Cardiology

Current efforts to control high blood pressure (BP) are failing in the United States and globally.

The first World Health Organization (WHO) global report on hypertension found that only 54% of adults with hypertension are diagnosed, 42% get treatment, and just 21% have their hypertension controlled.

In the United States, almost half (48%) of adults have high BP, defined as a systolic BP > 130 mm Hg, or a diastolic BP > 80 mm Hg, or are taking medication for high BP, according to the Centers for Disease Control and Prevention. Only about one in four adults (22.5%) with high BP have their BP under control.

High BP is a major risk factor for coronary heart disease, heart failure, and stroke, and the problem of controlling it is only getting worse. In 2024, the American Heart Association estimates that, “among adults, prevalence of hypertension will increase from 51.2% in 2020 to 61.0% in 2050.”
 

Pharmacists Most Effective

Though many factors contribute to hypertension, researchers have found that the kind of specialist leading the hypertension team may play a role in success. Currently, most BP control teams are led by physicians in primary care.

In a recent meta-analysis involving 100 randomized controlled trials and more than 90,000 patients in Circulation, Katherine T. Mills, PhD, School of Public Health, Tulane University, New Orleans, Louisiana, and colleagues found that, while all the groups studied who led BP control efforts were successful in reducing BP, pharmacist- and community health worker–led teams saw the biggest reductions.

Those groups’ efforts resulted in the greatest systolic BP drops: −7.3 mm Hg (pharmacists) and −7.1 mm Hg (community health workers). Groups led by nurses and physicians saw systolic changes of −3 and −2.4 mm Hg, respectively.

Similarly, pharmacist- and community health worker–led efforts saw the greatest diastolic BP reductions (−3.8 and −3.1 mm Hg), compared with nurse-led (−1.6) and physician-led (−1.2) efforts.
 

Reductions Enough to Cut Cardiovascular Disease Risk

The reduction numbers for pharmacists are clinically meaningful, Mills said in an interview. “It’s greater than a lot of what we see from individual lifestyle changes,” such as reducing sodium intake or increasing physical activity.

“It’s a big enough blood pressure change to have meaningful reduction in risk of cardiovascular disease,” she said.

This evidence that the leader of the team matters is particularly important because the treatment of hypertension is not in doubt. Something else is not working the way it should.

“We have basically all the scientific evidence we need in terms of what interventions work. But there’s a big gap between that and what’s actually being done in the real world,” she said.

Mills said she was not surprised that pharmacists got the best results “because so much of it has to do with titrating medications and finding the right kind of medications for each patient.”

Additionally, BP management and control falls right into pharmacists’ wheelhouse, Mills noted, including evaluating medication side effects and talking to patients about medication adherence.
 

Why Pharmacists May Be More Successful

In an accompanying editorial, Ross T. Tsuyuki, PharmD, with the EPICORE Centre, Division of Cardiology, University of Alberta in Edmonton, Canada, and coauthors said the Mills study provides further data to support pharmacists leading BP control efforts, but it’s not the data that have been keeping the model from changing. The barriers include turf wars and lack of legislative change.

The editorialists also said having pharmacist-led BP teams is only the first step. “We need pharmacists to independently prescribe,” they wrote.

“Since individual states govern the scope of practice of pharmacists,” the editorialists wrote, “we have the enormous task of changing regulations to allow pharmacists to independently prescribe for hypertension. But it can be done. The Canadian province of Alberta allows pharmacists to prescribe. And more recently, Idaho. While most states allow some sort of collaborative (dependent) prescribing, that is only a first step.”

Allowing pharmacists to independently prescribe will help populations who do not have a physician or can’t get access to a physician, the editorialists wrote. But changing state legislation would be a lengthy and complex effort.
 

Physician-Led BP Control Model ‘Seems to Fail Miserably’

Coauthor of the editorial, Florian Rader, MD, MSc, medical director of the Hypertension Center of Excellence at Cedars-Sinai Medical Center in Los Angeles, California, said in an interview that, currently, physician-led teams are the norm, “and that model seems to fail miserably.”

He offered several key reasons for that. In primary care, patients with hypertension often have other problems — they may have high cholesterol or diabetes. “They may have acute illnesses that bother them as well as hypertension that doesn’t bother them,” he said.

Physicians tend to find excuses not to increase or add BP medications, Rader said. “We tend then to blame ‘white coat effect’ or say ‘you’re just nervous today.’ ”

Pharmacists, comparatively, are more protocol driven, he said. “They essentially look at blood pressure and they have an algorithm in their mind. If the blood pressure hits the guideline-stated bar, start this medication. If it hits another bar, increase or add another medication.”

Rader said turf wars are also keeping physician-led teams from changing, fueled by fears that patients will seek care from pharmacists instead of physicians.

“I don’t think the pharmacists will steal a single patient,” Rader said. “If a physician had a healthcare partner like a pharmacist to optimize blood pressure, then [patients] come back to the physician with normalized BP on the right medications. I think it’s a total win-win. I think we just have to get over that.”

Pharmacist-led warfarin clinics are very well established, Rader said, “but for whatever reason, when it comes to blood pressure, physicians are a little bit more hesitant.”
 

Collaboration Yes, Independent No

Hypertension expert Donald J. DiPette, MD, Health Sciences Distinguished Professor in the Department of Internal Medicine at University of South Carolina, Columbia, said he completely agrees with Mills and colleagues’ conclusion. “Pharmacists and community health workers are most effective at leading BP intervention implementation and should be prioritized in future hypertension control efforts.”

The conclusion “is in line with the thinking of major organizations,” said DiPette, who helped develop the WHO’s most recent pharmacological treatment of hypertension guidelines. “WHO suggests that pharmacological treatment of hypertension can be provided by nonphysician professionals such as pharmacists and nurses as long as the following conditions are met: Proper training, prescribing authority, specific management protocols, and physician oversight.”

DiPette strongly believes BP control efforts should be supervised by a physician, but that could come in different ways. He suggested a collaborative but physician-supervised development of a protocol. Everyone contributes, but the physician signs off on it.

As for the Idaho example of independent practice for pharmacists, DiPette said he doesn’t think that will make a big difference in control rates. “That’s still not team-based care.”
 

Community Health Workers Key

He said he was also glad to see community healthcare workers emerge as the next-most-effective group after pharmacists to lead BP control teams. This is particularly important as BP control efforts globally need to consider the cultural experience of individual communities. “The community worker is on the ground, and can help overcome some of the cultural barriers,” he said.

“The key is to focus on team-based care and moving away from silo practice,” DiPette said.

Physicians, he said, often fall into “clinical or therapeutic inertia,” where BP is concerned. “We fail to titrate or add additional hypertensive medications even when they’re clearly indicated by the blood pressure. This is a problem not with the individual patient or the healthcare system, this is on us as physicians.”

Nonphysicians are more aligned with following protocols and guidelines, irrespective of the dynamics of what’s going on, he said.

And following protocols rigidly is a good thing for hypertension. “We’re not overtreating hypertension,” he emphasized. “We’re undertreating it.”

Reversing the trend on hypertension will take a sea change in medicine — changing institutions, systems, and individuals who have been doing things the same way for decades, he said.

“Our hypertension control rates are dismal,” DiPette said. “What’s more alarming is they’re going down. That’s the urgency. That’s the burning platform. We must strongly consider doing something different.”

Tsuyuki has received investigator-initiated arm’s length research grants from Merck, Pfizer, AstraZeneca, and Sanofi. He has been a speaker/consultant for Merck, Emergent BioSolutions, and Shoppers Drug Mart/Loblaw Companies Limited. Rader has been a consultant for Bristol Meyers Squibb, Cytokinetics, Idorsia, Medtronic, and ReCor Medical. Mills and coauthors reported no relevant financial relationships. DiPette declared no relevant financial relationships. He was part of a leadership team that developed WHO guidelines on hypertension.

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

Current efforts to control high blood pressure (BP) are failing in the United States and globally.

The first World Health Organization (WHO) global report on hypertension found that only 54% of adults with hypertension are diagnosed, 42% get treatment, and just 21% have their hypertension controlled.

In the United States, almost half (48%) of adults have high BP, defined as a systolic BP > 130 mm Hg, or a diastolic BP > 80 mm Hg, or are taking medication for high BP, according to the Centers for Disease Control and Prevention. Only about one in four adults (22.5%) with high BP have their BP under control.

High BP is a major risk factor for coronary heart disease, heart failure, and stroke, and the problem of controlling it is only getting worse. In 2024, the American Heart Association estimates that, “among adults, prevalence of hypertension will increase from 51.2% in 2020 to 61.0% in 2050.”
 

Pharmacists Most Effective

Though many factors contribute to hypertension, researchers have found that the kind of specialist leading the hypertension team may play a role in success. Currently, most BP control teams are led by physicians in primary care.

In a recent meta-analysis involving 100 randomized controlled trials and more than 90,000 patients in Circulation, Katherine T. Mills, PhD, School of Public Health, Tulane University, New Orleans, Louisiana, and colleagues found that, while all the groups studied who led BP control efforts were successful in reducing BP, pharmacist- and community health worker–led teams saw the biggest reductions.

Those groups’ efforts resulted in the greatest systolic BP drops: −7.3 mm Hg (pharmacists) and −7.1 mm Hg (community health workers). Groups led by nurses and physicians saw systolic changes of −3 and −2.4 mm Hg, respectively.

Similarly, pharmacist- and community health worker–led efforts saw the greatest diastolic BP reductions (−3.8 and −3.1 mm Hg), compared with nurse-led (−1.6) and physician-led (−1.2) efforts.
 

Reductions Enough to Cut Cardiovascular Disease Risk

The reduction numbers for pharmacists are clinically meaningful, Mills said in an interview. “It’s greater than a lot of what we see from individual lifestyle changes,” such as reducing sodium intake or increasing physical activity.

“It’s a big enough blood pressure change to have meaningful reduction in risk of cardiovascular disease,” she said.

This evidence that the leader of the team matters is particularly important because the treatment of hypertension is not in doubt. Something else is not working the way it should.

“We have basically all the scientific evidence we need in terms of what interventions work. But there’s a big gap between that and what’s actually being done in the real world,” she said.

Mills said she was not surprised that pharmacists got the best results “because so much of it has to do with titrating medications and finding the right kind of medications for each patient.”

Additionally, BP management and control falls right into pharmacists’ wheelhouse, Mills noted, including evaluating medication side effects and talking to patients about medication adherence.
 

Why Pharmacists May Be More Successful

In an accompanying editorial, Ross T. Tsuyuki, PharmD, with the EPICORE Centre, Division of Cardiology, University of Alberta in Edmonton, Canada, and coauthors said the Mills study provides further data to support pharmacists leading BP control efforts, but it’s not the data that have been keeping the model from changing. The barriers include turf wars and lack of legislative change.

The editorialists also said having pharmacist-led BP teams is only the first step. “We need pharmacists to independently prescribe,” they wrote.

“Since individual states govern the scope of practice of pharmacists,” the editorialists wrote, “we have the enormous task of changing regulations to allow pharmacists to independently prescribe for hypertension. But it can be done. The Canadian province of Alberta allows pharmacists to prescribe. And more recently, Idaho. While most states allow some sort of collaborative (dependent) prescribing, that is only a first step.”

Allowing pharmacists to independently prescribe will help populations who do not have a physician or can’t get access to a physician, the editorialists wrote. But changing state legislation would be a lengthy and complex effort.
 

Physician-Led BP Control Model ‘Seems to Fail Miserably’

Coauthor of the editorial, Florian Rader, MD, MSc, medical director of the Hypertension Center of Excellence at Cedars-Sinai Medical Center in Los Angeles, California, said in an interview that, currently, physician-led teams are the norm, “and that model seems to fail miserably.”

He offered several key reasons for that. In primary care, patients with hypertension often have other problems — they may have high cholesterol or diabetes. “They may have acute illnesses that bother them as well as hypertension that doesn’t bother them,” he said.

Physicians tend to find excuses not to increase or add BP medications, Rader said. “We tend then to blame ‘white coat effect’ or say ‘you’re just nervous today.’ ”

Pharmacists, comparatively, are more protocol driven, he said. “They essentially look at blood pressure and they have an algorithm in their mind. If the blood pressure hits the guideline-stated bar, start this medication. If it hits another bar, increase or add another medication.”

Rader said turf wars are also keeping physician-led teams from changing, fueled by fears that patients will seek care from pharmacists instead of physicians.

“I don’t think the pharmacists will steal a single patient,” Rader said. “If a physician had a healthcare partner like a pharmacist to optimize blood pressure, then [patients] come back to the physician with normalized BP on the right medications. I think it’s a total win-win. I think we just have to get over that.”

Pharmacist-led warfarin clinics are very well established, Rader said, “but for whatever reason, when it comes to blood pressure, physicians are a little bit more hesitant.”
 

Collaboration Yes, Independent No

Hypertension expert Donald J. DiPette, MD, Health Sciences Distinguished Professor in the Department of Internal Medicine at University of South Carolina, Columbia, said he completely agrees with Mills and colleagues’ conclusion. “Pharmacists and community health workers are most effective at leading BP intervention implementation and should be prioritized in future hypertension control efforts.”

The conclusion “is in line with the thinking of major organizations,” said DiPette, who helped develop the WHO’s most recent pharmacological treatment of hypertension guidelines. “WHO suggests that pharmacological treatment of hypertension can be provided by nonphysician professionals such as pharmacists and nurses as long as the following conditions are met: Proper training, prescribing authority, specific management protocols, and physician oversight.”

DiPette strongly believes BP control efforts should be supervised by a physician, but that could come in different ways. He suggested a collaborative but physician-supervised development of a protocol. Everyone contributes, but the physician signs off on it.

As for the Idaho example of independent practice for pharmacists, DiPette said he doesn’t think that will make a big difference in control rates. “That’s still not team-based care.”
 

Community Health Workers Key

He said he was also glad to see community healthcare workers emerge as the next-most-effective group after pharmacists to lead BP control teams. This is particularly important as BP control efforts globally need to consider the cultural experience of individual communities. “The community worker is on the ground, and can help overcome some of the cultural barriers,” he said.

“The key is to focus on team-based care and moving away from silo practice,” DiPette said.

Physicians, he said, often fall into “clinical or therapeutic inertia,” where BP is concerned. “We fail to titrate or add additional hypertensive medications even when they’re clearly indicated by the blood pressure. This is a problem not with the individual patient or the healthcare system, this is on us as physicians.”

Nonphysicians are more aligned with following protocols and guidelines, irrespective of the dynamics of what’s going on, he said.

And following protocols rigidly is a good thing for hypertension. “We’re not overtreating hypertension,” he emphasized. “We’re undertreating it.”

Reversing the trend on hypertension will take a sea change in medicine — changing institutions, systems, and individuals who have been doing things the same way for decades, he said.

“Our hypertension control rates are dismal,” DiPette said. “What’s more alarming is they’re going down. That’s the urgency. That’s the burning platform. We must strongly consider doing something different.”

Tsuyuki has received investigator-initiated arm’s length research grants from Merck, Pfizer, AstraZeneca, and Sanofi. He has been a speaker/consultant for Merck, Emergent BioSolutions, and Shoppers Drug Mart/Loblaw Companies Limited. Rader has been a consultant for Bristol Meyers Squibb, Cytokinetics, Idorsia, Medtronic, and ReCor Medical. Mills and coauthors reported no relevant financial relationships. DiPette declared no relevant financial relationships. He was part of a leadership team that developed WHO guidelines on hypertension.

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

Current efforts to control high blood pressure (BP) are failing in the United States and globally.

The first World Health Organization (WHO) global report on hypertension found that only 54% of adults with hypertension are diagnosed, 42% get treatment, and just 21% have their hypertension controlled.

In the United States, almost half (48%) of adults have high BP, defined as a systolic BP > 130 mm Hg, or a diastolic BP > 80 mm Hg, or are taking medication for high BP, according to the Centers for Disease Control and Prevention. Only about one in four adults (22.5%) with high BP have their BP under control.

High BP is a major risk factor for coronary heart disease, heart failure, and stroke, and the problem of controlling it is only getting worse. In 2024, the American Heart Association estimates that, “among adults, prevalence of hypertension will increase from 51.2% in 2020 to 61.0% in 2050.”
 

Pharmacists Most Effective

Though many factors contribute to hypertension, researchers have found that the kind of specialist leading the hypertension team may play a role in success. Currently, most BP control teams are led by physicians in primary care.

In a recent meta-analysis involving 100 randomized controlled trials and more than 90,000 patients in Circulation, Katherine T. Mills, PhD, School of Public Health, Tulane University, New Orleans, Louisiana, and colleagues found that, while all the groups studied who led BP control efforts were successful in reducing BP, pharmacist- and community health worker–led teams saw the biggest reductions.

Those groups’ efforts resulted in the greatest systolic BP drops: −7.3 mm Hg (pharmacists) and −7.1 mm Hg (community health workers). Groups led by nurses and physicians saw systolic changes of −3 and −2.4 mm Hg, respectively.

Similarly, pharmacist- and community health worker–led efforts saw the greatest diastolic BP reductions (−3.8 and −3.1 mm Hg), compared with nurse-led (−1.6) and physician-led (−1.2) efforts.
 

Reductions Enough to Cut Cardiovascular Disease Risk

The reduction numbers for pharmacists are clinically meaningful, Mills said in an interview. “It’s greater than a lot of what we see from individual lifestyle changes,” such as reducing sodium intake or increasing physical activity.

“It’s a big enough blood pressure change to have meaningful reduction in risk of cardiovascular disease,” she said.

This evidence that the leader of the team matters is particularly important because the treatment of hypertension is not in doubt. Something else is not working the way it should.

“We have basically all the scientific evidence we need in terms of what interventions work. But there’s a big gap between that and what’s actually being done in the real world,” she said.

Mills said she was not surprised that pharmacists got the best results “because so much of it has to do with titrating medications and finding the right kind of medications for each patient.”

Additionally, BP management and control falls right into pharmacists’ wheelhouse, Mills noted, including evaluating medication side effects and talking to patients about medication adherence.
 

Why Pharmacists May Be More Successful

In an accompanying editorial, Ross T. Tsuyuki, PharmD, with the EPICORE Centre, Division of Cardiology, University of Alberta in Edmonton, Canada, and coauthors said the Mills study provides further data to support pharmacists leading BP control efforts, but it’s not the data that have been keeping the model from changing. The barriers include turf wars and lack of legislative change.

The editorialists also said having pharmacist-led BP teams is only the first step. “We need pharmacists to independently prescribe,” they wrote.

“Since individual states govern the scope of practice of pharmacists,” the editorialists wrote, “we have the enormous task of changing regulations to allow pharmacists to independently prescribe for hypertension. But it can be done. The Canadian province of Alberta allows pharmacists to prescribe. And more recently, Idaho. While most states allow some sort of collaborative (dependent) prescribing, that is only a first step.”

Allowing pharmacists to independently prescribe will help populations who do not have a physician or can’t get access to a physician, the editorialists wrote. But changing state legislation would be a lengthy and complex effort.
 

Physician-Led BP Control Model ‘Seems to Fail Miserably’

Coauthor of the editorial, Florian Rader, MD, MSc, medical director of the Hypertension Center of Excellence at Cedars-Sinai Medical Center in Los Angeles, California, said in an interview that, currently, physician-led teams are the norm, “and that model seems to fail miserably.”

He offered several key reasons for that. In primary care, patients with hypertension often have other problems — they may have high cholesterol or diabetes. “They may have acute illnesses that bother them as well as hypertension that doesn’t bother them,” he said.

Physicians tend to find excuses not to increase or add BP medications, Rader said. “We tend then to blame ‘white coat effect’ or say ‘you’re just nervous today.’ ”

Pharmacists, comparatively, are more protocol driven, he said. “They essentially look at blood pressure and they have an algorithm in their mind. If the blood pressure hits the guideline-stated bar, start this medication. If it hits another bar, increase or add another medication.”

Rader said turf wars are also keeping physician-led teams from changing, fueled by fears that patients will seek care from pharmacists instead of physicians.

“I don’t think the pharmacists will steal a single patient,” Rader said. “If a physician had a healthcare partner like a pharmacist to optimize blood pressure, then [patients] come back to the physician with normalized BP on the right medications. I think it’s a total win-win. I think we just have to get over that.”

Pharmacist-led warfarin clinics are very well established, Rader said, “but for whatever reason, when it comes to blood pressure, physicians are a little bit more hesitant.”
 

Collaboration Yes, Independent No

Hypertension expert Donald J. DiPette, MD, Health Sciences Distinguished Professor in the Department of Internal Medicine at University of South Carolina, Columbia, said he completely agrees with Mills and colleagues’ conclusion. “Pharmacists and community health workers are most effective at leading BP intervention implementation and should be prioritized in future hypertension control efforts.”

The conclusion “is in line with the thinking of major organizations,” said DiPette, who helped develop the WHO’s most recent pharmacological treatment of hypertension guidelines. “WHO suggests that pharmacological treatment of hypertension can be provided by nonphysician professionals such as pharmacists and nurses as long as the following conditions are met: Proper training, prescribing authority, specific management protocols, and physician oversight.”

DiPette strongly believes BP control efforts should be supervised by a physician, but that could come in different ways. He suggested a collaborative but physician-supervised development of a protocol. Everyone contributes, but the physician signs off on it.

As for the Idaho example of independent practice for pharmacists, DiPette said he doesn’t think that will make a big difference in control rates. “That’s still not team-based care.”
 

Community Health Workers Key

He said he was also glad to see community healthcare workers emerge as the next-most-effective group after pharmacists to lead BP control teams. This is particularly important as BP control efforts globally need to consider the cultural experience of individual communities. “The community worker is on the ground, and can help overcome some of the cultural barriers,” he said.

“The key is to focus on team-based care and moving away from silo practice,” DiPette said.

Physicians, he said, often fall into “clinical or therapeutic inertia,” where BP is concerned. “We fail to titrate or add additional hypertensive medications even when they’re clearly indicated by the blood pressure. This is a problem not with the individual patient or the healthcare system, this is on us as physicians.”

Nonphysicians are more aligned with following protocols and guidelines, irrespective of the dynamics of what’s going on, he said.

And following protocols rigidly is a good thing for hypertension. “We’re not overtreating hypertension,” he emphasized. “We’re undertreating it.”

Reversing the trend on hypertension will take a sea change in medicine — changing institutions, systems, and individuals who have been doing things the same way for decades, he said.

“Our hypertension control rates are dismal,” DiPette said. “What’s more alarming is they’re going down. That’s the urgency. That’s the burning platform. We must strongly consider doing something different.”

Tsuyuki has received investigator-initiated arm’s length research grants from Merck, Pfizer, AstraZeneca, and Sanofi. He has been a speaker/consultant for Merck, Emergent BioSolutions, and Shoppers Drug Mart/Loblaw Companies Limited. Rader has been a consultant for Bristol Meyers Squibb, Cytokinetics, Idorsia, Medtronic, and ReCor Medical. Mills and coauthors reported no relevant financial relationships. DiPette declared no relevant financial relationships. He was part of a leadership team that developed WHO guidelines on hypertension.

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

This transcript has been edited for clarity .

Robert A. Harrington, MD: I’m here in London at the European Society of Cardiology meetings, at theheart.org | Medscape Cardiology booth, using the meetings as an opportunity to meet with colleagues to talk about recent things that they’ve been writing about.

