MDedge Cardiology

Vaccines for the world’s most deadly diseases, like cancer and heart disease, will likely be ready by 2030 and could save millions of lives, according to the top doctor at one of the world’s leading drug companies.

The announcement is yet another sign of what many are calling “the golden age” of vaccine development, which is largely credited to the pandemic’s use of mRNA technology to create COVID-19 vaccines.

“I think what we have learned in recent months is that if you ever thought that mRNA was just for infectious diseases, or just for COVID, the evidence now is that that’s absolutely not the case,” Moderna Chief Medical Officer Paul Burton, MD, PhD, told The Guardian. “It can be applied to all sorts of disease areas; we are in cancer, infectious disease, cardiovascular disease, autoimmune diseases, rare disease. We have studies in all of those areas, and they have all shown tremendous promise.”

The U.S. Food and Drug Administration recently designated two new Moderna vaccines as breakthrough therapies: a shot that prevents respiratory syncytial virus (RSV) in older people and a shot that helps prevent the recurrence of melanoma. The FDA’s breakthrough designation is given when a new treatment’s early trial results are substantially better than an existing therapy.

The mRNA vaccine technology that made headlines for its role in COVID-19 vaccines works by teaching the body how to make a specific protein to help the immune system prevent or target a certain disease.

Dr. Burton anticipates that mRNA technology will result in breakthroughs such as a cancer vaccine that can be personalized based on the features of a specific tumor.

“I think we will have mRNA-based therapies for rare diseases that were previously undruggable, and I think that 10 years from now, we will be approaching a world where you truly can identify the genetic cause of a disease and, with relative simplicity, go and edit that out and repair it using mRNA-based technology,” he said. 

The Moderna executive made the statements before its annual update on its vaccine pipeline projects, which the company calls “Vaccines Day.” The Massachusetts-based drugmaker said it has given someone the first dose of a “next-generation” COVID-19 vaccine in a phase III trial, has made progress on a Lyme disease shot, and is developing a vaccine for the highly contagious norovirus.

In all, Moderna expects “six major vaccine product launches in the next few years,” the company said in a statement, adding that it expects the COVID-19 booster market alone to be valued at $15 billion.

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

Vaccines for the world’s most deadly diseases, like cancer and heart disease, will likely be ready by 2030 and could save millions of lives, according to the top doctor at one of the world’s leading drug companies.

The announcement is yet another sign of what many are calling “the golden age” of vaccine development, which is largely credited to the pandemic’s use of mRNA technology to create COVID-19 vaccines.

“I think what we have learned in recent months is that if you ever thought that mRNA was just for infectious diseases, or just for COVID, the evidence now is that that’s absolutely not the case,” Moderna Chief Medical Officer Paul Burton, MD, PhD, told The Guardian. “It can be applied to all sorts of disease areas; we are in cancer, infectious disease, cardiovascular disease, autoimmune diseases, rare disease. We have studies in all of those areas, and they have all shown tremendous promise.”

The U.S. Food and Drug Administration recently designated two new Moderna vaccines as breakthrough therapies: a shot that prevents respiratory syncytial virus (RSV) in older people and a shot that helps prevent the recurrence of melanoma. The FDA’s breakthrough designation is given when a new treatment’s early trial results are substantially better than an existing therapy.

The mRNA vaccine technology that made headlines for its role in COVID-19 vaccines works by teaching the body how to make a specific protein to help the immune system prevent or target a certain disease.

Dr. Burton anticipates that mRNA technology will result in breakthroughs such as a cancer vaccine that can be personalized based on the features of a specific tumor.

“I think we will have mRNA-based therapies for rare diseases that were previously undruggable, and I think that 10 years from now, we will be approaching a world where you truly can identify the genetic cause of a disease and, with relative simplicity, go and edit that out and repair it using mRNA-based technology,” he said. 

The Moderna executive made the statements before its annual update on its vaccine pipeline projects, which the company calls “Vaccines Day.” The Massachusetts-based drugmaker said it has given someone the first dose of a “next-generation” COVID-19 vaccine in a phase III trial, has made progress on a Lyme disease shot, and is developing a vaccine for the highly contagious norovirus.

In all, Moderna expects “six major vaccine product launches in the next few years,” the company said in a statement, adding that it expects the COVID-19 booster market alone to be valued at $15 billion.

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

Vaccines for the world’s most deadly diseases, like cancer and heart disease, will likely be ready by 2030 and could save millions of lives, according to the top doctor at one of the world’s leading drug companies.

The announcement is yet another sign of what many are calling “the golden age” of vaccine development, which is largely credited to the pandemic’s use of mRNA technology to create COVID-19 vaccines.

“I think what we have learned in recent months is that if you ever thought that mRNA was just for infectious diseases, or just for COVID, the evidence now is that that’s absolutely not the case,” Moderna Chief Medical Officer Paul Burton, MD, PhD, told The Guardian. “It can be applied to all sorts of disease areas; we are in cancer, infectious disease, cardiovascular disease, autoimmune diseases, rare disease. We have studies in all of those areas, and they have all shown tremendous promise.”

The U.S. Food and Drug Administration recently designated two new Moderna vaccines as breakthrough therapies: a shot that prevents respiratory syncytial virus (RSV) in older people and a shot that helps prevent the recurrence of melanoma. The FDA’s breakthrough designation is given when a new treatment’s early trial results are substantially better than an existing therapy.

The mRNA vaccine technology that made headlines for its role in COVID-19 vaccines works by teaching the body how to make a specific protein to help the immune system prevent or target a certain disease.

Dr. Burton anticipates that mRNA technology will result in breakthroughs such as a cancer vaccine that can be personalized based on the features of a specific tumor.

“I think we will have mRNA-based therapies for rare diseases that were previously undruggable, and I think that 10 years from now, we will be approaching a world where you truly can identify the genetic cause of a disease and, with relative simplicity, go and edit that out and repair it using mRNA-based technology,” he said. 

The Moderna executive made the statements before its annual update on its vaccine pipeline projects, which the company calls “Vaccines Day.” The Massachusetts-based drugmaker said it has given someone the first dose of a “next-generation” COVID-19 vaccine in a phase III trial, has made progress on a Lyme disease shot, and is developing a vaccine for the highly contagious norovirus.

In all, Moderna expects “six major vaccine product launches in the next few years,” the company said in a statement, adding that it expects the COVID-19 booster market alone to be valued at $15 billion.

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

You and me and baby makes 10,003

If you were a virus hunter, looking for your next big virus discovery, where would you go? The wholesale seafood market in Wuhan? A gathering of unmasked anti-vaxxers in the heartland of America? The frozen snot fields of northwest Siberia?

Comstock/Thinkstock

How about babies? Well, it’s too late now, because that’s what Dennis Sandris Nielsen, PhD, of the University of Copenhagen, and his associates did, and they hit the mother lode. Actually, it was more like the infant load, if we’re being honest here.

“We found an exceptional number of unknown viruses in the faeces of these babies,” Dr. Nielsen said in a written statement from the university. (The study was published in Nature Microbiology, so we get the English spelling of feces.)

The investigators mapped the gut “viromes” of 647 healthy Danish 1-year-old children over the course of 5 years and found 10,000 species of viruses distributed across 248 different viral families, of which only 16 were already known. Incredible stuff, but then things took a turn for the cute. “The researchers named the remaining 232 unknown viral families after the children whose diapers made the study possible. As a result, new viral families include names like Sylvesterviridae, Rigmorviridae and Tristanviridae,” the university said.

About 90% of the viruses found in the feces are bacterial viruses, aka bacteriophages, which have bacteria as their hosts and don’t attack the children’s cells, so they don’t cause disease. The other 10%, however, are eukaryotic: They use human cells as hosts, so they can be either friend or foe. “It is thought-provoking that all children run around with 10-20 of these virus types that infect human cells. So, there is a constant viral infection taking place, which apparently doesn’t make them sick,” Dr. Nielsen said.

Doesn’t make them sick? Riiiight. The thought that this gives rise to now? People love babies. Everyone wants to pick up the baby. Now we know why. Because the viruses want us to! Well, those cute little faces aren’t fooling us anymore. No more babies for us. Everyone should stay away from babies and their evil little eukaryotic viruses. STOP THE BABIES!

[Editor’s note: After a short timeout, we explained to the staff that the human species actually needs babies for its survival. They calmed down, picked up their crayons, and quietly went back to work.]

Fooled them. _{Stop the babies!}

At least someone out there appreciates hospital food

Life in Alaska is not for the meek. It’s dark half the year. Summer is 3 weeks in July. And somehow, there’s a moose in line ahead of you at the doctor’s office. To make matters worse, it’s arguing about insurance. “What do you mean, you’ve heard the Moo Cross Moo Shield joke before?”

Jean Beaufort/PublicDomainPictures.net

One might expect that Providence Alaska Health Park, located near downtown Anchorage, the largest city in Alaska by a massive margin, might be safe from ungulate invasion. Nope. In recent days, a young moose has taken to hanging around Providence campus, and it just could not find anything to eat. Remember, it may be early April, but this is Alaska. It’s still winter there. The ground’s still covered in snow.

Eventually, the gears in our young moose friend’s mind turned and it settled on a course of action: “Hey, those are some nice-looking plants behind that door over there. …” And that’s how Providence Alaska Health ended up with a moose munching on decorative potted plants in the hospital lobby.

Funnily enough, the moose didn’t even make a big scene. It just walked through the automatic doors and started chowing down. Security only found out because a tenant called them. Naturally though, once security made the announcement that a massive wild animal had been spotted in the building, the lobby was evacuated. … What do you mean, half the hospital came around to see it? Apparently, even though Alaskans have to fight moose herds on their daily commute, a lot of people wanted to see our moose friend do its thing.

“That’s crazy,” a woman in scrubs said in a video as she snapped a photo with her phone.

“This is the best. Like, what’s the code for this?” asked another bystander.

Despite security’s best efforts to shoo the moose out with barricades and offers of tasty branches, our furry friend left of its own volition, presumably irritated that his breakfast had become a spectator sport. But it didn’t go far. It hung around the front drive for a while, then went around the back of the building for a nap. What has four hooves and still doesn’t give a crap? Bob Moose-o! How you doing?
 

That click sounded stressed

How can people tell that you’re stressed? Maybe you get irritable and a little snappy. Some people have an inability to concentrate or focus. Eating that muffin when you weren’t really hungry could be a sign you’re not relaxed.

Georgijevic/E+/Getty Images

Did you know that your computer can be an indicator of your stress levels?

We tend to be working when we’re using computers, right? That can be a stressor in itself. Well, some researchers at ETH Zürich decided to have a look at the situation. Surprisingly, at least to us, one in three Swiss employees experience workplace stress, which makes us wonder what the percentage is in this country.

The Swiss researchers developed a model that tells how stressed someone is just by the way they use their computer mouse or type. The results of their study showed that those who were stressed clicked and tapped differently than participants who were more relaxed.

Stressed people click “more often and less precisely and cover longer distances on the screen,” while the relaxed take “shorter, more direct routes to reach their destination and take more time doing so,” study author Mara Nägelin explained in a written statement from ETH (Eidgenössische Technische Hochschule, or Swiss Federal Institute of Technology) Zürich.

Ever find when you’re frustrated and in a rush you end up making more mistakes? Same deal. Coauthor Jasmine Kerr noted that “increased levels of stress negatively impact our brain’s ability to process information.” Which totally is going to affect how we move.

Hopefully, these results can give insight to companies on how stressed their employees are and the effect it has on their work performance, eventually leading to, guess what, more research on how to alleviate workplace stress in general, which can benefit us all.

So if you find yourself in the office working on your computer like it’s a game of Perfection and time is running out, take a beat. Maybe try a stress-relieving breathing technique. Nonstressed people, according to the study, take fewer and longer pauses on their computers. Perfection on the job may mean relaxing first.

You and me and baby makes 10,003

If you were a virus hunter, looking for your next big virus discovery, where would you go? The wholesale seafood market in Wuhan? A gathering of unmasked anti-vaxxers in the heartland of America? The frozen snot fields of northwest Siberia?

Comstock/Thinkstock

How about babies? Well, it’s too late now, because that’s what Dennis Sandris Nielsen, PhD, of the University of Copenhagen, and his associates did, and they hit the mother lode. Actually, it was more like the infant load, if we’re being honest here.

“We found an exceptional number of unknown viruses in the faeces of these babies,” Dr. Nielsen said in a written statement from the university. (The study was published in Nature Microbiology, so we get the English spelling of feces.)

The investigators mapped the gut “viromes” of 647 healthy Danish 1-year-old children over the course of 5 years and found 10,000 species of viruses distributed across 248 different viral families, of which only 16 were already known. Incredible stuff, but then things took a turn for the cute. “The researchers named the remaining 232 unknown viral families after the children whose diapers made the study possible. As a result, new viral families include names like Sylvesterviridae, Rigmorviridae and Tristanviridae,” the university said.

About 90% of the viruses found in the feces are bacterial viruses, aka bacteriophages, which have bacteria as their hosts and don’t attack the children’s cells, so they don’t cause disease. The other 10%, however, are eukaryotic: They use human cells as hosts, so they can be either friend or foe. “It is thought-provoking that all children run around with 10-20 of these virus types that infect human cells. So, there is a constant viral infection taking place, which apparently doesn’t make them sick,” Dr. Nielsen said.

