotective benefits. Michael Farkouh, MD, a professor of cardiology at Cedars-Sinai, estimates half the physicians still accept people having a drink or two a day. “That is still in practice, though the numbers are reducing,” he said.

But Farkouh no longer drinks alcohol, a position he has come to after getting more involved in research into the substance and his realization that many of the studies touting alcohol’s health benefits were flawed.

Today, alcohol sits alongside asbestos and tobacco as class 1 carcinogens. According to the World Health Organization, it has no known safe ingestible amount. In 2018, a blockbuster report in The Lancet found no amount of any kind of alcohol improves health. In early January, US Surgeon General Vivek Murthy called for adding cancer warnings to alcohol labels.

But the way doctors drink is far from black and white. For physicians, drinking habits are tied up in personal values, professional understanding of a substance with a confusing research history, and the fact alcohol is deeply ingrained in the social fabric of society — and in medicine. As thinking on alcohol shifts, this news organization spoke with physicians about their own drinking habits, how they counsel patients on it, and alcohol’s place in a field that works to keep people healthy.

 

Cultural Currency

From the days of Hippocrates, who believed alcohol could cure virtually every ailment, alcohol has held a large role in medicine. Through much of the 19th century, patent remedies like Hamlin’s Wizard Oil and the Seven Sutherland Sisters Hair Grower, contained alcohol — sometimes in concentrations exceeding 50%.

The first American Pharmacopoeia, published in 1820, even contained nine wine-based medicines. Throughout the second half of the 19th century, physicians largely debated alcohol’s role in medicine. However, a 1922 poll of members of the American Medical Association found that physicians were still using alcohol as a medicine for everything from heart attacks to animal bites.

Today, alcohol’s presence in medicine is, in some ways, representative of a realized cognitive dissonance.

“In my mind, alcohol has completely lost any illusion of benefit. It is a poison to almost every single organ in our body. Yet I’m currently engaged in a duel of being a physician who drinks in moderation and constantly judging myself for it,” said Tyra Fainstad, MD, an internist and an associate professor at CU Medicine in Denver.

Fainstad said every academic national conference she has attended has had a reception with multiple cash bars — and professional recruitment dinners regularly include at least the offering of alcohol. Private hospitals often have open bars at events.

“Drinking has historically been a way that people unwind, even in medicine,” said addiction psychiatrist Alexis Ritvo, MD. Ritvo — who said she drinks occasionally but much less than she used to after paying attention to how alcohol makes her feel and the harm alcohol can cause — noted that some occasions where alcohol is present socially in medicine don’t bother her. Alcohol is even an option at the addiction psychiatry conference, where attendees can exchange tickets for drinks. But last year, the event provided separate bars for alcoholic and nonalcoholic drinks.

“Our life is full of things that are contradictory or at odds,” Ritvo said. “We want things to either be wrong or right, appropriate or inappropriate, but just like all things, everything’s pretty nuanced.”

But there are examples of alcohol being a part of an event that are downright inappropriate, such as when she attended a fundraiser for a recovery facility that had an open bar.

Farkouh said alcohol at events can exclude others. (He recommends that instead of calling a social gathering “going out for drinks,” someone might say, “We’re getting together.”) He drinks mocktails or nonalcoholic beer at work events where alcohol is served.

Brian Dwinnell, MD, associate dean of student life at CU Medicine, said alcohol can quickly become the focus of an event — something he noticed at an annual kickball game between first- and second-year students that has historically served beer.

In recent years, school leadership has removed alcohol from his institution’s match day celebration and the kickball game. “Initially, there was some pushback from students,” he said of making these events dry, “but now, it’s just sort of accepted, and the events have been just as great as they were when we did provide alcohol.”

 

How Doctors Drink

Physicians may have a greater understanding of alcohol’s health harms. Still, they don’t necessarily drink less because of it, and whether they should becomes a question not just of health but also of the standards to which society holds medical professionals.

Data suggest physicians tend to drink at rates similar to those among the general population. A recent Medscape Medical News survey found nearly 60% of physicians have started drinking less.

Dwinnell said he is a long-time “wine connoisseur” and drinks on occasion. But he admitted that while he thinks about the health implications of alcohol more — and he has nixed it from various events for medical students — he does not believe his drinking habits have changed much.

Navya Mysore, MD, a family physician in New York City, said she has become interested in wine over the past few years, even taking classes to learn more about it. “I like understanding how it’s made, the regions it’s from, and how to pair it with food,” she said. Mysore admits she drank a little more than usual throughout the pandemic, yet today, she said her relationship with alcohol in moderation is related to family, community, and connection.

Fainstad, who drinks socially, said: “I think there’s an immeasurable quality to the social ritual of it. I think for better or worse — probably for worse — for many generations, alcohol has been a part of many meaningful traditions and rituals that we hold.”

Farkouh was quick to underscore the importance of social connection, and that alcohol reduces stress for some people. “I don’t want to take that away from people,” he said. But he also stated the importance of finding other ways to find social fulfillment and enjoyment — and said it’s essential for societal norms to shift to reflect this.

With emerging data, alcohol’s image in society is shifting. Ireland recently became the first country to pass regulation requiring all alcohol sold there to come with a cancer warning. All the clinicians interviewed for this article spoke about the increased acceptability of choosing not to drink for whatever reason.

In the context of alcohol, Dwinnell often asks his students, “What if you were out at a restaurant and you saw your mother’s surgeon there and they were intoxicated? Are you going to feel comfortable with that individual operating on your mother tomorrow or any time?” He added: “Physicians are held to a higher professional standard than those in other fields — and they should be. This is a high-stakes business.”

Dwinnell’s hypothetical question to students is a good one, albeit perhaps not always a fair one. “It’s important for people to realize that physicians are humans,” Mysore said. “We are people, we have lives, and we may choose to have habits that are not necessarily the healthiest for us.”

Fainstad said there’s no shame in medical professionals drinking on occasion. “You can’t be held accountable for something you don’t know about,” she said, acknowledging the known harms of alcohol and that there is still more to learn. But she does wonder how doctors who drank might be perceived in years to come. “I can imagine in a couple of decades, people could say, ‘Even doctors used to have a glass of wine with dinner.’”

 

‘Physicians Should Tighten Their Stances on Alcohol’

The 2020-2025 Dietary Guidelines suggest limiting intake to two alcoholic drinks or less daily for men and one drink or less for women or to choose not to drink. Farkouh said he skews toward the latter, encouraging patients to drink as little as possible or nothing at all. “If you take a holistic approach, physicians should tighten their stances on alcohol,” he said.

Ultimately, he said a randomized trial is warranted to address the risk for cardiovascular disease, in particular.

Of course, physicians vary in how they discuss the topic with patients.

Mysore said she regularly educates patients about pour size and ways to swap out alcoholic drinks with nonalcoholic ones. Outside of cases of addiction, she favors the idea of moderation. “I don’t really subscribe to all-or-nothing mindsets. If there’s something that you enjoy having as a part of your life, I don’t think there’s any reason why you need to eliminate it,” she said. “You just need to figure out what moderation looks like for you.”

Ritvo favors motivational interviewing and tries to understand someone’s relationship with alcohol.

Fainstad provides the Dietary Guidelines’ cutoffs to patients and educates them on the poisonous nature of the substance.

Clearer guidance from large governing bodies — potential changes around alcohol in the 2025-230 revision of the US Dietary Guidelines or cancer warnings on booze sold in the United States — are coming and could help streamline messaging.

And although he speaks with urgency about alcohol’s dangers, Farkouh emphasized the need for a judgment-free and patient-centered approach to conversations around drinking: “People have grown up with alcohol being acceptable, and it’s going to take time to change that.”

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

For millennia in medicine, alcohol, particularly red wine, carried a health halo; in small doses, it has historically been thought to have cardioprotective benefits. Michael Farkouh, MD, a professor of cardiology at Cedars-Sinai, estimates half the physicians still accept people having a drink or two a day. “That is still in practice, though the numbers are reducing,” he said.

But Farkouh no longer drinks alcohol, a position he has come to after getting more involved in research into the substance and his realization that many of the studies touting alcohol’s health benefits were flawed.

Today, alcohol sits alongside asbestos and tobacco as class 1 carcinogens. According to the World Health Organization, it has no known safe ingestible amount. In 2018, a blockbuster report in The Lancet found no amount of any kind of alcohol improves health. In early January, US Surgeon General Vivek Murthy called for adding cancer warnings to alcohol labels.

But the way doctors drink is far from black and white. For physicians, drinking habits are tied up in personal values, professional understanding of a substance with a confusing research history, and the fact alcohol is deeply ingrained in the social fabric of society — and in medicine. As thinking on alcohol shifts, this news organization spoke with physicians about their own drinking habits, how they counsel patients on it, and alcohol’s place in a field that works to keep people healthy.

 

Cultural Currency

From the days of Hippocrates, who believed alcohol could cure virtually every ailment, alcohol has held a large role in medicine. Through much of the 19th century, patent remedies like Hamlin’s Wizard Oil and the Seven Sutherland Sisters Hair Grower, contained alcohol — sometimes in concentrations exceeding 50%.

The first American Pharmacopoeia, published in 1820, even contained nine wine-based medicines. Throughout the second half of the 19th century, physicians largely debated alcohol’s role in medicine. However, a 1922 poll of members of the American Medical Association found that physicians were still using alcohol as a medicine for everything from heart attacks to animal bites.

Today, alcohol’s presence in medicine is, in some ways, representative of a realized cognitive dissonance.

“In my mind, alcohol has completely lost any illusion of benefit. It is a poison to almost every single organ in our body. Yet I’m currently engaged in a duel of being a physician who drinks in moderation and constantly judging myself for it,” said Tyra Fainstad, MD, an internist and an associate professor at CU Medicine in Denver.

Fainstad said every academic national conference she has attended has had a reception with multiple cash bars — and professional recruitment dinners regularly include at least the offering of alcohol. Private hospitals often have open bars at events.

“Drinking has historically been a way that people unwind, even in medicine,” said addiction psychiatrist Alexis Ritvo, MD. Ritvo — who said she drinks occasionally but much less than she used to after paying attention to how alcohol makes her feel and the harm alcohol can cause — noted that some occasions where alcohol is present socially in medicine don’t bother her. Alcohol is even an option at the addiction psychiatry conference, where attendees can exchange tickets for drinks. But last year, the event provided separate bars for alcoholic and nonalcoholic drinks.

“Our life is full of things that are contradictory or at odds,” Ritvo said. “We want things to either be wrong or right, appropriate or inappropriate, but just like all things, everything’s pretty nuanced.”

But there are examples of alcohol being a part of an event that are downright inappropriate, such as when she attended a fundraiser for a recovery facility that had an open bar.

Farkouh said alcohol at events can exclude others. (He recommends that instead of calling a social gathering “going out for drinks,” someone might say, “We’re getting together.”) He drinks mocktails or nonalcoholic beer at work events where alcohol is served.

Brian Dwinnell, MD, associate dean of student life at CU Medicine, said alcohol can quickly become the focus of an event — something he noticed at an annual kickball game between first- and second-year students that has historically served beer.

In recent years, school leadership has removed alcohol from his institution’s match day celebration and the kickball game. “Initially, there was some pushback from students,” he said of making these events dry, “but now, it’s just sort of accepted, and the events have been just as great as they were when we did provide alcohol.”

 

How Doctors Drink

Physicians may have a greater understanding of alcohol’s health harms. Still, they don’t necessarily drink less because of it, and whether they should becomes a question not just of health but also of the standards to which society holds medical professionals.

Data suggest physicians tend to drink at rates similar to those among the general population. A recent Medscape Medical News survey found nearly 60% of physicians have started drinking less.

Dwinnell said he is a long-time “wine connoisseur” and drinks on occasion. But he admitted that while he thinks about the health implications of alcohol more — and he has nixed it from various events for medical students — he does not believe his drinking habits have changed much.

Navya Mysore, MD, a family physician in New York City, said she has become interested in wine over the past few years, even taking classes to learn more about it. “I like understanding how it’s made, the regions it’s from, and how to pair it with food,” she said. Mysore admits she drank a little more than usual throughout the pandemic, yet today, she said her relationship with alcohol in moderation is related to family, community, and connection.

Fainstad, who drinks socially, said: “I think there’s an immeasurable quality to the social ritual of it. I think for better or worse — probably for worse — for many generations, alcohol has been a part of many meaningful traditions and rituals that we hold.”

Farkouh was quick to underscore the importance of social connection, and that alcohol reduces stress for some people. “I don’t want to take that away from people,” he said. But he also stated the importance of finding other ways to find social fulfillment and enjoyment — and said it’s essential for societal norms to shift to reflect this.

With emerging data, alcohol’s image in society is shifting. Ireland recently became the first country to pass regulation requiring all alcohol sold there to come with a cancer warning. All the clinicians interviewed for this article spoke about the increased acceptability of choosing not to drink for whatever reason.

In the context of alcohol, Dwinnell often asks his students, “What if you were out at a restaurant and you saw your mother’s surgeon there and they were intoxicated? Are you going to feel comfortable with that individual operating on your mother tomorrow or any time?” He added: “Physicians are held to a higher professional standard than those in other fields — and they should be. This is a high-stakes business.”

Dwinnell’s hypothetical question to students is a good one, albeit perhaps not always a fair one. “It’s important for people to realize that physicians are humans,” Mysore said. “We are people, we have lives, and we may choose to have habits that are not necessarily the healthiest for us.”

Fainstad said there’s no shame in medical professionals drinking on occasion. “You can’t be held accountable for something you don’t know about,” she said, acknowledging the known harms of alcohol and that there is still more to learn. But she does wonder how doctors who drank might be perceived in years to come. “I can imagine in a couple of decades, people could say, ‘Even doctors used to have a glass of wine with dinner.’”

