Cardiology

Emergencies happen anywhere, anytime, and sometimes, medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series by this news organization that tells these stories.

It was my first night off after 12 days. It was a Friday night, and I went to a bar in Naples to get a beer with some friends. As it turned out, it wasn’t a night off after all.

As soon as we got inside, we heard over the speaker that they needed medical personnel and to please go to the left side of the bar. I thought it would be syncope or something like that.

I went over there and saw a woman holding up a man. He was basically leaning all over her. The light was low, and the music was pounding. I started to assess him and tried to get him to answer me. No response. I checked for pulses — nothing.

Now, I’m in a bar, right? It’s a cardiac arrest. The first thing you think is overdose or alcohol. I asked the woman if the man was doing any drugs. She said she didn’t know. Turns out they were both employees. He was a bouncer and a DJ.

The woman helped me lower him to the floor. I checked again for a pulse. Still nothing. I said, “Call 911,” and started compressions.

The difficult part was the place was completely dark. I knew where his body was on the floor. I could see his chest. But I couldn’t see his face at all.

It was also extremely loud with the music thumping. After a while, they finally shut it off.

Pretty soon, the security personnel from the bar brought me an automated external defibrillator, and it showed the man was having V-fib arrest. I shocked him. Still no pulse. I continued with cardiopulmonary resuscitation (CPR).

I hadn’t noticed, but lots of people were crowding around us. Somebody came up and said, “He’s my friend. He has a 9-year-old daughter. He can’t die. Let me help with the compressions.” I was like, “Go for it.”

The guy started kind of pushing on the man’s abdomen. He had no idea how to do compressions. I said, “Okay, let me take over again.”

Out of the crowd, nobody else volunteered to help. No one asked me, “Hey, what can I do?” Meanwhile, I found out later that someone was filming the whole thing on their phone.

But what the guy said about the man’s young daughter stayed in my brain. I thought, we need to keep going.

I did more compressions and shocked him again. Still no pulse. At that point, the police and emergency medical services showed up. They checked, nothing had changed, so they got him into the ambulance.

I asked one of the paramedics, “Where are you taking him? I can call ahead.”

But he said, “That’s HIPAA. We can’t tell you.” They also wouldn’t let me go with him in the ambulance.

“I have an active Florida license, and I work in the ICU [intensive care unit],” I said.

“No, we need to follow our protocol,” he replied.

I understood that, but I just wanted to help.

It was around 10:30 PM by then, and I was drenched in sweat. I had to go home. The first thing I did after taking a shower was open the computer and check my system. I needed to find out what happened to the guy.

I was looking for admissions, and I didn’t see him. I called the main hospital downtown and the one in North Naples. I couldn’t find him anywhere. I stayed up until almost 1:00 AM checking for his name. At that point I thought, okay, maybe he died.

The next night, Saturday, I was home and got a call from one of my colleagues. “Hey, were you in a bar yesterday? Did you do CPR on somebody?”

“How did you know?” I said.

He said the paramedics had described me — “a tall doctor with glasses who was a nice guy.” It was funny that he knew that was me.

He told me, “The guy’s alive. He’s sick and needs to be put on dialysis, but he’s alive.”

Apparently, the guy had gone to the emergency department at North Naples, and the doctors in the emergency room (ER) worked on him for over an hour. They did continuous CPR and shocked him for close to 40 minutes. They finally got his pulse back, and after that, he was transferred to the main hospital ICU. They didn’t admit him at the ER, which was why I couldn’t find his name.

On Sunday, I was checking my patients’ charts for the ICU that coming week. And there he was. I saw his name and the documentation by the ED that CPR was provided by a critical care doctor in the field. He was still alive. That gave me so much joy.

So, the man I had helped became my patient. When I saw him on Monday, he was intubated and needed dialysis. I finally saw his face and thought, Oh, so that’s what you look like. I hadn’t realized he was only 39 years old.

When he was awake, I explained to him I was the doctor that provided CPR at the bar. He was very grateful, but of course, he didn’t remember anything.

Eventually, I met his daughter, and she just said, “Thank you for allowing me to have my dad.”

The funny part is that he broke his leg. Well, that’s not funny, but no one had any idea how it happened. That was his only complaint. He was asking me, “Doctor, how did you break my leg?”

“Hey, I have no idea how you broke your leg,” I replied. “I was trying to save your life.”

He was in the hospital for almost a month but made a full recovery. The amazing part: After all the evaluations, he has no neurological deficits. He’s back to a normal life now.

They never found a cause for the cardiac arrest. I mean, he had an ejection fraction of 10%. All my money was on something drug related, but that wasn’t the case. They’d done a cardiac cut, and there was no obstruction. They couldn’t find a reason.

We’ve become friends. He still works as a DJ at the bar. He changed his name to “DJ the Survivor” or something like that.

Sometimes, he’ll text me: “Doctor, what are you doing? You want to come down to the bar?”

I’m like, “No. I don’t.”

It’s been more than a year, but I remember every detail. When you go into medicine, you dream that one day you’ll be able to say, “I saved somebody.”

He texted me a year later and told me he’s celebrating two birthdays now. He said, “I’m turning 1 year old today!”

I think about the value of life. How we can take it for granted. We think, I’m young, nothing is going to happen to me. But this guy was 39. He went to work and died that night.

I was able to help bring him back. That makes me thankful for every day.

Jose Valle Giler, MD, is a pulmonary, critical care, and sleep medicine physician at NCH Healthcare System in Naples, Florida.

A version of this article appeared on Medscape.com .

Emergencies happen anywhere, anytime, and sometimes, medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series by this news organization that tells these stories.

It was my first night off after 12 days. It was a Friday night, and I went to a bar in Naples to get a beer with some friends. As it turned out, it wasn’t a night off after all.

As soon as we got inside, we heard over the speaker that they needed medical personnel and to please go to the left side of the bar. I thought it would be syncope or something like that.

I went over there and saw a woman holding up a man. He was basically leaning all over her. The light was low, and the music was pounding. I started to assess him and tried to get him to answer me. No response. I checked for pulses — nothing.

Now, I’m in a bar, right? It’s a cardiac arrest. The first thing you think is overdose or alcohol. I asked the woman if the man was doing any drugs. She said she didn’t know. Turns out they were both employees. He was a bouncer and a DJ.

The woman helped me lower him to the floor. I checked again for a pulse. Still nothing. I said, “Call 911,” and started compressions.

The difficult part was the place was completely dark. I knew where his body was on the floor. I could see his chest. But I couldn’t see his face at all.

It was also extremely loud with the music thumping. After a while, they finally shut it off.

Pretty soon, the security personnel from the bar brought me an automated external defibrillator, and it showed the man was having V-fib arrest. I shocked him. Still no pulse. I continued with cardiopulmonary resuscitation (CPR).

I hadn’t noticed, but lots of people were crowding around us. Somebody came up and said, “He’s my friend. He has a 9-year-old daughter. He can’t die. Let me help with the compressions.” I was like, “Go for it.”

The guy started kind of pushing on the man’s abdomen. He had no idea how to do compressions. I said, “Okay, let me take over again.”

Out of the crowd, nobody else volunteered to help. No one asked me, “Hey, what can I do?” Meanwhile, I found out later that someone was filming the whole thing on their phone.

But what the guy said about the man’s young daughter stayed in my brain. I thought, we need to keep going.

I did more compressions and shocked him again. Still no pulse. At that point, the police and emergency medical services showed up. They checked, nothing had changed, so they got him into the ambulance.

I asked one of the paramedics, “Where are you taking him? I can call ahead.”

But he said, “That’s HIPAA. We can’t tell you.” They also wouldn’t let me go with him in the ambulance.

“I have an active Florida license, and I work in the ICU [intensive care unit],” I said.

“No, we need to follow our protocol,” he replied.

I understood that, but I just wanted to help.

It was around 10:30 PM by then, and I was drenched in sweat. I had to go home. The first thing I did after taking a shower was open the computer and check my system. I needed to find out what happened to the guy.

I was looking for admissions, and I didn’t see him. I called the main hospital downtown and the one in North Naples. I couldn’t find him anywhere. I stayed up until almost 1:00 AM checking for his name. At that point I thought, okay, maybe he died.

The next night, Saturday, I was home and got a call from one of my colleagues. “Hey, were you in a bar yesterday? Did you do CPR on somebody?”

“How did you know?” I said.

He said the paramedics had described me — “a tall doctor with glasses who was a nice guy.” It was funny that he knew that was me.

He told me, “The guy’s alive. He’s sick and needs to be put on dialysis, but he’s alive.”

Apparently, the guy had gone to the emergency department at North Naples, and the doctors in the emergency room (ER) worked on him for over an hour. They did continuous CPR and shocked him for close to 40 minutes. They finally got his pulse back, and after that, he was transferred to the main hospital ICU. They didn’t admit him at the ER, which was why I couldn’t find his name.

On Sunday, I was checking my patients’ charts for the ICU that coming week. And there he was. I saw his name and the documentation by the ED that CPR was provided by a critical care doctor in the field. He was still alive. That gave me so much joy.

So, the man I had helped became my patient. When I saw him on Monday, he was intubated and needed dialysis. I finally saw his face and thought, Oh, so that’s what you look like. I hadn’t realized he was only 39 years old.

When he was awake, I explained to him I was the doctor that provided CPR at the bar. He was very grateful, but of course, he didn’t remember anything.

Eventually, I met his daughter, and she just said, “Thank you for allowing me to have my dad.”

The funny part is that he broke his leg. Well, that’s not funny, but no one had any idea how it happened. That was his only complaint. He was asking me, “Doctor, how did you break my leg?”

“Hey, I have no idea how you broke your leg,” I replied. “I was trying to save your life.”

He was in the hospital for almost a month but made a full recovery. The amazing part: After all the evaluations, he has no neurological deficits. He’s back to a normal life now.

They never found a cause for the cardiac arrest. I mean, he had an ejection fraction of 10%. All my money was on something drug related, but that wasn’t the case. They’d done a cardiac cut, and there was no obstruction. They couldn’t find a reason.

