You eat a credit card’s worth of plastic in a week. That may bother you. But does it harm you?

The answer depends on who you ask. Awareness of microplastics in general is certainly increasing; the most recent news is the detection of microplastics in human breast milk. Other research has suggested that we may be consuming up to 5 grams of plastic each week from our food, water, and certain consumer products.

The World Health Organization has been releasing reports on microplastics and human health since 2019. Their most recent report was released in late August 2022.

“Although the limited data provide little evidence that nano- and microplastic particles have adverse effects in humans, there is increasing public awareness and an overwhelming consensus among all stakeholders that plastics do not belong in the environment, and measures should be taken to mitigate exposure,” the WHO said at the time.

The WHO can’t go beyond what the data shows, of course. If microplastics are wreaking long-term havoc in our bodies as we speak, science hasn’t connected the dots enough to definitively say “this is the problem.”

But some researchers are willing to speculate – and, at the very least, the risks are becoming impossible to ignore. Dick Vethaak, PhD, a microplastics researcher and emeritus professor of ecotoxicology at Vrije Universiteit, Amsterdam, is blunt, calling them “a plastic time bomb.”
 

The plastic problem

Every piece of plastic that has ever been created is still on our planet today, apart from what has been burned. Past estimates show we only recycle about 9% of all plastic, leaving 9 billion tons in our landfills, oceans, and ecosystems. For context, that amount is 1,500 times heavier than the Great Pyramid of Khufu.

New data is even more dire. A 2022 report from Greenpeace showed a 5% U.S. recycling rate in 2021, with a large portion of what consumers think of as “recycled” still winding up in garbage piles or bodies of water.

And this plastic doesn’t disappear. Instead, it breaks down into smaller and smaller pieces known as microplastics and nanoplastics.

Microplastics have been confirmed in human blood, lung tissue, colons, placentas, stool, and breast milk. But how they impact our health is still unknown.

To assess risk, we must ask: “How hazardous is the material?” said Flemming Cassee, PhD, professor of inhalation toxicology at Utrecht (the Netherlands) University and coauthor of the WHO’s recent microplastics report.

There are three potential hazards of microplastics: their physical presence in our bodies, what they’re made of, and what they carry. To determine the extent of these risks, we need to know how much we’re exposed to, said Dr. Cassee.

The first initiative to research the impact of microplastics on human health came from the European Union in 2018. Although microplastics were around before then, we were unable to detect them, said Dr. Cassee.

That’s the real problem: Since the evidence is so new – and there hasn’t been enough of it – it’s not yet possible to draw definite conclusions.

“But looking into the future, I believe that we are likely facing a public health emergency,” warned Dr. Vethaak.
 

What, exactly, are microplastics?

Microplastics are plastic particles between 5 mm and 100 nm in diameter, or the width of a pencil eraser and something 10 times thinner than a human hair. Anything smaller than that is known as a nanoplastic.

“Microplastics include a wide range of different materials, different sizes, different shapes, different densities, and different colors,” said Evangelos Danopoulos, PhD, a microplastics researcher at Hull York (England) Medical School.

“Primary” microplastics are manufactured to be small and used in things like cosmetics and paints. “Secondary” microplastics result from the breaking down of larger plastic materials, like water bottles and plastic bags.

Secondary microplastics are more diverse than primary microplastics and can take forms ranging from fibers shed from synthetic clothing (like polyester) to pieces of a plastic spoon left in our rivers, lakes, and oceans. Any plastic in the environment will eventually become a secondary microplastic as natural forces such as wind, water currents, and UV radiation break it down into smaller and smaller pieces.

Plastic is a diverse material. Heather Leslie, PhD, senior researcher in Vrije Universiteit’s department of environment and health, likens it to spaghetti with sauce. The noodles are the long polymer backbone that all plastic shares. The sauces are “the pigments, the antioxidants, the flame retardants, etc., that make it functional,” she said.
 

What makes microplastics dangerous?

There are more than 10,000 different chemicals, or “sauces,” used to alter a plastic’s physical characteristics – making it softer, more rigid, or more flexible, said Hanna Dusza, PhD, of the Institute for Risk Assessment Sciences at Utrecht University.

As plastics degrade and become microplastics, these chemicals likely remain. Recent research has shown that microplastics leach these chemicals locally in human tissues, or other areas of accumulation, said Dr. Dusza. Some 2,400 of the 10,000 chemical additives were classified as substances of potential concern, meeting the European Union’s criteria for persistence, bioaccumulation, or toxicity.

Many of these chemicals also act as endocrine-disrupting compounds, or toxicants that imitate hormones when they enter the body. Hormones are active at very low concentrations in your bloodstream, explained Dr. Leslie. To your body, some chemical additives in plastic resemble hormones, so the body responds.

“Sometimes even a low dose of some of these additives can cause unwanted effects,” said Dr. Leslie.

Bisphenol A (BPA), for example, is one of the more infamous endocrine disruptors. It is used as an additive to make plastics more rigid and can be found in any number of plastic products, though areas of concern have been plastic water bottles, baby bottles, and the protective coatings in canned foods.

BPA may mimic estrogen, the female sex hormone essential for reproduction, neurodevelopment, and bone density. In men, estrogen regulates sperm count, sex drive, and erectile function. BPA exposure has been linked with – but not proven to cause – multiple cancer types, ADHD, obesity, and low sperm count. Most everyone has some amount of BPA circulating within their blood, but microplastics may retain BPA as they degrade, potentially increasing our exposure, leading to its unwanted consequences, said Dr. Dusza.

And BPA is just one of those 2,400 substances of “potential concern.”
 

The inflammation problem

A potentially larger health issue emerges from our bodies yet again doing what they are supposed to do when encountering microplastics. Particles can trigger an immune response when they enter your bloodstream, explains Nienke Vrisekoop, PhD, assistant professor at UMC Utrecht.

White blood cells have no issue breaking down things like bacteria, but microplastics cannot be degraded. When a white blood cell engulfs a certain mass of microplastics – either many small particles or a singular large one – it dies, releasing its enzymes and causing local inflammation.

Meanwhile, the plastic particle remains. So more white blood cells attack.

“This triggers continual activation that can result in various adverse effects, including oxidative stress and the release of cytokines that trigger inflammatory reactions, said Dr. Vethaak.

And “chronic inflammation is the prelude to chronic diseases,” said Dr. Leslie. “Every chronic disease, like cancer, heart disease, and even neuropsychiatric diseases like Parkinson’s or major depression, begins with inflammation.”

Meanwhile, inhaling microplastic particles can lead to respiratory diseases and cancer.

“The smallest particles – less than one-tenth of a micrometer – penetrate deep into the lungs and even into the bloodstream, causing damage to the heart, blood vessels and brain,” said Dr. Vetaak. “The only direct evidence comes from workers in the textile and plastic industries that had been exposed to very high amounts of plastic fibrous dust.”
 

Microplastics as carriers

Microplastics can also pick up harmful substances and deliver them into your body.

“When they’re in an environment, they basically can suck up [chemicals] like a sponge,” said Dr. Dusza. “These chemicals are known environmental pollutants, like pesticides, fluorinated compounds, flame retardants, and so on.”

Once in the body, these chemicals can be released, potentially leading to cancer, chronic inflammation, or other unknown effects.

Particles can also act as a vector for microbes, bacteria, and viruses. A September 2022 study found that infectious viruses can survive for 3 days in fresh water by “hitchhiking” on microplastics. Their porous nature provides microbes with a perfect environment in which to live and reproduce, said Dr. Dusza. If you ingest the plastics, you ingest the microbes.
 

How to minimize exposure

There is no way to avoid microplastics. They’re in the air we breathe, the products we use, the water we drink, and the food we eat.

Dr. Danopoulos reviewed 72 studies to quantify our consumption of microplastics in drinking water, salt, and seafood.

“We are exposed to millions of microplastics every year, and I was only looking at three food sources, so there are really a lot more,” he said. “Once plastic waste is mismanaged and it enters the environment, there is very little we can do to extract it.”

That said, we can take steps to lower our exposure and keep the problem from getting worse.

Water filtration is one option, though it is not perfect. Research has shown that municipal water treatment can be effective. An October 2021 study found that two methods – electrocoagulation-electroflotation and membrane filtration – can be 100% effective in removing microplastics from treated water. The problem? Not all municipal water treatment uses these methods – and you would have to investigate to find out if your locality does.

As for at-home filtration methods, they can be effective but can also be dicey. Some consumer brands claim they remove microplastics, but how well depends on not just the type of filter but the size of the particles in the water. Meanwhile, how do you know if a filter is working on your water without testing it, something few people will do? Best not to take a brand’s claims on face-value, but look for independent testing on at-home brands.

A longer-term project: Reduce our risk by reusing and recycling plastic waste. Limiting our consumption of plastic, especially single use plastic, decreases the amount available to become micro- and nanoplastics.

We must all learn to not treat plastic as waste, but rather as a renewable material, said Dr. Cassee. But if that seems like a tall order, it’s because it is.

“You’re a human being and you have a voice and there are a lot of other humans out there with voices,” said Dr. Leslie.

“You sign a petition in your community. You talk about it with your friends at the pub. If you’re a teacher, you discuss it in your class. You call your elected representatives and tell them what you think and how you want them to vote on bills.”

When people start working together, you can really amplify that voice, said Dr. Leslie.
 

What’s the bottom line right now, today?

Numerous sources have declared microplastics do not impact human health. But that’s largely because no direct evidence of this exists yet.

Even the WHO in its report suggests that progress must happen if we’re to fully understand the scope of the problem.

“Strengthening of the evidence necessary for reliable characterization and quantification of the risks to human health posed by [nano- and microplastics] will require active participation by all stakeholders,” it said.

All researchers interviewed for this article agree we don’t have enough evidence to draw any definite conclusions. But “if you look at the wrong endpoints, things will look safe, until you look at the endpoint where it’s really causing the problem,” said Dr. Leslie.

We must research our blind spots and continually ask: Where could we be wrong?

“It is a problem; it’s not going to go away,” said Dr. Danopoulos. “It’s going to get worse, and will continue to get worse, not by something that we are doing now but by something we did 5 years ago.”

Perhaps the question to be asked, then, is the hardest to answer: Are we willing to wait for the science?

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

You eat a credit card’s worth of plastic in a week. That may bother you. But does it harm you?

The answer depends on who you ask. Awareness of microplastics in general is certainly increasing; the most recent news is the detection of microplastics in human breast milk. Other research has suggested that we may be consuming up to 5 grams of plastic each week from our food, water, and certain consumer products.

The World Health Organization has been releasing reports on microplastics and human health since 2019. Their most recent report was released in late August 2022.

“Although the limited data provide little evidence that nano- and microplastic particles have adverse effects in humans, there is increasing public awareness and an overwhelming consensus among all stakeholders that plastics do not belong in the environment, and measures should be taken to mitigate exposure,” the WHO said at the time.

The WHO can’t go beyond what the data shows, of course. If microplastics are wreaking long-term havoc in our bodies as we speak, science hasn’t connected the dots enough to definitively say “this is the problem.”

But some researchers are willing to speculate – and, at the very least, the risks are becoming impossible to ignore. Dick Vethaak, PhD, a microplastics researcher and emeritus professor of ecotoxicology at Vrije Universiteit, Amsterdam, is blunt, calling them “a plastic time bomb.”
 

The plastic problem

Every piece of plastic that has ever been created is still on our planet today, apart from what has been burned. Past estimates show we only recycle about 9% of all plastic, leaving 9 billion tons in our landfills, oceans, and ecosystems. For context, that amount is 1,500 times heavier than the Great Pyramid of Khufu.

New data is even more dire. A 2022 report from Greenpeace showed a 5% U.S. recycling rate in 2021, with a large portion of what consumers think of as “recycled” still winding up in garbage piles or bodies of water.

And this plastic doesn’t disappear. Instead, it breaks down into smaller and smaller pieces known as microplastics and nanoplastics.

Microplastics have been confirmed in human blood, lung tissue, colons, placentas, stool, and breast milk. But how they impact our health is still unknown.

To assess risk, we must ask: “How hazardous is the material?” said Flemming Cassee, PhD, professor of inhalation toxicology at Utrecht (the Netherlands) University and coauthor of the WHO’s recent microplastics report.

There are three potential hazards of microplastics: their physical presence in our bodies, what they’re made of, and what they carry. To determine the extent of these risks, we need to know how much we’re exposed to, said Dr. Cassee.

The first initiative to research the impact of microplastics on human health came from the European Union in 2018. Although microplastics were around before then, we were unable to detect them, said Dr. Cassee.

That’s the real problem: Since the evidence is so new – and there hasn’t been enough of it – it’s not yet possible to draw definite conclusions.

“But looking into the future, I believe that we are likely facing a public health emergency,” warned Dr. Vethaak.
 

What, exactly, are microplastics?

Microplastics are plastic particles between 5 mm and 100 nm in diameter, or the width of a pencil eraser and something 10 times thinner than a human hair. Anything smaller than that is known as a nanoplastic.

“Microplastics include a wide range of different materials, different sizes, different shapes, different densities, and different colors,” said Evangelos Danopoulos, PhD, a microplastics researcher at Hull York (England) Medical School.

“Primary” microplastics are manufactured to be small and used in things like cosmetics and paints. “Secondary” microplastics result from the breaking down of larger plastic materials, like water bottles and plastic bags.

Secondary microplastics are more diverse than primary microplastics and can take forms ranging from fibers shed from synthetic clothing (like polyester) to pieces of a plastic spoon left in our rivers, lakes, and oceans. Any plastic in the environment will eventually become a secondary microplastic as natural forces such as wind, water currents, and UV radiation break it down into smaller and smaller pieces.

Plastic is a diverse material. Heather Leslie, PhD, senior researcher in Vrije Universiteit’s department of environment and health, likens it to spaghetti with sauce. The noodles are the long polymer backbone that all plastic shares. The sauces are “the pigments, the antioxidants, the flame retardants, etc., that make it functional,” she said.
 

What makes microplastics dangerous?

There are more than 10,000 different chemicals, or “sauces,” used to alter a plastic’s physical characteristics – making it softer, more rigid, or more flexible, said Hanna Dusza, PhD, of the Institute for Risk Assessment Sciences at Utrecht University.

As plastics degrade and become microplastics, these chemicals likely remain. Recent research has shown that microplastics leach these chemicals locally in human tissues, or other areas of accumulation, said Dr. Dusza. Some 2,400 of the 10,000 chemical additives were classified as substances of potential concern, meeting the European Union’s criteria for persistence, bioaccumulation, or toxicity.

Many of these chemicals also act as endocrine-disrupting compounds, or toxicants that imitate hormones when they enter the body. Hormones are active at very low concentrations in your bloodstream, explained Dr. Leslie. To your body, some chemical additives in plastic resemble hormones, so the body responds.

“Sometimes even a low dose of some of these additives can cause unwanted effects,” said Dr. Leslie.

Bisphenol A (BPA), for example, is one of the more infamous endocrine disruptors. It is used as an additive to make plastics more rigid and can be found in any number of plastic products, though areas of concern have been plastic water bottles, baby bottles, and the protective coatings in canned foods.

BPA may mimic estrogen, the female sex hormone essential for reproduction, neurodevelopment, and bone density. In men, estrogen regulates sperm count, sex drive, and erectile function. BPA exposure has been linked with – but not proven to cause – multiple cancer types, ADHD, obesity, and low sperm count. Most everyone has some amount of BPA circulating within their blood, but microplastics may retain BPA as they degrade, potentially increasing our exposure, leading to its unwanted consequences, said Dr. Dusza.

And BPA is just one of those 2,400 substances of “potential concern.”
 

The inflammation problem

A potentially larger health issue emerges from our bodies yet again doing what they are supposed to do when encountering microplastics. Particles can trigger an immune response when they enter your bloodstream, explains Nienke Vrisekoop, PhD, assistant professor at UMC Utrecht.

White blood cells have no issue breaking down things like bacteria, but microplastics cannot be degraded. When a white blood cell engulfs a certain mass of microplastics – either many small particles or a singular large one – it dies, releasing its enzymes and causing local inflammation.

Meanwhile, the plastic particle remains. So more white blood cells attack.

“This triggers continual activation that can result in various adverse effects, including oxidative stress and the release of cytokines that trigger inflammatory reactions, said Dr. Vethaak.

And “chronic inflammation is the prelude to chronic diseases,” said Dr. Leslie. “Every chronic disease, like cancer, heart disease, and even neuropsychiatric diseases like Parkinson’s or major depression, begins with inflammation.”

Meanwhile, inhaling microplastic particles can lead to respiratory diseases and cancer.

“The smallest particles – less than one-tenth of a micrometer – penetrate deep into the lungs and even into the bloodstream, causing damage to the heart, blood vessels and brain,” said Dr. Vetaak. “The only direct evidence comes from workers in the textile and plastic industries that had been exposed to very high amounts of plastic fibrous dust.”
 

Microplastics as carriers

Microplastics can also pick up harmful substances and deliver them into your body.

“When they’re in an environment, they basically can suck up [chemicals] like a sponge,” said Dr. Dusza. “These chemicals are known environmental pollutants, like pesticides, fluorinated compounds, flame retardants, and so on.”

Once in the body, these chemicals can be released, potentially leading to cancer, chronic inflammation, or other unknown effects.

Particles can also act as a vector for microbes, bacteria, and viruses. A September 2022 study found that infectious viruses can survive for 3 days in fresh water by “hitchhiking” on microplastics. Their porous nature provides microbes with a perfect environment in which to live and reproduce, said Dr. Dusza. If you ingest the plastics, you ingest the microbes.
 