 

‘Physicians Should Tighten Their Stances on Alcohol’

The 2020-2025 Dietary Guidelines suggest limiting intake to two alcoholic drinks or less daily for men and one drink or less for women or to choose not to drink. Farkouh said he skews toward the latter, encouraging patients to drink as little as possible or nothing at all. “If you take a holistic approach, physicians should tighten their stances on alcohol,” he said.

Ultimately, he said a randomized trial is warranted to address the risk for cardiovascular disease, in particular.

Of course, physicians vary in how they discuss the topic with patients.

Mysore said she regularly educates patients about pour size and ways to swap out alcoholic drinks with nonalcoholic ones. Outside of cases of addiction, she favors the idea of moderation. “I don’t really subscribe to all-or-nothing mindsets. If there’s something that you enjoy having as a part of your life, I don’t think there’s any reason why you need to eliminate it,” she said. “You just need to figure out what moderation looks like for you.”

Ritvo favors motivational interviewing and tries to understand someone’s relationship with alcohol.

Fainstad provides the Dietary Guidelines’ cutoffs to patients and educates them on the poisonous nature of the substance.

Clearer guidance from large governing bodies — potential changes around alcohol in the 2025-230 revision of the US Dietary Guidelines or cancer warnings on booze sold in the United States — are coming and could help streamline messaging.

And although he speaks with urgency about alcohol’s dangers, Farkouh emphasized the need for a judgment-free and patient-centered approach to conversations around drinking: “People have grown up with alcohol being acceptable, and it’s going to take time to change that.”

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

For millennia in medicine, alcohol, particularly red wine, carried a health halo; in small doses, it has historically been thought to have cardioprotective benefits. Michael Farkouh, MD, a professor of cardiology at Cedars-Sinai, estimates half the physicians still accept people having a drink or two a day. “That is still in practice, though the numbers are reducing,” he said.

But Farkouh no longer drinks alcohol, a position he has come to after getting more involved in research into the substance and his realization that many of the studies touting alcohol’s health benefits were flawed.

Today, alcohol sits alongside asbestos and tobacco as class 1 carcinogens. According to the World Health Organization, it has no known safe ingestible amount. In 2018, a blockbuster report in The Lancet found no amount of any kind of alcohol improves health. In early January, US Surgeon General Vivek Murthy called for adding cancer warnings to alcohol labels.

But the way doctors drink is far from black and white. For physicians, drinking habits are tied up in personal values, professional understanding of a substance with a confusing research history, and the fact alcohol is deeply ingrained in the social fabric of society — and in medicine. As thinking on alcohol shifts, this news organization spoke with physicians about their own drinking habits, how they counsel patients on it, and alcohol’s place in a field that works to keep people healthy.

 

Cultural Currency

From the days of Hippocrates, who believed alcohol could cure virtually every ailment, alcohol has held a large role in medicine. Through much of the 19th century, patent remedies like Hamlin’s Wizard Oil and the Seven Sutherland Sisters Hair Grower, contained alcohol — sometimes in concentrations exceeding 50%.

The first American Pharmacopoeia, published in 1820, even contained nine wine-based medicines. Throughout the second half of the 19th century, physicians largely debated alcohol’s role in medicine. However, a 1922 poll of members of the American Medical Association found that physicians were still using alcohol as a medicine for everything from heart attacks to animal bites.

Today, alcohol’s presence in medicine is, in some ways, representative of a realized cognitive dissonance.

“In my mind, alcohol has completely lost any illusion of benefit. It is a poison to almost every single organ in our body. Yet I’m currently engaged in a duel of being a physician who drinks in moderation and constantly judging myself for it,” said Tyra Fainstad, MD, an internist and an associate professor at CU Medicine in Denver.

Fainstad said every academic national conference she has attended has had a reception with multiple cash bars — and professional recruitment dinners regularly include at least the offering of alcohol. Private hospitals often have open bars at events.

“Drinking has historically been a way that people unwind, even in medicine,” said addiction psychiatrist Alexis Ritvo, MD. Ritvo — who said she drinks occasionally but much less than she used to after paying attention to how alcohol makes her feel and the harm alcohol can cause — noted that some occasions where alcohol is present socially in medicine don’t bother her. Alcohol is even an option at the addiction psychiatry conference, where attendees can exchange tickets for drinks. But last year, the event provided separate bars for alcoholic and nonalcoholic drinks.

“Our life is full of things that are contradictory or at odds,” Ritvo said. “We want things to either be wrong or right, appropriate or inappropriate, but just like all things, everything’s pretty nuanced.”

But there are examples of alcohol being a part of an event that are downright inappropriate, such as when she attended a fundraiser for a recovery facility that had an open bar.

Farkouh said alcohol at events can exclude others. (He recommends that instead of calling a social gathering “going out for drinks,” someone might say, “We’re getting together.”) He drinks mocktails or nonalcoholic beer at work events where alcohol is served.

Brian Dwinnell, MD, associate dean of student life at CU Medicine, said alcohol can quickly become the focus of an event — something he noticed at an annual kickball game between first- and second-year students that has historically served beer.

In recent years, school leadership has removed alcohol from his institution’s match day celebration and the kickball game. “Initially, there was some pushback from students,” he said of making these events dry, “but now, it’s just sort of accepted, and the events have been just as great as they were when we did provide alcohol.”

 

How Doctors Drink

Physicians may have a greater understanding of alcohol’s health harms. Still, they don’t necessarily drink less because of it, and whether they should becomes a question not just of health but also of the standards to which society holds medical professionals.

Data suggest physicians tend to drink at rates similar to those among the general population. A recent Medscape Medical News survey found nearly 60% of physicians have started drinking less.

Dwinnell said he is a long-time “wine connoisseur” and drinks on occasion. But he admitted that while he thinks about the health implications of alcohol more — and he has nixed it from various events for medical students — he does not believe his drinking habits have changed much.

Navya Mysore, MD, a family physician in New York City, said she has become interested in wine over the past few years, even taking classes to learn more about it. “I like understanding how it’s made, the regions it’s from, and how to pair it with food,” she said. Mysore admits she drank a little more than usual throughout the pandemic, yet today, she said her relationship with alcohol in moderation is related to family, community, and connection.

Fainstad, who drinks socially, said: “I think there’s an immeasurable quality to the social ritual of it. I think for better or worse — probably for worse — for many generations, alcohol has been a part of many meaningful traditions and rituals that we hold.”

Farkouh was quick to underscore the importance of social connection, and that alcohol reduces stress for some people. “I don’t want to take that away from people,” he said. But he also stated the importance of finding other ways to find social fulfillment and enjoyment — and said it’s essential for societal norms to shift to reflect this.

With emerging data, alcohol’s image in society is shifting. Ireland recently became the first country to pass regulation requiring all alcohol sold there to come with a cancer warning. All the clinicians interviewed for this article spoke about the increased acceptability of choosing not to drink for whatever reason.

In the context of alcohol, Dwinnell often asks his students, “What if you were out at a restaurant and you saw your mother’s surgeon there and they were intoxicated? Are you going to feel comfortable with that individual operating on your mother tomorrow or any time?” He added: “Physicians are held to a higher professional standard than those in other fields — and they should be. This is a high-stakes business.”

Dwinnell’s hypothetical question to students is a good one, albeit perhaps not always a fair one. “It’s important for people to realize that physicians are humans,” Mysore said. “We are people, we have lives, and we may choose to have habits that are not necessarily the healthiest for us.”

Fainstad said there’s no shame in medical professionals drinking on occasion. “You can’t be held accountable for something you don’t know about,” she said, acknowledging the known harms of alcohol and that there is still more to learn. But she does wonder how doctors who drank might be perceived in years to come. “I can imagine in a couple of decades, people could say, ‘Even doctors used to have a glass of wine with dinner.’”

 

‘Physicians Should Tighten Their Stances on Alcohol’

The 2020-2025 Dietary Guidelines suggest limiting intake to two alcoholic drinks or less daily for men and one drink or less for women or to choose not to drink. Farkouh said he skews toward the latter, encouraging patients to drink as little as possible or nothing at all. “If you take a holistic approach, physicians should tighten their stances on alcohol,” he said.

Ultimately, he said a randomized trial is warranted to address the risk for cardiovascular disease, in particular.

Of course, physicians vary in how they discuss the topic with patients.

Mysore said she regularly educates patients about pour size and ways to swap out alcoholic drinks with nonalcoholic ones. Outside of cases of addiction, she favors the idea of moderation. “I don’t really subscribe to all-or-nothing mindsets. If there’s something that you enjoy having as a part of your life, I don’t think there’s any reason why you need to eliminate it,” she said. “You just need to figure out what moderation looks like for you.”

Ritvo favors motivational interviewing and tries to understand someone’s relationship with alcohol.

Fainstad provides the Dietary Guidelines’ cutoffs to patients and educates them on the poisonous nature of the substance.

Clearer guidance from large governing bodies — potential changes around alcohol in the 2025-230 revision of the US Dietary Guidelines or cancer warnings on booze sold in the United States — are coming and could help streamline messaging.

And although he speaks with urgency about alcohol’s dangers, Farkouh emphasized the need for a judgment-free and patient-centered approach to conversations around drinking: “People have grown up with alcohol being acceptable, and it’s going to take time to change that.”

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

TOPLINE:

Patients with systemic lupus erythematosus (SLE) face more than double the risk for atherosclerotic plaque progression than healthy control individuals without the condition, but management of traditional cardiovascular risk factors and prolonged clinical remission can successfully mitigate it.

METHODOLOGY:

• Researchers performed a prospective study to assess the progression of subclinical atherosclerosis plaques and the development of cardiovascular events in patients with SLE over a 10-year follow-up period.
• They included 111 patients with SLE (mean age, 43 years; 91% women) and 94 matched healthy control individuals without prior atherosclerotic cardiovascular disease (CVD), active malignancy, pregnancy, or diabetes mellitus who underwent carotid ultrasound measurements.
• A total of 738 carotid measurements were analyzed from baseline to 3-, 7-, and 10-year follow-up periods for assessing new carotid plaque development; incident CVD events were also analyzed during follow-up.
• Disease remission was evaluated based on the Definition of Remission in SLE criteria.
• Target for management of cardiovascular risk factors was based on standard recommendations.
•  

TAKEAWAY:

• During the 10-year follow-up, patients with SLE showed a 2.3-fold higher risk for plaque progression than healthy control participants (adjusted incidence rate ratio [aIRR], 2.26; P = .002).
• Achieving risk reduction target for each standard cardiovascular risk factor (blood pressure, lipids, smoking, body weight, and physical activity) was associated with a 32% reduction in the risk for plaque progression (aIRR, 0.68; P = .004).
• Staying in remission for ≥ 75% of the follow-up period was significantly associated with a 43% reduction in the risk for plaque progression (aIRR, 0.57; P = .033).
• Patients with SLE also had a higher incidence of CVD events than healthy control participants (permutation-based log-rank P = .036).
•  

IN PRACTICE:

“These findings support the importance of prioritizing sustained remission rather than a low disease activity state for the prevention of atherosclerosis development and progression in SLE,” the authors wrote.

SOURCE:

The study was led by Nikolaos Papazoglou, MD, First Department of Propaedeutic Internal Medicine, Joint Academic Rheumatology Program, School of Medicine, National and Kapodistrian University of Athens in Greece. It was published online on December 25, 2024, in Arthritis & Rheumatology.

LIMITATIONS:

The study had limited statistical power to perform a multivariate analysis of incident CVD events due to low event rates. The cohort consisted solely of White Europeans, possibly limiting the generalizability of the findings to more ethnically diverse populations. Because antiphospholipid antibodies are known to be associated with CVD events in the general population, the lack of testing for antiphospholipid antibody positivity in healthy control participants could be another limitation.

DISCLOSURES:

The study did not receive any funding from public, commercial, or not-for-profit sectors. The authors reported 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 appeared on Medscape.com.

TOPLINE:

Patients with systemic lupus erythematosus (SLE) face more than double the risk for atherosclerotic plaque progression than healthy control individuals without the condition, but management of traditional cardiovascular risk factors and prolonged clinical remission can successfully mitigate it.

METHODOLOGY:

• Researchers performed a prospective study to assess the progression of subclinical atherosclerosis plaques and the development of cardiovascular events in patients with SLE over a 10-year follow-up period.
• They included 111 patients with SLE (mean age, 43 years; 91% women) and 94 matched healthy control individuals without prior atherosclerotic cardiovascular disease (CVD), active malignancy, pregnancy, or diabetes mellitus who underwent carotid ultrasound measurements.
• A total of 738 carotid measurements were analyzed from baseline to 3-, 7-, and 10-year follow-up periods for assessing new carotid plaque development; incident CVD events were also analyzed during follow-up.
• Disease remission was evaluated based on the Definition of Remission in SLE criteria.
• Target for management of cardiovascular risk factors was based on standard recommendations.
•  

TAKEAWAY:

• During the 10-year follow-up, patients with SLE showed a 2.3-fold higher risk for plaque progression than healthy control participants (adjusted incidence rate ratio [aIRR], 2.26; P = .002).
• Achieving risk reduction target for each standard cardiovascular risk factor (blood pressure, lipids, smoking, body weight, and physical activity) was associated with a 32% reduction in the risk for plaque progression (aIRR, 0.68; P = .004).
• Staying in remission for ≥ 75% of the follow-up period was significantly associated with a 43% reduction in the risk for plaque progression (aIRR, 0.57; P = .033).
• Patients with SLE also had a higher incidence of CVD events than healthy control participants (permutation-based log-rank P = .036).
•  

IN PRACTICE:

“These findings support the importance of prioritizing sustained remission rather than a low disease activity state for the prevention of atherosclerosis development and progression in SLE,” the authors wrote.