Doesn’t make them sick? Riiiight. The thought that this gives rise to now? People love babies. Everyone wants to pick up the baby. Now we know why. Because the viruses want us to! Well, those cute little faces aren’t fooling us anymore. No more babies for us. Everyone should stay away from babies and their evil little eukaryotic viruses. STOP THE BABIES!

[Editor’s note: After a short timeout, we explained to the staff that the human species actually needs babies for its survival. They calmed down, picked up their crayons, and quietly went back to work.]

Fooled them. _{Stop the babies!}

At least someone out there appreciates hospital food

Life in Alaska is not for the meek. It’s dark half the year. Summer is 3 weeks in July. And somehow, there’s a moose in line ahead of you at the doctor’s office. To make matters worse, it’s arguing about insurance. “What do you mean, you’ve heard the Moo Cross Moo Shield joke before?”

Jean Beaufort/PublicDomainPictures.net

One might expect that Providence Alaska Health Park, located near downtown Anchorage, the largest city in Alaska by a massive margin, might be safe from ungulate invasion. Nope. In recent days, a young moose has taken to hanging around Providence campus, and it just could not find anything to eat. Remember, it may be early April, but this is Alaska. It’s still winter there. The ground’s still covered in snow.

Eventually, the gears in our young moose friend’s mind turned and it settled on a course of action: “Hey, those are some nice-looking plants behind that door over there. …” And that’s how Providence Alaska Health ended up with a moose munching on decorative potted plants in the hospital lobby.

Funnily enough, the moose didn’t even make a big scene. It just walked through the automatic doors and started chowing down. Security only found out because a tenant called them. Naturally though, once security made the announcement that a massive wild animal had been spotted in the building, the lobby was evacuated. … What do you mean, half the hospital came around to see it? Apparently, even though Alaskans have to fight moose herds on their daily commute, a lot of people wanted to see our moose friend do its thing.

“That’s crazy,” a woman in scrubs said in a video as she snapped a photo with her phone.

“This is the best. Like, what’s the code for this?” asked another bystander.

Despite security’s best efforts to shoo the moose out with barricades and offers of tasty branches, our furry friend left of its own volition, presumably irritated that his breakfast had become a spectator sport. But it didn’t go far. It hung around the front drive for a while, then went around the back of the building for a nap. What has four hooves and still doesn’t give a crap? Bob Moose-o! How you doing?
 

That click sounded stressed

How can people tell that you’re stressed? Maybe you get irritable and a little snappy. Some people have an inability to concentrate or focus. Eating that muffin when you weren’t really hungry could be a sign you’re not relaxed.

Georgijevic/E+/Getty Images

Did you know that your computer can be an indicator of your stress levels?

We tend to be working when we’re using computers, right? That can be a stressor in itself. Well, some researchers at ETH Zürich decided to have a look at the situation. Surprisingly, at least to us, one in three Swiss employees experience workplace stress, which makes us wonder what the percentage is in this country.

The Swiss researchers developed a model that tells how stressed someone is just by the way they use their computer mouse or type. The results of their study showed that those who were stressed clicked and tapped differently than participants who were more relaxed.

Stressed people click “more often and less precisely and cover longer distances on the screen,” while the relaxed take “shorter, more direct routes to reach their destination and take more time doing so,” study author Mara Nägelin explained in a written statement from ETH (Eidgenössische Technische Hochschule, or Swiss Federal Institute of Technology) Zürich.

Ever find when you’re frustrated and in a rush you end up making more mistakes? Same deal. Coauthor Jasmine Kerr noted that “increased levels of stress negatively impact our brain’s ability to process information.” Which totally is going to affect how we move.

Hopefully, these results can give insight to companies on how stressed their employees are and the effect it has on their work performance, eventually leading to, guess what, more research on how to alleviate workplace stress in general, which can benefit us all.

So if you find yourself in the office working on your computer like it’s a game of Perfection and time is running out, take a beat. Maybe try a stress-relieving breathing technique. Nonstressed people, according to the study, take fewer and longer pauses on their computers. Perfection on the job may mean relaxing first.

You and me and baby makes 10,003

If you were a virus hunter, looking for your next big virus discovery, where would you go? The wholesale seafood market in Wuhan? A gathering of unmasked anti-vaxxers in the heartland of America? The frozen snot fields of northwest Siberia?

Comstock/Thinkstock

How about babies? Well, it’s too late now, because that’s what Dennis Sandris Nielsen, PhD, of the University of Copenhagen, and his associates did, and they hit the mother lode. Actually, it was more like the infant load, if we’re being honest here.

“We found an exceptional number of unknown viruses in the faeces of these babies,” Dr. Nielsen said in a written statement from the university. (The study was published in Nature Microbiology, so we get the English spelling of feces.)

The investigators mapped the gut “viromes” of 647 healthy Danish 1-year-old children over the course of 5 years and found 10,000 species of viruses distributed across 248 different viral families, of which only 16 were already known. Incredible stuff, but then things took a turn for the cute. “The researchers named the remaining 232 unknown viral families after the children whose diapers made the study possible. As a result, new viral families include names like Sylvesterviridae, Rigmorviridae and Tristanviridae,” the university said.

About 90% of the viruses found in the feces are bacterial viruses, aka bacteriophages, which have bacteria as their hosts and don’t attack the children’s cells, so they don’t cause disease. The other 10%, however, are eukaryotic: They use human cells as hosts, so they can be either friend or foe. “It is thought-provoking that all children run around with 10-20 of these virus types that infect human cells. So, there is a constant viral infection taking place, which apparently doesn’t make them sick,” Dr. Nielsen said.

Doesn’t make them sick? Riiiight. The thought that this gives rise to now? People love babies. Everyone wants to pick up the baby. Now we know why. Because the viruses want us to! Well, those cute little faces aren’t fooling us anymore. No more babies for us. Everyone should stay away from babies and their evil little eukaryotic viruses. STOP THE BABIES!

[Editor’s note: After a short timeout, we explained to the staff that the human species actually needs babies for its survival. They calmed down, picked up their crayons, and quietly went back to work.]

Fooled them. _{Stop the babies!}

At least someone out there appreciates hospital food

Life in Alaska is not for the meek. It’s dark half the year. Summer is 3 weeks in July. And somehow, there’s a moose in line ahead of you at the doctor’s office. To make matters worse, it’s arguing about insurance. “What do you mean, you’ve heard the Moo Cross Moo Shield joke before?”

Jean Beaufort/PublicDomainPictures.net

One might expect that Providence Alaska Health Park, located near downtown Anchorage, the largest city in Alaska by a massive margin, might be safe from ungulate invasion. Nope. In recent days, a young moose has taken to hanging around Providence campus, and it just could not find anything to eat. Remember, it may be early April, but this is Alaska. It’s still winter there. The ground’s still covered in snow.

Eventually, the gears in our young moose friend’s mind turned and it settled on a course of action: “Hey, those are some nice-looking plants behind that door over there. …” And that’s how Providence Alaska Health ended up with a moose munching on decorative potted plants in the hospital lobby.

Funnily enough, the moose didn’t even make a big scene. It just walked through the automatic doors and started chowing down. Security only found out because a tenant called them. Naturally though, once security made the announcement that a massive wild animal had been spotted in the building, the lobby was evacuated. … What do you mean, half the hospital came around to see it? Apparently, even though Alaskans have to fight moose herds on their daily commute, a lot of people wanted to see our moose friend do its thing.

“That’s crazy,” a woman in scrubs said in a video as she snapped a photo with her phone.

“This is the best. Like, what’s the code for this?” asked another bystander.

Despite security’s best efforts to shoo the moose out with barricades and offers of tasty branches, our furry friend left of its own volition, presumably irritated that his breakfast had become a spectator sport. But it didn’t go far. It hung around the front drive for a while, then went around the back of the building for a nap. What has four hooves and still doesn’t give a crap? Bob Moose-o! How you doing?
 

That click sounded stressed

How can people tell that you’re stressed? Maybe you get irritable and a little snappy. Some people have an inability to concentrate or focus. Eating that muffin when you weren’t really hungry could be a sign you’re not relaxed.

Georgijevic/E+/Getty Images

Did you know that your computer can be an indicator of your stress levels?

We tend to be working when we’re using computers, right? That can be a stressor in itself. Well, some researchers at ETH Zürich decided to have a look at the situation. Surprisingly, at least to us, one in three Swiss employees experience workplace stress, which makes us wonder what the percentage is in this country.

The Swiss researchers developed a model that tells how stressed someone is just by the way they use their computer mouse or type. The results of their study showed that those who were stressed clicked and tapped differently than participants who were more relaxed.

Stressed people click “more often and less precisely and cover longer distances on the screen,” while the relaxed take “shorter, more direct routes to reach their destination and take more time doing so,” study author Mara Nägelin explained in a written statement from ETH (Eidgenössische Technische Hochschule, or Swiss Federal Institute of Technology) Zürich.

Ever find when you’re frustrated and in a rush you end up making more mistakes? Same deal. Coauthor Jasmine Kerr noted that “increased levels of stress negatively impact our brain’s ability to process information.” Which totally is going to affect how we move.

Hopefully, these results can give insight to companies on how stressed their employees are and the effect it has on their work performance, eventually leading to, guess what, more research on how to alleviate workplace stress in general, which can benefit us all.

So if you find yourself in the office working on your computer like it’s a game of Perfection and time is running out, take a beat. Maybe try a stress-relieving breathing technique. Nonstressed people, according to the study, take fewer and longer pauses on their computers. Perfection on the job may mean relaxing first.

In a new scientific statement, the American Heart Association highlighted the importance of incorporating nonbiological risk factors and social determinants of health in cardiovascular disease (CVD) risk assessment for women, particularly women from different racial and ethnic backgrounds.
 

CVD risk assessment in women is multifaceted and goes well beyond traditional risk factors to include sex-specific biological risk factors, as well as social, behavioral, and environmental factors, the writing group noted.

They said a greater focus on addressing all CVD risk factors among women from underrepresented races and ethnicities is warranted to avert future CVD.

The scientific statement was published online in Circulation.
 

Look beyond traditional risk factors

“Risk assessment is the first step in preventing heart disease, yet there are many limitations to traditional risk factors and their ability to comprehensively estimate a woman’s risk for cardiovascular disease,” Jennifer H. Mieres, MD, vice chair of the writing group and professor of cardiology at Hofstra University, Hempstead, N.Y., said in a news release. 

“The delivery of equitable cardiovascular health care for women depends on improving the knowledge and awareness of all members of the healthcare team about the full spectrum of cardiovascular risk factors for women, including female-specific and female-predominant risk factors,” Dr. Mieres added.

Female-specific factors that should be included in CVD risk assessment include pregnancy-related conditions such as preeclampsia, preterm delivery, and gestational diabetes, the writing group said.

Other factors include menstrual cycle history; types of birth control and/or hormone replacement therapy used; polycystic ovarian syndrome (PCOS), which affects 10% of women of reproductive age and is associated with increased CVD risk; and autoimmune disorders, depression, and PTSD, all of which are more common in women and are also associated with higher risk for CVD.

The statement also highlights the key role that social determinants of health (SDOH) play in the development of CVD in women, particularly women from diverse racial and ethnic backgrounds. SDOH include education level, economic stability, neighborhood safety, working conditions, environmental hazards, and access to quality health care.

“It is critical that risk assessment be expanded to include [SDOH] as risk factors if we are to improve health outcomes in all women,” Laxmi Mehta, MD, chair of the writing group and director of preventative cardiology and women’s cardiovascular health at Ohio State University Wexner Medical Center, Columbus, said in the news release.

“It is also important for the health care team to consider [SDOH] when working with women on shared decisions about cardiovascular disease prevention and treatment,” Dr. Mehta noted.
 

No one-size-fits-all approach

The statement highlighted significant differences in CVD risk among women of different racial and ethnic backgrounds and provides detailed CV risk factor profiles for non-Hispanic Black, Hispanic/Latinx, Asian and American Indian/Alaska Native women.

It noted that language barriers, discrimination, acculturation, and health care access disproportionately affect women of underrepresented racial and ethnic groups. These factors result in a higher prevalence of CVD and significant challenges in CVD diagnosis and treatment.

“When customizing CVD prevention and treatment strategies to improve cardiovascular health for women, a one-size-fits-all approach is unlikely to be successful,” Dr. Mieres said.

“We must be cognizant of the complex interplay of sex, race and ethnicity, as well as social determinants of health, and how they impact the risk of cardiovascular disease and adverse outcomes in order to avert future CVD morbidity and mortality,” Dr. Mieres added.

Looking ahead, the writing group said future CVD prevention guidelines could be strengthened by including culturally-specific lifestyle recommendations.

They also said community-based approaches, faith-based community partnerships, and peer support to encourage a healthy lifestyle could play a key role in preventing CVD among all women.

This scientific statement was prepared by the volunteer writing group on behalf of the AHA’s Cardiovascular Disease and Stroke in Women and Underrepresented Populations Committee of the Council on Clinical Cardiology, the Council on Cardiovascular and Stroke Nursing, the Council on Hypertension, the Council on Lifelong Congenital Heart Disease and Heart Health in the Young, the Council on Lifestyle and Cardiometabolic Health, the Council on Peripheral Vascular Disease, and the Stroke Council.