How to minimize exposure

There is no way to avoid microplastics. They’re in the air we breathe, the products we use, the water we drink, and the food we eat.

Dr. Danopoulos reviewed 72 studies to quantify our consumption of microplastics in drinking water, salt, and seafood.

“We are exposed to millions of microplastics every year, and I was only looking at three food sources, so there are really a lot more,” he said. “Once plastic waste is mismanaged and it enters the environment, there is very little we can do to extract it.”

That said, we can take steps to lower our exposure and keep the problem from getting worse.

Water filtration is one option, though it is not perfect. Research has shown that municipal water treatment can be effective. An October 2021 study found that two methods – electrocoagulation-electroflotation and membrane filtration – can be 100% effective in removing microplastics from treated water. The problem? Not all municipal water treatment uses these methods – and you would have to investigate to find out if your locality does.

As for at-home filtration methods, they can be effective but can also be dicey. Some consumer brands claim they remove microplastics, but how well depends on not just the type of filter but the size of the particles in the water. Meanwhile, how do you know if a filter is working on your water without testing it, something few people will do? Best not to take a brand’s claims on face-value, but look for independent testing on at-home brands.

A longer-term project: Reduce our risk by reusing and recycling plastic waste. Limiting our consumption of plastic, especially single use plastic, decreases the amount available to become micro- and nanoplastics.

We must all learn to not treat plastic as waste, but rather as a renewable material, said Dr. Cassee. But if that seems like a tall order, it’s because it is.

“You’re a human being and you have a voice and there are a lot of other humans out there with voices,” said Dr. Leslie.

“You sign a petition in your community. You talk about it with your friends at the pub. If you’re a teacher, you discuss it in your class. You call your elected representatives and tell them what you think and how you want them to vote on bills.”

When people start working together, you can really amplify that voice, said Dr. Leslie.
 

What’s the bottom line right now, today?

Numerous sources have declared microplastics do not impact human health. But that’s largely because no direct evidence of this exists yet.

Even the WHO in its report suggests that progress must happen if we’re to fully understand the scope of the problem.

“Strengthening of the evidence necessary for reliable characterization and quantification of the risks to human health posed by [nano- and microplastics] will require active participation by all stakeholders,” it said.

All researchers interviewed for this article agree we don’t have enough evidence to draw any definite conclusions. But “if you look at the wrong endpoints, things will look safe, until you look at the endpoint where it’s really causing the problem,” said Dr. Leslie.

We must research our blind spots and continually ask: Where could we be wrong?

“It is a problem; it’s not going to go away,” said Dr. Danopoulos. “It’s going to get worse, and will continue to get worse, not by something that we are doing now but by something we did 5 years ago.”

Perhaps the question to be asked, then, is the hardest to answer: Are we willing to wait for the science?

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

You eat a credit card’s worth of plastic in a week. That may bother you. But does it harm you?

The answer depends on who you ask. Awareness of microplastics in general is certainly increasing; the most recent news is the detection of microplastics in human breast milk. Other research has suggested that we may be consuming up to 5 grams of plastic each week from our food, water, and certain consumer products.

The World Health Organization has been releasing reports on microplastics and human health since 2019. Their most recent report was released in late August 2022.

“Although the limited data provide little evidence that nano- and microplastic particles have adverse effects in humans, there is increasing public awareness and an overwhelming consensus among all stakeholders that plastics do not belong in the environment, and measures should be taken to mitigate exposure,” the WHO said at the time.

The WHO can’t go beyond what the data shows, of course. If microplastics are wreaking long-term havoc in our bodies as we speak, science hasn’t connected the dots enough to definitively say “this is the problem.”

But some researchers are willing to speculate – and, at the very least, the risks are becoming impossible to ignore. Dick Vethaak, PhD, a microplastics researcher and emeritus professor of ecotoxicology at Vrije Universiteit, Amsterdam, is blunt, calling them “a plastic time bomb.”
 

The plastic problem

Every piece of plastic that has ever been created is still on our planet today, apart from what has been burned. Past estimates show we only recycle about 9% of all plastic, leaving 9 billion tons in our landfills, oceans, and ecosystems. For context, that amount is 1,500 times heavier than the Great Pyramid of Khufu.

New data is even more dire. A 2022 report from Greenpeace showed a 5% U.S. recycling rate in 2021, with a large portion of what consumers think of as “recycled” still winding up in garbage piles or bodies of water.

And this plastic doesn’t disappear. Instead, it breaks down into smaller and smaller pieces known as microplastics and nanoplastics.

Microplastics have been confirmed in human blood, lung tissue, colons, placentas, stool, and breast milk. But how they impact our health is still unknown.

To assess risk, we must ask: “How hazardous is the material?” said Flemming Cassee, PhD, professor of inhalation toxicology at Utrecht (the Netherlands) University and coauthor of the WHO’s recent microplastics report.

There are three potential hazards of microplastics: their physical presence in our bodies, what they’re made of, and what they carry. To determine the extent of these risks, we need to know how much we’re exposed to, said Dr. Cassee.

The first initiative to research the impact of microplastics on human health came from the European Union in 2018. Although microplastics were around before then, we were unable to detect them, said Dr. Cassee.

That’s the real problem: Since the evidence is so new – and there hasn’t been enough of it – it’s not yet possible to draw definite conclusions.

“But looking into the future, I believe that we are likely facing a public health emergency,” warned Dr. Vethaak.
 

What, exactly, are microplastics?

Microplastics are plastic particles between 5 mm and 100 nm in diameter, or the width of a pencil eraser and something 10 times thinner than a human hair. Anything smaller than that is known as a nanoplastic.

“Microplastics include a wide range of different materials, different sizes, different shapes, different densities, and different colors,” said Evangelos Danopoulos, PhD, a microplastics researcher at Hull York (England) Medical School.

“Primary” microplastics are manufactured to be small and used in things like cosmetics and paints. “Secondary” microplastics result from the breaking down of larger plastic materials, like water bottles and plastic bags.

Secondary microplastics are more diverse than primary microplastics and can take forms ranging from fibers shed from synthetic clothing (like polyester) to pieces of a plastic spoon left in our rivers, lakes, and oceans. Any plastic in the environment will eventually become a secondary microplastic as natural forces such as wind, water currents, and UV radiation break it down into smaller and smaller pieces.

Plastic is a diverse material. Heather Leslie, PhD, senior researcher in Vrije Universiteit’s department of environment and health, likens it to spaghetti with sauce. The noodles are the long polymer backbone that all plastic shares. The sauces are “the pigments, the antioxidants, the flame retardants, etc., that make it functional,” she said.
 

What makes microplastics dangerous?

There are more than 10,000 different chemicals, or “sauces,” used to alter a plastic’s physical characteristics – making it softer, more rigid, or more flexible, said Hanna Dusza, PhD, of the Institute for Risk Assessment Sciences at Utrecht University.

As plastics degrade and become microplastics, these chemicals likely remain. Recent research has shown that microplastics leach these chemicals locally in human tissues, or other areas of accumulation, said Dr. Dusza. Some 2,400 of the 10,000 chemical additives were classified as substances of potential concern, meeting the European Union’s criteria for persistence, bioaccumulation, or toxicity.

Many of these chemicals also act as endocrine-disrupting compounds, or toxicants that imitate hormones when they enter the body. Hormones are active at very low concentrations in your bloodstream, explained Dr. Leslie. To your body, some chemical additives in plastic resemble hormones, so the body responds.

“Sometimes even a low dose of some of these additives can cause unwanted effects,” said Dr. Leslie.

Bisphenol A (BPA), for example, is one of the more infamous endocrine disruptors. It is used as an additive to make plastics more rigid and can be found in any number of plastic products, though areas of concern have been plastic water bottles, baby bottles, and the protective coatings in canned foods.

BPA may mimic estrogen, the female sex hormone essential for reproduction, neurodevelopment, and bone density. In men, estrogen regulates sperm count, sex drive, and erectile function. BPA exposure has been linked with – but not proven to cause – multiple cancer types, ADHD, obesity, and low sperm count. Most everyone has some amount of BPA circulating within their blood, but microplastics may retain BPA as they degrade, potentially increasing our exposure, leading to its unwanted consequences, said Dr. Dusza.

And BPA is just one of those 2,400 substances of “potential concern.”
 

The inflammation problem

A potentially larger health issue emerges from our bodies yet again doing what they are supposed to do when encountering microplastics. Particles can trigger an immune response when they enter your bloodstream, explains Nienke Vrisekoop, PhD, assistant professor at UMC Utrecht.

White blood cells have no issue breaking down things like bacteria, but microplastics cannot be degraded. When a white blood cell engulfs a certain mass of microplastics – either many small particles or a singular large one – it dies, releasing its enzymes and causing local inflammation.

Meanwhile, the plastic particle remains. So more white blood cells attack.

“This triggers continual activation that can result in various adverse effects, including oxidative stress and the release of cytokines that trigger inflammatory reactions, said Dr. Vethaak.

And “chronic inflammation is the prelude to chronic diseases,” said Dr. Leslie. “Every chronic disease, like cancer, heart disease, and even neuropsychiatric diseases like Parkinson’s or major depression, begins with inflammation.”

Meanwhile, inhaling microplastic particles can lead to respiratory diseases and cancer.

“The smallest particles – less than one-tenth of a micrometer – penetrate deep into the lungs and even into the bloodstream, causing damage to the heart, blood vessels and brain,” said Dr. Vetaak. “The only direct evidence comes from workers in the textile and plastic industries that had been exposed to very high amounts of plastic fibrous dust.”
 

Microplastics as carriers

Microplastics can also pick up harmful substances and deliver them into your body.

“When they’re in an environment, they basically can suck up [chemicals] like a sponge,” said Dr. Dusza. “These chemicals are known environmental pollutants, like pesticides, fluorinated compounds, flame retardants, and so on.”

Once in the body, these chemicals can be released, potentially leading to cancer, chronic inflammation, or other unknown effects.

Particles can also act as a vector for microbes, bacteria, and viruses. A September 2022 study found that infectious viruses can survive for 3 days in fresh water by “hitchhiking” on microplastics. Their porous nature provides microbes with a perfect environment in which to live and reproduce, said Dr. Dusza. If you ingest the plastics, you ingest the microbes.
 

How to minimize exposure

There is no way to avoid microplastics. They’re in the air we breathe, the products we use, the water we drink, and the food we eat.

Dr. Danopoulos reviewed 72 studies to quantify our consumption of microplastics in drinking water, salt, and seafood.

“We are exposed to millions of microplastics every year, and I was only looking at three food sources, so there are really a lot more,” he said. “Once plastic waste is mismanaged and it enters the environment, there is very little we can do to extract it.”

That said, we can take steps to lower our exposure and keep the problem from getting worse.

Water filtration is one option, though it is not perfect. Research has shown that municipal water treatment can be effective. An October 2021 study found that two methods – electrocoagulation-electroflotation and membrane filtration – can be 100% effective in removing microplastics from treated water. The problem? Not all municipal water treatment uses these methods – and you would have to investigate to find out if your locality does.

As for at-home filtration methods, they can be effective but can also be dicey. Some consumer brands claim they remove microplastics, but how well depends on not just the type of filter but the size of the particles in the water. Meanwhile, how do you know if a filter is working on your water without testing it, something few people will do? Best not to take a brand’s claims on face-value, but look for independent testing on at-home brands.

A longer-term project: Reduce our risk by reusing and recycling plastic waste. Limiting our consumption of plastic, especially single use plastic, decreases the amount available to become micro- and nanoplastics.

We must all learn to not treat plastic as waste, but rather as a renewable material, said Dr. Cassee. But if that seems like a tall order, it’s because it is.

“You’re a human being and you have a voice and there are a lot of other humans out there with voices,” said Dr. Leslie.

“You sign a petition in your community. You talk about it with your friends at the pub. If you’re a teacher, you discuss it in your class. You call your elected representatives and tell them what you think and how you want them to vote on bills.”

When people start working together, you can really amplify that voice, said Dr. Leslie.
 

What’s the bottom line right now, today?

Numerous sources have declared microplastics do not impact human health. But that’s largely because no direct evidence of this exists yet.

Even the WHO in its report suggests that progress must happen if we’re to fully understand the scope of the problem.

“Strengthening of the evidence necessary for reliable characterization and quantification of the risks to human health posed by [nano- and microplastics] will require active participation by all stakeholders,” it said.

All researchers interviewed for this article agree we don’t have enough evidence to draw any definite conclusions. But “if you look at the wrong endpoints, things will look safe, until you look at the endpoint where it’s really causing the problem,” said Dr. Leslie.

We must research our blind spots and continually ask: Where could we be wrong?

“It is a problem; it’s not going to go away,” said Dr. Danopoulos. “It’s going to get worse, and will continue to get worse, not by something that we are doing now but by something we did 5 years ago.”

Perhaps the question to be asked, then, is the hardest to answer: Are we willing to wait for the science?

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

Black veterans hospitalized with COVID-19 were less likely to be treated with evidence-based treatments, in a study conducted in 130 US Department of Veterans Affairs (VA) medical centers between March 1, 2020, and February 28, 2022.

The study involved 12,135 Black veterans and 40,717 White veterans. Most patients hospitalized during period 1 (March-September 2020) were Black veterans and the proportion of White patients increased over time. The latter 3 periods, which included the Delta- and Omicron-predominant periods, saw the most admissions.

Controlling for the site of treatment, Black patients were equally likely to be admitted to the intensive care unit (40% vs 43%). However, they were less likely to receive steroids, remdesivir, or immunomodulatory drugs.

The researchers say their data confirm other findings from 41 US health care systems participating in the National Patient-Centered Clinical Research Network (PCORNet), which found lower use of monoclonal antibody treatment for COVID infection for patients who identified as Asian, Black, Hispanic, American Indian or Alaska Native, Native Hawaiian or other Pacific Islander, or multiple races.

The researchers did not observe consistent differences in clinical outcomes between Black and White patients. After adjusting for demographics, chronic health conditions, severity of acute illness, and receipt of COVID-19–specific treatments, there was no association of Black race with hospital mortality or 30-day readmission. Black and White patients had a similar burden of preexisting health conditions. Of 38,782 patients discharged, 14% were readmitted within 30 days; the median time to readmission for both groups was 9 days.

Differences in care were partially explained by within- and between-hospital differences, the researchers say. They also cite research that demonstrated a poorer quality of care for hospitals with higher monthly COVID-19 discharges and hospital size.

The study results contradict the assumptions that differences in inpatient treatment by race and ethnicity may be due to differences in clinical indications for medication use based on age and comorbidities, such as chronic kidney or liver disease, the researchers say. For one thing, the VA issued a systemwide COVID-19 response plan that included specific treatment guidelines and distribution plans. But they also point to recent reports that have suggested that occult hypoxemia not detected by pulse oximetry occurs “far more often in Black patients than White patients,” which could result in delayed or missed opportunities to treat patients with COVID-19.

Black veterans hospitalized with COVID-19 were less likely to be treated with evidence-based treatments, in a study conducted in 130 US Department of Veterans Affairs (VA) medical centers between March 1, 2020, and February 28, 2022.

The study involved 12,135 Black veterans and 40,717 White veterans. Most patients hospitalized during period 1 (March-September 2020) were Black veterans and the proportion of White patients increased over time. The latter 3 periods, which included the Delta- and Omicron-predominant periods, saw the most admissions.

Controlling for the site of treatment, Black patients were equally likely to be admitted to the intensive care unit (40% vs 43%). However, they were less likely to receive steroids, remdesivir, or immunomodulatory drugs.

The researchers say their data confirm other findings from 41 US health care systems participating in the National Patient-Centered Clinical Research Network (PCORNet), which found lower use of monoclonal antibody treatment for COVID infection for patients who identified as Asian, Black, Hispanic, American Indian or Alaska Native, Native Hawaiian or other Pacific Islander, or multiple races.

The researchers did not observe consistent differences in clinical outcomes between Black and White patients. After adjusting for demographics, chronic health conditions, severity of acute illness, and receipt of COVID-19–specific treatments, there was no association of Black race with hospital mortality or 30-day readmission. Black and White patients had a similar burden of preexisting health conditions. Of 38,782 patients discharged, 14% were readmitted within 30 days; the median time to readmission for both groups was 9 days.

Differences in care were partially explained by within- and between-hospital differences, the researchers say. They also cite research that demonstrated a poorer quality of care for hospitals with higher monthly COVID-19 discharges and hospital size.

The study results contradict the assumptions that differences in inpatient treatment by race and ethnicity may be due to differences in clinical indications for medication use based on age and comorbidities, such as chronic kidney or liver disease, the researchers say. For one thing, the VA issued a systemwide COVID-19 response plan that included specific treatment guidelines and distribution plans. But they also point to recent reports that have suggested that occult hypoxemia not detected by pulse oximetry occurs “far more often in Black patients than White patients,” which could result in delayed or missed opportunities to treat patients with COVID-19.

Black veterans hospitalized with COVID-19 were less likely to be treated with evidence-based treatments, in a study conducted in 130 US Department of Veterans Affairs (VA) medical centers between March 1, 2020, and February 28, 2022.

The study involved 12,135 Black veterans and 40,717 White veterans. Most patients hospitalized during period 1 (March-September 2020) were Black veterans and the proportion of White patients increased over time. The latter 3 periods, which included the Delta- and Omicron-predominant periods, saw the most admissions.

Controlling for the site of treatment, Black patients were equally likely to be admitted to the intensive care unit (40% vs 43%). However, they were less likely to receive steroids, remdesivir, or immunomodulatory drugs.