SOURCE:

The study was led by Nikolaos Papazoglou, MD, First Department of Propaedeutic Internal Medicine, Joint Academic Rheumatology Program, School of Medicine, National and Kapodistrian University of Athens in Greece. It was published online on December 25, 2024, in Arthritis & Rheumatology.

LIMITATIONS:

The study had limited statistical power to perform a multivariate analysis of incident CVD events due to low event rates. The cohort consisted solely of White Europeans, possibly limiting the generalizability of the findings to more ethnically diverse populations. Because antiphospholipid antibodies are known to be associated with CVD events in the general population, the lack of testing for antiphospholipid antibody positivity in healthy control participants could be another limitation.

DISCLOSURES:

The study did not receive any funding from public, commercial, or not-for-profit sectors. The authors reported 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 appeared on Medscape.com.

TOPLINE:

Patients with systemic lupus erythematosus (SLE) face more than double the risk for atherosclerotic plaque progression than healthy control individuals without the condition, but management of traditional cardiovascular risk factors and prolonged clinical remission can successfully mitigate it.

METHODOLOGY:

• Researchers performed a prospective study to assess the progression of subclinical atherosclerosis plaques and the development of cardiovascular events in patients with SLE over a 10-year follow-up period.
• They included 111 patients with SLE (mean age, 43 years; 91% women) and 94 matched healthy control individuals without prior atherosclerotic cardiovascular disease (CVD), active malignancy, pregnancy, or diabetes mellitus who underwent carotid ultrasound measurements.
• A total of 738 carotid measurements were analyzed from baseline to 3-, 7-, and 10-year follow-up periods for assessing new carotid plaque development; incident CVD events were also analyzed during follow-up.
• Disease remission was evaluated based on the Definition of Remission in SLE criteria.
• Target for management of cardiovascular risk factors was based on standard recommendations.
•  

TAKEAWAY:

• During the 10-year follow-up, patients with SLE showed a 2.3-fold higher risk for plaque progression than healthy control participants (adjusted incidence rate ratio [aIRR], 2.26; P = .002).
• Achieving risk reduction target for each standard cardiovascular risk factor (blood pressure, lipids, smoking, body weight, and physical activity) was associated with a 32% reduction in the risk for plaque progression (aIRR, 0.68; P = .004).
• Staying in remission for ≥ 75% of the follow-up period was significantly associated with a 43% reduction in the risk for plaque progression (aIRR, 0.57; P = .033).
• Patients with SLE also had a higher incidence of CVD events than healthy control participants (permutation-based log-rank P = .036).
•  

IN PRACTICE:

“These findings support the importance of prioritizing sustained remission rather than a low disease activity state for the prevention of atherosclerosis development and progression in SLE,” the authors wrote.

SOURCE:

The study was led by Nikolaos Papazoglou, MD, First Department of Propaedeutic Internal Medicine, Joint Academic Rheumatology Program, School of Medicine, National and Kapodistrian University of Athens in Greece. It was published online on December 25, 2024, in Arthritis & Rheumatology.

LIMITATIONS:

The study had limited statistical power to perform a multivariate analysis of incident CVD events due to low event rates. The cohort consisted solely of White Europeans, possibly limiting the generalizability of the findings to more ethnically diverse populations. Because antiphospholipid antibodies are known to be associated with CVD events in the general population, the lack of testing for antiphospholipid antibody positivity in healthy control participants could be another limitation.

DISCLOSURES:

The study did not receive any funding from public, commercial, or not-for-profit sectors. The authors reported 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 appeared on Medscape.com.

TOPLINE:

The newer biologics — interleukin (IL)–17, IL-12/23, and IL-23 inhibitors — demonstrate comparable cardiovascular safety profiles to tumor necrosis factor (TNF) inhibitors in biologic-naive patients with psoriasis or psoriatic arthritis (PsA).

METHODOLOGY:

• In a retrospective cohort study, researchers conducted an emulated target trial analysis using data of 32,098 biologic-naive patients with psoriasis or PsA who were treated with one of the newer biologics (infliximab, adalimumab, etanercept, certolizumab pegol, secukinumab, ixekizumab, brodalumab, ustekinumab, risankizumab, guselkumab, and tildrakizumab) from the TriNetX Research Network between 2014 and 2022.
• Patients received TNF inhibitors (n = 20,314), IL-17 inhibitors (n = 5073), IL-12/23 inhibitors (n = 3573), or IL-23 inhibitors (n = 3138).
• A propensity-matched analysis compared each class of newer biologics with TNF inhibitors, adjusting for demographics, comorbidities, and medication use.
• The primary outcomes were major adverse cardiovascular events (MACE; myocardial infarction and stroke) or venous thromboembolic events (VTE).

TAKEAWAY:

• Compared with patients who received TNF inhibitors, the risk for MACE was not significantly different between patients who received IL-17 inhibitors (incidence rate ratio [IRR], 1.14; 95% CI, 0.86-1.52), IL-12/23 inhibitors (IRR, 1.24; 95% CI, 0.84-1.78), or IL-23 inhibitors (IRR, 0.93; 95% CI, 0.61-1.38)
• The VTE risk was also not significantly different between patients who received IL-17 inhibitors (IRR, 1.12; 95% CI, 0.63-2.08), IL-12/23 inhibitors (IRR, 1.51; 95% CI, 0.73-3.19), or IL-23 inhibitors (IRR, 1.42; 95% CI, 0.64-3.25) compared with those who received TNF inhibitors.
• Subgroup analyses for psoriasis or psoriatic arthritis alone confirmed consistent findings.
• Patients with preexisting hyperlipidemia and diabetes mellitus showed lower risks for MACE and VTE with newer biologics compared with TNF inhibitors. 

IN PRACTICE:

“No significant MACE and VTE risk differences were detected in patients with psoriasis or PsA between those receiving IL-17, IL-12/23, and IL-23 inhibitors and those with TNF inhibitors,” the authors concluded. These findings, they added “can be considered by physicians and patients when making treatment decisions” and also provide “evidence for future pharmacovigilance studies.”

SOURCE:

The study was led by Tai-Li Chen, MD, of the Department of Dermatology, Taipei Veterans General Hospital in Taipei, Taiwan. It was published online on December 27, 2024, in the Journal of the American Academy of Dermatology.

LIMITATIONS:

Study limitations included potential residual confounding factors, lack of information on disease severity, and inclusion of predominantly White individuals.

DISCLOSURES:

The study received support from Taipei Veterans General Hospital and Ministry of Science and Technology, Taiwan. The authors reported 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:

The newer biologics — interleukin (IL)–17, IL-12/23, and IL-23 inhibitors — demonstrate comparable cardiovascular safety profiles to tumor necrosis factor (TNF) inhibitors in biologic-naive patients with psoriasis or psoriatic arthritis (PsA).

METHODOLOGY:

• In a retrospective cohort study, researchers conducted an emulated target trial analysis using data of 32,098 biologic-naive patients with psoriasis or PsA who were treated with one of the newer biologics (infliximab, adalimumab, etanercept, certolizumab pegol, secukinumab, ixekizumab, brodalumab, ustekinumab, risankizumab, guselkumab, and tildrakizumab) from the TriNetX Research Network between 2014 and 2022.
• Patients received TNF inhibitors (n = 20,314), IL-17 inhibitors (n = 5073), IL-12/23 inhibitors (n = 3573), or IL-23 inhibitors (n = 3138).
• A propensity-matched analysis compared each class of newer biologics with TNF inhibitors, adjusting for demographics, comorbidities, and medication use.
• The primary outcomes were major adverse cardiovascular events (MACE; myocardial infarction and stroke) or venous thromboembolic events (VTE).

TAKEAWAY:

• Compared with patients who received TNF inhibitors, the risk for MACE was not significantly different between patients who received IL-17 inhibitors (incidence rate ratio [IRR], 1.14; 95% CI, 0.86-1.52), IL-12/23 inhibitors (IRR, 1.24; 95% CI, 0.84-1.78), or IL-23 inhibitors (IRR, 0.93; 95% CI, 0.61-1.38)
• The VTE risk was also not significantly different between patients who received IL-17 inhibitors (IRR, 1.12; 95% CI, 0.63-2.08), IL-12/23 inhibitors (IRR, 1.51; 95% CI, 0.73-3.19), or IL-23 inhibitors (IRR, 1.42; 95% CI, 0.64-3.25) compared with those who received TNF inhibitors.
• Subgroup analyses for psoriasis or psoriatic arthritis alone confirmed consistent findings.
• Patients with preexisting hyperlipidemia and diabetes mellitus showed lower risks for MACE and VTE with newer biologics compared with TNF inhibitors. 

IN PRACTICE:

“No significant MACE and VTE risk differences were detected in patients with psoriasis or PsA between those receiving IL-17, IL-12/23, and IL-23 inhibitors and those with TNF inhibitors,” the authors concluded. These findings, they added “can be considered by physicians and patients when making treatment decisions” and also provide “evidence for future pharmacovigilance studies.”

SOURCE:

The study was led by Tai-Li Chen, MD, of the Department of Dermatology, Taipei Veterans General Hospital in Taipei, Taiwan. It was published online on December 27, 2024, in the Journal of the American Academy of Dermatology.

LIMITATIONS:

Study limitations included potential residual confounding factors, lack of information on disease severity, and inclusion of predominantly White individuals.

DISCLOSURES:

The study received support from Taipei Veterans General Hospital and Ministry of Science and Technology, Taiwan. The authors reported 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:

The newer biologics — interleukin (IL)–17, IL-12/23, and IL-23 inhibitors — demonstrate comparable cardiovascular safety profiles to tumor necrosis factor (TNF) inhibitors in biologic-naive patients with psoriasis or psoriatic arthritis (PsA).

METHODOLOGY:

• In a retrospective cohort study, researchers conducted an emulated target trial analysis using data of 32,098 biologic-naive patients with psoriasis or PsA who were treated with one of the newer biologics (infliximab, adalimumab, etanercept, certolizumab pegol, secukinumab, ixekizumab, brodalumab, ustekinumab, risankizumab, guselkumab, and tildrakizumab) from the TriNetX Research Network between 2014 and 2022.
• Patients received TNF inhibitors (n = 20,314), IL-17 inhibitors (n = 5073), IL-12/23 inhibitors (n = 3573), or IL-23 inhibitors (n = 3138).
• A propensity-matched analysis compared each class of newer biologics with TNF inhibitors, adjusting for demographics, comorbidities, and medication use.
• The primary outcomes were major adverse cardiovascular events (MACE; myocardial infarction and stroke) or venous thromboembolic events (VTE).

TAKEAWAY:

• Compared with patients who received TNF inhibitors, the risk for MACE was not significantly different between patients who received IL-17 inhibitors (incidence rate ratio [IRR], 1.14; 95% CI, 0.86-1.52), IL-12/23 inhibitors (IRR, 1.24; 95% CI, 0.84-1.78), or IL-23 inhibitors (IRR, 0.93; 95% CI, 0.61-1.38)
• The VTE risk was also not significantly different between patients who received IL-17 inhibitors (IRR, 1.12; 95% CI, 0.63-2.08), IL-12/23 inhibitors (IRR, 1.51; 95% CI, 0.73-3.19), or IL-23 inhibitors (IRR, 1.42; 95% CI, 0.64-3.25) compared with those who received TNF inhibitors.
• Subgroup analyses for psoriasis or psoriatic arthritis alone confirmed consistent findings.
• Patients with preexisting hyperlipidemia and diabetes mellitus showed lower risks for MACE and VTE with newer biologics compared with TNF inhibitors. 

IN PRACTICE:

“No significant MACE and VTE risk differences were detected in patients with psoriasis or PsA between those receiving IL-17, IL-12/23, and IL-23 inhibitors and those with TNF inhibitors,” the authors concluded. These findings, they added “can be considered by physicians and patients when making treatment decisions” and also provide “evidence for future pharmacovigilance studies.”

SOURCE:

The study was led by Tai-Li Chen, MD, of the Department of Dermatology, Taipei Veterans General Hospital in Taipei, Taiwan. It was published online on December 27, 2024, in the Journal of the American Academy of Dermatology.

LIMITATIONS:

Study limitations included potential residual confounding factors, lack of information on disease severity, and inclusion of predominantly White individuals.

DISCLOSURES:

The study received support from Taipei Veterans General Hospital and Ministry of Science and Technology, Taiwan. The authors reported 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:

Patients with rheumatoid arthritis (RA) face a higher risk for heart failure (HF) than those without the condition, with the elevated risk primarily driven by HF with preserved ejection fraction (HFpEF).

METHODOLOGY:

• The researchers conducted a retrospective cohort study using data from the Mass General Brigham Biobank to investigate the risk for overall HF and its subtypes, particularly HF with reduced EF (HFrEF) and HFpEF, in patients with RA.
• They included 1445 patients newly diagnosed with RA (mean age, 51.4 years; 78.7% women) and 4335 matched comparators without RA.
• Patients with RA were identified using diagnosis codes and RA-related natural language processing concepts.
• HFpEF and HFrEF were defined as HF with an EF ≥ 50% and ≤ 40%, respectively; incidences for overall HF, HFpEF, and HFrEF were calculated per 1000 person-years.

TAKEAWAY:

• The study identified 92 incident HF cases in the RA cohort and 157 in the non-RA cohort over a median follow-up of 10.3 years per patient.
• HFpEF was the predominant HF subtype in both cohorts, with a higher incidence in patients with RA than in those without the condition (4.33 vs 2.11 per 1000 person-years).
• Patients with RA showed a 79% higher risk for HF than those without the condition (adjusted hazard ratio [aHR], 1.79; 95% CI, 1.38-2.32).
• Among the HF subtypes, patients with RA had a significantly increased risk for HFpEF (aHR, 1.99; 95% CI, 1.43-2.77) but not for HFrEF.

IN PRACTICE:

“RA can be considered a human model for inflammation, and findings from this study support the notion that chronic inflammation increases risk for HFpEF,” the authors wrote.