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

In a new scientific statement, the American Heart Association highlighted the importance of incorporating nonbiological risk factors and social determinants of health in cardiovascular disease (CVD) risk assessment for women, particularly women from different racial and ethnic backgrounds.
 

CVD risk assessment in women is multifaceted and goes well beyond traditional risk factors to include sex-specific biological risk factors, as well as social, behavioral, and environmental factors, the writing group noted.

They said a greater focus on addressing all CVD risk factors among women from underrepresented races and ethnicities is warranted to avert future CVD.

The scientific statement was published online in Circulation.
 

Look beyond traditional risk factors

“Risk assessment is the first step in preventing heart disease, yet there are many limitations to traditional risk factors and their ability to comprehensively estimate a woman’s risk for cardiovascular disease,” Jennifer H. Mieres, MD, vice chair of the writing group and professor of cardiology at Hofstra University, Hempstead, N.Y., said in a news release. 

“The delivery of equitable cardiovascular health care for women depends on improving the knowledge and awareness of all members of the healthcare team about the full spectrum of cardiovascular risk factors for women, including female-specific and female-predominant risk factors,” Dr. Mieres added.

Female-specific factors that should be included in CVD risk assessment include pregnancy-related conditions such as preeclampsia, preterm delivery, and gestational diabetes, the writing group said.

Other factors include menstrual cycle history; types of birth control and/or hormone replacement therapy used; polycystic ovarian syndrome (PCOS), which affects 10% of women of reproductive age and is associated with increased CVD risk; and autoimmune disorders, depression, and PTSD, all of which are more common in women and are also associated with higher risk for CVD.

The statement also highlights the key role that social determinants of health (SDOH) play in the development of CVD in women, particularly women from diverse racial and ethnic backgrounds. SDOH include education level, economic stability, neighborhood safety, working conditions, environmental hazards, and access to quality health care.

“It is critical that risk assessment be expanded to include [SDOH] as risk factors if we are to improve health outcomes in all women,” Laxmi Mehta, MD, chair of the writing group and director of preventative cardiology and women’s cardiovascular health at Ohio State University Wexner Medical Center, Columbus, said in the news release.

“It is also important for the health care team to consider [SDOH] when working with women on shared decisions about cardiovascular disease prevention and treatment,” Dr. Mehta noted.
 

No one-size-fits-all approach

The statement highlighted significant differences in CVD risk among women of different racial and ethnic backgrounds and provides detailed CV risk factor profiles for non-Hispanic Black, Hispanic/Latinx, Asian and American Indian/Alaska Native women.

It noted that language barriers, discrimination, acculturation, and health care access disproportionately affect women of underrepresented racial and ethnic groups. These factors result in a higher prevalence of CVD and significant challenges in CVD diagnosis and treatment.

“When customizing CVD prevention and treatment strategies to improve cardiovascular health for women, a one-size-fits-all approach is unlikely to be successful,” Dr. Mieres said.

“We must be cognizant of the complex interplay of sex, race and ethnicity, as well as social determinants of health, and how they impact the risk of cardiovascular disease and adverse outcomes in order to avert future CVD morbidity and mortality,” Dr. Mieres added.

Looking ahead, the writing group said future CVD prevention guidelines could be strengthened by including culturally-specific lifestyle recommendations.

They also said community-based approaches, faith-based community partnerships, and peer support to encourage a healthy lifestyle could play a key role in preventing CVD among all women.

This scientific statement was prepared by the volunteer writing group on behalf of the AHA’s Cardiovascular Disease and Stroke in Women and Underrepresented Populations Committee of the Council on Clinical Cardiology, the Council on Cardiovascular and Stroke Nursing, the Council on Hypertension, the Council on Lifelong Congenital Heart Disease and Heart Health in the Young, the Council on Lifestyle and Cardiometabolic Health, the Council on Peripheral Vascular Disease, and the Stroke Council.

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

In a new scientific statement, the American Heart Association highlighted the importance of incorporating nonbiological risk factors and social determinants of health in cardiovascular disease (CVD) risk assessment for women, particularly women from different racial and ethnic backgrounds.
 

CVD risk assessment in women is multifaceted and goes well beyond traditional risk factors to include sex-specific biological risk factors, as well as social, behavioral, and environmental factors, the writing group noted.

They said a greater focus on addressing all CVD risk factors among women from underrepresented races and ethnicities is warranted to avert future CVD.

The scientific statement was published online in Circulation.
 

Look beyond traditional risk factors

“Risk assessment is the first step in preventing heart disease, yet there are many limitations to traditional risk factors and their ability to comprehensively estimate a woman’s risk for cardiovascular disease,” Jennifer H. Mieres, MD, vice chair of the writing group and professor of cardiology at Hofstra University, Hempstead, N.Y., said in a news release. 

“The delivery of equitable cardiovascular health care for women depends on improving the knowledge and awareness of all members of the healthcare team about the full spectrum of cardiovascular risk factors for women, including female-specific and female-predominant risk factors,” Dr. Mieres added.

Female-specific factors that should be included in CVD risk assessment include pregnancy-related conditions such as preeclampsia, preterm delivery, and gestational diabetes, the writing group said.

Other factors include menstrual cycle history; types of birth control and/or hormone replacement therapy used; polycystic ovarian syndrome (PCOS), which affects 10% of women of reproductive age and is associated with increased CVD risk; and autoimmune disorders, depression, and PTSD, all of which are more common in women and are also associated with higher risk for CVD.

The statement also highlights the key role that social determinants of health (SDOH) play in the development of CVD in women, particularly women from diverse racial and ethnic backgrounds. SDOH include education level, economic stability, neighborhood safety, working conditions, environmental hazards, and access to quality health care.

“It is critical that risk assessment be expanded to include [SDOH] as risk factors if we are to improve health outcomes in all women,” Laxmi Mehta, MD, chair of the writing group and director of preventative cardiology and women’s cardiovascular health at Ohio State University Wexner Medical Center, Columbus, said in the news release.

“It is also important for the health care team to consider [SDOH] when working with women on shared decisions about cardiovascular disease prevention and treatment,” Dr. Mehta noted.
 

No one-size-fits-all approach

The statement highlighted significant differences in CVD risk among women of different racial and ethnic backgrounds and provides detailed CV risk factor profiles for non-Hispanic Black, Hispanic/Latinx, Asian and American Indian/Alaska Native women.

It noted that language barriers, discrimination, acculturation, and health care access disproportionately affect women of underrepresented racial and ethnic groups. These factors result in a higher prevalence of CVD and significant challenges in CVD diagnosis and treatment.

“When customizing CVD prevention and treatment strategies to improve cardiovascular health for women, a one-size-fits-all approach is unlikely to be successful,” Dr. Mieres said.

“We must be cognizant of the complex interplay of sex, race and ethnicity, as well as social determinants of health, and how they impact the risk of cardiovascular disease and adverse outcomes in order to avert future CVD morbidity and mortality,” Dr. Mieres added.

Looking ahead, the writing group said future CVD prevention guidelines could be strengthened by including culturally-specific lifestyle recommendations.

They also said community-based approaches, faith-based community partnerships, and peer support to encourage a healthy lifestyle could play a key role in preventing CVD among all women.

This scientific statement was prepared by the volunteer writing group on behalf of the AHA’s Cardiovascular Disease and Stroke in Women and Underrepresented Populations Committee of the Council on Clinical Cardiology, the Council on Cardiovascular and Stroke Nursing, the Council on Hypertension, the Council on Lifelong Congenital Heart Disease and Heart Health in the Young, the Council on Lifestyle and Cardiometabolic Health, the Council on Peripheral Vascular Disease, and the Stroke Council.

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

The American Society of Echocardiography (ASE) has issued guidance on all critical aspects of training for cardiology and anesthesiology trainees and postgraduate echocardiographers who plan to specialize in interventional echocardiography (IE).

The guideline outlines requirements of the training institution, the duration and core competencies of training, minimal procedural volume for competency in IE, and knowledge of specific structural health disease (SHD) procedures.

The 16-page guideline was published online  in the Journal of the American Society of Echocardiography.
 

Specific skill set

IE is the primary imaging modality used to support and guide SHD interventions, such as heart valve replacements and other cardiac catheterization procedures, the writing group notes.

They say the “emerging specialty” of IE requires a specific set of skills to support an array of transcatheter therapies, with successful outcomes highly dependent on the skill of the echocardiography team.

“IE techniques are unique since imaging is performed in real-time, it is highly dependent on 3D and non-standard views, and it has immediate and profound implications for patient management,” Stephen H. Little, MD, ASE president and co-chair of the guideline writing group, says in a news release.

“Additionally, IE requires candid, accurate, and timely communication with other members of the multidisciplinary SHD team,” Dr. Little adds.

The new ASE guideline expands on the 2019 statement on echocardiography training put forward by the American College of Cardiology, American Heart Association, and ASE, by focusing specifically on interventional echocardiographers.

It outlines core competencies common to all transcatheter therapies, as well as specific transcatheter procedures. It provides consensus recommendations for specific knowledge, experience, and skills to be learned and demonstrated within an IE training program or during postgraduate training.

A “core principle” in the guideline states that the length of IE training or achieved number of procedures performed are less important than the demonstration of procedure-specific competencies within the milestone domains of knowledge, skill, and communication.

“Transcatheter therapies for SHD continue to grow at a rapid pace, which means that the demand for skilled interventional echocardiographers has steadily increased,” Vera H. Rigolin, MD, co-chair of the guideline writing, says in the release.

“Training standards are needed to ensure that interventional echocardiographers have the necessary expertise to provide fast, accurate, and high-quality image acquisition and interpretation in real-time,” Dr. Rigolin adds.

In addition, the guidelines states that use of simulation training has a role in IE training.

Virtual and simulation training could shorten the learning curve for trainees and, when combined with remote learning, could permit societies to standardize a teaching curriculum and allow the trainee to complete training in a reasonable timeframe. Simulator training may also improve access to training and thus promote diversity and inclusivity, the writing group says.

The guideline has been endorsed by 21 ASE international partners.

Writing group co-chairs Little and Rigolin have declared no conflicts of interest. A complete list of disclosures for the writing group is available with the original article.

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

The American Society of Echocardiography (ASE) has issued guidance on all critical aspects of training for cardiology and anesthesiology trainees and postgraduate echocardiographers who plan to specialize in interventional echocardiography (IE).

The guideline outlines requirements of the training institution, the duration and core competencies of training, minimal procedural volume for competency in IE, and knowledge of specific structural health disease (SHD) procedures.

The 16-page guideline was published online  in the Journal of the American Society of Echocardiography.
 

Specific skill set

IE is the primary imaging modality used to support and guide SHD interventions, such as heart valve replacements and other cardiac catheterization procedures, the writing group notes.

They say the “emerging specialty” of IE requires a specific set of skills to support an array of transcatheter therapies, with successful outcomes highly dependent on the skill of the echocardiography team.

“IE techniques are unique since imaging is performed in real-time, it is highly dependent on 3D and non-standard views, and it has immediate and profound implications for patient management,” Stephen H. Little, MD, ASE president and co-chair of the guideline writing group, says in a news release.

“Additionally, IE requires candid, accurate, and timely communication with other members of the multidisciplinary SHD team,” Dr. Little adds.

The new ASE guideline expands on the 2019 statement on echocardiography training put forward by the American College of Cardiology, American Heart Association, and ASE, by focusing specifically on interventional echocardiographers.

It outlines core competencies common to all transcatheter therapies, as well as specific transcatheter procedures. It provides consensus recommendations for specific knowledge, experience, and skills to be learned and demonstrated within an IE training program or during postgraduate training.

A “core principle” in the guideline states that the length of IE training or achieved number of procedures performed are less important than the demonstration of procedure-specific competencies within the milestone domains of knowledge, skill, and communication.

“Transcatheter therapies for SHD continue to grow at a rapid pace, which means that the demand for skilled interventional echocardiographers has steadily increased,” Vera H. Rigolin, MD, co-chair of the guideline writing, says in the release.

“Training standards are needed to ensure that interventional echocardiographers have the necessary expertise to provide fast, accurate, and high-quality image acquisition and interpretation in real-time,” Dr. Rigolin adds.

In addition, the guidelines states that use of simulation training has a role in IE training.

Virtual and simulation training could shorten the learning curve for trainees and, when combined with remote learning, could permit societies to standardize a teaching curriculum and allow the trainee to complete training in a reasonable timeframe. Simulator training may also improve access to training and thus promote diversity and inclusivity, the writing group says.

The guideline has been endorsed by 21 ASE international partners.

Writing group co-chairs Little and Rigolin have declared no conflicts of interest. A complete list of disclosures for the writing group is available with the original article.

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

The American Society of Echocardiography (ASE) has issued guidance on all critical aspects of training for cardiology and anesthesiology trainees and postgraduate echocardiographers who plan to specialize in interventional echocardiography (IE).

The guideline outlines requirements of the training institution, the duration and core competencies of training, minimal procedural volume for competency in IE, and knowledge of specific structural health disease (SHD) procedures.

The 16-page guideline was published online  in the Journal of the American Society of Echocardiography.
 

