CHEST Physician

CHICAGO – For the chief patient officer of the American Cancer Society, this year’s annual meeting of the American Society of Clinical Oncology was a gem. And it didn’t just sparkle because of the sequined Taylor Swift fans clogging the nearby streets during the meeting.

Arif Kamal, MD, MBA, MHS, who is also an oncologist at Duke University, Durham, N.C., said he was impressed by a pair of landmark studies released at the meeting that show hidden cancer can be targeted with “really remarkable outcomes.” He also highlighted sessions that examined the role of artificial intelligence (AI) in oncology, during an interview.

Below are lightly edited excerpts from a conversation with Dr. Kamal:



Question: What are some of most groundbreaking studies released at ASCO?

Answer: One is an interim analysis of the NATALEE trial, which involved patients with early-stage hormone receptor-positive, HER2-negative (HR+/HER2–) breast tumors. This phase 3 randomized trial compared maintenance therapy with the cyclin-dependent kinase 4/6 (CDK4/6) inhibitor ribociclib (Kisqali) plus endocrine therapy with an aromatase inhibitor to endocrine therapy alone in patients with node-positive or node-negative and stage II or III HR+/HER– breast cancer.

For a long time, the standard care in these patients has been to use endocrine therapy alone. This is the first big trial to show that upstream usage of additional therapy in early stages is also beneficial for disease-free survival. The 3-year invasive disease-free survival rate was 90.4% in the rebociclib-endocrine therapy group vs. 87.1% for patients who received only endocrine therapy (P = .0014).



Q: How do these findings add to current knowledge?

A: Typically, we let people get metastatic disease before we use CDK4/6 inhibitors. These findings show that systemic treatment beyond endocrine therapy will be helpful in cases where you’ve got smaller disease that has not spread yet.

Even in patients with node-negative breast cancer, micrometastatic disease is clearly there, because the medication killed the negative lymph nodes.



Q: What else struck you as especially important research?

A: The NATALEE findings match what we saw in another study – the ADAURA trial, which looked at adjuvant osimertinib in non–small-cell lung cancer patients with EGFR-mutated, stage IB to IIIA disease – cancer that has not spread to the lymph nodes.

This is another example where you have a treatment being used in earlier-stage disease that’s showing really remarkable outcomes. The study found that 5-year overall survival was 88% in an osimertinib group vs. 78% in a placebo group (P < .001). This is a disease where, in stage IB, we wouldn’t even necessarily give these patients treatment at all, other than surgical resection of the tumor and maybe give them a little bit of chemotherapy.

Even in these smaller, early tumors, osimertinib makes a difference.



Q: As a whole, what are these studies telling us about cancer cells that can’t be easily detected?

A: To find a disease-free survival benefit with adding ribociclib in a stage II, stage III setting, particularly in node-negative disease, is remarkable because it says that the cells in hiding are bad actors, and they are going to cause trouble. The study shows that medications can find these cells and reverse that risk of bad outcomes.

If you think about the paradigm of cancer, that’s pretty remarkable because the ADAURA trial does the same thing: You do surgery for [early-stage] lung cancers that have not spread to the lymph nodes and you figure, “Well, I’ve got it all, right? The margins are real big, healthy, clean.” And yet, people still have recurrences, and you ask the same question: “Can any medicine find those few cells, the hundreds of cells that are still left somewhere in hiding?” And the answer is again, yes. It’s changing the paradigm of our understanding of minimal residual disease.

That’s why there’s so much interest in liquid biopsies. Let’s say that after treatment we don’t see any cancer radiologically, but there’s a signal from a liquid biopsy [detecting residual cancer]. These two trials demonstrate that there’s something we can do about it.



Q: There were quite a few studies about artificial intelligence released at ASCO. Where do we stand on that front?

A: We’re just at the beginning of people thinking about the use of generative AI for clinical decision support, clinical trial matching, and pathology review. But AI, at least for now, still has the issue of making up things that aren’t true. That’s not something patients are going to be okay with.



Q: How can AI be helpful to medical providers considering its limitations?

A: AI is going to be very good at the data-to-information transition. You’ll start seeing people use AI to start clinical notes for them and to match patients to the best clinical trials for them. But fundamentally, the clinician’s role will continue to be to check facts and offer wisdom.



Q: Will AI threaten the careers of oncologists?

A: The body of knowledge about oncology is growing exponentially, and no one can actually keep up. There’s so much data that’s out there that needs to be turned into usable information amid a shortage of oncologists. At the same time, the prevalence of cancer is going up, even though mortality is going down.

Synthesis of data is what oncologists are waiting for from AI. They’ll welcome it as opposed to being worried. That’s the sentiment I heard from my colleagues.

Dr. Kamal has no disclosures.

CHICAGO – For the chief patient officer of the American Cancer Society, this year’s annual meeting of the American Society of Clinical Oncology was a gem. And it didn’t just sparkle because of the sequined Taylor Swift fans clogging the nearby streets during the meeting.

Arif Kamal, MD, MBA, MHS, who is also an oncologist at Duke University, Durham, N.C., said he was impressed by a pair of landmark studies released at the meeting that show hidden cancer can be targeted with “really remarkable outcomes.” He also highlighted sessions that examined the role of artificial intelligence (AI) in oncology, during an interview.

Below are lightly edited excerpts from a conversation with Dr. Kamal:



Question: What are some of most groundbreaking studies released at ASCO?

Answer: One is an interim analysis of the NATALEE trial, which involved patients with early-stage hormone receptor-positive, HER2-negative (HR+/HER2–) breast tumors. This phase 3 randomized trial compared maintenance therapy with the cyclin-dependent kinase 4/6 (CDK4/6) inhibitor ribociclib (Kisqali) plus endocrine therapy with an aromatase inhibitor to endocrine therapy alone in patients with node-positive or node-negative and stage II or III HR+/HER– breast cancer.

For a long time, the standard care in these patients has been to use endocrine therapy alone. This is the first big trial to show that upstream usage of additional therapy in early stages is also beneficial for disease-free survival. The 3-year invasive disease-free survival rate was 90.4% in the rebociclib-endocrine therapy group vs. 87.1% for patients who received only endocrine therapy (P = .0014).



Q: How do these findings add to current knowledge?

A: Typically, we let people get metastatic disease before we use CDK4/6 inhibitors. These findings show that systemic treatment beyond endocrine therapy will be helpful in cases where you’ve got smaller disease that has not spread yet.

Even in patients with node-negative breast cancer, micrometastatic disease is clearly there, because the medication killed the negative lymph nodes.



Q: What else struck you as especially important research?

A: The NATALEE findings match what we saw in another study – the ADAURA trial, which looked at adjuvant osimertinib in non–small-cell lung cancer patients with EGFR-mutated, stage IB to IIIA disease – cancer that has not spread to the lymph nodes.

This is another example where you have a treatment being used in earlier-stage disease that’s showing really remarkable outcomes. The study found that 5-year overall survival was 88% in an osimertinib group vs. 78% in a placebo group (P < .001). This is a disease where, in stage IB, we wouldn’t even necessarily give these patients treatment at all, other than surgical resection of the tumor and maybe give them a little bit of chemotherapy.

Even in these smaller, early tumors, osimertinib makes a difference.



Q: As a whole, what are these studies telling us about cancer cells that can’t be easily detected?

A: To find a disease-free survival benefit with adding ribociclib in a stage II, stage III setting, particularly in node-negative disease, is remarkable because it says that the cells in hiding are bad actors, and they are going to cause trouble. The study shows that medications can find these cells and reverse that risk of bad outcomes.

If you think about the paradigm of cancer, that’s pretty remarkable because the ADAURA trial does the same thing: You do surgery for [early-stage] lung cancers that have not spread to the lymph nodes and you figure, “Well, I’ve got it all, right? The margins are real big, healthy, clean.” And yet, people still have recurrences, and you ask the same question: “Can any medicine find those few cells, the hundreds of cells that are still left somewhere in hiding?” And the answer is again, yes. It’s changing the paradigm of our understanding of minimal residual disease.

That’s why there’s so much interest in liquid biopsies. Let’s say that after treatment we don’t see any cancer radiologically, but there’s a signal from a liquid biopsy [detecting residual cancer]. These two trials demonstrate that there’s something we can do about it.



Q: There were quite a few studies about artificial intelligence released at ASCO. Where do we stand on that front?

A: We’re just at the beginning of people thinking about the use of generative AI for clinical decision support, clinical trial matching, and pathology review. But AI, at least for now, still has the issue of making up things that aren’t true. That’s not something patients are going to be okay with.



Q: How can AI be helpful to medical providers considering its limitations?

A: AI is going to be very good at the data-to-information transition. You’ll start seeing people use AI to start clinical notes for them and to match patients to the best clinical trials for them. But fundamentally, the clinician’s role will continue to be to check facts and offer wisdom.



Q: Will AI threaten the careers of oncologists?

A: The body of knowledge about oncology is growing exponentially, and no one can actually keep up. There’s so much data that’s out there that needs to be turned into usable information amid a shortage of oncologists. At the same time, the prevalence of cancer is going up, even though mortality is going down.

Synthesis of data is what oncologists are waiting for from AI. They’ll welcome it as opposed to being worried. That’s the sentiment I heard from my colleagues.

Dr. Kamal has no disclosures.

CHICAGO – For the chief patient officer of the American Cancer Society, this year’s annual meeting of the American Society of Clinical Oncology was a gem. And it didn’t just sparkle because of the sequined Taylor Swift fans clogging the nearby streets during the meeting.

Arif Kamal, MD, MBA, MHS, who is also an oncologist at Duke University, Durham, N.C., said he was impressed by a pair of landmark studies released at the meeting that show hidden cancer can be targeted with “really remarkable outcomes.” He also highlighted sessions that examined the role of artificial intelligence (AI) in oncology, during an interview.

Below are lightly edited excerpts from a conversation with Dr. Kamal:



Question: What are some of most groundbreaking studies released at ASCO?

Answer: One is an interim analysis of the NATALEE trial, which involved patients with early-stage hormone receptor-positive, HER2-negative (HR+/HER2–) breast tumors. This phase 3 randomized trial compared maintenance therapy with the cyclin-dependent kinase 4/6 (CDK4/6) inhibitor ribociclib (Kisqali) plus endocrine therapy with an aromatase inhibitor to endocrine therapy alone in patients with node-positive or node-negative and stage II or III HR+/HER– breast cancer.

For a long time, the standard care in these patients has been to use endocrine therapy alone. This is the first big trial to show that upstream usage of additional therapy in early stages is also beneficial for disease-free survival. The 3-year invasive disease-free survival rate was 90.4% in the rebociclib-endocrine therapy group vs. 87.1% for patients who received only endocrine therapy (P = .0014).



Q: How do these findings add to current knowledge?

A: Typically, we let people get metastatic disease before we use CDK4/6 inhibitors. These findings show that systemic treatment beyond endocrine therapy will be helpful in cases where you’ve got smaller disease that has not spread yet.

Even in patients with node-negative breast cancer, micrometastatic disease is clearly there, because the medication killed the negative lymph nodes.



Q: What else struck you as especially important research?

A: The NATALEE findings match what we saw in another study – the ADAURA trial, which looked at adjuvant osimertinib in non–small-cell lung cancer patients with EGFR-mutated, stage IB to IIIA disease – cancer that has not spread to the lymph nodes.

This is another example where you have a treatment being used in earlier-stage disease that’s showing really remarkable outcomes. The study found that 5-year overall survival was 88% in an osimertinib group vs. 78% in a placebo group (P < .001). This is a disease where, in stage IB, we wouldn’t even necessarily give these patients treatment at all, other than surgical resection of the tumor and maybe give them a little bit of chemotherapy.

Even in these smaller, early tumors, osimertinib makes a difference.



Q: As a whole, what are these studies telling us about cancer cells that can’t be easily detected?

A: To find a disease-free survival benefit with adding ribociclib in a stage II, stage III setting, particularly in node-negative disease, is remarkable because it says that the cells in hiding are bad actors, and they are going to cause trouble. The study shows that medications can find these cells and reverse that risk of bad outcomes.

If you think about the paradigm of cancer, that’s pretty remarkable because the ADAURA trial does the same thing: You do surgery for [early-stage] lung cancers that have not spread to the lymph nodes and you figure, “Well, I’ve got it all, right? The margins are real big, healthy, clean.” And yet, people still have recurrences, and you ask the same question: “Can any medicine find those few cells, the hundreds of cells that are still left somewhere in hiding?” And the answer is again, yes. It’s changing the paradigm of our understanding of minimal residual disease.

That’s why there’s so much interest in liquid biopsies. Let’s say that after treatment we don’t see any cancer radiologically, but there’s a signal from a liquid biopsy [detecting residual cancer]. These two trials demonstrate that there’s something we can do about it.



Q: There were quite a few studies about artificial intelligence released at ASCO. Where do we stand on that front?

A: We’re just at the beginning of people thinking about the use of generative AI for clinical decision support, clinical trial matching, and pathology review. But AI, at least for now, still has the issue of making up things that aren’t true. That’s not something patients are going to be okay with.



Q: How can AI be helpful to medical providers considering its limitations?

A: AI is going to be very good at the data-to-information transition. You’ll start seeing people use AI to start clinical notes for them and to match patients to the best clinical trials for them. But fundamentally, the clinician’s role will continue to be to check facts and offer wisdom.



Q: Will AI threaten the careers of oncologists?

A: The body of knowledge about oncology is growing exponentially, and no one can actually keep up. There’s so much data that’s out there that needs to be turned into usable information amid a shortage of oncologists. At the same time, the prevalence of cancer is going up, even though mortality is going down.

Synthesis of data is what oncologists are waiting for from AI. They’ll welcome it as opposed to being worried. That’s the sentiment I heard from my colleagues.

Dr. Kamal has no disclosures.

Three big bumps on the weight-loss journey

The search for the Holy Grail. The destruction of the One Ring. The never-ending struggle to Lose Weight.

Like most legendary quests, weight loss is a journey, and we need support to help us achieve our goal. Maybe it’s gaining a new workout partner or finding a similarly-goaled Facebook Group. For a lot of people, it’s as simple as your friends and family. A recent study, however, suggests that the people closest to you may be your worst weight-loss enemies, and they might not even know it.

Spencer Davis/Unsplash

Researchers at the University of Surrey reviewed the literature on the positives and negatives of social support when it comes to weight loss and identified three types of negative effects: acts of sabotage, feeding behavior, and collusion.

Let’s start with the softest of intentions and work our way up. Collusion is the least negative. Friends and family may just go with the flow, even if it doesn’t agree with the goals of the person who’s trying to lose weight. It can even happen when health care professionals try to help their patients navigate or avoid obesity, ultimately killing with kindness, so to speak.

Next up, feeding behavior. Maybe you know someone whose love language is cooking. There are also people who share food because they don’t want to waste it or because they’re trying to be polite. They act out of the goodness of their hearts, but they’re putting up roadblocks to someone’s goals. These types of acts are usually one-sided, the researchers found. Remember, it’s okay to say, “No thanks.”

The last method, sabotage, is the most sinister. The saboteur may discourage others from eating healthy, undermine their efforts to be physically active, or take jabs at their confidence or self-esteem. Something as simple as criticizing someone for eating a salad or refusing to go on a walk with them can cause a setback.

“We need to explore this area further to develop interventions which could target family and friends and help them be more supportive in helping those they are close to lose weight,” said lead author Jane Odgen, PhD, of the University of Surrey, Guildford, England.

Like we said before, weight loss is a journey. The right support can only improve the odds of success.
 

Robots vs. mosquitoes

If there’s one thing robots are bad at, it’s giving solid mental health advice to people in crisis. If there’s one thing robots are very, very good at, it’s causing apocalypses. And joyous day for humanity, this time we’re not the ones being apocalypsed.

Yet.

Liu et al., 2023, PLOS Neglected Tropical Diseases, CC-BY 4.0

Taiwan has a big mosquito problem. Not only do the mosquitoes in Taiwan carry dengue – among other dangerous diseases – but they’ve urbanized. Not urbanized in the sense that they’ve acquired a taste for organic coffee and avocado toast (that would be the millennial mosquito, a separate but even more terrifying creature), but more that they’ve adapted to reproduce literally anywhere and everywhere. Taiwanese mosquitoes like to breed in roadside sewer ditches, and this is where our genocidal robot comes in.

To combat the new, dangerous form of street-savvy mosquito, researchers built a robot armed with both insecticide and high-temperature, high-pressure water jets and sent it into the sewers of Kaohsiung City. The robot’s goal was simple: Whenever it came across signs of heavy mosquito breeding – eggs, larvae, pupae, and so on – the robot went to work. Utilizing both its primary weapons, the robot scrubbed numerous breeding sites across the city clean.

The researchers could just sit back and wait to see how effective their robot was. In the immediate aftermath, at various monitoring sites placed alongside the ditches, adult mosquito density fell by two-thirds in areas targeted by the robot. That’s nothing to sniff at, and it does make sense. After all, mosquitoes are quite difficult to kill in their adult stage, why not target them when they’re young and basically immobile?

The researchers saw promise with their mosquito-killing robot, but we’ve noticed a rather large issue. Killing two-thirds of mosquitoes is fine, but the third that’s left will be very angry. Very angry indeed. After all, we’re targeting the mosquito equivalent of children. Let’s hope our mosquito Terminator managed to kill mosquito Sarah Connor, or we’re going to have a big problem on our hands a bit later down the line.
 

This is knot what you were expecting

Physicians who aren’t surgeons probably don’t realize it, but the big thing that’s been getting between the knot-tying specialists and perfect suturing technique all these years is a lack of physics. Don’t believe us? Well, maybe you’ll believe plastic surgeon Samia Guerid, MD, of Lausanne, Switzerland: “The lack of physics-based analysis has been a limitation.” Nuff said.

Alain Herzog / EPFL

That’s not enough for you, is it? Fine, we were warned.