SOURCE:

This study was led by Yumeko Kawano, MD, Brigham and Women’s Hospital, Boston, Massachusetts, and was published online in Arthritis Care & Research.

LIMITATIONS:

This study was conducted within an academic tertiary hospital system and involved participants from a biobank, which may have introduced selection bias and limited generalizability. The study did not account for post-baseline variables that could mediate the observed associations, such as the chronic use of nonsteroidal anti-inflammatory drugs, steroids, or specific disease-modifying antirheumatic drugs. The study relied on the availability of clinically performed cardiology studies for HF subtyping, possibly introducing misclassification of HF.

DISCLOSURES:

This study was supported by grants from the National Institute of Arthritis and Musculoskeletal and Skin Diseases. One author received support from the Ruth L. Kirschstein Institutional National Research Service Award, National Institutes of Health.

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

TOPLINE:

Patients with rheumatoid arthritis (RA) face a higher risk for heart failure (HF) than those without the condition, with the elevated risk primarily driven by HF with preserved ejection fraction (HFpEF).

METHODOLOGY:

• The researchers conducted a retrospective cohort study using data from the Mass General Brigham Biobank to investigate the risk for overall HF and its subtypes, particularly HF with reduced EF (HFrEF) and HFpEF, in patients with RA.
• They included 1445 patients newly diagnosed with RA (mean age, 51.4 years; 78.7% women) and 4335 matched comparators without RA.
• Patients with RA were identified using diagnosis codes and RA-related natural language processing concepts.
• HFpEF and HFrEF were defined as HF with an EF ≥ 50% and ≤ 40%, respectively; incidences for overall HF, HFpEF, and HFrEF were calculated per 1000 person-years.

TAKEAWAY:

• The study identified 92 incident HF cases in the RA cohort and 157 in the non-RA cohort over a median follow-up of 10.3 years per patient.
• HFpEF was the predominant HF subtype in both cohorts, with a higher incidence in patients with RA than in those without the condition (4.33 vs 2.11 per 1000 person-years).
• Patients with RA showed a 79% higher risk for HF than those without the condition (adjusted hazard ratio [aHR], 1.79; 95% CI, 1.38-2.32).
• Among the HF subtypes, patients with RA had a significantly increased risk for HFpEF (aHR, 1.99; 95% CI, 1.43-2.77) but not for HFrEF.

IN PRACTICE:

“RA can be considered a human model for inflammation, and findings from this study support the notion that chronic inflammation increases risk for HFpEF,” the authors wrote.

SOURCE:

This study was led by Yumeko Kawano, MD, Brigham and Women’s Hospital, Boston, Massachusetts, and was published online in Arthritis Care & Research.

LIMITATIONS:

This study was conducted within an academic tertiary hospital system and involved participants from a biobank, which may have introduced selection bias and limited generalizability. The study did not account for post-baseline variables that could mediate the observed associations, such as the chronic use of nonsteroidal anti-inflammatory drugs, steroids, or specific disease-modifying antirheumatic drugs. The study relied on the availability of clinically performed cardiology studies for HF subtyping, possibly introducing misclassification of HF.

DISCLOSURES:

This study was supported by grants from the National Institute of Arthritis and Musculoskeletal and Skin Diseases. One author received support from the Ruth L. Kirschstein Institutional National Research Service Award, National Institutes of Health.

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

TOPLINE:

Patients with rheumatoid arthritis (RA) face a higher risk for heart failure (HF) than those without the condition, with the elevated risk primarily driven by HF with preserved ejection fraction (HFpEF).

METHODOLOGY:

• The researchers conducted a retrospective cohort study using data from the Mass General Brigham Biobank to investigate the risk for overall HF and its subtypes, particularly HF with reduced EF (HFrEF) and HFpEF, in patients with RA.
• They included 1445 patients newly diagnosed with RA (mean age, 51.4 years; 78.7% women) and 4335 matched comparators without RA.
• Patients with RA were identified using diagnosis codes and RA-related natural language processing concepts.
• HFpEF and HFrEF were defined as HF with an EF ≥ 50% and ≤ 40%, respectively; incidences for overall HF, HFpEF, and HFrEF were calculated per 1000 person-years.

TAKEAWAY:

• The study identified 92 incident HF cases in the RA cohort and 157 in the non-RA cohort over a median follow-up of 10.3 years per patient.
• HFpEF was the predominant HF subtype in both cohorts, with a higher incidence in patients with RA than in those without the condition (4.33 vs 2.11 per 1000 person-years).
• Patients with RA showed a 79% higher risk for HF than those without the condition (adjusted hazard ratio [aHR], 1.79; 95% CI, 1.38-2.32).
• Among the HF subtypes, patients with RA had a significantly increased risk for HFpEF (aHR, 1.99; 95% CI, 1.43-2.77) but not for HFrEF.

IN PRACTICE:

“RA can be considered a human model for inflammation, and findings from this study support the notion that chronic inflammation increases risk for HFpEF,” the authors wrote.

SOURCE:

This study was led by Yumeko Kawano, MD, Brigham and Women’s Hospital, Boston, Massachusetts, and was published online in Arthritis Care & Research.

LIMITATIONS:

This study was conducted within an academic tertiary hospital system and involved participants from a biobank, which may have introduced selection bias and limited generalizability. The study did not account for post-baseline variables that could mediate the observed associations, such as the chronic use of nonsteroidal anti-inflammatory drugs, steroids, or specific disease-modifying antirheumatic drugs. The study relied on the availability of clinically performed cardiology studies for HF subtyping, possibly introducing misclassification of HF.

DISCLOSURES:

This study was supported by grants from the National Institute of Arthritis and Musculoskeletal and Skin Diseases. One author received support from the Ruth L. Kirschstein Institutional National Research Service Award, National Institutes of Health.

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

This transcript has been edited for clarity. 

Blood pressure. If you’re a primary care provider trying to do right by your patients, you might be understandably confused by the current mishmash of guidelines with different blood pressure targets. But as chaotic as things are, at least it’s not the 1930s, when you might hear John Hay give a lecture to the British Medical Association and say, “The greatest danger to a man with high blood pressure lies in its discovery, because then some fool is certain to try and reduce it.”

Yeah, he said that. But what happened in the 1930s stays in the 1930s. And now we can at least agree that we should be treating high blood pressure. But what’s the goal we should be aiming for? This is On Second Thought. 

We’ve come a long way since FDR was recording blood pressures of 200 and his doctor prescribed him barbiturates and massage therapy.

That s#$# don’t fly no more. Over the past hundred years, we have become much more aggressive in treating blood pressure. Remember the Oslo study? It defined mild hypertension as a blood pressure between 150 and 180 mm Hg. Now, those numbers send people screaming to the emergency room. So, let’s acknowledge that things are substantially better than they once were. Let’s agree on that and we can start to heal this nation again. 

Before we get into the numbers, when we’re treating blood pressure, let’s make a few points about measuring it. Obviously, to treat something, you have to measure it properly. Two recent trials have illustrated that these details matter a lot.

The Cuff(SZ) randomized crossover trial — and it took me a minute to realize that Cuff(SZ) meant cuff size, so bravo, Ishigami et al — showed that picking the wrong cuff size could affect BP measurements by 4.5 points if you were one size off. If you were two sizes too small, you overestimated BP by almost 20 points.

Add on here another recent study, the ARMS crossover randomized clinical trial, looking at how arm position affected BP measures. If the arm was resting on your lap or hanging by your side, that overestimated blood pressure by 4 and 6.5 points. So sometimes you have to remember the fundamentals: cuff size, arm position — it might make the difference between increasing or maintaining the patient’s meds.

But on to the main show. What numbers should we be aiming for? We no longer live in the “BP 200, the president’s going to have a stroke” world of the 1940s, and even a BP of 150 is considered quite high these days. Studies like the MRC trial, INVEST, and SPRINT have pushed BP targets ever lower. SPRINT, in particular, randomized patients to a blood pressure target under 120 systolic vs under 140 systolic, and the under-120 arm won out with fewer cardiovascular events and lower all-cause mortality.

Pretty definitive slam dunk. But the more intensive treatment came with more hypotension, syncope, and kidney injury, because there is no free lunch in medicine. And ditto with BPROAD, just published in The New England Journal of Medicine and presented at the American Heart Association annual meeting. A diabetic population randomized to 120 vs 140 as a BP target showed that more aggressive treatment was better.

Fewer cardiovascular events, like stroke, but no mortality difference, and more hypotension. So a cardiovascular benefit at the cost of more side effects. Now, like all cardiologists, my motto is “Save the heart and screw the kidney.” But if you do care about the other organs in this meat sack that we call a human body, the question you need to wrestle with is, how much do you value cardiovascular protection vs how willing are you to tolerate side effects?

Hypotension may not sound dangerous, but gravity is an unforgiving mistress. If you painstakingly compile the summary of the various BP guidelines for easy perusal, you would notice something critical: One, I have too much free time on my hands; two, the disagreements are not really all that profound.

Arguing about 120 vs 130 vs 140 is not the same as saying, “Drugs schmugs; a good massage will fix what ails you, and here are some addictive sleeping pills for good measure.” Physicians from the 1930s were a little sketchy. So much of this controversy is about how you define high-risk patients and what are the age cutoffs.

Basically, the cardiovascular guidelines say, “Treat them all and let God sort it out” because they care about cardiovascular events and are concerned about cardiovascular endpoints. Whereas general practice guidelines put more emphasis on potential side effects and admittedly tend to treat a not so high-risk population, so they have laxer targets.

A 2014 analysis from the Blood Pressure Lowering Treatment Trialists’ Collaboration [The Lancet] had a good mathematical way of explaining this problem. Now, lowering blood pressure is obviously a good thing. That prevents heart attacks, strokes, kidney failure, and all that. Please don’t let hypertension denialism become a thing.

Let’s start with the basics. Treating high blood pressure led to a 15% to 18% decrease in cardiovascular events, pretty consistently across all risk categories, and other analyses have found that every 5-point decrease in blood pressure gives you about a 10% decrease in major cardiovascular events on the relative-risk scale. 

While the benefits are pretty consistent across all groups, that difference in baseline risk translates into different absolute benefits. In the Lancet paper, when the population was divided into four different groups based on their cardiovascular risk, the absolute risk reduction in the lowest-risk group was 14 fewer cardiovascular events if you treat 1000 patients for 5 years.

With each higher-risk group, it was 20 fewer, 24 fewer, and 38 fewer. At the lowest-risk group, the number needed to treat was 71, 50, 42, and 26 fewer cardiovascular events with 5 years of treatment. 

And herein lies the secret to the disagreement: If you have a high-risk patient, there is a big benefit to bringing that blood pressure down from 135 to 130. Whereas for a low-risk patient, it probably doesn’t matter as much. And the cardiovascular benefits are going to be offset by the side effects and the risks for hypotension. 

Of course, there’s a simple solution to this dilemma: Just speak to the patient in front of you. Treat high blood pressure, and if your patient’s blood pressure drops or they get dizzy or have fainting spells, then just ease up on the meds. It’s not rocket science; it’s just cardiology. 

Arguing about five millimeters of mercury of blood pressure is probably less important from the public health perspective than the fact that tens of millions of people in the United States are unaware that they have hypertension, and even those diagnosed are being inadequately treated.

So, let’s all do better as a medical community. Nobody should have untreated hypertension in this day and age. It’s not the 1930s. 
 

Dr Labos, Cardiologist, 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. 

Blood pressure. If you’re a primary care provider trying to do right by your patients, you might be understandably confused by the current mishmash of guidelines with different blood pressure targets. But as chaotic as things are, at least it’s not the 1930s, when you might hear John Hay give a lecture to the British Medical Association and say, “The greatest danger to a man with high blood pressure lies in its discovery, because then some fool is certain to try and reduce it.”

Yeah, he said that. But what happened in the 1930s stays in the 1930s. And now we can at least agree that we should be treating high blood pressure. But what’s the goal we should be aiming for? This is On Second Thought. 

We’ve come a long way since FDR was recording blood pressures of 200 and his doctor prescribed him barbiturates and massage therapy.

That s#$# don’t fly no more. Over the past hundred years, we have become much more aggressive in treating blood pressure. Remember the Oslo study? It defined mild hypertension as a blood pressure between 150 and 180 mm Hg. Now, those numbers send people screaming to the emergency room. So, let’s acknowledge that things are substantially better than they once were. Let’s agree on that and we can start to heal this nation again. 

Before we get into the numbers, when we’re treating blood pressure, let’s make a few points about measuring it. Obviously, to treat something, you have to measure it properly. Two recent trials have illustrated that these details matter a lot.

The Cuff(SZ) randomized crossover trial — and it took me a minute to realize that Cuff(SZ) meant cuff size, so bravo, Ishigami et al — showed that picking the wrong cuff size could affect BP measurements by 4.5 points if you were one size off. If you were two sizes too small, you overestimated BP by almost 20 points.

Add on here another recent study, the ARMS crossover randomized clinical trial, looking at how arm position affected BP measures. If the arm was resting on your lap or hanging by your side, that overestimated blood pressure by 4 and 6.5 points. So sometimes you have to remember the fundamentals: cuff size, arm position — it might make the difference between increasing or maintaining the patient’s meds.

But on to the main show. What numbers should we be aiming for? We no longer live in the “BP 200, the president’s going to have a stroke” world of the 1940s, and even a BP of 150 is considered quite high these days. Studies like the MRC trial, INVEST, and SPRINT have pushed BP targets ever lower. SPRINT, in particular, randomized patients to a blood pressure target under 120 systolic vs under 140 systolic, and the under-120 arm won out with fewer cardiovascular events and lower all-cause mortality.

Pretty definitive slam dunk. But the more intensive treatment came with more hypotension, syncope, and kidney injury, because there is no free lunch in medicine. And ditto with BPROAD, just published in The New England Journal of Medicine and presented at the American Heart Association annual meeting. A diabetic population randomized to 120 vs 140 as a BP target showed that more aggressive treatment was better.