We’ve become friends. He still works as a DJ at the bar. He changed his name to “DJ the Survivor” or something like that.

Sometimes, he’ll text me: “Doctor, what are you doing? You want to come down to the bar?”

I’m like, “No. I don’t.”

It’s been more than a year, but I remember every detail. When you go into medicine, you dream that one day you’ll be able to say, “I saved somebody.”

He texted me a year later and told me he’s celebrating two birthdays now. He said, “I’m turning 1 year old today!”

I think about the value of life. How we can take it for granted. We think, I’m young, nothing is going to happen to me. But this guy was 39. He went to work and died that night.

I was able to help bring him back. That makes me thankful for every day.

Jose Valle Giler, MD, is a pulmonary, critical care, and sleep medicine physician at NCH Healthcare System in Naples, Florida.

A version of this article appeared on Medscape.com .

Emergencies happen anywhere, anytime, and sometimes, medical professionals find themselves in situations where they are the only ones who can help. Is There a Doctor in the House? is a series by this news organization that tells these stories.

It was my first night off after 12 days. It was a Friday night, and I went to a bar in Naples to get a beer with some friends. As it turned out, it wasn’t a night off after all.

As soon as we got inside, we heard over the speaker that they needed medical personnel and to please go to the left side of the bar. I thought it would be syncope or something like that.

I went over there and saw a woman holding up a man. He was basically leaning all over her. The light was low, and the music was pounding. I started to assess him and tried to get him to answer me. No response. I checked for pulses — nothing.

Now, I’m in a bar, right? It’s a cardiac arrest. The first thing you think is overdose or alcohol. I asked the woman if the man was doing any drugs. She said she didn’t know. Turns out they were both employees. He was a bouncer and a DJ.

The woman helped me lower him to the floor. I checked again for a pulse. Still nothing. I said, “Call 911,” and started compressions.

The difficult part was the place was completely dark. I knew where his body was on the floor. I could see his chest. But I couldn’t see his face at all.

It was also extremely loud with the music thumping. After a while, they finally shut it off.

Pretty soon, the security personnel from the bar brought me an automated external defibrillator, and it showed the man was having V-fib arrest. I shocked him. Still no pulse. I continued with cardiopulmonary resuscitation (CPR).

I hadn’t noticed, but lots of people were crowding around us. Somebody came up and said, “He’s my friend. He has a 9-year-old daughter. He can’t die. Let me help with the compressions.” I was like, “Go for it.”

The guy started kind of pushing on the man’s abdomen. He had no idea how to do compressions. I said, “Okay, let me take over again.”

Out of the crowd, nobody else volunteered to help. No one asked me, “Hey, what can I do?” Meanwhile, I found out later that someone was filming the whole thing on their phone.

But what the guy said about the man’s young daughter stayed in my brain. I thought, we need to keep going.

I did more compressions and shocked him again. Still no pulse. At that point, the police and emergency medical services showed up. They checked, nothing had changed, so they got him into the ambulance.

I asked one of the paramedics, “Where are you taking him? I can call ahead.”

But he said, “That’s HIPAA. We can’t tell you.” They also wouldn’t let me go with him in the ambulance.

“I have an active Florida license, and I work in the ICU [intensive care unit],” I said.

“No, we need to follow our protocol,” he replied.

I understood that, but I just wanted to help.

It was around 10:30 PM by then, and I was drenched in sweat. I had to go home. The first thing I did after taking a shower was open the computer and check my system. I needed to find out what happened to the guy.

I was looking for admissions, and I didn’t see him. I called the main hospital downtown and the one in North Naples. I couldn’t find him anywhere. I stayed up until almost 1:00 AM checking for his name. At that point I thought, okay, maybe he died.

The next night, Saturday, I was home and got a call from one of my colleagues. “Hey, were you in a bar yesterday? Did you do CPR on somebody?”

“How did you know?” I said.

He said the paramedics had described me — “a tall doctor with glasses who was a nice guy.” It was funny that he knew that was me.

He told me, “The guy’s alive. He’s sick and needs to be put on dialysis, but he’s alive.”

Apparently, the guy had gone to the emergency department at North Naples, and the doctors in the emergency room (ER) worked on him for over an hour. They did continuous CPR and shocked him for close to 40 minutes. They finally got his pulse back, and after that, he was transferred to the main hospital ICU. They didn’t admit him at the ER, which was why I couldn’t find his name.

On Sunday, I was checking my patients’ charts for the ICU that coming week. And there he was. I saw his name and the documentation by the ED that CPR was provided by a critical care doctor in the field. He was still alive. That gave me so much joy.

So, the man I had helped became my patient. When I saw him on Monday, he was intubated and needed dialysis. I finally saw his face and thought, Oh, so that’s what you look like. I hadn’t realized he was only 39 years old.

When he was awake, I explained to him I was the doctor that provided CPR at the bar. He was very grateful, but of course, he didn’t remember anything.

Eventually, I met his daughter, and she just said, “Thank you for allowing me to have my dad.”

The funny part is that he broke his leg. Well, that’s not funny, but no one had any idea how it happened. That was his only complaint. He was asking me, “Doctor, how did you break my leg?”

“Hey, I have no idea how you broke your leg,” I replied. “I was trying to save your life.”

He was in the hospital for almost a month but made a full recovery. The amazing part: After all the evaluations, he has no neurological deficits. He’s back to a normal life now.

They never found a cause for the cardiac arrest. I mean, he had an ejection fraction of 10%. All my money was on something drug related, but that wasn’t the case. They’d done a cardiac cut, and there was no obstruction. They couldn’t find a reason.

We’ve become friends. He still works as a DJ at the bar. He changed his name to “DJ the Survivor” or something like that.

Sometimes, he’ll text me: “Doctor, what are you doing? You want to come down to the bar?”

I’m like, “No. I don’t.”

It’s been more than a year, but I remember every detail. When you go into medicine, you dream that one day you’ll be able to say, “I saved somebody.”

He texted me a year later and told me he’s celebrating two birthdays now. He said, “I’m turning 1 year old today!”

I think about the value of life. How we can take it for granted. We think, I’m young, nothing is going to happen to me. But this guy was 39. He went to work and died that night.

I was able to help bring him back. That makes me thankful for every day.

Jose Valle Giler, MD, is a pulmonary, critical care, and sleep medicine physician at NCH Healthcare System in Naples, Florida.

A version of this article appeared on Medscape.com .

Statins raise the risks for increased glucose levels and the development of type 2 diabetes among people who don’t have it at baseline, but those risks are outweighed by the cardiovascular benefit, new data suggested.

The findings come from an analysis of individual participant data from a total of 23 randomized trials of statin therapy involving 154,664 individuals. In people without diabetes at baseline, statin therapy produces a dose-dependent increase in the risk for diabetes diagnosis, particularly among those whose glycemia marker levels are already at the diagnostic threshold.

Statins also tend to raise glucose levels in people who already have diabetes, but “the diabetes-related risks arising from the small changes in glycemia resulting from statin therapy are greatly outweighed by the benefits of statins on major vascular events when the direct clinical consequences of these outcomes are taken into consideration,” wrote the authors of the Cholesterol Treatment Trialists’ (CTT) Collaboration in their paper, published online in The Lancet Diabetes & Endocrinology.

Moreover, they say, “since the effect of statin therapy on measures of glycemia within an individual is small, there is likely to be little clinical benefit in measuring glucose concentrations and A1c values routinely after starting statin therapy with the aim of making comparisons to values taken before the initiation of a statin. However, people should continue to be screened for diabetes and associated risk factors and have their glycemic control monitored in accordance with current clinical guidelines.”

The CTT is co-led by Christina Reith, MBChB, PhD, and David Preiss, PhD, FRCPath, MRCP, both of the Nuffield Department of Population Health, University of Oxford, England.

In an accompanying editorial, Hertzel C. Gerstein, MD, and Marie Pigeyre, MD, PhD, both of McMaster University and Hamilton Health Sciences, Hamilton, Ontario, Canada, noted that the decreased absolute annual incidence of life-threatening cardiovascular outcomes with statins in people at high risk for type 2 diabetes “clearly exceeds the 0.1%-1.3% per year increased absolute incidence of type 2 diabetes.”

Dr. Gerstein and Dr. Pigeyre also said “these findings emphasize the importance of holistic care. As people at risk for cardiovascular outcomes are also at risk for type 2 diabetes, any prescription of a statin should be accompanied by promoting proven strategies to prevent or delay diabetes, such as modest weight reduction and increased physical activity. Finally, these findings emphasize the importance of always being alert for harmful adverse effects, even with the most beneficial and successful preventive therapies.”
 

Statins Raise Diabetes Risk, Glucose Levels Slightly

The meta-analysis of trials in the CTT Collaboration included individual participant data from 19 double-blind randomized, controlled trials with a median follow-up of 4.3 years comparing statins with placebo in a total of 123,940 participants, including 18% who had known type 2 diabetes at randomization. Also analyzed were another four double-blind trials of lower- vs higher-intensity statins involving a total of 30,724 participants followed for a median of 4.9 years, with 15% having diabetes at baseline.

In the 19 trials of low- or moderate-intensity statins vs placebo, statins resulted in a significant 10% increase in new-onset diabetes compared with placebo (rate ratio, 1.10), while high-intensity statins raised the risk by an also significant 36% (1.36). This translated to a mean absolute excess of 0.12% per year of treatment.

Compared with less intensive statin therapy, more intensive statin therapy resulted in a significant 10% proportional increase in new-onset diabetes (1.10), giving an absolute annual excess of 0.22%.

In the statin vs placebo trials, differences in A1c values from placebo were 0.06 percentage points higher for low- or moderate-intensity statins and 0.08 points greater for high-intensity statins.

Nearly two thirds (62%) of the excess cases of new-onset diabetes occurred among participants in the highest quarter of the baseline glycemia distribution for both low-intensity or moderate-intensity and high-intensity statin therapy.