Any surgical knot, Dr. Guerid and associates explained in a written statement, involves the “complex interplay” between six key factors: topology, geometry, elasticity, contact, friction, and polymer plasticity of the suturing filament. The strength of a suture “depends on the tension applied during the tying of the knot, [which] permanently deforms, or stretches the filament, creating a holding force.” Not enough tension and the knot comes undone, while too much snaps the filament.

For the experiment, Dr. Guerid tied a few dozen surgical knots, which were then scanned using x-ray micro–computed tomography to facilitate finite element modeling with a “3D continuum-level constitutive model for elastic-viscoplastic mechanical behavior” – no, we have no idea what that means, either – developed by the research team.

That model, and a great deal of math – so much math – allowed the researchers to define a threshold between loose and tight knots and uncover “relationships between knot strength and pretension, friction, and number of throws,” they said.

But what about the big question? The one about the ideal amount of tension? You may want to sit down. The answer to the ultimate question of the relationship between knot pretension and strength is … Did we mention that the team had its own mathematician? Their predictive model for safe knot-tying is … You’re not going to like this. The best way to teach safe knot-tying to both trainees and robots is … not ready yet.

The secret to targeting the knot tension sweet spot, for now, anyway, is still intuition gained from years of experience. Nobody ever said science was perfect … or easy … or quick.

Three big bumps on the weight-loss journey

The search for the Holy Grail. The destruction of the One Ring. The never-ending struggle to Lose Weight.

Like most legendary quests, weight loss is a journey, and we need support to help us achieve our goal. Maybe it’s gaining a new workout partner or finding a similarly-goaled Facebook Group. For a lot of people, it’s as simple as your friends and family. A recent study, however, suggests that the people closest to you may be your worst weight-loss enemies, and they might not even know it.

Spencer Davis/Unsplash

Researchers at the University of Surrey reviewed the literature on the positives and negatives of social support when it comes to weight loss and identified three types of negative effects: acts of sabotage, feeding behavior, and collusion.

Let’s start with the softest of intentions and work our way up. Collusion is the least negative. Friends and family may just go with the flow, even if it doesn’t agree with the goals of the person who’s trying to lose weight. It can even happen when health care professionals try to help their patients navigate or avoid obesity, ultimately killing with kindness, so to speak.

Next up, feeding behavior. Maybe you know someone whose love language is cooking. There are also people who share food because they don’t want to waste it or because they’re trying to be polite. They act out of the goodness of their hearts, but they’re putting up roadblocks to someone’s goals. These types of acts are usually one-sided, the researchers found. Remember, it’s okay to say, “No thanks.”

The last method, sabotage, is the most sinister. The saboteur may discourage others from eating healthy, undermine their efforts to be physically active, or take jabs at their confidence or self-esteem. Something as simple as criticizing someone for eating a salad or refusing to go on a walk with them can cause a setback.

“We need to explore this area further to develop interventions which could target family and friends and help them be more supportive in helping those they are close to lose weight,” said lead author Jane Odgen, PhD, of the University of Surrey, Guildford, England.

Like we said before, weight loss is a journey. The right support can only improve the odds of success.
 

Robots vs. mosquitoes

If there’s one thing robots are bad at, it’s giving solid mental health advice to people in crisis. If there’s one thing robots are very, very good at, it’s causing apocalypses. And joyous day for humanity, this time we’re not the ones being apocalypsed.

Yet.

Liu et al., 2023, PLOS Neglected Tropical Diseases, CC-BY 4.0

Taiwan has a big mosquito problem. Not only do the mosquitoes in Taiwan carry dengue – among other dangerous diseases – but they’ve urbanized. Not urbanized in the sense that they’ve acquired a taste for organic coffee and avocado toast (that would be the millennial mosquito, a separate but even more terrifying creature), but more that they’ve adapted to reproduce literally anywhere and everywhere. Taiwanese mosquitoes like to breed in roadside sewer ditches, and this is where our genocidal robot comes in.

To combat the new, dangerous form of street-savvy mosquito, researchers built a robot armed with both insecticide and high-temperature, high-pressure water jets and sent it into the sewers of Kaohsiung City. The robot’s goal was simple: Whenever it came across signs of heavy mosquito breeding – eggs, larvae, pupae, and so on – the robot went to work. Utilizing both its primary weapons, the robot scrubbed numerous breeding sites across the city clean.

The researchers could just sit back and wait to see how effective their robot was. In the immediate aftermath, at various monitoring sites placed alongside the ditches, adult mosquito density fell by two-thirds in areas targeted by the robot. That’s nothing to sniff at, and it does make sense. After all, mosquitoes are quite difficult to kill in their adult stage, why not target them when they’re young and basically immobile?

The researchers saw promise with their mosquito-killing robot, but we’ve noticed a rather large issue. Killing two-thirds of mosquitoes is fine, but the third that’s left will be very angry. Very angry indeed. After all, we’re targeting the mosquito equivalent of children. Let’s hope our mosquito Terminator managed to kill mosquito Sarah Connor, or we’re going to have a big problem on our hands a bit later down the line.
 

This is knot what you were expecting

Physicians who aren’t surgeons probably don’t realize it, but the big thing that’s been getting between the knot-tying specialists and perfect suturing technique all these years is a lack of physics. Don’t believe us? Well, maybe you’ll believe plastic surgeon Samia Guerid, MD, of Lausanne, Switzerland: “The lack of physics-based analysis has been a limitation.” Nuff said.

Alain Herzog / EPFL

That’s not enough for you, is it? Fine, we were warned.

Any surgical knot, Dr. Guerid and associates explained in a written statement, involves the “complex interplay” between six key factors: topology, geometry, elasticity, contact, friction, and polymer plasticity of the suturing filament. The strength of a suture “depends on the tension applied during the tying of the knot, [which] permanently deforms, or stretches the filament, creating a holding force.” Not enough tension and the knot comes undone, while too much snaps the filament.

For the experiment, Dr. Guerid tied a few dozen surgical knots, which were then scanned using x-ray micro–computed tomography to facilitate finite element modeling with a “3D continuum-level constitutive model for elastic-viscoplastic mechanical behavior” – no, we have no idea what that means, either – developed by the research team.

That model, and a great deal of math – so much math – allowed the researchers to define a threshold between loose and tight knots and uncover “relationships between knot strength and pretension, friction, and number of throws,” they said.

But what about the big question? The one about the ideal amount of tension? You may want to sit down. The answer to the ultimate question of the relationship between knot pretension and strength is … Did we mention that the team had its own mathematician? Their predictive model for safe knot-tying is … You’re not going to like this. The best way to teach safe knot-tying to both trainees and robots is … not ready yet.

The secret to targeting the knot tension sweet spot, for now, anyway, is still intuition gained from years of experience. Nobody ever said science was perfect … or easy … or quick.

Three big bumps on the weight-loss journey

The search for the Holy Grail. The destruction of the One Ring. The never-ending struggle to Lose Weight.

Like most legendary quests, weight loss is a journey, and we need support to help us achieve our goal. Maybe it’s gaining a new workout partner or finding a similarly-goaled Facebook Group. For a lot of people, it’s as simple as your friends and family. A recent study, however, suggests that the people closest to you may be your worst weight-loss enemies, and they might not even know it.

Spencer Davis/Unsplash

Researchers at the University of Surrey reviewed the literature on the positives and negatives of social support when it comes to weight loss and identified three types of negative effects: acts of sabotage, feeding behavior, and collusion.

Let’s start with the softest of intentions and work our way up. Collusion is the least negative. Friends and family may just go with the flow, even if it doesn’t agree with the goals of the person who’s trying to lose weight. It can even happen when health care professionals try to help their patients navigate or avoid obesity, ultimately killing with kindness, so to speak.

Next up, feeding behavior. Maybe you know someone whose love language is cooking. There are also people who share food because they don’t want to waste it or because they’re trying to be polite. They act out of the goodness of their hearts, but they’re putting up roadblocks to someone’s goals. These types of acts are usually one-sided, the researchers found. Remember, it’s okay to say, “No thanks.”

The last method, sabotage, is the most sinister. The saboteur may discourage others from eating healthy, undermine their efforts to be physically active, or take jabs at their confidence or self-esteem. Something as simple as criticizing someone for eating a salad or refusing to go on a walk with them can cause a setback.

“We need to explore this area further to develop interventions which could target family and friends and help them be more supportive in helping those they are close to lose weight,” said lead author Jane Odgen, PhD, of the University of Surrey, Guildford, England.

Like we said before, weight loss is a journey. The right support can only improve the odds of success.
 

Robots vs. mosquitoes

If there’s one thing robots are bad at, it’s giving solid mental health advice to people in crisis. If there’s one thing robots are very, very good at, it’s causing apocalypses. And joyous day for humanity, this time we’re not the ones being apocalypsed.

Yet.

Liu et al., 2023, PLOS Neglected Tropical Diseases, CC-BY 4.0

Taiwan has a big mosquito problem. Not only do the mosquitoes in Taiwan carry dengue – among other dangerous diseases – but they’ve urbanized. Not urbanized in the sense that they’ve acquired a taste for organic coffee and avocado toast (that would be the millennial mosquito, a separate but even more terrifying creature), but more that they’ve adapted to reproduce literally anywhere and everywhere. Taiwanese mosquitoes like to breed in roadside sewer ditches, and this is where our genocidal robot comes in.

To combat the new, dangerous form of street-savvy mosquito, researchers built a robot armed with both insecticide and high-temperature, high-pressure water jets and sent it into the sewers of Kaohsiung City. The robot’s goal was simple: Whenever it came across signs of heavy mosquito breeding – eggs, larvae, pupae, and so on – the robot went to work. Utilizing both its primary weapons, the robot scrubbed numerous breeding sites across the city clean.

The researchers could just sit back and wait to see how effective their robot was. In the immediate aftermath, at various monitoring sites placed alongside the ditches, adult mosquito density fell by two-thirds in areas targeted by the robot. That’s nothing to sniff at, and it does make sense. After all, mosquitoes are quite difficult to kill in their adult stage, why not target them when they’re young and basically immobile?

The researchers saw promise with their mosquito-killing robot, but we’ve noticed a rather large issue. Killing two-thirds of mosquitoes is fine, but the third that’s left will be very angry. Very angry indeed. After all, we’re targeting the mosquito equivalent of children. Let’s hope our mosquito Terminator managed to kill mosquito Sarah Connor, or we’re going to have a big problem on our hands a bit later down the line.
 

This is knot what you were expecting

Physicians who aren’t surgeons probably don’t realize it, but the big thing that’s been getting between the knot-tying specialists and perfect suturing technique all these years is a lack of physics. Don’t believe us? Well, maybe you’ll believe plastic surgeon Samia Guerid, MD, of Lausanne, Switzerland: “The lack of physics-based analysis has been a limitation.” Nuff said.

Alain Herzog / EPFL

That’s not enough for you, is it? Fine, we were warned.

Any surgical knot, Dr. Guerid and associates explained in a written statement, involves the “complex interplay” between six key factors: topology, geometry, elasticity, contact, friction, and polymer plasticity of the suturing filament. The strength of a suture “depends on the tension applied during the tying of the knot, [which] permanently deforms, or stretches the filament, creating a holding force.” Not enough tension and the knot comes undone, while too much snaps the filament.

For the experiment, Dr. Guerid tied a few dozen surgical knots, which were then scanned using x-ray micro–computed tomography to facilitate finite element modeling with a “3D continuum-level constitutive model for elastic-viscoplastic mechanical behavior” – no, we have no idea what that means, either – developed by the research team.

That model, and a great deal of math – so much math – allowed the researchers to define a threshold between loose and tight knots and uncover “relationships between knot strength and pretension, friction, and number of throws,” they said.

But what about the big question? The one about the ideal amount of tension? You may want to sit down. The answer to the ultimate question of the relationship between knot pretension and strength is … Did we mention that the team had its own mathematician? Their predictive model for safe knot-tying is … You’re not going to like this. The best way to teach safe knot-tying to both trainees and robots is … not ready yet.

The secret to targeting the knot tension sweet spot, for now, anyway, is still intuition gained from years of experience. Nobody ever said science was perfect … or easy … or quick.

A bill in the Maine legislature would have the medical malpractice statute of limitations clock start running when a patient discovers the negligence, which could be years after treatment took place. And other states could follow suit with similar bills. What danger does this pose for doctors?

As it stands, the time limit for patients to be able to bring a medical malpractice lawsuit varies by state. The bill that was introduced in Maine would enable patients to bring suits many years after treatment took place. For physicians, this extends their period of liability and could potentially increase the number of lawsuits against them.

“The theory behind a statute of limitations is that states want to provide a reasonable, but not indefinite, amount of time for someone to bring a case to court,” says Patrick T. O’Rourke, Esq., adjunct professor at University of Colorado School of Law, Boulder.

Without a statute of limitations, people could bring claims many years after the fact, which makes it harder to obtain and preserve evidence, Mr. O’Rourke says.

In most cases, it isn’t necessary for a patient to know the full extent of their injury or that their physician acted wrongfully or negligently for the statute of limitations to begin running.
 

Time of injury versus time of discovery

Most states’ laws dictate that the statute of limitations begins at a set time “after the cause of action accrues.” That means that the clock starts ticking from the date of the procedure, surgery, or treatment. In most states, that time is 2 or 3 years.

This can bar some patients from taking any action at all because the statute of limitations ran out. Because of these hurdles, the proposed bill in Maine would extend the statute of limitations.

Proponents of the bill say that patients would still have 3 years to file suit; it just changes when the clock starts. But opponents feel it could open the door to a limitless system in which people have an indefinite time to sue.

Many states already have discovery rules that extend the statute of limitations when the harm was not immediately obvious to the patient. The legal expectation is that patients who have significant pain or unexpected health conditions will seek medical treatment to investigate what’s wrong. Patients who don’t address the situation promptly are not protected by the discovery rule.

“It is the injured person’s obligation, once learning of the injury, to take action to protect their rights,” says Mr. O’Rourke.

Some states have also enacted other claims requirements in medical malpractice cases that are prerequisites for bringing lawsuits that have periods attached to them. For instance, in Florida, parties have 10 days to provide relevant medical records during the investigation period for a malpractice suit, and in Maine, before filing any malpractice action, a plaintiff must file a complaint with a prelitigation screening panel.
 

Medical malpractice statutes of limitations by state

Although each state has a basic statute of limitations, many states also include clauses for discovery rules. For example, in Vermont, in addition to the 3-year statute of limitations, a patient can pursue legal recourse “2 years from the date the injury is or reasonably should have been discovered, whichever occurs later, but not later than 7 years from the date of the incident.”

In some states, such as Virginia, special extensions apply in cases in which fraud, concealment, or intentional misrepresentation prevented discovery of the injury within the statute of limitations. And in most states, the statute of limitations is much longer for cases in which medical malpractice involves a child, usually at least until the child turns 18.
 

Statutes of limitations by state

1 Year: California, Kentucky, Louisiana, Ohio, Tennessee

2 Years: Alabama, Alaska, Arizona, Arkansas, Colorado, Connecticut, Delaware, Florida, Georgia, Hawaii, Idaho, Illinois, Indiana, Iowa, Kansas, Michigan, Mississippi, Missouri, Nebraska, New Hampshire, New Jersey, North Dakota, Oklahoma, Oregon, Pennsylvania, South Dakota, Texas, Utah, Virginia, West Virginia, Wyoming

2.5 Years: New York

3 Years: Washington D.C., Maine, Maryland, Massachusetts, Montana, Nevada, New Mexico, North Carolina, Rhode Island, South Carolina, Vermont, Washington, Wisconsin

4 Years: Minnesota
 

To protect yourself

Mr. O’Rourke says that if your state enacts a law that extends the statute of limitations for medical malpractice, there aren’t any proactive changes you need to make in terms of your day-to-day practice of medicine.

“Physicians should continue to provide care that is consistent with the standards of care for their specialty and ensure that the documentation accurately reflects the care they rendered,” he says.

Always be candid and up-front about a patient’s condition, Mr. O’Rourke says, especially if malpractice is on the table.

“If a physician misleads a patient about the nature or extent of an injury, that could prevent the statute of limitations from beginning to run,” he says. “Being open and honest about an injury doesn’t mean that a physician must admit any fault. The patient is owed timely, accurate, and candid information about their condition.”
 

Keep good records

If the statute of limitations increases, you’ll need to have access to the medical records for as long as the statute is in place, but this shouldn’t have an effect on your records keeping if you’re up to date with HIPAA compliance, says Mr. O’Rourke.

“I don’t think an extension of the statute should cause physicians to change their practices, particularly with the retention of medical records, which should be maintained consistently with HIPAA requirements irrespective of the limitations period in a particular state,” he adds.
 

Keep an eye on malpractice insurance rates

It’s possible that your malpractice insurance could go up as a result of laws that increase the statute of limitations. But Mr. O’Rourke thinks it likely won’t be a significant amount.

He says it’s “theoretically possible” that an increase in a limitations period could result in an increase in your malpractice insurance, since some claims that would otherwise have been barred because of time could then proceed, but the increase would be nominal.

“I would expect any increase to be fairly marginal because the majority of claims will already be accounted for on an actuarial basis,” he says. “I also don’t think that the extension of a limitations period would increase the award of damages in a particular case. The injuries should be the same under either limitations period, so the compensable loss should not increase.”

Anything that makes it easier for patients to recover should increase the cost of professional liability insurance, and vice versa, says Charles Silver, McDonald Endowed Chair in Civil Procedure at University of Texas at Austin School of Law and coauthor of “Medical Malpractice Litigation: How It Works – Why Tort Reform Hasn’t Helped.” But the long-term trend across the country is toward declining rates of liability and declining payouts on claims.

“The likelihood of being sued successfully by a former patient is low, as is the risk of having to pay out of pocket to settle a claim,” he says. In 2022, the number of adverse reports nationally was 38,938, and out of those, 10,807 resulted in a payout.