Specific skill set

IE is the primary imaging modality used to support and guide SHD interventions, such as heart valve replacements and other cardiac catheterization procedures, the writing group notes.

They say the “emerging specialty” of IE requires a specific set of skills to support an array of transcatheter therapies, with successful outcomes highly dependent on the skill of the echocardiography team.

“IE techniques are unique since imaging is performed in real-time, it is highly dependent on 3D and non-standard views, and it has immediate and profound implications for patient management,” Stephen H. Little, MD, ASE president and co-chair of the guideline writing group, says in a news release.

“Additionally, IE requires candid, accurate, and timely communication with other members of the multidisciplinary SHD team,” Dr. Little adds.

The new ASE guideline expands on the 2019 statement on echocardiography training put forward by the American College of Cardiology, American Heart Association, and ASE, by focusing specifically on interventional echocardiographers.

It outlines core competencies common to all transcatheter therapies, as well as specific transcatheter procedures. It provides consensus recommendations for specific knowledge, experience, and skills to be learned and demonstrated within an IE training program or during postgraduate training.

A “core principle” in the guideline states that the length of IE training or achieved number of procedures performed are less important than the demonstration of procedure-specific competencies within the milestone domains of knowledge, skill, and communication.

“Transcatheter therapies for SHD continue to grow at a rapid pace, which means that the demand for skilled interventional echocardiographers has steadily increased,” Vera H. Rigolin, MD, co-chair of the guideline writing, says in the release.

“Training standards are needed to ensure that interventional echocardiographers have the necessary expertise to provide fast, accurate, and high-quality image acquisition and interpretation in real-time,” Dr. Rigolin adds.

In addition, the guidelines states that use of simulation training has a role in IE training.

Virtual and simulation training could shorten the learning curve for trainees and, when combined with remote learning, could permit societies to standardize a teaching curriculum and allow the trainee to complete training in a reasonable timeframe. Simulator training may also improve access to training and thus promote diversity and inclusivity, the writing group says.

The guideline has been endorsed by 21 ASE international partners.

Writing group co-chairs Little and Rigolin have declared no conflicts of interest. A complete list of disclosures for the writing group is available with the original article.

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

Among adults with diabetes but no history of heart failure (HF), taking a NSAID – even for only a month – sharply raises the risk of an HF hospitalization, suggests a prospective, controlled study.
 

Certain subgroups may account for much of the excess risk, the results suggest, including the very elderly, patients with uncontrolled diabetes, those prescribed an NSAID for the first time, and patients already taking both a renin-angiotensin system inhibitor (RASi) and a diuretic.

Such patients with a firm indication for NSAIDs potentially could “be the ones benefiting most from closer follow-up, reduced dosage, or other mitigation strategies,” Anders Holt, MD, said in an interview.

Dr. Holt, of Copenhagen University Hospital and Herlev-Gentofte Hospital in Hellerup, Denmark, is lead author on the analysis of Danish registry data published in the Journal of the American College of Cardiology. He presented essentially the same results in preliminary form at the 2022 annual congress of the European Society of Cardiology.

HF hospitalizations linked to NSAIDs, the published report notes, are often attributed to symptoms from temporary fluid overload, often without worsening cardiac function, that stem from the drugs’ renal effects.

“One could speculate,” Dr. Holt said, that such HF events might be less severe and even associated with better outcomes, compared with other forms of heart failure.

But the current analysis provides a hint to the contrary, he observed. The 5-year mortality was similar for patients with HF linked to NSAIDs and those with other forms of HF, “which could suggest that NSAID-associated heart failure is more than transient fluid overload.”

The drugs may promote HF through direct effects on the heart by any of several proposed mechanisms, including “induction of arrhythmias and heart fibrosis, vasoconstriction, subclinical inflammation, and blood pressure elevation,” Dr. Holt said.

The current study doesn’t determine whether NSAID-associated HF stems from transient fluid overload or direct cardiac effects, but it’s “most likely both.”

In other limitations, the analysis is unable to “reliably explore” whether promotion of HF is an NSAID class effect, a “clinically relevant” point given the drugs’ varying effects on cardiovascular risk, states an accompanying editorial. Nor was it able to determine whether the drugs exert a dose-response effect on HF risk, noted Hassan Khan, MD, PhD, Norton Healthcare, Louisville, Ky., and Setor K. Kunutsor, MD, PhD, University of Leicester (England).

Still, “given the well-established relationship between the use of NSAIDs and increased HF, these findings are not unexpected because type 2 diabetes is also a major risk factor for HF.”

But it may be “premature to issue guideline recommendations based on a single observational study,” the editorialists wrote. “Further robust clinical trial evidence is needed to replicate these results and investigate the relationship of the type and dose of NSAIDs with HF risk. However, it should be realized that short-term or long-term use of NSAIDs may be detrimental to cardiovascular health.”

The analysis covered 23,308 patients from throughout Denmark with a type 2 diabetes diagnosis and no HF history who experienced a first HF hospitalization; their age averaged 76 years and 39% were women.

They served as their own controls; their NSAID exposures at two 28-day periods preceding the HF event, the one immediately before and the other preceding it by 56 days, were compared as the index and control periods, respectively.

Exposure to NSAIDs was defined as obtaining a prescription for celecoxib, diclofenac, ibuprofen, or naproxen, “as these are NSAIDs used primarily in Denmark,” the report states.

The odds ratios for HF hospitalization associated with NSAID exposure within 28 days preceding the event were 1.43 (95% confidence interval, 1.27-1.63) overall, 1.41 (95% CI, 1.16-1.71) for an NSAID given on top of both RASi and diuretics, 1.68 (95% CI, 1.00-2.88) for patients with elevated hemoglobin A1c, 1.78 (95% CI, 1.39-2.28) for those 80 or older, and 2.71 (95% CI, 1.78-4.23) for those with prior NSAID use.

That NSAID use and diabetes are each associated with increased risk for HF is well established, Dr. Holt observed. Yet the drugs had been prescribed to 16% of patients in the study.

“One of the more surprising findings, to me, was the quite substantial use of prescribed NSAIDs in a population of patients with diabetes, a patient group with a well-established cardiovascular risk,” he said.

“This patient group is only growing, so emphasis on the possible associations between even short-term NSAID use and incident heart failure is probably timely and perhaps needed.”

Dr. Holt and the study were supported by grants from Ib Mogens Kristiansens Almene Fond, Helsefonden, Snedkermester Sophus Jacobsen og hustru Astrid Jacobsen Fond, Marie og M.B. Richters Fond, and the Dagmar Marshalls Fond. Dr. Khan and Dr. Kunutsor reported no relevant relationships.

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

Among adults with diabetes but no history of heart failure (HF), taking a NSAID – even for only a month – sharply raises the risk of an HF hospitalization, suggests a prospective, controlled study.
 

Certain subgroups may account for much of the excess risk, the results suggest, including the very elderly, patients with uncontrolled diabetes, those prescribed an NSAID for the first time, and patients already taking both a renin-angiotensin system inhibitor (RASi) and a diuretic.

Such patients with a firm indication for NSAIDs potentially could “be the ones benefiting most from closer follow-up, reduced dosage, or other mitigation strategies,” Anders Holt, MD, said in an interview.

Dr. Holt, of Copenhagen University Hospital and Herlev-Gentofte Hospital in Hellerup, Denmark, is lead author on the analysis of Danish registry data published in the Journal of the American College of Cardiology. He presented essentially the same results in preliminary form at the 2022 annual congress of the European Society of Cardiology.

HF hospitalizations linked to NSAIDs, the published report notes, are often attributed to symptoms from temporary fluid overload, often without worsening cardiac function, that stem from the drugs’ renal effects.

“One could speculate,” Dr. Holt said, that such HF events might be less severe and even associated with better outcomes, compared with other forms of heart failure.

But the current analysis provides a hint to the contrary, he observed. The 5-year mortality was similar for patients with HF linked to NSAIDs and those with other forms of HF, “which could suggest that NSAID-associated heart failure is more than transient fluid overload.”

The drugs may promote HF through direct effects on the heart by any of several proposed mechanisms, including “induction of arrhythmias and heart fibrosis, vasoconstriction, subclinical inflammation, and blood pressure elevation,” Dr. Holt said.

The current study doesn’t determine whether NSAID-associated HF stems from transient fluid overload or direct cardiac effects, but it’s “most likely both.”

In other limitations, the analysis is unable to “reliably explore” whether promotion of HF is an NSAID class effect, a “clinically relevant” point given the drugs’ varying effects on cardiovascular risk, states an accompanying editorial. Nor was it able to determine whether the drugs exert a dose-response effect on HF risk, noted Hassan Khan, MD, PhD, Norton Healthcare, Louisville, Ky., and Setor K. Kunutsor, MD, PhD, University of Leicester (England).

Still, “given the well-established relationship between the use of NSAIDs and increased HF, these findings are not unexpected because type 2 diabetes is also a major risk factor for HF.”

But it may be “premature to issue guideline recommendations based on a single observational study,” the editorialists wrote. “Further robust clinical trial evidence is needed to replicate these results and investigate the relationship of the type and dose of NSAIDs with HF risk. However, it should be realized that short-term or long-term use of NSAIDs may be detrimental to cardiovascular health.”

The analysis covered 23,308 patients from throughout Denmark with a type 2 diabetes diagnosis and no HF history who experienced a first HF hospitalization; their age averaged 76 years and 39% were women.

They served as their own controls; their NSAID exposures at two 28-day periods preceding the HF event, the one immediately before and the other preceding it by 56 days, were compared as the index and control periods, respectively.

Exposure to NSAIDs was defined as obtaining a prescription for celecoxib, diclofenac, ibuprofen, or naproxen, “as these are NSAIDs used primarily in Denmark,” the report states.

The odds ratios for HF hospitalization associated with NSAID exposure within 28 days preceding the event were 1.43 (95% confidence interval, 1.27-1.63) overall, 1.41 (95% CI, 1.16-1.71) for an NSAID given on top of both RASi and diuretics, 1.68 (95% CI, 1.00-2.88) for patients with elevated hemoglobin A1c, 1.78 (95% CI, 1.39-2.28) for those 80 or older, and 2.71 (95% CI, 1.78-4.23) for those with prior NSAID use.

That NSAID use and diabetes are each associated with increased risk for HF is well established, Dr. Holt observed. Yet the drugs had been prescribed to 16% of patients in the study.

“One of the more surprising findings, to me, was the quite substantial use of prescribed NSAIDs in a population of patients with diabetes, a patient group with a well-established cardiovascular risk,” he said.

“This patient group is only growing, so emphasis on the possible associations between even short-term NSAID use and incident heart failure is probably timely and perhaps needed.”

Dr. Holt and the study were supported by grants from Ib Mogens Kristiansens Almene Fond, Helsefonden, Snedkermester Sophus Jacobsen og hustru Astrid Jacobsen Fond, Marie og M.B. Richters Fond, and the Dagmar Marshalls Fond. Dr. Khan and Dr. Kunutsor reported no relevant relationships.

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

Among adults with diabetes but no history of heart failure (HF), taking a NSAID – even for only a month – sharply raises the risk of an HF hospitalization, suggests a prospective, controlled study.
 

Certain subgroups may account for much of the excess risk, the results suggest, including the very elderly, patients with uncontrolled diabetes, those prescribed an NSAID for the first time, and patients already taking both a renin-angiotensin system inhibitor (RASi) and a diuretic.

Such patients with a firm indication for NSAIDs potentially could “be the ones benefiting most from closer follow-up, reduced dosage, or other mitigation strategies,” Anders Holt, MD, said in an interview.

Dr. Holt, of Copenhagen University Hospital and Herlev-Gentofte Hospital in Hellerup, Denmark, is lead author on the analysis of Danish registry data published in the Journal of the American College of Cardiology. He presented essentially the same results in preliminary form at the 2022 annual congress of the European Society of Cardiology.

HF hospitalizations linked to NSAIDs, the published report notes, are often attributed to symptoms from temporary fluid overload, often without worsening cardiac function, that stem from the drugs’ renal effects.

“One could speculate,” Dr. Holt said, that such HF events might be less severe and even associated with better outcomes, compared with other forms of heart failure.

But the current analysis provides a hint to the contrary, he observed. The 5-year mortality was similar for patients with HF linked to NSAIDs and those with other forms of HF, “which could suggest that NSAID-associated heart failure is more than transient fluid overload.”

The drugs may promote HF through direct effects on the heart by any of several proposed mechanisms, including “induction of arrhythmias and heart fibrosis, vasoconstriction, subclinical inflammation, and blood pressure elevation,” Dr. Holt said.

The current study doesn’t determine whether NSAID-associated HF stems from transient fluid overload or direct cardiac effects, but it’s “most likely both.”

In other limitations, the analysis is unable to “reliably explore” whether promotion of HF is an NSAID class effect, a “clinically relevant” point given the drugs’ varying effects on cardiovascular risk, states an accompanying editorial. Nor was it able to determine whether the drugs exert a dose-response effect on HF risk, noted Hassan Khan, MD, PhD, Norton Healthcare, Louisville, Ky., and Setor K. Kunutsor, MD, PhD, University of Leicester (England).

Still, “given the well-established relationship between the use of NSAIDs and increased HF, these findings are not unexpected because type 2 diabetes is also a major risk factor for HF.”