And among participants who already had diabetes at baseline, there was a significant 10% relative increase in worsening glycemia (defined by adverse glycemic event, A1c increase of ≥ 0.5 percentage points, or medication escalation) with low- or moderate-intensity statins compared with placebo and a 24% relative increase in the high-intensity trials.

The Nuffield Department of Population Health has an explicit policy of not accepting any personal honoraria payments directly or indirectly from the pharmaceutical and food industries. It seeks reimbursement to the University of Oxford for the costs of travel and accommodation to participate in scientific meetings. Dr. Reith reported receiving funding to the University of Oxford from the UK National Institute for Health and Care Research Health Technology Assessment Programme and holding unpaid roles on the Clinical Data Interchange Standards Consortium as a board member and WHO as a scientific advisor. Dr. Preiss reported receiving funding to his research institution (but no personal funding) from Novartis for the ORION 4 trial of inclisiran, Novo Nordisk for the ASCEND PLUS trial of semaglutide, and Boehringer Ingelheim and Eli Lilly for the EMPA-KIDNEY trial and being a committee member for a National Institute for Health and Care Excellence guideline.

Dr. Gerstein holds the McMaster-Sanofi Population Health Institute Chair in Diabetes Research and Care. He reported research grants from Eli Lilly, AstraZeneca, Novo Nordisk, Hanmi, and Merck; continuing medical education grants to McMaster University from Eli Lilly, Abbott, Sanofi, Novo Nordisk, and Boehringer Ingelheim; honoraria for speaking from AstraZeneca, Eli Lilly, Novo Nordisk, DKSH, Zuellig Pharma, Sanofi, and Jiangsu Hanson; and consulting fees from Abbott, Eli Lilly, Novo Nordisk, Pfizer, Carbon Brand, Sanofi, Kowa, and Hanmi. Pigeyre had no disclosures.
 

A version of this article appeared on Medscape.com.

Statins raise the risks for increased glucose levels and the development of type 2 diabetes among people who don’t have it at baseline, but those risks are outweighed by the cardiovascular benefit, new data suggested.

The findings come from an analysis of individual participant data from a total of 23 randomized trials of statin therapy involving 154,664 individuals. In people without diabetes at baseline, statin therapy produces a dose-dependent increase in the risk for diabetes diagnosis, particularly among those whose glycemia marker levels are already at the diagnostic threshold.

Statins also tend to raise glucose levels in people who already have diabetes, but “the diabetes-related risks arising from the small changes in glycemia resulting from statin therapy are greatly outweighed by the benefits of statins on major vascular events when the direct clinical consequences of these outcomes are taken into consideration,” wrote the authors of the Cholesterol Treatment Trialists’ (CTT) Collaboration in their paper, published online in The Lancet Diabetes & Endocrinology.

Moreover, they say, “since the effect of statin therapy on measures of glycemia within an individual is small, there is likely to be little clinical benefit in measuring glucose concentrations and A1c values routinely after starting statin therapy with the aim of making comparisons to values taken before the initiation of a statin. However, people should continue to be screened for diabetes and associated risk factors and have their glycemic control monitored in accordance with current clinical guidelines.”

The CTT is co-led by Christina Reith, MBChB, PhD, and David Preiss, PhD, FRCPath, MRCP, both of the Nuffield Department of Population Health, University of Oxford, England.

In an accompanying editorial, Hertzel C. Gerstein, MD, and Marie Pigeyre, MD, PhD, both of McMaster University and Hamilton Health Sciences, Hamilton, Ontario, Canada, noted that the decreased absolute annual incidence of life-threatening cardiovascular outcomes with statins in people at high risk for type 2 diabetes “clearly exceeds the 0.1%-1.3% per year increased absolute incidence of type 2 diabetes.”

Dr. Gerstein and Dr. Pigeyre also said “these findings emphasize the importance of holistic care. As people at risk for cardiovascular outcomes are also at risk for type 2 diabetes, any prescription of a statin should be accompanied by promoting proven strategies to prevent or delay diabetes, such as modest weight reduction and increased physical activity. Finally, these findings emphasize the importance of always being alert for harmful adverse effects, even with the most beneficial and successful preventive therapies.”
 

Statins Raise Diabetes Risk, Glucose Levels Slightly

The meta-analysis of trials in the CTT Collaboration included individual participant data from 19 double-blind randomized, controlled trials with a median follow-up of 4.3 years comparing statins with placebo in a total of 123,940 participants, including 18% who had known type 2 diabetes at randomization. Also analyzed were another four double-blind trials of lower- vs higher-intensity statins involving a total of 30,724 participants followed for a median of 4.9 years, with 15% having diabetes at baseline.

In the 19 trials of low- or moderate-intensity statins vs placebo, statins resulted in a significant 10% increase in new-onset diabetes compared with placebo (rate ratio, 1.10), while high-intensity statins raised the risk by an also significant 36% (1.36). This translated to a mean absolute excess of 0.12% per year of treatment.

Compared with less intensive statin therapy, more intensive statin therapy resulted in a significant 10% proportional increase in new-onset diabetes (1.10), giving an absolute annual excess of 0.22%.

In the statin vs placebo trials, differences in A1c values from placebo were 0.06 percentage points higher for low- or moderate-intensity statins and 0.08 points greater for high-intensity statins.

Nearly two thirds (62%) of the excess cases of new-onset diabetes occurred among participants in the highest quarter of the baseline glycemia distribution for both low-intensity or moderate-intensity and high-intensity statin therapy.

And among participants who already had diabetes at baseline, there was a significant 10% relative increase in worsening glycemia (defined by adverse glycemic event, A1c increase of ≥ 0.5 percentage points, or medication escalation) with low- or moderate-intensity statins compared with placebo and a 24% relative increase in the high-intensity trials.

The Nuffield Department of Population Health has an explicit policy of not accepting any personal honoraria payments directly or indirectly from the pharmaceutical and food industries. It seeks reimbursement to the University of Oxford for the costs of travel and accommodation to participate in scientific meetings. Dr. Reith reported receiving funding to the University of Oxford from the UK National Institute for Health and Care Research Health Technology Assessment Programme and holding unpaid roles on the Clinical Data Interchange Standards Consortium as a board member and WHO as a scientific advisor. Dr. Preiss reported receiving funding to his research institution (but no personal funding) from Novartis for the ORION 4 trial of inclisiran, Novo Nordisk for the ASCEND PLUS trial of semaglutide, and Boehringer Ingelheim and Eli Lilly for the EMPA-KIDNEY trial and being a committee member for a National Institute for Health and Care Excellence guideline.

Dr. Gerstein holds the McMaster-Sanofi Population Health Institute Chair in Diabetes Research and Care. He reported research grants from Eli Lilly, AstraZeneca, Novo Nordisk, Hanmi, and Merck; continuing medical education grants to McMaster University from Eli Lilly, Abbott, Sanofi, Novo Nordisk, and Boehringer Ingelheim; honoraria for speaking from AstraZeneca, Eli Lilly, Novo Nordisk, DKSH, Zuellig Pharma, Sanofi, and Jiangsu Hanson; and consulting fees from Abbott, Eli Lilly, Novo Nordisk, Pfizer, Carbon Brand, Sanofi, Kowa, and Hanmi. Pigeyre had no disclosures.
 

A version of this article appeared on Medscape.com.

Statins raise the risks for increased glucose levels and the development of type 2 diabetes among people who don’t have it at baseline, but those risks are outweighed by the cardiovascular benefit, new data suggested.

The findings come from an analysis of individual participant data from a total of 23 randomized trials of statin therapy involving 154,664 individuals. In people without diabetes at baseline, statin therapy produces a dose-dependent increase in the risk for diabetes diagnosis, particularly among those whose glycemia marker levels are already at the diagnostic threshold.

Statins also tend to raise glucose levels in people who already have diabetes, but “the diabetes-related risks arising from the small changes in glycemia resulting from statin therapy are greatly outweighed by the benefits of statins on major vascular events when the direct clinical consequences of these outcomes are taken into consideration,” wrote the authors of the Cholesterol Treatment Trialists’ (CTT) Collaboration in their paper, published online in The Lancet Diabetes & Endocrinology.

Moreover, they say, “since the effect of statin therapy on measures of glycemia within an individual is small, there is likely to be little clinical benefit in measuring glucose concentrations and A1c values routinely after starting statin therapy with the aim of making comparisons to values taken before the initiation of a statin. However, people should continue to be screened for diabetes and associated risk factors and have their glycemic control monitored in accordance with current clinical guidelines.”

The CTT is co-led by Christina Reith, MBChB, PhD, and David Preiss, PhD, FRCPath, MRCP, both of the Nuffield Department of Population Health, University of Oxford, England.

In an accompanying editorial, Hertzel C. Gerstein, MD, and Marie Pigeyre, MD, PhD, both of McMaster University and Hamilton Health Sciences, Hamilton, Ontario, Canada, noted that the decreased absolute annual incidence of life-threatening cardiovascular outcomes with statins in people at high risk for type 2 diabetes “clearly exceeds the 0.1%-1.3% per year increased absolute incidence of type 2 diabetes.”

Dr. Gerstein and Dr. Pigeyre also said “these findings emphasize the importance of holistic care. As people at risk for cardiovascular outcomes are also at risk for type 2 diabetes, any prescription of a statin should be accompanied by promoting proven strategies to prevent or delay diabetes, such as modest weight reduction and increased physical activity. Finally, these findings emphasize the importance of always being alert for harmful adverse effects, even with the most beneficial and successful preventive therapies.”
 

Statins Raise Diabetes Risk, Glucose Levels Slightly

The meta-analysis of trials in the CTT Collaboration included individual participant data from 19 double-blind randomized, controlled trials with a median follow-up of 4.3 years comparing statins with placebo in a total of 123,940 participants, including 18% who had known type 2 diabetes at randomization. Also analyzed were another four double-blind trials of lower- vs higher-intensity statins involving a total of 30,724 participants followed for a median of 4.9 years, with 15% having diabetes at baseline.