In his research on medical malpractice in Texas, Mr. Silver says physicians who carried $1 million in coverage essentially never faced any personal liability on medical malpractice claims. “[This means] that they never had to write a check to a victim,” he says. “Insurers provided all the money. I suspect that the same is true nationwide.”
 

Key takeaways

Ultimately, to protect yourself and your practice, you can do the following:

• Know the statute of limitations and discovery rules for your state.
• Review your coverage with your insurer to better understand your liability.
• Keep accurate records for as long as your statute requires.
• Notify your insurer or risk management department as soon as possible in the event of an adverse outcome with a patient, Mr. O’Rourke advises.

“The most important thing a physician can do to avoid being sued, even when negligent, is to treat patients with kindness and respect,” says Mr. Silver. “Patients don’t expect doctors to be perfect, and they rarely sue doctors they like.”

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

A bill in the Maine legislature would have the medical malpractice statute of limitations clock start running when a patient discovers the negligence, which could be years after treatment took place. And other states could follow suit with similar bills. What danger does this pose for doctors?

As it stands, the time limit for patients to be able to bring a medical malpractice lawsuit varies by state. The bill that was introduced in Maine would enable patients to bring suits many years after treatment took place. For physicians, this extends their period of liability and could potentially increase the number of lawsuits against them.

“The theory behind a statute of limitations is that states want to provide a reasonable, but not indefinite, amount of time for someone to bring a case to court,” says Patrick T. O’Rourke, Esq., adjunct professor at University of Colorado School of Law, Boulder.

Without a statute of limitations, people could bring claims many years after the fact, which makes it harder to obtain and preserve evidence, Mr. O’Rourke says.

In most cases, it isn’t necessary for a patient to know the full extent of their injury or that their physician acted wrongfully or negligently for the statute of limitations to begin running.
 

Time of injury versus time of discovery

Most states’ laws dictate that the statute of limitations begins at a set time “after the cause of action accrues.” That means that the clock starts ticking from the date of the procedure, surgery, or treatment. In most states, that time is 2 or 3 years.

This can bar some patients from taking any action at all because the statute of limitations ran out. Because of these hurdles, the proposed bill in Maine would extend the statute of limitations.

Proponents of the bill say that patients would still have 3 years to file suit; it just changes when the clock starts. But opponents feel it could open the door to a limitless system in which people have an indefinite time to sue.

Many states already have discovery rules that extend the statute of limitations when the harm was not immediately obvious to the patient. The legal expectation is that patients who have significant pain or unexpected health conditions will seek medical treatment to investigate what’s wrong. Patients who don’t address the situation promptly are not protected by the discovery rule.

“It is the injured person’s obligation, once learning of the injury, to take action to protect their rights,” says Mr. O’Rourke.

Some states have also enacted other claims requirements in medical malpractice cases that are prerequisites for bringing lawsuits that have periods attached to them. For instance, in Florida, parties have 10 days to provide relevant medical records during the investigation period for a malpractice suit, and in Maine, before filing any malpractice action, a plaintiff must file a complaint with a prelitigation screening panel.
 

Medical malpractice statutes of limitations by state

Although each state has a basic statute of limitations, many states also include clauses for discovery rules. For example, in Vermont, in addition to the 3-year statute of limitations, a patient can pursue legal recourse “2 years from the date the injury is or reasonably should have been discovered, whichever occurs later, but not later than 7 years from the date of the incident.”

In some states, such as Virginia, special extensions apply in cases in which fraud, concealment, or intentional misrepresentation prevented discovery of the injury within the statute of limitations. And in most states, the statute of limitations is much longer for cases in which medical malpractice involves a child, usually at least until the child turns 18.
 

Statutes of limitations by state

1 Year: California, Kentucky, Louisiana, Ohio, Tennessee

2 Years: Alabama, Alaska, Arizona, Arkansas, Colorado, Connecticut, Delaware, Florida, Georgia, Hawaii, Idaho, Illinois, Indiana, Iowa, Kansas, Michigan, Mississippi, Missouri, Nebraska, New Hampshire, New Jersey, North Dakota, Oklahoma, Oregon, Pennsylvania, South Dakota, Texas, Utah, Virginia, West Virginia, Wyoming

2.5 Years: New York

3 Years: Washington D.C., Maine, Maryland, Massachusetts, Montana, Nevada, New Mexico, North Carolina, Rhode Island, South Carolina, Vermont, Washington, Wisconsin

4 Years: Minnesota
 

To protect yourself

Mr. O’Rourke says that if your state enacts a law that extends the statute of limitations for medical malpractice, there aren’t any proactive changes you need to make in terms of your day-to-day practice of medicine.

“Physicians should continue to provide care that is consistent with the standards of care for their specialty and ensure that the documentation accurately reflects the care they rendered,” he says.

Always be candid and up-front about a patient’s condition, Mr. O’Rourke says, especially if malpractice is on the table.

“If a physician misleads a patient about the nature or extent of an injury, that could prevent the statute of limitations from beginning to run,” he says. “Being open and honest about an injury doesn’t mean that a physician must admit any fault. The patient is owed timely, accurate, and candid information about their condition.”
 

Keep good records

If the statute of limitations increases, you’ll need to have access to the medical records for as long as the statute is in place, but this shouldn’t have an effect on your records keeping if you’re up to date with HIPAA compliance, says Mr. O’Rourke.

“I don’t think an extension of the statute should cause physicians to change their practices, particularly with the retention of medical records, which should be maintained consistently with HIPAA requirements irrespective of the limitations period in a particular state,” he adds.
 

Keep an eye on malpractice insurance rates

It’s possible that your malpractice insurance could go up as a result of laws that increase the statute of limitations. But Mr. O’Rourke thinks it likely won’t be a significant amount.

He says it’s “theoretically possible” that an increase in a limitations period could result in an increase in your malpractice insurance, since some claims that would otherwise have been barred because of time could then proceed, but the increase would be nominal.

“I would expect any increase to be fairly marginal because the majority of claims will already be accounted for on an actuarial basis,” he says. “I also don’t think that the extension of a limitations period would increase the award of damages in a particular case. The injuries should be the same under either limitations period, so the compensable loss should not increase.”

Anything that makes it easier for patients to recover should increase the cost of professional liability insurance, and vice versa, says Charles Silver, McDonald Endowed Chair in Civil Procedure at University of Texas at Austin School of Law and coauthor of “Medical Malpractice Litigation: How It Works – Why Tort Reform Hasn’t Helped.” But the long-term trend across the country is toward declining rates of liability and declining payouts on claims.

“The likelihood of being sued successfully by a former patient is low, as is the risk of having to pay out of pocket to settle a claim,” he says. In 2022, the number of adverse reports nationally was 38,938, and out of those, 10,807 resulted in a payout.

In his research on medical malpractice in Texas, Mr. Silver says physicians who carried $1 million in coverage essentially never faced any personal liability on medical malpractice claims. “[This means] that they never had to write a check to a victim,” he says. “Insurers provided all the money. I suspect that the same is true nationwide.”
 

Key takeaways

Ultimately, to protect yourself and your practice, you can do the following:

• Know the statute of limitations and discovery rules for your state.
• Review your coverage with your insurer to better understand your liability.
• Keep accurate records for as long as your statute requires.
• Notify your insurer or risk management department as soon as possible in the event of an adverse outcome with a patient, Mr. O’Rourke advises.

“The most important thing a physician can do to avoid being sued, even when negligent, is to treat patients with kindness and respect,” says Mr. Silver. “Patients don’t expect doctors to be perfect, and they rarely sue doctors they like.”

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

A bill in the Maine legislature would have the medical malpractice statute of limitations clock start running when a patient discovers the negligence, which could be years after treatment took place. And other states could follow suit with similar bills. What danger does this pose for doctors?

As it stands, the time limit for patients to be able to bring a medical malpractice lawsuit varies by state. The bill that was introduced in Maine would enable patients to bring suits many years after treatment took place. For physicians, this extends their period of liability and could potentially increase the number of lawsuits against them.

“The theory behind a statute of limitations is that states want to provide a reasonable, but not indefinite, amount of time for someone to bring a case to court,” says Patrick T. O’Rourke, Esq., adjunct professor at University of Colorado School of Law, Boulder.

Without a statute of limitations, people could bring claims many years after the fact, which makes it harder to obtain and preserve evidence, Mr. O’Rourke says.

In most cases, it isn’t necessary for a patient to know the full extent of their injury or that their physician acted wrongfully or negligently for the statute of limitations to begin running.
 

Time of injury versus time of discovery

Most states’ laws dictate that the statute of limitations begins at a set time “after the cause of action accrues.” That means that the clock starts ticking from the date of the procedure, surgery, or treatment. In most states, that time is 2 or 3 years.

This can bar some patients from taking any action at all because the statute of limitations ran out. Because of these hurdles, the proposed bill in Maine would extend the statute of limitations.

Proponents of the bill say that patients would still have 3 years to file suit; it just changes when the clock starts. But opponents feel it could open the door to a limitless system in which people have an indefinite time to sue.

Many states already have discovery rules that extend the statute of limitations when the harm was not immediately obvious to the patient. The legal expectation is that patients who have significant pain or unexpected health conditions will seek medical treatment to investigate what’s wrong. Patients who don’t address the situation promptly are not protected by the discovery rule.

“It is the injured person’s obligation, once learning of the injury, to take action to protect their rights,” says Mr. O’Rourke.

Some states have also enacted other claims requirements in medical malpractice cases that are prerequisites for bringing lawsuits that have periods attached to them. For instance, in Florida, parties have 10 days to provide relevant medical records during the investigation period for a malpractice suit, and in Maine, before filing any malpractice action, a plaintiff must file a complaint with a prelitigation screening panel.
 

Medical malpractice statutes of limitations by state

Although each state has a basic statute of limitations, many states also include clauses for discovery rules. For example, in Vermont, in addition to the 3-year statute of limitations, a patient can pursue legal recourse “2 years from the date the injury is or reasonably should have been discovered, whichever occurs later, but not later than 7 years from the date of the incident.”

In some states, such as Virginia, special extensions apply in cases in which fraud, concealment, or intentional misrepresentation prevented discovery of the injury within the statute of limitations. And in most states, the statute of limitations is much longer for cases in which medical malpractice involves a child, usually at least until the child turns 18.
 

Statutes of limitations by state

1 Year: California, Kentucky, Louisiana, Ohio, Tennessee

2 Years: Alabama, Alaska, Arizona, Arkansas, Colorado, Connecticut, Delaware, Florida, Georgia, Hawaii, Idaho, Illinois, Indiana, Iowa, Kansas, Michigan, Mississippi, Missouri, Nebraska, New Hampshire, New Jersey, North Dakota, Oklahoma, Oregon, Pennsylvania, South Dakota, Texas, Utah, Virginia, West Virginia, Wyoming

2.5 Years: New York

3 Years: Washington D.C., Maine, Maryland, Massachusetts, Montana, Nevada, New Mexico, North Carolina, Rhode Island, South Carolina, Vermont, Washington, Wisconsin

4 Years: Minnesota
 

To protect yourself

Mr. O’Rourke says that if your state enacts a law that extends the statute of limitations for medical malpractice, there aren’t any proactive changes you need to make in terms of your day-to-day practice of medicine.

“Physicians should continue to provide care that is consistent with the standards of care for their specialty and ensure that the documentation accurately reflects the care they rendered,” he says.

Always be candid and up-front about a patient’s condition, Mr. O’Rourke says, especially if malpractice is on the table.

“If a physician misleads a patient about the nature or extent of an injury, that could prevent the statute of limitations from beginning to run,” he says. “Being open and honest about an injury doesn’t mean that a physician must admit any fault. The patient is owed timely, accurate, and candid information about their condition.”
 

Keep good records

If the statute of limitations increases, you’ll need to have access to the medical records for as long as the statute is in place, but this shouldn’t have an effect on your records keeping if you’re up to date with HIPAA compliance, says Mr. O’Rourke.

“I don’t think an extension of the statute should cause physicians to change their practices, particularly with the retention of medical records, which should be maintained consistently with HIPAA requirements irrespective of the limitations period in a particular state,” he adds.
 

Keep an eye on malpractice insurance rates

It’s possible that your malpractice insurance could go up as a result of laws that increase the statute of limitations. But Mr. O’Rourke thinks it likely won’t be a significant amount.

He says it’s “theoretically possible” that an increase in a limitations period could result in an increase in your malpractice insurance, since some claims that would otherwise have been barred because of time could then proceed, but the increase would be nominal.

“I would expect any increase to be fairly marginal because the majority of claims will already be accounted for on an actuarial basis,” he says. “I also don’t think that the extension of a limitations period would increase the award of damages in a particular case. The injuries should be the same under either limitations period, so the compensable loss should not increase.”

Anything that makes it easier for patients to recover should increase the cost of professional liability insurance, and vice versa, says Charles Silver, McDonald Endowed Chair in Civil Procedure at University of Texas at Austin School of Law and coauthor of “Medical Malpractice Litigation: How It Works – Why Tort Reform Hasn’t Helped.” But the long-term trend across the country is toward declining rates of liability and declining payouts on claims.

“The likelihood of being sued successfully by a former patient is low, as is the risk of having to pay out of pocket to settle a claim,” he says. In 2022, the number of adverse reports nationally was 38,938, and out of those, 10,807 resulted in a payout.

In his research on medical malpractice in Texas, Mr. Silver says physicians who carried $1 million in coverage essentially never faced any personal liability on medical malpractice claims. “[This means] that they never had to write a check to a victim,” he says. “Insurers provided all the money. I suspect that the same is true nationwide.”
 

Key takeaways

Ultimately, to protect yourself and your practice, you can do the following:

• Know the statute of limitations and discovery rules for your state.
• Review your coverage with your insurer to better understand your liability.
• Keep accurate records for as long as your statute requires.
• Notify your insurer or risk management department as soon as possible in the event of an adverse outcome with a patient, Mr. O’Rourke advises.

“The most important thing a physician can do to avoid being sued, even when negligent, is to treat patients with kindness and respect,” says Mr. Silver. “Patients don’t expect doctors to be perfect, and they rarely sue doctors they like.”

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

Insomnia may increase vulnerability to influenza-like illness, a novel finding that was revealed by the passive collection of biometric data from a smart bed.

The study of smart-bed sleepers found that there was a statistically significant correlation between a higher number of episodes of influenza-like illnesses (ILI) per year with longer duration compared to people without insomnia.

However, more research is needed to determine causality and whether insomnia may predispose to ILI or whether ILI affects long-term sleep behavior, the researchers noted. 

“Several lines of evidence make me think that it’s more likely that insomnia makes one more vulnerable to influenza through pathways that involve decreased immune function,” study investigator Gary Garcia-Molina, PhD, with Sleep Number Labs, San Jose, Calif., said in an interview.

Sleep disorders, including insomnia, can dampen immune function and an individual’s ability to fight off illness, he noted.

The findings were presented at the annual meeting of the Associated Professional Sleep Societies.
 

Smart, connected devices

Pathophysiological responses to respiratory viral infection affect sleep duration and quality in addition to breathing function. “Smart” and “connected” devices that monitor biosignals over time have shown promise for monitoring infectious disease.

In an earlier study presented at SLEEP 2021, Dr. Garcia-Molina and colleagues found that real-world biometric data obtained from a smart bed can help predict and track symptoms of COVID-19 and other respiratory infections. They showed that worsening of COVID-19 symptoms correlated with an increase in sleep duration, breathing rate, and heart rate and a decrease in sleep quality.

In the new study, the researchers evaluated vulnerability to ILI in people with insomnia.

They quantified insomnia over time using the insomnia severity index (ISI). They quantified ILI vulnerability using an established artificial intelligence model they developed that estimates the daily probability of ILI symptoms from a Sleep Number smart bed using ballistocardiograph sensors.

Smart bed data – including daily and restful sleep duration, sleep latency, sleep quality, heart rate, breathing rate and motion level – were queried from 2019 (pre-COVID) and 2021.

A total of 1,680 smart sleepers had nearly constant ISI scores over the study period, with 249 having insomnia and 1,431 not having insomnia.

Data from both 2019 and 2021 show that smart sleepers with insomnia had significantly more and longer ILI episodes per year, compared with peers without insomnia.

For 2019, individuals without insomnia had 1.2 ILI episodes on average, which was significantly less (P < .01) than individuals with insomnia, at 1.5 episodes. The average ILI episode duration for those without insomnia was 4.3 days, which was significantly lower (P < .01) in those with insomnia group, at 6.1 days.

The data for 2021 show similar results, with the no-insomnia group having significantly fewer (P < .01) ILI episodes (about 1.2), compared with the insomnia group (about 1.5).

The average ILI episode duration for the no-insomnia group was 5 days, which was significantly less (P < .01) than the insomnia group, at 6.1 days.

The researchers said their study adds to other data on the relationship between sleep and overall health and well-being. It also highlights the potential health risk of insomnia and the importance of identifying and treating sleep disorders.

“Sleep has such a profound influence on health and wellness and the ability to capture these data unobtrusively in such an easy way and with such a large number of participants paves the way to investigate different aspects of health and disease,” Dr. Garcia-Molina said.
 

Rich data source

In a comment, Adam C. Powell, PhD, president of Payer+Provider Syndicate, a management advisory and operational consulting firm, said “smart beds provide a new data source for passively monitoring the health of individuals.”

“Unlike active monitoring methods requiring self-report, passive monitoring enables data to be captured without an individual taking any action. This data can be potentially integrated with data from other sources, such as pedometers, smart scales, and smart blood pressure cuffs, to gain a more holistic understanding of how an individual’s activities and behaviors impact their well-being,” said Dr. Powell, who wasn’t involved in the study.

There are some methodological limitations to the study, he noted.

“While the dependent variables examined were the duration and presence of episodes of influenza-like illness, they did not directly measure these episodes. Instead, they calculated the daily probability of influenza-like illness symptoms using a model that received input from the ballistocardiograph sensors in the smart beds,” Dr. Powell noted.