Today I’m joined by a good friend and colleague, Dr. Dhruv Kazi from Beth Israel Deaconess in Boston. Thanks for joining us.

Dhruv S. Kazi, MD, MS: Thank you for having me.

Harrington: Dr. Kazi is an associate professor of medicine at Harvard Medical School. He’s also the associate director of the Smith Center, which is an outcomes research center at the Beth Israel Deaconess. Thanks for joining us.

Kazi: Excited to be here.

Harrington: The topic I think you know that I want to discuss is a really important paper. There are two papers. They’re part of the American Heart Association’s 100th anniversary celebration, if you will. Many of the papers looked back at where science taken us.

With your coauthor, Karen Joynt Maddox, your papers are looking forward. They’re about the burden of cardiovascular disease in 2050. One paper really focused on what I would call the clinical and public health issues. Yours is focused on the economics. Is that a good description?

Kazi: Perfect.

Harrington: Tell us what you, Karen, and the other writers set out to do. What were you asked to do?

Kazi: As you know, the American Heart Association is entering its second century. Part of this was an exercise to say, where will the country be in 2050, which is a long enough time horizon for us to start planning for the future. What are the conditions that affect the magnitude of the disease, and the kinds of people who will be affected, that we should be aware of?

We looked back and said, if prior trends remain the same, where will we be in 2050, accounting for changes in demographics, changes in the composition of the population, and knowing that some of the cardiovascular risk factors are getting worse?

Harrington: For me, what was really striking is that, when I first saw the title and read “2050,” I thought, Oh, that’s a long way away. Then as I started reading it, I realized that this is not so far away.

Kazi: Absolutely.

Harrington: If we’re going to make a difference, it might take us 25 years.

Kazi: Especially if we set ourselves ambitious goals, we›re going to have to dig deep. Business-as-usual is not going to get us there.

Harrington: No. What I think has happened is we›ve spent so much time taking care of acute illness. Case fatality rates are fantastic. I was actually making the comment yesterday to a colleague that when I was an intern, the 30-day death rate from acute myocardial infarction was about 20%.

Kazi: Oh, wow.

Harrington: Now it’s 5%. That’s a big difference in a career.
 

Trends in the Wrong Direction

Kazi: There are fundamental trends. The decline in case fatalities is a really positive development, and I would hope that, going forward, that would continue. Those are risk-adjusted death rates and what is happening is that risk is going up. This is a function of the fact that the US population is aging; 2030 will be the first year that all the baby boomers will be over the age of 65.

By the mid-2030s, we’ll have more adults over the age of 65 than kids. That aging of the population is going to increase risk. The second is — and this is a positive development — we are a more diverse population, but the populations that are minoritized have higher cardiovascular risk, for a variety of reasons.

As the population of Asian Americans increases and doubles, in fact, as the population of Hispanic Americans doubles, we’re going to see an increase in risk related to cardiovascular disease. The third is that, over the past decade, there are some risk factors that are going in the wrong direction.

Harrington: Let’s talk about that because that’s humbling. I’m involved, as you know, with the American Heart Association, as are you. Despite all the work on Life’s Simple 7 and now Life’s Essential 8, we still have some issues.

Kazi: The big ones that come to mind are hypertension, diabetes, and obesity, all of which are trending in the wrong direction. Hypertension, we were gaining traction; and then over the past decade, we’ve slipped again. As you know, national blood pressure control rates have declined in many populations.

Harrington: Rather substantially.

Kazi: Substantially so, which has implications, in particular, for stroke rates in the future and stroke rates in young adults in the future. Obesity is a problem that we have very little control over. We’re already at 40% on average, which means that some populations are already in the 60% range.

Harrington: We also have obesity in kids — the burden, I’ll call it, of obesity. It’s not that you become obese in your thirties or your forties; you›re becoming obese as a teenager or even younger.

Kazi: Exactly. Since the 1990s, obesity in US adults has doubled, but obesity in US children has quadrupled. It’s starting from a lower base, but it’s very much an escalating problem.

Harrington: Diabetes is tightly linked to it but not totally explained.

Kazi: Exactly. The increase in diabetes is largely driven by obesity, but it›s probably also driven by changes in diet and lifestyle that don›t go through obesity.

Harrington: Yeah, it’s interesting. I think I have this figure correctly. It used to be rare that you saw a child with type 2 diabetes or what we call type 2 diabetes.

Kazi: Yeah.

Harrington: Now, the vast majority of kids with diabetes have type 2 diabetes.

Kazi: In the adolescents/young adults age group, most of it is type 2.

Harrington: Diabetes going up, obesity up, hypertension not well controlled, smoking combustible cigarettes way down.

Kazi: Yeah.

Harrington: Cholesterol levels. I was surprised. Cholesterol looked better. You said — because I was at a meeting where somebody asked you — that’s not explained by treatment.

Kazi: No, it’s not, at least going back to the ‘70s, but likely even sooner. I think that can only be attributed to substantial dietary changes. We are consuming less fat and less trans-fat. It’s possible that those collectively are improving our cholesterol levels, possibly at the expense of our glucose levels, because we basically substituted fats in our diet with more carbs at a population level.
 

Cigarettes and Vaping

Harrington: Some things certainly trend in the right direction but others in a really difficult direction. It’s going to lead to pretty large changes in risk for coronary disease, atrial fibrillation, and heart failure.

Kazi: I want to go back to the tobacco point. There are definitely marked declines in tobacco, still tightly related to income in the country. You see much higher prevalence of tobacco use in lower-income populations, but it’s unclear to me where it’s going in kids. We know that combustible tobacco use is going down but e-cigarettes went up. What that leads to over the next 30 years is unclear to me.

Harrington: That is a really important comment that’s worth sidebarring. The vaping use has been a terrible epidemic among our high schoolers. What is that going to lead to? Is it going to lead to the use of combustible cigarettes and we’re going to see that go back up? It remains to be seen.

Kazi: Yes, it remains to be seen. Going back to your point about this change in risk factors and this change in demographics, both aging and becoming a more diverse population means that we have large increases in some healthcare conditions.

Coronary heart disease goes up some, there›s a big jump in stroke — nearly a doubling in stroke — which is related to hypertension, obesity, an aging population, and a more diverse population. There are changes in stroke in the young, and atrial fibrillation related to, again, hypertension. We’re seeing these projections, and with them come these pretty large projections in changes in healthcare spending.
 

Healthcare Spending Not Sustainable

Harrington: Big. I mean, it’s not sustainable. Give the audience the number — it’s pretty frightening.

Kazi: We’re talking about a quadrupling of healthcare costs related to cardiovascular disease over 25 years. We’ve gotten used to the narrative that healthcare in the US is expensive and drugs are expensive, but this is an enormous problem — an unsustainable problem, like you called it.

It’s a doubling as a proportion of the economy. I was looking this up this morning. If the US healthcare economy were its own economy, it would be the fourth largest economy in the world.

Harrington: Healthcare as it is today, is it 21% of our economy?

Kazi: It’s 17% now. If it were its own economy, it would be the fourth largest in the world. We are spending more on healthcare than all but two other countries’ total economies. It’s kind of crazy.

Harrington: We’re talking about a quadrupling.

Kazi: Within that, the cardiovascular piece is a big piece, and we›re talking about a quadrupling.

Harrington: That’s both direct and indirect costs.

Kazi: The quadrupling of costs is just the direct costs. Indirect costs, for the listeners, refer to costs unrelated to healthcare but changes in productivity, either because people are disabled and unable to participate fully in the workforce or they die early.

The productivity costs are also increased substantially as a result. If you look at both healthcare and productivity, that goes up threefold. These are very large changes.

Harrington: Let’s now get to what we can do about it. I made the comment to you when I first read the papers that I was very depressed. Then, after I went through my Kübler-Ross stages of depression, death, and dying, I came to acceptance.

What are we going to do about it? This is a focus on policy, but also a focus on how we deliver healthcare, how we think about healthcare, and how we develop drugs and devices.

The drug question is going to be the one the audience is thinking about. They say, well, what about GLP-1 agonists? Aren’t those going to save the day?

Kazi: Yes and no. I’ll say that, early in my career, I used to be very attracted to simple solutions to complex problems. I’ve come to realize that simple solutions are elegant, attractive, and wrong. We›re dealing with a very complex issue and I think we’re going to need a multipronged approach.

The way I think about it is that there was a group of people who are at very high risk today. How do we help those individuals? Then how do we help the future generation so that they’re not dealing with the projections that we’re talking about.

My colleague, Karen Joynt Maddox, who led one of the papers, as you mentioned, has an elegant line in the paper where she says projections are not destiny. These are things we can change.

Harrington: If nothing changes, this is what it’s going to look like.

Kazi: This is where we’re headed.

Harrington: We can change. We’ve got some time to change, but we don’t have forever.

Kazi: Yes, exactly. We picked the 25-year timeline instead of a “let’s plan for the next century” timeline because we want something concrete and actionable. It’s close enough to be meaningful but far enough to give us the runway we need to act.

Harrington: Give me two things from the policy perspective, because it’s mostly policy.

Kazi: There are policy and clinical interventions. From the policy perspective, if I had to list two things, one is expansion of access to care. As we talk about this big increase in the burden of disease and risk factors, if you have a large proportion of your population that has hypertension or diabetes, you’re going to have to expand access to care to ensure that people get treated so they can get access to this care before they develop the complications that we worry about, like stroke and heart disease, that are very expensive to treat downstream.

The second, more broadly related to access to care, is the access to medications that are effective. You bring up GLP-1s. I think we need a real strategy for how we can give people access to GLP-1s at a price that is affordable to individuals but also affordable to the health system, and to help them stay on the drugs.

GLP-1s are transformative in what they do for weight loss and for diabetes, but more than 50% of people who start one are off it at 12 months. There’s something fundamentally wrong about how we’re delivering GLP-1s today. It’s not just about the cost of the drugs but the support system people need to stay on.

Harrington: I’ve made the comment, in many forms now, that we know the drugs work. We have to figure out how to use them.

Kazi: Exactly, yes.

Harrington: Using them includes chronicity. This is a chronic condition. Some people can come off the drugs, but many can’t. We’re going to have to figure this out, and maybe the newer generations of drugs will help us address what people call the off-ramping. How are we going to do that? I think you’re spot-on. Those are critically important questions.

Kazi: As we looked at this modeling, I’ll tell you — I had a come-to-Jesus moment where I was like, there is no way to fix cardiovascular disease in the US without going through obesity and diabetes. We have to address obesity in the US. We can’t just treat our way out of it. Obesity is fundamentally a food problem and we’ve got to engage again with food policy in a meaningful way.

Harrington: As you know, with the American Heart Association, we›re doing a large amount of work now on food as medicine and food is medicine. We are trying to figure out what the levers are that we can pull to actually help people eat healthier diets.

Kazi: Yes. Rather than framing it as an individual choice that people are eating poorly, it’s, how do we make healthy diets the default in the environment?

Harrington: This is where you get to the children as well.

Kazi: Exactly.

Harrington: I could talk about this all day. I’ve had the benefit of reading the papers now a few times and talking to you on several occasions. Thank you for joining us.

Kazi: Thank you.
 

Dr. Harrington, Stephen and Suzanne Weiss Dean, Weill Cornell Medicine; Provost for Medical Affairs, Cornell University, New York, NY, disclosed ties with Baim Institute (DSMB); CSL (RCT Executive Committee); Janssen (RCT Char), NHLBI (RCT Executive Committee, DSMB Chair); PCORI (RCT Co-Chair); DCRI, Atropos Health; Bitterroot Bio; Bristol Myers Squibb; BridgeBio; Element Science; Edwards Lifesciences; Foresite Labs; Medscape/WebMD Board of Directors for: American Heart Association; College of the Holy Cross; and Cytokinetics. Dr. Kazi, Associate Director, Smith Center for Outcomes Research, Associate Professor, Department of Medicine (Cardiology), Harvard Medical School, Director, Department of Cardiac Critical Care Unit, Beth Israel Deaconess Medical Center, Boston, Massachusetts, has disclosed receiving a research grant from Boston Scientific (grant to examine the economics of stroke prevention).

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity .

Robert A. Harrington, MD: I’m here in London at the European Society of Cardiology meetings, at theheart.org | Medscape Cardiology booth, using the meetings as an opportunity to meet with colleagues to talk about recent things that they’ve been writing about.

Today I’m joined by a good friend and colleague, Dr. Dhruv Kazi from Beth Israel Deaconess in Boston. Thanks for joining us.

Dhruv S. Kazi, MD, MS: Thank you for having me.

Harrington: Dr. Kazi is an associate professor of medicine at Harvard Medical School. He’s also the associate director of the Smith Center, which is an outcomes research center at the Beth Israel Deaconess. Thanks for joining us.

Kazi: Excited to be here.

Harrington: The topic I think you know that I want to discuss is a really important paper. There are two papers. They’re part of the American Heart Association’s 100th anniversary celebration, if you will. Many of the papers looked back at where science taken us.

With your coauthor, Karen Joynt Maddox, your papers are looking forward. They’re about the burden of cardiovascular disease in 2050. One paper really focused on what I would call the clinical and public health issues. Yours is focused on the economics. Is that a good description?

Kazi: Perfect.

Harrington: Tell us what you, Karen, and the other writers set out to do. What were you asked to do?

Kazi: As you know, the American Heart Association is entering its second century. Part of this was an exercise to say, where will the country be in 2050, which is a long enough time horizon for us to start planning for the future. What are the conditions that affect the magnitude of the disease, and the kinds of people who will be affected, that we should be aware of?

We looked back and said, if prior trends remain the same, where will we be in 2050, accounting for changes in demographics, changes in the composition of the population, and knowing that some of the cardiovascular risk factors are getting worse?

Harrington: For me, what was really striking is that, when I first saw the title and read “2050,” I thought, Oh, that’s a long way away. Then as I started reading it, I realized that this is not so far away.

Kazi: Absolutely.

Harrington: If we’re going to make a difference, it might take us 25 years.

Kazi: Especially if we set ourselves ambitious goals, we›re going to have to dig deep. Business-as-usual is not going to get us there.

Harrington: No. What I think has happened is we›ve spent so much time taking care of acute illness. Case fatality rates are fantastic. I was actually making the comment yesterday to a colleague that when I was an intern, the 30-day death rate from acute myocardial infarction was about 20%.

Kazi: Oh, wow.

Harrington: Now it’s 5%. That’s a big difference in a career.
 

Trends in the Wrong Direction

Kazi: There are fundamental trends. The decline in case fatalities is a really positive development, and I would hope that, going forward, that would continue. Those are risk-adjusted death rates and what is happening is that risk is going up. This is a function of the fact that the US population is aging; 2030 will be the first year that all the baby boomers will be over the age of 65.

By the mid-2030s, we’ll have more adults over the age of 65 than kids. That aging of the population is going to increase risk. The second is — and this is a positive development — we are a more diverse population, but the populations that are minoritized have higher cardiovascular risk, for a variety of reasons.

As the population of Asian Americans increases and doubles, in fact, as the population of Hispanic Americans doubles, we’re going to see an increase in risk related to cardiovascular disease. The third is that, over the past decade, there are some risk factors that are going in the wrong direction.

Harrington: Let’s talk about that because that’s humbling. I’m involved, as you know, with the American Heart Association, as are you. Despite all the work on Life’s Simple 7 and now Life’s Essential 8, we still have some issues.

Kazi: The big ones that come to mind are hypertension, diabetes, and obesity, all of which are trending in the wrong direction. Hypertension, we were gaining traction; and then over the past decade, we’ve slipped again. As you know, national blood pressure control rates have declined in many populations.

Harrington: Rather substantially.

Kazi: Substantially so, which has implications, in particular, for stroke rates in the future and stroke rates in young adults in the future. Obesity is a problem that we have very little control over. We’re already at 40% on average, which means that some populations are already in the 60% range.

Harrington: We also have obesity in kids — the burden, I’ll call it, of obesity. It’s not that you become obese in your thirties or your forties; you›re becoming obese as a teenager or even younger.

Kazi: Exactly. Since the 1990s, obesity in US adults has doubled, but obesity in US children has quadrupled. It’s starting from a lower base, but it’s very much an escalating problem.

Harrington: Diabetes is tightly linked to it but not totally explained.

Kazi: Exactly. The increase in diabetes is largely driven by obesity, but it›s probably also driven by changes in diet and lifestyle that don›t go through obesity.

Harrington: Yeah, it’s interesting. I think I have this figure correctly. It used to be rare that you saw a child with type 2 diabetes or what we call type 2 diabetes.

Kazi: Yeah.

Harrington: Now, the vast majority of kids with diabetes have type 2 diabetes.

Kazi: In the adolescents/young adults age group, most of it is type 2.

Harrington: Diabetes going up, obesity up, hypertension not well controlled, smoking combustible cigarettes way down.

Kazi: Yeah.

Harrington: Cholesterol levels. I was surprised. Cholesterol looked better. You said — because I was at a meeting where somebody asked you — that’s not explained by treatment.

Kazi: No, it’s not, at least going back to the ‘70s, but likely even sooner. I think that can only be attributed to substantial dietary changes. We are consuming less fat and less trans-fat. It’s possible that those collectively are improving our cholesterol levels, possibly at the expense of our glucose levels, because we basically substituted fats in our diet with more carbs at a population level.
 

Cigarettes and Vaping

Harrington: Some things certainly trend in the right direction but others in a really difficult direction. It’s going to lead to pretty large changes in risk for coronary disease, atrial fibrillation, and heart failure.

Kazi: I want to go back to the tobacco point. There are definitely marked declines in tobacco, still tightly related to income in the country. You see much higher prevalence of tobacco use in lower-income populations, but it’s unclear to me where it’s going in kids. We know that combustible tobacco use is going down but e-cigarettes went up. What that leads to over the next 30 years is unclear to me.

Harrington: That is a really important comment that’s worth sidebarring. The vaping use has been a terrible epidemic among our high schoolers. What is that going to lead to? Is it going to lead to the use of combustible cigarettes and we’re going to see that go back up? It remains to be seen.

Kazi: Yes, it remains to be seen. Going back to your point about this change in risk factors and this change in demographics, both aging and becoming a more diverse population means that we have large increases in some healthcare conditions.

Coronary heart disease goes up some, there›s a big jump in stroke — nearly a doubling in stroke — which is related to hypertension, obesity, an aging population, and a more diverse population. There are changes in stroke in the young, and atrial fibrillation related to, again, hypertension. We’re seeing these projections, and with them come these pretty large projections in changes in healthcare spending.
 

Healthcare Spending Not Sustainable

Harrington: Big. I mean, it’s not sustainable. Give the audience the number — it’s pretty frightening.

Kazi: We’re talking about a quadrupling of healthcare costs related to cardiovascular disease over 25 years. We’ve gotten used to the narrative that healthcare in the US is expensive and drugs are expensive, but this is an enormous problem — an unsustainable problem, like you called it.

It’s a doubling as a proportion of the economy. I was looking this up this morning. If the US healthcare economy were its own economy, it would be the fourth largest economy in the world.

Harrington: Healthcare as it is today, is it 21% of our economy?

Kazi: It’s 17% now. If it were its own economy, it would be the fourth largest in the world. We are spending more on healthcare than all but two other countries’ total economies. It’s kind of crazy.

Harrington: We’re talking about a quadrupling.

Kazi: Within that, the cardiovascular piece is a big piece, and we›re talking about a quadrupling.

Harrington: That’s both direct and indirect costs.

Kazi: The quadrupling of costs is just the direct costs. Indirect costs, for the listeners, refer to costs unrelated to healthcare but changes in productivity, either because people are disabled and unable to participate fully in the workforce or they die early.

The productivity costs are also increased substantially as a result. If you look at both healthcare and productivity, that goes up threefold. These are very large changes.

Harrington: Let’s now get to what we can do about it. I made the comment to you when I first read the papers that I was very depressed. Then, after I went through my Kübler-Ross stages of depression, death, and dying, I came to acceptance.

What are we going to do about it? This is a focus on policy, but also a focus on how we deliver healthcare, how we think about healthcare, and how we develop drugs and devices.

The drug question is going to be the one the audience is thinking about. They say, well, what about GLP-1 agonists? Aren’t those going to save the day?

Kazi: Yes and no. I’ll say that, early in my career, I used to be very attracted to simple solutions to complex problems. I’ve come to realize that simple solutions are elegant, attractive, and wrong. We›re dealing with a very complex issue and I think we’re going to need a multipronged approach.

The way I think about it is that there was a group of people who are at very high risk today. How do we help those individuals? Then how do we help the future generation so that they’re not dealing with the projections that we’re talking about.

My colleague, Karen Joynt Maddox, who led one of the papers, as you mentioned, has an elegant line in the paper where she says projections are not destiny. These are things we can change.

Harrington: If nothing changes, this is what it’s going to look like.

Kazi: This is where we’re headed.

Harrington: We can change. We’ve got some time to change, but we don’t have forever.

Kazi: Yes, exactly. We picked the 25-year timeline instead of a “let’s plan for the next century” timeline because we want something concrete and actionable. It’s close enough to be meaningful but far enough to give us the runway we need to act.

Harrington: Give me two things from the policy perspective, because it’s mostly policy.

Kazi: There are policy and clinical interventions. From the policy perspective, if I had to list two things, one is expansion of access to care. As we talk about this big increase in the burden of disease and risk factors, if you have a large proportion of your population that has hypertension or diabetes, you’re going to have to expand access to care to ensure that people get treated so they can get access to this care before they develop the complications that we worry about, like stroke and heart disease, that are very expensive to treat downstream.

The second, more broadly related to access to care, is the access to medications that are effective. You bring up GLP-1s. I think we need a real strategy for how we can give people access to GLP-1s at a price that is affordable to individuals but also affordable to the health system, and to help them stay on the drugs.

GLP-1s are transformative in what they do for weight loss and for diabetes, but more than 50% of people who start one are off it at 12 months. There’s something fundamentally wrong about how we’re delivering GLP-1s today. It’s not just about the cost of the drugs but the support system people need to stay on.

Harrington: I’ve made the comment, in many forms now, that we know the drugs work. We have to figure out how to use them.

Kazi: Exactly, yes.

Harrington: Using them includes chronicity. This is a chronic condition. Some people can come off the drugs, but many can’t. We’re going to have to figure this out, and maybe the newer generations of drugs will help us address what people call the off-ramping. How are we going to do that? I think you’re spot-on. Those are critically important questions.

Kazi: As we looked at this modeling, I’ll tell you — I had a come-to-Jesus moment where I was like, there is no way to fix cardiovascular disease in the US without going through obesity and diabetes. We have to address obesity in the US. We can’t just treat our way out of it. Obesity is fundamentally a food problem and we’ve got to engage again with food policy in a meaningful way.

Harrington: As you know, with the American Heart Association, we›re doing a large amount of work now on food as medicine and food is medicine. We are trying to figure out what the levers are that we can pull to actually help people eat healthier diets.

Kazi: Yes. Rather than framing it as an individual choice that people are eating poorly, it’s, how do we make healthy diets the default in the environment?

Harrington: This is where you get to the children as well.

Kazi: Exactly.

Harrington: I could talk about this all day. I’ve had the benefit of reading the papers now a few times and talking to you on several occasions. Thank you for joining us.

Kazi: Thank you.
 