In the 19 trials of low- or moderate-intensity statins vs placebo, statins resulted in a significant 10% increase in new-onset diabetes compared with placebo (rate ratio, 1.10), while high-intensity statins raised the risk by an also significant 36% (1.36). This translated to a mean absolute excess of 0.12% per year of treatment.

Compared with less intensive statin therapy, more intensive statin therapy resulted in a significant 10% proportional increase in new-onset diabetes (1.10), giving an absolute annual excess of 0.22%.

In the statin vs placebo trials, differences in A1c values from placebo were 0.06 percentage points higher for low- or moderate-intensity statins and 0.08 points greater for high-intensity statins.

Nearly two thirds (62%) of the excess cases of new-onset diabetes occurred among participants in the highest quarter of the baseline glycemia distribution for both low-intensity or moderate-intensity and high-intensity statin therapy.

And among participants who already had diabetes at baseline, there was a significant 10% relative increase in worsening glycemia (defined by adverse glycemic event, A1c increase of ≥ 0.5 percentage points, or medication escalation) with low- or moderate-intensity statins compared with placebo and a 24% relative increase in the high-intensity trials.

The Nuffield Department of Population Health has an explicit policy of not accepting any personal honoraria payments directly or indirectly from the pharmaceutical and food industries. It seeks reimbursement to the University of Oxford for the costs of travel and accommodation to participate in scientific meetings. Dr. Reith reported receiving funding to the University of Oxford from the UK National Institute for Health and Care Research Health Technology Assessment Programme and holding unpaid roles on the Clinical Data Interchange Standards Consortium as a board member and WHO as a scientific advisor. Dr. Preiss reported receiving funding to his research institution (but no personal funding) from Novartis for the ORION 4 trial of inclisiran, Novo Nordisk for the ASCEND PLUS trial of semaglutide, and Boehringer Ingelheim and Eli Lilly for the EMPA-KIDNEY trial and being a committee member for a National Institute for Health and Care Excellence guideline.

Dr. Gerstein holds the McMaster-Sanofi Population Health Institute Chair in Diabetes Research and Care. He reported research grants from Eli Lilly, AstraZeneca, Novo Nordisk, Hanmi, and Merck; continuing medical education grants to McMaster University from Eli Lilly, Abbott, Sanofi, Novo Nordisk, and Boehringer Ingelheim; honoraria for speaking from AstraZeneca, Eli Lilly, Novo Nordisk, DKSH, Zuellig Pharma, Sanofi, and Jiangsu Hanson; and consulting fees from Abbott, Eli Lilly, Novo Nordisk, Pfizer, Carbon Brand, Sanofi, Kowa, and Hanmi. Pigeyre had no disclosures.
 

A version of this article appeared on Medscape.com.

ATLANTA — A novel antisense therapy called olezarsen reduced triglycerides (TGs) by approximately 50% with either of the two study doses relative to placebo and did so with a low relative risk for adverse events, new data from a phase 2b trial showed.

“The reduction in triglycerides was greater than that currently possible with any available therapy,” reported Brian A. Bergmark, MD, an interventional cardiologist at Brigham and Women’s Hospital, Boston.

The drug also produced meaningful improvements in multiple other lipid subfractions associated with increased cardiovascular (CV) risk, including ApoC-III, very low–density lipoprotein (VLDL) cholesterol, ApoB, and non-LDL cholesterol. High-density lipoprotein (HDL) cholesterol levels were significantly raised.

The results were presented on April 7 as a late breaker at the American College of Cardiology (ACC) Scientific Session 2024 and published online simultaneously in The New England Journal of Medicine.
 

No Major Subgroup Failed to Respond

The effect was seen across all the key subgroups evaluated, including women and patients with diabetes, obesity, and severe as well as moderate elevations in TGs at baseline, Dr. Bergmark reported.

Olezarsen is a N-acetylgalactosamine–conjugated antisense oligonucleotide targeting APOC3 RNA. The results of this randomized trial, called BRIDGE-TIMI 73a, are consistent with other evidence that inhibiting expression of ApoC-III lowers the levels of TGs and other lipid subfractions to a degree that would predict clinical benefit.

In this study, 154 patients at 24 sites in North America were randomized in a 1:1 ratio to 50 or 80 mg olezarsen. Those in each of these cohorts were then randomized in a 3:1 ratio to active therapy or placebo. All therapies were administered by subcutaneous injection once per month.

Patients were eligible for the trial if they had moderate hypertriglyceridemia, defined as a level of 150-499 mg/dL, and elevated CV risk or if they had severe hypertriglyceridemia (≥ 500 mg/dL) with or without other evidence of elevated CV risk. The primary endpoint was a change in TGs at 6 months. Complete follow-up was available in about 97% of patients regardless of treatment assignment.

With a slight numerical advantage for the higher dose, the TG reductions were 49.1% for the 50-mg dose and 53.1% for the 80-mg dose relative to no significant change in the placebo group (P < .001 for both olezarsen doses). The reductions in ApoC-III, an upstream driver of TG production and a CV risk factor, were 64.2% and 73.2% relative to placebo (both P < .001), respectively, Dr. Bergmark reported.

In those with moderate hypertriglyceridemia, normal TG levels, defined as < 150 mg/dL, were reached at 6 months in 85.7% and 93.3% in the 40-mg and 80-mg dose groups, respectively. Relative to these reductions, normalization was seen in only 11.8% of placebo patients (P < .001).
 

TG Lowering Might Not Be Best Endpoint

The primary endpoint in this trial was a change in TGs, but this target was questioned by an invited ACC discussant, Daniel Soffer, MD, who is both an adjunct professor assistant professor of medicine at Penn Medicine, Philadelphia, and current president of the National Lipid Association.

Dr. Soffer noted that highly elevated TGs are a major risk factor for acute pancreatitis, so this predicts a clinical benefit for this purpose, but he thought the other lipid subfractions are far more important for the goal of reducing atherosclerotic cardiovascular disease (ASCVD).

Indeed, he said categorically that it is not TGs that drive ASCVD risk and therefore not what is the real importance of these data. Rather, “it is the non-HDL cholesterol and ApoB lowering” that will drive the likely benefits from this therapy in CV disease.

In addition to the TG reductions, olezarsen did, in fact, produce significant reductions in many of the lipid subfractions associated with increased CV risk. While slightly more favorable in most cases with the higher dose of olezarsen, even the lower dose reduced Apo C-III from baseline by 64.2% (P < .001), VLDL by 46.2% (P < .001), remnant cholesterol by 46.6% (P < .001), ApoB by 18.2% (P < .001), and non-HDL cholesterol by 25.4% (P < .001). HDL cholesterol was increased by 39.6% (P < .001).

These favorable effects on TG and other lipid subfractions were achieved with a safety profile that was reassuring, Dr. Bergmark said. Serious adverse events leading to discontinuation occurred in 0%, 1.7%, and 1.8% of the placebo, lower-dose, and higher-dose arms, respectively. These rates did not differ significantly.
 

Increased Liver Enzymes Is Common

Liver enzymes were significantly elevated (P < .001) for both doses of olezarsen vs placebo, but liver enzymes > 3× the upper limit of normal did not reach significance on either dose of olezarsen relative to placebo. Low platelet counts and reductions in kidney function were observed in a minority of patients but were generally manageable, according to Dr. Bergmark. There was no impact on hemoglobin A1c levels.

Further evaluation of change in hepatic function is planned in the ongoing extension studies.

Characterizing these results as “exciting,” Neha J. Pagidipati, MD, a member of the Duke Clinical Research Institute and an assistant professor at the Duke School of Medicine, Durham, North Carolina, said that identifying a drug effective for hypertriglyceridemia is likely to be a major advance. While elevated TGs are “one of the toughest” lipid abnormalities to manage, “there is not much out there to offer for treatment.”

She, like Dr. Soffer, was encouraged by the favorable effects on multiple lipid abnormalities associated with increased CV risk, but she said the ultimate clinical utility of this or other agents that lower TGs for ASCVD requires a study showing a change in CV events.

Dr. Bergmark reported financial relationships with 15 pharmaceutical companies, including Ionis, which provided funding for the BRIDGE-TIMI 73a trial. Soffer had financial relationships with Akcea, Amgen, Amryt, AstraZeneca, Ionis, Novartis, Regeneron, and Verve. Dr. Pagidipati had financial relationships with more than 10 pharmaceutical companies but was not involved in the design of management of the BRIDGE-TIMI 73a trial.

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

ATLANTA — A novel antisense therapy called olezarsen reduced triglycerides (TGs) by approximately 50% with either of the two study doses relative to placebo and did so with a low relative risk for adverse events, new data from a phase 2b trial showed.

“The reduction in triglycerides was greater than that currently possible with any available therapy,” reported Brian A. Bergmark, MD, an interventional cardiologist at Brigham and Women’s Hospital, Boston.

The drug also produced meaningful improvements in multiple other lipid subfractions associated with increased cardiovascular (CV) risk, including ApoC-III, very low–density lipoprotein (VLDL) cholesterol, ApoB, and non-LDL cholesterol. High-density lipoprotein (HDL) cholesterol levels were significantly raised.

The results were presented on April 7 as a late breaker at the American College of Cardiology (ACC) Scientific Session 2024 and published online simultaneously in The New England Journal of Medicine.
 

No Major Subgroup Failed to Respond

The effect was seen across all the key subgroups evaluated, including women and patients with diabetes, obesity, and severe as well as moderate elevations in TGs at baseline, Dr. Bergmark reported.

Olezarsen is a N-acetylgalactosamine–conjugated antisense oligonucleotide targeting APOC3 RNA. The results of this randomized trial, called BRIDGE-TIMI 73a, are consistent with other evidence that inhibiting expression of ApoC-III lowers the levels of TGs and other lipid subfractions to a degree that would predict clinical benefit.

In this study, 154 patients at 24 sites in North America were randomized in a 1:1 ratio to 50 or 80 mg olezarsen. Those in each of these cohorts were then randomized in a 3:1 ratio to active therapy or placebo. All therapies were administered by subcutaneous injection once per month.