“The model used to calculate daily probability of influenza-like illness was created by examining associations between individuals’ smart-bed sensor data and population-level trends in influenza-like illness reported by the Centers for Disease Control and Prevention,” he explained.

Nonetheless, the findings are “consistent with the literature. It has been established by other researchers that impaired sleep is associated with greater risk of influenza, as well as other illnesses,” Dr. Powell said.

Funding for the study was provided by Sleep Number. Dr. Garcia-Molina and five coauthors are employed by Sleep Number. Dr. Powell reported no relevant financial relationships.

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

Insomnia may increase vulnerability to influenza-like illness, a novel finding that was revealed by the passive collection of biometric data from a smart bed.

The study of smart-bed sleepers found that there was a statistically significant correlation between a higher number of episodes of influenza-like illnesses (ILI) per year with longer duration compared to people without insomnia.

However, more research is needed to determine causality and whether insomnia may predispose to ILI or whether ILI affects long-term sleep behavior, the researchers noted. 

“Several lines of evidence make me think that it’s more likely that insomnia makes one more vulnerable to influenza through pathways that involve decreased immune function,” study investigator Gary Garcia-Molina, PhD, with Sleep Number Labs, San Jose, Calif., said in an interview.

Sleep disorders, including insomnia, can dampen immune function and an individual’s ability to fight off illness, he noted.

The findings were presented at the annual meeting of the Associated Professional Sleep Societies.
 

Smart, connected devices

Pathophysiological responses to respiratory viral infection affect sleep duration and quality in addition to breathing function. “Smart” and “connected” devices that monitor biosignals over time have shown promise for monitoring infectious disease.

In an earlier study presented at SLEEP 2021, Dr. Garcia-Molina and colleagues found that real-world biometric data obtained from a smart bed can help predict and track symptoms of COVID-19 and other respiratory infections. They showed that worsening of COVID-19 symptoms correlated with an increase in sleep duration, breathing rate, and heart rate and a decrease in sleep quality.

In the new study, the researchers evaluated vulnerability to ILI in people with insomnia.

They quantified insomnia over time using the insomnia severity index (ISI). They quantified ILI vulnerability using an established artificial intelligence model they developed that estimates the daily probability of ILI symptoms from a Sleep Number smart bed using ballistocardiograph sensors.

Smart bed data – including daily and restful sleep duration, sleep latency, sleep quality, heart rate, breathing rate and motion level – were queried from 2019 (pre-COVID) and 2021.

A total of 1,680 smart sleepers had nearly constant ISI scores over the study period, with 249 having insomnia and 1,431 not having insomnia.

Data from both 2019 and 2021 show that smart sleepers with insomnia had significantly more and longer ILI episodes per year, compared with peers without insomnia.

For 2019, individuals without insomnia had 1.2 ILI episodes on average, which was significantly less (P < .01) than individuals with insomnia, at 1.5 episodes. The average ILI episode duration for those without insomnia was 4.3 days, which was significantly lower (P < .01) in those with insomnia group, at 6.1 days.

The data for 2021 show similar results, with the no-insomnia group having significantly fewer (P < .01) ILI episodes (about 1.2), compared with the insomnia group (about 1.5).

The average ILI episode duration for the no-insomnia group was 5 days, which was significantly less (P < .01) than the insomnia group, at 6.1 days.

The researchers said their study adds to other data on the relationship between sleep and overall health and well-being. It also highlights the potential health risk of insomnia and the importance of identifying and treating sleep disorders.

“Sleep has such a profound influence on health and wellness and the ability to capture these data unobtrusively in such an easy way and with such a large number of participants paves the way to investigate different aspects of health and disease,” Dr. Garcia-Molina said.
 

Rich data source

In a comment, Adam C. Powell, PhD, president of Payer+Provider Syndicate, a management advisory and operational consulting firm, said “smart beds provide a new data source for passively monitoring the health of individuals.”

“Unlike active monitoring methods requiring self-report, passive monitoring enables data to be captured without an individual taking any action. This data can be potentially integrated with data from other sources, such as pedometers, smart scales, and smart blood pressure cuffs, to gain a more holistic understanding of how an individual’s activities and behaviors impact their well-being,” said Dr. Powell, who wasn’t involved in the study.

There are some methodological limitations to the study, he noted.

“While the dependent variables examined were the duration and presence of episodes of influenza-like illness, they did not directly measure these episodes. Instead, they calculated the daily probability of influenza-like illness symptoms using a model that received input from the ballistocardiograph sensors in the smart beds,” Dr. Powell noted.

“The model used to calculate daily probability of influenza-like illness was created by examining associations between individuals’ smart-bed sensor data and population-level trends in influenza-like illness reported by the Centers for Disease Control and Prevention,” he explained.

Nonetheless, the findings are “consistent with the literature. It has been established by other researchers that impaired sleep is associated with greater risk of influenza, as well as other illnesses,” Dr. Powell said.

Funding for the study was provided by Sleep Number. Dr. Garcia-Molina and five coauthors are employed by Sleep Number. Dr. Powell reported no relevant financial relationships.

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

Insomnia may increase vulnerability to influenza-like illness, a novel finding that was revealed by the passive collection of biometric data from a smart bed.

The study of smart-bed sleepers found that there was a statistically significant correlation between a higher number of episodes of influenza-like illnesses (ILI) per year with longer duration compared to people without insomnia.

However, more research is needed to determine causality and whether insomnia may predispose to ILI or whether ILI affects long-term sleep behavior, the researchers noted. 

“Several lines of evidence make me think that it’s more likely that insomnia makes one more vulnerable to influenza through pathways that involve decreased immune function,” study investigator Gary Garcia-Molina, PhD, with Sleep Number Labs, San Jose, Calif., said in an interview.

Sleep disorders, including insomnia, can dampen immune function and an individual’s ability to fight off illness, he noted.

The findings were presented at the annual meeting of the Associated Professional Sleep Societies.
 

Smart, connected devices

Pathophysiological responses to respiratory viral infection affect sleep duration and quality in addition to breathing function. “Smart” and “connected” devices that monitor biosignals over time have shown promise for monitoring infectious disease.

In an earlier study presented at SLEEP 2021, Dr. Garcia-Molina and colleagues found that real-world biometric data obtained from a smart bed can help predict and track symptoms of COVID-19 and other respiratory infections. They showed that worsening of COVID-19 symptoms correlated with an increase in sleep duration, breathing rate, and heart rate and a decrease in sleep quality.

In the new study, the researchers evaluated vulnerability to ILI in people with insomnia.

They quantified insomnia over time using the insomnia severity index (ISI). They quantified ILI vulnerability using an established artificial intelligence model they developed that estimates the daily probability of ILI symptoms from a Sleep Number smart bed using ballistocardiograph sensors.

Smart bed data – including daily and restful sleep duration, sleep latency, sleep quality, heart rate, breathing rate and motion level – were queried from 2019 (pre-COVID) and 2021.

A total of 1,680 smart sleepers had nearly constant ISI scores over the study period, with 249 having insomnia and 1,431 not having insomnia.

Data from both 2019 and 2021 show that smart sleepers with insomnia had significantly more and longer ILI episodes per year, compared with peers without insomnia.

For 2019, individuals without insomnia had 1.2 ILI episodes on average, which was significantly less (P < .01) than individuals with insomnia, at 1.5 episodes. The average ILI episode duration for those without insomnia was 4.3 days, which was significantly lower (P < .01) in those with insomnia group, at 6.1 days.

The data for 2021 show similar results, with the no-insomnia group having significantly fewer (P < .01) ILI episodes (about 1.2), compared with the insomnia group (about 1.5).

The average ILI episode duration for the no-insomnia group was 5 days, which was significantly less (P < .01) than the insomnia group, at 6.1 days.

The researchers said their study adds to other data on the relationship between sleep and overall health and well-being. It also highlights the potential health risk of insomnia and the importance of identifying and treating sleep disorders.

“Sleep has such a profound influence on health and wellness and the ability to capture these data unobtrusively in such an easy way and with such a large number of participants paves the way to investigate different aspects of health and disease,” Dr. Garcia-Molina said.
 

Rich data source

In a comment, Adam C. Powell, PhD, president of Payer+Provider Syndicate, a management advisory and operational consulting firm, said “smart beds provide a new data source for passively monitoring the health of individuals.”

“Unlike active monitoring methods requiring self-report, passive monitoring enables data to be captured without an individual taking any action. This data can be potentially integrated with data from other sources, such as pedometers, smart scales, and smart blood pressure cuffs, to gain a more holistic understanding of how an individual’s activities and behaviors impact their well-being,” said Dr. Powell, who wasn’t involved in the study.

There are some methodological limitations to the study, he noted.

“While the dependent variables examined were the duration and presence of episodes of influenza-like illness, they did not directly measure these episodes. Instead, they calculated the daily probability of influenza-like illness symptoms using a model that received input from the ballistocardiograph sensors in the smart beds,” Dr. Powell noted.

“The model used to calculate daily probability of influenza-like illness was created by examining associations between individuals’ smart-bed sensor data and population-level trends in influenza-like illness reported by the Centers for Disease Control and Prevention,” he explained.

Nonetheless, the findings are “consistent with the literature. It has been established by other researchers that impaired sleep is associated with greater risk of influenza, as well as other illnesses,” Dr. Powell said.

Funding for the study was provided by Sleep Number. Dr. Garcia-Molina and five coauthors are employed by Sleep Number. Dr. Powell reported no relevant financial relationships.

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

Chronic pulmonary disease continues to be a major cause of morbidity and mortality in individuals living with the human immunodeficiency virus, even with optimal HIV control. And this is independent, as seen in many studies, of age, smoking, and pulmonary infections.

Both chronic pulmonary obstructive disease (COPD) and lung cancer occur more frequently in people living with HIV than in the general population, and at earlier ages, and with worse outcomes. The risk for emphysema and interstitial lung abnormalities also appears to be higher, research has shown. And asthma has also recently emerged as another important lung disease in people with HIV (PWH).

“There is evidence that the severity of immunocompromise associated with HIV infection is linked with chronic lung diseases. People who have a lower CD4 cell count or a higher viral load do have an increased risk of COPD and emphysema as well as potentially lung cancer. But [while] immunocompromise plays a role, it isn’t the only story, given that even with well-controlled HIV there is increased risk,” said Kristina Crothers, MD, professor in the division of pulmonary, critical care, and sleep medicine at the University of Washington, Seattle.

Research has evolved from a focus on the epidemiology of HIV-related chronic lung diseases to a current emphasis on “trying to understand further the mechanisms [behind the heightened risk] through more benchwork and corollary translational studies, and then to the next level of trying to understand what this means for how we should manage people with HIV who have chronic lung diseases,” Dr. Crothers said. “Should management be tailored for people with HIV infection?”

Impairments in immune pathways, local and systemic inflammation, oxidative stress, dysbiosis, and accelerated cellular senescence are among potential mechanisms, but until ongoing mechanistic research yields more answers, pulmonologists should simply – but importantly – be aware of the increased risk and have a low threshold for investigating respiratory symptoms, she and other experts said in interviews. Referral of eligible patients for lung cancer screening is also a priority, as is smoking cessation, they said.

Notably, while spirometry has been the most commonly studied lung function measure in PWH, another noninvasive measure, diffusing capacity for carbon monoxide (DLCO), has garnered attention in the past decade and thus far appears to be the more frequent lung function abnormality.

In an analysis published in 2020 from the longitudinal Multicenter AIDS Cohort Study (MACS) – a study of a subcohort of 591 men with HIV and 476 without HIV – those with HIV were found to have a 1.6-fold increased risk of mild DLCO impairment (< 80% of predicted normal) and a 3-fold higher risk of more severe DLCO impairment (< 60% of predicted normal). There was no significant difference in spirometry findings by HIV status.

Such findings on DLCO are worthy of consideration in clinical practice, even in the absence of HIV-specific screening guidelines for noncommunicable lung diseases, Dr. Crothers said. “In thinking about screening and diagnosing chronic lung diseases in these patients, I’d not only consider spirometry, but also diffusing capacity” when possible, she said. Impaired DLCO is seen with emphysema and pulmonary vascular diseases like pulmonary hypertension and also interstitial lung diseases.
 

Key chronic lung diseases

Ken M. Kunisaki, MD, MS, associate professor of medicine at the University of Minnesota, Minneapolis, and the first author of the MACS analysis of lung function – one of the most recent and largest reports of DLCO impairment – points out that studies of chest computed tomography (CT) have also documented higher rates of emphysema and interstitial lung abnormalities.

A chest CT analysis from a cohort in Denmark (the Copenhagen Comorbidity in HIV Infection [COCOMO] cohort) found interstitial lung abnormalities in 10.9% of more than 700 PWH which represented a 1.8-fold increased risk compared to HIV-negative controls. And a study from an Italian sample of never-smoking PWH and controls reported emphysema in 18% and 4%, respectively. These studies, which did not measure DLCO, are among those discussed in a 2021 review by Dr. Kunisaki of advances in HIV-associated chronic lung disease research.

COPD is the best studied and most commonly encountered chronic lung disease in PWH. “Particularly for COPD, what’s both interesting and unfortunate is that we haven’t really seen any changes in the epidemiology with ART (antiretroviral therapy) – we’re still seeing the same findings, like the association of HIV with worse COPD at younger ages,” said Alison Morris, MD, MS, professor of medicine, immunology, and clinical and translational research at the University of Pittsburgh. “It doesn’t seem to have improved.”

Its prevalence has varied widely from cohort to cohort, from as low as 3% (similar to the general population) to over 40%, Dr. Kunisaki said, emphasizing that many studies, including studies showing higher rates, have controlled for current and past smoking. In evaluating patients with low or no smoking burden, “don’t discount respiratory symptoms as possibly reflecting underlying lung disease because COPD can develop with low to no smoking history in those with HIV,” he advised.

A better understanding of how a chronic viral infection like HIV leads to heightened COPD risk will not only help those with HIV, he notes, but also people without HIV who have COPD but have never smoked – a woefully underappreciated and understudied population. Ongoing research, he said, “should help us understand COPD pathogenesis generally.”

Research on asthma is relatively limited thus far, but it does appear that PWH may be more prone to developing severe asthma, just as with COPD, said Dr. Kunisaki, also a staff physician at the Minneapolis Veterans Administration Health Care System. Research has shown, for instance, that people with HIV more frequently needed aggressive respiratory support when hospitalized for asthma exacerbations.

It’s unclear how much of this potentially increased severity is attributable to the biology of HIV’s impact on the body and how much relates to social factors like disparities in income and access to care, Dr. Kunisaki said, noting that the same questions apply to the more frequent COPD exacerbations documented in PWH.

Dr. Crothers points out that, while most studies do not suggest a difference in the incidence of asthma in PWH, “there is some data from researchers looking at asthma profiles [suggesting] that the biomarkers associated with asthma may be different in people with and without HIV,” signaling potentially different molecular or biologic underpinnings of the disease.

Incidence rates of lung cancer in PWH, meanwhile, have declined over the last 2 decades, but lung cancer remains the leading cause of cancer-related mortality in PWH and occurs at a rate that is 2-2.5 times higher than that of individuals not infected with HIV, according to

Janice Leung, MD, of the division of respiratory medicine at the University of British Columbia and the Centre for Heart Lung Innovation at St. Paul’s Hospital in Vancouver.

Patients with HIV have “worse outcomes overall and a higher risk of mortality, even when presenting at the same stage,” said Dr. Leung, who reviewed trends in COPD and lung cancer in a recently published opinion piece.
 

Potential drivers

A bird’s eye view of potential – and likely interrelated – mechanisms for chronic lung disease includes chronic immune activation that impairs innate and adaptive immune pathways; chronic inflammation systemically and in the lung despite viral suppression; persistence of the virus in latent reservoirs in the lung, particularly in alveolar macrophages and T cells; HIV-related proteins contributing to oxidative stress; accelerated cellular aging; dysbiosis; and ongoing injury from inhaled toxins.

All are described in the literature and are being further explored. “It’s likely that multiple pathways are playing a role,” said Dr. Crothers, “and it could be that the balance of one to another leads to different manifestations of disease.”

Biomarkers that have been elevated and associated with different features of chronic lung disease – such as airflow obstruction, low DLCO, and emphysema – include markers of inflammation (e.g., C-reactive protein, interleukin-6), monocyte activation (e.g., soluble CD14), and markers of endothelial dysfunction, she noted in a 2021 commentary marking 40 years since the first reported cases of acquired immunodeficiency syndrome.

In her laboratory, Dr. Leung is using new epigenetic markers to look at the pathogenesis of accelerated aging in the lung. By profiling bronchial epithelial brushings for DNA methylation and gene expression, they have found that “people living with both HIV and COPD have the fastest epigenetic age acceleration in their airway epithelium,” she said. The findings “suggest that the HIV lung is aging faster.”

They reported their findings in 2022, describing methylation disruptions along age-related pathways such as cellular senescence, longevity regulation, and insulin signaling.

Dr. Leung and her team have also studied the lung microbiome and found lower microbial diversity in the airway epithelium in patients with HIV than those without, especially in those with HIV and COPD. The National Institutes of Health–sponsored Lung HIV Microbiome Project found that changes in the lung microbiome are most pronounced in patients who haven’t yet initiated ART, but research in her lab suggests ongoing suppression of microbial diversity even after ART, she said.

Dr. Morris is particularly interested in the oral microbiome, having found through her research that changes in the oral microbiome in PWH were more related to impaired lung function than alterations in the lung and gut microbiome. “That may be in part because of the way we measure things,” she said. “But we also think that the oral microbiome probably seeds the lung [through micro-aspiration].” A study published in 2020 from the Pittsburgh site of the MACS described alterations in oral microbial communities in PWH with abnormal lung function.

Preliminary research suggests that improved dental cleaning and periodontal work in PWH and COPD may influence the severity of COPD, she noted.