Dr. Harrington, Stephen and Suzanne Weiss Dean, Weill Cornell Medicine; Provost for Medical Affairs, Cornell University, New York, NY, disclosed ties with Baim Institute (DSMB); CSL (RCT Executive Committee); Janssen (RCT Char), NHLBI (RCT Executive Committee, DSMB Chair); PCORI (RCT Co-Chair); DCRI, Atropos Health; Bitterroot Bio; Bristol Myers Squibb; BridgeBio; Element Science; Edwards Lifesciences; Foresite Labs; Medscape/WebMD Board of Directors for: American Heart Association; College of the Holy Cross; and Cytokinetics. Dr. Kazi, Associate Director, Smith Center for Outcomes Research, Associate Professor, Department of Medicine (Cardiology), Harvard Medical School, Director, Department of Cardiac Critical Care Unit, Beth Israel Deaconess Medical Center, Boston, Massachusetts, has disclosed receiving a research grant from Boston Scientific (grant to examine the economics of stroke prevention).

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity .

Robert A. Harrington, MD: I’m here in London at the European Society of Cardiology meetings, at theheart.org | Medscape Cardiology booth, using the meetings as an opportunity to meet with colleagues to talk about recent things that they’ve been writing about.

Today I’m joined by a good friend and colleague, Dr. Dhruv Kazi from Beth Israel Deaconess in Boston. Thanks for joining us.

Dhruv S. Kazi, MD, MS: Thank you for having me.

Harrington: Dr. Kazi is an associate professor of medicine at Harvard Medical School. He’s also the associate director of the Smith Center, which is an outcomes research center at the Beth Israel Deaconess. Thanks for joining us.

Kazi: Excited to be here.

Harrington: The topic I think you know that I want to discuss is a really important paper. There are two papers. They’re part of the American Heart Association’s 100th anniversary celebration, if you will. Many of the papers looked back at where science taken us.

With your coauthor, Karen Joynt Maddox, your papers are looking forward. They’re about the burden of cardiovascular disease in 2050. One paper really focused on what I would call the clinical and public health issues. Yours is focused on the economics. Is that a good description?

Kazi: Perfect.

Harrington: Tell us what you, Karen, and the other writers set out to do. What were you asked to do?

Kazi: As you know, the American Heart Association is entering its second century. Part of this was an exercise to say, where will the country be in 2050, which is a long enough time horizon for us to start planning for the future. What are the conditions that affect the magnitude of the disease, and the kinds of people who will be affected, that we should be aware of?

We looked back and said, if prior trends remain the same, where will we be in 2050, accounting for changes in demographics, changes in the composition of the population, and knowing that some of the cardiovascular risk factors are getting worse?

Harrington: For me, what was really striking is that, when I first saw the title and read “2050,” I thought, Oh, that’s a long way away. Then as I started reading it, I realized that this is not so far away.

Kazi: Absolutely.

Harrington: If we’re going to make a difference, it might take us 25 years.

Kazi: Especially if we set ourselves ambitious goals, we›re going to have to dig deep. Business-as-usual is not going to get us there.

Harrington: No. What I think has happened is we›ve spent so much time taking care of acute illness. Case fatality rates are fantastic. I was actually making the comment yesterday to a colleague that when I was an intern, the 30-day death rate from acute myocardial infarction was about 20%.

Kazi: Oh, wow.

Harrington: Now it’s 5%. That’s a big difference in a career.
 

Trends in the Wrong Direction

Kazi: There are fundamental trends. The decline in case fatalities is a really positive development, and I would hope that, going forward, that would continue. Those are risk-adjusted death rates and what is happening is that risk is going up. This is a function of the fact that the US population is aging; 2030 will be the first year that all the baby boomers will be over the age of 65.

By the mid-2030s, we’ll have more adults over the age of 65 than kids. That aging of the population is going to increase risk. The second is — and this is a positive development — we are a more diverse population, but the populations that are minoritized have higher cardiovascular risk, for a variety of reasons.

As the population of Asian Americans increases and doubles, in fact, as the population of Hispanic Americans doubles, we’re going to see an increase in risk related to cardiovascular disease. The third is that, over the past decade, there are some risk factors that are going in the wrong direction.

Harrington: Let’s talk about that because that’s humbling. I’m involved, as you know, with the American Heart Association, as are you. Despite all the work on Life’s Simple 7 and now Life’s Essential 8, we still have some issues.

Kazi: The big ones that come to mind are hypertension, diabetes, and obesity, all of which are trending in the wrong direction. Hypertension, we were gaining traction; and then over the past decade, we’ve slipped again. As you know, national blood pressure control rates have declined in many populations.

Harrington: Rather substantially.

Kazi: Substantially so, which has implications, in particular, for stroke rates in the future and stroke rates in young adults in the future. Obesity is a problem that we have very little control over. We’re already at 40% on average, which means that some populations are already in the 60% range.

Harrington: We also have obesity in kids — the burden, I’ll call it, of obesity. It’s not that you become obese in your thirties or your forties; you›re becoming obese as a teenager or even younger.

Kazi: Exactly. Since the 1990s, obesity in US adults has doubled, but obesity in US children has quadrupled. It’s starting from a lower base, but it’s very much an escalating problem.

Harrington: Diabetes is tightly linked to it but not totally explained.

Kazi: Exactly. The increase in diabetes is largely driven by obesity, but it›s probably also driven by changes in diet and lifestyle that don›t go through obesity.

Harrington: Yeah, it’s interesting. I think I have this figure correctly. It used to be rare that you saw a child with type 2 diabetes or what we call type 2 diabetes.

Kazi: Yeah.

Harrington: Now, the vast majority of kids with diabetes have type 2 diabetes.

Kazi: In the adolescents/young adults age group, most of it is type 2.

Harrington: Diabetes going up, obesity up, hypertension not well controlled, smoking combustible cigarettes way down.

Kazi: Yeah.

Harrington: Cholesterol levels. I was surprised. Cholesterol looked better. You said — because I was at a meeting where somebody asked you — that’s not explained by treatment.

Kazi: No, it’s not, at least going back to the ‘70s, but likely even sooner. I think that can only be attributed to substantial dietary changes. We are consuming less fat and less trans-fat. It’s possible that those collectively are improving our cholesterol levels, possibly at the expense of our glucose levels, because we basically substituted fats in our diet with more carbs at a population level.
 

Cigarettes and Vaping

Harrington: Some things certainly trend in the right direction but others in a really difficult direction. It’s going to lead to pretty large changes in risk for coronary disease, atrial fibrillation, and heart failure.

Kazi: I want to go back to the tobacco point. There are definitely marked declines in tobacco, still tightly related to income in the country. You see much higher prevalence of tobacco use in lower-income populations, but it’s unclear to me where it’s going in kids. We know that combustible tobacco use is going down but e-cigarettes went up. What that leads to over the next 30 years is unclear to me.

Harrington: That is a really important comment that’s worth sidebarring. The vaping use has been a terrible epidemic among our high schoolers. What is that going to lead to? Is it going to lead to the use of combustible cigarettes and we’re going to see that go back up? It remains to be seen.

Kazi: Yes, it remains to be seen. Going back to your point about this change in risk factors and this change in demographics, both aging and becoming a more diverse population means that we have large increases in some healthcare conditions.

Coronary heart disease goes up some, there›s a big jump in stroke — nearly a doubling in stroke — which is related to hypertension, obesity, an aging population, and a more diverse population. There are changes in stroke in the young, and atrial fibrillation related to, again, hypertension. We’re seeing these projections, and with them come these pretty large projections in changes in healthcare spending.
 

Healthcare Spending Not Sustainable

Harrington: Big. I mean, it’s not sustainable. Give the audience the number — it’s pretty frightening.

Kazi: We’re talking about a quadrupling of healthcare costs related to cardiovascular disease over 25 years. We’ve gotten used to the narrative that healthcare in the US is expensive and drugs are expensive, but this is an enormous problem — an unsustainable problem, like you called it.

It’s a doubling as a proportion of the economy. I was looking this up this morning. If the US healthcare economy were its own economy, it would be the fourth largest economy in the world.

Harrington: Healthcare as it is today, is it 21% of our economy?

Kazi: It’s 17% now. If it were its own economy, it would be the fourth largest in the world. We are spending more on healthcare than all but two other countries’ total economies. It’s kind of crazy.

Harrington: We’re talking about a quadrupling.

Kazi: Within that, the cardiovascular piece is a big piece, and we›re talking about a quadrupling.

Harrington: That’s both direct and indirect costs.

Kazi: The quadrupling of costs is just the direct costs. Indirect costs, for the listeners, refer to costs unrelated to healthcare but changes in productivity, either because people are disabled and unable to participate fully in the workforce or they die early.

The productivity costs are also increased substantially as a result. If you look at both healthcare and productivity, that goes up threefold. These are very large changes.

Harrington: Let’s now get to what we can do about it. I made the comment to you when I first read the papers that I was very depressed. Then, after I went through my Kübler-Ross stages of depression, death, and dying, I came to acceptance.

What are we going to do about it? This is a focus on policy, but also a focus on how we deliver healthcare, how we think about healthcare, and how we develop drugs and devices.

The drug question is going to be the one the audience is thinking about. They say, well, what about GLP-1 agonists? Aren’t those going to save the day?

Kazi: Yes and no. I’ll say that, early in my career, I used to be very attracted to simple solutions to complex problems. I’ve come to realize that simple solutions are elegant, attractive, and wrong. We›re dealing with a very complex issue and I think we’re going to need a multipronged approach.

The way I think about it is that there was a group of people who are at very high risk today. How do we help those individuals? Then how do we help the future generation so that they’re not dealing with the projections that we’re talking about.

My colleague, Karen Joynt Maddox, who led one of the papers, as you mentioned, has an elegant line in the paper where she says projections are not destiny. These are things we can change.

Harrington: If nothing changes, this is what it’s going to look like.

Kazi: This is where we’re headed.

Harrington: We can change. We’ve got some time to change, but we don’t have forever.

Kazi: Yes, exactly. We picked the 25-year timeline instead of a “let’s plan for the next century” timeline because we want something concrete and actionable. It’s close enough to be meaningful but far enough to give us the runway we need to act.

Harrington: Give me two things from the policy perspective, because it’s mostly policy.

Kazi: There are policy and clinical interventions. From the policy perspective, if I had to list two things, one is expansion of access to care. As we talk about this big increase in the burden of disease and risk factors, if you have a large proportion of your population that has hypertension or diabetes, you’re going to have to expand access to care to ensure that people get treated so they can get access to this care before they develop the complications that we worry about, like stroke and heart disease, that are very expensive to treat downstream.

The second, more broadly related to access to care, is the access to medications that are effective. You bring up GLP-1s. I think we need a real strategy for how we can give people access to GLP-1s at a price that is affordable to individuals but also affordable to the health system, and to help them stay on the drugs.

GLP-1s are transformative in what they do for weight loss and for diabetes, but more than 50% of people who start one are off it at 12 months. There’s something fundamentally wrong about how we’re delivering GLP-1s today. It’s not just about the cost of the drugs but the support system people need to stay on.

Harrington: I’ve made the comment, in many forms now, that we know the drugs work. We have to figure out how to use them.

Kazi: Exactly, yes.

Harrington: Using them includes chronicity. This is a chronic condition. Some people can come off the drugs, but many can’t. We’re going to have to figure this out, and maybe the newer generations of drugs will help us address what people call the off-ramping. How are we going to do that? I think you’re spot-on. Those are critically important questions.

Kazi: As we looked at this modeling, I’ll tell you — I had a come-to-Jesus moment where I was like, there is no way to fix cardiovascular disease in the US without going through obesity and diabetes. We have to address obesity in the US. We can’t just treat our way out of it. Obesity is fundamentally a food problem and we’ve got to engage again with food policy in a meaningful way.

Harrington: As you know, with the American Heart Association, we›re doing a large amount of work now on food as medicine and food is medicine. We are trying to figure out what the levers are that we can pull to actually help people eat healthier diets.

Kazi: Yes. Rather than framing it as an individual choice that people are eating poorly, it’s, how do we make healthy diets the default in the environment?

Harrington: This is where you get to the children as well.

Kazi: Exactly.

Harrington: I could talk about this all day. I’ve had the benefit of reading the papers now a few times and talking to you on several occasions. Thank you for joining us.

Kazi: Thank you.
 

Dr. Harrington, Stephen and Suzanne Weiss Dean, Weill Cornell Medicine; Provost for Medical Affairs, Cornell University, New York, NY, disclosed ties with Baim Institute (DSMB); CSL (RCT Executive Committee); Janssen (RCT Char), NHLBI (RCT Executive Committee, DSMB Chair); PCORI (RCT Co-Chair); DCRI, Atropos Health; Bitterroot Bio; Bristol Myers Squibb; BridgeBio; Element Science; Edwards Lifesciences; Foresite Labs; Medscape/WebMD Board of Directors for: American Heart Association; College of the Holy Cross; and Cytokinetics. Dr. Kazi, Associate Director, Smith Center for Outcomes Research, Associate Professor, Department of Medicine (Cardiology), Harvard Medical School, Director, Department of Cardiac Critical Care Unit, Beth Israel Deaconess Medical Center, Boston, Massachusetts, has disclosed receiving a research grant from Boston Scientific (grant to examine the economics of stroke prevention).

A version of this article appeared on Medscape.com.

TOPLINE:

Stroke rates in Californians with sickle cell disease (SCD) have increased in both children and adults in the post-STOP era. The cumulative incidence of first ischemic stroke was 2.1% by age 20 and 13.5% by age 60.

METHODOLOGY:

• Researchers analyzed data from the California Department of Health Care Access and Innovation (HCAI), covering emergency department and hospitalization records from 1991 to 2019.
• A total of 7636 patients with SCD were included in the study cohort.
• Cumulative incidence and rates for primary and recurrent strokes and transient ischemic attacks (TIAs) were determined pre- and post STOP trial.
• Patients with SCD were identified using ICD-9 and ICD-10 codes, with specific criteria for inclusion based on hospitalization records.
• The study utilized Fine and Gray methodology to calculate cumulative incidence functions, accounting for the competing risk for death.

TAKEAWAY:

• The cumulative incidence of first ischemic stroke in patients with SCD was 2.1% by age 20 and 13.5% by age 60.
• Ischemic stroke rates increased significantly in children and adults in the 2010-2019 period, compared with the preceding decade.
• Risk factors for stroke and TIA included increasing age, hypertension, and hyperlipidemia.
• The study found a significant increase in rates of intracranial hemorrhage in adults aged 18-30 years and TIAs in children younger than 18 years from 2010 to 2019, compared with the prior decade.

IN PRACTICE:

“Neurovascular complications, including strokes and transient ischemic attacks (TIAs), are common and cause significant morbidity in individuals with sickle cell disease (SCD). The STOP trial (1998) established chronic transfusions as the standard of care for children with SCD at high risk for stroke,” the study’s authors wrote.

SOURCE:

This study was led by Olubusola B. Oluwole, MD, MS, University of Pittsburgh in Pennsylvania, and was published online in Blood.

LIMITATIONS:

This study’s reliance on administrative data may have introduced systematic errors, particularly with the transition from ICD-9 to ICD-10 codes. The lack of laboratory results and medication data in the HCAI database limited the ability to fully assess patient conditions and treatments. Additionally, the methodology changes in 2014 likely underreported death rates in people without PDD/EDU encounters in the calendar year preceding their death.

DISCLOSURES:

The authors reported no relevant 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:

Stroke rates in Californians with sickle cell disease (SCD) have increased in both children and adults in the post-STOP era. The cumulative incidence of first ischemic stroke was 2.1% by age 20 and 13.5% by age 60.

METHODOLOGY:

• Researchers analyzed data from the California Department of Health Care Access and Innovation (HCAI), covering emergency department and hospitalization records from 1991 to 2019.
• A total of 7636 patients with SCD were included in the study cohort.
• Cumulative incidence and rates for primary and recurrent strokes and transient ischemic attacks (TIAs) were determined pre- and post STOP trial.
• Patients with SCD were identified using ICD-9 and ICD-10 codes, with specific criteria for inclusion based on hospitalization records.
• The study utilized Fine and Gray methodology to calculate cumulative incidence functions, accounting for the competing risk for death.

TAKEAWAY:

• The cumulative incidence of first ischemic stroke in patients with SCD was 2.1% by age 20 and 13.5% by age 60.
• Ischemic stroke rates increased significantly in children and adults in the 2010-2019 period, compared with the preceding decade.
• Risk factors for stroke and TIA included increasing age, hypertension, and hyperlipidemia.
• The study found a significant increase in rates of intracranial hemorrhage in adults aged 18-30 years and TIAs in children younger than 18 years from 2010 to 2019, compared with the prior decade.

IN PRACTICE:

“Neurovascular complications, including strokes and transient ischemic attacks (TIAs), are common and cause significant morbidity in individuals with sickle cell disease (SCD). The STOP trial (1998) established chronic transfusions as the standard of care for children with SCD at high risk for stroke,” the study’s authors wrote.

SOURCE:

This study was led by Olubusola B. Oluwole, MD, MS, University of Pittsburgh in Pennsylvania, and was published online in Blood.

LIMITATIONS:

This study’s reliance on administrative data may have introduced systematic errors, particularly with the transition from ICD-9 to ICD-10 codes. The lack of laboratory results and medication data in the HCAI database limited the ability to fully assess patient conditions and treatments. Additionally, the methodology changes in 2014 likely underreported death rates in people without PDD/EDU encounters in the calendar year preceding their death.

DISCLOSURES:

The authors reported no relevant 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:

Stroke rates in Californians with sickle cell disease (SCD) have increased in both children and adults in the post-STOP era. The cumulative incidence of first ischemic stroke was 2.1% by age 20 and 13.5% by age 60.

METHODOLOGY:

• Researchers analyzed data from the California Department of Health Care Access and Innovation (HCAI), covering emergency department and hospitalization records from 1991 to 2019.
• A total of 7636 patients with SCD were included in the study cohort.
• Cumulative incidence and rates for primary and recurrent strokes and transient ischemic attacks (TIAs) were determined pre- and post STOP trial.
• Patients with SCD were identified using ICD-9 and ICD-10 codes, with specific criteria for inclusion based on hospitalization records.
• The study utilized Fine and Gray methodology to calculate cumulative incidence functions, accounting for the competing risk for death.

TAKEAWAY:

• The cumulative incidence of first ischemic stroke in patients with SCD was 2.1% by age 20 and 13.5% by age 60.
• Ischemic stroke rates increased significantly in children and adults in the 2010-2019 period, compared with the preceding decade.
• Risk factors for stroke and TIA included increasing age, hypertension, and hyperlipidemia.
• The study found a significant increase in rates of intracranial hemorrhage in adults aged 18-30 years and TIAs in children younger than 18 years from 2010 to 2019, compared with the prior decade.

IN PRACTICE:

“Neurovascular complications, including strokes and transient ischemic attacks (TIAs), are common and cause significant morbidity in individuals with sickle cell disease (SCD). The STOP trial (1998) established chronic transfusions as the standard of care for children with SCD at high risk for stroke,” the study’s authors wrote.

SOURCE:

This study was led by Olubusola B. Oluwole, MD, MS, University of Pittsburgh in Pennsylvania, and was published online in Blood.

LIMITATIONS:

This study’s reliance on administrative data may have introduced systematic errors, particularly with the transition from ICD-9 to ICD-10 codes. The lack of laboratory results and medication data in the HCAI database limited the ability to fully assess patient conditions and treatments. Additionally, the methodology changes in 2014 likely underreported death rates in people without PDD/EDU encounters in the calendar year preceding their death.

DISCLOSURES:

The authors reported no relevant 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.

ABU DHABI, UAE — The long-standing debate as to when to start anticoagulation in patients with an acute ischemic stroke and atrial fibrillation (AF) looks as though it’s settled.

Results of the OPTIMAS trial, the largest trial to address this question, showed that initiation of a direct oral anticoagulant (DOAC) within 4 days after ischemic stroke associated with AF was noninferior to delayed initiation (7-14 days) for the composite outcome of ischemic stroke, intracranial hemorrhage, unclassifiable stroke, or systemic embolism at 90 days. Importantly, early DOAC initiation was safe with a low rate of symptomatic hemorrhage, regardless of stroke severity.

In addition, a new meta-analysis, known as CATALYST, which included all four randomized trials now available on this issue, showed a clear benefit of earlier initiation (within 4 days) versus later (5 days and up) on its primary endpoint of new ischemic stroke, symptomatic intracerebral hemorrhage, and unclassified stroke at 30 days.

The results of the OPTIMAS trial and the meta-analysis were both presented at the 16th World Stroke Congress (WSC) 2024. The OPTIMAS trial was also simultaneously published online in The Lancet.

“Our findings do not support the guideline recommended practice of delaying DOAC initiation after ischemic stroke with AF regardless of clinical stroke severity, reperfusion or prior anticoagulation,” said OPTIMAS investigator David Werring, PhD, University College London in England.

Presenting the meta-analysis, Signild Åsberg, MD, Uppsala University, Uppsala, Sweden, said his group’s findings “support the early start of DOACs (within 4 days) in clinical practice.”

Werring pointed out that starting anticoagulation early also had important logistical advantages.

“This means we can start anticoagulation before patients are discharged from hospital, thus ensuring that this important secondary prevention medication is always prescribed, when appropriate. That’s going to be a key benefit in the real world.”
 

Clinical Dilemma

Werring noted that AF accounts for 20%-30% of ischemic strokes, which tend to be more severe than other stroke types. The pivotal trials of DOACs did not include patients within 30 days of an acute ischemic stroke, creating a clinical dilemma on when to start this treatment.

“On the one hand, we wish to start anticoagulation early to reduce early recurrence of ischemic stroke. But on the other hand, there are concerns that if we start anticoagulation early, it could cause intracranial bleeding, including hemorrhagic transformation of the acute infarct. Guidelines on this issue are inconsistent and have called for randomized control trials in this area,” he noted.

So far, three randomized trials on DOAC timing have been conducted, which Werring said suggested early DOAC treatment is safe. However, these trials have provided limited data on moderate to severe stroke, patients with hemorrhagic transformation, or those already taking oral anticoagulants — subgroups in which there are particular concerns about early oral anticoagulation.

The OPTIMAS trial included a broad population of patients with acute ischemic stroke associated with AF including these critical subgroups.

The trial, conducted at 100 hospitals in the United Kingdom, included 3648 patients with AF and acute ischemic stroke who were randomly assigned to early (≤ 4 days from stroke symptom onset) or delayed (7-14 days) anticoagulation initiation with any DOAC.

There was no restriction on stroke severity, and patients with hemorrhagic transformation were allowed, with the exception of parenchymal hematoma type 2, a rare and severe type of hemorrhagic transformation.

Approximately 35% of patients had been taking an oral anticoagulant, mainly DOACs, prior to their stroke, and about 30% had revascularization with thrombolysis, thrombectomy, or both. Nearly 900 participants (25%) had moderate to severe stroke (National Institutes of Health Stroke Scale [NIHSS] score ≥ 11).

The primary outcome was a composite of recurrent ischemic stroke, symptomatic intracranial hemorrhage, unclassifiable stroke, or systemic embolism incidence at 90 days. The initial analysis aimed to show noninferiority of early DOAC initiation, with a noninferiority margin of 2 percentage points, followed by testing for superiority.

Results showed that the primary outcome occurred in 3.3% of both groups (adjusted risk difference, 0.000; 95% CI, −0.011 to 0.012), with noninferiority criteria fulfilled. Superiority was not achieved.