But it may be “premature to issue guideline recommendations based on a single observational study,” the editorialists wrote. “Further robust clinical trial evidence is needed to replicate these results and investigate the relationship of the type and dose of NSAIDs with HF risk. However, it should be realized that short-term or long-term use of NSAIDs may be detrimental to cardiovascular health.”

The analysis covered 23,308 patients from throughout Denmark with a type 2 diabetes diagnosis and no HF history who experienced a first HF hospitalization; their age averaged 76 years and 39% were women.

They served as their own controls; their NSAID exposures at two 28-day periods preceding the HF event, the one immediately before and the other preceding it by 56 days, were compared as the index and control periods, respectively.

Exposure to NSAIDs was defined as obtaining a prescription for celecoxib, diclofenac, ibuprofen, or naproxen, “as these are NSAIDs used primarily in Denmark,” the report states.

The odds ratios for HF hospitalization associated with NSAID exposure within 28 days preceding the event were 1.43 (95% confidence interval, 1.27-1.63) overall, 1.41 (95% CI, 1.16-1.71) for an NSAID given on top of both RASi and diuretics, 1.68 (95% CI, 1.00-2.88) for patients with elevated hemoglobin A1c, 1.78 (95% CI, 1.39-2.28) for those 80 or older, and 2.71 (95% CI, 1.78-4.23) for those with prior NSAID use.

That NSAID use and diabetes are each associated with increased risk for HF is well established, Dr. Holt observed. Yet the drugs had been prescribed to 16% of patients in the study.

“One of the more surprising findings, to me, was the quite substantial use of prescribed NSAIDs in a population of patients with diabetes, a patient group with a well-established cardiovascular risk,” he said.

“This patient group is only growing, so emphasis on the possible associations between even short-term NSAID use and incident heart failure is probably timely and perhaps needed.”

Dr. Holt and the study were supported by grants from Ib Mogens Kristiansens Almene Fond, Helsefonden, Snedkermester Sophus Jacobsen og hustru Astrid Jacobsen Fond, Marie og M.B. Richters Fond, and the Dagmar Marshalls Fond. Dr. Khan and Dr. Kunutsor reported no relevant relationships.

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

Atrial fibrillation (AFib) is a known and serious side effect of some cancer treatments, but it is underreported in cancer drug trials, French investigators said in a new report.

As a result, oncologists likely underestimate the risk of atrial fibrillation when new cancer drugs come to market, they said.

The team came to these conclusions after conducting a meta-analysis of 191 phase 2 or 3 clinical trials that included 26,604 patients. The trials investigated 15 anticancer drugs used as monotherapy.

The meta-analysis showed that the annualized incidence rate of AFib ranged from 0.26 cases per 100 person-years – about the same as placebo – to 4.92 cases, a nearly 20 times’ higher risk.

Rates were the highest for ibrutinib, clofarabine, and ponatinib.

The study was published in JACC: CardioOncology, a journal of the American College of Cardiology.

Actual rates of AFib are probably higher than what they found in this meta-analysis, the authors suspect, because most oncology trials only identify and report severe cases of AFib that require immediate medical attention. Less severe cases can also lead to serious complications, including strokes, but they go unreported, said the investigators, led by Joachim Alexandre, MD, PhD, a member of the cardio-oncology program at the University of Caen Normandie Hospital Center, France.

“These findings suggest a global and systemic underreporting and/or underidentification of cardiotoxicity among cancer clinical trial participants,” and AFib reporting is “particularly affected,” they said.
 

Call for routine monitoring

The root of the problem is the lack of routine rhythm monitoring in cancer trials. This in turn “leads to a significant underestimation of AFib incidence” and rates “markedly lower than those observed among real-life” patients, the authors pointed out.

To address the issue, Dr. Alexandre and his team called for routine cardiac monitoring in trials to capture the true incidence of AFib and to “clearly define which anticancer drugs are significantly associated” with the condition.

Approached for comment, Michael G. Fradley, MD, medical director of cardio-oncology at the University of Pennsylvania, Philadelphia, agreed.

“It’s incredibly important” to “identify the drugs most likely to cause arrhythmias and determine the best prevention and treatment strategies. Unfortunately, systematic evaluation of arrhythmias in cancer clinical trials has often been lacking,” Dr. Fradley told this news organization.

The investigators said the issue is particularly pressing for drugs known to be associated with AFib. For Bruton’s tyrosine kinase inhibitors such as ibrutinib, for instance, they call for standardize AFib detection in trials “not only on 12-lead ECGs” for symptomatic AFib but also with “longer-term ambulatory monitoring or insertable cardiac monitors to detect subclinical AFib.”

Dr. Fradley said there might also be a role for newer wearable technologies that can detect arrhythmias through a skin patch or by other means.
 

Details of the meta-analysis

The investigators pulled the 191 studies they used in their meta-analysis from the ClinicalTrials.gov database.

The trials covered anticancer drugs used as monotherapy up to Sept. 18, 2020. Almost half were randomized trials, but only seven had placebo arms. Trials involving hematologic cancers outnumbered those involving solid tumors.

The 15 drugs examined were dacarbazine, abiraterone, clofarabine, azacitidine, ibrutinib, nilotinib, ponatinib, midostaurin, ipilimumab, aldesleukin, lenalidomide, pomalidomide, rituximab, bortezomib, and docetaxel.

The annualized incidence AFib rates per 100 person-years were 4.92 cases for ibrutinib, 2.38 cases for clofarabine, and 2.35 cases for ponatinib.

The lowest AFib rates were for ipilimumab (0.26 cases), rituximab (0.27), and nilotinib (0.29).

For placebo, the annualized rate was 0.25 cases per 100 person-years.

The team said caution is warranted regarding their estimations for clofarabine and midostaurin (0.65 cases) because no trials were registered after September 2009, when adverse event reporting became mandatory. As a result, estimates may be artificially low.

One of the limits of the study is that it focused on monotherapy in an age when combination treatment is generally the rule for cancer, the authors noted.

No external funding was reported for the study. Dr. Alexandre has received honoraria for presentations and consulting fees from Bayer, BMS, Pfizer, Amgen, and Bioserenity.
 

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

Atrial fibrillation (AFib) is a known and serious side effect of some cancer treatments, but it is underreported in cancer drug trials, French investigators said in a new report.

As a result, oncologists likely underestimate the risk of atrial fibrillation when new cancer drugs come to market, they said.

The team came to these conclusions after conducting a meta-analysis of 191 phase 2 or 3 clinical trials that included 26,604 patients. The trials investigated 15 anticancer drugs used as monotherapy.

The meta-analysis showed that the annualized incidence rate of AFib ranged from 0.26 cases per 100 person-years – about the same as placebo – to 4.92 cases, a nearly 20 times’ higher risk.

Rates were the highest for ibrutinib, clofarabine, and ponatinib.

The study was published in JACC: CardioOncology, a journal of the American College of Cardiology.

Actual rates of AFib are probably higher than what they found in this meta-analysis, the authors suspect, because most oncology trials only identify and report severe cases of AFib that require immediate medical attention. Less severe cases can also lead to serious complications, including strokes, but they go unreported, said the investigators, led by Joachim Alexandre, MD, PhD, a member of the cardio-oncology program at the University of Caen Normandie Hospital Center, France.

“These findings suggest a global and systemic underreporting and/or underidentification of cardiotoxicity among cancer clinical trial participants,” and AFib reporting is “particularly affected,” they said.
 

Call for routine monitoring

The root of the problem is the lack of routine rhythm monitoring in cancer trials. This in turn “leads to a significant underestimation of AFib incidence” and rates “markedly lower than those observed among real-life” patients, the authors pointed out.

To address the issue, Dr. Alexandre and his team called for routine cardiac monitoring in trials to capture the true incidence of AFib and to “clearly define which anticancer drugs are significantly associated” with the condition.

Approached for comment, Michael G. Fradley, MD, medical director of cardio-oncology at the University of Pennsylvania, Philadelphia, agreed.

“It’s incredibly important” to “identify the drugs most likely to cause arrhythmias and determine the best prevention and treatment strategies. Unfortunately, systematic evaluation of arrhythmias in cancer clinical trials has often been lacking,” Dr. Fradley told this news organization.

The investigators said the issue is particularly pressing for drugs known to be associated with AFib. For Bruton’s tyrosine kinase inhibitors such as ibrutinib, for instance, they call for standardize AFib detection in trials “not only on 12-lead ECGs” for symptomatic AFib but also with “longer-term ambulatory monitoring or insertable cardiac monitors to detect subclinical AFib.”

Dr. Fradley said there might also be a role for newer wearable technologies that can detect arrhythmias through a skin patch or by other means.
 

Details of the meta-analysis

The investigators pulled the 191 studies they used in their meta-analysis from the ClinicalTrials.gov database.

The trials covered anticancer drugs used as monotherapy up to Sept. 18, 2020. Almost half were randomized trials, but only seven had placebo arms. Trials involving hematologic cancers outnumbered those involving solid tumors.

The 15 drugs examined were dacarbazine, abiraterone, clofarabine, azacitidine, ibrutinib, nilotinib, ponatinib, midostaurin, ipilimumab, aldesleukin, lenalidomide, pomalidomide, rituximab, bortezomib, and docetaxel.

The annualized incidence AFib rates per 100 person-years were 4.92 cases for ibrutinib, 2.38 cases for clofarabine, and 2.35 cases for ponatinib.

The lowest AFib rates were for ipilimumab (0.26 cases), rituximab (0.27), and nilotinib (0.29).

For placebo, the annualized rate was 0.25 cases per 100 person-years.

The team said caution is warranted regarding their estimations for clofarabine and midostaurin (0.65 cases) because no trials were registered after September 2009, when adverse event reporting became mandatory. As a result, estimates may be artificially low.

One of the limits of the study is that it focused on monotherapy in an age when combination treatment is generally the rule for cancer, the authors noted.

No external funding was reported for the study. Dr. Alexandre has received honoraria for presentations and consulting fees from Bayer, BMS, Pfizer, Amgen, and Bioserenity.
 

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

Atrial fibrillation (AFib) is a known and serious side effect of some cancer treatments, but it is underreported in cancer drug trials, French investigators said in a new report.

As a result, oncologists likely underestimate the risk of atrial fibrillation when new cancer drugs come to market, they said.

The team came to these conclusions after conducting a meta-analysis of 191 phase 2 or 3 clinical trials that included 26,604 patients. The trials investigated 15 anticancer drugs used as monotherapy.

The meta-analysis showed that the annualized incidence rate of AFib ranged from 0.26 cases per 100 person-years – about the same as placebo – to 4.92 cases, a nearly 20 times’ higher risk.

Rates were the highest for ibrutinib, clofarabine, and ponatinib.

The study was published in JACC: CardioOncology, a journal of the American College of Cardiology.

Actual rates of AFib are probably higher than what they found in this meta-analysis, the authors suspect, because most oncology trials only identify and report severe cases of AFib that require immediate medical attention. Less severe cases can also lead to serious complications, including strokes, but they go unreported, said the investigators, led by Joachim Alexandre, MD, PhD, a member of the cardio-oncology program at the University of Caen Normandie Hospital Center, France.

“These findings suggest a global and systemic underreporting and/or underidentification of cardiotoxicity among cancer clinical trial participants,” and AFib reporting is “particularly affected,” they said.
 

Call for routine monitoring

The root of the problem is the lack of routine rhythm monitoring in cancer trials. This in turn “leads to a significant underestimation of AFib incidence” and rates “markedly lower than those observed among real-life” patients, the authors pointed out.

To address the issue, Dr. Alexandre and his team called for routine cardiac monitoring in trials to capture the true incidence of AFib and to “clearly define which anticancer drugs are significantly associated” with the condition.

Approached for comment, Michael G. Fradley, MD, medical director of cardio-oncology at the University of Pennsylvania, Philadelphia, agreed.

“It’s incredibly important” to “identify the drugs most likely to cause arrhythmias and determine the best prevention and treatment strategies. Unfortunately, systematic evaluation of arrhythmias in cancer clinical trials has often been lacking,” Dr. Fradley told this news organization.

The investigators said the issue is particularly pressing for drugs known to be associated with AFib. For Bruton’s tyrosine kinase inhibitors such as ibrutinib, for instance, they call for standardize AFib detection in trials “not only on 12-lead ECGs” for symptomatic AFib but also with “longer-term ambulatory monitoring or insertable cardiac monitors to detect subclinical AFib.”

Dr. Fradley said there might also be a role for newer wearable technologies that can detect arrhythmias through a skin patch or by other means.
 

Details of the meta-analysis

The investigators pulled the 191 studies they used in their meta-analysis from the ClinicalTrials.gov database.

The trials covered anticancer drugs used as monotherapy up to Sept. 18, 2020. Almost half were randomized trials, but only seven had placebo arms. Trials involving hematologic cancers outnumbered those involving solid tumors.

The 15 drugs examined were dacarbazine, abiraterone, clofarabine, azacitidine, ibrutinib, nilotinib, ponatinib, midostaurin, ipilimumab, aldesleukin, lenalidomide, pomalidomide, rituximab, bortezomib, and docetaxel.

The annualized incidence AFib rates per 100 person-years were 4.92 cases for ibrutinib, 2.38 cases for clofarabine, and 2.35 cases for ponatinib.