“We don’t see as much of a signal with the gut microbiome [and HIV status or lung function], though there could still be ways in which gut microbiome influences the lung,” through systemic inflammation, the release of metabolites into the bloodstream, or microbial translocation, for instance, she said.

The potential role of translocation of members of the microbiome, in fact, is an area of active research for Dr. Morris. Members of the microbiome – viruses and fungi in addition to bacteria – “can get into the bloodstream from the mouth, from the lung, from the gut, to stimulate inflammation and worsen lung disease,” she said.
 

Key questions in an evolving research landscape

Dr. Kunisaki looks forward to research providing a more longitudinal look at lung function decline– a move beyond a dominance of cross-sectional studies – as well as research that is more comprehensive, with simultaneous collection of various functional measures (eg., DLCO with chest imaging and fractional excretion of nitric oxide (FENO – a standardized breath measure of Th2 airway inflammation).

The several-year-old NIH-supported MACS/WIHS (Women’s Interagency HIV Study) Combined Cohort study, in which Dr. Kunisaki and Dr. Morris participate, aims in part to identity biomarkers of increased risk for chronic lung disease and other chronic disorders and to develop strategies for more effective interventions and treatments.

Researchers will also share biospecimens, “which will allow more mechanistic work,” Dr. Kunisaki noted. (The combined cohort study includes participants from the earlier, separate MACS and WIHS studies.)

Questions about treatment strategies include the risks versus benefits of inhaled corticosteroids, which may increase an already elevated risk of respiratory infections like bacterial pneumonia in PWH, Dr. Kunisaki said.

[An aside: Inhaled corticosteroids also have well-described interactions with ART regimens that contain CYP3A4 inhibitors (e.g., ritonavir and cobicistat) that can lead to hypercortisolism. In patients who require both types of drugs, he said, beclomethasone has the least interactions and is the preferred inhaled corticosteroid.]

For Dr. Crothers, unanswered critical questions include – as she wrote in her 2021 commentary – the question of how guidelines for the management of COPD and asthma should be adapted for PWH. Is COPD in PWH more or less responsive to inhaled corticosteroids, for instance? And are antifibrotic treatments for interstitial lung disease and immunotherapies for asthma or lung cancer similarly effective, and are there any increased risks for harms in people with HIV?

There’s also the question of whether PWH should be screened for lung cancer earlier and with a lower smoking exposure than is advised under current guidelines for the general population, she said in the interview. “And should the approach to shared decision-making be modified for people with HIV?” she said. “We’re doing some work on these questions” right now.

None of the researchers interviewed reported any conflicts of interest relevant to the story. Dr. Kunisaki reported that he has no relevant disclosures, and said that his comments are his personal views and not official views of the U.S. Government, Department of Veterans Affairs, the Minneapolis VA, or the University of Minnesota.

Chronic pulmonary disease continues to be a major cause of morbidity and mortality in individuals living with the human immunodeficiency virus, even with optimal HIV control. And this is independent, as seen in many studies, of age, smoking, and pulmonary infections.

Both chronic pulmonary obstructive disease (COPD) and lung cancer occur more frequently in people living with HIV than in the general population, and at earlier ages, and with worse outcomes. The risk for emphysema and interstitial lung abnormalities also appears to be higher, research has shown. And asthma has also recently emerged as another important lung disease in people with HIV (PWH).

“There is evidence that the severity of immunocompromise associated with HIV infection is linked with chronic lung diseases. People who have a lower CD4 cell count or a higher viral load do have an increased risk of COPD and emphysema as well as potentially lung cancer. But [while] immunocompromise plays a role, it isn’t the only story, given that even with well-controlled HIV there is increased risk,” said Kristina Crothers, MD, professor in the division of pulmonary, critical care, and sleep medicine at the University of Washington, Seattle.

Research has evolved from a focus on the epidemiology of HIV-related chronic lung diseases to a current emphasis on “trying to understand further the mechanisms [behind the heightened risk] through more benchwork and corollary translational studies, and then to the next level of trying to understand what this means for how we should manage people with HIV who have chronic lung diseases,” Dr. Crothers said. “Should management be tailored for people with HIV infection?”

Impairments in immune pathways, local and systemic inflammation, oxidative stress, dysbiosis, and accelerated cellular senescence are among potential mechanisms, but until ongoing mechanistic research yields more answers, pulmonologists should simply – but importantly – be aware of the increased risk and have a low threshold for investigating respiratory symptoms, she and other experts said in interviews. Referral of eligible patients for lung cancer screening is also a priority, as is smoking cessation, they said.

Notably, while spirometry has been the most commonly studied lung function measure in PWH, another noninvasive measure, diffusing capacity for carbon monoxide (DLCO), has garnered attention in the past decade and thus far appears to be the more frequent lung function abnormality.

In an analysis published in 2020 from the longitudinal Multicenter AIDS Cohort Study (MACS) – a study of a subcohort of 591 men with HIV and 476 without HIV – those with HIV were found to have a 1.6-fold increased risk of mild DLCO impairment (< 80% of predicted normal) and a 3-fold higher risk of more severe DLCO impairment (< 60% of predicted normal). There was no significant difference in spirometry findings by HIV status.

Such findings on DLCO are worthy of consideration in clinical practice, even in the absence of HIV-specific screening guidelines for noncommunicable lung diseases, Dr. Crothers said. “In thinking about screening and diagnosing chronic lung diseases in these patients, I’d not only consider spirometry, but also diffusing capacity” when possible, she said. Impaired DLCO is seen with emphysema and pulmonary vascular diseases like pulmonary hypertension and also interstitial lung diseases.
 

Key chronic lung diseases

Ken M. Kunisaki, MD, MS, associate professor of medicine at the University of Minnesota, Minneapolis, and the first author of the MACS analysis of lung function – one of the most recent and largest reports of DLCO impairment – points out that studies of chest computed tomography (CT) have also documented higher rates of emphysema and interstitial lung abnormalities.

A chest CT analysis from a cohort in Denmark (the Copenhagen Comorbidity in HIV Infection [COCOMO] cohort) found interstitial lung abnormalities in 10.9% of more than 700 PWH which represented a 1.8-fold increased risk compared to HIV-negative controls. And a study from an Italian sample of never-smoking PWH and controls reported emphysema in 18% and 4%, respectively. These studies, which did not measure DLCO, are among those discussed in a 2021 review by Dr. Kunisaki of advances in HIV-associated chronic lung disease research.

COPD is the best studied and most commonly encountered chronic lung disease in PWH. “Particularly for COPD, what’s both interesting and unfortunate is that we haven’t really seen any changes in the epidemiology with ART (antiretroviral therapy) – we’re still seeing the same findings, like the association of HIV with worse COPD at younger ages,” said Alison Morris, MD, MS, professor of medicine, immunology, and clinical and translational research at the University of Pittsburgh. “It doesn’t seem to have improved.”

Its prevalence has varied widely from cohort to cohort, from as low as 3% (similar to the general population) to over 40%, Dr. Kunisaki said, emphasizing that many studies, including studies showing higher rates, have controlled for current and past smoking. In evaluating patients with low or no smoking burden, “don’t discount respiratory symptoms as possibly reflecting underlying lung disease because COPD can develop with low to no smoking history in those with HIV,” he advised.

A better understanding of how a chronic viral infection like HIV leads to heightened COPD risk will not only help those with HIV, he notes, but also people without HIV who have COPD but have never smoked – a woefully underappreciated and understudied population. Ongoing research, he said, “should help us understand COPD pathogenesis generally.”

Research on asthma is relatively limited thus far, but it does appear that PWH may be more prone to developing severe asthma, just as with COPD, said Dr. Kunisaki, also a staff physician at the Minneapolis Veterans Administration Health Care System. Research has shown, for instance, that people with HIV more frequently needed aggressive respiratory support when hospitalized for asthma exacerbations.

It’s unclear how much of this potentially increased severity is attributable to the biology of HIV’s impact on the body and how much relates to social factors like disparities in income and access to care, Dr. Kunisaki said, noting that the same questions apply to the more frequent COPD exacerbations documented in PWH.

Dr. Crothers points out that, while most studies do not suggest a difference in the incidence of asthma in PWH, “there is some data from researchers looking at asthma profiles [suggesting] that the biomarkers associated with asthma may be different in people with and without HIV,” signaling potentially different molecular or biologic underpinnings of the disease.

Incidence rates of lung cancer in PWH, meanwhile, have declined over the last 2 decades, but lung cancer remains the leading cause of cancer-related mortality in PWH and occurs at a rate that is 2-2.5 times higher than that of individuals not infected with HIV, according to

Janice Leung, MD, of the division of respiratory medicine at the University of British Columbia and the Centre for Heart Lung Innovation at St. Paul’s Hospital in Vancouver.

Patients with HIV have “worse outcomes overall and a higher risk of mortality, even when presenting at the same stage,” said Dr. Leung, who reviewed trends in COPD and lung cancer in a recently published opinion piece.
 

Potential drivers

A bird’s eye view of potential – and likely interrelated – mechanisms for chronic lung disease includes chronic immune activation that impairs innate and adaptive immune pathways; chronic inflammation systemically and in the lung despite viral suppression; persistence of the virus in latent reservoirs in the lung, particularly in alveolar macrophages and T cells; HIV-related proteins contributing to oxidative stress; accelerated cellular aging; dysbiosis; and ongoing injury from inhaled toxins.

All are described in the literature and are being further explored. “It’s likely that multiple pathways are playing a role,” said Dr. Crothers, “and it could be that the balance of one to another leads to different manifestations of disease.”

Biomarkers that have been elevated and associated with different features of chronic lung disease – such as airflow obstruction, low DLCO, and emphysema – include markers of inflammation (e.g., C-reactive protein, interleukin-6), monocyte activation (e.g., soluble CD14), and markers of endothelial dysfunction, she noted in a 2021 commentary marking 40 years since the first reported cases of acquired immunodeficiency syndrome.

In her laboratory, Dr. Leung is using new epigenetic markers to look at the pathogenesis of accelerated aging in the lung. By profiling bronchial epithelial brushings for DNA methylation and gene expression, they have found that “people living with both HIV and COPD have the fastest epigenetic age acceleration in their airway epithelium,” she said. The findings “suggest that the HIV lung is aging faster.”

They reported their findings in 2022, describing methylation disruptions along age-related pathways such as cellular senescence, longevity regulation, and insulin signaling.

Dr. Leung and her team have also studied the lung microbiome and found lower microbial diversity in the airway epithelium in patients with HIV than those without, especially in those with HIV and COPD. The National Institutes of Health–sponsored Lung HIV Microbiome Project found that changes in the lung microbiome are most pronounced in patients who haven’t yet initiated ART, but research in her lab suggests ongoing suppression of microbial diversity even after ART, she said.

Dr. Morris is particularly interested in the oral microbiome, having found through her research that changes in the oral microbiome in PWH were more related to impaired lung function than alterations in the lung and gut microbiome. “That may be in part because of the way we measure things,” she said. “But we also think that the oral microbiome probably seeds the lung [through micro-aspiration].” A study published in 2020 from the Pittsburgh site of the MACS described alterations in oral microbial communities in PWH with abnormal lung function.

Preliminary research suggests that improved dental cleaning and periodontal work in PWH and COPD may influence the severity of COPD, she noted.

“We don’t see as much of a signal with the gut microbiome [and HIV status or lung function], though there could still be ways in which gut microbiome influences the lung,” through systemic inflammation, the release of metabolites into the bloodstream, or microbial translocation, for instance, she said.

The potential role of translocation of members of the microbiome, in fact, is an area of active research for Dr. Morris. Members of the microbiome – viruses and fungi in addition to bacteria – “can get into the bloodstream from the mouth, from the lung, from the gut, to stimulate inflammation and worsen lung disease,” she said.
 

Key questions in an evolving research landscape

Dr. Kunisaki looks forward to research providing a more longitudinal look at lung function decline– a move beyond a dominance of cross-sectional studies – as well as research that is more comprehensive, with simultaneous collection of various functional measures (eg., DLCO with chest imaging and fractional excretion of nitric oxide (FENO – a standardized breath measure of Th2 airway inflammation).

The several-year-old NIH-supported MACS/WIHS (Women’s Interagency HIV Study) Combined Cohort study, in which Dr. Kunisaki and Dr. Morris participate, aims in part to identity biomarkers of increased risk for chronic lung disease and other chronic disorders and to develop strategies for more effective interventions and treatments.

Researchers will also share biospecimens, “which will allow more mechanistic work,” Dr. Kunisaki noted. (The combined cohort study includes participants from the earlier, separate MACS and WIHS studies.)

Questions about treatment strategies include the risks versus benefits of inhaled corticosteroids, which may increase an already elevated risk of respiratory infections like bacterial pneumonia in PWH, Dr. Kunisaki said.

[An aside: Inhaled corticosteroids also have well-described interactions with ART regimens that contain CYP3A4 inhibitors (e.g., ritonavir and cobicistat) that can lead to hypercortisolism. In patients who require both types of drugs, he said, beclomethasone has the least interactions and is the preferred inhaled corticosteroid.]

For Dr. Crothers, unanswered critical questions include – as she wrote in her 2021 commentary – the question of how guidelines for the management of COPD and asthma should be adapted for PWH. Is COPD in PWH more or less responsive to inhaled corticosteroids, for instance? And are antifibrotic treatments for interstitial lung disease and immunotherapies for asthma or lung cancer similarly effective, and are there any increased risks for harms in people with HIV?

There’s also the question of whether PWH should be screened for lung cancer earlier and with a lower smoking exposure than is advised under current guidelines for the general population, she said in the interview. “And should the approach to shared decision-making be modified for people with HIV?” she said. “We’re doing some work on these questions” right now.

None of the researchers interviewed reported any conflicts of interest relevant to the story. Dr. Kunisaki reported that he has no relevant disclosures, and said that his comments are his personal views and not official views of the U.S. Government, Department of Veterans Affairs, the Minneapolis VA, or the University of Minnesota.

Chronic pulmonary disease continues to be a major cause of morbidity and mortality in individuals living with the human immunodeficiency virus, even with optimal HIV control. And this is independent, as seen in many studies, of age, smoking, and pulmonary infections.

Both chronic pulmonary obstructive disease (COPD) and lung cancer occur more frequently in people living with HIV than in the general population, and at earlier ages, and with worse outcomes. The risk for emphysema and interstitial lung abnormalities also appears to be higher, research has shown. And asthma has also recently emerged as another important lung disease in people with HIV (PWH).

“There is evidence that the severity of immunocompromise associated with HIV infection is linked with chronic lung diseases. People who have a lower CD4 cell count or a higher viral load do have an increased risk of COPD and emphysema as well as potentially lung cancer. But [while] immunocompromise plays a role, it isn’t the only story, given that even with well-controlled HIV there is increased risk,” said Kristina Crothers, MD, professor in the division of pulmonary, critical care, and sleep medicine at the University of Washington, Seattle.

Research has evolved from a focus on the epidemiology of HIV-related chronic lung diseases to a current emphasis on “trying to understand further the mechanisms [behind the heightened risk] through more benchwork and corollary translational studies, and then to the next level of trying to understand what this means for how we should manage people with HIV who have chronic lung diseases,” Dr. Crothers said. “Should management be tailored for people with HIV infection?”

Impairments in immune pathways, local and systemic inflammation, oxidative stress, dysbiosis, and accelerated cellular senescence are among potential mechanisms, but until ongoing mechanistic research yields more answers, pulmonologists should simply – but importantly – be aware of the increased risk and have a low threshold for investigating respiratory symptoms, she and other experts said in interviews. Referral of eligible patients for lung cancer screening is also a priority, as is smoking cessation, they said.

Notably, while spirometry has been the most commonly studied lung function measure in PWH, another noninvasive measure, diffusing capacity for carbon monoxide (DLCO), has garnered attention in the past decade and thus far appears to be the more frequent lung function abnormality.

In an analysis published in 2020 from the longitudinal Multicenter AIDS Cohort Study (MACS) – a study of a subcohort of 591 men with HIV and 476 without HIV – those with HIV were found to have a 1.6-fold increased risk of mild DLCO impairment (< 80% of predicted normal) and a 3-fold higher risk of more severe DLCO impairment (< 60% of predicted normal). There was no significant difference in spirometry findings by HIV status.

Such findings on DLCO are worthy of consideration in clinical practice, even in the absence of HIV-specific screening guidelines for noncommunicable lung diseases, Dr. Crothers said. “In thinking about screening and diagnosing chronic lung diseases in these patients, I’d not only consider spirometry, but also diffusing capacity” when possible, she said. Impaired DLCO is seen with emphysema and pulmonary vascular diseases like pulmonary hypertension and also interstitial lung diseases.
 

Key chronic lung diseases

Ken M. Kunisaki, MD, MS, associate professor of medicine at the University of Minnesota, Minneapolis, and the first author of the MACS analysis of lung function – one of the most recent and largest reports of DLCO impairment – points out that studies of chest computed tomography (CT) have also documented higher rates of emphysema and interstitial lung abnormalities.

A chest CT analysis from a cohort in Denmark (the Copenhagen Comorbidity in HIV Infection [COCOMO] cohort) found interstitial lung abnormalities in 10.9% of more than 700 PWH which represented a 1.8-fold increased risk compared to HIV-negative controls. And a study from an Italian sample of never-smoking PWH and controls reported emphysema in 18% and 4%, respectively. These studies, which did not measure DLCO, are among those discussed in a 2021 review by Dr. Kunisaki of advances in HIV-associated chronic lung disease research.

COPD is the best studied and most commonly encountered chronic lung disease in PWH. “Particularly for COPD, what’s both interesting and unfortunate is that we haven’t really seen any changes in the epidemiology with ART (antiretroviral therapy) – we’re still seeing the same findings, like the association of HIV with worse COPD at younger ages,” said Alison Morris, MD, MS, professor of medicine, immunology, and clinical and translational research at the University of Pittsburgh. “It doesn’t seem to have improved.”