Symptomatic intracranial hemorrhage occurred in 0.6% of patients in the early DOAC initiation group vs 0.7% of those in the delayed group — a nonsignificant difference.
 

Applicable to Real-World Practice

A time-to-event analysis of the primary outcome showed that there were fewer outcomes in the first 30 days in the early DOAC initiation group, but the curves subsequently came together.

Subgroup analysis showed consistent results across all whole trial population, with no modification of the effect of early DOAC initiation according to stroke severity, reperfusion treatment, or previous anticoagulation.

Werring said that strengths of the OPTIMAS trial included a large sample size, a broad population with generalizability to real-world practice, and the inclusion of patients at higher bleeding risk than included in previous studies.

During the discussion, it was noted that the trial included few (about 3%) patients — about 3% — with very severe stroke (NIHSS score > 21), with the question of whether the findings could be applied to this group.

Werring noted that there was no evidence of heterogeneity, and if anything, patients with more severe strokes may have had a slightly greater benefit with early DOAC initiation. “So my feeling is probably these results do generalize to the more severe patients,” he said.

In a commentary accompanying The Lancet publication of the OPTIMAS trial, Else Charlotte Sandset, MD, University of Oslo, in Norway, and Diana Aguiar de Sousa, MD, Central Lisbon University Hospital Centre, Lisbon, Portugal, noted that the “increasing body of evidence strongly supports the message that initiating anticoagulation early for patients with ischaemic stroke is safe. The consistent absence of heterogeneity in safety outcomes suggests that the risk of symptomatic intracranial haemorrhage is not a major concern, even in patients with large infarcts.”

Regardless of the size of the treatment effect, initiating early anticoagulation makes sense when it can be done safely, as it helps prevent recurrent ischemic strokes and other embolic events. Early intervention reduces embolization risk, particularly in high-risk patients, and allows secondary prevention measures to begin while patients are still hospitalized, they added.
 

CATALYST Findings

The CATALYST meta-analysis included four trials, namely, TIMING, ELAN, OPTIMAS, and START, of early versus later DOAC administration in a total of 5411 patients with acute ischemic stroke and AF. In this meta-analysis, early was defined as within 4 days of stroke and later as 5 days or more.

The primary outcome was a composite of ischemic stroke, symptomatic, intracerebral hemorrhage, or unclassified stroke at 30 days. This was significantly reduced in the early group (2.12%) versus 3.02% in the later group, giving an odds ratio of 0.70 (95% CI, 0.50-0.98; P =.04).

The results were consistent across all subgroups, all suggesting an advantage for early DOAC.

Further analysis showed a clear benefit of early DOAC initiation in ischemic stroke with the curves separating early.

The rate of symptomatic intracerebral hemorrhage was low in both groups (0.45% in the early group and 0.40% in the later group) as was extracranial hemorrhage (0.45% vs 0.55%).

At 90 days, there were still lower event rates in the early group than the later one, but the difference was no longer statistically significant.
 

‘Practice Changing’ Results

Commenting on both studies, chair of the WSC session where the results of both OPTIMAS trial and the meta-analysis were presented, Craig Anderson, MD, The George Institute for Global Health, Sydney, Australia, described these latest results as “practice changing.”

“When to start anticoagulation in acute ischemic stroke patients with AF has been uncertain for a long time. The dogma has always been that we should wait. Over the years, we’ve become a little bit more confident, but now we’ve got good data from randomized trials showing that early initiation is safe, with the meta-analysis showing benefit,” he said.

“These new data from OPTIMAS will reassure clinicians that there’s no excessive harm and, more importantly, no excessive harm across all patient groups. And the meta-analysis clearly showed an upfront benefit of starting anticoagulation early. That’s a very convincing result,” he added.

Anderson cautioned that there still may be concerns about starting DOACs early in some groups, including Asian populations that have a higher bleeding risk (these trials included predominantly White patients) and people who are older or frail, who may have extensive small vessel disease.

During the discussion, several questions centered on the lack of imaging data available on the patients in the studies. Anderson said imaging data would help reassure clinicians on the safety of early anticoagulation in patients with large infarcts.

“Stroke clinicians make decisions on the basis of the patient and on the basis of the brain, and we only have the patient information at the moment. We don’t have information on the brain — that comes from imaging.”

Regardless, he believes these new data will lead to a shift in practice. “But maybe, it won’t be as dramatic as we would hope because I think some clinicians may still hesitate to apply these results to patients at high risk of bleeding. With imaging data from the studies that might change.”

The OPTIMAS trial was funded by University College London and the British Heart Foundation. Werring reported consulting fees from Novo Nordisk, National Institute for Health and Care Excellence, and Alnylam; payments or speaker honoraria from Novo Nordisk, Bayer, and AstraZeneca/Alexion; participation on a data safety monitoring board for the OXHARP trial; and participation as steering committee chair for the MACE-ICH and PLINTH trials. Åsberg received institutional research grants and lecture fees to her institution from AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, and Institut Produits Synthése. Sandset and de Sousa were both steering committee members of the ELAN trial. Anderson reported grant funding from Penumbra and Takeda China.
 

A version of this article appeared on Medscape.com.

ABU DHABI, UAE — The long-standing debate as to when to start anticoagulation in patients with an acute ischemic stroke and atrial fibrillation (AF) looks as though it’s settled.

Results of the OPTIMAS trial, the largest trial to address this question, showed that initiation of a direct oral anticoagulant (DOAC) within 4 days after ischemic stroke associated with AF was noninferior to delayed initiation (7-14 days) for the composite outcome of ischemic stroke, intracranial hemorrhage, unclassifiable stroke, or systemic embolism at 90 days. Importantly, early DOAC initiation was safe with a low rate of symptomatic hemorrhage, regardless of stroke severity.

In addition, a new meta-analysis, known as CATALYST, which included all four randomized trials now available on this issue, showed a clear benefit of earlier initiation (within 4 days) versus later (5 days and up) on its primary endpoint of new ischemic stroke, symptomatic intracerebral hemorrhage, and unclassified stroke at 30 days.

The results of the OPTIMAS trial and the meta-analysis were both presented at the 16th World Stroke Congress (WSC) 2024. The OPTIMAS trial was also simultaneously published online in The Lancet.

“Our findings do not support the guideline recommended practice of delaying DOAC initiation after ischemic stroke with AF regardless of clinical stroke severity, reperfusion or prior anticoagulation,” said OPTIMAS investigator David Werring, PhD, University College London in England.

Presenting the meta-analysis, Signild Åsberg, MD, Uppsala University, Uppsala, Sweden, said his group’s findings “support the early start of DOACs (within 4 days) in clinical practice.”

Werring pointed out that starting anticoagulation early also had important logistical advantages.

“This means we can start anticoagulation before patients are discharged from hospital, thus ensuring that this important secondary prevention medication is always prescribed, when appropriate. That’s going to be a key benefit in the real world.”
 

Clinical Dilemma

Werring noted that AF accounts for 20%-30% of ischemic strokes, which tend to be more severe than other stroke types. The pivotal trials of DOACs did not include patients within 30 days of an acute ischemic stroke, creating a clinical dilemma on when to start this treatment.

“On the one hand, we wish to start anticoagulation early to reduce early recurrence of ischemic stroke. But on the other hand, there are concerns that if we start anticoagulation early, it could cause intracranial bleeding, including hemorrhagic transformation of the acute infarct. Guidelines on this issue are inconsistent and have called for randomized control trials in this area,” he noted.

So far, three randomized trials on DOAC timing have been conducted, which Werring said suggested early DOAC treatment is safe. However, these trials have provided limited data on moderate to severe stroke, patients with hemorrhagic transformation, or those already taking oral anticoagulants — subgroups in which there are particular concerns about early oral anticoagulation.

The OPTIMAS trial included a broad population of patients with acute ischemic stroke associated with AF including these critical subgroups.

The trial, conducted at 100 hospitals in the United Kingdom, included 3648 patients with AF and acute ischemic stroke who were randomly assigned to early (≤ 4 days from stroke symptom onset) or delayed (7-14 days) anticoagulation initiation with any DOAC.

There was no restriction on stroke severity, and patients with hemorrhagic transformation were allowed, with the exception of parenchymal hematoma type 2, a rare and severe type of hemorrhagic transformation.

Approximately 35% of patients had been taking an oral anticoagulant, mainly DOACs, prior to their stroke, and about 30% had revascularization with thrombolysis, thrombectomy, or both. Nearly 900 participants (25%) had moderate to severe stroke (National Institutes of Health Stroke Scale [NIHSS] score ≥ 11).

The primary outcome was a composite of recurrent ischemic stroke, symptomatic intracranial hemorrhage, unclassifiable stroke, or systemic embolism incidence at 90 days. The initial analysis aimed to show noninferiority of early DOAC initiation, with a noninferiority margin of 2 percentage points, followed by testing for superiority.

Results showed that the primary outcome occurred in 3.3% of both groups (adjusted risk difference, 0.000; 95% CI, −0.011 to 0.012), with noninferiority criteria fulfilled. Superiority was not achieved.

Symptomatic intracranial hemorrhage occurred in 0.6% of patients in the early DOAC initiation group vs 0.7% of those in the delayed group — a nonsignificant difference.
 

Applicable to Real-World Practice

A time-to-event analysis of the primary outcome showed that there were fewer outcomes in the first 30 days in the early DOAC initiation group, but the curves subsequently came together.

Subgroup analysis showed consistent results across all whole trial population, with no modification of the effect of early DOAC initiation according to stroke severity, reperfusion treatment, or previous anticoagulation.

Werring said that strengths of the OPTIMAS trial included a large sample size, a broad population with generalizability to real-world practice, and the inclusion of patients at higher bleeding risk than included in previous studies.

During the discussion, it was noted that the trial included few (about 3%) patients — about 3% — with very severe stroke (NIHSS score > 21), with the question of whether the findings could be applied to this group.

Werring noted that there was no evidence of heterogeneity, and if anything, patients with more severe strokes may have had a slightly greater benefit with early DOAC initiation. “So my feeling is probably these results do generalize to the more severe patients,” he said.

In a commentary accompanying The Lancet publication of the OPTIMAS trial, Else Charlotte Sandset, MD, University of Oslo, in Norway, and Diana Aguiar de Sousa, MD, Central Lisbon University Hospital Centre, Lisbon, Portugal, noted that the “increasing body of evidence strongly supports the message that initiating anticoagulation early for patients with ischaemic stroke is safe. The consistent absence of heterogeneity in safety outcomes suggests that the risk of symptomatic intracranial haemorrhage is not a major concern, even in patients with large infarcts.”

Regardless of the size of the treatment effect, initiating early anticoagulation makes sense when it can be done safely, as it helps prevent recurrent ischemic strokes and other embolic events. Early intervention reduces embolization risk, particularly in high-risk patients, and allows secondary prevention measures to begin while patients are still hospitalized, they added.
 

CATALYST Findings

The CATALYST meta-analysis included four trials, namely, TIMING, ELAN, OPTIMAS, and START, of early versus later DOAC administration in a total of 5411 patients with acute ischemic stroke and AF. In this meta-analysis, early was defined as within 4 days of stroke and later as 5 days or more.

The primary outcome was a composite of ischemic stroke, symptomatic, intracerebral hemorrhage, or unclassified stroke at 30 days. This was significantly reduced in the early group (2.12%) versus 3.02% in the later group, giving an odds ratio of 0.70 (95% CI, 0.50-0.98; P =.04).

The results were consistent across all subgroups, all suggesting an advantage for early DOAC.

Further analysis showed a clear benefit of early DOAC initiation in ischemic stroke with the curves separating early.

The rate of symptomatic intracerebral hemorrhage was low in both groups (0.45% in the early group and 0.40% in the later group) as was extracranial hemorrhage (0.45% vs 0.55%).

At 90 days, there were still lower event rates in the early group than the later one, but the difference was no longer statistically significant.
 

‘Practice Changing’ Results

Commenting on both studies, chair of the WSC session where the results of both OPTIMAS trial and the meta-analysis were presented, Craig Anderson, MD, The George Institute for Global Health, Sydney, Australia, described these latest results as “practice changing.”

“When to start anticoagulation in acute ischemic stroke patients with AF has been uncertain for a long time. The dogma has always been that we should wait. Over the years, we’ve become a little bit more confident, but now we’ve got good data from randomized trials showing that early initiation is safe, with the meta-analysis showing benefit,” he said.

“These new data from OPTIMAS will reassure clinicians that there’s no excessive harm and, more importantly, no excessive harm across all patient groups. And the meta-analysis clearly showed an upfront benefit of starting anticoagulation early. That’s a very convincing result,” he added.

Anderson cautioned that there still may be concerns about starting DOACs early in some groups, including Asian populations that have a higher bleeding risk (these trials included predominantly White patients) and people who are older or frail, who may have extensive small vessel disease.

During the discussion, several questions centered on the lack of imaging data available on the patients in the studies. Anderson said imaging data would help reassure clinicians on the safety of early anticoagulation in patients with large infarcts.

“Stroke clinicians make decisions on the basis of the patient and on the basis of the brain, and we only have the patient information at the moment. We don’t have information on the brain — that comes from imaging.”

Regardless, he believes these new data will lead to a shift in practice. “But maybe, it won’t be as dramatic as we would hope because I think some clinicians may still hesitate to apply these results to patients at high risk of bleeding. With imaging data from the studies that might change.”

The OPTIMAS trial was funded by University College London and the British Heart Foundation. Werring reported consulting fees from Novo Nordisk, National Institute for Health and Care Excellence, and Alnylam; payments or speaker honoraria from Novo Nordisk, Bayer, and AstraZeneca/Alexion; participation on a data safety monitoring board for the OXHARP trial; and participation as steering committee chair for the MACE-ICH and PLINTH trials. Åsberg received institutional research grants and lecture fees to her institution from AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, and Institut Produits Synthése. Sandset and de Sousa were both steering committee members of the ELAN trial. Anderson reported grant funding from Penumbra and Takeda China.
 

A version of this article appeared on Medscape.com.

ABU DHABI, UAE — The long-standing debate as to when to start anticoagulation in patients with an acute ischemic stroke and atrial fibrillation (AF) looks as though it’s settled.

Results of the OPTIMAS trial, the largest trial to address this question, showed that initiation of a direct oral anticoagulant (DOAC) within 4 days after ischemic stroke associated with AF was noninferior to delayed initiation (7-14 days) for the composite outcome of ischemic stroke, intracranial hemorrhage, unclassifiable stroke, or systemic embolism at 90 days. Importantly, early DOAC initiation was safe with a low rate of symptomatic hemorrhage, regardless of stroke severity.

In addition, a new meta-analysis, known as CATALYST, which included all four randomized trials now available on this issue, showed a clear benefit of earlier initiation (within 4 days) versus later (5 days and up) on its primary endpoint of new ischemic stroke, symptomatic intracerebral hemorrhage, and unclassified stroke at 30 days.

The results of the OPTIMAS trial and the meta-analysis were both presented at the 16th World Stroke Congress (WSC) 2024. The OPTIMAS trial was also simultaneously published online in The Lancet.

“Our findings do not support the guideline recommended practice of delaying DOAC initiation after ischemic stroke with AF regardless of clinical stroke severity, reperfusion or prior anticoagulation,” said OPTIMAS investigator David Werring, PhD, University College London in England.

Presenting the meta-analysis, Signild Åsberg, MD, Uppsala University, Uppsala, Sweden, said his group’s findings “support the early start of DOACs (within 4 days) in clinical practice.”

Werring pointed out that starting anticoagulation early also had important logistical advantages.

“This means we can start anticoagulation before patients are discharged from hospital, thus ensuring that this important secondary prevention medication is always prescribed, when appropriate. That’s going to be a key benefit in the real world.”
 

Clinical Dilemma

Werring noted that AF accounts for 20%-30% of ischemic strokes, which tend to be more severe than other stroke types. The pivotal trials of DOACs did not include patients within 30 days of an acute ischemic stroke, creating a clinical dilemma on when to start this treatment.

“On the one hand, we wish to start anticoagulation early to reduce early recurrence of ischemic stroke. But on the other hand, there are concerns that if we start anticoagulation early, it could cause intracranial bleeding, including hemorrhagic transformation of the acute infarct. Guidelines on this issue are inconsistent and have called for randomized control trials in this area,” he noted.

So far, three randomized trials on DOAC timing have been conducted, which Werring said suggested early DOAC treatment is safe. However, these trials have provided limited data on moderate to severe stroke, patients with hemorrhagic transformation, or those already taking oral anticoagulants — subgroups in which there are particular concerns about early oral anticoagulation.

The OPTIMAS trial included a broad population of patients with acute ischemic stroke associated with AF including these critical subgroups.

The trial, conducted at 100 hospitals in the United Kingdom, included 3648 patients with AF and acute ischemic stroke who were randomly assigned to early (≤ 4 days from stroke symptom onset) or delayed (7-14 days) anticoagulation initiation with any DOAC.

There was no restriction on stroke severity, and patients with hemorrhagic transformation were allowed, with the exception of parenchymal hematoma type 2, a rare and severe type of hemorrhagic transformation.

Approximately 35% of patients had been taking an oral anticoagulant, mainly DOACs, prior to their stroke, and about 30% had revascularization with thrombolysis, thrombectomy, or both. Nearly 900 participants (25%) had moderate to severe stroke (National Institutes of Health Stroke Scale [NIHSS] score ≥ 11).

The primary outcome was a composite of recurrent ischemic stroke, symptomatic intracranial hemorrhage, unclassifiable stroke, or systemic embolism incidence at 90 days. The initial analysis aimed to show noninferiority of early DOAC initiation, with a noninferiority margin of 2 percentage points, followed by testing for superiority.

Results showed that the primary outcome occurred in 3.3% of both groups (adjusted risk difference, 0.000; 95% CI, −0.011 to 0.012), with noninferiority criteria fulfilled. Superiority was not achieved.

Symptomatic intracranial hemorrhage occurred in 0.6% of patients in the early DOAC initiation group vs 0.7% of those in the delayed group — a nonsignificant difference.
 

Applicable to Real-World Practice

A time-to-event analysis of the primary outcome showed that there were fewer outcomes in the first 30 days in the early DOAC initiation group, but the curves subsequently came together.

Subgroup analysis showed consistent results across all whole trial population, with no modification of the effect of early DOAC initiation according to stroke severity, reperfusion treatment, or previous anticoagulation.

Werring said that strengths of the OPTIMAS trial included a large sample size, a broad population with generalizability to real-world practice, and the inclusion of patients at higher bleeding risk than included in previous studies.

During the discussion, it was noted that the trial included few (about 3%) patients — about 3% — with very severe stroke (NIHSS score > 21), with the question of whether the findings could be applied to this group.

Werring noted that there was no evidence of heterogeneity, and if anything, patients with more severe strokes may have had a slightly greater benefit with early DOAC initiation. “So my feeling is probably these results do generalize to the more severe patients,” he said.

In a commentary accompanying The Lancet publication of the OPTIMAS trial, Else Charlotte Sandset, MD, University of Oslo, in Norway, and Diana Aguiar de Sousa, MD, Central Lisbon University Hospital Centre, Lisbon, Portugal, noted that the “increasing body of evidence strongly supports the message that initiating anticoagulation early for patients with ischaemic stroke is safe. The consistent absence of heterogeneity in safety outcomes suggests that the risk of symptomatic intracranial haemorrhage is not a major concern, even in patients with large infarcts.”

Regardless of the size of the treatment effect, initiating early anticoagulation makes sense when it can be done safely, as it helps prevent recurrent ischemic strokes and other embolic events. Early intervention reduces embolization risk, particularly in high-risk patients, and allows secondary prevention measures to begin while patients are still hospitalized, they added.
 

CATALYST Findings

The CATALYST meta-analysis included four trials, namely, TIMING, ELAN, OPTIMAS, and START, of early versus later DOAC administration in a total of 5411 patients with acute ischemic stroke and AF. In this meta-analysis, early was defined as within 4 days of stroke and later as 5 days or more.

The primary outcome was a composite of ischemic stroke, symptomatic, intracerebral hemorrhage, or unclassified stroke at 30 days. This was significantly reduced in the early group (2.12%) versus 3.02% in the later group, giving an odds ratio of 0.70 (95% CI, 0.50-0.98; P =.04).

The results were consistent across all subgroups, all suggesting an advantage for early DOAC.

Further analysis showed a clear benefit of early DOAC initiation in ischemic stroke with the curves separating early.

The rate of symptomatic intracerebral hemorrhage was low in both groups (0.45% in the early group and 0.40% in the later group) as was extracranial hemorrhage (0.45% vs 0.55%).

At 90 days, there were still lower event rates in the early group than the later one, but the difference was no longer statistically significant.
 

‘Practice Changing’ Results

Commenting on both studies, chair of the WSC session where the results of both OPTIMAS trial and the meta-analysis were presented, Craig Anderson, MD, The George Institute for Global Health, Sydney, Australia, described these latest results as “practice changing.”

“When to start anticoagulation in acute ischemic stroke patients with AF has been uncertain for a long time. The dogma has always been that we should wait. Over the years, we’ve become a little bit more confident, but now we’ve got good data from randomized trials showing that early initiation is safe, with the meta-analysis showing benefit,” he said.

“These new data from OPTIMAS will reassure clinicians that there’s no excessive harm and, more importantly, no excessive harm across all patient groups. And the meta-analysis clearly showed an upfront benefit of starting anticoagulation early. That’s a very convincing result,” he added.

Anderson cautioned that there still may be concerns about starting DOACs early in some groups, including Asian populations that have a higher bleeding risk (these trials included predominantly White patients) and people who are older or frail, who may have extensive small vessel disease.

During the discussion, several questions centered on the lack of imaging data available on the patients in the studies. Anderson said imaging data would help reassure clinicians on the safety of early anticoagulation in patients with large infarcts.

“Stroke clinicians make decisions on the basis of the patient and on the basis of the brain, and we only have the patient information at the moment. We don’t have information on the brain — that comes from imaging.”

Regardless, he believes these new data will lead to a shift in practice. “But maybe, it won’t be as dramatic as we would hope because I think some clinicians may still hesitate to apply these results to patients at high risk of bleeding. With imaging data from the studies that might change.”

The OPTIMAS trial was funded by University College London and the British Heart Foundation. Werring reported consulting fees from Novo Nordisk, National Institute for Health and Care Excellence, and Alnylam; payments or speaker honoraria from Novo Nordisk, Bayer, and AstraZeneca/Alexion; participation on a data safety monitoring board for the OXHARP trial; and participation as steering committee chair for the MACE-ICH and PLINTH trials. Åsberg received institutional research grants and lecture fees to her institution from AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, and Institut Produits Synthése. Sandset and de Sousa were both steering committee members of the ELAN trial. Anderson reported grant funding from Penumbra and Takeda China.
 

A version of this article appeared on Medscape.com.

Plant-based diets have become increasingly popular over the last decade as the evidence supporting their health benefits becomes stronger. 

Research pooled from nearly 100 studies has indicated that people who adhere to a vegan diet (ie, completely devoid of animal products) or a vegetarian diet (ie, devoid of meat, but may include dairy and eggs) are able to ward off some chronic diseases, such as cardiovascular disease, optimize glycemic control, and decrease their risk for cancer compared with those who consume omnivorous diets. 

Vegan and vegetarian diets, or flexitarian diets — which are less reliant on animal protein than the standard US diet but do not completely exclude meat, fish, eggs, or dairy — may promote homeostasis and decrease inflammation by providing more fiber, antioxidants, and unsaturated fatty acids than the typical Western diet. 
 