The lowest AFib rates were for ipilimumab (0.26 cases), rituximab (0.27), and nilotinib (0.29).

For placebo, the annualized rate was 0.25 cases per 100 person-years.

The team said caution is warranted regarding their estimations for clofarabine and midostaurin (0.65 cases) because no trials were registered after September 2009, when adverse event reporting became mandatory. As a result, estimates may be artificially low.

One of the limits of the study is that it focused on monotherapy in an age when combination treatment is generally the rule for cancer, the authors noted.

No external funding was reported for the study. Dr. Alexandre has received honoraria for presentations and consulting fees from Bayer, BMS, Pfizer, Amgen, and Bioserenity.
 

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

The presence of antiphospholipid antibodies is associated with an increased risk for future cardiovascular events, according to a new study.

The findings point to possible new approaches to risk stratification and the potential for new therapeutic targets in heart disease.

“In this study of the general population, we found that two antiphospholipid antibodies were associated with an increased risk of having a serious cardiovascular event over a follow-up of 8 years,” coauthor Jason Knight, MD, University of Michigan, Ann Arbor, said in an interview.

“If confirmed in further studies, these findings could be used to identify a subgroup of patients who need more careful monitoring and more aggressive risk-factor modification, and if the increased risk linked to these antibodies is high enough, it may also justify preemptive treatments such as the anticoagulants that are routinely used in antiphospholipid syndrome,” Dr. Knight said.

“The long-term vision is that we may identify some people in the general population who would benefit from treating the immune system for the prevention and treatment of cardiovascular disease instead of, or in addition to, using typical cardiovascular medications,” he added.

The study was published online in JAMA Network Open.

Individuals with autoimmune and inflammatory diseases have a greater risk for cardiovascular events than expected based on traditional cardiovascular risk factors, with mechanisms proposed to explain this risk including inflammation-mediated disruption of vascular integrity and activation of platelets and coagulation pathways, the authors explained. However, the role of autoantibodies remains unclear.

They noted that antiphospholipid antibodies can activate endothelial cells, platelets, and neutrophils, and some patients with persistently circulating antiphospholipid antibodies can develop antiphospholipid syndrome – an acquired thromboinflammatory disease characterized by arterial, venous, and microvascular thrombotic events and obstetric complications.

Cross-sectional studies have shown that antiphospholipid antibodies are acutely present in up to 17.4% of patients with stroke or transient ischemic attack, and small cohort studies have suggested that such antibodies may be present in 1%-12% of seemingly healthy individuals. However, the impact of sex, race, and ethnicity on the prevalence of antiphospholipid antibodies and their association with atherosclerotic cardiovascular disease is not known.

The researchers conducted the current study to look at the association between antiphospholipid antibodies and future risk for atherosclerotic cardiovascular events.

They analyzed data from 2,427 participants in the population-based Dallas Heart Study who had no history of atherosclerotic cardiovascular disease or autoimmune diseases requiring immunosuppressive medications at the time of blood sampling at study entry in 2007-2009.

Eight different types of antiphospholipid antibodies were measured, and data on cardiovascular events over the next 8 years was recorded.

Results showed that 14.5% of the cohort tested positive for one of these antiphospholipid antibodies at the start of the study, with approximately one-third of those detected at a moderate or high titer.

The researchers also found that the IgA isotypes of two antiphospholipid antibodies – anticardiolipin and anti-beta-2 glycoprotein – were associated with future atherosclerotic cardiovascular events.

After adjustment for other known risk factors, individuals testing positive for the IgA isotype of anticardiolipin had an almost five times increased risk (hazard ratio, 4.92) of the primary endpoint (myocardial infarction, stroke, coronary revascularization, or cardiovascular death); while those testing positive for anti–beta₂-glycoprotein had an almost three times increased risk (HR, 2.91).

Furthermore, there was what appeared to be a dose effect. People with the highest levels of these antibodies also had the highest risk for cardiovascular events, with up to an almost 10-fold increased risk with the higher level of anticardiolipin. 

Dr. Knight said that more research into the IgA isotypes of these antiphospholipid antibodies is needed.

“Most of the mechanistic work in the antiphospholipid syndrome field has focused on IgG antiphospholipid antibodies. While we commonly find these IgA antibodies in patients with APS, the extent to which they contribute to disease has not been firmly established,” he said. “The fact that IgA was the primary hit in our unbiased screen suggests that there is more to the story and we need to better understand the implications of having these antibodies in circulation, and what specific problems they may be causing.”

Noting that antiphospholipid antibodies can form transiently after certain situations, such as infections, Dr. Knight said that further studies were needed with repeat blood testing to detect the chronic presence of the antibodies.

He added that information of venous thromboses was not available in this study and “perhaps some of the other antibodies might have stood out if we were able to analyze for different outcomes.”

This study was supported by a Pfizer Aspire Award. Dr. Knight reported receiving research funding and consulting fees from Jazz Pharmaceuticals outside the submitted work.

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

The presence of antiphospholipid antibodies is associated with an increased risk for future cardiovascular events, according to a new study.

The findings point to possible new approaches to risk stratification and the potential for new therapeutic targets in heart disease.

“In this study of the general population, we found that two antiphospholipid antibodies were associated with an increased risk of having a serious cardiovascular event over a follow-up of 8 years,” coauthor Jason Knight, MD, University of Michigan, Ann Arbor, said in an interview.

“If confirmed in further studies, these findings could be used to identify a subgroup of patients who need more careful monitoring and more aggressive risk-factor modification, and if the increased risk linked to these antibodies is high enough, it may also justify preemptive treatments such as the anticoagulants that are routinely used in antiphospholipid syndrome,” Dr. Knight said.

“The long-term vision is that we may identify some people in the general population who would benefit from treating the immune system for the prevention and treatment of cardiovascular disease instead of, or in addition to, using typical cardiovascular medications,” he added.

The study was published online in JAMA Network Open.

Individuals with autoimmune and inflammatory diseases have a greater risk for cardiovascular events than expected based on traditional cardiovascular risk factors, with mechanisms proposed to explain this risk including inflammation-mediated disruption of vascular integrity and activation of platelets and coagulation pathways, the authors explained. However, the role of autoantibodies remains unclear.

They noted that antiphospholipid antibodies can activate endothelial cells, platelets, and neutrophils, and some patients with persistently circulating antiphospholipid antibodies can develop antiphospholipid syndrome – an acquired thromboinflammatory disease characterized by arterial, venous, and microvascular thrombotic events and obstetric complications.

Cross-sectional studies have shown that antiphospholipid antibodies are acutely present in up to 17.4% of patients with stroke or transient ischemic attack, and small cohort studies have suggested that such antibodies may be present in 1%-12% of seemingly healthy individuals. However, the impact of sex, race, and ethnicity on the prevalence of antiphospholipid antibodies and their association with atherosclerotic cardiovascular disease is not known.

The researchers conducted the current study to look at the association between antiphospholipid antibodies and future risk for atherosclerotic cardiovascular events.

They analyzed data from 2,427 participants in the population-based Dallas Heart Study who had no history of atherosclerotic cardiovascular disease or autoimmune diseases requiring immunosuppressive medications at the time of blood sampling at study entry in 2007-2009.

Eight different types of antiphospholipid antibodies were measured, and data on cardiovascular events over the next 8 years was recorded.

Results showed that 14.5% of the cohort tested positive for one of these antiphospholipid antibodies at the start of the study, with approximately one-third of those detected at a moderate or high titer.

The researchers also found that the IgA isotypes of two antiphospholipid antibodies – anticardiolipin and anti-beta-2 glycoprotein – were associated with future atherosclerotic cardiovascular events.

After adjustment for other known risk factors, individuals testing positive for the IgA isotype of anticardiolipin had an almost five times increased risk (hazard ratio, 4.92) of the primary endpoint (myocardial infarction, stroke, coronary revascularization, or cardiovascular death); while those testing positive for anti–beta₂-glycoprotein had an almost three times increased risk (HR, 2.91).

Furthermore, there was what appeared to be a dose effect. People with the highest levels of these antibodies also had the highest risk for cardiovascular events, with up to an almost 10-fold increased risk with the higher level of anticardiolipin. 

Dr. Knight said that more research into the IgA isotypes of these antiphospholipid antibodies is needed.

“Most of the mechanistic work in the antiphospholipid syndrome field has focused on IgG antiphospholipid antibodies. While we commonly find these IgA antibodies in patients with APS, the extent to which they contribute to disease has not been firmly established,” he said. “The fact that IgA was the primary hit in our unbiased screen suggests that there is more to the story and we need to better understand the implications of having these antibodies in circulation, and what specific problems they may be causing.”

Noting that antiphospholipid antibodies can form transiently after certain situations, such as infections, Dr. Knight said that further studies were needed with repeat blood testing to detect the chronic presence of the antibodies.

He added that information of venous thromboses was not available in this study and “perhaps some of the other antibodies might have stood out if we were able to analyze for different outcomes.”

This study was supported by a Pfizer Aspire Award. Dr. Knight reported receiving research funding and consulting fees from Jazz Pharmaceuticals outside the submitted work.

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

The presence of antiphospholipid antibodies is associated with an increased risk for future cardiovascular events, according to a new study.

The findings point to possible new approaches to risk stratification and the potential for new therapeutic targets in heart disease.

“In this study of the general population, we found that two antiphospholipid antibodies were associated with an increased risk of having a serious cardiovascular event over a follow-up of 8 years,” coauthor Jason Knight, MD, University of Michigan, Ann Arbor, said in an interview.

“If confirmed in further studies, these findings could be used to identify a subgroup of patients who need more careful monitoring and more aggressive risk-factor modification, and if the increased risk linked to these antibodies is high enough, it may also justify preemptive treatments such as the anticoagulants that are routinely used in antiphospholipid syndrome,” Dr. Knight said.

“The long-term vision is that we may identify some people in the general population who would benefit from treating the immune system for the prevention and treatment of cardiovascular disease instead of, or in addition to, using typical cardiovascular medications,” he added.

The study was published online in JAMA Network Open.

Individuals with autoimmune and inflammatory diseases have a greater risk for cardiovascular events than expected based on traditional cardiovascular risk factors, with mechanisms proposed to explain this risk including inflammation-mediated disruption of vascular integrity and activation of platelets and coagulation pathways, the authors explained. However, the role of autoantibodies remains unclear.

They noted that antiphospholipid antibodies can activate endothelial cells, platelets, and neutrophils, and some patients with persistently circulating antiphospholipid antibodies can develop antiphospholipid syndrome – an acquired thromboinflammatory disease characterized by arterial, venous, and microvascular thrombotic events and obstetric complications.

Cross-sectional studies have shown that antiphospholipid antibodies are acutely present in up to 17.4% of patients with stroke or transient ischemic attack, and small cohort studies have suggested that such antibodies may be present in 1%-12% of seemingly healthy individuals. However, the impact of sex, race, and ethnicity on the prevalence of antiphospholipid antibodies and their association with atherosclerotic cardiovascular disease is not known.

The researchers conducted the current study to look at the association between antiphospholipid antibodies and future risk for atherosclerotic cardiovascular events.

They analyzed data from 2,427 participants in the population-based Dallas Heart Study who had no history of atherosclerotic cardiovascular disease or autoimmune diseases requiring immunosuppressive medications at the time of blood sampling at study entry in 2007-2009.

Eight different types of antiphospholipid antibodies were measured, and data on cardiovascular events over the next 8 years was recorded.

Results showed that 14.5% of the cohort tested positive for one of these antiphospholipid antibodies at the start of the study, with approximately one-third of those detected at a moderate or high titer.

The researchers also found that the IgA isotypes of two antiphospholipid antibodies – anticardiolipin and anti-beta-2 glycoprotein – were associated with future atherosclerotic cardiovascular events.

After adjustment for other known risk factors, individuals testing positive for the IgA isotype of anticardiolipin had an almost five times increased risk (hazard ratio, 4.92) of the primary endpoint (myocardial infarction, stroke, coronary revascularization, or cardiovascular death); while those testing positive for anti–beta₂-glycoprotein had an almost three times increased risk (HR, 2.91).

Furthermore, there was what appeared to be a dose effect. People with the highest levels of these antibodies also had the highest risk for cardiovascular events, with up to an almost 10-fold increased risk with the higher level of anticardiolipin. 

Dr. Knight said that more research into the IgA isotypes of these antiphospholipid antibodies is needed.

“Most of the mechanistic work in the antiphospholipid syndrome field has focused on IgG antiphospholipid antibodies. While we commonly find these IgA antibodies in patients with APS, the extent to which they contribute to disease has not been firmly established,” he said. “The fact that IgA was the primary hit in our unbiased screen suggests that there is more to the story and we need to better understand the implications of having these antibodies in circulation, and what specific problems they may be causing.”

Noting that antiphospholipid antibodies can form transiently after certain situations, such as infections, Dr. Knight said that further studies were needed with repeat blood testing to detect the chronic presence of the antibodies.

He added that information of venous thromboses was not available in this study and “perhaps some of the other antibodies might have stood out if we were able to analyze for different outcomes.”

This study was supported by a Pfizer Aspire Award. Dr. Knight reported receiving research funding and consulting fees from Jazz Pharmaceuticals outside the submitted work.