The researchers say their data confirm other findings from 41 US health care systems participating in the National Patient-Centered Clinical Research Network (PCORNet), which found lower use of monoclonal antibody treatment for COVID infection for patients who identified as Asian, Black, Hispanic, American Indian or Alaska Native, Native Hawaiian or other Pacific Islander, or multiple races.

The researchers did not observe consistent differences in clinical outcomes between Black and White patients. After adjusting for demographics, chronic health conditions, severity of acute illness, and receipt of COVID-19–specific treatments, there was no association of Black race with hospital mortality or 30-day readmission. Black and White patients had a similar burden of preexisting health conditions. Of 38,782 patients discharged, 14% were readmitted within 30 days; the median time to readmission for both groups was 9 days.

Differences in care were partially explained by within- and between-hospital differences, the researchers say. They also cite research that demonstrated a poorer quality of care for hospitals with higher monthly COVID-19 discharges and hospital size.

The study results contradict the assumptions that differences in inpatient treatment by race and ethnicity may be due to differences in clinical indications for medication use based on age and comorbidities, such as chronic kidney or liver disease, the researchers say. For one thing, the VA issued a systemwide COVID-19 response plan that included specific treatment guidelines and distribution plans. But they also point to recent reports that have suggested that occult hypoxemia not detected by pulse oximetry occurs “far more often in Black patients than White patients,” which could result in delayed or missed opportunities to treat patients with COVID-19.

A study evaluating a new approach using a combination of two thrombolytics designed to reduce bleeding risk in patients with acute ischemic stroke has not shown any benefit on the primary outcome of all intracranial hemorrhage (ICH).

However, there were some encouraging findings including a trend towards a reduction in symptomatic ICH, researchers report, and the combination approach did not show any depletion of fibrinogen levels, which suggests a potential lower bleeding risk.

“Although the main results of this study are neutral, we are encouraged that the combination approach with a low dose of alteplase followed by the new mutant pro-urokinase product looked as effective as full-dose alteplase alone, and there were some promising signs signaling a potential lower bleeding risk,” senior investigator, Diederik Dippel, MD, Erasmus University Medical Center, Rotterdam, the Netherlands, told this news organization.  

The DUMAS study (Dual Thrombolytic Therapy With Mutant Pro-Urokinase and Low Dose Alteplase for Ischemic Stroke) was presented at the World Stroke Congress in Singapore by study coauthor Nadinda van der Ende, MD, also from Erasmus University Medical Center. 

She pointed out that thrombolysis with intravenous alteplase increases the likelihood of a good outcome in acute ischemic stroke but can cause symptomatic intracranial hemorrhage, which can be associated with death and major disability.

Mutant pro-urokinase is a new thrombolytic agent, in development by Thrombolytic Science, Cambridge, Mass., formed by changing one amino acid in pro-urokinase to make it more stable. It is more fibrin specific than alteplase and therefore believed to have a lower risk of intracranial hemorrhage.

Fibrin is formed as the last step in the clotting process, and the precursor of fibrin in the blood is fibrinogen, Dr. van der Ende noted. Alteplase depletes fibrinogen, contributing to its increased bleeding risk, but mutant pro-urokinase is not believed to affect fibrinogen.

“Mutant pro-urokinase does not bind to intact fibrin. It only binds to fibrin that has already been primed by alteplase,” she explained.

The hypothesis behind the current study is that giving a small dose of alteplase will break down fibrin in the clot enough to expose the binding sites for mutant pro-urokinase, which can then be given to continue to lyse the clot.  

As alteplase has a short half-life, it disappears quickly, and new fibrin is not affected. As mutant pro-urokinase can only lyse fibrin that is primed with alteplase, new hemostatic clots should stay intact. Animal studies have shown less bleeding from distant sites with this approach, Dr. van der Ende said.

The primary analysis of the phase 2 DUMAS study included 238 patients with mild ischemic stroke (median National Institutes of Health Stroke Scale [NIHSS] score 3) who met the standard criteria for IV alteplase.

They were randomized to alteplase alone at the regular dose of 0.9 mg/kg (max 90 mg) with a 10% bolus and the remaining given over 60 minutes; or to a combination of a 5-mg bolus of IV alteplase followed by mutant pro-urokinase at a dose of 40 mg given over 60 minutes.

The primary outcome was the rate of all intracranial hemorrhage (symptomatic and asymptomatic) detected by neuroimaging.  

This occurred in 14% of patients in the full-dose alteplase group vs. 13% of patients in the combined alteplase/mutant pro-urokinase group, a nonsignificant difference: adjusted odds ratio, 0.99 (95% confidence interval, 0.46-2.14).

Secondary outcomes showed no significant differences in NIHSS scores at 24 hours or 5-7 days; functional outcome as measured by a shift analysis of the Modified Rankin Scale (mRS); final infarct volume; or perfusion deficit.

However, blood fibrinogen levels were not depleted and significantly higher in the alteplase/mutant pro-urokinase group than in the full-dose alteplase alone group.

In terms of safety, symptomatic ICH occurred in three patients in the alteplase group (3%) and in none (0%) in the combined alteplase/mutant pro-urokinase group; death occurred in 4% vs. 2% patients respectively; and major extracranial hemorrhage occurred in 1% in both groups.

Dr. Van der Ende concluded that the study showed an overall low rate of ICH; a combination of alteplase and mutant pro-urokinase was not superior to alteplase alone in reducing ICH rates in this population of patients with minor stroke; and mutant pro-urokinase appeared to be safe and, unlike alteplase, did not show any reduction in fibrinogen levels.

“We think the lack of an effect on fibrinogen with this new combination of a small alteplase bolus followed by mutant pro-urokinase infusion is promising,” Dr. Dippel commented. “The fact that there was no symptomatic ICH with the combination treatment is also encouraging. Although the primary endpoint of this trial was neutral, we still believe this is a very interesting approach, with the potential for reduced bleeding, compared with alteplase alone, but we need larger numbers to see an effect on outcomes.”

Dr. Dippel also pointed out that the study included only patients with minor stroke who were not eligible for endovascular therapy, and these patients have a low risk of a poor outcome and a low bleeding risk. 

They are hoping to do another study in patients with more severe stroke, who have a higher bleeding risk and would have more to gain from this combination approach.

Because many patients with severe stroke now have immediate thrombectomy if they present to a comprehensive stroke center, a trial in severe stroke patients would have to be done in primary stroke centers, so if the patents are referred to thrombectomy, the thrombolytic would have a chance to work, Dr. Dippel added.

Commenting on the study for this news organization, Stefan Kiechl, MD, Medical University of Innsbruck (Austria), who is cochair of the World Stroke Congress scientific committee, said, “Alteplase is not fibrin specific, and also causes a degeneration of fibrinogen, which results in ‘fibrinogen depletion coagulopathy.’ It is assumed that 20%-40% of intracerebral bleeding after thrombolysis with alteplase is caused by this problem. DUMAS tests the combination of a substantially reduced alteplase [5 mg] dose plus mutant pro-urokinase to avoid this problem.”

The new thrombolysis protocol, however, did not result in a lower bleeding risk, compared to the comparator alteplase,” he added. “The main limitation of this study is that mainly patients with minor strokes were included. Patients with moderate and severe strokes, who have a substantial risk of bleeding, were not adequately addressed.”

The DUMAS trial was funded by an unrestricted grant from Thrombolytic Science, paid to the institution. Dr. Van der Ende and Dr. Dippel report no relevant disclosures.
 

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

A study evaluating a new approach using a combination of two thrombolytics designed to reduce bleeding risk in patients with acute ischemic stroke has not shown any benefit on the primary outcome of all intracranial hemorrhage (ICH).

However, there were some encouraging findings including a trend towards a reduction in symptomatic ICH, researchers report, and the combination approach did not show any depletion of fibrinogen levels, which suggests a potential lower bleeding risk.

“Although the main results of this study are neutral, we are encouraged that the combination approach with a low dose of alteplase followed by the new mutant pro-urokinase product looked as effective as full-dose alteplase alone, and there were some promising signs signaling a potential lower bleeding risk,” senior investigator, Diederik Dippel, MD, Erasmus University Medical Center, Rotterdam, the Netherlands, told this news organization.  

The DUMAS study (Dual Thrombolytic Therapy With Mutant Pro-Urokinase and Low Dose Alteplase for Ischemic Stroke) was presented at the World Stroke Congress in Singapore by study coauthor Nadinda van der Ende, MD, also from Erasmus University Medical Center. 

She pointed out that thrombolysis with intravenous alteplase increases the likelihood of a good outcome in acute ischemic stroke but can cause symptomatic intracranial hemorrhage, which can be associated with death and major disability.

Mutant pro-urokinase is a new thrombolytic agent, in development by Thrombolytic Science, Cambridge, Mass., formed by changing one amino acid in pro-urokinase to make it more stable. It is more fibrin specific than alteplase and therefore believed to have a lower risk of intracranial hemorrhage.

Fibrin is formed as the last step in the clotting process, and the precursor of fibrin in the blood is fibrinogen, Dr. van der Ende noted. Alteplase depletes fibrinogen, contributing to its increased bleeding risk, but mutant pro-urokinase is not believed to affect fibrinogen.

“Mutant pro-urokinase does not bind to intact fibrin. It only binds to fibrin that has already been primed by alteplase,” she explained.

The hypothesis behind the current study is that giving a small dose of alteplase will break down fibrin in the clot enough to expose the binding sites for mutant pro-urokinase, which can then be given to continue to lyse the clot.  

As alteplase has a short half-life, it disappears quickly, and new fibrin is not affected. As mutant pro-urokinase can only lyse fibrin that is primed with alteplase, new hemostatic clots should stay intact. Animal studies have shown less bleeding from distant sites with this approach, Dr. van der Ende said.

The primary analysis of the phase 2 DUMAS study included 238 patients with mild ischemic stroke (median National Institutes of Health Stroke Scale [NIHSS] score 3) who met the standard criteria for IV alteplase.

They were randomized to alteplase alone at the regular dose of 0.9 mg/kg (max 90 mg) with a 10% bolus and the remaining given over 60 minutes; or to a combination of a 5-mg bolus of IV alteplase followed by mutant pro-urokinase at a dose of 40 mg given over 60 minutes.

The primary outcome was the rate of all intracranial hemorrhage (symptomatic and asymptomatic) detected by neuroimaging.  

This occurred in 14% of patients in the full-dose alteplase group vs. 13% of patients in the combined alteplase/mutant pro-urokinase group, a nonsignificant difference: adjusted odds ratio, 0.99 (95% confidence interval, 0.46-2.14).

Secondary outcomes showed no significant differences in NIHSS scores at 24 hours or 5-7 days; functional outcome as measured by a shift analysis of the Modified Rankin Scale (mRS); final infarct volume; or perfusion deficit.

However, blood fibrinogen levels were not depleted and significantly higher in the alteplase/mutant pro-urokinase group than in the full-dose alteplase alone group.

In terms of safety, symptomatic ICH occurred in three patients in the alteplase group (3%) and in none (0%) in the combined alteplase/mutant pro-urokinase group; death occurred in 4% vs. 2% patients respectively; and major extracranial hemorrhage occurred in 1% in both groups.

Dr. Van der Ende concluded that the study showed an overall low rate of ICH; a combination of alteplase and mutant pro-urokinase was not superior to alteplase alone in reducing ICH rates in this population of patients with minor stroke; and mutant pro-urokinase appeared to be safe and, unlike alteplase, did not show any reduction in fibrinogen levels.

“We think the lack of an effect on fibrinogen with this new combination of a small alteplase bolus followed by mutant pro-urokinase infusion is promising,” Dr. Dippel commented. “The fact that there was no symptomatic ICH with the combination treatment is also encouraging. Although the primary endpoint of this trial was neutral, we still believe this is a very interesting approach, with the potential for reduced bleeding, compared with alteplase alone, but we need larger numbers to see an effect on outcomes.”

Dr. Dippel also pointed out that the study included only patients with minor stroke who were not eligible for endovascular therapy, and these patients have a low risk of a poor outcome and a low bleeding risk. 

They are hoping to do another study in patients with more severe stroke, who have a higher bleeding risk and would have more to gain from this combination approach.

Because many patients with severe stroke now have immediate thrombectomy if they present to a comprehensive stroke center, a trial in severe stroke patients would have to be done in primary stroke centers, so if the patents are referred to thrombectomy, the thrombolytic would have a chance to work, Dr. Dippel added.

Commenting on the study for this news organization, Stefan Kiechl, MD, Medical University of Innsbruck (Austria), who is cochair of the World Stroke Congress scientific committee, said, “Alteplase is not fibrin specific, and also causes a degeneration of fibrinogen, which results in ‘fibrinogen depletion coagulopathy.’ It is assumed that 20%-40% of intracerebral bleeding after thrombolysis with alteplase is caused by this problem. DUMAS tests the combination of a substantially reduced alteplase [5 mg] dose plus mutant pro-urokinase to avoid this problem.”

The new thrombolysis protocol, however, did not result in a lower bleeding risk, compared to the comparator alteplase,” he added. “The main limitation of this study is that mainly patients with minor strokes were included. Patients with moderate and severe strokes, who have a substantial risk of bleeding, were not adequately addressed.”

The DUMAS trial was funded by an unrestricted grant from Thrombolytic Science, paid to the institution. Dr. Van der Ende and Dr. Dippel report no relevant disclosures.
 

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

A study evaluating a new approach using a combination of two thrombolytics designed to reduce bleeding risk in patients with acute ischemic stroke has not shown any benefit on the primary outcome of all intracranial hemorrhage (ICH).

However, there were some encouraging findings including a trend towards a reduction in symptomatic ICH, researchers report, and the combination approach did not show any depletion of fibrinogen levels, which suggests a potential lower bleeding risk.

“Although the main results of this study are neutral, we are encouraged that the combination approach with a low dose of alteplase followed by the new mutant pro-urokinase product looked as effective as full-dose alteplase alone, and there were some promising signs signaling a potential lower bleeding risk,” senior investigator, Diederik Dippel, MD, Erasmus University Medical Center, Rotterdam, the Netherlands, told this news organization.  

The DUMAS study (Dual Thrombolytic Therapy With Mutant Pro-Urokinase and Low Dose Alteplase for Ischemic Stroke) was presented at the World Stroke Congress in Singapore by study coauthor Nadinda van der Ende, MD, also from Erasmus University Medical Center. 

She pointed out that thrombolysis with intravenous alteplase increases the likelihood of a good outcome in acute ischemic stroke but can cause symptomatic intracranial hemorrhage, which can be associated with death and major disability.

Mutant pro-urokinase is a new thrombolytic agent, in development by Thrombolytic Science, Cambridge, Mass., formed by changing one amino acid in pro-urokinase to make it more stable. It is more fibrin specific than alteplase and therefore believed to have a lower risk of intracranial hemorrhage.

Fibrin is formed as the last step in the clotting process, and the precursor of fibrin in the blood is fibrinogen, Dr. van der Ende noted. Alteplase depletes fibrinogen, contributing to its increased bleeding risk, but mutant pro-urokinase is not believed to affect fibrinogen.

“Mutant pro-urokinase does not bind to intact fibrin. It only binds to fibrin that has already been primed by alteplase,” she explained.

The hypothesis behind the current study is that giving a small dose of alteplase will break down fibrin in the clot enough to expose the binding sites for mutant pro-urokinase, which can then be given to continue to lyse the clot.  

As alteplase has a short half-life, it disappears quickly, and new fibrin is not affected. As mutant pro-urokinase can only lyse fibrin that is primed with alteplase, new hemostatic clots should stay intact. Animal studies have shown less bleeding from distant sites with this approach, Dr. van der Ende said.

The primary analysis of the phase 2 DUMAS study included 238 patients with mild ischemic stroke (median National Institutes of Health Stroke Scale [NIHSS] score 3) who met the standard criteria for IV alteplase.

They were randomized to alteplase alone at the regular dose of 0.9 mg/kg (max 90 mg) with a 10% bolus and the remaining given over 60 minutes; or to a combination of a 5-mg bolus of IV alteplase followed by mutant pro-urokinase at a dose of 40 mg given over 60 minutes.

The primary outcome was the rate of all intracranial hemorrhage (symptomatic and asymptomatic) detected by neuroimaging.  

This occurred in 14% of patients in the full-dose alteplase group vs. 13% of patients in the combined alteplase/mutant pro-urokinase group, a nonsignificant difference: adjusted odds ratio, 0.99 (95% confidence interval, 0.46-2.14).

Secondary outcomes showed no significant differences in NIHSS scores at 24 hours or 5-7 days; functional outcome as measured by a shift analysis of the Modified Rankin Scale (mRS); final infarct volume; or perfusion deficit.

However, blood fibrinogen levels were not depleted and significantly higher in the alteplase/mutant pro-urokinase group than in the full-dose alteplase alone group.

In terms of safety, symptomatic ICH occurred in three patients in the alteplase group (3%) and in none (0%) in the combined alteplase/mutant pro-urokinase group; death occurred in 4% vs. 2% patients respectively; and major extracranial hemorrhage occurred in 1% in both groups.

Dr. Van der Ende concluded that the study showed an overall low rate of ICH; a combination of alteplase and mutant pro-urokinase was not superior to alteplase alone in reducing ICH rates in this population of patients with minor stroke; and mutant pro-urokinase appeared to be safe and, unlike alteplase, did not show any reduction in fibrinogen levels.