Patients were eligible for the trial if they had moderate hypertriglyceridemia, defined as a level of 150-499 mg/dL, and elevated CV risk or if they had severe hypertriglyceridemia (≥ 500 mg/dL) with or without other evidence of elevated CV risk. The primary endpoint was a change in TGs at 6 months. Complete follow-up was available in about 97% of patients regardless of treatment assignment.

With a slight numerical advantage for the higher dose, the TG reductions were 49.1% for the 50-mg dose and 53.1% for the 80-mg dose relative to no significant change in the placebo group (P < .001 for both olezarsen doses). The reductions in ApoC-III, an upstream driver of TG production and a CV risk factor, were 64.2% and 73.2% relative to placebo (both P < .001), respectively, Dr. Bergmark reported.

In those with moderate hypertriglyceridemia, normal TG levels, defined as < 150 mg/dL, were reached at 6 months in 85.7% and 93.3% in the 40-mg and 80-mg dose groups, respectively. Relative to these reductions, normalization was seen in only 11.8% of placebo patients (P < .001).
 

TG Lowering Might Not Be Best Endpoint

The primary endpoint in this trial was a change in TGs, but this target was questioned by an invited ACC discussant, Daniel Soffer, MD, who is both an adjunct professor assistant professor of medicine at Penn Medicine, Philadelphia, and current president of the National Lipid Association.

Dr. Soffer noted that highly elevated TGs are a major risk factor for acute pancreatitis, so this predicts a clinical benefit for this purpose, but he thought the other lipid subfractions are far more important for the goal of reducing atherosclerotic cardiovascular disease (ASCVD).

Indeed, he said categorically that it is not TGs that drive ASCVD risk and therefore not what is the real importance of these data. Rather, “it is the non-HDL cholesterol and ApoB lowering” that will drive the likely benefits from this therapy in CV disease.

In addition to the TG reductions, olezarsen did, in fact, produce significant reductions in many of the lipid subfractions associated with increased CV risk. While slightly more favorable in most cases with the higher dose of olezarsen, even the lower dose reduced Apo C-III from baseline by 64.2% (P < .001), VLDL by 46.2% (P < .001), remnant cholesterol by 46.6% (P < .001), ApoB by 18.2% (P < .001), and non-HDL cholesterol by 25.4% (P < .001). HDL cholesterol was increased by 39.6% (P < .001).

These favorable effects on TG and other lipid subfractions were achieved with a safety profile that was reassuring, Dr. Bergmark said. Serious adverse events leading to discontinuation occurred in 0%, 1.7%, and 1.8% of the placebo, lower-dose, and higher-dose arms, respectively. These rates did not differ significantly.
 

Increased Liver Enzymes Is Common

Liver enzymes were significantly elevated (P < .001) for both doses of olezarsen vs placebo, but liver enzymes > 3× the upper limit of normal did not reach significance on either dose of olezarsen relative to placebo. Low platelet counts and reductions in kidney function were observed in a minority of patients but were generally manageable, according to Dr. Bergmark. There was no impact on hemoglobin A1c levels.

Further evaluation of change in hepatic function is planned in the ongoing extension studies.

Characterizing these results as “exciting,” Neha J. Pagidipati, MD, a member of the Duke Clinical Research Institute and an assistant professor at the Duke School of Medicine, Durham, North Carolina, said that identifying a drug effective for hypertriglyceridemia is likely to be a major advance. While elevated TGs are “one of the toughest” lipid abnormalities to manage, “there is not much out there to offer for treatment.”

She, like Dr. Soffer, was encouraged by the favorable effects on multiple lipid abnormalities associated with increased CV risk, but she said the ultimate clinical utility of this or other agents that lower TGs for ASCVD requires a study showing a change in CV events.

Dr. Bergmark reported financial relationships with 15 pharmaceutical companies, including Ionis, which provided funding for the BRIDGE-TIMI 73a trial. Soffer had financial relationships with Akcea, Amgen, Amryt, AstraZeneca, Ionis, Novartis, Regeneron, and Verve. Dr. Pagidipati had financial relationships with more than 10 pharmaceutical companies but was not involved in the design of management of the BRIDGE-TIMI 73a trial.

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

ATLANTA — A novel antisense therapy called olezarsen reduced triglycerides (TGs) by approximately 50% with either of the two study doses relative to placebo and did so with a low relative risk for adverse events, new data from a phase 2b trial showed.

“The reduction in triglycerides was greater than that currently possible with any available therapy,” reported Brian A. Bergmark, MD, an interventional cardiologist at Brigham and Women’s Hospital, Boston.

The drug also produced meaningful improvements in multiple other lipid subfractions associated with increased cardiovascular (CV) risk, including ApoC-III, very low–density lipoprotein (VLDL) cholesterol, ApoB, and non-LDL cholesterol. High-density lipoprotein (HDL) cholesterol levels were significantly raised.

The results were presented on April 7 as a late breaker at the American College of Cardiology (ACC) Scientific Session 2024 and published online simultaneously in The New England Journal of Medicine.
 

No Major Subgroup Failed to Respond

The effect was seen across all the key subgroups evaluated, including women and patients with diabetes, obesity, and severe as well as moderate elevations in TGs at baseline, Dr. Bergmark reported.

Olezarsen is a N-acetylgalactosamine–conjugated antisense oligonucleotide targeting APOC3 RNA. The results of this randomized trial, called BRIDGE-TIMI 73a, are consistent with other evidence that inhibiting expression of ApoC-III lowers the levels of TGs and other lipid subfractions to a degree that would predict clinical benefit.

In this study, 154 patients at 24 sites in North America were randomized in a 1:1 ratio to 50 or 80 mg olezarsen. Those in each of these cohorts were then randomized in a 3:1 ratio to active therapy or placebo. All therapies were administered by subcutaneous injection once per month.

Patients were eligible for the trial if they had moderate hypertriglyceridemia, defined as a level of 150-499 mg/dL, and elevated CV risk or if they had severe hypertriglyceridemia (≥ 500 mg/dL) with or without other evidence of elevated CV risk. The primary endpoint was a change in TGs at 6 months. Complete follow-up was available in about 97% of patients regardless of treatment assignment.

With a slight numerical advantage for the higher dose, the TG reductions were 49.1% for the 50-mg dose and 53.1% for the 80-mg dose relative to no significant change in the placebo group (P < .001 for both olezarsen doses). The reductions in ApoC-III, an upstream driver of TG production and a CV risk factor, were 64.2% and 73.2% relative to placebo (both P < .001), respectively, Dr. Bergmark reported.

In those with moderate hypertriglyceridemia, normal TG levels, defined as < 150 mg/dL, were reached at 6 months in 85.7% and 93.3% in the 40-mg and 80-mg dose groups, respectively. Relative to these reductions, normalization was seen in only 11.8% of placebo patients (P < .001).
 

TG Lowering Might Not Be Best Endpoint

The primary endpoint in this trial was a change in TGs, but this target was questioned by an invited ACC discussant, Daniel Soffer, MD, who is both an adjunct professor assistant professor of medicine at Penn Medicine, Philadelphia, and current president of the National Lipid Association.

Dr. Soffer noted that highly elevated TGs are a major risk factor for acute pancreatitis, so this predicts a clinical benefit for this purpose, but he thought the other lipid subfractions are far more important for the goal of reducing atherosclerotic cardiovascular disease (ASCVD).

Indeed, he said categorically that it is not TGs that drive ASCVD risk and therefore not what is the real importance of these data. Rather, “it is the non-HDL cholesterol and ApoB lowering” that will drive the likely benefits from this therapy in CV disease.

In addition to the TG reductions, olezarsen did, in fact, produce significant reductions in many of the lipid subfractions associated with increased CV risk. While slightly more favorable in most cases with the higher dose of olezarsen, even the lower dose reduced Apo C-III from baseline by 64.2% (P < .001), VLDL by 46.2% (P < .001), remnant cholesterol by 46.6% (P < .001), ApoB by 18.2% (P < .001), and non-HDL cholesterol by 25.4% (P < .001). HDL cholesterol was increased by 39.6% (P < .001).

These favorable effects on TG and other lipid subfractions were achieved with a safety profile that was reassuring, Dr. Bergmark said. Serious adverse events leading to discontinuation occurred in 0%, 1.7%, and 1.8% of the placebo, lower-dose, and higher-dose arms, respectively. These rates did not differ significantly.
 

Increased Liver Enzymes Is Common

Liver enzymes were significantly elevated (P < .001) for both doses of olezarsen vs placebo, but liver enzymes > 3× the upper limit of normal did not reach significance on either dose of olezarsen relative to placebo. Low platelet counts and reductions in kidney function were observed in a minority of patients but were generally manageable, according to Dr. Bergmark. There was no impact on hemoglobin A1c levels.

Further evaluation of change in hepatic function is planned in the ongoing extension studies.

Characterizing these results as “exciting,” Neha J. Pagidipati, MD, a member of the Duke Clinical Research Institute and an assistant professor at the Duke School of Medicine, Durham, North Carolina, said that identifying a drug effective for hypertriglyceridemia is likely to be a major advance. While elevated TGs are “one of the toughest” lipid abnormalities to manage, “there is not much out there to offer for treatment.”

She, like Dr. Soffer, was encouraged by the favorable effects on multiple lipid abnormalities associated with increased CV risk, but she said the ultimate clinical utility of this or other agents that lower TGs for ASCVD requires a study showing a change in CV events.

Dr. Bergmark reported financial relationships with 15 pharmaceutical companies, including Ionis, which provided funding for the BRIDGE-TIMI 73a trial. Soffer had financial relationships with Akcea, Amgen, Amryt, AstraZeneca, Ionis, Novartis, Regeneron, and Verve. Dr. Pagidipati had financial relationships with more than 10 pharmaceutical companies but was not involved in the design of management of the BRIDGE-TIMI 73a trial.

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

TOPLINE:

In people with type 2 diabetes (T2D), higher levels of arm and trunk fat are associated with an increased risk for cardiovascular disease (CVD) and mortality, while higher levels of leg fat are associated with a reduced risk for these conditions.