Inflammation and Obesity

Adipose tissue is a major producer of pro-inflammatory cytokines like interleukin (IL)-6, whose presence then triggers a rush of acute-phase reactants such as C-reactive protein (CRP) by the liver. This process develops into chronic low-grade inflammation that can increase a person’s chances of developing diabetes, cardiovascular disease, kidney disease, metabolic syndrome, and related complications.

Adopting a plant-based diet can improve markers of chronic low-grade inflammation that can lead to chronic disease and worsen existent chronic disease. A meta-analysis of 29 studies encompassing nearly 2700 participants found that initiation of a plant-based diet showed significant improvement in CRP, IL-6, and soluble intercellular adhesion molecule 1. 

If we want to prevent these inflammatory disease states and their complications, the obvious response is to counsel patients to avoid excessive weight gain or to lose weight if obesity is their baseline. This can be tough for some patients, but it is nonetheless an important step in chronic disease prevention and management.
 

Plant-Based Diet for Type 2 Diabetes

According to a review of nine studies of patients living with type 2 diabetes who adhered to a plant-based diet, all but one found that this approach led to significantly lower A1c values than those seen in control groups. Six of the included studies reported that participants were able to decrease or discontinue medications for the management of diabetes. Researchers across all included studies also noted a decrease in total cholesterol, low-density lipoprotein cholesterol, and triglycerides, as well as increased weight loss in participants in each intervention group. 

Such improvements are probably the result of the increase in fiber intake that occurs with a plant-based diet. A high-fiber diet is known to promote improved glucose and lipid metabolism as well as weight loss. 

It is also worth noting that participants in the intervention groups also experienced improvements in depression and less chronic pain than did those in the control groups. 
 

Plant-Based Diet for Chronic Kidney Disease (CKD)

Although the use of a plant-based diet in the prevention of CKD is well documented, adopting such diets for the treatment of CKD may intimidate both patients and practitioners owing to the high potassium and phosphorus content of many fruits and vegetables.

However, research indicates that the bioavailability of both potassium and phosphorus is lower in plant-based, whole foods than in preservatives and the highly processed food items that incorporate them. This makes a plant-based diet more viable than previously thought. 

Diets rich in vegetables, whole grains, nuts, and legumes have been shown to decrease dietary acid load, both preventing and treating metabolic acidosis. Such diets have also been shown to decrease blood pressure and the risk for a decline in estimated glomerular filtration rate. This type of diet would also prioritize the unsaturated fatty acids and fiber-rich proteins such as avocados, beans, and nuts shown to improve dyslipidemia, which may occur alongside CKD.
 

Realistic Options for Patients on Medical Diets

There is one question that I always seem to get from when recommending a plant-based diet: “These patients already have so many restrictions. Why would you add more?” And my answer is also always the same: I don’t. 

I rarely, if ever, recommend completely cutting out any food item or food group. Instead, I ask the patient to increase their intake of plant-based foods and only limit highly processed foods and fatty meats. By shifting a patient’s focus to beans; nuts; and low-carbohydrate, high-fiber fruits and vegetables, I am often opening up a whole new world of possibilities. 

Instead of a sandwich with low-sodium turkey and cheese on white bread with a side of unsalted pretzels, I recommend a caprese salad with blueberries and almonds or a Southwest salad with black beans, corn, and avocado. I don’t encourage my patients to skip the foods that they love, but instead to only think about all the delicious plant-based options that will provide them with more than just calories.

Meat, dairy, seafood, and eggs can certainly be a part of a healthy diet, but what if our chronically ill patients, especially those with diabetes, had more options than just grilled chicken and green beans for every meal? What if we focus on decreasing dietary restrictions, incorporating a variety of nourishing foods, and educating our patients, instead of on portion control and moderation? 

This is how I choose to incorporate plant-based diets into my practice to treat and prevent these chronic inflammatory conditions and promote sustainable, realistic change in my clients’ health.

Brandy Winfree Root, a renal dietitian in private practice in Mary Esther, Florida, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Plant-based diets have become increasingly popular over the last decade as the evidence supporting their health benefits becomes stronger. 

Research pooled from nearly 100 studies has indicated that people who adhere to a vegan diet (ie, completely devoid of animal products) or a vegetarian diet (ie, devoid of meat, but may include dairy and eggs) are able to ward off some chronic diseases, such as cardiovascular disease, optimize glycemic control, and decrease their risk for cancer compared with those who consume omnivorous diets. 

Vegan and vegetarian diets, or flexitarian diets — which are less reliant on animal protein than the standard US diet but do not completely exclude meat, fish, eggs, or dairy — may promote homeostasis and decrease inflammation by providing more fiber, antioxidants, and unsaturated fatty acids than the typical Western diet. 
 

Inflammation and Obesity

Adipose tissue is a major producer of pro-inflammatory cytokines like interleukin (IL)-6, whose presence then triggers a rush of acute-phase reactants such as C-reactive protein (CRP) by the liver. This process develops into chronic low-grade inflammation that can increase a person’s chances of developing diabetes, cardiovascular disease, kidney disease, metabolic syndrome, and related complications.

Adopting a plant-based diet can improve markers of chronic low-grade inflammation that can lead to chronic disease and worsen existent chronic disease. A meta-analysis of 29 studies encompassing nearly 2700 participants found that initiation of a plant-based diet showed significant improvement in CRP, IL-6, and soluble intercellular adhesion molecule 1. 

If we want to prevent these inflammatory disease states and their complications, the obvious response is to counsel patients to avoid excessive weight gain or to lose weight if obesity is their baseline. This can be tough for some patients, but it is nonetheless an important step in chronic disease prevention and management.
 

Plant-Based Diet for Type 2 Diabetes

According to a review of nine studies of patients living with type 2 diabetes who adhered to a plant-based diet, all but one found that this approach led to significantly lower A1c values than those seen in control groups. Six of the included studies reported that participants were able to decrease or discontinue medications for the management of diabetes. Researchers across all included studies also noted a decrease in total cholesterol, low-density lipoprotein cholesterol, and triglycerides, as well as increased weight loss in participants in each intervention group. 

Such improvements are probably the result of the increase in fiber intake that occurs with a plant-based diet. A high-fiber diet is known to promote improved glucose and lipid metabolism as well as weight loss. 

It is also worth noting that participants in the intervention groups also experienced improvements in depression and less chronic pain than did those in the control groups. 
 

Plant-Based Diet for Chronic Kidney Disease (CKD)

Although the use of a plant-based diet in the prevention of CKD is well documented, adopting such diets for the treatment of CKD may intimidate both patients and practitioners owing to the high potassium and phosphorus content of many fruits and vegetables.

However, research indicates that the bioavailability of both potassium and phosphorus is lower in plant-based, whole foods than in preservatives and the highly processed food items that incorporate them. This makes a plant-based diet more viable than previously thought. 

Diets rich in vegetables, whole grains, nuts, and legumes have been shown to decrease dietary acid load, both preventing and treating metabolic acidosis. Such diets have also been shown to decrease blood pressure and the risk for a decline in estimated glomerular filtration rate. This type of diet would also prioritize the unsaturated fatty acids and fiber-rich proteins such as avocados, beans, and nuts shown to improve dyslipidemia, which may occur alongside CKD.
 

Realistic Options for Patients on Medical Diets

There is one question that I always seem to get from when recommending a plant-based diet: “These patients already have so many restrictions. Why would you add more?” And my answer is also always the same: I don’t. 

I rarely, if ever, recommend completely cutting out any food item or food group. Instead, I ask the patient to increase their intake of plant-based foods and only limit highly processed foods and fatty meats. By shifting a patient’s focus to beans; nuts; and low-carbohydrate, high-fiber fruits and vegetables, I am often opening up a whole new world of possibilities. 

Instead of a sandwich with low-sodium turkey and cheese on white bread with a side of unsalted pretzels, I recommend a caprese salad with blueberries and almonds or a Southwest salad with black beans, corn, and avocado. I don’t encourage my patients to skip the foods that they love, but instead to only think about all the delicious plant-based options that will provide them with more than just calories.

Meat, dairy, seafood, and eggs can certainly be a part of a healthy diet, but what if our chronically ill patients, especially those with diabetes, had more options than just grilled chicken and green beans for every meal? What if we focus on decreasing dietary restrictions, incorporating a variety of nourishing foods, and educating our patients, instead of on portion control and moderation? 

This is how I choose to incorporate plant-based diets into my practice to treat and prevent these chronic inflammatory conditions and promote sustainable, realistic change in my clients’ health.

Brandy Winfree Root, a renal dietitian in private practice in Mary Esther, Florida, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Plant-based diets have become increasingly popular over the last decade as the evidence supporting their health benefits becomes stronger. 

Research pooled from nearly 100 studies has indicated that people who adhere to a vegan diet (ie, completely devoid of animal products) or a vegetarian diet (ie, devoid of meat, but may include dairy and eggs) are able to ward off some chronic diseases, such as cardiovascular disease, optimize glycemic control, and decrease their risk for cancer compared with those who consume omnivorous diets. 

Vegan and vegetarian diets, or flexitarian diets — which are less reliant on animal protein than the standard US diet but do not completely exclude meat, fish, eggs, or dairy — may promote homeostasis and decrease inflammation by providing more fiber, antioxidants, and unsaturated fatty acids than the typical Western diet. 
 

Inflammation and Obesity

Adipose tissue is a major producer of pro-inflammatory cytokines like interleukin (IL)-6, whose presence then triggers a rush of acute-phase reactants such as C-reactive protein (CRP) by the liver. This process develops into chronic low-grade inflammation that can increase a person’s chances of developing diabetes, cardiovascular disease, kidney disease, metabolic syndrome, and related complications.

Adopting a plant-based diet can improve markers of chronic low-grade inflammation that can lead to chronic disease and worsen existent chronic disease. A meta-analysis of 29 studies encompassing nearly 2700 participants found that initiation of a plant-based diet showed significant improvement in CRP, IL-6, and soluble intercellular adhesion molecule 1. 

If we want to prevent these inflammatory disease states and their complications, the obvious response is to counsel patients to avoid excessive weight gain or to lose weight if obesity is their baseline. This can be tough for some patients, but it is nonetheless an important step in chronic disease prevention and management.
 

Plant-Based Diet for Type 2 Diabetes

According to a review of nine studies of patients living with type 2 diabetes who adhered to a plant-based diet, all but one found that this approach led to significantly lower A1c values than those seen in control groups. Six of the included studies reported that participants were able to decrease or discontinue medications for the management of diabetes. Researchers across all included studies also noted a decrease in total cholesterol, low-density lipoprotein cholesterol, and triglycerides, as well as increased weight loss in participants in each intervention group. 

Such improvements are probably the result of the increase in fiber intake that occurs with a plant-based diet. A high-fiber diet is known to promote improved glucose and lipid metabolism as well as weight loss. 

It is also worth noting that participants in the intervention groups also experienced improvements in depression and less chronic pain than did those in the control groups. 
 

Plant-Based Diet for Chronic Kidney Disease (CKD)

Although the use of a plant-based diet in the prevention of CKD is well documented, adopting such diets for the treatment of CKD may intimidate both patients and practitioners owing to the high potassium and phosphorus content of many fruits and vegetables.

However, research indicates that the bioavailability of both potassium and phosphorus is lower in plant-based, whole foods than in preservatives and the highly processed food items that incorporate them. This makes a plant-based diet more viable than previously thought. 

Diets rich in vegetables, whole grains, nuts, and legumes have been shown to decrease dietary acid load, both preventing and treating metabolic acidosis. Such diets have also been shown to decrease blood pressure and the risk for a decline in estimated glomerular filtration rate. This type of diet would also prioritize the unsaturated fatty acids and fiber-rich proteins such as avocados, beans, and nuts shown to improve dyslipidemia, which may occur alongside CKD.
 

Realistic Options for Patients on Medical Diets

There is one question that I always seem to get from when recommending a plant-based diet: “These patients already have so many restrictions. Why would you add more?” And my answer is also always the same: I don’t. 

I rarely, if ever, recommend completely cutting out any food item or food group. Instead, I ask the patient to increase their intake of plant-based foods and only limit highly processed foods and fatty meats. By shifting a patient’s focus to beans; nuts; and low-carbohydrate, high-fiber fruits and vegetables, I am often opening up a whole new world of possibilities. 

Instead of a sandwich with low-sodium turkey and cheese on white bread with a side of unsalted pretzels, I recommend a caprese salad with blueberries and almonds or a Southwest salad with black beans, corn, and avocado. I don’t encourage my patients to skip the foods that they love, but instead to only think about all the delicious plant-based options that will provide them with more than just calories.

Meat, dairy, seafood, and eggs can certainly be a part of a healthy diet, but what if our chronically ill patients, especially those with diabetes, had more options than just grilled chicken and green beans for every meal? What if we focus on decreasing dietary restrictions, incorporating a variety of nourishing foods, and educating our patients, instead of on portion control and moderation? 

This is how I choose to incorporate plant-based diets into my practice to treat and prevent these chronic inflammatory conditions and promote sustainable, realistic change in my clients’ health.

Brandy Winfree Root, a renal dietitian in private practice in Mary Esther, Florida, has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

This October, millions of Americans missed out on two of the most spectacular shows in the universe: the northern lights and a rare comet. Even if you were aware of them, light pollution made them difficult to see, unless you went to a dark area and let your eyes adjust.

It’s not getting any easier — the night sky over North America has been growing brighter by about 10% per year since 2011. More and more research is linking all that light pollution to a surprising range of health consequences: cancer, heart disease, diabetes, Alzheimer’s disease, and even low sperm quality, though the reasons for these troubling associations are not always clear. 

“We’ve lost the contrast between light and dark, and we are confusing our physiology on a regular basis,” said John Hanifin, PhD, associate director of Thomas Jefferson University’s Light Research Program. 

Our own galaxy is invisible to nearly 80% of people in North America. In 1994, an earthquake-triggered blackout in Los Angeles led to calls to the Griffith Observatory from people wondering about that hazy blob of light in the night sky. It was the Milky Way.

Glaring headlights, illuminated buildings, blazing billboards, and streetlights fill our urban skies with a glow that even affects rural residents. Inside, since the invention of the lightbulb, we’ve kept our homes bright at night. Now, we’ve also added blue light-emitting devices — smartphones, television screens, tablets — which have been linked to sleep problems.

But outdoor light may matter for our health, too. “Every photon counts,” Hanifin said. 
 

Bright Lights, Big Problems

For one 2024 study researchers used satellite data to measure light pollution at residential addresses of over 13,000 people. They found that those who lived in places with the brightest skies at night had a 31% higher risk of high blood pressure. Another study out of Hong Kong showed a 29% higher risk of death from coronary heart disease. And yet another found a 17%higher risk of cerebrovascular disease, such as strokes or brain aneurysms. 

Of course, urban areas also have air pollution, noise, and a lack of greenery. So, for some studies, scientists controlled for these factors, and the correlation remained strong (although air pollution with fine particulate matter appeared to be worse for heart health than outdoor light). 

Research has found links between the nighttime glow outside and other diseases:

Breast cancer. “It’s a very strong correlation,” said Randy Nelson, PhD, a neuroscientist at West Virginia University. A study of over 100,000 teachers in California revealed that women living in areas with the most light pollution had a 12%higher risk. That effect is comparable to increasing your intake of ultra-processed foods by 10%. 

Alzheimer’s disease. In a study published this fall, outdoor light at night was more strongly linked to the disease than even alcohol misuse or obesity.

Diabetes. In one recent study, people living in the most illuminated areas had a 28% higher risk of diabetes than those residing in much darker places. In a country like China, scientists concluded that 9 million cases of diabetes could be linked to light pollution. 
 

What Happens in Your Body When You’re Exposed to Light at Night

Research has revealed that light at night (indoors or out) disrupts circadian clocks, increases inflammation, affects cell division, and suppresses melatonin, the “hormone of darkness.” “Darkness is very important,” Hanifin said. When he and his colleagues decades ago started studying the effects of light on human physiology, “people thought we were borderline crazy,” he said.

Nighttime illumination affects the health and behavior of species as diverse as Siberian hamsters, zebra finches, mice, crickets, and mosquitoes. Like most creatures on Earth, humans have internal clocks that are synced to the 24-hour cycle of day and night. The master clock is in your hypothalamus, a diamond-shaped part of the brain, but every cell in your body has its own clock, too. Many physiological processes run on circadian rhythms (a term derived from a Latin phrase meaning “about a day”), from sleep-wake cycle to hormone secretion, as well as processes involved in cancer progression, such as cell division.

“There are special photoreceptors in the eye that don’t deal with visual information. They just send light information,” Nelson said. “If you get light at the wrong time, you’re resetting the clocks.” 

This internal clock “prepares the body for various recurrent challenges, such as eating,” said Christian Benedict, PhD, a sleep researcher at Uppsala University, Sweden. “Light exposure [at night] can mess up this very important system.” This could mean, for instance, that your insulin is released at the wrong time, Benedict said, causing “a jet lag-ish condition that will then impair the ability to handle blood sugar.” Animal studies confirm that exposure to light at night can reduce glucose tolerance and alter insulin secretion – potential pathways to diabetes.

The hormone melatonin, produced when it’s dark by the pineal gland in the brain, is a key player in this modern struggle. Melatonin helps you sleep, synchronizes the body’s circadian rhythms, protects neurons from damage, regulates the immune system, and fights inflammation. But even a sliver of light at night can suppress its secretion. Less than 30 lux of light, about the level of a pedestrian street at night, can slash melatonin by half. 

When lab animals are exposed to nighttime light, they “show enormous neuroinflammation” — that is, inflammation of nervous tissue, Nelson said. In one experiment on humans, those who slept immersed in weak light had higher levels of C-reactive protein in their blood, a marker of inflammation.

Low melatonin has also been linked to cancer. It “allows the metabolic machinery of the cancer cells to be active,” Hanifin said. One of melatonin’s effects is stimulation of natural killer cells, which can recognize and destroy cancer cells. What’s more, when melatonin plunges, estrogen may go up, which could explain the link between light at night and breast cancer (estrogen fuels tumor growth in breast cancers). 

Researchers concede that satellite data might be too coarse to estimate how much light people are actually exposed to while they sleep. Plus, many of us are staring at bright screens. “But the studies keep coming,” Nelson said, suggesting that outdoor light pollution does have an impact. 

When researchers put wrist-worn light sensors on over 80,000 British people, they found that the more light the device registered between half-past midnight and 6 a.m., the more its wearer was at risk of having diabetes several years down the road — no matter how long they’ve actually slept. This, according to the study’s authors, supports the findings of satellite data.

A similar study that used actigraphy with built-in light sensors, measuring whether people had been sleeping in complete darkness for at least five hours, found that light pollution upped the risk of heart disease by 74%.
 

What Can You Do About This?

Not everyone’s melatonin is affected by nighttime light to the same degree. “Some people are very much sensitive to very dim light, whereas others are not as sensitive and need far, far more light stimulation [to impact melatonin],” Benedict said. In one study, some volunteers needed 350 lux to lower their melatonin by half. For such people, flipping on the light in the bathroom at night wouldn’t matter; for others, though, a mere 6 lux was already as harmful – which is darker than twilight. 

You can protect yourself by keeping your bedroom lights off and your screens stashed away, but avoiding outdoor light pollution may be harder. You can invest in high-quality blackout curtains, of course, although some light may still seep inside. You can plant trees in front of your windows, reorient any motion-detector lights, and even petition your local government to reduce over-illumination of buildings and to choose better streetlights. You can support organizations, such as the International Dark-Sky Association, that work to preserve darkness.

Last but not least, you might want to change your habits. If you live in a particularly light-polluted area, such as the District of Columbia, America’s top place for urban blaze, you might reconsider late-night walks or drives around the neighborhood. Instead, Hanifin said, read a book in bed, while keeping the light “as dim as you can.” It’s “a much better idea versus being outside in midtown Manhattan,” he said. According to recent recommendations published by Hanifin and his colleagues, when you sleep, there should be no more than 1 lux of illumination at the level of your eyes — about as much as you’d get from having a lit candle 1 meter away. 

And if we manage to preserve outdoor darkness, and the stars reappear (including the breathtaking Milky Way), we could reap more benefits — some research suggests that stargazing can elicit positive emotions, a sense of personal growth, and “a variety of transcendent thoughts and experiences.” 
 

A version of this article appeared on WebMD.com.

This October, millions of Americans missed out on two of the most spectacular shows in the universe: the northern lights and a rare comet. Even if you were aware of them, light pollution made them difficult to see, unless you went to a dark area and let your eyes adjust.

It’s not getting any easier — the night sky over North America has been growing brighter by about 10% per year since 2011. More and more research is linking all that light pollution to a surprising range of health consequences: cancer, heart disease, diabetes, Alzheimer’s disease, and even low sperm quality, though the reasons for these troubling associations are not always clear. 

“We’ve lost the contrast between light and dark, and we are confusing our physiology on a regular basis,” said John Hanifin, PhD, associate director of Thomas Jefferson University’s Light Research Program. 

Our own galaxy is invisible to nearly 80% of people in North America. In 1994, an earthquake-triggered blackout in Los Angeles led to calls to the Griffith Observatory from people wondering about that hazy blob of light in the night sky. It was the Milky Way.

Glaring headlights, illuminated buildings, blazing billboards, and streetlights fill our urban skies with a glow that even affects rural residents. Inside, since the invention of the lightbulb, we’ve kept our homes bright at night. Now, we’ve also added blue light-emitting devices — smartphones, television screens, tablets — which have been linked to sleep problems.

But outdoor light may matter for our health, too. “Every photon counts,” Hanifin said. 
 

Bright Lights, Big Problems

For one 2024 study researchers used satellite data to measure light pollution at residential addresses of over 13,000 people. They found that those who lived in places with the brightest skies at night had a 31% higher risk of high blood pressure. Another study out of Hong Kong showed a 29% higher risk of death from coronary heart disease. And yet another found a 17%higher risk of cerebrovascular disease, such as strokes or brain aneurysms. 

Of course, urban areas also have air pollution, noise, and a lack of greenery. So, for some studies, scientists controlled for these factors, and the correlation remained strong (although air pollution with fine particulate matter appeared to be worse for heart health than outdoor light). 

Research has found links between the nighttime glow outside and other diseases:

Breast cancer. “It’s a very strong correlation,” said Randy Nelson, PhD, a neuroscientist at West Virginia University. A study of over 100,000 teachers in California revealed that women living in areas with the most light pollution had a 12%higher risk. That effect is comparable to increasing your intake of ultra-processed foods by 10%. 

Alzheimer’s disease. In a study published this fall, outdoor light at night was more strongly linked to the disease than even alcohol misuse or obesity.

Diabetes. In one recent study, people living in the most illuminated areas had a 28% higher risk of diabetes than those residing in much darker places. In a country like China, scientists concluded that 9 million cases of diabetes could be linked to light pollution. 
 

What Happens in Your Body When You’re Exposed to Light at Night

Research has revealed that light at night (indoors or out) disrupts circadian clocks, increases inflammation, affects cell division, and suppresses melatonin, the “hormone of darkness.” “Darkness is very important,” Hanifin said. When he and his colleagues decades ago started studying the effects of light on human physiology, “people thought we were borderline crazy,” he said.