“We think the lack of an effect on fibrinogen with this new combination of a small alteplase bolus followed by mutant pro-urokinase infusion is promising,” Dr. Dippel commented. “The fact that there was no symptomatic ICH with the combination treatment is also encouraging. Although the primary endpoint of this trial was neutral, we still believe this is a very interesting approach, with the potential for reduced bleeding, compared with alteplase alone, but we need larger numbers to see an effect on outcomes.”

Dr. Dippel also pointed out that the study included only patients with minor stroke who were not eligible for endovascular therapy, and these patients have a low risk of a poor outcome and a low bleeding risk. 

They are hoping to do another study in patients with more severe stroke, who have a higher bleeding risk and would have more to gain from this combination approach.

Because many patients with severe stroke now have immediate thrombectomy if they present to a comprehensive stroke center, a trial in severe stroke patients would have to be done in primary stroke centers, so if the patents are referred to thrombectomy, the thrombolytic would have a chance to work, Dr. Dippel added.

Commenting on the study for this news organization, Stefan Kiechl, MD, Medical University of Innsbruck (Austria), who is cochair of the World Stroke Congress scientific committee, said, “Alteplase is not fibrin specific, and also causes a degeneration of fibrinogen, which results in ‘fibrinogen depletion coagulopathy.’ It is assumed that 20%-40% of intracerebral bleeding after thrombolysis with alteplase is caused by this problem. DUMAS tests the combination of a substantially reduced alteplase [5 mg] dose plus mutant pro-urokinase to avoid this problem.”

The new thrombolysis protocol, however, did not result in a lower bleeding risk, compared to the comparator alteplase,” he added. “The main limitation of this study is that mainly patients with minor strokes were included. Patients with moderate and severe strokes, who have a substantial risk of bleeding, were not adequately addressed.”

The DUMAS trial was funded by an unrestricted grant from Thrombolytic Science, paid to the institution. Dr. Van der Ende and Dr. Dippel report no relevant disclosures.
 

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

The US Department of Veterans Affairs (VA) is pushing further deployments of the system to June 2023 “to address challenges” and make sure it’s functioning optimally.

Among the challenges: Safety concerns “voluminous enough and prevalent enough” to prompt the VA to disclose to 41,500 veterans enrolled in Washington, Idaho, Oregon, Montana, and Ohio that their care “may have been impacted as a result of the system’s deployment as it is currently configured,” VA Undersecretary for Health Shereef Elnahal said in a news conference.

The plan was to launch in the first quarter of 2023 in Western Washington, Michigan, and Ohio. But in a recent release, the VA said an investigation had found several technical and system issues, such as latency and slowness, and problems with patient scheduling, referrals, medication management, and other types of medical orders. During this “assess and address” period, the VA says, it will correct outstanding issues—especially those that may have patient safety implications—before restarting deployments at other VA medical centers.

“Right now, the Oracle Cerner [EHR] system is not delivering for veterans or VA health care providers—and we are holding Oracle Cerner and ourselves accountable to get this right,” said VA Deputy Secretary Donald Remy, who has oversight over the EHR program. “We are delaying all future deployments of the new EHR while we fully assess performance and address every concern. Veterans and clinicians deserve a seamless, modernized health record system, and we will not rest until they get it.”

The modernized EHR, intended to replace the Veterans Health Information Systems and Technology Architecture (VistA), has been plagued by problems from the very first launch in October 2020 at Mann-Grandstaff VA Medical Center and associated clinics in the Northwest. Deputy Inspector David Case, of the Office of Inspector General (OIG), reported to the House Committee on Veterans’ Affairs on oversight between 2020 and July 2021. Among other things, the OIG identified problems with the infrastructure and with users’ experiences. Clinical and administrative staff at Mann-Grandstaff and a Columbus clinic shared their frustration with OIG personnel about the “significant system and process limitations that raised concerns about the continuity of and prompt access to quality patient care.”

For example, according to an OIG report from July 2022, the new EHR sent thousands of orders for medical care to an “undetectable location, or unknown queue” instead of the intended location. The mis-delivery caused 149 patient harm events.

On October 11, the VA confirmed to The Spokesman-Review, a Spokane-based newspaper, that a patient had died at the VA clinic in Columbus. The death was attributed to the patient not receiving medication due to incorrect information. The incident is being treated as a potential “sentinel event.”

Elnahal, who met with employees in September at the Columbus clinic where the Oracle Cerner system was launched in April, said he found that the highly complex system made it hard for clinicians to perform routine tasks, such as ordering tests or follow-up appointments. Delays in follow-ups—including a yearlong delay in treatment for a veteran ultimately diagnosed with terminal cancer—were the main cause of the cases of harm cited in the July OIG report.

The veterans who received the letter about the potential impact on their health care “got caught up in this phenomenon of commands not getting where they need to go,” Elnahal said in a news conference in September.

Senator Patty Murray (D-WA), a senior member of the Veterans Affairs Committee, has been consistently pressing the VA to do something about the EHR system’s flaws. “It’s painfully clear,” she said in a statement, “we need to stop this program until the VA can fix these serious issues before they hurt anyone else.”

After finding more than 200 orders in the unknown queue in May 2022, the OIG said, it “has concerns with the effectiveness of Cerner’s plan to mitigate the safety risk.” While executing its “assess and address” plan, the VA will continue to focus on the 5 facilities where the new system has been deployed. “Sometimes, you’re not presented with options to immediately resolve the safety concerns that are in front of you,” Elnahal told reporters. “It is simply the case that the best option in front of us to resolve these patient safety concerns is to work with Oracle Cerner over the next several months to resolve the Cerner system issues at the sites where it exists. We know that this is possible, because other health systems have gone through this journey before, and I think we can do it.”

Veterans who believe their care may have been affected can call a dedicated call center at 800.319.9446. A VA health care team will follow up within 5 days.

The US Department of Veterans Affairs (VA) is pushing further deployments of the system to June 2023 “to address challenges” and make sure it’s functioning optimally.

Among the challenges: Safety concerns “voluminous enough and prevalent enough” to prompt the VA to disclose to 41,500 veterans enrolled in Washington, Idaho, Oregon, Montana, and Ohio that their care “may have been impacted as a result of the system’s deployment as it is currently configured,” VA Undersecretary for Health Shereef Elnahal said in a news conference.

The plan was to launch in the first quarter of 2023 in Western Washington, Michigan, and Ohio. But in a recent release, the VA said an investigation had found several technical and system issues, such as latency and slowness, and problems with patient scheduling, referrals, medication management, and other types of medical orders. During this “assess and address” period, the VA says, it will correct outstanding issues—especially those that may have patient safety implications—before restarting deployments at other VA medical centers.

“Right now, the Oracle Cerner [EHR] system is not delivering for veterans or VA health care providers—and we are holding Oracle Cerner and ourselves accountable to get this right,” said VA Deputy Secretary Donald Remy, who has oversight over the EHR program. “We are delaying all future deployments of the new EHR while we fully assess performance and address every concern. Veterans and clinicians deserve a seamless, modernized health record system, and we will not rest until they get it.”

The modernized EHR, intended to replace the Veterans Health Information Systems and Technology Architecture (VistA), has been plagued by problems from the very first launch in October 2020 at Mann-Grandstaff VA Medical Center and associated clinics in the Northwest. Deputy Inspector David Case, of the Office of Inspector General (OIG), reported to the House Committee on Veterans’ Affairs on oversight between 2020 and July 2021. Among other things, the OIG identified problems with the infrastructure and with users’ experiences. Clinical and administrative staff at Mann-Grandstaff and a Columbus clinic shared their frustration with OIG personnel about the “significant system and process limitations that raised concerns about the continuity of and prompt access to quality patient care.”

For example, according to an OIG report from July 2022, the new EHR sent thousands of orders for medical care to an “undetectable location, or unknown queue” instead of the intended location. The mis-delivery caused 149 patient harm events.

On October 11, the VA confirmed to The Spokesman-Review, a Spokane-based newspaper, that a patient had died at the VA clinic in Columbus. The death was attributed to the patient not receiving medication due to incorrect information. The incident is being treated as a potential “sentinel event.”

Elnahal, who met with employees in September at the Columbus clinic where the Oracle Cerner system was launched in April, said he found that the highly complex system made it hard for clinicians to perform routine tasks, such as ordering tests or follow-up appointments. Delays in follow-ups—including a yearlong delay in treatment for a veteran ultimately diagnosed with terminal cancer—were the main cause of the cases of harm cited in the July OIG report.

The veterans who received the letter about the potential impact on their health care “got caught up in this phenomenon of commands not getting where they need to go,” Elnahal said in a news conference in September.

Senator Patty Murray (D-WA), a senior member of the Veterans Affairs Committee, has been consistently pressing the VA to do something about the EHR system’s flaws. “It’s painfully clear,” she said in a statement, “we need to stop this program until the VA can fix these serious issues before they hurt anyone else.”

After finding more than 200 orders in the unknown queue in May 2022, the OIG said, it “has concerns with the effectiveness of Cerner’s plan to mitigate the safety risk.” While executing its “assess and address” plan, the VA will continue to focus on the 5 facilities where the new system has been deployed. “Sometimes, you’re not presented with options to immediately resolve the safety concerns that are in front of you,” Elnahal told reporters. “It is simply the case that the best option in front of us to resolve these patient safety concerns is to work with Oracle Cerner over the next several months to resolve the Cerner system issues at the sites where it exists. We know that this is possible, because other health systems have gone through this journey before, and I think we can do it.”

Veterans who believe their care may have been affected can call a dedicated call center at 800.319.9446. A VA health care team will follow up within 5 days.

The US Department of Veterans Affairs (VA) is pushing further deployments of the system to June 2023 “to address challenges” and make sure it’s functioning optimally.

Among the challenges: Safety concerns “voluminous enough and prevalent enough” to prompt the VA to disclose to 41,500 veterans enrolled in Washington, Idaho, Oregon, Montana, and Ohio that their care “may have been impacted as a result of the system’s deployment as it is currently configured,” VA Undersecretary for Health Shereef Elnahal said in a news conference.

The plan was to launch in the first quarter of 2023 in Western Washington, Michigan, and Ohio. But in a recent release, the VA said an investigation had found several technical and system issues, such as latency and slowness, and problems with patient scheduling, referrals, medication management, and other types of medical orders. During this “assess and address” period, the VA says, it will correct outstanding issues—especially those that may have patient safety implications—before restarting deployments at other VA medical centers.

“Right now, the Oracle Cerner [EHR] system is not delivering for veterans or VA health care providers—and we are holding Oracle Cerner and ourselves accountable to get this right,” said VA Deputy Secretary Donald Remy, who has oversight over the EHR program. “We are delaying all future deployments of the new EHR while we fully assess performance and address every concern. Veterans and clinicians deserve a seamless, modernized health record system, and we will not rest until they get it.”

The modernized EHR, intended to replace the Veterans Health Information Systems and Technology Architecture (VistA), has been plagued by problems from the very first launch in October 2020 at Mann-Grandstaff VA Medical Center and associated clinics in the Northwest. Deputy Inspector David Case, of the Office of Inspector General (OIG), reported to the House Committee on Veterans’ Affairs on oversight between 2020 and July 2021. Among other things, the OIG identified problems with the infrastructure and with users’ experiences. Clinical and administrative staff at Mann-Grandstaff and a Columbus clinic shared their frustration with OIG personnel about the “significant system and process limitations that raised concerns about the continuity of and prompt access to quality patient care.”

For example, according to an OIG report from July 2022, the new EHR sent thousands of orders for medical care to an “undetectable location, or unknown queue” instead of the intended location. The mis-delivery caused 149 patient harm events.

On October 11, the VA confirmed to The Spokesman-Review, a Spokane-based newspaper, that a patient had died at the VA clinic in Columbus. The death was attributed to the patient not receiving medication due to incorrect information. The incident is being treated as a potential “sentinel event.”

Elnahal, who met with employees in September at the Columbus clinic where the Oracle Cerner system was launched in April, said he found that the highly complex system made it hard for clinicians to perform routine tasks, such as ordering tests or follow-up appointments. Delays in follow-ups—including a yearlong delay in treatment for a veteran ultimately diagnosed with terminal cancer—were the main cause of the cases of harm cited in the July OIG report.

The veterans who received the letter about the potential impact on their health care “got caught up in this phenomenon of commands not getting where they need to go,” Elnahal said in a news conference in September.

Senator Patty Murray (D-WA), a senior member of the Veterans Affairs Committee, has been consistently pressing the VA to do something about the EHR system’s flaws. “It’s painfully clear,” she said in a statement, “we need to stop this program until the VA can fix these serious issues before they hurt anyone else.”

After finding more than 200 orders in the unknown queue in May 2022, the OIG said, it “has concerns with the effectiveness of Cerner’s plan to mitigate the safety risk.” While executing its “assess and address” plan, the VA will continue to focus on the 5 facilities where the new system has been deployed. “Sometimes, you’re not presented with options to immediately resolve the safety concerns that are in front of you,” Elnahal told reporters. “It is simply the case that the best option in front of us to resolve these patient safety concerns is to work with Oracle Cerner over the next several months to resolve the Cerner system issues at the sites where it exists. We know that this is possible, because other health systems have gone through this journey before, and I think we can do it.”

Veterans who believe their care may have been affected can call a dedicated call center at 800.319.9446. A VA health care team will follow up within 5 days.

Most hospitals in the United States have yet to transition from conventional to high-sensitivity cardiac troponin (hs-cTn) assays, despite their greater sensitivity for myocardial injury, a new National Cardiovascular Data Registry (NCDR) registry study indicates.

hs-cTn assays have been used in routine clinical practice in Europe, Canada, and Australia since 2010, but the first such assay did not gain approval in the United States until 2017. Although single-center studies have examined their efficacy and potential downstream consequences, few data exist on hs-cTn implementation nationally, explained study author Cian McCarthy, MB, BCh, BAO, Massachusetts General Hospital, Boston.

The results were published online in the Journal of the American College of Cardiology and will be presented Nov. 5 at the American Heart Association scientific sessions.

For the study, Dr. McCarthy and colleagues examined 550 hospitals participating in the NCDR Chest Pain-MI registry from January 2019 through September 2021.

Of the 251,000 patients included in the analysis (mean age, 64 years; 41.5% female), 155,049 had a non–ST-segment myocardial infarction (NSTEMI), 15,989 had unstable angina, and 79,962 had low-risk chest pain.

The hs-cTn assays included Roche Diagnostic’s Elecsys Gen5 STAT troponin T assay (23%); Abbott’s ARCHITECT STAT (17%); Beckman Coulter’s ACCESS (21%); and Siemens’ Atellica IM (18%), Dimension VISTA (14%), Dimension EXL (4%), and ADVIA Centaur (2%) troponin I assays.

During the study period, 11.5% of patients were evaluated with hs-cTn assays and the remainder were evaluated with conventional troponin assays. These patients were slightly older (65.0 vs. 64.0 years), more commonly White (83.1% vs. 79.9%), less likely to be of Hispanic or Latino ethnicity (8.9% vs. 10.0%), and less likely to be uninsured (6.8% vs. 8.3%; P for all < .001).

A slightly higher proportion of patients evaluated with hs-cTn assays were diagnosed with unstable angina (7.1% vs. 6.3%), a lower proportion with NSTEMI (61.1% vs. 61.9%), and a similar proportion with low-risk chest pain (31.8% vs. 31.9%) compared with those evaluated by conventional troponin assays.

Implementation, defined as at least 25% of patients evaluated by hs-cTn in each quarter, increased from 3.3% in the first quarter of 2019 to 32.6% in the third quarter of 2021 (P trend < .001).

Using higher implementation thresholds of at least 50% and 75% of patients evaluated by hs-cTn, the prevalence in 2021 was 28.9% and 24.7%, respectively.

“So still, the majority of the hospitals by the end of the third quarter 2021 were not using these assays,” Dr. McCarthy said.

Potential explanations for the slow uptake are that prospective comparative effectiveness trials of These assays have predominantly been in international populations and real-world data on U.S. implementation have been limited to integrated health networks at academic institutions.

Approval of several assays was also delayed and the study data cut off just before the October publication of the 2021 AHA/ACC Chest Pain guideline. “So, whether the chest pain guideline with the new class 1 recommendation for hs-cTn will lead to further uptake is something that will need to be looked at in the future,” he said.
 

Downstream testing

In adjusted analyses, hs-cTn use was associated with more echocardiography among patients with non-ST elevation–acute coronary syndrome (NSTE-ACS) (82.4% vs. 75.0%; odds ratio [OR], 1.43; 95% confidence interval [CI], 1.19-1.73), but not among those with low-risk chest pain (19.7% vs. 19.4%; OR, 0.93; 95% CI, 0.71-1.22) compared with conventional cTn assays.

Importantly, hs-cTn was not associated with a difference in stress testing or CT coronary angiography utilization.

Use of hs-cTn was associated with lower use of invasive coronary angiography among patients with low-risk chest pain (3.7% vs. 4.5%; OR, 0.73, 95% CI, 0.58-0.92) but similar use for NSTE-ACS (96.3% vs. 95.8%; OR, 0.99, 95% CI, 0.82-1.19).

Among patients with NSTE-ACS, there also was no difference in revascularization with percutaneous coronary intervention (PCI) (52.7% vs. 52.3%; OR, 0.99; 95% CI, 0.94-1.04) or coronary bypass graft surgery (9.4% vs. 9.1%; OR, 1.06; 95% CI, 0.94-1.18).

PCI (0.1% vs. 0.2%; P = .05) and bypass graft surgery (both 0.1%) were uncommon among patients with low-risk chest pain.