Its prevalence has varied widely from cohort to cohort, from as low as 3% (similar to the general population) to over 40%, Dr. Kunisaki said, emphasizing that many studies, including studies showing higher rates, have controlled for current and past smoking. In evaluating patients with low or no smoking burden, “don’t discount respiratory symptoms as possibly reflecting underlying lung disease because COPD can develop with low to no smoking history in those with HIV,” he advised.

A better understanding of how a chronic viral infection like HIV leads to heightened COPD risk will not only help those with HIV, he notes, but also people without HIV who have COPD but have never smoked – a woefully underappreciated and understudied population. Ongoing research, he said, “should help us understand COPD pathogenesis generally.”

Research on asthma is relatively limited thus far, but it does appear that PWH may be more prone to developing severe asthma, just as with COPD, said Dr. Kunisaki, also a staff physician at the Minneapolis Veterans Administration Health Care System. Research has shown, for instance, that people with HIV more frequently needed aggressive respiratory support when hospitalized for asthma exacerbations.

It’s unclear how much of this potentially increased severity is attributable to the biology of HIV’s impact on the body and how much relates to social factors like disparities in income and access to care, Dr. Kunisaki said, noting that the same questions apply to the more frequent COPD exacerbations documented in PWH.

Dr. Crothers points out that, while most studies do not suggest a difference in the incidence of asthma in PWH, “there is some data from researchers looking at asthma profiles [suggesting] that the biomarkers associated with asthma may be different in people with and without HIV,” signaling potentially different molecular or biologic underpinnings of the disease.

Incidence rates of lung cancer in PWH, meanwhile, have declined over the last 2 decades, but lung cancer remains the leading cause of cancer-related mortality in PWH and occurs at a rate that is 2-2.5 times higher than that of individuals not infected with HIV, according to

Janice Leung, MD, of the division of respiratory medicine at the University of British Columbia and the Centre for Heart Lung Innovation at St. Paul’s Hospital in Vancouver.

Patients with HIV have “worse outcomes overall and a higher risk of mortality, even when presenting at the same stage,” said Dr. Leung, who reviewed trends in COPD and lung cancer in a recently published opinion piece.
 

Potential drivers

A bird’s eye view of potential – and likely interrelated – mechanisms for chronic lung disease includes chronic immune activation that impairs innate and adaptive immune pathways; chronic inflammation systemically and in the lung despite viral suppression; persistence of the virus in latent reservoirs in the lung, particularly in alveolar macrophages and T cells; HIV-related proteins contributing to oxidative stress; accelerated cellular aging; dysbiosis; and ongoing injury from inhaled toxins.

All are described in the literature and are being further explored. “It’s likely that multiple pathways are playing a role,” said Dr. Crothers, “and it could be that the balance of one to another leads to different manifestations of disease.”

Biomarkers that have been elevated and associated with different features of chronic lung disease – such as airflow obstruction, low DLCO, and emphysema – include markers of inflammation (e.g., C-reactive protein, interleukin-6), monocyte activation (e.g., soluble CD14), and markers of endothelial dysfunction, she noted in a 2021 commentary marking 40 years since the first reported cases of acquired immunodeficiency syndrome.

In her laboratory, Dr. Leung is using new epigenetic markers to look at the pathogenesis of accelerated aging in the lung. By profiling bronchial epithelial brushings for DNA methylation and gene expression, they have found that “people living with both HIV and COPD have the fastest epigenetic age acceleration in their airway epithelium,” she said. The findings “suggest that the HIV lung is aging faster.”

They reported their findings in 2022, describing methylation disruptions along age-related pathways such as cellular senescence, longevity regulation, and insulin signaling.

Dr. Leung and her team have also studied the lung microbiome and found lower microbial diversity in the airway epithelium in patients with HIV than those without, especially in those with HIV and COPD. The National Institutes of Health–sponsored Lung HIV Microbiome Project found that changes in the lung microbiome are most pronounced in patients who haven’t yet initiated ART, but research in her lab suggests ongoing suppression of microbial diversity even after ART, she said.

Dr. Morris is particularly interested in the oral microbiome, having found through her research that changes in the oral microbiome in PWH were more related to impaired lung function than alterations in the lung and gut microbiome. “That may be in part because of the way we measure things,” she said. “But we also think that the oral microbiome probably seeds the lung [through micro-aspiration].” A study published in 2020 from the Pittsburgh site of the MACS described alterations in oral microbial communities in PWH with abnormal lung function.

Preliminary research suggests that improved dental cleaning and periodontal work in PWH and COPD may influence the severity of COPD, she noted.

“We don’t see as much of a signal with the gut microbiome [and HIV status or lung function], though there could still be ways in which gut microbiome influences the lung,” through systemic inflammation, the release of metabolites into the bloodstream, or microbial translocation, for instance, she said.

The potential role of translocation of members of the microbiome, in fact, is an area of active research for Dr. Morris. Members of the microbiome – viruses and fungi in addition to bacteria – “can get into the bloodstream from the mouth, from the lung, from the gut, to stimulate inflammation and worsen lung disease,” she said.
 

Key questions in an evolving research landscape

Dr. Kunisaki looks forward to research providing a more longitudinal look at lung function decline– a move beyond a dominance of cross-sectional studies – as well as research that is more comprehensive, with simultaneous collection of various functional measures (eg., DLCO with chest imaging and fractional excretion of nitric oxide (FENO – a standardized breath measure of Th2 airway inflammation).

The several-year-old NIH-supported MACS/WIHS (Women’s Interagency HIV Study) Combined Cohort study, in which Dr. Kunisaki and Dr. Morris participate, aims in part to identity biomarkers of increased risk for chronic lung disease and other chronic disorders and to develop strategies for more effective interventions and treatments.

Researchers will also share biospecimens, “which will allow more mechanistic work,” Dr. Kunisaki noted. (The combined cohort study includes participants from the earlier, separate MACS and WIHS studies.)

Questions about treatment strategies include the risks versus benefits of inhaled corticosteroids, which may increase an already elevated risk of respiratory infections like bacterial pneumonia in PWH, Dr. Kunisaki said.

[An aside: Inhaled corticosteroids also have well-described interactions with ART regimens that contain CYP3A4 inhibitors (e.g., ritonavir and cobicistat) that can lead to hypercortisolism. In patients who require both types of drugs, he said, beclomethasone has the least interactions and is the preferred inhaled corticosteroid.]

For Dr. Crothers, unanswered critical questions include – as she wrote in her 2021 commentary – the question of how guidelines for the management of COPD and asthma should be adapted for PWH. Is COPD in PWH more or less responsive to inhaled corticosteroids, for instance? And are antifibrotic treatments for interstitial lung disease and immunotherapies for asthma or lung cancer similarly effective, and are there any increased risks for harms in people with HIV?

There’s also the question of whether PWH should be screened for lung cancer earlier and with a lower smoking exposure than is advised under current guidelines for the general population, she said in the interview. “And should the approach to shared decision-making be modified for people with HIV?” she said. “We’re doing some work on these questions” right now.

None of the researchers interviewed reported any conflicts of interest relevant to the story. Dr. Kunisaki reported that he has no relevant disclosures, and said that his comments are his personal views and not official views of the U.S. Government, Department of Veterans Affairs, the Minneapolis VA, or the University of Minnesota.

In patients with fibrotic interstitial lung disease, nocturnal hypoxemia is associated with poor clinical outcomes, according to results of a prospective observational cohort study. Obstructive sleep apnea in the absence of nocturnal hypoxemia was not independently associated with poor clinical outcomes.

While both obstructive sleep apnea (OSA) and nocturnal hypoxemia (NH) are known to be common in patients with fibrotic interstitial lung disease (F-ILD), how they affect disease outcomes has remained unclear, Katherine J. Myall, MBChB, and colleagues reported in their published study. They noted that deposition of extracellular matrix within the lung parenchyma found in F-ILD is associated with restrictive lung disease and impaired gas exchange leading to progressive breathlessness and exercise intolerance and ultimately respiratory failure.

Prior research has suggested that sleep architecture is disrupted in F-ILD, with nocturnal desaturations from relative hypoventilation during rapid-eye movement sleep and higher incidence of OSA. While disrupted sleep architecture has been associated with poorer outcomes including worse survival, the relationship between sleep and F-ILD is not well understood, especially whether either total time spent in sleep with hypoxemia or repeated desaturations and arousals seen in OSA might promote disease progression, the researchers wrote.

They conducted a prospective observational cohort study among 102 idiopathic pulmonary fibrosis patients without daytime hypoxemia (74.5% male; age 73.0 years), among whom 91.1% and 31.4% had nocturnal hypoxemia (NH) and obstructive sleep apnea (OSA), respectively. There were no significant differences between those with and without NH or OSA at baseline. The study’s primary outcome measure was change in King’s Brief Interstitial Lung Disease questionnaire (KBILD) at 12 months from baseline. The secondary outcome measures were annualized change in forced vital capacity (FVC), transfer factor for carbon monoxide (TLCO), and mortality at 12 months.
 

Mortality association?

The analysis showed NH was associated with a more rapid decline in both quality of life (KBILD change –11.3 in the NH group vs. –6.7 in those without NH, P = .005) and higher all-cause mortality at 1 year (hazard ratio [HR], 8.21; 95% confidence interval [CI], 2.40-28.1, P < .001). There was no increased risk of death in patients with OSA compared with those without (HR, 2.78; 95% CI 0.85-9.12, P = .19), and OSA in the absence of NH was not associated with worsening of KBILD scores (P = .30). Analysis of findings did not reveal any relationship between disease severity and sleep characteristics.

“This suggests that the excess mortality demonstrated in earlier studies of patients with OSA may be related to prolonged hypoxemia rather than sleep disruption or the other deleterious physiological effects of OSA, such as sympathetic excitation,” noted Dr. Myall and colleagues. Underscoring that the current study is the first to elucidate the contribution of prolonged NH to disease progression and death in this population, they added that since the central process in the development of idiopathic pulmonary fibrosis is thought to be one of repeated or sustained lung injury, one hypothesis is that prolonged hypoxia of the alveolar epithelium due to prolonged nocturnal hypoxemia may be the source of this insult.

“These data provide support for screening for nocturnal hypoxemia, as well as obstructive sleep apnea in patients with F-ILD to allow early identification of these potentially modifiable conditions. Trials of CPAP and nocturnal oxygen therapy would offer a potential intervention to correct prolonged nocturnal hypoxemia, offering the potential to improve quality of life and survival for patients who otherwise have limited treatment options,” the researchers concluded.

A possible limitations of the study was the fact that patients were offered referral for CPAP therapy, and were used in the analysis only if they elected not to commence therapy. This may have introduced a bias, although there was no statistically significant difference between patients who opted to be referred and those who did not, according to the authors.

Dr. Myall reported having no conflicts of interest to declare.

In patients with fibrotic interstitial lung disease, nocturnal hypoxemia is associated with poor clinical outcomes, according to results of a prospective observational cohort study. Obstructive sleep apnea in the absence of nocturnal hypoxemia was not independently associated with poor clinical outcomes.

While both obstructive sleep apnea (OSA) and nocturnal hypoxemia (NH) are known to be common in patients with fibrotic interstitial lung disease (F-ILD), how they affect disease outcomes has remained unclear, Katherine J. Myall, MBChB, and colleagues reported in their published study. They noted that deposition of extracellular matrix within the lung parenchyma found in F-ILD is associated with restrictive lung disease and impaired gas exchange leading to progressive breathlessness and exercise intolerance and ultimately respiratory failure.

Prior research has suggested that sleep architecture is disrupted in F-ILD, with nocturnal desaturations from relative hypoventilation during rapid-eye movement sleep and higher incidence of OSA. While disrupted sleep architecture has been associated with poorer outcomes including worse survival, the relationship between sleep and F-ILD is not well understood, especially whether either total time spent in sleep with hypoxemia or repeated desaturations and arousals seen in OSA might promote disease progression, the researchers wrote.

They conducted a prospective observational cohort study among 102 idiopathic pulmonary fibrosis patients without daytime hypoxemia (74.5% male; age 73.0 years), among whom 91.1% and 31.4% had nocturnal hypoxemia (NH) and obstructive sleep apnea (OSA), respectively. There were no significant differences between those with and without NH or OSA at baseline. The study’s primary outcome measure was change in King’s Brief Interstitial Lung Disease questionnaire (KBILD) at 12 months from baseline. The secondary outcome measures were annualized change in forced vital capacity (FVC), transfer factor for carbon monoxide (TLCO), and mortality at 12 months.
 

Mortality association?

The analysis showed NH was associated with a more rapid decline in both quality of life (KBILD change –11.3 in the NH group vs. –6.7 in those without NH, P = .005) and higher all-cause mortality at 1 year (hazard ratio [HR], 8.21; 95% confidence interval [CI], 2.40-28.1, P < .001). There was no increased risk of death in patients with OSA compared with those without (HR, 2.78; 95% CI 0.85-9.12, P = .19), and OSA in the absence of NH was not associated with worsening of KBILD scores (P = .30). Analysis of findings did not reveal any relationship between disease severity and sleep characteristics.

“This suggests that the excess mortality demonstrated in earlier studies of patients with OSA may be related to prolonged hypoxemia rather than sleep disruption or the other deleterious physiological effects of OSA, such as sympathetic excitation,” noted Dr. Myall and colleagues. Underscoring that the current study is the first to elucidate the contribution of prolonged NH to disease progression and death in this population, they added that since the central process in the development of idiopathic pulmonary fibrosis is thought to be one of repeated or sustained lung injury, one hypothesis is that prolonged hypoxia of the alveolar epithelium due to prolonged nocturnal hypoxemia may be the source of this insult.

“These data provide support for screening for nocturnal hypoxemia, as well as obstructive sleep apnea in patients with F-ILD to allow early identification of these potentially modifiable conditions. Trials of CPAP and nocturnal oxygen therapy would offer a potential intervention to correct prolonged nocturnal hypoxemia, offering the potential to improve quality of life and survival for patients who otherwise have limited treatment options,” the researchers concluded.

A possible limitations of the study was the fact that patients were offered referral for CPAP therapy, and were used in the analysis only if they elected not to commence therapy. This may have introduced a bias, although there was no statistically significant difference between patients who opted to be referred and those who did not, according to the authors.

Dr. Myall reported having no conflicts of interest to declare.

In patients with fibrotic interstitial lung disease, nocturnal hypoxemia is associated with poor clinical outcomes, according to results of a prospective observational cohort study. Obstructive sleep apnea in the absence of nocturnal hypoxemia was not independently associated with poor clinical outcomes.

While both obstructive sleep apnea (OSA) and nocturnal hypoxemia (NH) are known to be common in patients with fibrotic interstitial lung disease (F-ILD), how they affect disease outcomes has remained unclear, Katherine J. Myall, MBChB, and colleagues reported in their published study. They noted that deposition of extracellular matrix within the lung parenchyma found in F-ILD is associated with restrictive lung disease and impaired gas exchange leading to progressive breathlessness and exercise intolerance and ultimately respiratory failure.

Prior research has suggested that sleep architecture is disrupted in F-ILD, with nocturnal desaturations from relative hypoventilation during rapid-eye movement sleep and higher incidence of OSA. While disrupted sleep architecture has been associated with poorer outcomes including worse survival, the relationship between sleep and F-ILD is not well understood, especially whether either total time spent in sleep with hypoxemia or repeated desaturations and arousals seen in OSA might promote disease progression, the researchers wrote.

They conducted a prospective observational cohort study among 102 idiopathic pulmonary fibrosis patients without daytime hypoxemia (74.5% male; age 73.0 years), among whom 91.1% and 31.4% had nocturnal hypoxemia (NH) and obstructive sleep apnea (OSA), respectively. There were no significant differences between those with and without NH or OSA at baseline. The study’s primary outcome measure was change in King’s Brief Interstitial Lung Disease questionnaire (KBILD) at 12 months from baseline. The secondary outcome measures were annualized change in forced vital capacity (FVC), transfer factor for carbon monoxide (TLCO), and mortality at 12 months.
 

Mortality association?

The analysis showed NH was associated with a more rapid decline in both quality of life (KBILD change –11.3 in the NH group vs. –6.7 in those without NH, P = .005) and higher all-cause mortality at 1 year (hazard ratio [HR], 8.21; 95% confidence interval [CI], 2.40-28.1, P < .001). There was no increased risk of death in patients with OSA compared with those without (HR, 2.78; 95% CI 0.85-9.12, P = .19), and OSA in the absence of NH was not associated with worsening of KBILD scores (P = .30). Analysis of findings did not reveal any relationship between disease severity and sleep characteristics.

“This suggests that the excess mortality demonstrated in earlier studies of patients with OSA may be related to prolonged hypoxemia rather than sleep disruption or the other deleterious physiological effects of OSA, such as sympathetic excitation,” noted Dr. Myall and colleagues. Underscoring that the current study is the first to elucidate the contribution of prolonged NH to disease progression and death in this population, they added that since the central process in the development of idiopathic pulmonary fibrosis is thought to be one of repeated or sustained lung injury, one hypothesis is that prolonged hypoxia of the alveolar epithelium due to prolonged nocturnal hypoxemia may be the source of this insult.

“These data provide support for screening for nocturnal hypoxemia, as well as obstructive sleep apnea in patients with F-ILD to allow early identification of these potentially modifiable conditions. Trials of CPAP and nocturnal oxygen therapy would offer a potential intervention to correct prolonged nocturnal hypoxemia, offering the potential to improve quality of life and survival for patients who otherwise have limited treatment options,” the researchers concluded.

A possible limitations of the study was the fact that patients were offered referral for CPAP therapy, and were used in the analysis only if they elected not to commence therapy. This may have introduced a bias, although there was no statistically significant difference between patients who opted to be referred and those who did not, according to the authors.

Dr. Myall reported having no conflicts of interest to declare.