Nighttime illumination affects the health and behavior of species as diverse as Siberian hamsters, zebra finches, mice, crickets, and mosquitoes. Like most creatures on Earth, humans have internal clocks that are synced to the 24-hour cycle of day and night. The master clock is in your hypothalamus, a diamond-shaped part of the brain, but every cell in your body has its own clock, too. Many physiological processes run on circadian rhythms (a term derived from a Latin phrase meaning “about a day”), from sleep-wake cycle to hormone secretion, as well as processes involved in cancer progression, such as cell division.

“There are special photoreceptors in the eye that don’t deal with visual information. They just send light information,” Nelson said. “If you get light at the wrong time, you’re resetting the clocks.” 

This internal clock “prepares the body for various recurrent challenges, such as eating,” said Christian Benedict, PhD, a sleep researcher at Uppsala University, Sweden. “Light exposure [at night] can mess up this very important system.” This could mean, for instance, that your insulin is released at the wrong time, Benedict said, causing “a jet lag-ish condition that will then impair the ability to handle blood sugar.” Animal studies confirm that exposure to light at night can reduce glucose tolerance and alter insulin secretion – potential pathways to diabetes.

The hormone melatonin, produced when it’s dark by the pineal gland in the brain, is a key player in this modern struggle. Melatonin helps you sleep, synchronizes the body’s circadian rhythms, protects neurons from damage, regulates the immune system, and fights inflammation. But even a sliver of light at night can suppress its secretion. Less than 30 lux of light, about the level of a pedestrian street at night, can slash melatonin by half. 

When lab animals are exposed to nighttime light, they “show enormous neuroinflammation” — that is, inflammation of nervous tissue, Nelson said. In one experiment on humans, those who slept immersed in weak light had higher levels of C-reactive protein in their blood, a marker of inflammation.

Low melatonin has also been linked to cancer. It “allows the metabolic machinery of the cancer cells to be active,” Hanifin said. One of melatonin’s effects is stimulation of natural killer cells, which can recognize and destroy cancer cells. What’s more, when melatonin plunges, estrogen may go up, which could explain the link between light at night and breast cancer (estrogen fuels tumor growth in breast cancers). 

Researchers concede that satellite data might be too coarse to estimate how much light people are actually exposed to while they sleep. Plus, many of us are staring at bright screens. “But the studies keep coming,” Nelson said, suggesting that outdoor light pollution does have an impact. 

When researchers put wrist-worn light sensors on over 80,000 British people, they found that the more light the device registered between half-past midnight and 6 a.m., the more its wearer was at risk of having diabetes several years down the road — no matter how long they’ve actually slept. This, according to the study’s authors, supports the findings of satellite data.

A similar study that used actigraphy with built-in light sensors, measuring whether people had been sleeping in complete darkness for at least five hours, found that light pollution upped the risk of heart disease by 74%.
 

What Can You Do About This?

Not everyone’s melatonin is affected by nighttime light to the same degree. “Some people are very much sensitive to very dim light, whereas others are not as sensitive and need far, far more light stimulation [to impact melatonin],” Benedict said. In one study, some volunteers needed 350 lux to lower their melatonin by half. For such people, flipping on the light in the bathroom at night wouldn’t matter; for others, though, a mere 6 lux was already as harmful – which is darker than twilight. 

You can protect yourself by keeping your bedroom lights off and your screens stashed away, but avoiding outdoor light pollution may be harder. You can invest in high-quality blackout curtains, of course, although some light may still seep inside. You can plant trees in front of your windows, reorient any motion-detector lights, and even petition your local government to reduce over-illumination of buildings and to choose better streetlights. You can support organizations, such as the International Dark-Sky Association, that work to preserve darkness.

Last but not least, you might want to change your habits. If you live in a particularly light-polluted area, such as the District of Columbia, America’s top place for urban blaze, you might reconsider late-night walks or drives around the neighborhood. Instead, Hanifin said, read a book in bed, while keeping the light “as dim as you can.” It’s “a much better idea versus being outside in midtown Manhattan,” he said. According to recent recommendations published by Hanifin and his colleagues, when you sleep, there should be no more than 1 lux of illumination at the level of your eyes — about as much as you’d get from having a lit candle 1 meter away. 

And if we manage to preserve outdoor darkness, and the stars reappear (including the breathtaking Milky Way), we could reap more benefits — some research suggests that stargazing can elicit positive emotions, a sense of personal growth, and “a variety of transcendent thoughts and experiences.” 
 

A version of this article appeared on WebMD.com.

This October, millions of Americans missed out on two of the most spectacular shows in the universe: the northern lights and a rare comet. Even if you were aware of them, light pollution made them difficult to see, unless you went to a dark area and let your eyes adjust.

It’s not getting any easier — the night sky over North America has been growing brighter by about 10% per year since 2011. More and more research is linking all that light pollution to a surprising range of health consequences: cancer, heart disease, diabetes, Alzheimer’s disease, and even low sperm quality, though the reasons for these troubling associations are not always clear. 

“We’ve lost the contrast between light and dark, and we are confusing our physiology on a regular basis,” said John Hanifin, PhD, associate director of Thomas Jefferson University’s Light Research Program. 

Our own galaxy is invisible to nearly 80% of people in North America. In 1994, an earthquake-triggered blackout in Los Angeles led to calls to the Griffith Observatory from people wondering about that hazy blob of light in the night sky. It was the Milky Way.

Glaring headlights, illuminated buildings, blazing billboards, and streetlights fill our urban skies with a glow that even affects rural residents. Inside, since the invention of the lightbulb, we’ve kept our homes bright at night. Now, we’ve also added blue light-emitting devices — smartphones, television screens, tablets — which have been linked to sleep problems.

But outdoor light may matter for our health, too. “Every photon counts,” Hanifin said. 
 

Bright Lights, Big Problems

For one 2024 study researchers used satellite data to measure light pollution at residential addresses of over 13,000 people. They found that those who lived in places with the brightest skies at night had a 31% higher risk of high blood pressure. Another study out of Hong Kong showed a 29% higher risk of death from coronary heart disease. And yet another found a 17%higher risk of cerebrovascular disease, such as strokes or brain aneurysms. 

Of course, urban areas also have air pollution, noise, and a lack of greenery. So, for some studies, scientists controlled for these factors, and the correlation remained strong (although air pollution with fine particulate matter appeared to be worse for heart health than outdoor light). 

Research has found links between the nighttime glow outside and other diseases:

Breast cancer. “It’s a very strong correlation,” said Randy Nelson, PhD, a neuroscientist at West Virginia University. A study of over 100,000 teachers in California revealed that women living in areas with the most light pollution had a 12%higher risk. That effect is comparable to increasing your intake of ultra-processed foods by 10%. 

Alzheimer’s disease. In a study published this fall, outdoor light at night was more strongly linked to the disease than even alcohol misuse or obesity.

Diabetes. In one recent study, people living in the most illuminated areas had a 28% higher risk of diabetes than those residing in much darker places. In a country like China, scientists concluded that 9 million cases of diabetes could be linked to light pollution. 
 

What Happens in Your Body When You’re Exposed to Light at Night

Research has revealed that light at night (indoors or out) disrupts circadian clocks, increases inflammation, affects cell division, and suppresses melatonin, the “hormone of darkness.” “Darkness is very important,” Hanifin said. When he and his colleagues decades ago started studying the effects of light on human physiology, “people thought we were borderline crazy,” he said.

Nighttime illumination affects the health and behavior of species as diverse as Siberian hamsters, zebra finches, mice, crickets, and mosquitoes. Like most creatures on Earth, humans have internal clocks that are synced to the 24-hour cycle of day and night. The master clock is in your hypothalamus, a diamond-shaped part of the brain, but every cell in your body has its own clock, too. Many physiological processes run on circadian rhythms (a term derived from a Latin phrase meaning “about a day”), from sleep-wake cycle to hormone secretion, as well as processes involved in cancer progression, such as cell division.

“There are special photoreceptors in the eye that don’t deal with visual information. They just send light information,” Nelson said. “If you get light at the wrong time, you’re resetting the clocks.” 

This internal clock “prepares the body for various recurrent challenges, such as eating,” said Christian Benedict, PhD, a sleep researcher at Uppsala University, Sweden. “Light exposure [at night] can mess up this very important system.” This could mean, for instance, that your insulin is released at the wrong time, Benedict said, causing “a jet lag-ish condition that will then impair the ability to handle blood sugar.” Animal studies confirm that exposure to light at night can reduce glucose tolerance and alter insulin secretion – potential pathways to diabetes.

The hormone melatonin, produced when it’s dark by the pineal gland in the brain, is a key player in this modern struggle. Melatonin helps you sleep, synchronizes the body’s circadian rhythms, protects neurons from damage, regulates the immune system, and fights inflammation. But even a sliver of light at night can suppress its secretion. Less than 30 lux of light, about the level of a pedestrian street at night, can slash melatonin by half. 

When lab animals are exposed to nighttime light, they “show enormous neuroinflammation” — that is, inflammation of nervous tissue, Nelson said. In one experiment on humans, those who slept immersed in weak light had higher levels of C-reactive protein in their blood, a marker of inflammation.

Low melatonin has also been linked to cancer. It “allows the metabolic machinery of the cancer cells to be active,” Hanifin said. One of melatonin’s effects is stimulation of natural killer cells, which can recognize and destroy cancer cells. What’s more, when melatonin plunges, estrogen may go up, which could explain the link between light at night and breast cancer (estrogen fuels tumor growth in breast cancers). 

Researchers concede that satellite data might be too coarse to estimate how much light people are actually exposed to while they sleep. Plus, many of us are staring at bright screens. “But the studies keep coming,” Nelson said, suggesting that outdoor light pollution does have an impact. 

When researchers put wrist-worn light sensors on over 80,000 British people, they found that the more light the device registered between half-past midnight and 6 a.m., the more its wearer was at risk of having diabetes several years down the road — no matter how long they’ve actually slept. This, according to the study’s authors, supports the findings of satellite data.

A similar study that used actigraphy with built-in light sensors, measuring whether people had been sleeping in complete darkness for at least five hours, found that light pollution upped the risk of heart disease by 74%.
 

What Can You Do About This?

Not everyone’s melatonin is affected by nighttime light to the same degree. “Some people are very much sensitive to very dim light, whereas others are not as sensitive and need far, far more light stimulation [to impact melatonin],” Benedict said. In one study, some volunteers needed 350 lux to lower their melatonin by half. For such people, flipping on the light in the bathroom at night wouldn’t matter; for others, though, a mere 6 lux was already as harmful – which is darker than twilight. 

You can protect yourself by keeping your bedroom lights off and your screens stashed away, but avoiding outdoor light pollution may be harder. You can invest in high-quality blackout curtains, of course, although some light may still seep inside. You can plant trees in front of your windows, reorient any motion-detector lights, and even petition your local government to reduce over-illumination of buildings and to choose better streetlights. You can support organizations, such as the International Dark-Sky Association, that work to preserve darkness.

Last but not least, you might want to change your habits. If you live in a particularly light-polluted area, such as the District of Columbia, America’s top place for urban blaze, you might reconsider late-night walks or drives around the neighborhood. Instead, Hanifin said, read a book in bed, while keeping the light “as dim as you can.” It’s “a much better idea versus being outside in midtown Manhattan,” he said. According to recent recommendations published by Hanifin and his colleagues, when you sleep, there should be no more than 1 lux of illumination at the level of your eyes — about as much as you’d get from having a lit candle 1 meter away. 

And if we manage to preserve outdoor darkness, and the stars reappear (including the breathtaking Milky Way), we could reap more benefits — some research suggests that stargazing can elicit positive emotions, a sense of personal growth, and “a variety of transcendent thoughts and experiences.” 
 

A version of this article appeared on WebMD.com.

The incidence of atrial fibrillation (AF) is on the rise, and recent joint guidelines from the American College of Cardiology and American Heart Association (ACC/AHA) stress the role of primary care clinicians in prevention and management.

One in three White and one in five Black Americans will develop AF in their lifetime, and the projected number of individuals diagnosed with AF in the United States is expected to double by 2050.

Cardiologists who spoke to Medscape Medical News said primary care clinicians can help control AF by focusing on diabetes and hypertension, along with lifestyle factors such as diet, exercise, and alcohol intake.

“It’s not just a rhythm abnormality, but a complex disease that needs to be addressed in a multidisciplinary, holistic way,” said Jose Joglar, MD, a professor in the Department of Internal Medicine at the UT Southwestern Medical Center in Dallas and lead author of the guidelines.

Joglar said primary care clinicians can play an important role in counseling on lifestyle changes for patients with the most common etiologies such as poorly controlled hypertension, diabetes, and obesity.
 

The Primary Care Physicians ABCs: Risk Factors and Comorbidities

The three pillars of the new ACC/AHA guidelines include: Stroke risk assessment and management; optimize the patient’s risks; and symptom management.

“As a primary care physician or as a cardiologist, I often think that if I do these things, I’m going to help with a lot of conditions, not just atrial fibrillation,” said Manesh Patel, MD, chief of the Divisions of Cardiology and Clinical Pharmacology at the Duke University School of Medicine in Durham, North Carolina.

Lifestyle choices such as sleeping habits can play a big part in AF outcomes. Although the guidelines specifically address obstructive sleep apnea as a risk factor, he said more data are needed on the effect of sleep hygiene — getting 8 hours of sleep a night — a goal few people attain.

“What we do know is people that can routinely try to go to sleep and sleep with some regularity seem to have less cardiovascular risk,” Patel said.

Although existing data are limited, literature reviews have found evidence that sleep disruptions, sleep duration, circadian rhythm, and insomnia are associated with heart disease, independent of obstructive sleep apnea.

Use of alcohol should also be discussed with patients, as many are unaware of the effects of the drug on cardiovascular disease, said Joglar, who is also the program director of the Clinical Cardiac Electrophysiology Fellowship program at the UT Southwestern Medical Center.

“Doctors can inform the patient that this is not a judgment call but simple medical fact,” he said.

Joglar also said many physicians need to become educated on a common misconception.

“Every time a patient develops palpitations or atrial fibrillation, the first thing every patient tells me is, I quit drinking coffee,” Joglar said.

However, as the guidelines point out, the link between caffeine and AF is uncertain at best.
 

Preventing AF

A newer class of drugs may help clinicians manage comorbidities that contribute to AF, such as hypertension, sleep apnea, and obesity, said John Mandrola, MD, an electrophysiologist in Louisville, Kentucky, who hosts This Week in Cardiology on Medscape.

Although originally approved for treatment of diabetes, sodium-glucose cotransporter-2 inhibitors are also approved for management of heart failure. Mandrola started prescribing these drugs 2 years ago for patients, given the links of both conditions with AF.

“I think the next frontier for us in cardiology and AF management will be the GLP-1 agonists,” Mandrola said. He hasn’t started prescribing these drugs for his patients yet but said they will likely play a role in the management of patients with AF with the common constellation of comorbidities such as obesity, hypertension, and sleep apnea. 

“The GLP-1 agonists have a really good chance of competing with AF ablation for rhythm control over the long term,” he said.
 

Decisions, Decisions: Stroke Risk Scoring Systems

The risk for stroke varies widely among patients with AF, so primary care clinicians can pick among several scoring systems to estimate the risk for stroke and guide the decision on whether to initiate anticoagulation therapy.

The ACC/AHA guidelines do not state a preference for a particular instrument. The Congestive heart failure, Hypertension, Age, Diabetes mellitus, Stroke, Vascular disease, Sex (CHA2DS2-VASc) score is the most widely used and validated instrument, Joglar said. He usually recommends anticoagulation if the CHA2DS2-VASc score is > 2, dependent on individual patient factors.

“If you have a CHA2DS2-VASc score of 1, and you only had one episode of AF for a few hours a year ago, then your risk of stroke is not as high as somebody who has a score of 1 but has more frequent or persistent AF,” Joglar said.

None of the systems is perfect at predicting risk for stroke, so clinicians should discuss options with patients.

“The real message is, are you talking about the risk of stroke and systemic embolism to your patient, so that the patient understands that risk?” he said.

Patel also said measuring creatine clearance can be analogous to using an instrument like CHA2DS2-VASc.

“I often think about renal disease as a very good risk marker and something that does elevate your risk,” he said.
 

Which Anticoagulant?

Although the ACC/AHA guidelines still recommend warfarin for patients with AF with mechanical heart valves or moderate to severe rheumatic fever, direct oral anticoagulants (DOACs) are the first-line therapy for all other patients with AF.

In terms of which DOACs to use, the differences are subtle, according to Patel.

“I don’t know that they’re that different from each other,” he said. “All of the new drugs are better than warfarin by far.”

Patel pointed out that dabigatran at 150 mg is the only DOAC shown to reduce the incidence of ischemic stroke. For patients with renal dysfunction, he has a slight preference for a 15-mg dose of rivaroxaban.

Mandrola said he mainly prescribes apixaban and rivaroxaban, the latter of which requires only once a day dosing.

“We stopped using dabigatran because 10% of people get gastrointestinal upset,” he said.

Although studies suggest aspirin is less effective than either warfarin or DOACs for the prevention of stroke, Joglar said he still sees patients who come to him after being prescribed low-dose aspirin from primary care clinicians.

“We made it very clear that it should not be recommended just for mitigating stroke risk in atrial fibrillation,” Joglar said. “You could use it if the patient has another indication, such as a prior heart attack.”
 

Does My Patient Have to Be in Normal Sinus Rhythm?

The new guidelines present evidence maintaining sinus rhythm should be favored over controlling heart rate for managing AF.

“We’ve focused on rhythm control as a better strategy, especially catheter ablation, which seems to be particularly effective in parallel to lifestyle interventions and management of comorbidities,” Joglar said. Rhythm control is of particular benefit for patients with AF triggered by heart failure. Control of rhythm in these patients has been shown to improve multiple outcomes such as ejection fraction, symptoms, and survival.

Patel said as a patient’s symptoms increase, the more likely a clinician will be able to control sinus rhythm. Some patients do not notice their arrhythmia, but others feel dizzy or have chest pain.

“The less symptomatic the patient is, the more likely they’re going to tolerate it, especially if they’re older, and it’s hard to get them into sinus rhythm,” Patel said.
 

When to Refer for Catheter Ablation?

The new guidelines upgraded the recommendation for catheter ablation to class I (strong recommendation) for patients with symptomatic AF in whom anti-arrhythmic therapy is unsuccessful, not tolerated, or contraindicated; patients with symptomatic paroxysmal AF (typically younger patients with few comorbidities); and patients with symptomatic or clinically significant atrial flutter. The previous iteration recommended trying drug therapy first.

Multiple randomized clinical trials have demonstrated the effectiveness of catheter ablation.

“In somebody who is younger, with a healthy heart, the 1-year success rate of the procedure might be about 70%,” Joglar said. While 70% of patients receiving a catheter have no AF episodes in the following year, Joglar said 20%-25% of those who do have recurrences will experience fewer or shorter episodes.

Conversations about rate vs rhythm control and whether to pursue catheter ablation often come down to preference, Patel said. He would tend to intervene earlier using ablation in patients with heart failure or those experiencing symptoms of AF who cannot be controlled with a heart rate < 100 beats/min.

But he said he prefers using medication for rate control in many of his patients who are older, have chronic AF, and do not have heart failure.

Mandrola takes a more conservative approach, reserving catheter ablation for patients in whom risk factor management and anti-arrhythmic drugs have not been successful.

“In my hospital, it’s done for patients who have symptomatic AF that’s really impacting their quality of life,” he said. But for those with fewer symptoms, his advice is to provide education, reassurance, and time because AF can resolve on its own.
 

What About Data From Implantables and Wearables?

The guidelines provide an algorithm for when to treat non-symptomatic atrial high-rate episodes detected by a cardiovascular implantable electronic device such as a pacemaker or defibrillator. Episodes less than 5 minutes can be ignored, while treatment could be considered for those with episodes lasting 5 minutes up to 24 hours with a CHA2DS2-VASc score ≥ 3, or lasting longer than 24 hours with a CHA2DS2-VASc score ≥ 2.

But whether anticoagulation improves outcomes is unclear.

“That is a $64,000 question,” Mandrola said. “I would bet every day I get a notification in the electronic health record that says Mr. Smith had 2 hours of AFib 2 weeks ago.”

He also hears from patients who report their Apple Watch has detected an episode of AF.

Mandrola cited evidence from two recent studies of patients who had an atrial high-rate episode longer than 6 minutes detected by implantable devices. The NOAH-AFNET 6 trial randomized patients over 65 years with one or more risk factors for stroke to receive a DOAC or placebo, while the ARTESIA trial used similar inclusion criteria to assign patients to receive either DOAC or aspirin. Both studies reported modest reductions in stroke that were outweighed by a higher incidence of major bleeding in the group receiving anticoagulation.

Shared decision-making should play a role in deciding how aggressively to treat episodes of AF detected by implantable or wearable devices.

He said some patients fear having a stroke, while others are adamantly opposed to taking an anticoagulant.

For patients who present with a documented episode of AF but who otherwise have no symptoms, Patel said clinicians should consider risk for stroke and frequency and duration of episodes.

“One way clinicians should be thinking about it is, the more risk factors they have, the lower burden of AF I need to treat,” Patel said. Even for patients who are having only short episodes of AF, he has a low threshold for recommending an anticoagulation drug if the patient’s CHA2DS2-VASc score is high.

Patel reported research grants from Bayer, Novartis, Idorsia, NHLBI, and Janssen Pharmaceuticals and served as a consultant on the advisory boards of Bayer, Janssen Pharmaceuticals, and Esperion Therapeutics. 

Joglar and Mandrola had no disclosures. 

A version of this article appeared on Medscape.com.

The incidence of atrial fibrillation (AF) is on the rise, and recent joint guidelines from the American College of Cardiology and American Heart Association (ACC/AHA) stress the role of primary care clinicians in prevention and management.

One in three White and one in five Black Americans will develop AF in their lifetime, and the projected number of individuals diagnosed with AF in the United States is expected to double by 2050.

Cardiologists who spoke to Medscape Medical News said primary care clinicians can help control AF by focusing on diabetes and hypertension, along with lifestyle factors such as diet, exercise, and alcohol intake.

“It’s not just a rhythm abnormality, but a complex disease that needs to be addressed in a multidisciplinary, holistic way,” said Jose Joglar, MD, a professor in the Department of Internal Medicine at the UT Southwestern Medical Center in Dallas and lead author of the guidelines.

Joglar said primary care clinicians can play an important role in counseling on lifestyle changes for patients with the most common etiologies such as poorly controlled hypertension, diabetes, and obesity.
 

The Primary Care Physicians ABCs: Risk Factors and Comorbidities

The three pillars of the new ACC/AHA guidelines include: Stroke risk assessment and management; optimize the patient’s risks; and symptom management.

“As a primary care physician or as a cardiologist, I often think that if I do these things, I’m going to help with a lot of conditions, not just atrial fibrillation,” said Manesh Patel, MD, chief of the Divisions of Cardiology and Clinical Pharmacology at the Duke University School of Medicine in Durham, North Carolina.

Lifestyle choices such as sleeping habits can play a big part in AF outcomes. Although the guidelines specifically address obstructive sleep apnea as a risk factor, he said more data are needed on the effect of sleep hygiene — getting 8 hours of sleep a night — a goal few people attain.

“What we do know is people that can routinely try to go to sleep and sleep with some regularity seem to have less cardiovascular risk,” Patel said.

Although existing data are limited, literature reviews have found evidence that sleep disruptions, sleep duration, circadian rhythm, and insomnia are associated with heart disease, independent of obstructive sleep apnea.