In-hospital mortality was similar among patients with low-risk chest pain evaluated using hs-cTn assays vs. conventional troponin assays (0% vs. 0.02%; P = .16) and among patients with NSTE-ACS (2.8% vs. 3.2%; OR, 0.98, 95% CI, 0.87-1.11).

Length of stay was slightly shorter with hs-cTn use for patients with low-risk chest pain (median, 5.8 vs. 6.2 hours; P < .001) and patients with NSTE-ACS (66.9 vs. 67.8 hours; P = .01).

“There was always a concern that maybe high-sensitivity cardiac troponin would dramatically increase testing and could even increase length of stay, but I think these data are reassuring, in that this study suggests high-sensitivity cardiac troponin is associated with a small reduction in length of stay and possibly more appropriate use of testing with echocardiography in STEMI and a reduction in invasive angiography in low-risk patients,” Dr. McCarthy said. “But the majority of hospitals haven’t implemented the assay.”

The authors pointed out that because registry entry of patients with low-risk chest pain and unstable angina is optional for participating sites, the percentage of patients with NSTEMI is higher than in typical chest pain analyses. This higher pretest probability for MI may thus affect post-test accuracy for a true positive result. “That stated, this is the exact scenario where higher sensitivity might be associated with favorable impact on utilization.”

Among other limitations: There was the potential for unmeasured confounders, the accuracy of diagnoses could not be confirmed, patients with type 2 MI were excluded from the registry, and post-discharge safety was not assessed.

“These data indicate further opportunities to more widely and effectively implement hs-cTn in the U.S. hospitals persist that could optimize care for patients with possible or definitive ACS,” Dr. McCarthy and colleagues concluded.

The study was funded by the American College of Cardiology’s National Cardiovascular Data Registry. Dr. McCarthy is supported by the National Heart, Lung, and Blood Institute and has received consulting income from Abbott Laboratories.

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

Most hospitals in the United States have yet to transition from conventional to high-sensitivity cardiac troponin (hs-cTn) assays, despite their greater sensitivity for myocardial injury, a new National Cardiovascular Data Registry (NCDR) registry study indicates.

hs-cTn assays have been used in routine clinical practice in Europe, Canada, and Australia since 2010, but the first such assay did not gain approval in the United States until 2017. Although single-center studies have examined their efficacy and potential downstream consequences, few data exist on hs-cTn implementation nationally, explained study author Cian McCarthy, MB, BCh, BAO, Massachusetts General Hospital, Boston.

The results were published online in the Journal of the American College of Cardiology and will be presented Nov. 5 at the American Heart Association scientific sessions.

For the study, Dr. McCarthy and colleagues examined 550 hospitals participating in the NCDR Chest Pain-MI registry from January 2019 through September 2021.

Of the 251,000 patients included in the analysis (mean age, 64 years; 41.5% female), 155,049 had a non–ST-segment myocardial infarction (NSTEMI), 15,989 had unstable angina, and 79,962 had low-risk chest pain.

The hs-cTn assays included Roche Diagnostic’s Elecsys Gen5 STAT troponin T assay (23%); Abbott’s ARCHITECT STAT (17%); Beckman Coulter’s ACCESS (21%); and Siemens’ Atellica IM (18%), Dimension VISTA (14%), Dimension EXL (4%), and ADVIA Centaur (2%) troponin I assays.

During the study period, 11.5% of patients were evaluated with hs-cTn assays and the remainder were evaluated with conventional troponin assays. These patients were slightly older (65.0 vs. 64.0 years), more commonly White (83.1% vs. 79.9%), less likely to be of Hispanic or Latino ethnicity (8.9% vs. 10.0%), and less likely to be uninsured (6.8% vs. 8.3%; P for all < .001).

A slightly higher proportion of patients evaluated with hs-cTn assays were diagnosed with unstable angina (7.1% vs. 6.3%), a lower proportion with NSTEMI (61.1% vs. 61.9%), and a similar proportion with low-risk chest pain (31.8% vs. 31.9%) compared with those evaluated by conventional troponin assays.

Implementation, defined as at least 25% of patients evaluated by hs-cTn in each quarter, increased from 3.3% in the first quarter of 2019 to 32.6% in the third quarter of 2021 (P trend < .001).

Using higher implementation thresholds of at least 50% and 75% of patients evaluated by hs-cTn, the prevalence in 2021 was 28.9% and 24.7%, respectively.

“So still, the majority of the hospitals by the end of the third quarter 2021 were not using these assays,” Dr. McCarthy said.

Potential explanations for the slow uptake are that prospective comparative effectiveness trials of These assays have predominantly been in international populations and real-world data on U.S. implementation have been limited to integrated health networks at academic institutions.

Approval of several assays was also delayed and the study data cut off just before the October publication of the 2021 AHA/ACC Chest Pain guideline. “So, whether the chest pain guideline with the new class 1 recommendation for hs-cTn will lead to further uptake is something that will need to be looked at in the future,” he said.
 

Downstream testing

In adjusted analyses, hs-cTn use was associated with more echocardiography among patients with non-ST elevation–acute coronary syndrome (NSTE-ACS) (82.4% vs. 75.0%; odds ratio [OR], 1.43; 95% confidence interval [CI], 1.19-1.73), but not among those with low-risk chest pain (19.7% vs. 19.4%; OR, 0.93; 95% CI, 0.71-1.22) compared with conventional cTn assays.

Importantly, hs-cTn was not associated with a difference in stress testing or CT coronary angiography utilization.

Use of hs-cTn was associated with lower use of invasive coronary angiography among patients with low-risk chest pain (3.7% vs. 4.5%; OR, 0.73, 95% CI, 0.58-0.92) but similar use for NSTE-ACS (96.3% vs. 95.8%; OR, 0.99, 95% CI, 0.82-1.19).

Among patients with NSTE-ACS, there also was no difference in revascularization with percutaneous coronary intervention (PCI) (52.7% vs. 52.3%; OR, 0.99; 95% CI, 0.94-1.04) or coronary bypass graft surgery (9.4% vs. 9.1%; OR, 1.06; 95% CI, 0.94-1.18).

PCI (0.1% vs. 0.2%; P = .05) and bypass graft surgery (both 0.1%) were uncommon among patients with low-risk chest pain.

In-hospital mortality was similar among patients with low-risk chest pain evaluated using hs-cTn assays vs. conventional troponin assays (0% vs. 0.02%; P = .16) and among patients with NSTE-ACS (2.8% vs. 3.2%; OR, 0.98, 95% CI, 0.87-1.11).

Length of stay was slightly shorter with hs-cTn use for patients with low-risk chest pain (median, 5.8 vs. 6.2 hours; P < .001) and patients with NSTE-ACS (66.9 vs. 67.8 hours; P = .01).

“There was always a concern that maybe high-sensitivity cardiac troponin would dramatically increase testing and could even increase length of stay, but I think these data are reassuring, in that this study suggests high-sensitivity cardiac troponin is associated with a small reduction in length of stay and possibly more appropriate use of testing with echocardiography in STEMI and a reduction in invasive angiography in low-risk patients,” Dr. McCarthy said. “But the majority of hospitals haven’t implemented the assay.”

The authors pointed out that because registry entry of patients with low-risk chest pain and unstable angina is optional for participating sites, the percentage of patients with NSTEMI is higher than in typical chest pain analyses. This higher pretest probability for MI may thus affect post-test accuracy for a true positive result. “That stated, this is the exact scenario where higher sensitivity might be associated with favorable impact on utilization.”

Among other limitations: There was the potential for unmeasured confounders, the accuracy of diagnoses could not be confirmed, patients with type 2 MI were excluded from the registry, and post-discharge safety was not assessed.

“These data indicate further opportunities to more widely and effectively implement hs-cTn in the U.S. hospitals persist that could optimize care for patients with possible or definitive ACS,” Dr. McCarthy and colleagues concluded.

The study was funded by the American College of Cardiology’s National Cardiovascular Data Registry. Dr. McCarthy is supported by the National Heart, Lung, and Blood Institute and has received consulting income from Abbott Laboratories.

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

Most hospitals in the United States have yet to transition from conventional to high-sensitivity cardiac troponin (hs-cTn) assays, despite their greater sensitivity for myocardial injury, a new National Cardiovascular Data Registry (NCDR) registry study indicates.

hs-cTn assays have been used in routine clinical practice in Europe, Canada, and Australia since 2010, but the first such assay did not gain approval in the United States until 2017. Although single-center studies have examined their efficacy and potential downstream consequences, few data exist on hs-cTn implementation nationally, explained study author Cian McCarthy, MB, BCh, BAO, Massachusetts General Hospital, Boston.

The results were published online in the Journal of the American College of Cardiology and will be presented Nov. 5 at the American Heart Association scientific sessions.

For the study, Dr. McCarthy and colleagues examined 550 hospitals participating in the NCDR Chest Pain-MI registry from January 2019 through September 2021.

Of the 251,000 patients included in the analysis (mean age, 64 years; 41.5% female), 155,049 had a non–ST-segment myocardial infarction (NSTEMI), 15,989 had unstable angina, and 79,962 had low-risk chest pain.

The hs-cTn assays included Roche Diagnostic’s Elecsys Gen5 STAT troponin T assay (23%); Abbott’s ARCHITECT STAT (17%); Beckman Coulter’s ACCESS (21%); and Siemens’ Atellica IM (18%), Dimension VISTA (14%), Dimension EXL (4%), and ADVIA Centaur (2%) troponin I assays.

During the study period, 11.5% of patients were evaluated with hs-cTn assays and the remainder were evaluated with conventional troponin assays. These patients were slightly older (65.0 vs. 64.0 years), more commonly White (83.1% vs. 79.9%), less likely to be of Hispanic or Latino ethnicity (8.9% vs. 10.0%), and less likely to be uninsured (6.8% vs. 8.3%; P for all < .001).

A slightly higher proportion of patients evaluated with hs-cTn assays were diagnosed with unstable angina (7.1% vs. 6.3%), a lower proportion with NSTEMI (61.1% vs. 61.9%), and a similar proportion with low-risk chest pain (31.8% vs. 31.9%) compared with those evaluated by conventional troponin assays.

Implementation, defined as at least 25% of patients evaluated by hs-cTn in each quarter, increased from 3.3% in the first quarter of 2019 to 32.6% in the third quarter of 2021 (P trend < .001).

Using higher implementation thresholds of at least 50% and 75% of patients evaluated by hs-cTn, the prevalence in 2021 was 28.9% and 24.7%, respectively.

“So still, the majority of the hospitals by the end of the third quarter 2021 were not using these assays,” Dr. McCarthy said.

Potential explanations for the slow uptake are that prospective comparative effectiveness trials of These assays have predominantly been in international populations and real-world data on U.S. implementation have been limited to integrated health networks at academic institutions.

Approval of several assays was also delayed and the study data cut off just before the October publication of the 2021 AHA/ACC Chest Pain guideline. “So, whether the chest pain guideline with the new class 1 recommendation for hs-cTn will lead to further uptake is something that will need to be looked at in the future,” he said.
 

Downstream testing

In adjusted analyses, hs-cTn use was associated with more echocardiography among patients with non-ST elevation–acute coronary syndrome (NSTE-ACS) (82.4% vs. 75.0%; odds ratio [OR], 1.43; 95% confidence interval [CI], 1.19-1.73), but not among those with low-risk chest pain (19.7% vs. 19.4%; OR, 0.93; 95% CI, 0.71-1.22) compared with conventional cTn assays.

Importantly, hs-cTn was not associated with a difference in stress testing or CT coronary angiography utilization.

Use of hs-cTn was associated with lower use of invasive coronary angiography among patients with low-risk chest pain (3.7% vs. 4.5%; OR, 0.73, 95% CI, 0.58-0.92) but similar use for NSTE-ACS (96.3% vs. 95.8%; OR, 0.99, 95% CI, 0.82-1.19).

Among patients with NSTE-ACS, there also was no difference in revascularization with percutaneous coronary intervention (PCI) (52.7% vs. 52.3%; OR, 0.99; 95% CI, 0.94-1.04) or coronary bypass graft surgery (9.4% vs. 9.1%; OR, 1.06; 95% CI, 0.94-1.18).

PCI (0.1% vs. 0.2%; P = .05) and bypass graft surgery (both 0.1%) were uncommon among patients with low-risk chest pain.

In-hospital mortality was similar among patients with low-risk chest pain evaluated using hs-cTn assays vs. conventional troponin assays (0% vs. 0.02%; P = .16) and among patients with NSTE-ACS (2.8% vs. 3.2%; OR, 0.98, 95% CI, 0.87-1.11).

Length of stay was slightly shorter with hs-cTn use for patients with low-risk chest pain (median, 5.8 vs. 6.2 hours; P < .001) and patients with NSTE-ACS (66.9 vs. 67.8 hours; P = .01).

“There was always a concern that maybe high-sensitivity cardiac troponin would dramatically increase testing and could even increase length of stay, but I think these data are reassuring, in that this study suggests high-sensitivity cardiac troponin is associated with a small reduction in length of stay and possibly more appropriate use of testing with echocardiography in STEMI and a reduction in invasive angiography in low-risk patients,” Dr. McCarthy said. “But the majority of hospitals haven’t implemented the assay.”

The authors pointed out that because registry entry of patients with low-risk chest pain and unstable angina is optional for participating sites, the percentage of patients with NSTEMI is higher than in typical chest pain analyses. This higher pretest probability for MI may thus affect post-test accuracy for a true positive result. “That stated, this is the exact scenario where higher sensitivity might be associated with favorable impact on utilization.”

Among other limitations: There was the potential for unmeasured confounders, the accuracy of diagnoses could not be confirmed, patients with type 2 MI were excluded from the registry, and post-discharge safety was not assessed.

“These data indicate further opportunities to more widely and effectively implement hs-cTn in the U.S. hospitals persist that could optimize care for patients with possible or definitive ACS,” Dr. McCarthy and colleagues concluded.

The study was funded by the American College of Cardiology’s National Cardiovascular Data Registry. Dr. McCarthy is supported by the National Heart, Lung, and Blood Institute and has received consulting income from Abbott Laboratories.

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

New trial data from drugmaker Pfizer shows promising results of a vaccine given to mothers during pregnancy that later protects infants in their first months from the worst effects of respiratory syncytial virus, or RSV.

Pfizer will apply for FDA approval by the end of the year, the company said in a statement Nov. 1.

Trial results are so promising that – after talking with government regulators – the company will stop enrolling new people in the study.

Specifically, the company reported that the vaccine prevented severe illness particularly well during the first 90 days of life, with measurable protection against severe illness continuing through 6 months of age. (That period is when infants are the most fragile if they get sick with RSV.)

RSV is a respiratory illness than can affect anyone, usually resulting in no symptoms or those similar to the common cold. But it can be particularly dangerous – and even deadly – for babies and for people over the age of 65. Pfizer and another drug company, GSK, are developing promising vaccines for older adults, the Washington Post reported.

RSV is the leading cause of hospitalization for infants, the Post noted.

The Pfizer study, called MATISSE, enrolled 7,400 pregnant women in 18 countries worldwide. Those who received the vaccine were given it during the late second to third trimester of pregnancy. Women in the study were monitored for safety through the rest of their pregnancy and 6 months after their children were born. Infants were monitored for at least 1 year for safety and effectiveness; more than half of them were monitored for 2 years.

The Pfizer vaccine works by passing maternal antibodies to the infant during pregnancy, the Post reported, noting that other vaccines transmitted via maternal immunization include those for influenza, diphtheria, tetanus, and pertussis.

Annually, RSV has a devastating impact on young children, hospitalizing tens of thousands and causing up to 300 deaths, data show.

For every 100 children who get RSV under 6 months of age, one or two of them may need to be hospitalized, according to the CDC. Those hospitalized infants may need oxygen, intubation, or even mechanical ventilation to help with breathing.

“Most improve with this type of supportive care and are discharged in a few days,” the CDC said.

“I think this is a big step for protecting babies against RSV and improving overall lung health,” vaccine researcher Barney Graham, PhD, told the Post. “Overall, it’s an exciting time for RSV. It’s also a troubling time, because you see how the patterns of infection have been changed by COVID, and we’re having an earlier, bigger season this year than we have for a couple of years – and it’s causing a lot of hospitalization and misery for people.”

As many as four RSV vaccines may have applications submitted to the FDA in 2022, according to CNN. Also in development is an antibody shot given to infants just after they are born, the news outlet reported.

Pfizer’s data, announced Tuesday, has not yet been published or peer-reviewed, but the company said it is seeking peer-reviewed publication.

“We are thrilled by these data, as this is the first-ever investigational vaccine shown to help protect newborns against severe RSV-related respiratory illness immediately at birth,” Annaliesa Anderson, PhD, Pfizer chief scientific officer for vaccine research & development, said in a statement. “We look forward to working with the FDA and other regulatory agencies to bring this vaccine candidate to expectant mothers to help protect their infants against severe RSV during their most vulnerable first six months of life, which has the highest burden of RSV illness in infants.”

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

New trial data from drugmaker Pfizer shows promising results of a vaccine given to mothers during pregnancy that later protects infants in their first months from the worst effects of respiratory syncytial virus, or RSV.

Pfizer will apply for FDA approval by the end of the year, the company said in a statement Nov. 1.

Trial results are so promising that – after talking with government regulators – the company will stop enrolling new people in the study.

Specifically, the company reported that the vaccine prevented severe illness particularly well during the first 90 days of life, with measurable protection against severe illness continuing through 6 months of age. (That period is when infants are the most fragile if they get sick with RSV.)

RSV is a respiratory illness than can affect anyone, usually resulting in no symptoms or those similar to the common cold. But it can be particularly dangerous – and even deadly – for babies and for people over the age of 65. Pfizer and another drug company, GSK, are developing promising vaccines for older adults, the Washington Post reported.