METHODOLOGY:

• People with T2D have a twofold to fourfold higher risk for CVD and mortality, and evidence shows obesity management helps delay complications and premature death, but an elevated body mass index (BMI) may be insufficient to measure obesity.
• In the “obesity paradox,” people with elevated BMI may have a lower CVD risk than people of normal weight.
• Researchers prospectively investigated how regional body fat accumulation was associated with CVD risk in 21,472 people with T2D (mean age, 58.9 years; 60.7% men; BMI about 29-33) from the UK Biobank (2006-2010), followed up for a median of 7.7 years.
• The regional body fat distribution in arms, trunk, and legs was assessed using bioelectrical impedance analysis.
• The primary outcomes were the incidence of CVD, all-cause mortality, and CVD mortality.

TAKEAWAY:

• Participants in the highest quartile of arm fat percentage (multivariate-adjusted hazard ratio [HR], 1.63; 95% CI, 1.29-2.05) and trunk fat percentage (HR, 1.27; 95% CI, 1.06-1.52) were at a higher risk for CVD than those in the lowest quartile.
• However, participants in the highest quartile of leg fat percentage had a lower risk for CVD than those in the lowest quartile (HR, 0.72; 95% CI, 0.58-0.90).
• A nonlinear relationship was observed between higher leg fat percentage and lower CVD risk and between higher trunk fat percentage and higher CVD risk, whereas a linear relationship was noted between higher arm fat percentage and higher CVD risk.
• The patterns of association were similar for both all-cause mortality and CVD mortality. Overall patterns were similar for men and women.

IN PRACTICE:

“Our findings add to the understanding of body fat distribution in patients with T2D, which highlights the importance of considering both the amount and the location of body fat when assessing CVD and mortality risk among patients with T2D,” wrote the authors.

SOURCE:

The study led by Zixin Qiu, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China, was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

As body fat was measured only once at the beginning of the study, its changing association over time could not be assessed. Moreover, the findings were primarily based on predominantly White UK adults, potentially restricting their generalizability to other population groups. Furthermore, diabetes was diagnosed using self-reported medical history, medication, and hemoglobin A1c levels, implying that some cases may have gone undetected at baseline. 

DISCLOSURES:

This study was funded by grants from the National Natural Science Foundation of China, Hubei Province Science Fund for Distinguished Young Scholars, and Fundamental Research Funds for the Central Universities. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

In people with type 2 diabetes (T2D), higher levels of arm and trunk fat are associated with an increased risk for cardiovascular disease (CVD) and mortality, while higher levels of leg fat are associated with a reduced risk for these conditions.

METHODOLOGY:

• People with T2D have a twofold to fourfold higher risk for CVD and mortality, and evidence shows obesity management helps delay complications and premature death, but an elevated body mass index (BMI) may be insufficient to measure obesity.
• In the “obesity paradox,” people with elevated BMI may have a lower CVD risk than people of normal weight.
• Researchers prospectively investigated how regional body fat accumulation was associated with CVD risk in 21,472 people with T2D (mean age, 58.9 years; 60.7% men; BMI about 29-33) from the UK Biobank (2006-2010), followed up for a median of 7.7 years.
• The regional body fat distribution in arms, trunk, and legs was assessed using bioelectrical impedance analysis.
• The primary outcomes were the incidence of CVD, all-cause mortality, and CVD mortality.

TAKEAWAY:

• Participants in the highest quartile of arm fat percentage (multivariate-adjusted hazard ratio [HR], 1.63; 95% CI, 1.29-2.05) and trunk fat percentage (HR, 1.27; 95% CI, 1.06-1.52) were at a higher risk for CVD than those in the lowest quartile.
• However, participants in the highest quartile of leg fat percentage had a lower risk for CVD than those in the lowest quartile (HR, 0.72; 95% CI, 0.58-0.90).
• A nonlinear relationship was observed between higher leg fat percentage and lower CVD risk and between higher trunk fat percentage and higher CVD risk, whereas a linear relationship was noted between higher arm fat percentage and higher CVD risk.
• The patterns of association were similar for both all-cause mortality and CVD mortality. Overall patterns were similar for men and women.

IN PRACTICE:

“Our findings add to the understanding of body fat distribution in patients with T2D, which highlights the importance of considering both the amount and the location of body fat when assessing CVD and mortality risk among patients with T2D,” wrote the authors.

SOURCE:

The study led by Zixin Qiu, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China, was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

As body fat was measured only once at the beginning of the study, its changing association over time could not be assessed. Moreover, the findings were primarily based on predominantly White UK adults, potentially restricting their generalizability to other population groups. Furthermore, diabetes was diagnosed using self-reported medical history, medication, and hemoglobin A1c levels, implying that some cases may have gone undetected at baseline. 

DISCLOSURES:

This study was funded by grants from the National Natural Science Foundation of China, Hubei Province Science Fund for Distinguished Young Scholars, and Fundamental Research Funds for the Central Universities. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

TOPLINE:

In people with type 2 diabetes (T2D), higher levels of arm and trunk fat are associated with an increased risk for cardiovascular disease (CVD) and mortality, while higher levels of leg fat are associated with a reduced risk for these conditions.

METHODOLOGY:

• People with T2D have a twofold to fourfold higher risk for CVD and mortality, and evidence shows obesity management helps delay complications and premature death, but an elevated body mass index (BMI) may be insufficient to measure obesity.
• In the “obesity paradox,” people with elevated BMI may have a lower CVD risk than people of normal weight.
• Researchers prospectively investigated how regional body fat accumulation was associated with CVD risk in 21,472 people with T2D (mean age, 58.9 years; 60.7% men; BMI about 29-33) from the UK Biobank (2006-2010), followed up for a median of 7.7 years.
• The regional body fat distribution in arms, trunk, and legs was assessed using bioelectrical impedance analysis.
• The primary outcomes were the incidence of CVD, all-cause mortality, and CVD mortality.

TAKEAWAY:

• Participants in the highest quartile of arm fat percentage (multivariate-adjusted hazard ratio [HR], 1.63; 95% CI, 1.29-2.05) and trunk fat percentage (HR, 1.27; 95% CI, 1.06-1.52) were at a higher risk for CVD than those in the lowest quartile.
• However, participants in the highest quartile of leg fat percentage had a lower risk for CVD than those in the lowest quartile (HR, 0.72; 95% CI, 0.58-0.90).
• A nonlinear relationship was observed between higher leg fat percentage and lower CVD risk and between higher trunk fat percentage and higher CVD risk, whereas a linear relationship was noted between higher arm fat percentage and higher CVD risk.
• The patterns of association were similar for both all-cause mortality and CVD mortality. Overall patterns were similar for men and women.

IN PRACTICE:

“Our findings add to the understanding of body fat distribution in patients with T2D, which highlights the importance of considering both the amount and the location of body fat when assessing CVD and mortality risk among patients with T2D,” wrote the authors.

SOURCE:

The study led by Zixin Qiu, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China, was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

As body fat was measured only once at the beginning of the study, its changing association over time could not be assessed. Moreover, the findings were primarily based on predominantly White UK adults, potentially restricting their generalizability to other population groups. Furthermore, diabetes was diagnosed using self-reported medical history, medication, and hemoglobin A1c levels, implying that some cases may have gone undetected at baseline. 

DISCLOSURES:

This study was funded by grants from the National Natural Science Foundation of China, Hubei Province Science Fund for Distinguished Young Scholars, and Fundamental Research Funds for the Central Universities. The authors declared no conflicts of interest.

A version of this article appeared on Medscape.com.

ATLANTA — Patients with acute coronary syndrome (ACS) who had a myocardial infarction or unstable angina and underwent percutaneous coronary intervention (PCI) had a 76% lower rate of hospital readmission after 6 months if they participated in a remote monitoring protocol compared with similar patients who had standard post-discharge care, results of a new trial suggest.

The TELE-ACS trial showed that at 6 months, telemedicine patients also had statistically significantly lower rates of post-discharge emergency department visits, unplanned coronary revascularizations, and cardiovascular symptoms, such as chest pain, shortness of breath and dizziness. However, the rates of major adverse cardiovascular events (MACE) were similar between the two groups. The protocol included consultation with a cardiologist who reviewed home-monitoring data.

“The team was able to aid in preventing unnecessary presentations and advised the patients to seek emergency care whenever was necessary,” Nasser Alshahrani, MSc, a clinical research fellow at Imperial College London, said while presenting the results at the American College of Cardiology meeting. “The TELE-ACS protocol provided a significant reduction in readmission rates post-ACS and other adverse events.” 

The study findings were published online simultaneously in the Journal of the American College of Cardiology.
 

Telemedicine Protocol

The trial, conducted from January 2022 to April 2023, randomly assigned 337 patients to telemedicine or standard care when they were discharged after PCI and had at least one cardiovascular risk factor. The telemedicine protocol consisted of 12-lead electrocardiogram belt, an automated blood-pressure monitor, and a pulse oximeter. 

Patients in the telemedicine arm initiated the remote monitoring protocol if they thought they had cardiac symptoms. The majority (86%) were men with what the study described as “a high preponderance of cardiovascular risk factors.” Average age was 58.1 years. 

If a telemedicine patient initiated the protocol, a cardiologist remotely assessed the patient’s symptoms and channeled the patient to the appropriate care pathway, whether reassuring the patient or sending them to a primary care physician or emergency department, or to call emergency services. Patients who didn’t get a call back from the cardiologist within 15 minutes were told to seek care in the standard clinical pathway.

Telemedicine patients were given the telemonitoring package and training in how to use the devices before they were discharged. They also received three follow-up quality control calls in the first two months to ensure they were using the equipment correctly. They kept the telemonitoring equipment for 8 months, but were followed out to 9 months. Six telemedicine patients dropped out while one standard care patient withdrew from the study.