Use of alcohol should also be discussed with patients, as many are unaware of the effects of the drug on cardiovascular disease, said Joglar, who is also the program director of the Clinical Cardiac Electrophysiology Fellowship program at the UT Southwestern Medical Center.

“Doctors can inform the patient that this is not a judgment call but simple medical fact,” he said.

Joglar also said many physicians need to become educated on a common misconception.

“Every time a patient develops palpitations or atrial fibrillation, the first thing every patient tells me is, I quit drinking coffee,” Joglar said.

However, as the guidelines point out, the link between caffeine and AF is uncertain at best.
 

Preventing AF

A newer class of drugs may help clinicians manage comorbidities that contribute to AF, such as hypertension, sleep apnea, and obesity, said John Mandrola, MD, an electrophysiologist in Louisville, Kentucky, who hosts This Week in Cardiology on Medscape.

Although originally approved for treatment of diabetes, sodium-glucose cotransporter-2 inhibitors are also approved for management of heart failure. Mandrola started prescribing these drugs 2 years ago for patients, given the links of both conditions with AF.

“I think the next frontier for us in cardiology and AF management will be the GLP-1 agonists,” Mandrola said. He hasn’t started prescribing these drugs for his patients yet but said they will likely play a role in the management of patients with AF with the common constellation of comorbidities such as obesity, hypertension, and sleep apnea. 

“The GLP-1 agonists have a really good chance of competing with AF ablation for rhythm control over the long term,” he said.
 

Decisions, Decisions: Stroke Risk Scoring Systems

The risk for stroke varies widely among patients with AF, so primary care clinicians can pick among several scoring systems to estimate the risk for stroke and guide the decision on whether to initiate anticoagulation therapy.

The ACC/AHA guidelines do not state a preference for a particular instrument. The Congestive heart failure, Hypertension, Age, Diabetes mellitus, Stroke, Vascular disease, Sex (CHA2DS2-VASc) score is the most widely used and validated instrument, Joglar said. He usually recommends anticoagulation if the CHA2DS2-VASc score is > 2, dependent on individual patient factors.

“If you have a CHA2DS2-VASc score of 1, and you only had one episode of AF for a few hours a year ago, then your risk of stroke is not as high as somebody who has a score of 1 but has more frequent or persistent AF,” Joglar said.

None of the systems is perfect at predicting risk for stroke, so clinicians should discuss options with patients.

“The real message is, are you talking about the risk of stroke and systemic embolism to your patient, so that the patient understands that risk?” he said.

Patel also said measuring creatine clearance can be analogous to using an instrument like CHA2DS2-VASc.

“I often think about renal disease as a very good risk marker and something that does elevate your risk,” he said.
 

Which Anticoagulant?

Although the ACC/AHA guidelines still recommend warfarin for patients with AF with mechanical heart valves or moderate to severe rheumatic fever, direct oral anticoagulants (DOACs) are the first-line therapy for all other patients with AF.

In terms of which DOACs to use, the differences are subtle, according to Patel.

“I don’t know that they’re that different from each other,” he said. “All of the new drugs are better than warfarin by far.”

Patel pointed out that dabigatran at 150 mg is the only DOAC shown to reduce the incidence of ischemic stroke. For patients with renal dysfunction, he has a slight preference for a 15-mg dose of rivaroxaban.

Mandrola said he mainly prescribes apixaban and rivaroxaban, the latter of which requires only once a day dosing.

“We stopped using dabigatran because 10% of people get gastrointestinal upset,” he said.

Although studies suggest aspirin is less effective than either warfarin or DOACs for the prevention of stroke, Joglar said he still sees patients who come to him after being prescribed low-dose aspirin from primary care clinicians.

“We made it very clear that it should not be recommended just for mitigating stroke risk in atrial fibrillation,” Joglar said. “You could use it if the patient has another indication, such as a prior heart attack.”
 

Does My Patient Have to Be in Normal Sinus Rhythm?

The new guidelines present evidence maintaining sinus rhythm should be favored over controlling heart rate for managing AF.

“We’ve focused on rhythm control as a better strategy, especially catheter ablation, which seems to be particularly effective in parallel to lifestyle interventions and management of comorbidities,” Joglar said. Rhythm control is of particular benefit for patients with AF triggered by heart failure. Control of rhythm in these patients has been shown to improve multiple outcomes such as ejection fraction, symptoms, and survival.

Patel said as a patient’s symptoms increase, the more likely a clinician will be able to control sinus rhythm. Some patients do not notice their arrhythmia, but others feel dizzy or have chest pain.

“The less symptomatic the patient is, the more likely they’re going to tolerate it, especially if they’re older, and it’s hard to get them into sinus rhythm,” Patel said.
 

When to Refer for Catheter Ablation?

The new guidelines upgraded the recommendation for catheter ablation to class I (strong recommendation) for patients with symptomatic AF in whom anti-arrhythmic therapy is unsuccessful, not tolerated, or contraindicated; patients with symptomatic paroxysmal AF (typically younger patients with few comorbidities); and patients with symptomatic or clinically significant atrial flutter. The previous iteration recommended trying drug therapy first.

Multiple randomized clinical trials have demonstrated the effectiveness of catheter ablation.

“In somebody who is younger, with a healthy heart, the 1-year success rate of the procedure might be about 70%,” Joglar said. While 70% of patients receiving a catheter have no AF episodes in the following year, Joglar said 20%-25% of those who do have recurrences will experience fewer or shorter episodes.

Conversations about rate vs rhythm control and whether to pursue catheter ablation often come down to preference, Patel said. He would tend to intervene earlier using ablation in patients with heart failure or those experiencing symptoms of AF who cannot be controlled with a heart rate < 100 beats/min.

But he said he prefers using medication for rate control in many of his patients who are older, have chronic AF, and do not have heart failure.

Mandrola takes a more conservative approach, reserving catheter ablation for patients in whom risk factor management and anti-arrhythmic drugs have not been successful.

“In my hospital, it’s done for patients who have symptomatic AF that’s really impacting their quality of life,” he said. But for those with fewer symptoms, his advice is to provide education, reassurance, and time because AF can resolve on its own.
 

What About Data From Implantables and Wearables?

The guidelines provide an algorithm for when to treat non-symptomatic atrial high-rate episodes detected by a cardiovascular implantable electronic device such as a pacemaker or defibrillator. Episodes less than 5 minutes can be ignored, while treatment could be considered for those with episodes lasting 5 minutes up to 24 hours with a CHA2DS2-VASc score ≥ 3, or lasting longer than 24 hours with a CHA2DS2-VASc score ≥ 2.

But whether anticoagulation improves outcomes is unclear.

“That is a $64,000 question,” Mandrola said. “I would bet every day I get a notification in the electronic health record that says Mr. Smith had 2 hours of AFib 2 weeks ago.”

He also hears from patients who report their Apple Watch has detected an episode of AF.

Mandrola cited evidence from two recent studies of patients who had an atrial high-rate episode longer than 6 minutes detected by implantable devices. The NOAH-AFNET 6 trial randomized patients over 65 years with one or more risk factors for stroke to receive a DOAC or placebo, while the ARTESIA trial used similar inclusion criteria to assign patients to receive either DOAC or aspirin. Both studies reported modest reductions in stroke that were outweighed by a higher incidence of major bleeding in the group receiving anticoagulation.

Shared decision-making should play a role in deciding how aggressively to treat episodes of AF detected by implantable or wearable devices.

He said some patients fear having a stroke, while others are adamantly opposed to taking an anticoagulant.

For patients who present with a documented episode of AF but who otherwise have no symptoms, Patel said clinicians should consider risk for stroke and frequency and duration of episodes.

“One way clinicians should be thinking about it is, the more risk factors they have, the lower burden of AF I need to treat,” Patel said. Even for patients who are having only short episodes of AF, he has a low threshold for recommending an anticoagulation drug if the patient’s CHA2DS2-VASc score is high.

Patel reported research grants from Bayer, Novartis, Idorsia, NHLBI, and Janssen Pharmaceuticals and served as a consultant on the advisory boards of Bayer, Janssen Pharmaceuticals, and Esperion Therapeutics. 

Joglar and Mandrola had no disclosures. 

A version of this article appeared on Medscape.com.

The incidence of atrial fibrillation (AF) is on the rise, and recent joint guidelines from the American College of Cardiology and American Heart Association (ACC/AHA) stress the role of primary care clinicians in prevention and management.

One in three White and one in five Black Americans will develop AF in their lifetime, and the projected number of individuals diagnosed with AF in the United States is expected to double by 2050.

Cardiologists who spoke to Medscape Medical News said primary care clinicians can help control AF by focusing on diabetes and hypertension, along with lifestyle factors such as diet, exercise, and alcohol intake.

“It’s not just a rhythm abnormality, but a complex disease that needs to be addressed in a multidisciplinary, holistic way,” said Jose Joglar, MD, a professor in the Department of Internal Medicine at the UT Southwestern Medical Center in Dallas and lead author of the guidelines.

Joglar said primary care clinicians can play an important role in counseling on lifestyle changes for patients with the most common etiologies such as poorly controlled hypertension, diabetes, and obesity.
 

The Primary Care Physicians ABCs: Risk Factors and Comorbidities

The three pillars of the new ACC/AHA guidelines include: Stroke risk assessment and management; optimize the patient’s risks; and symptom management.

“As a primary care physician or as a cardiologist, I often think that if I do these things, I’m going to help with a lot of conditions, not just atrial fibrillation,” said Manesh Patel, MD, chief of the Divisions of Cardiology and Clinical Pharmacology at the Duke University School of Medicine in Durham, North Carolina.

Lifestyle choices such as sleeping habits can play a big part in AF outcomes. Although the guidelines specifically address obstructive sleep apnea as a risk factor, he said more data are needed on the effect of sleep hygiene — getting 8 hours of sleep a night — a goal few people attain.

“What we do know is people that can routinely try to go to sleep and sleep with some regularity seem to have less cardiovascular risk,” Patel said.

Although existing data are limited, literature reviews have found evidence that sleep disruptions, sleep duration, circadian rhythm, and insomnia are associated with heart disease, independent of obstructive sleep apnea.

Use of alcohol should also be discussed with patients, as many are unaware of the effects of the drug on cardiovascular disease, said Joglar, who is also the program director of the Clinical Cardiac Electrophysiology Fellowship program at the UT Southwestern Medical Center.

“Doctors can inform the patient that this is not a judgment call but simple medical fact,” he said.

Joglar also said many physicians need to become educated on a common misconception.

“Every time a patient develops palpitations or atrial fibrillation, the first thing every patient tells me is, I quit drinking coffee,” Joglar said.

However, as the guidelines point out, the link between caffeine and AF is uncertain at best.
 

Preventing AF

A newer class of drugs may help clinicians manage comorbidities that contribute to AF, such as hypertension, sleep apnea, and obesity, said John Mandrola, MD, an electrophysiologist in Louisville, Kentucky, who hosts This Week in Cardiology on Medscape.

Although originally approved for treatment of diabetes, sodium-glucose cotransporter-2 inhibitors are also approved for management of heart failure. Mandrola started prescribing these drugs 2 years ago for patients, given the links of both conditions with AF.

“I think the next frontier for us in cardiology and AF management will be the GLP-1 agonists,” Mandrola said. He hasn’t started prescribing these drugs for his patients yet but said they will likely play a role in the management of patients with AF with the common constellation of comorbidities such as obesity, hypertension, and sleep apnea. 

“The GLP-1 agonists have a really good chance of competing with AF ablation for rhythm control over the long term,” he said.
 

Decisions, Decisions: Stroke Risk Scoring Systems

The risk for stroke varies widely among patients with AF, so primary care clinicians can pick among several scoring systems to estimate the risk for stroke and guide the decision on whether to initiate anticoagulation therapy.

The ACC/AHA guidelines do not state a preference for a particular instrument. The Congestive heart failure, Hypertension, Age, Diabetes mellitus, Stroke, Vascular disease, Sex (CHA2DS2-VASc) score is the most widely used and validated instrument, Joglar said. He usually recommends anticoagulation if the CHA2DS2-VASc score is > 2, dependent on individual patient factors.

“If you have a CHA2DS2-VASc score of 1, and you only had one episode of AF for a few hours a year ago, then your risk of stroke is not as high as somebody who has a score of 1 but has more frequent or persistent AF,” Joglar said.

None of the systems is perfect at predicting risk for stroke, so clinicians should discuss options with patients.

“The real message is, are you talking about the risk of stroke and systemic embolism to your patient, so that the patient understands that risk?” he said.

Patel also said measuring creatine clearance can be analogous to using an instrument like CHA2DS2-VASc.

“I often think about renal disease as a very good risk marker and something that does elevate your risk,” he said.
 

Which Anticoagulant?

Although the ACC/AHA guidelines still recommend warfarin for patients with AF with mechanical heart valves or moderate to severe rheumatic fever, direct oral anticoagulants (DOACs) are the first-line therapy for all other patients with AF.

In terms of which DOACs to use, the differences are subtle, according to Patel.

“I don’t know that they’re that different from each other,” he said. “All of the new drugs are better than warfarin by far.”

Patel pointed out that dabigatran at 150 mg is the only DOAC shown to reduce the incidence of ischemic stroke. For patients with renal dysfunction, he has a slight preference for a 15-mg dose of rivaroxaban.

Mandrola said he mainly prescribes apixaban and rivaroxaban, the latter of which requires only once a day dosing.

“We stopped using dabigatran because 10% of people get gastrointestinal upset,” he said.

Although studies suggest aspirin is less effective than either warfarin or DOACs for the prevention of stroke, Joglar said he still sees patients who come to him after being prescribed low-dose aspirin from primary care clinicians.

“We made it very clear that it should not be recommended just for mitigating stroke risk in atrial fibrillation,” Joglar said. “You could use it if the patient has another indication, such as a prior heart attack.”
 

Does My Patient Have to Be in Normal Sinus Rhythm?

The new guidelines present evidence maintaining sinus rhythm should be favored over controlling heart rate for managing AF.

“We’ve focused on rhythm control as a better strategy, especially catheter ablation, which seems to be particularly effective in parallel to lifestyle interventions and management of comorbidities,” Joglar said. Rhythm control is of particular benefit for patients with AF triggered by heart failure. Control of rhythm in these patients has been shown to improve multiple outcomes such as ejection fraction, symptoms, and survival.

Patel said as a patient’s symptoms increase, the more likely a clinician will be able to control sinus rhythm. Some patients do not notice their arrhythmia, but others feel dizzy or have chest pain.

“The less symptomatic the patient is, the more likely they’re going to tolerate it, especially if they’re older, and it’s hard to get them into sinus rhythm,” Patel said.
 

When to Refer for Catheter Ablation?

The new guidelines upgraded the recommendation for catheter ablation to class I (strong recommendation) for patients with symptomatic AF in whom anti-arrhythmic therapy is unsuccessful, not tolerated, or contraindicated; patients with symptomatic paroxysmal AF (typically younger patients with few comorbidities); and patients with symptomatic or clinically significant atrial flutter. The previous iteration recommended trying drug therapy first.

Multiple randomized clinical trials have demonstrated the effectiveness of catheter ablation.

“In somebody who is younger, with a healthy heart, the 1-year success rate of the procedure might be about 70%,” Joglar said. While 70% of patients receiving a catheter have no AF episodes in the following year, Joglar said 20%-25% of those who do have recurrences will experience fewer or shorter episodes.

Conversations about rate vs rhythm control and whether to pursue catheter ablation often come down to preference, Patel said. He would tend to intervene earlier using ablation in patients with heart failure or those experiencing symptoms of AF who cannot be controlled with a heart rate < 100 beats/min.

But he said he prefers using medication for rate control in many of his patients who are older, have chronic AF, and do not have heart failure.

Mandrola takes a more conservative approach, reserving catheter ablation for patients in whom risk factor management and anti-arrhythmic drugs have not been successful.

“In my hospital, it’s done for patients who have symptomatic AF that’s really impacting their quality of life,” he said. But for those with fewer symptoms, his advice is to provide education, reassurance, and time because AF can resolve on its own.
 

What About Data From Implantables and Wearables?

The guidelines provide an algorithm for when to treat non-symptomatic atrial high-rate episodes detected by a cardiovascular implantable electronic device such as a pacemaker or defibrillator. Episodes less than 5 minutes can be ignored, while treatment could be considered for those with episodes lasting 5 minutes up to 24 hours with a CHA2DS2-VASc score ≥ 3, or lasting longer than 24 hours with a CHA2DS2-VASc score ≥ 2.

But whether anticoagulation improves outcomes is unclear.

“That is a $64,000 question,” Mandrola said. “I would bet every day I get a notification in the electronic health record that says Mr. Smith had 2 hours of AFib 2 weeks ago.”

He also hears from patients who report their Apple Watch has detected an episode of AF.

Mandrola cited evidence from two recent studies of patients who had an atrial high-rate episode longer than 6 minutes detected by implantable devices. The NOAH-AFNET 6 trial randomized patients over 65 years with one or more risk factors for stroke to receive a DOAC or placebo, while the ARTESIA trial used similar inclusion criteria to assign patients to receive either DOAC or aspirin. Both studies reported modest reductions in stroke that were outweighed by a higher incidence of major bleeding in the group receiving anticoagulation.

Shared decision-making should play a role in deciding how aggressively to treat episodes of AF detected by implantable or wearable devices.

He said some patients fear having a stroke, while others are adamantly opposed to taking an anticoagulant.

For patients who present with a documented episode of AF but who otherwise have no symptoms, Patel said clinicians should consider risk for stroke and frequency and duration of episodes.

“One way clinicians should be thinking about it is, the more risk factors they have, the lower burden of AF I need to treat,” Patel said. Even for patients who are having only short episodes of AF, he has a low threshold for recommending an anticoagulation drug if the patient’s CHA2DS2-VASc score is high.

Patel reported research grants from Bayer, Novartis, Idorsia, NHLBI, and Janssen Pharmaceuticals and served as a consultant on the advisory boards of Bayer, Janssen Pharmaceuticals, and Esperion Therapeutics. 

Joglar and Mandrola had no disclosures. 

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Rachel S. Rubin, MD: I’m Dr. Rachel Rubin, a urologist and sexual medicine specialist in the Washington, DC, area. And I am so thrilled because my co-fellow, the brilliant and famous Dr. Ashley Winter, a board-certified urologist and a certified menopause practitioner, who sees patients in our practice from Los Angeles, is joining us today to talk about sex as a vital sign.

Ashley Winter, MD: To have the best sexual function, you need many different systems to work. You need your hormones to be in the right place. You need your blood vessels to dilate when you want them to. You need your nerves to connect to your genitalia to make them responsive. The way people say, “The eyes are the window into the soul” — well, the genitals are the window into the cardiovascular system, the peripheral nervous system, and the hormonal system. It’s so dynamic. Patients can understand how this reflects their health. We just need healthcare providers to hammer home how those things connect.

Rubin: If you’re a primary care doctor seeing a patient and you want to educate them on diabetes or high blood pressure, how can you “ ‘sell it with ‘sex”? How can you use sex to educate them about these important medical conditions?

Winter: I hate using it as a fear tactic, but sometimes you have to. Time and again, I’ve seen men with severe profound erectile dysfunction at a young age, with chronically uncontrolled diabetes.

Diabetes can impair the peripheral nerves, resulting in peripheral neuropathy. The same way that it can affect the fingers and toes, diabetes can affect the penis, even before those other areas. Diabetes can also lead to other conditions such as low testosterone, which also affects the function of the penis.

I’m being brutally honest when I tell patients that diabetes control is critical to having a wonderful sexspan — the duration of your life where you’re able to be sexually active and have great sex and do it in the way that you want.

Chronic conditions such as high cholesterol or hypertension can affect your ability to become erect or aroused whether you have a penis or a vulva, and even your ability to have an orgasm.

Rubin: None of my doctors has ever asked me about these issues. But we have to bring them up with patients because they›re not going to bring them up to us. I always say in the review of systems, we shouldn›t just ask, “Do you have any sexual problems?” (which nobody ever does) and move past the question about men, women or both. We should be asking, “Do you have any issues with libido? Do you want to talk about it? Any issues with erection, arousal, orgasm, or sexual pain?”

When you can talk about those things, you can treat the patient from a whole physiologic perspective. For example, how does their sciatica affect their sexual pain? How does their antidepressant cause a delayed orgasm? How does their low testosterone level affect their energy level, their libido, and their desire? 

We see so much shame and guilt in sexual health, to the extent that patients feel broken. We can help them understand the anatomy and physiology and explain that they aren’t broken. Instead, it’s “You need this medicine for your crippling anxiety, and that’s why your orgasm is delayed, and so can we augment it or add or subtract something to help you with it.”

Winter: In a primary care setting, where we are considering the patient›s overall health, we strive for medication compliance, but a huge part of medication noncompliance is sexual side effects, whether it›s antidepressants, beta-blockers, birth control, or this new world of GLP-1 agonists.

Rubin: I would add breast cancer treatments. Many patients go off their anastrozole or their tamoxifen because of the sexual side effects. 

Winter: This is where we get to the crux of this discussion about sex being a vital sign — something you need to check routinely. We need to become comfortable with it, because then we are unlocking the ability to treat every patient like a whole person, give them better outcomes, improve their compliance, and have a really powerful tool for education.

Rubin: We have a growing toolbox for all genders when it comes to sexual health. We have FDA- approved medications for low libido in women. We use testosterone in men in an evidence-based way to safely improve libido. We use medications to help with the genitourinary syndrome of menopause. Orgasm is a challenging one, but we have devices that can help with those reflexes. And working with people who specialize in sexual pain can be extremely helpful for patients.

Dr. Winter, having practiced in different settings, what would you tell the primary care doctors who don’t want to talk about libido or who minimize sexual complaints because they don’t know how to navigate them?

Winter: I do not envy the challenge of being a primary care provider in the healthcare world we are living in. I think it is the hardest job. The ultimate takeaway is to just normalize the conversation and be able to validate what is happening. Have a few basic tools, and then have referrals. It›s not that you have to have all the time in the world or you have to treat every condition, but you have to start the conversation, be comfortable with it, and then get patients hooked up with the right resources.

Rubin: Every doctor of every kind can connect with patients and try to understand what they care about. What are their goals? What do they want for their families, for their relationships, for their quality of life? And how can we work collaboratively as a team to help them with those things? 

Sex is a huge part of people’s lives. If we don’t ask about it; if we don’t look into it; and if we don’t admit that our physiology, our medications, and our surgeries can affect sexual health and functioning, how can we improve people’s lives? We can do so much as a team when we consider sex as a true vital sign.
 

Dr. Rubin, Assistant Clinical Professor, Department of Urology, Georgetown University, Washington, DC, has disclosed ties with Maternal Medical, Absorption Pharmaceuticals, GlaxoSmithKline, and Endo.

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

This transcript has been edited for clarity.

Rachel S. Rubin, MD: I’m Dr. Rachel Rubin, a urologist and sexual medicine specialist in the Washington, DC, area. And I am so thrilled because my co-fellow, the brilliant and famous Dr. Ashley Winter, a board-certified urologist and a certified menopause practitioner, who sees patients in our practice from Los Angeles, is joining us today to talk about sex as a vital sign.