The U.K. Mini Mitral trial, showing that mitral valve repair with the less invasive minithoracotomy approach achieved similar outcomes, compared with sternotomy, has now been published.

The trial, which was first presented earlier this year at the American College of Cardiology meeting, showed that minimally invasive mitral valve repair does not improve physical function at 12 weeks, compared with sternotomy, but outcomes at 1 year show minimally invasive repair is as safe and effective as sternotomy for degenerative mitral regurgitation.

The full results are now published online in JAMA.

The authors, led by Enoch Akowuah, MD, South Tees Hospitals NHS Foundation Trust, Middlesbrough, United Kingdom, explain that mitral valve repair surgery is the preferred treatment for patients with degenerative mitral regurgitation and is routinely performed via full sternotomy, enabling easy access to the heart, flexibility in myocardial protection strategies, and multiple ways of accessing the mitral valve and easing de-airing to prevent air emboli, which cause cerebrovascular accidents. 

However, the invasiveness of sternotomy is associated with delayed return to presurgery physical function levels and an increase in postoperative complications.

An alternative new video-guided minimally invasive approach involving a 4- to 7-cm lateral thoracotomy, completely avoiding sternotomy, has been developed, with the hope that it should speed physical recovery function after surgery and reduce postoperative complications and costs by reducing hospital stay.

Dr. Akowuah et al. note that uptake of minithoracotomy is variable, with low rates in the United States and the United Kingdom but high rates in Germany. They say that this variation is attributable to the absence of high-quality evidence from randomized trials demonstrating equivalent or superior benefits, compared with sternotomy, and there are also concerns that the increased technical complexity of minithoracotomy may impair the ability to repair complex valve lesions or increase perioperative complications, particularly vascular injuries and stroke.

The U.K. Mini Mitral trial was therefore conducted to compare the effectiveness and safety of minithoracotomy versus sternotomy mitral valve repair.

For the trial, 330 patients with degenerative mitral regurgitation were randomized to receive either minithoracotomy or sternotomy mitral valve repair performed by an expert surgeon.

The primary outcome was physical functioning and associated return to usual activities measured by change from baseline in the 36-Item Short Form Health Survey (SF-36) physical functioning scale 12 weeks after the surgery.  

This failed to show superiority of minithoracotomy, with a mean difference of 0.68 (95% confidence interval, −1.89 to 3.26) between the two groups.

Analysis of secondary outcomes demonstrated that time spent undertaking moderate to vigorous physical activity was higher among participants receiving minithoracotomy at 6 weeks, although the treatment effect was small at an average of 9 minutes and was not different at 12 weeks.  

Postoperative length of hospital stay was reduced after minithoracotomy by 1 day, with a median of 5 days, compared with 6 days after sternotomy.

Although repair techniques were at the discretion of the surgeons and differed between the two procedures, high rates of valve repair and low rates of recurrent mitral regurgitation were observed in both groups. Cardiopulmonary bypass times were longer with minithoracotomy, but postoperative complications and adverse events were similar.

There was no difference between the two groups with respect to the prespecified safety outcome of death, repeat mitral valve surgery, or heart failure hospitalization up to 1 year, which occurred in 5.4% of patients undergoing minithoracotomy and 6.1% of those undergoing sternotomy.

“These findings can inform shared decision-making and treatment guidelines,” the authors conclude.
 

Approach ‘may appeal to patients’

In an editorial accompanying the publication of the study in JAMA, Maurice Enriquez-Sarano, MD, Minneapolis Heart Institute, Minnesota, says the results should be integrated into patient management.

“Mini-thoracotomy mitral repair carried low risk and was highly effective compared with sternotomy. It can thus be applied successfully by surgeons who achieve the necessary expertise,” he notes.

“Mini-thoracotomy may appeal to patients because the procedure is less disfiguring than sternotomy. The early (6-week) benefit, albeit small and transient, is important to patients,” he adds.

The study was funded by the United Kingdom’s National Institute for Health and Care Research. Dr. Akowuah reports no relevant financial relationships with industry. Dr. Enriquez-Sarano reports receiving consulting fees from Edwards Lifesciences, Artivion, ChemImage, HighLife, and Corcym.

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

The U.K. Mini Mitral trial, showing that mitral valve repair with the less invasive minithoracotomy approach achieved similar outcomes, compared with sternotomy, has now been published.

The trial, which was first presented earlier this year at the American College of Cardiology meeting, showed that minimally invasive mitral valve repair does not improve physical function at 12 weeks, compared with sternotomy, but outcomes at 1 year show minimally invasive repair is as safe and effective as sternotomy for degenerative mitral regurgitation.

The full results are now published online in JAMA.

The authors, led by Enoch Akowuah, MD, South Tees Hospitals NHS Foundation Trust, Middlesbrough, United Kingdom, explain that mitral valve repair surgery is the preferred treatment for patients with degenerative mitral regurgitation and is routinely performed via full sternotomy, enabling easy access to the heart, flexibility in myocardial protection strategies, and multiple ways of accessing the mitral valve and easing de-airing to prevent air emboli, which cause cerebrovascular accidents. 

However, the invasiveness of sternotomy is associated with delayed return to presurgery physical function levels and an increase in postoperative complications.

An alternative new video-guided minimally invasive approach involving a 4- to 7-cm lateral thoracotomy, completely avoiding sternotomy, has been developed, with the hope that it should speed physical recovery function after surgery and reduce postoperative complications and costs by reducing hospital stay.

Dr. Akowuah et al. note that uptake of minithoracotomy is variable, with low rates in the United States and the United Kingdom but high rates in Germany. They say that this variation is attributable to the absence of high-quality evidence from randomized trials demonstrating equivalent or superior benefits, compared with sternotomy, and there are also concerns that the increased technical complexity of minithoracotomy may impair the ability to repair complex valve lesions or increase perioperative complications, particularly vascular injuries and stroke.

The U.K. Mini Mitral trial was therefore conducted to compare the effectiveness and safety of minithoracotomy versus sternotomy mitral valve repair.

For the trial, 330 patients with degenerative mitral regurgitation were randomized to receive either minithoracotomy or sternotomy mitral valve repair performed by an expert surgeon.

The primary outcome was physical functioning and associated return to usual activities measured by change from baseline in the 36-Item Short Form Health Survey (SF-36) physical functioning scale 12 weeks after the surgery.  

This failed to show superiority of minithoracotomy, with a mean difference of 0.68 (95% confidence interval, −1.89 to 3.26) between the two groups.

Analysis of secondary outcomes demonstrated that time spent undertaking moderate to vigorous physical activity was higher among participants receiving minithoracotomy at 6 weeks, although the treatment effect was small at an average of 9 minutes and was not different at 12 weeks.  

Postoperative length of hospital stay was reduced after minithoracotomy by 1 day, with a median of 5 days, compared with 6 days after sternotomy.

Although repair techniques were at the discretion of the surgeons and differed between the two procedures, high rates of valve repair and low rates of recurrent mitral regurgitation were observed in both groups. Cardiopulmonary bypass times were longer with minithoracotomy, but postoperative complications and adverse events were similar.

There was no difference between the two groups with respect to the prespecified safety outcome of death, repeat mitral valve surgery, or heart failure hospitalization up to 1 year, which occurred in 5.4% of patients undergoing minithoracotomy and 6.1% of those undergoing sternotomy.

“These findings can inform shared decision-making and treatment guidelines,” the authors conclude.
 

Approach ‘may appeal to patients’

In an editorial accompanying the publication of the study in JAMA, Maurice Enriquez-Sarano, MD, Minneapolis Heart Institute, Minnesota, says the results should be integrated into patient management.

“Mini-thoracotomy mitral repair carried low risk and was highly effective compared with sternotomy. It can thus be applied successfully by surgeons who achieve the necessary expertise,” he notes.

“Mini-thoracotomy may appeal to patients because the procedure is less disfiguring than sternotomy. The early (6-week) benefit, albeit small and transient, is important to patients,” he adds.

The study was funded by the United Kingdom’s National Institute for Health and Care Research. Dr. Akowuah reports no relevant financial relationships with industry. Dr. Enriquez-Sarano reports receiving consulting fees from Edwards Lifesciences, Artivion, ChemImage, HighLife, and Corcym.

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

The U.K. Mini Mitral trial, showing that mitral valve repair with the less invasive minithoracotomy approach achieved similar outcomes, compared with sternotomy, has now been published.

The trial, which was first presented earlier this year at the American College of Cardiology meeting, showed that minimally invasive mitral valve repair does not improve physical function at 12 weeks, compared with sternotomy, but outcomes at 1 year show minimally invasive repair is as safe and effective as sternotomy for degenerative mitral regurgitation.

The full results are now published online in JAMA.

The authors, led by Enoch Akowuah, MD, South Tees Hospitals NHS Foundation Trust, Middlesbrough, United Kingdom, explain that mitral valve repair surgery is the preferred treatment for patients with degenerative mitral regurgitation and is routinely performed via full sternotomy, enabling easy access to the heart, flexibility in myocardial protection strategies, and multiple ways of accessing the mitral valve and easing de-airing to prevent air emboli, which cause cerebrovascular accidents. 

However, the invasiveness of sternotomy is associated with delayed return to presurgery physical function levels and an increase in postoperative complications.

An alternative new video-guided minimally invasive approach involving a 4- to 7-cm lateral thoracotomy, completely avoiding sternotomy, has been developed, with the hope that it should speed physical recovery function after surgery and reduce postoperative complications and costs by reducing hospital stay.

Dr. Akowuah et al. note that uptake of minithoracotomy is variable, with low rates in the United States and the United Kingdom but high rates in Germany. They say that this variation is attributable to the absence of high-quality evidence from randomized trials demonstrating equivalent or superior benefits, compared with sternotomy, and there are also concerns that the increased technical complexity of minithoracotomy may impair the ability to repair complex valve lesions or increase perioperative complications, particularly vascular injuries and stroke.

The U.K. Mini Mitral trial was therefore conducted to compare the effectiveness and safety of minithoracotomy versus sternotomy mitral valve repair.

For the trial, 330 patients with degenerative mitral regurgitation were randomized to receive either minithoracotomy or sternotomy mitral valve repair performed by an expert surgeon.

The primary outcome was physical functioning and associated return to usual activities measured by change from baseline in the 36-Item Short Form Health Survey (SF-36) physical functioning scale 12 weeks after the surgery.  

This failed to show superiority of minithoracotomy, with a mean difference of 0.68 (95% confidence interval, −1.89 to 3.26) between the two groups.

Analysis of secondary outcomes demonstrated that time spent undertaking moderate to vigorous physical activity was higher among participants receiving minithoracotomy at 6 weeks, although the treatment effect was small at an average of 9 minutes and was not different at 12 weeks.  

Postoperative length of hospital stay was reduced after minithoracotomy by 1 day, with a median of 5 days, compared with 6 days after sternotomy.

Although repair techniques were at the discretion of the surgeons and differed between the two procedures, high rates of valve repair and low rates of recurrent mitral regurgitation were observed in both groups. Cardiopulmonary bypass times were longer with minithoracotomy, but postoperative complications and adverse events were similar.

There was no difference between the two groups with respect to the prespecified safety outcome of death, repeat mitral valve surgery, or heart failure hospitalization up to 1 year, which occurred in 5.4% of patients undergoing minithoracotomy and 6.1% of those undergoing sternotomy.

“These findings can inform shared decision-making and treatment guidelines,” the authors conclude.
 

Approach ‘may appeal to patients’

In an editorial accompanying the publication of the study in JAMA, Maurice Enriquez-Sarano, MD, Minneapolis Heart Institute, Minnesota, says the results should be integrated into patient management.

“Mini-thoracotomy mitral repair carried low risk and was highly effective compared with sternotomy. It can thus be applied successfully by surgeons who achieve the necessary expertise,” he notes.

“Mini-thoracotomy may appeal to patients because the procedure is less disfiguring than sternotomy. The early (6-week) benefit, albeit small and transient, is important to patients,” he adds.

The study was funded by the United Kingdom’s National Institute for Health and Care Research. Dr. Akowuah reports no relevant financial relationships with industry. Dr. Enriquez-Sarano reports receiving consulting fees from Edwards Lifesciences, Artivion, ChemImage, HighLife, and Corcym.

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

A simple measurement – the cardiorespiratory optimal point (COP) – could predict how long someone will live or the severity of their heart failure, according to clinicians who champion the assessment. The COP is easier to obtain than cardiorespiratory measures that require people to exercise to their limit, advocates say; rather than running full speed, someone can walk or lightly jog on a treadmill, with a COP value obtained easily. 
 

But other clinicians argue that maximal exercise tests have many prognostic benefits, and that physicians should do everything in their power to push patients to exercise as hard as possible. In particular, the VO₂ max test captures the maximum amount of oxygen someone uses when exercising at their capacity and is the preferred method for measuring cardiovascular endurance.

The COP is a measure of the minimum number of liters of air during breathing required to move one liter of oxygen through the bloodstream. The lower the COP the better, because this means that someone is working less strenuously than someone else to transport the same amount of oxygen, denoting a more efficient interaction between their heart and lungs.

The COP for a fit person might be 15, about 20-25 for a healthy person, and 35 for someone with heart failure, according to Claudio Gil Araújo, MD, PhD, director of research and education at CLINIMEX, an exercise medicine clinic in Rio de Janeiro.

“Max VO₂ is very important, that’s indisputable. But when do you use max VO₂ in your daily life? Never,” Dr. Araújo said. But almost anyone can generate a COP.
 

Emerging uses for the COP

“I can put someone on the treadmill or bike, and after 3 or 4 minutes I have the COP. It’s like a walking pace,” Dr. Araújo said. Yet the values are obtained with roughly half the effort as VO₂ max. Other clinicians argue exercising to the limits of endurance offers unique clinical insights.

“We should do everything in our power to exercise our patients to maximum. How long a patient is able to go is really important,” said Anu Lala, MD, a cardiologist who specializes in heart failure treatment at Mount Sinai Hospital in New York. A full-capacity exercise test gives useful insights into someone’s heart rate, heart rate recovery, blood pressure, and ECG response to vigorous exercise, Dr. Lala added, all of which are important clues to someone’s overall health.

In 2012 Dr. Araújo coauthored a study that first defined the COP, which is calculated by measuring expired gasses people produce while gently exercising, perhaps to the point where they begin to perspire, and then dividing their breathing capacity by their oxygen uptake every minute. The lowest value obtained during any exercise session is the COP.

Various studies show that higher COP values are associated with more severe heart lesions in patients with congenital heart disease; higher levels of mortality in seemingly healthy male adults; and with worse prognoses in patients with heart failure. These studies all appeared within the last 7 months.

The mortality study, which Dr. Araújo coauthored, compared COP in more than 3,000 U.S. men and women who completed an exercise test from 1973 to 2018 and were tracked for an average of 23 years. Although COP was introduced as an assessment in 2012, calculating the value from tests prior to that date was possible because those tests had captured the relevant breathing rate and oxygen uptake. In males aged 18-85 years, a worse COP was significantly associated with an increased risk for earlier death. This finding did not hold for females, however; Dr. Araújo noted that more research is needed to understand the discrepancy in COP’s predictive power by sex.

In the heart failure study, everyone enrolled had heart failure and completed a COP test. People with the worse COPs also had the worst symptoms of heart failure, but completing an exercise rehabilitation program improved COP values when researchers measured them again. Dr. Araújo was also part of this study, based in the Netherlands.

“I think the COP could become a novel parameter in clinical care,” for most people, said Thijs Eijsvogels, PhD, an exercise physiologist at Radboud University in Nijmegen, the Netherlands, and the senior author of the heart failure study. That said, Dr. Eijsvogels said elite athletes will always be more interested in measuring VO₂ max.

Dr. Lala agreed that tests such as the COP have some value. Her own work has shown that measuring the efficiency of someone’s breathing patterns for exhaling carbon dioxide, which can also be done without making people exercise full strength, has prognostic value for patients with advanced heart failure. Even so, she said she would like to see maximal effort tests used as much as possible.

“I worry about saying we’re going to settle for a parameter that can be achieved at 50% of peak VO₂ and then we don’t exercise our patients,” Dr. Lala said.

Dr. Araújo said he plans to continue to measure VO₂ max but he believes COP has utility – even for elite athletes. One of his patients is a frequent Ironman competitor who competes well despite having a solid but not amazing VO₂ max level. But her COP is quite low, Dr. Araújo said, which to him suggests an especially efficient interaction between her respiratory and cardiovascular systems.

“We have a new player in the game,” Dr. Araújo said.

The sources in this study report no relevant financial relationships.

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

A simple measurement – the cardiorespiratory optimal point (COP) – could predict how long someone will live or the severity of their heart failure, according to clinicians who champion the assessment. The COP is easier to obtain than cardiorespiratory measures that require people to exercise to their limit, advocates say; rather than running full speed, someone can walk or lightly jog on a treadmill, with a COP value obtained easily. 
 

But other clinicians argue that maximal exercise tests have many prognostic benefits, and that physicians should do everything in their power to push patients to exercise as hard as possible. In particular, the VO₂ max test captures the maximum amount of oxygen someone uses when exercising at their capacity and is the preferred method for measuring cardiovascular endurance.

The COP is a measure of the minimum number of liters of air during breathing required to move one liter of oxygen through the bloodstream. The lower the COP the better, because this means that someone is working less strenuously than someone else to transport the same amount of oxygen, denoting a more efficient interaction between their heart and lungs.

The COP for a fit person might be 15, about 20-25 for a healthy person, and 35 for someone with heart failure, according to Claudio Gil Araújo, MD, PhD, director of research and education at CLINIMEX, an exercise medicine clinic in Rio de Janeiro.

“Max VO₂ is very important, that’s indisputable. But when do you use max VO₂ in your daily life? Never,” Dr. Araújo said. But almost anyone can generate a COP.
 