Results showed that at 6 months, telemedicine patients had statistically significantly lower rates of post-discharge emergency department visits (25% vs 37%, P < .001), unplanned coronary revascularizations (3% vs 9%, P < .01) and cardiovascular symptoms, such as chest pain, shortness of breath and dizziness (a 13% to 18% difference for each symptom, P < .01).

MACE rates were similar between the two groups.

At 9 months, 3 months after the protocol ended, 20 telemedicine patients and 50 standard-care patients were readmitted to the hospital, while 52 and 73, respectively, went to the emergency department.

The telemedicine patients also had shorter hospital stays: an average of 0.5 and 1.2 days at 6 and 9 months, respectively, vs 1.5 and 1.8 days in the standard treatment arm (P < .001 for both).

Mr. Alshahrani noted several limitations with the study, namely that 86% of participants were men, and that the intervention was only offered to people who had smartphones. “The high level of support for the telemedicine group, with prompt cardiology responses, may be challenging to replicate outside a trial setting, requiring significant investment and training,” he added.
 

Human Element Key

In an interview from London after the presentation, lead author Ramzi Khamis, MB ChB, PhD, said, “This was quite a basic study. Really what we did was we integrated a clinical decision-making algorithm that we perfected with some quite novel but basic technology.” Future research should strive to add a home troponin test to the protocol and an artificial intelligence component, he said.

However, Dr. Khamis noted that human interaction was key to the success of the TELE-ACS trial. “The human factor is very important here and I think it would be really interesting to have a head-to-head comparison of human interaction with remote monitoring vs an AI-driven interaction,” he said. “I have my doubts that AI would be able to beat the human factor here.”

Lawrence Phillips, MD, medical director of outpatient cardiology at NYU Langone Heart, told this news organization that the study was appropriately powered to evaluate the telemedicine protocol, and that it could serve as a template for other studies of remote monitoring in cardiology. 

“I think that this study is forming the foundation of evolving telemedicine data,” he said. “It shows really interesting results, and I’m sure it’s going to be reproduced in different ways going forward.”

While other studies have shown the utility of telemedicine to decrease unnecessary hospitalizations, this study went one step further, Dr. Phillips said. “What was unique about this study was the package that they put together,” he added. “It was a combination of telehealth and being able to speak with someone when you have concerns with objective data of an electrocardiogram, blood-pressure cuff, and oxygen level assessment, which is an interesting approach having that ejective data with [a] subjective element.”

The trial received funding from the British Heart Foundation; King Khalid University, Abha, Saudi Arabia via The Saudi Arabian Cultural Bureau; Sansour Fund, Imperial Healthcare Charity; and Safwan Sobhan Fund at Imperial College London. Mr. Alshahrani and Dr. Khamis have no relevant relationships to disclose. Dr. Phillips has no relevant disclosures.

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

ATLANTA — Patients with acute coronary syndrome (ACS) who had a myocardial infarction or unstable angina and underwent percutaneous coronary intervention (PCI) had a 76% lower rate of hospital readmission after 6 months if they participated in a remote monitoring protocol compared with similar patients who had standard post-discharge care, results of a new trial suggest.

The TELE-ACS trial showed that at 6 months, telemedicine patients also had statistically significantly lower rates of post-discharge emergency department visits, unplanned coronary revascularizations, and cardiovascular symptoms, such as chest pain, shortness of breath and dizziness. However, the rates of major adverse cardiovascular events (MACE) were similar between the two groups. The protocol included consultation with a cardiologist who reviewed home-monitoring data.

“The team was able to aid in preventing unnecessary presentations and advised the patients to seek emergency care whenever was necessary,” Nasser Alshahrani, MSc, a clinical research fellow at Imperial College London, said while presenting the results at the American College of Cardiology meeting. “The TELE-ACS protocol provided a significant reduction in readmission rates post-ACS and other adverse events.” 

The study findings were published online simultaneously in the Journal of the American College of Cardiology.
 

Telemedicine Protocol

The trial, conducted from January 2022 to April 2023, randomly assigned 337 patients to telemedicine or standard care when they were discharged after PCI and had at least one cardiovascular risk factor. The telemedicine protocol consisted of 12-lead electrocardiogram belt, an automated blood-pressure monitor, and a pulse oximeter. 

Patients in the telemedicine arm initiated the remote monitoring protocol if they thought they had cardiac symptoms. The majority (86%) were men with what the study described as “a high preponderance of cardiovascular risk factors.” Average age was 58.1 years. 

If a telemedicine patient initiated the protocol, a cardiologist remotely assessed the patient’s symptoms and channeled the patient to the appropriate care pathway, whether reassuring the patient or sending them to a primary care physician or emergency department, or to call emergency services. Patients who didn’t get a call back from the cardiologist within 15 minutes were told to seek care in the standard clinical pathway.

Telemedicine patients were given the telemonitoring package and training in how to use the devices before they were discharged. They also received three follow-up quality control calls in the first two months to ensure they were using the equipment correctly. They kept the telemonitoring equipment for 8 months, but were followed out to 9 months. Six telemedicine patients dropped out while one standard care patient withdrew from the study.

Results showed that at 6 months, telemedicine patients had statistically significantly lower rates of post-discharge emergency department visits (25% vs 37%, P < .001), unplanned coronary revascularizations (3% vs 9%, P < .01) and cardiovascular symptoms, such as chest pain, shortness of breath and dizziness (a 13% to 18% difference for each symptom, P < .01).

MACE rates were similar between the two groups.

At 9 months, 3 months after the protocol ended, 20 telemedicine patients and 50 standard-care patients were readmitted to the hospital, while 52 and 73, respectively, went to the emergency department.

The telemedicine patients also had shorter hospital stays: an average of 0.5 and 1.2 days at 6 and 9 months, respectively, vs 1.5 and 1.8 days in the standard treatment arm (P < .001 for both).

Mr. Alshahrani noted several limitations with the study, namely that 86% of participants were men, and that the intervention was only offered to people who had smartphones. “The high level of support for the telemedicine group, with prompt cardiology responses, may be challenging to replicate outside a trial setting, requiring significant investment and training,” he added.
 

Human Element Key

In an interview from London after the presentation, lead author Ramzi Khamis, MB ChB, PhD, said, “This was quite a basic study. Really what we did was we integrated a clinical decision-making algorithm that we perfected with some quite novel but basic technology.” Future research should strive to add a home troponin test to the protocol and an artificial intelligence component, he said.

However, Dr. Khamis noted that human interaction was key to the success of the TELE-ACS trial. “The human factor is very important here and I think it would be really interesting to have a head-to-head comparison of human interaction with remote monitoring vs an AI-driven interaction,” he said. “I have my doubts that AI would be able to beat the human factor here.”

Lawrence Phillips, MD, medical director of outpatient cardiology at NYU Langone Heart, told this news organization that the study was appropriately powered to evaluate the telemedicine protocol, and that it could serve as a template for other studies of remote monitoring in cardiology. 

“I think that this study is forming the foundation of evolving telemedicine data,” he said. “It shows really interesting results, and I’m sure it’s going to be reproduced in different ways going forward.”

While other studies have shown the utility of telemedicine to decrease unnecessary hospitalizations, this study went one step further, Dr. Phillips said. “What was unique about this study was the package that they put together,” he added. “It was a combination of telehealth and being able to speak with someone when you have concerns with objective data of an electrocardiogram, blood-pressure cuff, and oxygen level assessment, which is an interesting approach having that ejective data with [a] subjective element.”

The trial received funding from the British Heart Foundation; King Khalid University, Abha, Saudi Arabia via The Saudi Arabian Cultural Bureau; Sansour Fund, Imperial Healthcare Charity; and Safwan Sobhan Fund at Imperial College London. Mr. Alshahrani and Dr. Khamis have no relevant relationships to disclose. Dr. Phillips has no relevant disclosures.

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

ATLANTA — Patients with acute coronary syndrome (ACS) who had a myocardial infarction or unstable angina and underwent percutaneous coronary intervention (PCI) had a 76% lower rate of hospital readmission after 6 months if they participated in a remote monitoring protocol compared with similar patients who had standard post-discharge care, results of a new trial suggest.

The TELE-ACS trial showed that at 6 months, telemedicine patients also had statistically significantly lower rates of post-discharge emergency department visits, unplanned coronary revascularizations, and cardiovascular symptoms, such as chest pain, shortness of breath and dizziness. However, the rates of major adverse cardiovascular events (MACE) were similar between the two groups. The protocol included consultation with a cardiologist who reviewed home-monitoring data.

“The team was able to aid in preventing unnecessary presentations and advised the patients to seek emergency care whenever was necessary,” Nasser Alshahrani, MSc, a clinical research fellow at Imperial College London, said while presenting the results at the American College of Cardiology meeting. “The TELE-ACS protocol provided a significant reduction in readmission rates post-ACS and other adverse events.” 

The study findings were published online simultaneously in the Journal of the American College of Cardiology.
 

Telemedicine Protocol

The trial, conducted from January 2022 to April 2023, randomly assigned 337 patients to telemedicine or standard care when they were discharged after PCI and had at least one cardiovascular risk factor. The telemedicine protocol consisted of 12-lead electrocardiogram belt, an automated blood-pressure monitor, and a pulse oximeter. 

Patients in the telemedicine arm initiated the remote monitoring protocol if they thought they had cardiac symptoms. The majority (86%) were men with what the study described as “a high preponderance of cardiovascular risk factors.” Average age was 58.1 years. 

If a telemedicine patient initiated the protocol, a cardiologist remotely assessed the patient’s symptoms and channeled the patient to the appropriate care pathway, whether reassuring the patient or sending them to a primary care physician or emergency department, or to call emergency services. Patients who didn’t get a call back from the cardiologist within 15 minutes were told to seek care in the standard clinical pathway.

Telemedicine patients were given the telemonitoring package and training in how to use the devices before they were discharged. They also received three follow-up quality control calls in the first two months to ensure they were using the equipment correctly. They kept the telemonitoring equipment for 8 months, but were followed out to 9 months. Six telemedicine patients dropped out while one standard care patient withdrew from the study.