Fewer cardiovascular events, like stroke, but no mortality difference, and more hypotension. So a cardiovascular benefit at the cost of more side effects. Now, like all cardiologists, my motto is “Save the heart and screw the kidney.” But if you do care about the other organs in this meat sack that we call a human body, the question you need to wrestle with is, how much do you value cardiovascular protection vs how willing are you to tolerate side effects?

Hypotension may not sound dangerous, but gravity is an unforgiving mistress. If you painstakingly compile the summary of the various BP guidelines for easy perusal, you would notice something critical: One, I have too much free time on my hands; two, the disagreements are not really all that profound.

Arguing about 120 vs 130 vs 140 is not the same as saying, “Drugs schmugs; a good massage will fix what ails you, and here are some addictive sleeping pills for good measure.” Physicians from the 1930s were a little sketchy. So much of this controversy is about how you define high-risk patients and what are the age cutoffs.

Basically, the cardiovascular guidelines say, “Treat them all and let God sort it out” because they care about cardiovascular events and are concerned about cardiovascular endpoints. Whereas general practice guidelines put more emphasis on potential side effects and admittedly tend to treat a not so high-risk population, so they have laxer targets.

A 2014 analysis from the Blood Pressure Lowering Treatment Trialists’ Collaboration [The Lancet] had a good mathematical way of explaining this problem. Now, lowering blood pressure is obviously a good thing. That prevents heart attacks, strokes, kidney failure, and all that. Please don’t let hypertension denialism become a thing.

Let’s start with the basics. Treating high blood pressure led to a 15% to 18% decrease in cardiovascular events, pretty consistently across all risk categories, and other analyses have found that every 5-point decrease in blood pressure gives you about a 10% decrease in major cardiovascular events on the relative-risk scale. 

While the benefits are pretty consistent across all groups, that difference in baseline risk translates into different absolute benefits. In the Lancet paper, when the population was divided into four different groups based on their cardiovascular risk, the absolute risk reduction in the lowest-risk group was 14 fewer cardiovascular events if you treat 1000 patients for 5 years.

With each higher-risk group, it was 20 fewer, 24 fewer, and 38 fewer. At the lowest-risk group, the number needed to treat was 71, 50, 42, and 26 fewer cardiovascular events with 5 years of treatment. 

And herein lies the secret to the disagreement: If you have a high-risk patient, there is a big benefit to bringing that blood pressure down from 135 to 130. Whereas for a low-risk patient, it probably doesn’t matter as much. And the cardiovascular benefits are going to be offset by the side effects and the risks for hypotension. 

Of course, there’s a simple solution to this dilemma: Just speak to the patient in front of you. Treat high blood pressure, and if your patient’s blood pressure drops or they get dizzy or have fainting spells, then just ease up on the meds. It’s not rocket science; it’s just cardiology. 

Arguing about five millimeters of mercury of blood pressure is probably less important from the public health perspective than the fact that tens of millions of people in the United States are unaware that they have hypertension, and even those diagnosed are being inadequately treated.

So, let’s all do better as a medical community. Nobody should have untreated hypertension in this day and age. It’s not the 1930s. 
 

Dr Labos, Cardiologist, 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. 

Blood pressure. If you’re a primary care provider trying to do right by your patients, you might be understandably confused by the current mishmash of guidelines with different blood pressure targets. But as chaotic as things are, at least it’s not the 1930s, when you might hear John Hay give a lecture to the British Medical Association and say, “The greatest danger to a man with high blood pressure lies in its discovery, because then some fool is certain to try and reduce it.”

Yeah, he said that. But what happened in the 1930s stays in the 1930s. And now we can at least agree that we should be treating high blood pressure. But what’s the goal we should be aiming for? This is On Second Thought. 

We’ve come a long way since FDR was recording blood pressures of 200 and his doctor prescribed him barbiturates and massage therapy.

That s#$# don’t fly no more. Over the past hundred years, we have become much more aggressive in treating blood pressure. Remember the Oslo study? It defined mild hypertension as a blood pressure between 150 and 180 mm Hg. Now, those numbers send people screaming to the emergency room. So, let’s acknowledge that things are substantially better than they once were. Let’s agree on that and we can start to heal this nation again. 

Before we get into the numbers, when we’re treating blood pressure, let’s make a few points about measuring it. Obviously, to treat something, you have to measure it properly. Two recent trials have illustrated that these details matter a lot.

The Cuff(SZ) randomized crossover trial — and it took me a minute to realize that Cuff(SZ) meant cuff size, so bravo, Ishigami et al — showed that picking the wrong cuff size could affect BP measurements by 4.5 points if you were one size off. If you were two sizes too small, you overestimated BP by almost 20 points.

Add on here another recent study, the ARMS crossover randomized clinical trial, looking at how arm position affected BP measures. If the arm was resting on your lap or hanging by your side, that overestimated blood pressure by 4 and 6.5 points. So sometimes you have to remember the fundamentals: cuff size, arm position — it might make the difference between increasing or maintaining the patient’s meds.

But on to the main show. What numbers should we be aiming for? We no longer live in the “BP 200, the president’s going to have a stroke” world of the 1940s, and even a BP of 150 is considered quite high these days. Studies like the MRC trial, INVEST, and SPRINT have pushed BP targets ever lower. SPRINT, in particular, randomized patients to a blood pressure target under 120 systolic vs under 140 systolic, and the under-120 arm won out with fewer cardiovascular events and lower all-cause mortality.

Pretty definitive slam dunk. But the more intensive treatment came with more hypotension, syncope, and kidney injury, because there is no free lunch in medicine. And ditto with BPROAD, just published in The New England Journal of Medicine and presented at the American Heart Association annual meeting. A diabetic population randomized to 120 vs 140 as a BP target showed that more aggressive treatment was better.

Fewer cardiovascular events, like stroke, but no mortality difference, and more hypotension. So a cardiovascular benefit at the cost of more side effects. Now, like all cardiologists, my motto is “Save the heart and screw the kidney.” But if you do care about the other organs in this meat sack that we call a human body, the question you need to wrestle with is, how much do you value cardiovascular protection vs how willing are you to tolerate side effects?

Hypotension may not sound dangerous, but gravity is an unforgiving mistress. If you painstakingly compile the summary of the various BP guidelines for easy perusal, you would notice something critical: One, I have too much free time on my hands; two, the disagreements are not really all that profound.

Arguing about 120 vs 130 vs 140 is not the same as saying, “Drugs schmugs; a good massage will fix what ails you, and here are some addictive sleeping pills for good measure.” Physicians from the 1930s were a little sketchy. So much of this controversy is about how you define high-risk patients and what are the age cutoffs.

Basically, the cardiovascular guidelines say, “Treat them all and let God sort it out” because they care about cardiovascular events and are concerned about cardiovascular endpoints. Whereas general practice guidelines put more emphasis on potential side effects and admittedly tend to treat a not so high-risk population, so they have laxer targets.

A 2014 analysis from the Blood Pressure Lowering Treatment Trialists’ Collaboration [The Lancet] had a good mathematical way of explaining this problem. Now, lowering blood pressure is obviously a good thing. That prevents heart attacks, strokes, kidney failure, and all that. Please don’t let hypertension denialism become a thing.

Let’s start with the basics. Treating high blood pressure led to a 15% to 18% decrease in cardiovascular events, pretty consistently across all risk categories, and other analyses have found that every 5-point decrease in blood pressure gives you about a 10% decrease in major cardiovascular events on the relative-risk scale. 

While the benefits are pretty consistent across all groups, that difference in baseline risk translates into different absolute benefits. In the Lancet paper, when the population was divided into four different groups based on their cardiovascular risk, the absolute risk reduction in the lowest-risk group was 14 fewer cardiovascular events if you treat 1000 patients for 5 years.

With each higher-risk group, it was 20 fewer, 24 fewer, and 38 fewer. At the lowest-risk group, the number needed to treat was 71, 50, 42, and 26 fewer cardiovascular events with 5 years of treatment. 

And herein lies the secret to the disagreement: If you have a high-risk patient, there is a big benefit to bringing that blood pressure down from 135 to 130. Whereas for a low-risk patient, it probably doesn’t matter as much. And the cardiovascular benefits are going to be offset by the side effects and the risks for hypotension. 

Of course, there’s a simple solution to this dilemma: Just speak to the patient in front of you. Treat high blood pressure, and if your patient’s blood pressure drops or they get dizzy or have fainting spells, then just ease up on the meds. It’s not rocket science; it’s just cardiology. 

Arguing about five millimeters of mercury of blood pressure is probably less important from the public health perspective than the fact that tens of millions of people in the United States are unaware that they have hypertension, and even those diagnosed are being inadequately treated.

So, let’s all do better as a medical community. Nobody should have untreated hypertension in this day and age. It’s not the 1930s. 
 

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

A version of this article appeared on Medscape.com.

TOPLINE:

Fragmented sleep — that is, increased wakefulness and reduced sleep efficiency — is a sign of metabolic dysfunction–associated steatotic liver disease (MASLD), a study using actigraphy showed.

METHODOLOGY:

• Researchers assessed sleep-wake rhythms in 35 patients with MASLD (median age, 58 years; 66% were men; 80% with metabolic syndrome) and 16 matched healthy controls (median age, 61 years; 50% were men) using data collected 24/7 via actigraphy for 4 weeks.
• Sub-analyses were conducted with MASLD comparator groups: 16 patients with MASH, 8 with MASH with cirrhosis, and 11 with non-MASH–related cirrhosis.
• All participants visited the clinic at baseline, week 2, and week 4 to undergo a clinical investigation and complete questionnaires about their sleep.
• A standardized sleep hygiene education session was conducted at week 2.

TAKEAWAY:

• Actigraphy data from patients with MASLD did not reveal significant differences in bedtime, sleep-onset latency, sleep duration, wake-up time, or time in bed compared with controls.
• However, compared with controls, those with MASLD woke 55% more often at night (8.5 vs 5.5), lay awake 113% longer after having first fallen asleep (45.4 minutes vs 21.3 minutes), and slept more often and longer during the day (decreased sleep efficiency).
• Subgroup analyses showed that actigraphy-measured sleep patterns and quality were similarly impaired in patients with MASH, MASH with cirrhosis, and non–MASH-related cirrhosis.
• Patients with MASLD self-reported their fragmented sleep as shorter sleep with a delayed onset. In sleep diaries, 32% of patients with MASLD reported sleep disturbances caused by psychological stress, compared with only 6.25% of controls and 9% of patients with cirrhosis.
• The sleep education session did not change the actigraphy measures or the sleep parameters assessed with sleep questionnaires at the end of the study.

IN PRACTICE:

“We concluded from our data that sleep fragmentation plays a role in the pathogenesis of human MASLD. Whether MASLD causes sleep disorders or vice versa remains unknown. The underlying mechanism presumably involves genetics, environmental factors, and the activation of immune responses — ultimately driven by obesity and metabolic syndrome,” said corresponding author.

SOURCE:

The study, led by Sofia Schaeffer, PhD, University of Basel, Switzerland, was published online in Frontiers in Network Physiology.

LIMITATIONS:

The study had several limitations. There was a significant difference in body mass index between patients with MASLD (median, 31) and controls (median, 23.5), representing a potential confounder that could explain the differences in sleep behavior. Undetected obstructive sleep apnea could also be a confounding factor. The small number of participants limited the interpretation and generalization of the data, especially in the MASLD subgroups.

DISCLOSURES:

This study was supported by a grant from the University of Basel. One coauthor received a research grant from the University Center for Gastrointestinal and Liver Diseases, Basel, Switzerland. Another coauthor was employed by NovoLytiX. Schaeffer and the remaining coauthors declared that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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

TOPLINE:

Fragmented sleep — that is, increased wakefulness and reduced sleep efficiency — is a sign of metabolic dysfunction–associated steatotic liver disease (MASLD), a study using actigraphy showed.

METHODOLOGY:

• Researchers assessed sleep-wake rhythms in 35 patients with MASLD (median age, 58 years; 66% were men; 80% with metabolic syndrome) and 16 matched healthy controls (median age, 61 years; 50% were men) using data collected 24/7 via actigraphy for 4 weeks.
• Sub-analyses were conducted with MASLD comparator groups: 16 patients with MASH, 8 with MASH with cirrhosis, and 11 with non-MASH–related cirrhosis.
• All participants visited the clinic at baseline, week 2, and week 4 to undergo a clinical investigation and complete questionnaires about their sleep.
• A standardized sleep hygiene education session was conducted at week 2.

TAKEAWAY:

• Actigraphy data from patients with MASLD did not reveal significant differences in bedtime, sleep-onset latency, sleep duration, wake-up time, or time in bed compared with controls.
• However, compared with controls, those with MASLD woke 55% more often at night (8.5 vs 5.5), lay awake 113% longer after having first fallen asleep (45.4 minutes vs 21.3 minutes), and slept more often and longer during the day (decreased sleep efficiency).
• Subgroup analyses showed that actigraphy-measured sleep patterns and quality were similarly impaired in patients with MASH, MASH with cirrhosis, and non–MASH-related cirrhosis.
• Patients with MASLD self-reported their fragmented sleep as shorter sleep with a delayed onset. In sleep diaries, 32% of patients with MASLD reported sleep disturbances caused by psychological stress, compared with only 6.25% of controls and 9% of patients with cirrhosis.
• The sleep education session did not change the actigraphy measures or the sleep parameters assessed with sleep questionnaires at the end of the study.

IN PRACTICE:

“We concluded from our data that sleep fragmentation plays a role in the pathogenesis of human MASLD. Whether MASLD causes sleep disorders or vice versa remains unknown. The underlying mechanism presumably involves genetics, environmental factors, and the activation of immune responses — ultimately driven by obesity and metabolic syndrome,” said corresponding author.