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

More than 3 years into the COVID-19 pandemic, lasting symptoms are becoming quite common, with residents of certain states, women, Hispanic people, and transgender people more at risk, a new report shows. 

More than one in four adults sickened by the virus go on to have long COVID, according to a new report from the U.S. Census Bureau. Overall, nearly 15% of all American adults – more than 38 million people nationwide – have had long COVID at some point since the start of the pandemic, according to the report. 

The report, based on survey data collected between March 1 and 13, defines long COVID as symptoms lasting at least 3 months that people didn’t have before getting infected with the virus. 

It is the second recent look at who is most likely to face long COVID. A similar study, published in March, found that women, smokers, and those who had severe COVID-19 infections are most likely to have the disorder

The Census Bureau report found that while 27% of adults nationwide have had long COVID after getting infected with the virus, the condition has impacted some states more than others. The proportion of residents hit with long COVID ranged from a low of 18.8% in New Jersey to a high of 40.7% in West Virginia. 

Other states with long COVID rates well below the national average include Alaska, Maryland, New York, and Wisconsin. At the other end of the spectrum, the states with rates well above the national average include Kentucky, Mississippi, New Mexico, Nevada, South Carolina, South Dakota, and Wyoming.

Long COVID rates also varied by age, gender, and race. People in their 50s were most at risk, with about 31% of those infected by the virus going on to have long COVID, followed by those in their 40s, at more than 29%. 

Far more women (almost 33%) than men (21%) with COVID infections got long COVID. And when researchers looked at long COVID rates based on gender identity, they found that transgender adults were more than twice as likely to have long COVID than cisgender males. Bisexual adults also had much higher long COVID rates than straight, gay, or lesbian people. 

Long COVID was also much more common among Hispanic adults, affecting almost 29% of those infected with the virus, than among White or Black people, who had long COVID rates similar to the national average of 27%. Asian adults had lower long COVID rates than the national average, at less than 20%.

People with disabilities were also at higher risk, with long COVID rates of almost 47%, compared with 24% among adults without disabilities.
 

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

More than 3 years into the COVID-19 pandemic, lasting symptoms are becoming quite common, with residents of certain states, women, Hispanic people, and transgender people more at risk, a new report shows. 

More than one in four adults sickened by the virus go on to have long COVID, according to a new report from the U.S. Census Bureau. Overall, nearly 15% of all American adults – more than 38 million people nationwide – have had long COVID at some point since the start of the pandemic, according to the report. 

The report, based on survey data collected between March 1 and 13, defines long COVID as symptoms lasting at least 3 months that people didn’t have before getting infected with the virus. 

It is the second recent look at who is most likely to face long COVID. A similar study, published in March, found that women, smokers, and those who had severe COVID-19 infections are most likely to have the disorder

The Census Bureau report found that while 27% of adults nationwide have had long COVID after getting infected with the virus, the condition has impacted some states more than others. The proportion of residents hit with long COVID ranged from a low of 18.8% in New Jersey to a high of 40.7% in West Virginia. 

Other states with long COVID rates well below the national average include Alaska, Maryland, New York, and Wisconsin. At the other end of the spectrum, the states with rates well above the national average include Kentucky, Mississippi, New Mexico, Nevada, South Carolina, South Dakota, and Wyoming.

Long COVID rates also varied by age, gender, and race. People in their 50s were most at risk, with about 31% of those infected by the virus going on to have long COVID, followed by those in their 40s, at more than 29%. 

Far more women (almost 33%) than men (21%) with COVID infections got long COVID. And when researchers looked at long COVID rates based on gender identity, they found that transgender adults were more than twice as likely to have long COVID than cisgender males. Bisexual adults also had much higher long COVID rates than straight, gay, or lesbian people. 

Long COVID was also much more common among Hispanic adults, affecting almost 29% of those infected with the virus, than among White or Black people, who had long COVID rates similar to the national average of 27%. Asian adults had lower long COVID rates than the national average, at less than 20%.

People with disabilities were also at higher risk, with long COVID rates of almost 47%, compared with 24% among adults without disabilities.
 

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

More than 3 years into the COVID-19 pandemic, lasting symptoms are becoming quite common, with residents of certain states, women, Hispanic people, and transgender people more at risk, a new report shows. 

More than one in four adults sickened by the virus go on to have long COVID, according to a new report from the U.S. Census Bureau. Overall, nearly 15% of all American adults – more than 38 million people nationwide – have had long COVID at some point since the start of the pandemic, according to the report. 

The report, based on survey data collected between March 1 and 13, defines long COVID as symptoms lasting at least 3 months that people didn’t have before getting infected with the virus. 

It is the second recent look at who is most likely to face long COVID. A similar study, published in March, found that women, smokers, and those who had severe COVID-19 infections are most likely to have the disorder

The Census Bureau report found that while 27% of adults nationwide have had long COVID after getting infected with the virus, the condition has impacted some states more than others. The proportion of residents hit with long COVID ranged from a low of 18.8% in New Jersey to a high of 40.7% in West Virginia. 

Other states with long COVID rates well below the national average include Alaska, Maryland, New York, and Wisconsin. At the other end of the spectrum, the states with rates well above the national average include Kentucky, Mississippi, New Mexico, Nevada, South Carolina, South Dakota, and Wyoming.

Long COVID rates also varied by age, gender, and race. People in their 50s were most at risk, with about 31% of those infected by the virus going on to have long COVID, followed by those in their 40s, at more than 29%. 

Far more women (almost 33%) than men (21%) with COVID infections got long COVID. And when researchers looked at long COVID rates based on gender identity, they found that transgender adults were more than twice as likely to have long COVID than cisgender males. Bisexual adults also had much higher long COVID rates than straight, gay, or lesbian people. 

Long COVID was also much more common among Hispanic adults, affecting almost 29% of those infected with the virus, than among White or Black people, who had long COVID rates similar to the national average of 27%. Asian adults had lower long COVID rates than the national average, at less than 20%.

People with disabilities were also at higher risk, with long COVID rates of almost 47%, compared with 24% among adults without disabilities.
 

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

Disordered sleep is associated with a significantly increased risk for stroke, new research shows.

Results of a large international study show stroke risk was more than three times higher in those who slept too little, more than twice as high in those who sleep too much, and two to three times higher in those with symptoms of severe obstructive sleep apnea.

The study also showed that the greater the number of sleep disorder symptoms, the greater the stroke risk. The 11% of study participants with five or more symptoms of disordered sleep had a fivefold increased risk for stroke.

Jupiterimages/Thinkstock

More symptoms, more risk

Previous research shows severe OSA doubles the risk of stroke and increases the chance of recurrent stroke. A 2019 study showed that people with insomnia had a small increased risk of stroke.

“Both snoring and extremes of sleep duration have been previously associated with an increased risk of stroke in observational research, but less is known about other symptoms of sleep impairment, with less consistent findings,” Dr. McCarthy said.

Prior studies have also generally come from a single geographic region, which Dr. McCarthy noted could limit their generalizability.

For this effort, investigators used data from 4,496 participants in INTERSTROKE, an international case-control study of risk factors for a first acute stroke. About half of the participants had a history of stroke.

Using information collected from a survey of sleep habits, researchers found an elevated stroke risk in those who received less than 5 hours of sleep per night (odds ratio, 3.15; 95% confidence interval, 2.09-4.76) or more than 9 hours of sleep per night (OR, 2.67; 95% CI, 1.89-3.78), compared with those who slept 7 hours a night.

Participants who took unplanned naps or naps lasting an hour or more (OR, 2.46; 95% CI, 1.69-3.57) and participants who reported poor quality sleep (OR,1.52; 95% CI, 1.32-1.75) were also at an increased risk for stroke.

Symptoms of OSA were also strongly associated with increased stroke risk, including snoring (OR, 1.91; 95% CI, 1.62-2.24), snorting (OR, 2.64; 95% CI, 2.17-3.20), and breathing cessation (OR, 2.87; 95% CI, 2.28-2.60).

Stroke risk increased as the number of sleep disturbance symptoms rose, with the greatest risk in the 11% of participants who had five or more symptoms (OR, 5.38; 95% CI, 4.03-7.18).

“This study finds an association between a broad range of sleep impairment symptoms and stroke, and a graded association with increasing symptoms, in an international setting,” Dr. McCarthy said.

Researchers aren’t sure what’s driving the higher stroke risk among people with sleep disturbances. Although the study did control for potential confounders, it wasn’t designed to get at what’s driving the association.

“Sleep disturbance may also have a bi-directional relationship with many stroke risk factors; for example, sleep disturbance may be a symptom of disease and exacerbate disease,” Dr. McCarthy said. “Future interventional studies are required to determine the true direction of the relationship.”
 

A marker of stroke risk

Daniel Lackland, DrPH, professor of neurology at the Medical University of South Carolina, Charleston, said the findings provide additional evidence of the link between sleep and stroke risk.

“The results confirm sleep disorders as a potential marker and part of the risk profile,” he said.

Collecting information about sleep using a validated assessment tool is an important piece of clinical care, Dr. Lackland said, especially among patients with other stroke risk factors.

One limitation of the study was that data on sleep was collected only at one point, and participants were not followed over time to see if changes in sleep affected stroke risk.

“This is an important point and should be a focus for future studies, as it is critical in the design of interventions,” Dr. Lackland said.

The INTERSTROKE study is funded by the Canadian Institutes of Health Research, Heart and Stroke Foundation of Canada, Canadian Stroke Network, Swedish Research Council, Swedish Heart and Lung Foundation, The Health & Medical Care Committee of the Regional Executive Board, Region Västra Götaland, Astra Zeneca, Boehringer Ingelheim (Canada), Pfizer (Canada), MERCK, Sharp and Dohme, Swedish Heart and Lung Foundation, U.K. Chest, and U.K. Heart and Stroke. Dr. McCarthy and Lackland report no relevant financial relationships.

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

Disordered sleep is associated with a significantly increased risk for stroke, new research shows.

Results of a large international study show stroke risk was more than three times higher in those who slept too little, more than twice as high in those who sleep too much, and two to three times higher in those with symptoms of severe obstructive sleep apnea.

The study also showed that the greater the number of sleep disorder symptoms, the greater the stroke risk. The 11% of study participants with five or more symptoms of disordered sleep had a fivefold increased risk for stroke.

Jupiterimages/Thinkstock

More symptoms, more risk

Previous research shows severe OSA doubles the risk of stroke and increases the chance of recurrent stroke. A 2019 study showed that people with insomnia had a small increased risk of stroke.

“Both snoring and extremes of sleep duration have been previously associated with an increased risk of stroke in observational research, but less is known about other symptoms of sleep impairment, with less consistent findings,” Dr. McCarthy said.

Prior studies have also generally come from a single geographic region, which Dr. McCarthy noted could limit their generalizability.

For this effort, investigators used data from 4,496 participants in INTERSTROKE, an international case-control study of risk factors for a first acute stroke. About half of the participants had a history of stroke.

Using information collected from a survey of sleep habits, researchers found an elevated stroke risk in those who received less than 5 hours of sleep per night (odds ratio, 3.15; 95% confidence interval, 2.09-4.76) or more than 9 hours of sleep per night (OR, 2.67; 95% CI, 1.89-3.78), compared with those who slept 7 hours a night.

Participants who took unplanned naps or naps lasting an hour or more (OR, 2.46; 95% CI, 1.69-3.57) and participants who reported poor quality sleep (OR,1.52; 95% CI, 1.32-1.75) were also at an increased risk for stroke.

Symptoms of OSA were also strongly associated with increased stroke risk, including snoring (OR, 1.91; 95% CI, 1.62-2.24), snorting (OR, 2.64; 95% CI, 2.17-3.20), and breathing cessation (OR, 2.87; 95% CI, 2.28-2.60).

Stroke risk increased as the number of sleep disturbance symptoms rose, with the greatest risk in the 11% of participants who had five or more symptoms (OR, 5.38; 95% CI, 4.03-7.18).

“This study finds an association between a broad range of sleep impairment symptoms and stroke, and a graded association with increasing symptoms, in an international setting,” Dr. McCarthy said.

Researchers aren’t sure what’s driving the higher stroke risk among people with sleep disturbances. Although the study did control for potential confounders, it wasn’t designed to get at what’s driving the association.

“Sleep disturbance may also have a bi-directional relationship with many stroke risk factors; for example, sleep disturbance may be a symptom of disease and exacerbate disease,” Dr. McCarthy said. “Future interventional studies are required to determine the true direction of the relationship.”
 

A marker of stroke risk

Daniel Lackland, DrPH, professor of neurology at the Medical University of South Carolina, Charleston, said the findings provide additional evidence of the link between sleep and stroke risk.

“The results confirm sleep disorders as a potential marker and part of the risk profile,” he said.

Collecting information about sleep using a validated assessment tool is an important piece of clinical care, Dr. Lackland said, especially among patients with other stroke risk factors.

One limitation of the study was that data on sleep was collected only at one point, and participants were not followed over time to see if changes in sleep affected stroke risk.

“This is an important point and should be a focus for future studies, as it is critical in the design of interventions,” Dr. Lackland said.