Emerging uses for the COP

“I can put someone on the treadmill or bike, and after 3 or 4 minutes I have the COP. It’s like a walking pace,” Dr. Araújo said. Yet the values are obtained with roughly half the effort as VO₂ max. Other clinicians argue exercising to the limits of endurance offers unique clinical insights.

“We should do everything in our power to exercise our patients to maximum. How long a patient is able to go is really important,” said Anu Lala, MD, a cardiologist who specializes in heart failure treatment at Mount Sinai Hospital in New York. A full-capacity exercise test gives useful insights into someone’s heart rate, heart rate recovery, blood pressure, and ECG response to vigorous exercise, Dr. Lala added, all of which are important clues to someone’s overall health.

In 2012 Dr. Araújo coauthored a study that first defined the COP, which is calculated by measuring expired gasses people produce while gently exercising, perhaps to the point where they begin to perspire, and then dividing their breathing capacity by their oxygen uptake every minute. The lowest value obtained during any exercise session is the COP.

Various studies show that higher COP values are associated with more severe heart lesions in patients with congenital heart disease; higher levels of mortality in seemingly healthy male adults; and with worse prognoses in patients with heart failure. These studies all appeared within the last 7 months.

The mortality study, which Dr. Araújo coauthored, compared COP in more than 3,000 U.S. men and women who completed an exercise test from 1973 to 2018 and were tracked for an average of 23 years. Although COP was introduced as an assessment in 2012, calculating the value from tests prior to that date was possible because those tests had captured the relevant breathing rate and oxygen uptake. In males aged 18-85 years, a worse COP was significantly associated with an increased risk for earlier death. This finding did not hold for females, however; Dr. Araújo noted that more research is needed to understand the discrepancy in COP’s predictive power by sex.

In the heart failure study, everyone enrolled had heart failure and completed a COP test. People with the worse COPs also had the worst symptoms of heart failure, but completing an exercise rehabilitation program improved COP values when researchers measured them again. Dr. Araújo was also part of this study, based in the Netherlands.

“I think the COP could become a novel parameter in clinical care,” for most people, said Thijs Eijsvogels, PhD, an exercise physiologist at Radboud University in Nijmegen, the Netherlands, and the senior author of the heart failure study. That said, Dr. Eijsvogels said elite athletes will always be more interested in measuring VO₂ max.

Dr. Lala agreed that tests such as the COP have some value. Her own work has shown that measuring the efficiency of someone’s breathing patterns for exhaling carbon dioxide, which can also be done without making people exercise full strength, has prognostic value for patients with advanced heart failure. Even so, she said she would like to see maximal effort tests used as much as possible.

“I worry about saying we’re going to settle for a parameter that can be achieved at 50% of peak VO₂ and then we don’t exercise our patients,” Dr. Lala said.

Dr. Araújo said he plans to continue to measure VO₂ max but he believes COP has utility – even for elite athletes. One of his patients is a frequent Ironman competitor who competes well despite having a solid but not amazing VO₂ max level. But her COP is quite low, Dr. Araújo said, which to him suggests an especially efficient interaction between her respiratory and cardiovascular systems.

“We have a new player in the game,” Dr. Araújo said.

The sources in this study report no relevant financial relationships.

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

A simple measurement – the cardiorespiratory optimal point (COP) – could predict how long someone will live or the severity of their heart failure, according to clinicians who champion the assessment. The COP is easier to obtain than cardiorespiratory measures that require people to exercise to their limit, advocates say; rather than running full speed, someone can walk or lightly jog on a treadmill, with a COP value obtained easily. 
 

But other clinicians argue that maximal exercise tests have many prognostic benefits, and that physicians should do everything in their power to push patients to exercise as hard as possible. In particular, the VO₂ max test captures the maximum amount of oxygen someone uses when exercising at their capacity and is the preferred method for measuring cardiovascular endurance.

The COP is a measure of the minimum number of liters of air during breathing required to move one liter of oxygen through the bloodstream. The lower the COP the better, because this means that someone is working less strenuously than someone else to transport the same amount of oxygen, denoting a more efficient interaction between their heart and lungs.

The COP for a fit person might be 15, about 20-25 for a healthy person, and 35 for someone with heart failure, according to Claudio Gil Araújo, MD, PhD, director of research and education at CLINIMEX, an exercise medicine clinic in Rio de Janeiro.

“Max VO₂ is very important, that’s indisputable. But when do you use max VO₂ in your daily life? Never,” Dr. Araújo said. But almost anyone can generate a COP.
 

Emerging uses for the COP

“I can put someone on the treadmill or bike, and after 3 or 4 minutes I have the COP. It’s like a walking pace,” Dr. Araújo said. Yet the values are obtained with roughly half the effort as VO₂ max. Other clinicians argue exercising to the limits of endurance offers unique clinical insights.

“We should do everything in our power to exercise our patients to maximum. How long a patient is able to go is really important,” said Anu Lala, MD, a cardiologist who specializes in heart failure treatment at Mount Sinai Hospital in New York. A full-capacity exercise test gives useful insights into someone’s heart rate, heart rate recovery, blood pressure, and ECG response to vigorous exercise, Dr. Lala added, all of which are important clues to someone’s overall health.

In 2012 Dr. Araújo coauthored a study that first defined the COP, which is calculated by measuring expired gasses people produce while gently exercising, perhaps to the point where they begin to perspire, and then dividing their breathing capacity by their oxygen uptake every minute. The lowest value obtained during any exercise session is the COP.

Various studies show that higher COP values are associated with more severe heart lesions in patients with congenital heart disease; higher levels of mortality in seemingly healthy male adults; and with worse prognoses in patients with heart failure. These studies all appeared within the last 7 months.

The mortality study, which Dr. Araújo coauthored, compared COP in more than 3,000 U.S. men and women who completed an exercise test from 1973 to 2018 and were tracked for an average of 23 years. Although COP was introduced as an assessment in 2012, calculating the value from tests prior to that date was possible because those tests had captured the relevant breathing rate and oxygen uptake. In males aged 18-85 years, a worse COP was significantly associated with an increased risk for earlier death. This finding did not hold for females, however; Dr. Araújo noted that more research is needed to understand the discrepancy in COP’s predictive power by sex.

In the heart failure study, everyone enrolled had heart failure and completed a COP test. People with the worse COPs also had the worst symptoms of heart failure, but completing an exercise rehabilitation program improved COP values when researchers measured them again. Dr. Araújo was also part of this study, based in the Netherlands.

“I think the COP could become a novel parameter in clinical care,” for most people, said Thijs Eijsvogels, PhD, an exercise physiologist at Radboud University in Nijmegen, the Netherlands, and the senior author of the heart failure study. That said, Dr. Eijsvogels said elite athletes will always be more interested in measuring VO₂ max.

Dr. Lala agreed that tests such as the COP have some value. Her own work has shown that measuring the efficiency of someone’s breathing patterns for exhaling carbon dioxide, which can also be done without making people exercise full strength, has prognostic value for patients with advanced heart failure. Even so, she said she would like to see maximal effort tests used as much as possible.

“I worry about saying we’re going to settle for a parameter that can be achieved at 50% of peak VO₂ and then we don’t exercise our patients,” Dr. Lala said.

Dr. Araújo said he plans to continue to measure VO₂ max but he believes COP has utility – even for elite athletes. One of his patients is a frequent Ironman competitor who competes well despite having a solid but not amazing VO₂ max level. But her COP is quite low, Dr. Araújo said, which to him suggests an especially efficient interaction between her respiratory and cardiovascular systems.

“We have a new player in the game,” Dr. Araújo said.

The sources in this study report no relevant financial relationships.

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

Thoracic Oncology & Chest Imaging Network

Pleural Disease Section

Lobectomy with intrathoracic nodal dissection remains the standard of care for early stage (tumor size ≤ 3.0 cm) peripheral non–small cell lung cancer (NSCLC). This practice is primarily influenced by data from the mid-1990s associating limited resection (segmentectomy or wedge resection) with increased recurrence rate and mortality compared with lobectomy (Ginsberg et al. Ann Thorac Surg. 1995;60:615). Recent advances in video and robot-assisted thoracic surgery, as well as the implementation of lung cancer screening, improvement in minimally invasive diagnostic modalities, and neoadjuvant therapies have driven the medical community to revisit the role of sublobar lung resection.

Two newly published large randomized control multicenter multinational trials (Saji et al. Lancet. 2022;399:1670 and Altorki et al. N Engl J Med. 2023;388:489) have challenged our well-established practices. They compared overall and disease-free survival sublobar to lobar resection of early stage NSCLC (tumor size ≤ 2.0 cm and negative intraoperative nodal disease) and demonstrated noninferiority of sublobar resection with respect to overall survival and disease-free survival. While the sublobar resection in the Saji et al. trial consisted strictly of segmentectomy, the majority of sublobar resections in the Altorki et al. trial were wedge resections. Interestingly, both trials chose lower cut-offs for tumor size (≤ 2.0 cm) compared with the Ginsberg trial (≤ 3.0 cm), which could arguably have accounted for this difference in outcomes. In summary, these emerging data are here to tell us a new story by supporting more limited anatomical lung resection options for our patients with early stage NSCLC.

Christopher Yurosko, DO – Section Fellow-in-Training

Melissa Rosas, MD – Section Member-at-Large

Labib Debiane, MD - Section Member-at-Large

Thoracic Oncology & Chest Imaging Network

Pleural Disease Section

Lobectomy with intrathoracic nodal dissection remains the standard of care for early stage (tumor size ≤ 3.0 cm) peripheral non–small cell lung cancer (NSCLC). This practice is primarily influenced by data from the mid-1990s associating limited resection (segmentectomy or wedge resection) with increased recurrence rate and mortality compared with lobectomy (Ginsberg et al. Ann Thorac Surg. 1995;60:615). Recent advances in video and robot-assisted thoracic surgery, as well as the implementation of lung cancer screening, improvement in minimally invasive diagnostic modalities, and neoadjuvant therapies have driven the medical community to revisit the role of sublobar lung resection.

Two newly published large randomized control multicenter multinational trials (Saji et al. Lancet. 2022;399:1670 and Altorki et al. N Engl J Med. 2023;388:489) have challenged our well-established practices. They compared overall and disease-free survival sublobar to lobar resection of early stage NSCLC (tumor size ≤ 2.0 cm and negative intraoperative nodal disease) and demonstrated noninferiority of sublobar resection with respect to overall survival and disease-free survival. While the sublobar resection in the Saji et al. trial consisted strictly of segmentectomy, the majority of sublobar resections in the Altorki et al. trial were wedge resections. Interestingly, both trials chose lower cut-offs for tumor size (≤ 2.0 cm) compared with the Ginsberg trial (≤ 3.0 cm), which could arguably have accounted for this difference in outcomes. In summary, these emerging data are here to tell us a new story by supporting more limited anatomical lung resection options for our patients with early stage NSCLC.

Christopher Yurosko, DO – Section Fellow-in-Training

Melissa Rosas, MD – Section Member-at-Large

Labib Debiane, MD - Section Member-at-Large

Thoracic Oncology & Chest Imaging Network

Pleural Disease Section

Lobectomy with intrathoracic nodal dissection remains the standard of care for early stage (tumor size ≤ 3.0 cm) peripheral non–small cell lung cancer (NSCLC). This practice is primarily influenced by data from the mid-1990s associating limited resection (segmentectomy or wedge resection) with increased recurrence rate and mortality compared with lobectomy (Ginsberg et al. Ann Thorac Surg. 1995;60:615). Recent advances in video and robot-assisted thoracic surgery, as well as the implementation of lung cancer screening, improvement in minimally invasive diagnostic modalities, and neoadjuvant therapies have driven the medical community to revisit the role of sublobar lung resection.

Two newly published large randomized control multicenter multinational trials (Saji et al. Lancet. 2022;399:1670 and Altorki et al. N Engl J Med. 2023;388:489) have challenged our well-established practices. They compared overall and disease-free survival sublobar to lobar resection of early stage NSCLC (tumor size ≤ 2.0 cm and negative intraoperative nodal disease) and demonstrated noninferiority of sublobar resection with respect to overall survival and disease-free survival. While the sublobar resection in the Saji et al. trial consisted strictly of segmentectomy, the majority of sublobar resections in the Altorki et al. trial were wedge resections. Interestingly, both trials chose lower cut-offs for tumor size (≤ 2.0 cm) compared with the Ginsberg trial (≤ 3.0 cm), which could arguably have accounted for this difference in outcomes. In summary, these emerging data are here to tell us a new story by supporting more limited anatomical lung resection options for our patients with early stage NSCLC.

Christopher Yurosko, DO – Section Fellow-in-Training

Melissa Rosas, MD – Section Member-at-Large

Labib Debiane, MD - Section Member-at-Large

Sleep Medicine Network

Non-Respiratory Sleep Section

Want to feel your best when enjoying CHEST 2023 sessions, games, vendors, networking events, and much more on the island paradise of Hawai’i? It’s time to start making plans to align your circadian rhythm with Hawai’i Standard Time (HST).

Dr. Sabra Abbott, a circadian rhythm expert and the Director of the Circadian Medicine Clinic at Northwestern University, recommends “to best adapt to the time zone change, you can take advantage of the time-of-day specific phase shifting properties of light and melatonin.”

Before heading west to the meeting, Dr. Abbott recommends mainland USA travelers get extra light exposure in the evening. On arrival in Hawai’i, morning bright-light exposure should be limited. Luckily, afternoon/early evening light exposure is encouraged, which will help get some extra hours on the beach! Don’t forget your sunglasses to help with blocking light in the morning.

Once the meeting has concluded, attendees from mainland USA will need to advance their internal clocks earlier as they travel east back home. This can be achieved by taking melatonin 0.5 mg around bedtime and seeking bright-light during the mid-to-late morning.

To develop a personalized sleep prescription based on your time zone and preferred sleep times, you can use an online jet lag calculator, such as Jet Lag Rooster (jetlag.sleepopolis.com; no affiliations with authors or Dr. Abbott).

To learn more about circadian rhythm alignment when working and traveling, we’ll see you at the CHEST 2023 session “Shifting to Hawai’i – Jet Lag, Shift Workers, and Sleep for Health Care Providers” (10/8/2023 at 0815-HST).  If you haven't registered for the meeting, make sure to do so soon! You'll find the full schedule, pricing, and more at the CHEST 2023 website.

Paul Chung, DO – Section Fellow-in-Training
Lisa Wolfe, MD – Section Member-at-Large
William Healy, MD – Section Member-at-Large

Sleep Medicine Network

Non-Respiratory Sleep Section

Want to feel your best when enjoying CHEST 2023 sessions, games, vendors, networking events, and much more on the island paradise of Hawai’i? It’s time to start making plans to align your circadian rhythm with Hawai’i Standard Time (HST).

Dr. Sabra Abbott, a circadian rhythm expert and the Director of the Circadian Medicine Clinic at Northwestern University, recommends “to best adapt to the time zone change, you can take advantage of the time-of-day specific phase shifting properties of light and melatonin.”

Before heading west to the meeting, Dr. Abbott recommends mainland USA travelers get extra light exposure in the evening. On arrival in Hawai’i, morning bright-light exposure should be limited. Luckily, afternoon/early evening light exposure is encouraged, which will help get some extra hours on the beach! Don’t forget your sunglasses to help with blocking light in the morning.

Once the meeting has concluded, attendees from mainland USA will need to advance their internal clocks earlier as they travel east back home. This can be achieved by taking melatonin 0.5 mg around bedtime and seeking bright-light during the mid-to-late morning.

To develop a personalized sleep prescription based on your time zone and preferred sleep times, you can use an online jet lag calculator, such as Jet Lag Rooster (jetlag.sleepopolis.com; no affiliations with authors or Dr. Abbott).

To learn more about circadian rhythm alignment when working and traveling, we’ll see you at the CHEST 2023 session “Shifting to Hawai’i – Jet Lag, Shift Workers, and Sleep for Health Care Providers” (10/8/2023 at 0815-HST).  If you haven't registered for the meeting, make sure to do so soon! You'll find the full schedule, pricing, and more at the CHEST 2023 website.

Paul Chung, DO – Section Fellow-in-Training
Lisa Wolfe, MD – Section Member-at-Large
William Healy, MD – Section Member-at-Large

Sleep Medicine Network

Non-Respiratory Sleep Section

Want to feel your best when enjoying CHEST 2023 sessions, games, vendors, networking events, and much more on the island paradise of Hawai’i? It’s time to start making plans to align your circadian rhythm with Hawai’i Standard Time (HST).

Dr. Sabra Abbott, a circadian rhythm expert and the Director of the Circadian Medicine Clinic at Northwestern University, recommends “to best adapt to the time zone change, you can take advantage of the time-of-day specific phase shifting properties of light and melatonin.”

Before heading west to the meeting, Dr. Abbott recommends mainland USA travelers get extra light exposure in the evening. On arrival in Hawai’i, morning bright-light exposure should be limited. Luckily, afternoon/early evening light exposure is encouraged, which will help get some extra hours on the beach! Don’t forget your sunglasses to help with blocking light in the morning.

Once the meeting has concluded, attendees from mainland USA will need to advance their internal clocks earlier as they travel east back home. This can be achieved by taking melatonin 0.5 mg around bedtime and seeking bright-light during the mid-to-late morning.

To develop a personalized sleep prescription based on your time zone and preferred sleep times, you can use an online jet lag calculator, such as Jet Lag Rooster (jetlag.sleepopolis.com; no affiliations with authors or Dr. Abbott).

To learn more about circadian rhythm alignment when working and traveling, we’ll see you at the CHEST 2023 session “Shifting to Hawai’i – Jet Lag, Shift Workers, and Sleep for Health Care Providers” (10/8/2023 at 0815-HST).  If you haven't registered for the meeting, make sure to do so soon! You'll find the full schedule, pricing, and more at the CHEST 2023 website.

Paul Chung, DO – Section Fellow-in-Training
Lisa Wolfe, MD – Section Member-at-Large
William Healy, MD – Section Member-at-Large