Ashley Winter, MD: To have the best sexual function, you need many different systems to work. You need your hormones to be in the right place. You need your blood vessels to dilate when you want them to. You need your nerves to connect to your genitalia to make them responsive. The way people say, “The eyes are the window into the soul” — well, the genitals are the window into the cardiovascular system, the peripheral nervous system, and the hormonal system. It’s so dynamic. Patients can understand how this reflects their health. We just need healthcare providers to hammer home how those things connect.

Rubin: If you’re a primary care doctor seeing a patient and you want to educate them on diabetes or high blood pressure, how can you “ ‘sell it with ‘sex”? How can you use sex to educate them about these important medical conditions?

Winter: I hate using it as a fear tactic, but sometimes you have to. Time and again, I’ve seen men with severe profound erectile dysfunction at a young age, with chronically uncontrolled diabetes.

Diabetes can impair the peripheral nerves, resulting in peripheral neuropathy. The same way that it can affect the fingers and toes, diabetes can affect the penis, even before those other areas. Diabetes can also lead to other conditions such as low testosterone, which also affects the function of the penis.

I’m being brutally honest when I tell patients that diabetes control is critical to having a wonderful sexspan — the duration of your life where you’re able to be sexually active and have great sex and do it in the way that you want.

Chronic conditions such as high cholesterol or hypertension can affect your ability to become erect or aroused whether you have a penis or a vulva, and even your ability to have an orgasm.

Rubin: None of my doctors has ever asked me about these issues. But we have to bring them up with patients because they›re not going to bring them up to us. I always say in the review of systems, we shouldn›t just ask, “Do you have any sexual problems?” (which nobody ever does) and move past the question about men, women or both. We should be asking, “Do you have any issues with libido? Do you want to talk about it? Any issues with erection, arousal, orgasm, or sexual pain?”

When you can talk about those things, you can treat the patient from a whole physiologic perspective. For example, how does their sciatica affect their sexual pain? How does their antidepressant cause a delayed orgasm? How does their low testosterone level affect their energy level, their libido, and their desire? 

We see so much shame and guilt in sexual health, to the extent that patients feel broken. We can help them understand the anatomy and physiology and explain that they aren’t broken. Instead, it’s “You need this medicine for your crippling anxiety, and that’s why your orgasm is delayed, and so can we augment it or add or subtract something to help you with it.”

Winter: In a primary care setting, where we are considering the patient›s overall health, we strive for medication compliance, but a huge part of medication noncompliance is sexual side effects, whether it›s antidepressants, beta-blockers, birth control, or this new world of GLP-1 agonists.

Rubin: I would add breast cancer treatments. Many patients go off their anastrozole or their tamoxifen because of the sexual side effects. 

Winter: This is where we get to the crux of this discussion about sex being a vital sign — something you need to check routinely. We need to become comfortable with it, because then we are unlocking the ability to treat every patient like a whole person, give them better outcomes, improve their compliance, and have a really powerful tool for education.

Rubin: We have a growing toolbox for all genders when it comes to sexual health. We have FDA- approved medications for low libido in women. We use testosterone in men in an evidence-based way to safely improve libido. We use medications to help with the genitourinary syndrome of menopause. Orgasm is a challenging one, but we have devices that can help with those reflexes. And working with people who specialize in sexual pain can be extremely helpful for patients.

Dr. Winter, having practiced in different settings, what would you tell the primary care doctors who don’t want to talk about libido or who minimize sexual complaints because they don’t know how to navigate them?

Winter: I do not envy the challenge of being a primary care provider in the healthcare world we are living in. I think it is the hardest job. The ultimate takeaway is to just normalize the conversation and be able to validate what is happening. Have a few basic tools, and then have referrals. It›s not that you have to have all the time in the world or you have to treat every condition, but you have to start the conversation, be comfortable with it, and then get patients hooked up with the right resources.

Rubin: Every doctor of every kind can connect with patients and try to understand what they care about. What are their goals? What do they want for their families, for their relationships, for their quality of life? And how can we work collaboratively as a team to help them with those things? 

Sex is a huge part of people’s lives. If we don’t ask about it; if we don’t look into it; and if we don’t admit that our physiology, our medications, and our surgeries can affect sexual health and functioning, how can we improve people’s lives? We can do so much as a team when we consider sex as a true vital sign.
 

Dr. Rubin, Assistant Clinical Professor, Department of Urology, Georgetown University, Washington, DC, has disclosed ties with Maternal Medical, Absorption Pharmaceuticals, GlaxoSmithKline, and Endo.

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

This transcript has been edited for clarity.

Rachel S. Rubin, MD: I’m Dr. Rachel Rubin, a urologist and sexual medicine specialist in the Washington, DC, area. And I am so thrilled because my co-fellow, the brilliant and famous Dr. Ashley Winter, a board-certified urologist and a certified menopause practitioner, who sees patients in our practice from Los Angeles, is joining us today to talk about sex as a vital sign.

Ashley Winter, MD: To have the best sexual function, you need many different systems to work. You need your hormones to be in the right place. You need your blood vessels to dilate when you want them to. You need your nerves to connect to your genitalia to make them responsive. The way people say, “The eyes are the window into the soul” — well, the genitals are the window into the cardiovascular system, the peripheral nervous system, and the hormonal system. It’s so dynamic. Patients can understand how this reflects their health. We just need healthcare providers to hammer home how those things connect.

Rubin: If you’re a primary care doctor seeing a patient and you want to educate them on diabetes or high blood pressure, how can you “ ‘sell it with ‘sex”? How can you use sex to educate them about these important medical conditions?

Winter: I hate using it as a fear tactic, but sometimes you have to. Time and again, I’ve seen men with severe profound erectile dysfunction at a young age, with chronically uncontrolled diabetes.

Diabetes can impair the peripheral nerves, resulting in peripheral neuropathy. The same way that it can affect the fingers and toes, diabetes can affect the penis, even before those other areas. Diabetes can also lead to other conditions such as low testosterone, which also affects the function of the penis.

I’m being brutally honest when I tell patients that diabetes control is critical to having a wonderful sexspan — the duration of your life where you’re able to be sexually active and have great sex and do it in the way that you want.

Chronic conditions such as high cholesterol or hypertension can affect your ability to become erect or aroused whether you have a penis or a vulva, and even your ability to have an orgasm.

Rubin: None of my doctors has ever asked me about these issues. But we have to bring them up with patients because they›re not going to bring them up to us. I always say in the review of systems, we shouldn›t just ask, “Do you have any sexual problems?” (which nobody ever does) and move past the question about men, women or both. We should be asking, “Do you have any issues with libido? Do you want to talk about it? Any issues with erection, arousal, orgasm, or sexual pain?”

When you can talk about those things, you can treat the patient from a whole physiologic perspective. For example, how does their sciatica affect their sexual pain? How does their antidepressant cause a delayed orgasm? How does their low testosterone level affect their energy level, their libido, and their desire? 

We see so much shame and guilt in sexual health, to the extent that patients feel broken. We can help them understand the anatomy and physiology and explain that they aren’t broken. Instead, it’s “You need this medicine for your crippling anxiety, and that’s why your orgasm is delayed, and so can we augment it or add or subtract something to help you with it.”

Winter: In a primary care setting, where we are considering the patient›s overall health, we strive for medication compliance, but a huge part of medication noncompliance is sexual side effects, whether it›s antidepressants, beta-blockers, birth control, or this new world of GLP-1 agonists.

Rubin: I would add breast cancer treatments. Many patients go off their anastrozole or their tamoxifen because of the sexual side effects. 

Winter: This is where we get to the crux of this discussion about sex being a vital sign — something you need to check routinely. We need to become comfortable with it, because then we are unlocking the ability to treat every patient like a whole person, give them better outcomes, improve their compliance, and have a really powerful tool for education.

Rubin: We have a growing toolbox for all genders when it comes to sexual health. We have FDA- approved medications for low libido in women. We use testosterone in men in an evidence-based way to safely improve libido. We use medications to help with the genitourinary syndrome of menopause. Orgasm is a challenging one, but we have devices that can help with those reflexes. And working with people who specialize in sexual pain can be extremely helpful for patients.

Dr. Winter, having practiced in different settings, what would you tell the primary care doctors who don’t want to talk about libido or who minimize sexual complaints because they don’t know how to navigate them?

Winter: I do not envy the challenge of being a primary care provider in the healthcare world we are living in. I think it is the hardest job. The ultimate takeaway is to just normalize the conversation and be able to validate what is happening. Have a few basic tools, and then have referrals. It›s not that you have to have all the time in the world or you have to treat every condition, but you have to start the conversation, be comfortable with it, and then get patients hooked up with the right resources.

Rubin: Every doctor of every kind can connect with patients and try to understand what they care about. What are their goals? What do they want for their families, for their relationships, for their quality of life? And how can we work collaboratively as a team to help them with those things? 

Sex is a huge part of people’s lives. If we don’t ask about it; if we don’t look into it; and if we don’t admit that our physiology, our medications, and our surgeries can affect sexual health and functioning, how can we improve people’s lives? We can do so much as a team when we consider sex as a true vital sign.
 

Dr. Rubin, Assistant Clinical Professor, Department of Urology, Georgetown University, Washington, DC, has disclosed ties with Maternal Medical, Absorption Pharmaceuticals, GlaxoSmithKline, and Endo.

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

TOPLINE:

Adolescent girls with polycystic ovary syndrome (PCOS) have an increased risk for hypertension, according to a new study which underscores the importance of blood pressure surveillance in this population.

METHODOLOGY:

• The retrospective cohort study examined the association between PCOS and hypertension in adolescent girls within a diverse community-based US healthcare population.
• The researchers analyzed data from 224,418 adolescent girls (mean age at index visit, 14.9 years; 15.8% classified as having obesity) who had a well-child visit between 2013 and 2019, during which their systolic blood pressure and diastolic blood pressure were measured.
• Blood pressure in the hypertensive range was classified using the 2017 American Academy of Pediatrics Practice Guideline, with thresholds of 130/80 mm Hg or greater.

TAKEAWAY:

• The proportion of adolescent girls with high blood pressure was significantly greater among those with PCOS than among those without the condition (18.2% vs 7.1%; P < .001).
• Adolescent girls with PCOS had a 25% higher risk for hypertension than those without the disorder (adjusted odds ratio [aOR], 1.25; 95% CI, 1.10-1.42).
• Similarly, adolescent girls with obesity and PCOS had a 23% higher risk for high blood pressure than those without PCOS (aOR, 1.23; 95% CI, 1.06-1.42).

IN PRACTICE:

“The high prevalence of [hypertension] associated with PCOS emphasizes the key role of early [blood pressure] monitoring in this high-risk group,” the authors of the study wrote.

SOURCE:

The study was led by Sherry Zhang, MD, Kaiser Permanente Oakland Medical Center, Oakland, California, and was published online in the American Journal of Preventive Medicine.

LIMITATIONS:

The study relied on coded diagnoses of PCOS from clinical settings, which may have led to detection and referral biases. The findings may not be generalizable to an unselected population in which adolescent girls are systematically screened for both PCOS and hypertension.

DISCLOSURES:

This study was funded by the Cardiovascular and Metabolic Conditions Research Section and the Biostatistical Consulting Unit at the Division of Research, Kaiser Permanente Northern California and by the Kaiser Permanente Northern California Community Health Program. The authors declared having 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:

Adolescent girls with polycystic ovary syndrome (PCOS) have an increased risk for hypertension, according to a new study which underscores the importance of blood pressure surveillance in this population.

METHODOLOGY:

• The retrospective cohort study examined the association between PCOS and hypertension in adolescent girls within a diverse community-based US healthcare population.
• The researchers analyzed data from 224,418 adolescent girls (mean age at index visit, 14.9 years; 15.8% classified as having obesity) who had a well-child visit between 2013 and 2019, during which their systolic blood pressure and diastolic blood pressure were measured.
• Blood pressure in the hypertensive range was classified using the 2017 American Academy of Pediatrics Practice Guideline, with thresholds of 130/80 mm Hg or greater.

TAKEAWAY:

• The proportion of adolescent girls with high blood pressure was significantly greater among those with PCOS than among those without the condition (18.2% vs 7.1%; P < .001).
• Adolescent girls with PCOS had a 25% higher risk for hypertension than those without the disorder (adjusted odds ratio [aOR], 1.25; 95% CI, 1.10-1.42).
• Similarly, adolescent girls with obesity and PCOS had a 23% higher risk for high blood pressure than those without PCOS (aOR, 1.23; 95% CI, 1.06-1.42).

IN PRACTICE:

“The high prevalence of [hypertension] associated with PCOS emphasizes the key role of early [blood pressure] monitoring in this high-risk group,” the authors of the study wrote.

SOURCE:

The study was led by Sherry Zhang, MD, Kaiser Permanente Oakland Medical Center, Oakland, California, and was published online in the American Journal of Preventive Medicine.

LIMITATIONS:

The study relied on coded diagnoses of PCOS from clinical settings, which may have led to detection and referral biases. The findings may not be generalizable to an unselected population in which adolescent girls are systematically screened for both PCOS and hypertension.

DISCLOSURES:

This study was funded by the Cardiovascular and Metabolic Conditions Research Section and the Biostatistical Consulting Unit at the Division of Research, Kaiser Permanente Northern California and by the Kaiser Permanente Northern California Community Health Program. The authors declared having 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:

Adolescent girls with polycystic ovary syndrome (PCOS) have an increased risk for hypertension, according to a new study which underscores the importance of blood pressure surveillance in this population.

METHODOLOGY:

• The retrospective cohort study examined the association between PCOS and hypertension in adolescent girls within a diverse community-based US healthcare population.
• The researchers analyzed data from 224,418 adolescent girls (mean age at index visit, 14.9 years; 15.8% classified as having obesity) who had a well-child visit between 2013 and 2019, during which their systolic blood pressure and diastolic blood pressure were measured.
• Blood pressure in the hypertensive range was classified using the 2017 American Academy of Pediatrics Practice Guideline, with thresholds of 130/80 mm Hg or greater.

TAKEAWAY:

• The proportion of adolescent girls with high blood pressure was significantly greater among those with PCOS than among those without the condition (18.2% vs 7.1%; P < .001).
• Adolescent girls with PCOS had a 25% higher risk for hypertension than those without the disorder (adjusted odds ratio [aOR], 1.25; 95% CI, 1.10-1.42).
• Similarly, adolescent girls with obesity and PCOS had a 23% higher risk for high blood pressure than those without PCOS (aOR, 1.23; 95% CI, 1.06-1.42).

IN PRACTICE:

“The high prevalence of [hypertension] associated with PCOS emphasizes the key role of early [blood pressure] monitoring in this high-risk group,” the authors of the study wrote.

SOURCE:

The study was led by Sherry Zhang, MD, Kaiser Permanente Oakland Medical Center, Oakland, California, and was published online in the American Journal of Preventive Medicine.

LIMITATIONS:

The study relied on coded diagnoses of PCOS from clinical settings, which may have led to detection and referral biases. The findings may not be generalizable to an unselected population in which adolescent girls are systematically screened for both PCOS and hypertension.

DISCLOSURES:

This study was funded by the Cardiovascular and Metabolic Conditions Research Section and the Biostatistical Consulting Unit at the Division of Research, Kaiser Permanente Northern California and by the Kaiser Permanente Northern California Community Health Program. The authors declared having 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:

Higher doses of vitamin D3 supplementation did not significantly reduce cardiac biomarkers in older adults with low serum vitamin D levels. The STURDY trial found no significant differences in high-sensitivity cardiac troponin I (hs-cTnI) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) between low- and high-dose groups.

METHODOLOGY:

• A total of 688 participants aged 70 years or older with low serum 25-hydroxy vitamin D levels (10-29 ng/mL) were included in the STURDY trial.
• Participants were randomized to receive one of four doses of vitamin D3 supplementation: 200, 1000, 2000, or 4000 IU/d, with 200 IU/d as the reference dose.
• Cardiac biomarkers, including hs-cTnI and NT-proBNP, were measured at baseline, 3 months, 12 months, and 24 months.
• The trial was conducted at two community-based research institutions in the United States between July 2015 and March 2019.
• The effects of vitamin D3 dose on biomarkers were assessed via mixed-effects tobit models, with participants followed up to 24 months or until study termination.

TAKEAWAY:

• Higher doses of vitamin D3 supplementation did not significantly affect hs-cTnI levels compared with the low-dose group (1.6% difference; 95% CI, −5.3 to 8.9).
• No significant differences were observed in NT-proBNP levels between the high-dose and low-dose groups (−1.8% difference; 95% CI, −9.3 to 6.3).
• Both hs-cTnI and NT-proBNP levels increased in both low- and high-dose groups over time, with hs-cTnI increasing by 5.2% and 7.0%, respectively, and NT-proBNP increasing by 11.3% and 9.3%, respectively.
• The findings suggest that higher doses of vitamin D3 supplementation do not reduce markers of subclinical cardiovascular disease in older adults with low serum vitamin D levels.

IN PRACTICE:

“We can speculate that the systemic effects of vitamin D deficiency are more profound among the very old, and there may be an inverse relationship between supplementation and inflammation. It is also possible that serum vitamin D level is a risk marker but not a risk factor for CVD risk and related underlying mechanisms,” wrote the authors of the study.

SOURCE:

The study was led by Katharine W. Rainer, MD, Beth Israel Deaconess Medical Center in Boston. It was published online in the Journal of the American College of Cardiology.

LIMITATIONS:

The study’s community-based population may limit the generalizability of the findings to populations at higher risk for cardiovascular disease. Additionally, the baseline cardiac biomarkers were lower than those in some high-risk populations, which may affect the precision of the assay performance. The study may not have had adequate power for cross-sectional and subgroup analyses. Both groups received some vitamin D3 supplementation, making it difficult to determine the impact of lower-dose supplementation vs no supplementation.

DISCLOSURES:

The study was supported by grants from the National Institute on Aging, the Office of Dietary Supplements, the Mid-Atlantic Nutrition Obesity Research Center, and the Johns Hopkins Institute for Clinical and Translational Research. Rainer disclosed receiving grants from these organizations.

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:

Higher doses of vitamin D3 supplementation did not significantly reduce cardiac biomarkers in older adults with low serum vitamin D levels. The STURDY trial found no significant differences in high-sensitivity cardiac troponin I (hs-cTnI) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) between low- and high-dose groups.

METHODOLOGY:

• A total of 688 participants aged 70 years or older with low serum 25-hydroxy vitamin D levels (10-29 ng/mL) were included in the STURDY trial.
• Participants were randomized to receive one of four doses of vitamin D3 supplementation: 200, 1000, 2000, or 4000 IU/d, with 200 IU/d as the reference dose.
• Cardiac biomarkers, including hs-cTnI and NT-proBNP, were measured at baseline, 3 months, 12 months, and 24 months.
• The trial was conducted at two community-based research institutions in the United States between July 2015 and March 2019.
• The effects of vitamin D3 dose on biomarkers were assessed via mixed-effects tobit models, with participants followed up to 24 months or until study termination.

TAKEAWAY:

• Higher doses of vitamin D3 supplementation did not significantly affect hs-cTnI levels compared with the low-dose group (1.6% difference; 95% CI, −5.3 to 8.9).
• No significant differences were observed in NT-proBNP levels between the high-dose and low-dose groups (−1.8% difference; 95% CI, −9.3 to 6.3).
• Both hs-cTnI and NT-proBNP levels increased in both low- and high-dose groups over time, with hs-cTnI increasing by 5.2% and 7.0%, respectively, and NT-proBNP increasing by 11.3% and 9.3%, respectively.
• The findings suggest that higher doses of vitamin D3 supplementation do not reduce markers of subclinical cardiovascular disease in older adults with low serum vitamin D levels.

IN PRACTICE:

“We can speculate that the systemic effects of vitamin D deficiency are more profound among the very old, and there may be an inverse relationship between supplementation and inflammation. It is also possible that serum vitamin D level is a risk marker but not a risk factor for CVD risk and related underlying mechanisms,” wrote the authors of the study.

SOURCE:

The study was led by Katharine W. Rainer, MD, Beth Israel Deaconess Medical Center in Boston. It was published online in the Journal of the American College of Cardiology.

LIMITATIONS:

The study’s community-based population may limit the generalizability of the findings to populations at higher risk for cardiovascular disease. Additionally, the baseline cardiac biomarkers were lower than those in some high-risk populations, which may affect the precision of the assay performance. The study may not have had adequate power for cross-sectional and subgroup analyses. Both groups received some vitamin D3 supplementation, making it difficult to determine the impact of lower-dose supplementation vs no supplementation.

DISCLOSURES:

The study was supported by grants from the National Institute on Aging, the Office of Dietary Supplements, the Mid-Atlantic Nutrition Obesity Research Center, and the Johns Hopkins Institute for Clinical and Translational Research. Rainer disclosed receiving grants from these organizations.

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:

Higher doses of vitamin D3 supplementation did not significantly reduce cardiac biomarkers in older adults with low serum vitamin D levels. The STURDY trial found no significant differences in high-sensitivity cardiac troponin I (hs-cTnI) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) between low- and high-dose groups.

METHODOLOGY:

• A total of 688 participants aged 70 years or older with low serum 25-hydroxy vitamin D levels (10-29 ng/mL) were included in the STURDY trial.
• Participants were randomized to receive one of four doses of vitamin D3 supplementation: 200, 1000, 2000, or 4000 IU/d, with 200 IU/d as the reference dose.
• Cardiac biomarkers, including hs-cTnI and NT-proBNP, were measured at baseline, 3 months, 12 months, and 24 months.
• The trial was conducted at two community-based research institutions in the United States between July 2015 and March 2019.
• The effects of vitamin D3 dose on biomarkers were assessed via mixed-effects tobit models, with participants followed up to 24 months or until study termination.

TAKEAWAY:

• Higher doses of vitamin D3 supplementation did not significantly affect hs-cTnI levels compared with the low-dose group (1.6% difference; 95% CI, −5.3 to 8.9).
• No significant differences were observed in NT-proBNP levels between the high-dose and low-dose groups (−1.8% difference; 95% CI, −9.3 to 6.3).
• Both hs-cTnI and NT-proBNP levels increased in both low- and high-dose groups over time, with hs-cTnI increasing by 5.2% and 7.0%, respectively, and NT-proBNP increasing by 11.3% and 9.3%, respectively.
• The findings suggest that higher doses of vitamin D3 supplementation do not reduce markers of subclinical cardiovascular disease in older adults with low serum vitamin D levels.

IN PRACTICE:

“We can speculate that the systemic effects of vitamin D deficiency are more profound among the very old, and there may be an inverse relationship between supplementation and inflammation. It is also possible that serum vitamin D level is a risk marker but not a risk factor for CVD risk and related underlying mechanisms,” wrote the authors of the study.

SOURCE:

The study was led by Katharine W. Rainer, MD, Beth Israel Deaconess Medical Center in Boston. It was published online in the Journal of the American College of Cardiology.

LIMITATIONS:

The study’s community-based population may limit the generalizability of the findings to populations at higher risk for cardiovascular disease. Additionally, the baseline cardiac biomarkers were lower than those in some high-risk populations, which may affect the precision of the assay performance. The study may not have had adequate power for cross-sectional and subgroup analyses. Both groups received some vitamin D3 supplementation, making it difficult to determine the impact of lower-dose supplementation vs no supplementation.

DISCLOSURES:

The study was supported by grants from the National Institute on Aging, the Office of Dietary Supplements, the Mid-Atlantic Nutrition Obesity Research Center, and the Johns Hopkins Institute for Clinical and Translational Research. Rainer disclosed receiving grants from these organizations.

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.