The INTERSTROKE study is funded by the Canadian Institutes of Health Research, Heart and Stroke Foundation of Canada, Canadian Stroke Network, Swedish Research Council, Swedish Heart and Lung Foundation, The Health & Medical Care Committee of the Regional Executive Board, Region Västra Götaland, Astra Zeneca, Boehringer Ingelheim (Canada), Pfizer (Canada), MERCK, Sharp and Dohme, Swedish Heart and Lung Foundation, U.K. Chest, and U.K. Heart and Stroke. Dr. McCarthy and Lackland report no relevant financial relationships.

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

Disordered sleep is associated with a significantly increased risk for stroke, new research shows.

Results of a large international study show stroke risk was more than three times higher in those who slept too little, more than twice as high in those who sleep too much, and two to three times higher in those with symptoms of severe obstructive sleep apnea.

The study also showed that the greater the number of sleep disorder symptoms, the greater the stroke risk. The 11% of study participants with five or more symptoms of disordered sleep had a fivefold increased risk for stroke.

Jupiterimages/Thinkstock

More symptoms, more risk

Previous research shows severe OSA doubles the risk of stroke and increases the chance of recurrent stroke. A 2019 study showed that people with insomnia had a small increased risk of stroke.

“Both snoring and extremes of sleep duration have been previously associated with an increased risk of stroke in observational research, but less is known about other symptoms of sleep impairment, with less consistent findings,” Dr. McCarthy said.

Prior studies have also generally come from a single geographic region, which Dr. McCarthy noted could limit their generalizability.

For this effort, investigators used data from 4,496 participants in INTERSTROKE, an international case-control study of risk factors for a first acute stroke. About half of the participants had a history of stroke.

Using information collected from a survey of sleep habits, researchers found an elevated stroke risk in those who received less than 5 hours of sleep per night (odds ratio, 3.15; 95% confidence interval, 2.09-4.76) or more than 9 hours of sleep per night (OR, 2.67; 95% CI, 1.89-3.78), compared with those who slept 7 hours a night.

Participants who took unplanned naps or naps lasting an hour or more (OR, 2.46; 95% CI, 1.69-3.57) and participants who reported poor quality sleep (OR,1.52; 95% CI, 1.32-1.75) were also at an increased risk for stroke.

Symptoms of OSA were also strongly associated with increased stroke risk, including snoring (OR, 1.91; 95% CI, 1.62-2.24), snorting (OR, 2.64; 95% CI, 2.17-3.20), and breathing cessation (OR, 2.87; 95% CI, 2.28-2.60).

Stroke risk increased as the number of sleep disturbance symptoms rose, with the greatest risk in the 11% of participants who had five or more symptoms (OR, 5.38; 95% CI, 4.03-7.18).

“This study finds an association between a broad range of sleep impairment symptoms and stroke, and a graded association with increasing symptoms, in an international setting,” Dr. McCarthy said.

Researchers aren’t sure what’s driving the higher stroke risk among people with sleep disturbances. Although the study did control for potential confounders, it wasn’t designed to get at what’s driving the association.

“Sleep disturbance may also have a bi-directional relationship with many stroke risk factors; for example, sleep disturbance may be a symptom of disease and exacerbate disease,” Dr. McCarthy said. “Future interventional studies are required to determine the true direction of the relationship.”
 

A marker of stroke risk

Daniel Lackland, DrPH, professor of neurology at the Medical University of South Carolina, Charleston, said the findings provide additional evidence of the link between sleep and stroke risk.

“The results confirm sleep disorders as a potential marker and part of the risk profile,” he said.

Collecting information about sleep using a validated assessment tool is an important piece of clinical care, Dr. Lackland said, especially among patients with other stroke risk factors.

One limitation of the study was that data on sleep was collected only at one point, and participants were not followed over time to see if changes in sleep affected stroke risk.

“This is an important point and should be a focus for future studies, as it is critical in the design of interventions,” Dr. Lackland said.

The INTERSTROKE study is funded by the Canadian Institutes of Health Research, Heart and Stroke Foundation of Canada, Canadian Stroke Network, Swedish Research Council, Swedish Heart and Lung Foundation, The Health & Medical Care Committee of the Regional Executive Board, Region Västra Götaland, Astra Zeneca, Boehringer Ingelheim (Canada), Pfizer (Canada), MERCK, Sharp and Dohme, Swedish Heart and Lung Foundation, U.K. Chest, and U.K. Heart and Stroke. Dr. McCarthy and Lackland report no relevant financial relationships.

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

Women with better indicators of cardiovascular health at midlife saw reduced risk of later dementia, according to results of a study that was released early, ahead of its scheduled presentation at the annual meeting of the American Academy of Neurology.

Epidemiologist Pamela M. Rist, ScD, assistant professor of medicine at Harvard Medical School and associate epidemiologist at Brigham and Women’s Hospital, both in Boston, and colleagues, used data from 13,720 women whose mean age was 54 when they enrolled in the Harvard-based Women’s Health Study between 1992 and 1995. Subjects in that study were followed up in 2004.

Brigham and Women's Hospital

Putting ‘Life’s Simple 7’ to the test

Dr. Rist and colleagues used the Harvard data to discern how well closely women conformed, during the initial study period and at 10-year follow up, to what the American Heart Association describes as “Life’s Simple 7,” a list of behavioral and biometric measures that indicate and predict cardiovascular health. The measures include four modifiable behaviors – not smoking, healthy weight, a healthy diet, and being physically active – along with three biometric measures of blood pressure, cholesterol, and blood sugar (AHA has since added a sleep component).

Researchers assigned women one point for each desirable habit or measure on the list, with subjects’ average Simple 7 score at baseline 4.3, and 4.2 at 10 years’ follow-up.

The investigators then looked at Medicare data for the study subjects from 2011 to 2018 – approximately 20 years after their enrollment in the Women’s Health Study – seeking dementia diagnoses. Some 13% of the study cohort (n = 1,771) had gone on to develop dementia.

Each point on the Simple 7 score at baseline corresponded with a 6% reduction in later dementia risk, Dr. Rist and her colleagues found after adjusting for variables including age and education (odds ratio per one unit change in score, 0.94; 95% CI, 0.90-0.98). This effect was similar for Simple 7 scores measured at 10 years of follow-up (OR, 0.95; 95% CI, 0.91-1.00).

“It can be empowering for people to know that by taking steps such as exercising for a half an hour a day or keeping their blood pressure under control, they can reduce their risk of dementia,” Dr. Rist said in a statement on the findings.
 

‘A simple take-home message’

Reached for comment, Andrew E. Budson, MD, chief of cognitive-behavioral neurology at the VA Boston Healthcare System, praised Dr. Rist and colleagues’ study as one that “builds on existing knowledge to provide a simple take-home message that empowers women to take control of their dementia risk.”

VA Boston Healthcare System

Each of the seven known risk factors – being active, eating better, maintaining a healthy weight, not smoking, maintaining a healthy blood pressure, controlling cholesterol, and having low blood sugar – “was associated with a 6% reduced risk of dementia,” Dr. Budson continued. “So, women who work to address all seven risk factors can reduce their risk of developing dementia by 42%: a huge amount. Moreover, although this study only looked at women, I am confident that if men follow this same advice they will also be able to reduce their risk of dementia, although we don’t know if the size of the effect will be the same.”

Dr. Rist and colleagues’ study was supported by the National Institutes of Health. None of the study authors reported conflicts of interest. Dr. Budson has reported receiving past compensation as a speaker for Eli Lilly.

Women with better indicators of cardiovascular health at midlife saw reduced risk of later dementia, according to results of a study that was released early, ahead of its scheduled presentation at the annual meeting of the American Academy of Neurology.

Epidemiologist Pamela M. Rist, ScD, assistant professor of medicine at Harvard Medical School and associate epidemiologist at Brigham and Women’s Hospital, both in Boston, and colleagues, used data from 13,720 women whose mean age was 54 when they enrolled in the Harvard-based Women’s Health Study between 1992 and 1995. Subjects in that study were followed up in 2004.

Brigham and Women's Hospital

Putting ‘Life’s Simple 7’ to the test

Dr. Rist and colleagues used the Harvard data to discern how well closely women conformed, during the initial study period and at 10-year follow up, to what the American Heart Association describes as “Life’s Simple 7,” a list of behavioral and biometric measures that indicate and predict cardiovascular health. The measures include four modifiable behaviors – not smoking, healthy weight, a healthy diet, and being physically active – along with three biometric measures of blood pressure, cholesterol, and blood sugar (AHA has since added a sleep component).

Researchers assigned women one point for each desirable habit or measure on the list, with subjects’ average Simple 7 score at baseline 4.3, and 4.2 at 10 years’ follow-up.

The investigators then looked at Medicare data for the study subjects from 2011 to 2018 – approximately 20 years after their enrollment in the Women’s Health Study – seeking dementia diagnoses. Some 13% of the study cohort (n = 1,771) had gone on to develop dementia.

Each point on the Simple 7 score at baseline corresponded with a 6% reduction in later dementia risk, Dr. Rist and her colleagues found after adjusting for variables including age and education (odds ratio per one unit change in score, 0.94; 95% CI, 0.90-0.98). This effect was similar for Simple 7 scores measured at 10 years of follow-up (OR, 0.95; 95% CI, 0.91-1.00).

“It can be empowering for people to know that by taking steps such as exercising for a half an hour a day or keeping their blood pressure under control, they can reduce their risk of dementia,” Dr. Rist said in a statement on the findings.
 

‘A simple take-home message’

Reached for comment, Andrew E. Budson, MD, chief of cognitive-behavioral neurology at the VA Boston Healthcare System, praised Dr. Rist and colleagues’ study as one that “builds on existing knowledge to provide a simple take-home message that empowers women to take control of their dementia risk.”

VA Boston Healthcare System

Each of the seven known risk factors – being active, eating better, maintaining a healthy weight, not smoking, maintaining a healthy blood pressure, controlling cholesterol, and having low blood sugar – “was associated with a 6% reduced risk of dementia,” Dr. Budson continued. “So, women who work to address all seven risk factors can reduce their risk of developing dementia by 42%: a huge amount. Moreover, although this study only looked at women, I am confident that if men follow this same advice they will also be able to reduce their risk of dementia, although we don’t know if the size of the effect will be the same.”

Dr. Rist and colleagues’ study was supported by the National Institutes of Health. None of the study authors reported conflicts of interest. Dr. Budson has reported receiving past compensation as a speaker for Eli Lilly.

Women with better indicators of cardiovascular health at midlife saw reduced risk of later dementia, according to results of a study that was released early, ahead of its scheduled presentation at the annual meeting of the American Academy of Neurology.

Epidemiologist Pamela M. Rist, ScD, assistant professor of medicine at Harvard Medical School and associate epidemiologist at Brigham and Women’s Hospital, both in Boston, and colleagues, used data from 13,720 women whose mean age was 54 when they enrolled in the Harvard-based Women’s Health Study between 1992 and 1995. Subjects in that study were followed up in 2004.

Brigham and Women's Hospital

Putting ‘Life’s Simple 7’ to the test

Dr. Rist and colleagues used the Harvard data to discern how well closely women conformed, during the initial study period and at 10-year follow up, to what the American Heart Association describes as “Life’s Simple 7,” a list of behavioral and biometric measures that indicate and predict cardiovascular health. The measures include four modifiable behaviors – not smoking, healthy weight, a healthy diet, and being physically active – along with three biometric measures of blood pressure, cholesterol, and blood sugar (AHA has since added a sleep component).

Researchers assigned women one point for each desirable habit or measure on the list, with subjects’ average Simple 7 score at baseline 4.3, and 4.2 at 10 years’ follow-up.

The investigators then looked at Medicare data for the study subjects from 2011 to 2018 – approximately 20 years after their enrollment in the Women’s Health Study – seeking dementia diagnoses. Some 13% of the study cohort (n = 1,771) had gone on to develop dementia.

Each point on the Simple 7 score at baseline corresponded with a 6% reduction in later dementia risk, Dr. Rist and her colleagues found after adjusting for variables including age and education (odds ratio per one unit change in score, 0.94; 95% CI, 0.90-0.98). This effect was similar for Simple 7 scores measured at 10 years of follow-up (OR, 0.95; 95% CI, 0.91-1.00).

“It can be empowering for people to know that by taking steps such as exercising for a half an hour a day or keeping their blood pressure under control, they can reduce their risk of dementia,” Dr. Rist said in a statement on the findings.
 

‘A simple take-home message’

Reached for comment, Andrew E. Budson, MD, chief of cognitive-behavioral neurology at the VA Boston Healthcare System, praised Dr. Rist and colleagues’ study as one that “builds on existing knowledge to provide a simple take-home message that empowers women to take control of their dementia risk.”

VA Boston Healthcare System

Each of the seven known risk factors – being active, eating better, maintaining a healthy weight, not smoking, maintaining a healthy blood pressure, controlling cholesterol, and having low blood sugar – “was associated with a 6% reduced risk of dementia,” Dr. Budson continued. “So, women who work to address all seven risk factors can reduce their risk of developing dementia by 42%: a huge amount. Moreover, although this study only looked at women, I am confident that if men follow this same advice they will also be able to reduce their risk of dementia, although we don’t know if the size of the effect will be the same.”

Dr. Rist and colleagues’ study was supported by the National Institutes of Health. None of the study authors reported conflicts of interest. Dr. Budson has reported receiving past compensation as a speaker for Eli Lilly.