SOURCE:

The study, led by Sofia Schaeffer, PhD, University of Basel, Switzerland, was published online in Frontiers in Network Physiology.

LIMITATIONS:

The study had several limitations. There was a significant difference in body mass index between patients with MASLD (median, 31) and controls (median, 23.5), representing a potential confounder that could explain the differences in sleep behavior. Undetected obstructive sleep apnea could also be a confounding factor. The small number of participants limited the interpretation and generalization of the data, especially in the MASLD subgroups.

DISCLOSURES:

This study was supported by a grant from the University of Basel. One coauthor received a research grant from the University Center for Gastrointestinal and Liver Diseases, Basel, Switzerland. Another coauthor was employed by NovoLytiX. Schaeffer and the remaining coauthors declared that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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

TOPLINE:

Fragmented sleep — that is, increased wakefulness and reduced sleep efficiency — is a sign of metabolic dysfunction–associated steatotic liver disease (MASLD), a study using actigraphy showed.

METHODOLOGY:

• Researchers assessed sleep-wake rhythms in 35 patients with MASLD (median age, 58 years; 66% were men; 80% with metabolic syndrome) and 16 matched healthy controls (median age, 61 years; 50% were men) using data collected 24/7 via actigraphy for 4 weeks.
• Sub-analyses were conducted with MASLD comparator groups: 16 patients with MASH, 8 with MASH with cirrhosis, and 11 with non-MASH–related cirrhosis.
• All participants visited the clinic at baseline, week 2, and week 4 to undergo a clinical investigation and complete questionnaires about their sleep.
• A standardized sleep hygiene education session was conducted at week 2.

TAKEAWAY:

• Actigraphy data from patients with MASLD did not reveal significant differences in bedtime, sleep-onset latency, sleep duration, wake-up time, or time in bed compared with controls.
• However, compared with controls, those with MASLD woke 55% more often at night (8.5 vs 5.5), lay awake 113% longer after having first fallen asleep (45.4 minutes vs 21.3 minutes), and slept more often and longer during the day (decreased sleep efficiency).
• Subgroup analyses showed that actigraphy-measured sleep patterns and quality were similarly impaired in patients with MASH, MASH with cirrhosis, and non–MASH-related cirrhosis.
• Patients with MASLD self-reported their fragmented sleep as shorter sleep with a delayed onset. In sleep diaries, 32% of patients with MASLD reported sleep disturbances caused by psychological stress, compared with only 6.25% of controls and 9% of patients with cirrhosis.
• The sleep education session did not change the actigraphy measures or the sleep parameters assessed with sleep questionnaires at the end of the study.

IN PRACTICE:

“We concluded from our data that sleep fragmentation plays a role in the pathogenesis of human MASLD. Whether MASLD causes sleep disorders or vice versa remains unknown. The underlying mechanism presumably involves genetics, environmental factors, and the activation of immune responses — ultimately driven by obesity and metabolic syndrome,” said corresponding author.

SOURCE:

The study, led by Sofia Schaeffer, PhD, University of Basel, Switzerland, was published online in Frontiers in Network Physiology.

LIMITATIONS:

The study had several limitations. There was a significant difference in body mass index between patients with MASLD (median, 31) and controls (median, 23.5), representing a potential confounder that could explain the differences in sleep behavior. Undetected obstructive sleep apnea could also be a confounding factor. The small number of participants limited the interpretation and generalization of the data, especially in the MASLD subgroups.

DISCLOSURES:

This study was supported by a grant from the University of Basel. One coauthor received a research grant from the University Center for Gastrointestinal and Liver Diseases, Basel, Switzerland. Another coauthor was employed by NovoLytiX. Schaeffer and the remaining coauthors declared that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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

Forty-five circulating proteins in plasma are linked to the risk for myocardial infarction (MI), showed a new study that confirms some known associations and identifies new ones. Several proteins are associated with MI in women but not men, and some proteins linked with MI in both men and women are more strongly associated with MI in women.

“We hope that our study will shed light on pathways in MI,” said principal author Olga Titova, PhD, an epidemiologist at Uppsala University in Uppsala, Sweden. The work was published in the European Heart Journal.

Martha Gulati, MD, a cardiologist and associate director of the Barbra Streisand Women’s Heart Center at Cedars-Sinai Medical Center in Los Angeles and coauthor of an accompanying editorial, said the novel discovery of different patterns between men and women makes this an exciting study. The findings “highlight that sex differences in disease phenotype begin at the molecular level,” she said.

Titova and her team analyzed thousands of patients in two databases — one in Sweden (11,751 patients), the other in the United Kingdom (51,613 patients) — to discover proteins in the patients who went on to have an MI. Using one database to discover biomarkers and a second to replicate the findings is a common approach, said Titova.

Casting a Wide Net to Catch Proteins

The two databases “make findings more generalizable, allow us to confirm robust associations, and help minimize the risk of false positives.” The two databases mean researchers are more confident that the findings can be applied across populations, Titova added.

A total of 44 proteins were associated with later MI in both databases, adjusted for common MI risk factors as well as such factors as education, diet, physical activity, and alcohol intake, Titova explained. An additional protein was included from the first database that was unavailable in the second. Some of the proteins have been found in other studies, and this study confirms the link. Others were new, and a few appear to protect patients from MI.

“Most of the proteins are related to or involved in inflammation and atherosclerosis,” said Titova.

This is the first study to cast such a wide net, Titova pointed out. While several proteins have previously been linked to MI, most earlier studies have focused on specific proteins in populations that already have coronary artery disease or have involved cohorts of men only.

But she stresses that this study poses more questions than it answers. More research is needed to determine how proteins are involved in pathways leading to MI. The study found that some proteins may be mediators of general cardiovascular disease risk, whereas others are involved in mechanisms specifically linked to MI. Many proteins are involved in atherosclerosis, thrombosis, inflammation, immune system–related pathways, injury and tissue repair, coagulation, bone homeostasis, and iron metabolism.

“At this point, some [proteins] appear to be causal, some seem to be an association,” said Titova. It remains to be determined “which are on the causal path, which are potential biomarkers, which are going to shed light on the mechanisms” of MI.

The study took a step toward determining which proteins might be involved in causing MI through an analysis of some protein levels determined by genetics. This found three proteins linked to a higher risk for MI and three linked to a lower risk.

It’s Different for Women

Thirteen of the proteins were linked with later MI in women, either exclusively or more strongly than in men. Many of these associations were replicated in the second database, showing an alignment across populations.

Titova said the reason for the sex difference remains a mystery. “We have to go to the molecular level. It could be a consequence of risk factors affecting the sexes differently or different biology” between men and women.

Gulati, who specializes in women’s heart health, explained, “We know inflammation is much more prevalent in women and is the pathway to cardiovascular disease.” She points out that noncardiac inflammatory diseases are also more prevalent in women. Other biomarkers for inflammation, such as C-reactive protein, are higher in women than in men. She thinks the underlying mechanisms could involve “how we [women] make our proteins and how we respond to hormones.”

By identifying proteins linked to MI in women, the study helps to fill an important gap in our knowledge. “I can’t tell you how many papers don’t even look at sex differences. If we don’t look, we won’t know there are differences,” Gulati said. “In much of our cardiac research, women are underrepresented.”

The findings of this trial and others like it may lead to new approaches to prevention and treatment, Titova and Gulati agreed. Several proteins found in this study that may have a causal link with MI are already targets of drug development, they added.

Titova said other proteins may be useful in the future as biomarkers that indicate a need for preventive action.

Gulati asked, “If we can show some of the proteins are involved in the inflammatory response — if they are causal and we can prevent them upfront — can we reduce the chance of MI?” She and Titova said the many questions remaining should prove a rewarding avenue for research.

A version of this article appeared on Medscape.com.

Forty-five circulating proteins in plasma are linked to the risk for myocardial infarction (MI), showed a new study that confirms some known associations and identifies new ones. Several proteins are associated with MI in women but not men, and some proteins linked with MI in both men and women are more strongly associated with MI in women.

“We hope that our study will shed light on pathways in MI,” said principal author Olga Titova, PhD, an epidemiologist at Uppsala University in Uppsala, Sweden. The work was published in the European Heart Journal.

Martha Gulati, MD, a cardiologist and associate director of the Barbra Streisand Women’s Heart Center at Cedars-Sinai Medical Center in Los Angeles and coauthor of an accompanying editorial, said the novel discovery of different patterns between men and women makes this an exciting study. The findings “highlight that sex differences in disease phenotype begin at the molecular level,” she said.

Titova and her team analyzed thousands of patients in two databases — one in Sweden (11,751 patients), the other in the United Kingdom (51,613 patients) — to discover proteins in the patients who went on to have an MI. Using one database to discover biomarkers and a second to replicate the findings is a common approach, said Titova.

Casting a Wide Net to Catch Proteins

The two databases “make findings more generalizable, allow us to confirm robust associations, and help minimize the risk of false positives.” The two databases mean researchers are more confident that the findings can be applied across populations, Titova added.

A total of 44 proteins were associated with later MI in both databases, adjusted for common MI risk factors as well as such factors as education, diet, physical activity, and alcohol intake, Titova explained. An additional protein was included from the first database that was unavailable in the second. Some of the proteins have been found in other studies, and this study confirms the link. Others were new, and a few appear to protect patients from MI.

“Most of the proteins are related to or involved in inflammation and atherosclerosis,” said Titova.

This is the first study to cast such a wide net, Titova pointed out. While several proteins have previously been linked to MI, most earlier studies have focused on specific proteins in populations that already have coronary artery disease or have involved cohorts of men only.

But she stresses that this study poses more questions than it answers. More research is needed to determine how proteins are involved in pathways leading to MI. The study found that some proteins may be mediators of general cardiovascular disease risk, whereas others are involved in mechanisms specifically linked to MI. Many proteins are involved in atherosclerosis, thrombosis, inflammation, immune system–related pathways, injury and tissue repair, coagulation, bone homeostasis, and iron metabolism.

“At this point, some [proteins] appear to be causal, some seem to be an association,” said Titova. It remains to be determined “which are on the causal path, which are potential biomarkers, which are going to shed light on the mechanisms” of MI.

The study took a step toward determining which proteins might be involved in causing MI through an analysis of some protein levels determined by genetics. This found three proteins linked to a higher risk for MI and three linked to a lower risk.

It’s Different for Women

Thirteen of the proteins were linked with later MI in women, either exclusively or more strongly than in men. Many of these associations were replicated in the second database, showing an alignment across populations.

Titova said the reason for the sex difference remains a mystery. “We have to go to the molecular level. It could be a consequence of risk factors affecting the sexes differently or different biology” between men and women.

Gulati, who specializes in women’s heart health, explained, “We know inflammation is much more prevalent in women and is the pathway to cardiovascular disease.” She points out that noncardiac inflammatory diseases are also more prevalent in women. Other biomarkers for inflammation, such as C-reactive protein, are higher in women than in men. She thinks the underlying mechanisms could involve “how we [women] make our proteins and how we respond to hormones.”

By identifying proteins linked to MI in women, the study helps to fill an important gap in our knowledge. “I can’t tell you how many papers don’t even look at sex differences. If we don’t look, we won’t know there are differences,” Gulati said. “In much of our cardiac research, women are underrepresented.”

The findings of this trial and others like it may lead to new approaches to prevention and treatment, Titova and Gulati agreed. Several proteins found in this study that may have a causal link with MI are already targets of drug development, they added.

Titova said other proteins may be useful in the future as biomarkers that indicate a need for preventive action.

Gulati asked, “If we can show some of the proteins are involved in the inflammatory response — if they are causal and we can prevent them upfront — can we reduce the chance of MI?” She and Titova said the many questions remaining should prove a rewarding avenue for research.

A version of this article appeared on Medscape.com.

Forty-five circulating proteins in plasma are linked to the risk for myocardial infarction (MI), showed a new study that confirms some known associations and identifies new ones. Several proteins are associated with MI in women but not men, and some proteins linked with MI in both men and women are more strongly associated with MI in women.

“We hope that our study will shed light on pathways in MI,” said principal author Olga Titova, PhD, an epidemiologist at Uppsala University in Uppsala, Sweden. The work was published in the European Heart Journal.

Martha Gulati, MD, a cardiologist and associate director of the Barbra Streisand Women’s Heart Center at Cedars-Sinai Medical Center in Los Angeles and coauthor of an accompanying editorial, said the novel discovery of different patterns between men and women makes this an exciting study. The findings “highlight that sex differences in disease phenotype begin at the molecular level,” she said.

Titova and her team analyzed thousands of patients in two databases — one in Sweden (11,751 patients), the other in the United Kingdom (51,613 patients) — to discover proteins in the patients who went on to have an MI. Using one database to discover biomarkers and a second to replicate the findings is a common approach, said Titova.

Casting a Wide Net to Catch Proteins

The two databases “make findings more generalizable, allow us to confirm robust associations, and help minimize the risk of false positives.” The two databases mean researchers are more confident that the findings can be applied across populations, Titova added.

A total of 44 proteins were associated with later MI in both databases, adjusted for common MI risk factors as well as such factors as education, diet, physical activity, and alcohol intake, Titova explained. An additional protein was included from the first database that was unavailable in the second. Some of the proteins have been found in other studies, and this study confirms the link. Others were new, and a few appear to protect patients from MI.

“Most of the proteins are related to or involved in inflammation and atherosclerosis,” said Titova.

This is the first study to cast such a wide net, Titova pointed out. While several proteins have previously been linked to MI, most earlier studies have focused on specific proteins in populations that already have coronary artery disease or have involved cohorts of men only.

But she stresses that this study poses more questions than it answers. More research is needed to determine how proteins are involved in pathways leading to MI. The study found that some proteins may be mediators of general cardiovascular disease risk, whereas others are involved in mechanisms specifically linked to MI. Many proteins are involved in atherosclerosis, thrombosis, inflammation, immune system–related pathways, injury and tissue repair, coagulation, bone homeostasis, and iron metabolism.