RSV is the leading cause of hospitalization for infants, the Post noted.

The Pfizer study, called MATISSE, enrolled 7,400 pregnant women in 18 countries worldwide. Those who received the vaccine were given it during the late second to third trimester of pregnancy. Women in the study were monitored for safety through the rest of their pregnancy and 6 months after their children were born. Infants were monitored for at least 1 year for safety and effectiveness; more than half of them were monitored for 2 years.

The Pfizer vaccine works by passing maternal antibodies to the infant during pregnancy, the Post reported, noting that other vaccines transmitted via maternal immunization include those for influenza, diphtheria, tetanus, and pertussis.

Annually, RSV has a devastating impact on young children, hospitalizing tens of thousands and causing up to 300 deaths, data show.

For every 100 children who get RSV under 6 months of age, one or two of them may need to be hospitalized, according to the CDC. Those hospitalized infants may need oxygen, intubation, or even mechanical ventilation to help with breathing.

“Most improve with this type of supportive care and are discharged in a few days,” the CDC said.

“I think this is a big step for protecting babies against RSV and improving overall lung health,” vaccine researcher Barney Graham, PhD, told the Post. “Overall, it’s an exciting time for RSV. It’s also a troubling time, because you see how the patterns of infection have been changed by COVID, and we’re having an earlier, bigger season this year than we have for a couple of years – and it’s causing a lot of hospitalization and misery for people.”

As many as four RSV vaccines may have applications submitted to the FDA in 2022, according to CNN. Also in development is an antibody shot given to infants just after they are born, the news outlet reported.

Pfizer’s data, announced Tuesday, has not yet been published or peer-reviewed, but the company said it is seeking peer-reviewed publication.

“We are thrilled by these data, as this is the first-ever investigational vaccine shown to help protect newborns against severe RSV-related respiratory illness immediately at birth,” Annaliesa Anderson, PhD, Pfizer chief scientific officer for vaccine research & development, said in a statement. “We look forward to working with the FDA and other regulatory agencies to bring this vaccine candidate to expectant mothers to help protect their infants against severe RSV during their most vulnerable first six months of life, which has the highest burden of RSV illness in infants.”

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

New trial data from drugmaker Pfizer shows promising results of a vaccine given to mothers during pregnancy that later protects infants in their first months from the worst effects of respiratory syncytial virus, or RSV.

Pfizer will apply for FDA approval by the end of the year, the company said in a statement Nov. 1.

Trial results are so promising that – after talking with government regulators – the company will stop enrolling new people in the study.

Specifically, the company reported that the vaccine prevented severe illness particularly well during the first 90 days of life, with measurable protection against severe illness continuing through 6 months of age. (That period is when infants are the most fragile if they get sick with RSV.)

RSV is a respiratory illness than can affect anyone, usually resulting in no symptoms or those similar to the common cold. But it can be particularly dangerous – and even deadly – for babies and for people over the age of 65. Pfizer and another drug company, GSK, are developing promising vaccines for older adults, the Washington Post reported.

RSV is the leading cause of hospitalization for infants, the Post noted.

The Pfizer study, called MATISSE, enrolled 7,400 pregnant women in 18 countries worldwide. Those who received the vaccine were given it during the late second to third trimester of pregnancy. Women in the study were monitored for safety through the rest of their pregnancy and 6 months after their children were born. Infants were monitored for at least 1 year for safety and effectiveness; more than half of them were monitored for 2 years.

The Pfizer vaccine works by passing maternal antibodies to the infant during pregnancy, the Post reported, noting that other vaccines transmitted via maternal immunization include those for influenza, diphtheria, tetanus, and pertussis.

Annually, RSV has a devastating impact on young children, hospitalizing tens of thousands and causing up to 300 deaths, data show.

For every 100 children who get RSV under 6 months of age, one or two of them may need to be hospitalized, according to the CDC. Those hospitalized infants may need oxygen, intubation, or even mechanical ventilation to help with breathing.

“Most improve with this type of supportive care and are discharged in a few days,” the CDC said.

“I think this is a big step for protecting babies against RSV and improving overall lung health,” vaccine researcher Barney Graham, PhD, told the Post. “Overall, it’s an exciting time for RSV. It’s also a troubling time, because you see how the patterns of infection have been changed by COVID, and we’re having an earlier, bigger season this year than we have for a couple of years – and it’s causing a lot of hospitalization and misery for people.”

As many as four RSV vaccines may have applications submitted to the FDA in 2022, according to CNN. Also in development is an antibody shot given to infants just after they are born, the news outlet reported.

Pfizer’s data, announced Tuesday, has not yet been published or peer-reviewed, but the company said it is seeking peer-reviewed publication.

“We are thrilled by these data, as this is the first-ever investigational vaccine shown to help protect newborns against severe RSV-related respiratory illness immediately at birth,” Annaliesa Anderson, PhD, Pfizer chief scientific officer for vaccine research & development, said in a statement. “We look forward to working with the FDA and other regulatory agencies to bring this vaccine candidate to expectant mothers to help protect their infants against severe RSV during their most vulnerable first six months of life, which has the highest burden of RSV illness in infants.”

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

Severe marital stress was associated with worse recovery after myocardial infarction in a large U.S. cohort of married/partnered patients aged 55 years or younger.

Compared with patients who reported no or mild marital stress a month after their MI, patients who reported severe marital stress had worse physical and mental health, worse generic and cardiovascular quality of life, more frequent angina symptoms, and a greater likelihood of having a hospital readmission a year later.

These findings held true after adjusting for gender, age, race/ethnicity, and baseline health status (model 1) and after further adjusting for education and income levels and employment and insurance status (model 2).

A greater percentage of women than men reported having severe marital stress (39% vs. 30%; P = .001).

Cenjing Zhu, MPhil, a PhD candidate at Yale University, New Haven, Conn., and colleagues will present this study at the American Heart Association scientific sessions.

The results show that “both patients and care providers should be aware that stress experienced in one’s everyday life, such as marital stress, can affect AMI [acute MI] recovery,” Ms. Zhu said in an email.

Health care providers should consider incorporating screening for everyday stress during follow-up patient visits to better spot people at high risk of a poor recovery and further hospitalizations, she added. When possible, they could guide patients to resources to help them manage and reduce their stress levels.

According to Ms. Zhu, the findings suggest that “managing personal stress may be as important as managing other clinical risk factors during the recovery process.”

This study in younger patients with MI “shows that high levels of marital stress impair heart attack recovery, and women have greater impairment in their heart attack recovery compared to men,” AHA spokesperson Nieca Goldberg, MD, who was not involved with this research, told this news organization.

The study shows that “clinicians have to incorporate mental health as part of their assessment of all patients,” said Dr. Goldberg, a clinical associate professor of medicine at New York University and medical director of Atria New York City.

“Our mental health impacts our physical health,” she noted. “Questions about marital stress should be included as part of an overall assessment of mental health. This means assessing all patients for stress, anxiety, and depression.”

Patients who are experiencing marital stress should share the information with their doctor and discuss ways to be referred to therapists and cardiac rehabilitation providers, she said. “My final thought is, women have often been told that their cardiac symptoms are due to stress by doctors. Now we know stress impacts physical health and [is] no longer an excuse but a contributing factor to our physical health.”
 

Does marital stress affect young MI recovery?

Previous literature has linked psychological stress with worse cardiovascular outcomes, Ms. Zhu noted.

However, little is known about the prognostic impact of marital stress on 1-year health outcomes for younger people who survive an MI.

To investigate this, the researchers analyzed data from participants in the Variation in Recovery: Role of Gender on Outcomes of Young AMI Patients (VIRGO) study.

The current study comprised 1,593 adults, including 1,020 female participants (64%), who were treated for MI at 103 hospitals in 30 U.S. states.

VIRGO enrolled participants in a 2:1 female-to-male ratio so as to enrich the inclusion of women, Ms. Zhu explained.

In the study, “partnered” participants were individuals who self-reported as “living as married/living with a partner.” There were 126 such patients (8%) in the current study.

The mean age of the patients was 47, and about 90% were 40-55 years old. Three quarters were White, 13% were Black, and 7% were Hispanic.

Marital stress was assessed on the basis of patients’ replies to 17 questions in the Stockholm Marital Stress Scale regarding the quality of their emotional and sexual relationships with their spouses/partners.

The researchers divided patients into three groups on the basis of their marital stress: mild or absent (lowest quartile), moderate (second quartile), and severe (upper two quartiles).

At 1 year after their MI, patients replied to questionnaires that assessed their health, quality of life, and depressive and angina symptoms. Hospital readmissions were determined on the basis of self-reports and medical records.

Compared to participants who reported no or mild marital stress, those who reported severe mental stress had significantly worse scores for physical and mental health and generic and cardiovascular quality of life, after adjusting for baseline health and demographics. They had worse scores for mental health and quality of life, after further adjusting for socioeconomic status.

In the fully adjusted model, patients who reported severe marital stress were significantly more likely to report more frequent chest pain/angina (odds ratio, 1.49; 95% confidence interval, 1.06-2.10; P = .023) and to have been readmitted to hospital for any cause (OR, 1.45; 95% CI, 1.04-2.00; P = .006), compared with the patients who reported no or mild marital stress.

Study limitations include the fact that the findings are based on self-reported questionnaire replies; they may not be generalizable to patients in other countries; and they do not extend beyond a period of 1 year.

The researchers call for further research “to understand this complex relationship and potential causal pathway associated with these findings.”

“Additional stressors beyond marital stress, such as financial strain or work stress, may also play a role in young adults’ recovery, and the interaction between these factors require further research,” Ms. Zhu noted in a press release from the AHA.

The study was funded by Canadian Institutes of Health Research. The VIRGO study was funded by the National Heart, Lung, and Blood Institute. Ms. Zhu and Dr. Goldberg have disclosed no relevant financial relationships.

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

Severe marital stress was associated with worse recovery after myocardial infarction in a large U.S. cohort of married/partnered patients aged 55 years or younger.

Compared with patients who reported no or mild marital stress a month after their MI, patients who reported severe marital stress had worse physical and mental health, worse generic and cardiovascular quality of life, more frequent angina symptoms, and a greater likelihood of having a hospital readmission a year later.

These findings held true after adjusting for gender, age, race/ethnicity, and baseline health status (model 1) and after further adjusting for education and income levels and employment and insurance status (model 2).

A greater percentage of women than men reported having severe marital stress (39% vs. 30%; P = .001).

Cenjing Zhu, MPhil, a PhD candidate at Yale University, New Haven, Conn., and colleagues will present this study at the American Heart Association scientific sessions.

The results show that “both patients and care providers should be aware that stress experienced in one’s everyday life, such as marital stress, can affect AMI [acute MI] recovery,” Ms. Zhu said in an email.

Health care providers should consider incorporating screening for everyday stress during follow-up patient visits to better spot people at high risk of a poor recovery and further hospitalizations, she added. When possible, they could guide patients to resources to help them manage and reduce their stress levels.

According to Ms. Zhu, the findings suggest that “managing personal stress may be as important as managing other clinical risk factors during the recovery process.”

This study in younger patients with MI “shows that high levels of marital stress impair heart attack recovery, and women have greater impairment in their heart attack recovery compared to men,” AHA spokesperson Nieca Goldberg, MD, who was not involved with this research, told this news organization.

The study shows that “clinicians have to incorporate mental health as part of their assessment of all patients,” said Dr. Goldberg, a clinical associate professor of medicine at New York University and medical director of Atria New York City.

“Our mental health impacts our physical health,” she noted. “Questions about marital stress should be included as part of an overall assessment of mental health. This means assessing all patients for stress, anxiety, and depression.”

Patients who are experiencing marital stress should share the information with their doctor and discuss ways to be referred to therapists and cardiac rehabilitation providers, she said. “My final thought is, women have often been told that their cardiac symptoms are due to stress by doctors. Now we know stress impacts physical health and [is] no longer an excuse but a contributing factor to our physical health.”
 

Does marital stress affect young MI recovery?

Previous literature has linked psychological stress with worse cardiovascular outcomes, Ms. Zhu noted.

However, little is known about the prognostic impact of marital stress on 1-year health outcomes for younger people who survive an MI.

To investigate this, the researchers analyzed data from participants in the Variation in Recovery: Role of Gender on Outcomes of Young AMI Patients (VIRGO) study.

The current study comprised 1,593 adults, including 1,020 female participants (64%), who were treated for MI at 103 hospitals in 30 U.S. states.

VIRGO enrolled participants in a 2:1 female-to-male ratio so as to enrich the inclusion of women, Ms. Zhu explained.

In the study, “partnered” participants were individuals who self-reported as “living as married/living with a partner.” There were 126 such patients (8%) in the current study.

The mean age of the patients was 47, and about 90% were 40-55 years old. Three quarters were White, 13% were Black, and 7% were Hispanic.

Marital stress was assessed on the basis of patients’ replies to 17 questions in the Stockholm Marital Stress Scale regarding the quality of their emotional and sexual relationships with their spouses/partners.

The researchers divided patients into three groups on the basis of their marital stress: mild or absent (lowest quartile), moderate (second quartile), and severe (upper two quartiles).

At 1 year after their MI, patients replied to questionnaires that assessed their health, quality of life, and depressive and angina symptoms. Hospital readmissions were determined on the basis of self-reports and medical records.

Compared to participants who reported no or mild marital stress, those who reported severe mental stress had significantly worse scores for physical and mental health and generic and cardiovascular quality of life, after adjusting for baseline health and demographics. They had worse scores for mental health and quality of life, after further adjusting for socioeconomic status.

In the fully adjusted model, patients who reported severe marital stress were significantly more likely to report more frequent chest pain/angina (odds ratio, 1.49; 95% confidence interval, 1.06-2.10; P = .023) and to have been readmitted to hospital for any cause (OR, 1.45; 95% CI, 1.04-2.00; P = .006), compared with the patients who reported no or mild marital stress.

Study limitations include the fact that the findings are based on self-reported questionnaire replies; they may not be generalizable to patients in other countries; and they do not extend beyond a period of 1 year.

The researchers call for further research “to understand this complex relationship and potential causal pathway associated with these findings.”

“Additional stressors beyond marital stress, such as financial strain or work stress, may also play a role in young adults’ recovery, and the interaction between these factors require further research,” Ms. Zhu noted in a press release from the AHA.

The study was funded by Canadian Institutes of Health Research. The VIRGO study was funded by the National Heart, Lung, and Blood Institute. Ms. Zhu and Dr. Goldberg have disclosed no relevant financial relationships.

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

Severe marital stress was associated with worse recovery after myocardial infarction in a large U.S. cohort of married/partnered patients aged 55 years or younger.

Compared with patients who reported no or mild marital stress a month after their MI, patients who reported severe marital stress had worse physical and mental health, worse generic and cardiovascular quality of life, more frequent angina symptoms, and a greater likelihood of having a hospital readmission a year later.

These findings held true after adjusting for gender, age, race/ethnicity, and baseline health status (model 1) and after further adjusting for education and income levels and employment and insurance status (model 2).

A greater percentage of women than men reported having severe marital stress (39% vs. 30%; P = .001).

Cenjing Zhu, MPhil, a PhD candidate at Yale University, New Haven, Conn., and colleagues will present this study at the American Heart Association scientific sessions.

The results show that “both patients and care providers should be aware that stress experienced in one’s everyday life, such as marital stress, can affect AMI [acute MI] recovery,” Ms. Zhu said in an email.

Health care providers should consider incorporating screening for everyday stress during follow-up patient visits to better spot people at high risk of a poor recovery and further hospitalizations, she added. When possible, they could guide patients to resources to help them manage and reduce their stress levels.

According to Ms. Zhu, the findings suggest that “managing personal stress may be as important as managing other clinical risk factors during the recovery process.”

This study in younger patients with MI “shows that high levels of marital stress impair heart attack recovery, and women have greater impairment in their heart attack recovery compared to men,” AHA spokesperson Nieca Goldberg, MD, who was not involved with this research, told this news organization.

The study shows that “clinicians have to incorporate mental health as part of their assessment of all patients,” said Dr. Goldberg, a clinical associate professor of medicine at New York University and medical director of Atria New York City.

“Our mental health impacts our physical health,” she noted. “Questions about marital stress should be included as part of an overall assessment of mental health. This means assessing all patients for stress, anxiety, and depression.”

Patients who are experiencing marital stress should share the information with their doctor and discuss ways to be referred to therapists and cardiac rehabilitation providers, she said. “My final thought is, women have often been told that their cardiac symptoms are due to stress by doctors. Now we know stress impacts physical health and [is] no longer an excuse but a contributing factor to our physical health.”
 

Does marital stress affect young MI recovery?

Previous literature has linked psychological stress with worse cardiovascular outcomes, Ms. Zhu noted.

However, little is known about the prognostic impact of marital stress on 1-year health outcomes for younger people who survive an MI.

To investigate this, the researchers analyzed data from participants in the Variation in Recovery: Role of Gender on Outcomes of Young AMI Patients (VIRGO) study.

The current study comprised 1,593 adults, including 1,020 female participants (64%), who were treated for MI at 103 hospitals in 30 U.S. states.

VIRGO enrolled participants in a 2:1 female-to-male ratio so as to enrich the inclusion of women, Ms. Zhu explained.

In the study, “partnered” participants were individuals who self-reported as “living as married/living with a partner.” There were 126 such patients (8%) in the current study.

The mean age of the patients was 47, and about 90% were 40-55 years old. Three quarters were White, 13% were Black, and 7% were Hispanic.