“At this point, some [proteins] appear to be causal, some seem to be an association,” said Titova. It remains to be determined “which are on the causal path, which are potential biomarkers, which are going to shed light on the mechanisms” of MI.

The study took a step toward determining which proteins might be involved in causing MI through an analysis of some protein levels determined by genetics. This found three proteins linked to a higher risk for MI and three linked to a lower risk.

It’s Different for Women

Thirteen of the proteins were linked with later MI in women, either exclusively or more strongly than in men. Many of these associations were replicated in the second database, showing an alignment across populations.

Titova said the reason for the sex difference remains a mystery. “We have to go to the molecular level. It could be a consequence of risk factors affecting the sexes differently or different biology” between men and women.

Gulati, who specializes in women’s heart health, explained, “We know inflammation is much more prevalent in women and is the pathway to cardiovascular disease.” She points out that noncardiac inflammatory diseases are also more prevalent in women. Other biomarkers for inflammation, such as C-reactive protein, are higher in women than in men. She thinks the underlying mechanisms could involve “how we [women] make our proteins and how we respond to hormones.”

By identifying proteins linked to MI in women, the study helps to fill an important gap in our knowledge. “I can’t tell you how many papers don’t even look at sex differences. If we don’t look, we won’t know there are differences,” Gulati said. “In much of our cardiac research, women are underrepresented.”

The findings of this trial and others like it may lead to new approaches to prevention and treatment, Titova and Gulati agreed. Several proteins found in this study that may have a causal link with MI are already targets of drug development, they added.

Titova said other proteins may be useful in the future as biomarkers that indicate a need for preventive action.

Gulati asked, “If we can show some of the proteins are involved in the inflammatory response — if they are causal and we can prevent them upfront — can we reduce the chance of MI?” She and Titova said the many questions remaining should prove a rewarding avenue for research.

A version of this article appeared on Medscape.com.

An individual’s estimated risk of having a heart attack or stroke in the next 10 years is widely used to guide preventative medication prescriptions with statins or antihypertensive drugs in those who have not yet had such an event.

To estimate that risk, doctors use equations that include different risk factors, such as age, cholesterol levels, and blood pressure. The current equations, known as the pooled cohort equations, are considered to be outdated as they were developed in 2013 based on population data from the 1960s and 70s. A new set of risk equations — known as the PREVENT equations — were developed by the American Heart Association (AHA) in 2023, and are based on a more contemporary population. It is anticipated that AHA will recommend these new risk equations be used in clinical practice in the next primary prevention guidelines.

But could these new risk equations do more harm than good?

Two recent studies found that applying the PREVENT risk equations to the US population results in a much lower overall level of risk compared with the pooled cohort equations. And, if the current threshold for starting statin treatment — which is an estimated 7.5% risk of having a heart attack or stroke in the next 10 years — is kept the same, this would result in many fewer patients being eligible for statin treatment.

As cardiovascular risk is also used to guide antihypertensive treatment, the new risk equations would also result in fewer people with borderline high blood pressure being eligible for those medications.

This has raised concerns in the medical community, where there is a widespread view that many more people would benefit from primary prevention treatment, and that anything that may cause fewer people to receive these medications would be harmful. 

“I believe the new equations more accurately predict the risk of the current US population, but we need to be aware of what effect that may have on use of statins,” said Tim Anderson, MD, who studies healthcare delivery at the University of Pittsburgh in Pennsylvania and is lead author of one of the studies evaluating the equations.

Anderson told this news organization that the pooled cohort equations have long been viewed as problematic. 

“Because these equations were based on cohorts from the 1960s and 70s, it is believed they overestimate the current population’s risk of MI and stroke as the burden of disease has shifted in the intervening 50-60 years,” he said.

 

Current Equations Overestimate Risk

The new equations are based on more recent, representative, and diverse cohorts that capture a wider spectrum of the population in terms of race, ethnicity, and socioeconomic status. They also include factors that are now known to be relevant to cardiovascular risk, such as chronic kidney disease.

Anderson compared how the two sets of equations estimated risk of cardiovascular disease in the next 10 years in the US population using the NHANES survey — a large nationally representative survey conducted between 2017 and 2020. 

He found that the pooled cohort equations estimated the population average 10-year risk of cardiovascular disease to be about 8%, but the PREVENT equations estimated it at just over 4%.

“The new equations estimate that the middle-aged US population have almost half the level of risk of MI and stroke over next 10 years compared with the equations used currently. So, we will substantially change risk estimates if the new equations are introduced into practice,” Anderson said. 

The study found that, if the PREVENT equations are adopted in the next set of primary prevention guidelines and the current threshold of a 7.5% risk of having an MI or stroke in the next 10 years is maintained as the starting point for statin treatment, then 17.3 million adults who were previously recommended primary prevention statin therapy would no longer be eligible.

A second, similar study, conducted by a different team of US researchers, estimated that using PREVENT would decrease the number of US adults receiving or recommended for statin therapy by 14.3 million and antihypertensive therapy by 2.62 million.

The researchers, led by James A. Diao, MD, from Harvard Medical School, Boston, Massachusetts, also suggested that over 10 years, reductions in treatment eligibility could result in an estimated 107,000 additional MI or stroke events.

Anderson points out that using the new equations would not affect the highest-risk patients. “They are still going to be high risk whichever equations are used. If you smoke a pack of cigarettes a day, have very high blood pressure or cholesterol and are older, then you are high risk. That part hasn’t changed. These people will qualify for statin treatment many times over with both sets of guidelines,” he said. 

Rather it will be the large population at moderate risk of cardiovascular disease that will be affected, with far fewer of these individuals likely to get statins.

“If you are on the fence about whether to take a statin or not and you’re currently just on the threshold where they might be recommended then these new equations could mean that you’ll be less likely to be offered them,” he said. “Using the new equations may result in a delay of a couple of years to have that conversation.”

 

A Red Flag

Steve Nissen, MD, a cardiologist at the Cleveland Clinic in Ohio, is not a fan of cardiovascular risk equations in general. He points out that less than half of those currently eligible for statins are actually treated. And he believes the studies suggesting fewer people will be eligible with the new risk equations raise a red flag on whether they should be used.

“Anything that may result in fewer people being treated is a huge problem,” he told this news organization. “We have abundant evidence that we should be treating more people, not fewer people. Every study we have done has shown benefit with statins.”

The risk calculators were initially developed to limit use of statins and other medications to high-risk patients, he said, but now that we know more about safety of these drugs, it’s clear that the risks are almost nonexistent. 

“We really need something else to guide the prescription of statins,” said Nissen.

Nissen suggests the risk calculators and guidelines have resulted in undertreatment of the population because they lack nuance and put too much emphasis on age. We should be more interested in reducing the lifetime risk of cardiovascular events, he said. “Calculators don’t do a good job of that. Their time horizons are too short. Young people with a family history of cardiovascular disease may have a low 10-year risk on a risk calculator but their lifetime risk is elevated, and as such, they should be considered for statin treatment. We need to find a more nuanced approach to understanding the lifetime risk of individuals,” he said. 

Nissen said risk calculators can be useful in high-risk patients to help demonstrate their need for treatment. “I can show them the calculator and that they have a 20% chance of an event — that can help convince them to take a statin.” 

But at the lower end of the risk scale, “all it does is keep patients who should be getting treatment from having that treatment.”

Nissen said changing the risk calculator won’t affect how he treats patients. “I use judgment to decide who to treat based on scientific literature and the patient in front of me. We will engage in a discussion and make a shared decision on what is the best course of action. Calculators will never be a substitute for medical judgment,” he said.

 

Equations Don’t Decide

Sadiya Khan, MD, a cardiologist at Northwestern University, Evanston, Illinois, and lead author of the PREVENT equations, told this news organization that it is important to put this discussion into context.

“The two recent papers do a good job of describing differences in predictive risk between the two sets of equations but that’s where they stop,” she said. “The translation from that to the decision on who should or should not be on statins or other medications is a step too far.”

Clinical guidelines will need to be updated to take the PREVENT equations into account, as Khan argued in a JAMA editorial. So it is not clear whether the current 7.5% 10-year risk figure will remain the threshold to start treatment. Khan anticipates the guidelines committee will have to re-evaluate that threshold.

“The 7.5% risk threshold was advised in the 2013 guidelines, based on what we knew then about the balance between benefit and harm and with the knowledge that the risk equations overestimated risk,” she said. “We now have a lot more data on the safety of statin therapy. We see this frequently in preventive care. Treatments often becomes more widespread in time and use expands into lower-risk patients.”

She also pointed out that the current primary prevention guidelines encourage consideration of other factors, not just predictive risk scores, when thinking about starting statins, including very high LDL cholesterol, family history, and apo B and Lp(a) levels.

“The recommendation on who would qualify for statin therapy is not based on one number,” she said. “It is based on many considerations, including both qualitative and quantitative factors, and discussions between the patient and the doctor. It is not a straightforward yes or no based on a 7.5% risk threshold.”

The equations, she said, should only be viewed as the first step in the process, and she said she agrees with Nissen that when applying the equations, doctors need to use additional data from each individual patient to make a judgment. “Equations do not decide who gets treated. Clinical practice guidelines do that.” 

Khan also agreed with Nissen that more effort is needed to identify longer term cardiovascular risk in younger people, and so the PREVENT equations include 30-year risk estimates.

“I totally agree that we need to start earlier in having these prevention conversations. The PREVENT model starts at age 30 which is 10 years earlier than the pooled cohort equations and they add a 30-year time horizon as well as the 10-year period for these discussions on predicted risk estimates,” she said. “We need to make sure we are not missing risk in young adults just because we are waiting for them to get into some arbitrary age category.”

Khan says she believes that, used correctly, the new equations will not limit access to statins or other cardiovascular treatments. “Because they are a more accurate reflection of risk in the contemporary population, the new PREVENT equations should identify the correct patients to be treated, within the confines of knowing that no risk prediction equation is perfect,” she said. “And if everything else is considered as well, not just the numbers in the risk equations, it shouldn’t result in fewer patients being treated.”

Anderson reported receiving grants from the American Heart Association, the American College of Cardiology, and the US Deprescribing Research Network. Nissen is leading a development program for a nonprescription low dose of rosuvastatin. He is also involved in trials of a new cholesterol lowering drug, obicetrapib, and on trials on drugs that lower Lp(a). Khan reported receiving grants from the American Heart Association and National Heart, Lung, and Blood Institute.

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

An individual’s estimated risk of having a heart attack or stroke in the next 10 years is widely used to guide preventative medication prescriptions with statins or antihypertensive drugs in those who have not yet had such an event.

To estimate that risk, doctors use equations that include different risk factors, such as age, cholesterol levels, and blood pressure. The current equations, known as the pooled cohort equations, are considered to be outdated as they were developed in 2013 based on population data from the 1960s and 70s. A new set of risk equations — known as the PREVENT equations — were developed by the American Heart Association (AHA) in 2023, and are based on a more contemporary population. It is anticipated that AHA will recommend these new risk equations be used in clinical practice in the next primary prevention guidelines.

But could these new risk equations do more harm than good?

Two recent studies found that applying the PREVENT risk equations to the US population results in a much lower overall level of risk compared with the pooled cohort equations. And, if the current threshold for starting statin treatment — which is an estimated 7.5% risk of having a heart attack or stroke in the next 10 years — is kept the same, this would result in many fewer patients being eligible for statin treatment.

As cardiovascular risk is also used to guide antihypertensive treatment, the new risk equations would also result in fewer people with borderline high blood pressure being eligible for those medications.

This has raised concerns in the medical community, where there is a widespread view that many more people would benefit from primary prevention treatment, and that anything that may cause fewer people to receive these medications would be harmful. 

“I believe the new equations more accurately predict the risk of the current US population, but we need to be aware of what effect that may have on use of statins,” said Tim Anderson, MD, who studies healthcare delivery at the University of Pittsburgh in Pennsylvania and is lead author of one of the studies evaluating the equations.

Anderson told this news organization that the pooled cohort equations have long been viewed as problematic. 

“Because these equations were based on cohorts from the 1960s and 70s, it is believed they overestimate the current population’s risk of MI and stroke as the burden of disease has shifted in the intervening 50-60 years,” he said.

 

Current Equations Overestimate Risk

The new equations are based on more recent, representative, and diverse cohorts that capture a wider spectrum of the population in terms of race, ethnicity, and socioeconomic status. They also include factors that are now known to be relevant to cardiovascular risk, such as chronic kidney disease.

Anderson compared how the two sets of equations estimated risk of cardiovascular disease in the next 10 years in the US population using the NHANES survey — a large nationally representative survey conducted between 2017 and 2020. 

He found that the pooled cohort equations estimated the population average 10-year risk of cardiovascular disease to be about 8%, but the PREVENT equations estimated it at just over 4%.

“The new equations estimate that the middle-aged US population have almost half the level of risk of MI and stroke over next 10 years compared with the equations used currently. So, we will substantially change risk estimates if the new equations are introduced into practice,” Anderson said. 

The study found that, if the PREVENT equations are adopted in the next set of primary prevention guidelines and the current threshold of a 7.5% risk of having an MI or stroke in the next 10 years is maintained as the starting point for statin treatment, then 17.3 million adults who were previously recommended primary prevention statin therapy would no longer be eligible.

A second, similar study, conducted by a different team of US researchers, estimated that using PREVENT would decrease the number of US adults receiving or recommended for statin therapy by 14.3 million and antihypertensive therapy by 2.62 million.

The researchers, led by James A. Diao, MD, from Harvard Medical School, Boston, Massachusetts, also suggested that over 10 years, reductions in treatment eligibility could result in an estimated 107,000 additional MI or stroke events.