Marital stress was assessed on the basis of patients’ replies to 17 questions in the Stockholm Marital Stress Scale regarding the quality of their emotional and sexual relationships with their spouses/partners.

The researchers divided patients into three groups on the basis of their marital stress: mild or absent (lowest quartile), moderate (second quartile), and severe (upper two quartiles).

At 1 year after their MI, patients replied to questionnaires that assessed their health, quality of life, and depressive and angina symptoms. Hospital readmissions were determined on the basis of self-reports and medical records.

Compared to participants who reported no or mild marital stress, those who reported severe mental stress had significantly worse scores for physical and mental health and generic and cardiovascular quality of life, after adjusting for baseline health and demographics. They had worse scores for mental health and quality of life, after further adjusting for socioeconomic status.

In the fully adjusted model, patients who reported severe marital stress were significantly more likely to report more frequent chest pain/angina (odds ratio, 1.49; 95% confidence interval, 1.06-2.10; P = .023) and to have been readmitted to hospital for any cause (OR, 1.45; 95% CI, 1.04-2.00; P = .006), compared with the patients who reported no or mild marital stress.

Study limitations include the fact that the findings are based on self-reported questionnaire replies; they may not be generalizable to patients in other countries; and they do not extend beyond a period of 1 year.

The researchers call for further research “to understand this complex relationship and potential causal pathway associated with these findings.”

“Additional stressors beyond marital stress, such as financial strain or work stress, may also play a role in young adults’ recovery, and the interaction between these factors require further research,” Ms. Zhu noted in a press release from the AHA.

The study was funded by Canadian Institutes of Health Research. The VIRGO study was funded by the National Heart, Lung, and Blood Institute. Ms. Zhu and Dr. Goldberg have disclosed no relevant financial relationships.

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

The liquid form of the antibiotic amoxicillin often used to treat ear infections and strep throat in children is in short supply, just as Americans head into the season when they use the bacteria-fighting drug the most.

The FDA officially listed the shortage Oct. 28, but pharmacists, hospitals, and a supply tracking database sounded alarms earlier this month.

“The scary part is, we’re coming into the time of the year where you have the greatest need,” independent pharmacy owner Hugh Chancy, PharmD, of Georgia, told NBC News. 

Thus far, reports indicate the impact of the shortages is not widespread but does affect some pharmacies, and at least one hospital has published an algorithm for offering treatment alternatives. 

CVS told Bloomberg News that some stores are experiencing shortages of certain doses of amoxicillin, but a Walmart spokesperson said its diverse supply chain meant none of its pharmacies were affected.

“Hypothetically, if amoxicillin doesn’t come into stock for some time, then we’re potentially having to use less effective antibiotics with more side effects,” said Ohio pediatrician Sean Gallagher, MD, according to Bloomberg.

The shortage impacts three of the four largest amoxicillin manufacturers worldwide, according to the Center for Infectious Disease Research and Policy (CIDRAP) at the University of Minnesota. The FDA listed the reason for the shortage as “demand increase for drug,” except in the case of manufacturer Sandoz, for which the reason listed read “information pending.”

A company spokesperson told Bloomberg the reasons were complex.

“The combination in rapid succession of the pandemic impact and consequent demand swings, manufacturing capacity constraints, scarcity of raw materials, and the current energy crisis means we face a uniquely difficult situation in the short term,” Sandoz spokesperson Leslie Pott told Bloomberg.

According to Bloomberg, other major manufacturers are still delivering the product, but limiting new orders.

The American Society of Health-System Pharmacists issued an alert for the shortage last week via its real time drug shortage database.

“Amoxicillin comes in many forms – including capsules, powders and chewable tablets – but the most common type children take is the liquid form, which makes up at least 19 products that are part of the” shortage, Becker’s Hospital Review summarized of the database reports.

The pediatric health system Children’s Minnesota told CIDRAP that supplies are low and that alternatives are being prescribed “when appropriate.”

“As a final step, we temporarily discontinued our standard procedure of dispensing the entire bottle of amoxicillin (which comes in multiple sizes),” a spokesperson told CIDRAP. “We are instead mixing and pouring the exact amount for each course of therapy, to eliminate waste.” 

The Minnesota pediatric clinic and others are particularly on alert because of the surge nationwide of a respiratory virus that particularly impacts children known as RSV.

“We have certainly observed an increase in recent use most likely correlating with the surge in RSV and other respiratory viruses with concern for superimposed bacterial infection in our critically ill and hospitalized patient population,” Laura Bio, PharmD, a clinical pharmacy specialist at Stanford Medicine Children’s Health told CIDRAP.

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

The liquid form of the antibiotic amoxicillin often used to treat ear infections and strep throat in children is in short supply, just as Americans head into the season when they use the bacteria-fighting drug the most.

The FDA officially listed the shortage Oct. 28, but pharmacists, hospitals, and a supply tracking database sounded alarms earlier this month.

“The scary part is, we’re coming into the time of the year where you have the greatest need,” independent pharmacy owner Hugh Chancy, PharmD, of Georgia, told NBC News. 

Thus far, reports indicate the impact of the shortages is not widespread but does affect some pharmacies, and at least one hospital has published an algorithm for offering treatment alternatives. 

CVS told Bloomberg News that some stores are experiencing shortages of certain doses of amoxicillin, but a Walmart spokesperson said its diverse supply chain meant none of its pharmacies were affected.

“Hypothetically, if amoxicillin doesn’t come into stock for some time, then we’re potentially having to use less effective antibiotics with more side effects,” said Ohio pediatrician Sean Gallagher, MD, according to Bloomberg.

The shortage impacts three of the four largest amoxicillin manufacturers worldwide, according to the Center for Infectious Disease Research and Policy (CIDRAP) at the University of Minnesota. The FDA listed the reason for the shortage as “demand increase for drug,” except in the case of manufacturer Sandoz, for which the reason listed read “information pending.”

A company spokesperson told Bloomberg the reasons were complex.

“The combination in rapid succession of the pandemic impact and consequent demand swings, manufacturing capacity constraints, scarcity of raw materials, and the current energy crisis means we face a uniquely difficult situation in the short term,” Sandoz spokesperson Leslie Pott told Bloomberg.

According to Bloomberg, other major manufacturers are still delivering the product, but limiting new orders.

The American Society of Health-System Pharmacists issued an alert for the shortage last week via its real time drug shortage database.

“Amoxicillin comes in many forms – including capsules, powders and chewable tablets – but the most common type children take is the liquid form, which makes up at least 19 products that are part of the” shortage, Becker’s Hospital Review summarized of the database reports.

The pediatric health system Children’s Minnesota told CIDRAP that supplies are low and that alternatives are being prescribed “when appropriate.”

“As a final step, we temporarily discontinued our standard procedure of dispensing the entire bottle of amoxicillin (which comes in multiple sizes),” a spokesperson told CIDRAP. “We are instead mixing and pouring the exact amount for each course of therapy, to eliminate waste.” 

The Minnesota pediatric clinic and others are particularly on alert because of the surge nationwide of a respiratory virus that particularly impacts children known as RSV.

“We have certainly observed an increase in recent use most likely correlating with the surge in RSV and other respiratory viruses with concern for superimposed bacterial infection in our critically ill and hospitalized patient population,” Laura Bio, PharmD, a clinical pharmacy specialist at Stanford Medicine Children’s Health told CIDRAP.

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

The liquid form of the antibiotic amoxicillin often used to treat ear infections and strep throat in children is in short supply, just as Americans head into the season when they use the bacteria-fighting drug the most.

The FDA officially listed the shortage Oct. 28, but pharmacists, hospitals, and a supply tracking database sounded alarms earlier this month.

“The scary part is, we’re coming into the time of the year where you have the greatest need,” independent pharmacy owner Hugh Chancy, PharmD, of Georgia, told NBC News. 

Thus far, reports indicate the impact of the shortages is not widespread but does affect some pharmacies, and at least one hospital has published an algorithm for offering treatment alternatives. 

CVS told Bloomberg News that some stores are experiencing shortages of certain doses of amoxicillin, but a Walmart spokesperson said its diverse supply chain meant none of its pharmacies were affected.

“Hypothetically, if amoxicillin doesn’t come into stock for some time, then we’re potentially having to use less effective antibiotics with more side effects,” said Ohio pediatrician Sean Gallagher, MD, according to Bloomberg.

The shortage impacts three of the four largest amoxicillin manufacturers worldwide, according to the Center for Infectious Disease Research and Policy (CIDRAP) at the University of Minnesota. The FDA listed the reason for the shortage as “demand increase for drug,” except in the case of manufacturer Sandoz, for which the reason listed read “information pending.”

A company spokesperson told Bloomberg the reasons were complex.

“The combination in rapid succession of the pandemic impact and consequent demand swings, manufacturing capacity constraints, scarcity of raw materials, and the current energy crisis means we face a uniquely difficult situation in the short term,” Sandoz spokesperson Leslie Pott told Bloomberg.

According to Bloomberg, other major manufacturers are still delivering the product, but limiting new orders.

The American Society of Health-System Pharmacists issued an alert for the shortage last week via its real time drug shortage database.

“Amoxicillin comes in many forms – including capsules, powders and chewable tablets – but the most common type children take is the liquid form, which makes up at least 19 products that are part of the” shortage, Becker’s Hospital Review summarized of the database reports.

The pediatric health system Children’s Minnesota told CIDRAP that supplies are low and that alternatives are being prescribed “when appropriate.”

“As a final step, we temporarily discontinued our standard procedure of dispensing the entire bottle of amoxicillin (which comes in multiple sizes),” a spokesperson told CIDRAP. “We are instead mixing and pouring the exact amount for each course of therapy, to eliminate waste.” 

The Minnesota pediatric clinic and others are particularly on alert because of the surge nationwide of a respiratory virus that particularly impacts children known as RSV.

“We have certainly observed an increase in recent use most likely correlating with the surge in RSV and other respiratory viruses with concern for superimposed bacterial infection in our critically ill and hospitalized patient population,” Laura Bio, PharmD, a clinical pharmacy specialist at Stanford Medicine Children’s Health told CIDRAP.

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

A machine-learning risk model that incorporates childhood characteristics can predict development of bipolar disorder up to a decade later, according to investigators.

This is the first quantitative approach to predict bipolar disorder, offering sensitivity and specificity of 75% and 76%, respectively, reported lead author Mai Uchida, MD, director of the pediatric depression program at Massachusetts General Hospital and assistant professor of psychiatry at Harvard Medical School, Boston, and colleagues. With further development, the model could be used to identify at-risk children via electronic medical records, enabling earlier monitoring and intervention.

“Although longitudinal studies have found the prognosis of early-onset mood disorders to be unfavorable, research has also shown there are effective treatments and therapies that could significantly alleviate the patients’ and their families’ struggles from the diagnoses,” the investigators wrote in the Journal of Psychiatric Research. “Thus, early identification of the risks and interventions for early symptoms of pediatric mood disorders is crucial.”

To this end, Dr. Uchida and colleagues teamed up with the Gabrieli Lab at MIT, who have published extensively in the realm of neurodevelopment. They sourced data from 492 children, 6-18 years at baseline, who were involved in two longitudinal case-control family studies focused on ADHD. Inputs included psychometric scales, structured diagnostic interviews, social and cognitive functioning assessments, and sociodemographic data.

At 10-year follow-up, 10% of these children had developed bipolar disorder, a notably higher rate than the 3%-4% prevalence in the general population.

“This is a population that’s overrepresented,” Dr. Uchida said in an interview.

She offered two primary reasons for this: First, the families involved in the study were probably willing to be followed for 10 years because they had ongoing concerns about their child’s mental health. Second, the studies enrolled children diagnosed with ADHD, a condition associated with increased risk of bipolar disorder.

Using machine learning algorithms that processed the baseline data while accounting for the skewed distribution, the investigators were able to predict which of the children in the population would go on to develop bipolar disorder. The final model offered a sensitivity of 75%, a specificity of 76%, and an area under the receiver operating characteristic curve of 75%.

“To the best of our knowledge, this represents the first study using machine-learning algorithms for this purpose in pediatric psychiatry,” the investigators wrote.
 

Integrating models into electronic medical records

In the future, this model, or one like it, could be incorporated into software that automatically analyzes electronic medical records and notifies physicians about high-risk patients, Dr. Uchida predicted.

“Not all patients would connect to intervention,” she said. “Maybe it just means that you invite them in for a visit, or you observe them a little bit more carefully. I think that’s where we are hoping that machine learning and medical practice will go.”

When asked about the potential bias posed by psychiatric evaluation, compared with something like blood work results, Dr. Uchida suggested that this subjectivity can be overcome.

“I’m not entirely bothered by that,” she said, offering a list of objective data points that could be harvested from records, such as number of referrals, medications, and hospitalizations. Narrative text in medical records could also be analyzed, she said, potentially detecting key words that are more often associated with high-risk patients.

“Risk prediction is never going to be 100% accurate,” Dr. Uchida said. “But I do think that there will be things [in electronic medical records] that could guide how worried we should be, or how quickly we should intervene.”
 

Opening doors to personalized care

Martin Gignac, MD, chief of psychiatry at Montreal Children’s Hospital and associate professor at McGill University, Montreal, said the present study offers further support for the existence of pediatric-onset bipolar disorder, which “remains controversial” despite “solid evidence.”

“I’m impressed that we have 10-year-long longitudinal follow-up studies that corroborate the importance of this disorder, and show strong predictors of who is at risk,” Dr. Gignac said in an interview. “Clinicians treating a pediatric population should be aware that some of those children with mental health problems might have severe mental health problems, and you have to have the appropriate tools to screen them.”

Advanced tools like the one developed by Dr. Uchida and colleagues should lead to more personalized care, he said.

“We’re going to be able to define what your individual risk is, and maybe most importantly, what you can do to prevent the development of certain disorders,” Dr. Gignac said. “Are there any risks that are dynamic in nature, and that we can act upon? Exposure to stress, for example.”

While more work is needed to bring machine learning into daily psychiatric practice, Dr. Gignac concluded on an optimistic note.

“These instruments should translate from research into clinical practice in order to make difference for the patients we care for,” he said. “This is the type of hope that I hold – that it’s going to be applicable in clinical practice, hopefully, in the near future.”

The investigators disclosed relationships with InCarda, Baylis Medical, Johnson & Johnson, and others. Dr. Gignac disclosed no relevant competing interests.

A machine-learning risk model that incorporates childhood characteristics can predict development of bipolar disorder up to a decade later, according to investigators.

This is the first quantitative approach to predict bipolar disorder, offering sensitivity and specificity of 75% and 76%, respectively, reported lead author Mai Uchida, MD, director of the pediatric depression program at Massachusetts General Hospital and assistant professor of psychiatry at Harvard Medical School, Boston, and colleagues. With further development, the model could be used to identify at-risk children via electronic medical records, enabling earlier monitoring and intervention.

“Although longitudinal studies have found the prognosis of early-onset mood disorders to be unfavorable, research has also shown there are effective treatments and therapies that could significantly alleviate the patients’ and their families’ struggles from the diagnoses,” the investigators wrote in the Journal of Psychiatric Research. “Thus, early identification of the risks and interventions for early symptoms of pediatric mood disorders is crucial.”

To this end, Dr. Uchida and colleagues teamed up with the Gabrieli Lab at MIT, who have published extensively in the realm of neurodevelopment. They sourced data from 492 children, 6-18 years at baseline, who were involved in two longitudinal case-control family studies focused on ADHD. Inputs included psychometric scales, structured diagnostic interviews, social and cognitive functioning assessments, and sociodemographic data.

At 10-year follow-up, 10% of these children had developed bipolar disorder, a notably higher rate than the 3%-4% prevalence in the general population.

“This is a population that’s overrepresented,” Dr. Uchida said in an interview.

She offered two primary reasons for this: First, the families involved in the study were probably willing to be followed for 10 years because they had ongoing concerns about their child’s mental health. Second, the studies enrolled children diagnosed with ADHD, a condition associated with increased risk of bipolar disorder.

Using machine learning algorithms that processed the baseline data while accounting for the skewed distribution, the investigators were able to predict which of the children in the population would go on to develop bipolar disorder. The final model offered a sensitivity of 75%, a specificity of 76%, and an area under the receiver operating characteristic curve of 75%.

“To the best of our knowledge, this represents the first study using machine-learning algorithms for this purpose in pediatric psychiatry,” the investigators wrote.
 

Integrating models into electronic medical records

In the future, this model, or one like it, could be incorporated into software that automatically analyzes electronic medical records and notifies physicians about high-risk patients, Dr. Uchida predicted.

“Not all patients would connect to intervention,” she said. “Maybe it just means that you invite them in for a visit, or you observe them a little bit more carefully. I think that’s where we are hoping that machine learning and medical practice will go.”

When asked about the potential bias posed by psychiatric evaluation, compared with something like blood work results, Dr. Uchida suggested that this subjectivity can be overcome.

“I’m not entirely bothered by that,” she said, offering a list of objective data points that could be harvested from records, such as number of referrals, medications, and hospitalizations. Narrative text in medical records could also be analyzed, she said, potentially detecting key words that are more often associated with high-risk patients.

“Risk prediction is never going to be 100% accurate,” Dr. Uchida said. “But I do think that there will be things [in electronic medical records] that could guide how worried we should be, or how quickly we should intervene.”
 

Opening doors to personalized care

Martin Gignac, MD, chief of psychiatry at Montreal Children’s Hospital and associate professor at McGill University, Montreal, said the present study offers further support for the existence of pediatric-onset bipolar disorder, which “remains controversial” despite “solid evidence.”