Anderson points out that using the new equations would not affect the highest-risk patients. “They are still going to be high risk whichever equations are used. If you smoke a pack of cigarettes a day, have very high blood pressure or cholesterol and are older, then you are high risk. That part hasn’t changed. These people will qualify for statin treatment many times over with both sets of guidelines,” he said. 

Rather it will be the large population at moderate risk of cardiovascular disease that will be affected, with far fewer of these individuals likely to get statins.

“If you are on the fence about whether to take a statin or not and you’re currently just on the threshold where they might be recommended then these new equations could mean that you’ll be less likely to be offered them,” he said. “Using the new equations may result in a delay of a couple of years to have that conversation.”

 

A Red Flag

Steve Nissen, MD, a cardiologist at the Cleveland Clinic in Ohio, is not a fan of cardiovascular risk equations in general. He points out that less than half of those currently eligible for statins are actually treated. And he believes the studies suggesting fewer people will be eligible with the new risk equations raise a red flag on whether they should be used.

“Anything that may result in fewer people being treated is a huge problem,” he told this news organization. “We have abundant evidence that we should be treating more people, not fewer people. Every study we have done has shown benefit with statins.”

The risk calculators were initially developed to limit use of statins and other medications to high-risk patients, he said, but now that we know more about safety of these drugs, it’s clear that the risks are almost nonexistent. 

“We really need something else to guide the prescription of statins,” said Nissen.

Nissen suggests the risk calculators and guidelines have resulted in undertreatment of the population because they lack nuance and put too much emphasis on age. We should be more interested in reducing the lifetime risk of cardiovascular events, he said. “Calculators don’t do a good job of that. Their time horizons are too short. Young people with a family history of cardiovascular disease may have a low 10-year risk on a risk calculator but their lifetime risk is elevated, and as such, they should be considered for statin treatment. We need to find a more nuanced approach to understanding the lifetime risk of individuals,” he said. 

Nissen said risk calculators can be useful in high-risk patients to help demonstrate their need for treatment. “I can show them the calculator and that they have a 20% chance of an event — that can help convince them to take a statin.” 

But at the lower end of the risk scale, “all it does is keep patients who should be getting treatment from having that treatment.”

Nissen said changing the risk calculator won’t affect how he treats patients. “I use judgment to decide who to treat based on scientific literature and the patient in front of me. We will engage in a discussion and make a shared decision on what is the best course of action. Calculators will never be a substitute for medical judgment,” he said.

 

Equations Don’t Decide

Sadiya Khan, MD, a cardiologist at Northwestern University, Evanston, Illinois, and lead author of the PREVENT equations, told this news organization that it is important to put this discussion into context.

“The two recent papers do a good job of describing differences in predictive risk between the two sets of equations but that’s where they stop,” she said. “The translation from that to the decision on who should or should not be on statins or other medications is a step too far.”

Clinical guidelines will need to be updated to take the PREVENT equations into account, as Khan argued in a JAMA editorial. So it is not clear whether the current 7.5% 10-year risk figure will remain the threshold to start treatment. Khan anticipates the guidelines committee will have to re-evaluate that threshold.

“The 7.5% risk threshold was advised in the 2013 guidelines, based on what we knew then about the balance between benefit and harm and with the knowledge that the risk equations overestimated risk,” she said. “We now have a lot more data on the safety of statin therapy. We see this frequently in preventive care. Treatments often becomes more widespread in time and use expands into lower-risk patients.”

She also pointed out that the current primary prevention guidelines encourage consideration of other factors, not just predictive risk scores, when thinking about starting statins, including very high LDL cholesterol, family history, and apo B and Lp(a) levels.

“The recommendation on who would qualify for statin therapy is not based on one number,” she said. “It is based on many considerations, including both qualitative and quantitative factors, and discussions between the patient and the doctor. It is not a straightforward yes or no based on a 7.5% risk threshold.”

The equations, she said, should only be viewed as the first step in the process, and she said she agrees with Nissen that when applying the equations, doctors need to use additional data from each individual patient to make a judgment. “Equations do not decide who gets treated. Clinical practice guidelines do that.” 

Khan also agreed with Nissen that more effort is needed to identify longer term cardiovascular risk in younger people, and so the PREVENT equations include 30-year risk estimates.

“I totally agree that we need to start earlier in having these prevention conversations. The PREVENT model starts at age 30 which is 10 years earlier than the pooled cohort equations and they add a 30-year time horizon as well as the 10-year period for these discussions on predicted risk estimates,” she said. “We need to make sure we are not missing risk in young adults just because we are waiting for them to get into some arbitrary age category.”

Khan says she believes that, used correctly, the new equations will not limit access to statins or other cardiovascular treatments. “Because they are a more accurate reflection of risk in the contemporary population, the new PREVENT equations should identify the correct patients to be treated, within the confines of knowing that no risk prediction equation is perfect,” she said. “And if everything else is considered as well, not just the numbers in the risk equations, it shouldn’t result in fewer patients being treated.”

Anderson reported receiving grants from the American Heart Association, the American College of Cardiology, and the US Deprescribing Research Network. Nissen is leading a development program for a nonprescription low dose of rosuvastatin. He is also involved in trials of a new cholesterol lowering drug, obicetrapib, and on trials on drugs that lower Lp(a). Khan reported receiving grants from the American Heart Association and National Heart, Lung, and Blood Institute.

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

An individual’s estimated risk of having a heart attack or stroke in the next 10 years is widely used to guide preventative medication prescriptions with statins or antihypertensive drugs in those who have not yet had such an event.

To estimate that risk, doctors use equations that include different risk factors, such as age, cholesterol levels, and blood pressure. The current equations, known as the pooled cohort equations, are considered to be outdated as they were developed in 2013 based on population data from the 1960s and 70s. A new set of risk equations — known as the PREVENT equations — were developed by the American Heart Association (AHA) in 2023, and are based on a more contemporary population. It is anticipated that AHA will recommend these new risk equations be used in clinical practice in the next primary prevention guidelines.

But could these new risk equations do more harm than good?

Two recent studies found that applying the PREVENT risk equations to the US population results in a much lower overall level of risk compared with the pooled cohort equations. And, if the current threshold for starting statin treatment — which is an estimated 7.5% risk of having a heart attack or stroke in the next 10 years — is kept the same, this would result in many fewer patients being eligible for statin treatment.

As cardiovascular risk is also used to guide antihypertensive treatment, the new risk equations would also result in fewer people with borderline high blood pressure being eligible for those medications.

This has raised concerns in the medical community, where there is a widespread view that many more people would benefit from primary prevention treatment, and that anything that may cause fewer people to receive these medications would be harmful. 

“I believe the new equations more accurately predict the risk of the current US population, but we need to be aware of what effect that may have on use of statins,” said Tim Anderson, MD, who studies healthcare delivery at the University of Pittsburgh in Pennsylvania and is lead author of one of the studies evaluating the equations.

Anderson told this news organization that the pooled cohort equations have long been viewed as problematic. 

“Because these equations were based on cohorts from the 1960s and 70s, it is believed they overestimate the current population’s risk of MI and stroke as the burden of disease has shifted in the intervening 50-60 years,” he said.

 

Current Equations Overestimate Risk

The new equations are based on more recent, representative, and diverse cohorts that capture a wider spectrum of the population in terms of race, ethnicity, and socioeconomic status. They also include factors that are now known to be relevant to cardiovascular risk, such as chronic kidney disease.

Anderson compared how the two sets of equations estimated risk of cardiovascular disease in the next 10 years in the US population using the NHANES survey — a large nationally representative survey conducted between 2017 and 2020. 

He found that the pooled cohort equations estimated the population average 10-year risk of cardiovascular disease to be about 8%, but the PREVENT equations estimated it at just over 4%.

“The new equations estimate that the middle-aged US population have almost half the level of risk of MI and stroke over next 10 years compared with the equations used currently. So, we will substantially change risk estimates if the new equations are introduced into practice,” Anderson said. 

The study found that, if the PREVENT equations are adopted in the next set of primary prevention guidelines and the current threshold of a 7.5% risk of having an MI or stroke in the next 10 years is maintained as the starting point for statin treatment, then 17.3 million adults who were previously recommended primary prevention statin therapy would no longer be eligible.

A second, similar study, conducted by a different team of US researchers, estimated that using PREVENT would decrease the number of US adults receiving or recommended for statin therapy by 14.3 million and antihypertensive therapy by 2.62 million.

The researchers, led by James A. Diao, MD, from Harvard Medical School, Boston, Massachusetts, also suggested that over 10 years, reductions in treatment eligibility could result in an estimated 107,000 additional MI or stroke events.

Anderson points out that using the new equations would not affect the highest-risk patients. “They are still going to be high risk whichever equations are used. If you smoke a pack of cigarettes a day, have very high blood pressure or cholesterol and are older, then you are high risk. That part hasn’t changed. These people will qualify for statin treatment many times over with both sets of guidelines,” he said. 

Rather it will be the large population at moderate risk of cardiovascular disease that will be affected, with far fewer of these individuals likely to get statins.

“If you are on the fence about whether to take a statin or not and you’re currently just on the threshold where they might be recommended then these new equations could mean that you’ll be less likely to be offered them,” he said. “Using the new equations may result in a delay of a couple of years to have that conversation.”

 

A Red Flag

Steve Nissen, MD, a cardiologist at the Cleveland Clinic in Ohio, is not a fan of cardiovascular risk equations in general. He points out that less than half of those currently eligible for statins are actually treated. And he believes the studies suggesting fewer people will be eligible with the new risk equations raise a red flag on whether they should be used.

“Anything that may result in fewer people being treated is a huge problem,” he told this news organization. “We have abundant evidence that we should be treating more people, not fewer people. Every study we have done has shown benefit with statins.”

The risk calculators were initially developed to limit use of statins and other medications to high-risk patients, he said, but now that we know more about safety of these drugs, it’s clear that the risks are almost nonexistent. 

“We really need something else to guide the prescription of statins,” said Nissen.

Nissen suggests the risk calculators and guidelines have resulted in undertreatment of the population because they lack nuance and put too much emphasis on age. We should be more interested in reducing the lifetime risk of cardiovascular events, he said. “Calculators don’t do a good job of that. Their time horizons are too short. Young people with a family history of cardiovascular disease may have a low 10-year risk on a risk calculator but their lifetime risk is elevated, and as such, they should be considered for statin treatment. We need to find a more nuanced approach to understanding the lifetime risk of individuals,” he said. 

Nissen said risk calculators can be useful in high-risk patients to help demonstrate their need for treatment. “I can show them the calculator and that they have a 20% chance of an event — that can help convince them to take a statin.” 

But at the lower end of the risk scale, “all it does is keep patients who should be getting treatment from having that treatment.”

Nissen said changing the risk calculator won’t affect how he treats patients. “I use judgment to decide who to treat based on scientific literature and the patient in front of me. We will engage in a discussion and make a shared decision on what is the best course of action. Calculators will never be a substitute for medical judgment,” he said.

 

Equations Don’t Decide

Sadiya Khan, MD, a cardiologist at Northwestern University, Evanston, Illinois, and lead author of the PREVENT equations, told this news organization that it is important to put this discussion into context.

“The two recent papers do a good job of describing differences in predictive risk between the two sets of equations but that’s where they stop,” she said. “The translation from that to the decision on who should or should not be on statins or other medications is a step too far.”

Clinical guidelines will need to be updated to take the PREVENT equations into account, as Khan argued in a JAMA editorial. So it is not clear whether the current 7.5% 10-year risk figure will remain the threshold to start treatment. Khan anticipates the guidelines committee will have to re-evaluate that threshold.

“The 7.5% risk threshold was advised in the 2013 guidelines, based on what we knew then about the balance between benefit and harm and with the knowledge that the risk equations overestimated risk,” she said. “We now have a lot more data on the safety of statin therapy. We see this frequently in preventive care. Treatments often becomes more widespread in time and use expands into lower-risk patients.”

She also pointed out that the current primary prevention guidelines encourage consideration of other factors, not just predictive risk scores, when thinking about starting statins, including very high LDL cholesterol, family history, and apo B and Lp(a) levels.

“The recommendation on who would qualify for statin therapy is not based on one number,” she said. “It is based on many considerations, including both qualitative and quantitative factors, and discussions between the patient and the doctor. It is not a straightforward yes or no based on a 7.5% risk threshold.”

The equations, she said, should only be viewed as the first step in the process, and she said she agrees with Nissen that when applying the equations, doctors need to use additional data from each individual patient to make a judgment. “Equations do not decide who gets treated. Clinical practice guidelines do that.” 

Khan also agreed with Nissen that more effort is needed to identify longer term cardiovascular risk in younger people, and so the PREVENT equations include 30-year risk estimates.

“I totally agree that we need to start earlier in having these prevention conversations. The PREVENT model starts at age 30 which is 10 years earlier than the pooled cohort equations and they add a 30-year time horizon as well as the 10-year period for these discussions on predicted risk estimates,” she said. “We need to make sure we are not missing risk in young adults just because we are waiting for them to get into some arbitrary age category.”

Khan says she believes that, used correctly, the new equations will not limit access to statins or other cardiovascular treatments. “Because they are a more accurate reflection of risk in the contemporary population, the new PREVENT equations should identify the correct patients to be treated, within the confines of knowing that no risk prediction equation is perfect,” she said. “And if everything else is considered as well, not just the numbers in the risk equations, it shouldn’t result in fewer patients being treated.”

Anderson reported receiving grants from the American Heart Association, the American College of Cardiology, and the US Deprescribing Research Network. Nissen is leading a development program for a nonprescription low dose of rosuvastatin. He is also involved in trials of a new cholesterol lowering drug, obicetrapib, and on trials on drugs that lower Lp(a). Khan reported receiving grants from the American Heart Association and National Heart, Lung, and Blood Institute.

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