“I’m impressed that we have 10-year-long longitudinal follow-up studies that corroborate the importance of this disorder, and show strong predictors of who is at risk,” Dr. Gignac said in an interview. “Clinicians treating a pediatric population should be aware that some of those children with mental health problems might have severe mental health problems, and you have to have the appropriate tools to screen them.”

Advanced tools like the one developed by Dr. Uchida and colleagues should lead to more personalized care, he said.

“We’re going to be able to define what your individual risk is, and maybe most importantly, what you can do to prevent the development of certain disorders,” Dr. Gignac said. “Are there any risks that are dynamic in nature, and that we can act upon? Exposure to stress, for example.”

While more work is needed to bring machine learning into daily psychiatric practice, Dr. Gignac concluded on an optimistic note.

“These instruments should translate from research into clinical practice in order to make difference for the patients we care for,” he said. “This is the type of hope that I hold – that it’s going to be applicable in clinical practice, hopefully, in the near future.”

The investigators disclosed relationships with InCarda, Baylis Medical, Johnson & Johnson, and others. Dr. Gignac disclosed no relevant competing interests.

A machine-learning risk model that incorporates childhood characteristics can predict development of bipolar disorder up to a decade later, according to investigators.

This is the first quantitative approach to predict bipolar disorder, offering sensitivity and specificity of 75% and 76%, respectively, reported lead author Mai Uchida, MD, director of the pediatric depression program at Massachusetts General Hospital and assistant professor of psychiatry at Harvard Medical School, Boston, and colleagues. With further development, the model could be used to identify at-risk children via electronic medical records, enabling earlier monitoring and intervention.

“Although longitudinal studies have found the prognosis of early-onset mood disorders to be unfavorable, research has also shown there are effective treatments and therapies that could significantly alleviate the patients’ and their families’ struggles from the diagnoses,” the investigators wrote in the Journal of Psychiatric Research. “Thus, early identification of the risks and interventions for early symptoms of pediatric mood disorders is crucial.”

To this end, Dr. Uchida and colleagues teamed up with the Gabrieli Lab at MIT, who have published extensively in the realm of neurodevelopment. They sourced data from 492 children, 6-18 years at baseline, who were involved in two longitudinal case-control family studies focused on ADHD. Inputs included psychometric scales, structured diagnostic interviews, social and cognitive functioning assessments, and sociodemographic data.

At 10-year follow-up, 10% of these children had developed bipolar disorder, a notably higher rate than the 3%-4% prevalence in the general population.

“This is a population that’s overrepresented,” Dr. Uchida said in an interview.

She offered two primary reasons for this: First, the families involved in the study were probably willing to be followed for 10 years because they had ongoing concerns about their child’s mental health. Second, the studies enrolled children diagnosed with ADHD, a condition associated with increased risk of bipolar disorder.

Using machine learning algorithms that processed the baseline data while accounting for the skewed distribution, the investigators were able to predict which of the children in the population would go on to develop bipolar disorder. The final model offered a sensitivity of 75%, a specificity of 76%, and an area under the receiver operating characteristic curve of 75%.

“To the best of our knowledge, this represents the first study using machine-learning algorithms for this purpose in pediatric psychiatry,” the investigators wrote.
 

Integrating models into electronic medical records

In the future, this model, or one like it, could be incorporated into software that automatically analyzes electronic medical records and notifies physicians about high-risk patients, Dr. Uchida predicted.

“Not all patients would connect to intervention,” she said. “Maybe it just means that you invite them in for a visit, or you observe them a little bit more carefully. I think that’s where we are hoping that machine learning and medical practice will go.”

When asked about the potential bias posed by psychiatric evaluation, compared with something like blood work results, Dr. Uchida suggested that this subjectivity can be overcome.

“I’m not entirely bothered by that,” she said, offering a list of objective data points that could be harvested from records, such as number of referrals, medications, and hospitalizations. Narrative text in medical records could also be analyzed, she said, potentially detecting key words that are more often associated with high-risk patients.

“Risk prediction is never going to be 100% accurate,” Dr. Uchida said. “But I do think that there will be things [in electronic medical records] that could guide how worried we should be, or how quickly we should intervene.”
 

Opening doors to personalized care

Martin Gignac, MD, chief of psychiatry at Montreal Children’s Hospital and associate professor at McGill University, Montreal, said the present study offers further support for the existence of pediatric-onset bipolar disorder, which “remains controversial” despite “solid evidence.”

“I’m impressed that we have 10-year-long longitudinal follow-up studies that corroborate the importance of this disorder, and show strong predictors of who is at risk,” Dr. Gignac said in an interview. “Clinicians treating a pediatric population should be aware that some of those children with mental health problems might have severe mental health problems, and you have to have the appropriate tools to screen them.”

Advanced tools like the one developed by Dr. Uchida and colleagues should lead to more personalized care, he said.

“We’re going to be able to define what your individual risk is, and maybe most importantly, what you can do to prevent the development of certain disorders,” Dr. Gignac said. “Are there any risks that are dynamic in nature, and that we can act upon? Exposure to stress, for example.”

While more work is needed to bring machine learning into daily psychiatric practice, Dr. Gignac concluded on an optimistic note.

“These instruments should translate from research into clinical practice in order to make difference for the patients we care for,” he said. “This is the type of hope that I hold – that it’s going to be applicable in clinical practice, hopefully, in the near future.”

The investigators disclosed relationships with InCarda, Baylis Medical, Johnson & Johnson, and others. Dr. Gignac disclosed no relevant competing interests.

Bad drinking consequence No. 87: Joining the LOTME team

Alcohol and college students go together like peanut butter and jelly. Or peanut butter and chocolate. Or peanut butter and toothpaste. Peanut butter goes with a lot of things.

Naturally, when you combine alcohol and college students, bad decisions are sure to follow. But have you ever wondered just how many bad decisions alcohol causes? A team of researchers from Penn State University, the undisputed champion of poor drinking decisions (trust us, we know), sure has. They’ve even conducted a 4-year study of 1,700 students as they carved a drunken swath through the many fine local drinking establishments, such as East Halls or that one frat house that hosts medieval battle–style ping pong tournaments.

elevate/PxHere

The students were surveyed twice a year throughout the study, and the researchers compiled a list of all the various consequences their subjects experienced. Ultimately, college students will experience an average of 102 consequences from drinking during their 4-year college careers, which is an impressive number. Try thinking up a hundred consequences for anything.

Some consequences are less common than others – we imagine “missing the Renaissance Faire because you felt drunker the morning after than while you were drinking” is pretty low on the list – but more than 96% of students reported that they’d experienced a hangover and that drinking had caused them to say or do embarrassing things. Also, more than 70% said they needed additional alcohol to feel any effect, a potential sign of alcohol use disorder.

Once they had their list, the researchers focused on 12 of the more common and severe consequences, such as blacking out, hangovers, and missing work/class, and asked the study participants how their parents would react to their drinking and those specific consequences. Students who believed their parents would disapprove of alcohol-related consequences actually experienced fewer consequences overall.

College students, it seems, really do care what their parents think, even if they don’t express it, the researchers said. That gives space for parents to offer advice about the consequences of hard drinking, making decisions while drunk, or bringing godawful Fireball whiskey to parties. Seriously, don’t do that. Stuff’s bad, and you should feel bad for bringing it. Your parents raised you better than that.
 

COVID ‘expert’ discusses data sharing

We interrupt our regularly scheduled programming to bring you this special news event. Elon Musk, the world’s second-most annoying human, is holding a press conference to discuss, of all things, COVID-19.

Reporter: Hey, Mr. Musketeer, what qualifies you to talk about a global pandemic?

EM: As the official king of the Twitterverse, I’m pretty much an expert on any topic.

Reporter: Okay then, Mr. Muskmelon, what can you tell us about the new study in Agricultural Economics, which looked at consumers’ knowledge of local COVID infection rates and their willingness to eat at restaurants?

Dmitry Zvolskiy

That’s all the time I have to chat with you today. I’m off to fire some more Twitter employees.

In case you hadn’t already guessed, Vlad Putin is officially more annoying than Elon Musk. We now return to this week’s typical LOTME shenanigans, already in progress.
 

The deadliest month

With climate change making the world hotter, leading to more heat stroke and organ failure, you would think the summer months would be the most deadly. In reality, though, it’s quite the opposite.

Nothing Ahead

There are multiple factors that make January the most deadly month out of the year, as LiveScience discovered in a recent analysis.

Let’s go through them, shall we?

Respiratory viruses: Robert Glatter, MD, of Lenox Hill Hospital in New York, told LiveScence that winter is the time for illnesses like the flu, bacterial pneumonia, and RSV. Millions of people worldwide die from the flu, according to the CDC. And the World Health Organization reported lower respiratory infections as the fourth-leading cause of death worldwide before COVID came along.

Heart disease: Heart conditions are actually more fatal in the winter months, according to a study published in Circulation. The cold puts more stress on the heart to keep the body warm, which can be a challenge for people who already have preexisting heart conditions.

Space heaters: Dr. Glatter also told Live Science that the use of space heaters could be a factor in the cold winter months since they can lead to carbon monoxide poisoning and even fires. Silent killers.

Holiday season: A time for joy and merriment, certainly, but Christmas et al. have their downsides. By January we’re coming off a 3-month food and alcohol binge, which leads to cardiac stress. There’s also the psychological stress that comes with the season. Sometimes the most wonderful time of the year just isn’t.

So even though summer is hot, fall has hurricanes, and spring tends to have the highest suicide rate, winter still ends up being the deadliest season.

Bad drinking consequence No. 87: Joining the LOTME team

Alcohol and college students go together like peanut butter and jelly. Or peanut butter and chocolate. Or peanut butter and toothpaste. Peanut butter goes with a lot of things.

Naturally, when you combine alcohol and college students, bad decisions are sure to follow. But have you ever wondered just how many bad decisions alcohol causes? A team of researchers from Penn State University, the undisputed champion of poor drinking decisions (trust us, we know), sure has. They’ve even conducted a 4-year study of 1,700 students as they carved a drunken swath through the many fine local drinking establishments, such as East Halls or that one frat house that hosts medieval battle–style ping pong tournaments.

elevate/PxHere

The students were surveyed twice a year throughout the study, and the researchers compiled a list of all the various consequences their subjects experienced. Ultimately, college students will experience an average of 102 consequences from drinking during their 4-year college careers, which is an impressive number. Try thinking up a hundred consequences for anything.

Some consequences are less common than others – we imagine “missing the Renaissance Faire because you felt drunker the morning after than while you were drinking” is pretty low on the list – but more than 96% of students reported that they’d experienced a hangover and that drinking had caused them to say or do embarrassing things. Also, more than 70% said they needed additional alcohol to feel any effect, a potential sign of alcohol use disorder.

Once they had their list, the researchers focused on 12 of the more common and severe consequences, such as blacking out, hangovers, and missing work/class, and asked the study participants how their parents would react to their drinking and those specific consequences. Students who believed their parents would disapprove of alcohol-related consequences actually experienced fewer consequences overall.

College students, it seems, really do care what their parents think, even if they don’t express it, the researchers said. That gives space for parents to offer advice about the consequences of hard drinking, making decisions while drunk, or bringing godawful Fireball whiskey to parties. Seriously, don’t do that. Stuff’s bad, and you should feel bad for bringing it. Your parents raised you better than that.
 

COVID ‘expert’ discusses data sharing

We interrupt our regularly scheduled programming to bring you this special news event. Elon Musk, the world’s second-most annoying human, is holding a press conference to discuss, of all things, COVID-19.

Reporter: Hey, Mr. Musketeer, what qualifies you to talk about a global pandemic?

EM: As the official king of the Twitterverse, I’m pretty much an expert on any topic.

Reporter: Okay then, Mr. Muskmelon, what can you tell us about the new study in Agricultural Economics, which looked at consumers’ knowledge of local COVID infection rates and their willingness to eat at restaurants?

Dmitry Zvolskiy

That’s all the time I have to chat with you today. I’m off to fire some more Twitter employees.

In case you hadn’t already guessed, Vlad Putin is officially more annoying than Elon Musk. We now return to this week’s typical LOTME shenanigans, already in progress.
 

The deadliest month

With climate change making the world hotter, leading to more heat stroke and organ failure, you would think the summer months would be the most deadly. In reality, though, it’s quite the opposite.

Nothing Ahead

There are multiple factors that make January the most deadly month out of the year, as LiveScience discovered in a recent analysis.

Let’s go through them, shall we?

Respiratory viruses: Robert Glatter, MD, of Lenox Hill Hospital in New York, told LiveScence that winter is the time for illnesses like the flu, bacterial pneumonia, and RSV. Millions of people worldwide die from the flu, according to the CDC. And the World Health Organization reported lower respiratory infections as the fourth-leading cause of death worldwide before COVID came along.

Heart disease: Heart conditions are actually more fatal in the winter months, according to a study published in Circulation. The cold puts more stress on the heart to keep the body warm, which can be a challenge for people who already have preexisting heart conditions.

Space heaters: Dr. Glatter also told Live Science that the use of space heaters could be a factor in the cold winter months since they can lead to carbon monoxide poisoning and even fires. Silent killers.

Holiday season: A time for joy and merriment, certainly, but Christmas et al. have their downsides. By January we’re coming off a 3-month food and alcohol binge, which leads to cardiac stress. There’s also the psychological stress that comes with the season. Sometimes the most wonderful time of the year just isn’t.

So even though summer is hot, fall has hurricanes, and spring tends to have the highest suicide rate, winter still ends up being the deadliest season.

Bad drinking consequence No. 87: Joining the LOTME team

Alcohol and college students go together like peanut butter and jelly. Or peanut butter and chocolate. Or peanut butter and toothpaste. Peanut butter goes with a lot of things.

Naturally, when you combine alcohol and college students, bad decisions are sure to follow. But have you ever wondered just how many bad decisions alcohol causes? A team of researchers from Penn State University, the undisputed champion of poor drinking decisions (trust us, we know), sure has. They’ve even conducted a 4-year study of 1,700 students as they carved a drunken swath through the many fine local drinking establishments, such as East Halls or that one frat house that hosts medieval battle–style ping pong tournaments.

elevate/PxHere

The students were surveyed twice a year throughout the study, and the researchers compiled a list of all the various consequences their subjects experienced. Ultimately, college students will experience an average of 102 consequences from drinking during their 4-year college careers, which is an impressive number. Try thinking up a hundred consequences for anything.

Some consequences are less common than others – we imagine “missing the Renaissance Faire because you felt drunker the morning after than while you were drinking” is pretty low on the list – but more than 96% of students reported that they’d experienced a hangover and that drinking had caused them to say or do embarrassing things. Also, more than 70% said they needed additional alcohol to feel any effect, a potential sign of alcohol use disorder.

Once they had their list, the researchers focused on 12 of the more common and severe consequences, such as blacking out, hangovers, and missing work/class, and asked the study participants how their parents would react to their drinking and those specific consequences. Students who believed their parents would disapprove of alcohol-related consequences actually experienced fewer consequences overall.

College students, it seems, really do care what their parents think, even if they don’t express it, the researchers said. That gives space for parents to offer advice about the consequences of hard drinking, making decisions while drunk, or bringing godawful Fireball whiskey to parties. Seriously, don’t do that. Stuff’s bad, and you should feel bad for bringing it. Your parents raised you better than that.
 

COVID ‘expert’ discusses data sharing

We interrupt our regularly scheduled programming to bring you this special news event. Elon Musk, the world’s second-most annoying human, is holding a press conference to discuss, of all things, COVID-19.

Reporter: Hey, Mr. Musketeer, what qualifies you to talk about a global pandemic?

EM: As the official king of the Twitterverse, I’m pretty much an expert on any topic.

Reporter: Okay then, Mr. Muskmelon, what can you tell us about the new study in Agricultural Economics, which looked at consumers’ knowledge of local COVID infection rates and their willingness to eat at restaurants?

Dmitry Zvolskiy

That’s all the time I have to chat with you today. I’m off to fire some more Twitter employees.

In case you hadn’t already guessed, Vlad Putin is officially more annoying than Elon Musk. We now return to this week’s typical LOTME shenanigans, already in progress.
 

The deadliest month

With climate change making the world hotter, leading to more heat stroke and organ failure, you would think the summer months would be the most deadly. In reality, though, it’s quite the opposite.

Nothing Ahead

There are multiple factors that make January the most deadly month out of the year, as LiveScience discovered in a recent analysis.

Let’s go through them, shall we?

Respiratory viruses: Robert Glatter, MD, of Lenox Hill Hospital in New York, told LiveScence that winter is the time for illnesses like the flu, bacterial pneumonia, and RSV. Millions of people worldwide die from the flu, according to the CDC. And the World Health Organization reported lower respiratory infections as the fourth-leading cause of death worldwide before COVID came along.

Heart disease: Heart conditions are actually more fatal in the winter months, according to a study published in Circulation. The cold puts more stress on the heart to keep the body warm, which can be a challenge for people who already have preexisting heart conditions.

Space heaters: Dr. Glatter also told Live Science that the use of space heaters could be a factor in the cold winter months since they can lead to carbon monoxide poisoning and even fires. Silent killers.

Holiday season: A time for joy and merriment, certainly, but Christmas et al. have their downsides. By January we’re coming off a 3-month food and alcohol binge, which leads to cardiac stress. There’s also the psychological stress that comes with the season. Sometimes the most wonderful time of the year just isn’t.

So even though summer is hot, fall has hurricanes, and spring tends to have the highest suicide rate, winter still ends up being the deadliest season.