Results showed that at 6 months, telemedicine patients had statistically significantly lower rates of post-discharge emergency department visits (25% vs 37%, P < .001), unplanned coronary revascularizations (3% vs 9%, P < .01) and cardiovascular symptoms, such as chest pain, shortness of breath and dizziness (a 13% to 18% difference for each symptom, P < .01).

MACE rates were similar between the two groups.

At 9 months, 3 months after the protocol ended, 20 telemedicine patients and 50 standard-care patients were readmitted to the hospital, while 52 and 73, respectively, went to the emergency department.

The telemedicine patients also had shorter hospital stays: an average of 0.5 and 1.2 days at 6 and 9 months, respectively, vs 1.5 and 1.8 days in the standard treatment arm (P < .001 for both).

Mr. Alshahrani noted several limitations with the study, namely that 86% of participants were men, and that the intervention was only offered to people who had smartphones. “The high level of support for the telemedicine group, with prompt cardiology responses, may be challenging to replicate outside a trial setting, requiring significant investment and training,” he added.
 

Human Element Key

In an interview from London after the presentation, lead author Ramzi Khamis, MB ChB, PhD, said, “This was quite a basic study. Really what we did was we integrated a clinical decision-making algorithm that we perfected with some quite novel but basic technology.” Future research should strive to add a home troponin test to the protocol and an artificial intelligence component, he said.

However, Dr. Khamis noted that human interaction was key to the success of the TELE-ACS trial. “The human factor is very important here and I think it would be really interesting to have a head-to-head comparison of human interaction with remote monitoring vs an AI-driven interaction,” he said. “I have my doubts that AI would be able to beat the human factor here.”

Lawrence Phillips, MD, medical director of outpatient cardiology at NYU Langone Heart, told this news organization that the study was appropriately powered to evaluate the telemedicine protocol, and that it could serve as a template for other studies of remote monitoring in cardiology. 

“I think that this study is forming the foundation of evolving telemedicine data,” he said. “It shows really interesting results, and I’m sure it’s going to be reproduced in different ways going forward.”

While other studies have shown the utility of telemedicine to decrease unnecessary hospitalizations, this study went one step further, Dr. Phillips said. “What was unique about this study was the package that they put together,” he added. “It was a combination of telehealth and being able to speak with someone when you have concerns with objective data of an electrocardiogram, blood-pressure cuff, and oxygen level assessment, which is an interesting approach having that ejective data with [a] subjective element.”

The trial received funding from the British Heart Foundation; King Khalid University, Abha, Saudi Arabia via The Saudi Arabian Cultural Bureau; Sansour Fund, Imperial Healthcare Charity; and Safwan Sobhan Fund at Imperial College London. Mr. Alshahrani and Dr. Khamis have no relevant relationships to disclose. Dr. Phillips has no relevant disclosures.

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

Little blue pill meets a little blue light.

A digital application can improve erectile function, according to new research presented at the European Association of Urology (EAU) Annual Congress on April 8, 2024.

Researchers developed a 12-week, self-managed program to treat erectile dysfunction (ED). The program is delivered to patients’ mobile devices and encourages users to do cardiovascular training, pelvic floor exercises, and physiotherapy. It also provides information about ED, sexual therapy, and stress management.

“The treatment of ED through physical activity and/or lifestyle changes is recommended in current European guidelines but is not well established in clinical practice,” according to the researchers.

App or Waitlist

The app, known as Kranus Edera, was created by Kranus Health. It is available by prescription in Germany and France.

To study the effectiveness of the app, investigators conducted a randomized controlled trial at the University Hospital Münster in Germany.

The study included 241 men who had scores of 21 or less on the International Index of Erectile Function (IIEF-5).

About half of the participants were randomly assigned to get the app. The rest were placed on a waiting list for the technology and served as a control group.

After 12 weeks, those who received the app reported significantly greater improvement on the IIEF-5, with a gain of 4.5 points vs a 0.2-point improvement for men in the control group (P < .0001).

Men who received the app also reported gains in measures of quality of life (20.5 vs −0.04) and patient activation (11.1 vs 0.64).

Nearly nine in 10 people who used the app did so several times per week, the researchers reported.

Sabine Kliesch, MD, with University Hospital Münster, led the study, which was presented at a poster session on April 8 at the EAU Congress in Paris.

Fully Reimbursed in Germany

In Germany, Kranus Edera has been included on a government list of digital health apps that are fully reimbursed by insurers, partly based on the results of the clinical trial. The cost there is €235 (about $255).

Patients typically notice improvements in 2-4 weeks, according to the company’s website. Patients who are taking a phosphodiesterase-5 enzyme inhibitor for ED may continue taking the medication, although they may no longer need it or they may be able to reduce the dose after treatment with the app, it says.

Kranus also has virtual treatments for incontinence in women and voiding dysfunction.

The app is meant to save doctors time by providing patients with detailed explanations and guidance within the app itself, said Laura Wiemer, MD, senior medical director of Kranus.

The app’s modules help reinforce guideline-recommended approaches to the treatment of ED “in playful ways with awards, motivational messages, and individual adjustments to help achieve better adherence and compliance of the patient,” Dr. Wiemer told this news organization.

Kranus plans to expand to the United States in 2024, she said.

A version of this article appeared on Medscape.com.

Little blue pill meets a little blue light.

A digital application can improve erectile function, according to new research presented at the European Association of Urology (EAU) Annual Congress on April 8, 2024.

Researchers developed a 12-week, self-managed program to treat erectile dysfunction (ED). The program is delivered to patients’ mobile devices and encourages users to do cardiovascular training, pelvic floor exercises, and physiotherapy. It also provides information about ED, sexual therapy, and stress management.

“The treatment of ED through physical activity and/or lifestyle changes is recommended in current European guidelines but is not well established in clinical practice,” according to the researchers.

App or Waitlist

The app, known as Kranus Edera, was created by Kranus Health. It is available by prescription in Germany and France.

To study the effectiveness of the app, investigators conducted a randomized controlled trial at the University Hospital Münster in Germany.

The study included 241 men who had scores of 21 or less on the International Index of Erectile Function (IIEF-5).

About half of the participants were randomly assigned to get the app. The rest were placed on a waiting list for the technology and served as a control group.

After 12 weeks, those who received the app reported significantly greater improvement on the IIEF-5, with a gain of 4.5 points vs a 0.2-point improvement for men in the control group (P < .0001).

Men who received the app also reported gains in measures of quality of life (20.5 vs −0.04) and patient activation (11.1 vs 0.64).

Nearly nine in 10 people who used the app did so several times per week, the researchers reported.

Sabine Kliesch, MD, with University Hospital Münster, led the study, which was presented at a poster session on April 8 at the EAU Congress in Paris.

Fully Reimbursed in Germany

In Germany, Kranus Edera has been included on a government list of digital health apps that are fully reimbursed by insurers, partly based on the results of the clinical trial. The cost there is €235 (about $255).

Patients typically notice improvements in 2-4 weeks, according to the company’s website. Patients who are taking a phosphodiesterase-5 enzyme inhibitor for ED may continue taking the medication, although they may no longer need it or they may be able to reduce the dose after treatment with the app, it says.

Kranus also has virtual treatments for incontinence in women and voiding dysfunction.

The app is meant to save doctors time by providing patients with detailed explanations and guidance within the app itself, said Laura Wiemer, MD, senior medical director of Kranus.

The app’s modules help reinforce guideline-recommended approaches to the treatment of ED “in playful ways with awards, motivational messages, and individual adjustments to help achieve better adherence and compliance of the patient,” Dr. Wiemer told this news organization.

Kranus plans to expand to the United States in 2024, she said.

A version of this article appeared on Medscape.com.

Little blue pill meets a little blue light.

A digital application can improve erectile function, according to new research presented at the European Association of Urology (EAU) Annual Congress on April 8, 2024.

Researchers developed a 12-week, self-managed program to treat erectile dysfunction (ED). The program is delivered to patients’ mobile devices and encourages users to do cardiovascular training, pelvic floor exercises, and physiotherapy. It also provides information about ED, sexual therapy, and stress management.

“The treatment of ED through physical activity and/or lifestyle changes is recommended in current European guidelines but is not well established in clinical practice,” according to the researchers.

App or Waitlist

The app, known as Kranus Edera, was created by Kranus Health. It is available by prescription in Germany and France.

To study the effectiveness of the app, investigators conducted a randomized controlled trial at the University Hospital Münster in Germany.

The study included 241 men who had scores of 21 or less on the International Index of Erectile Function (IIEF-5).

About half of the participants were randomly assigned to get the app. The rest were placed on a waiting list for the technology and served as a control group.

After 12 weeks, those who received the app reported significantly greater improvement on the IIEF-5, with a gain of 4.5 points vs a 0.2-point improvement for men in the control group (P < .0001).

Men who received the app also reported gains in measures of quality of life (20.5 vs −0.04) and patient activation (11.1 vs 0.64).

Nearly nine in 10 people who used the app did so several times per week, the researchers reported.

Sabine Kliesch, MD, with University Hospital Münster, led the study, which was presented at a poster session on April 8 at the EAU Congress in Paris.

Fully Reimbursed in Germany

In Germany, Kranus Edera has been included on a government list of digital health apps that are fully reimbursed by insurers, partly based on the results of the clinical trial. The cost there is €235 (about $255).

Patients typically notice improvements in 2-4 weeks, according to the company’s website. Patients who are taking a phosphodiesterase-5 enzyme inhibitor for ED may continue taking the medication, although they may no longer need it or they may be able to reduce the dose after treatment with the app, it says.

Kranus also has virtual treatments for incontinence in women and voiding dysfunction.

The app is meant to save doctors time by providing patients with detailed explanations and guidance within the app itself, said Laura Wiemer, MD, senior medical director of Kranus.

The app’s modules help reinforce guideline-recommended approaches to the treatment of ED “in playful ways with awards, motivational messages, and individual adjustments to help achieve better adherence and compliance of the patient,” Dr. Wiemer told this news organization.

Kranus plans to expand to the United States in 2024, she said.

A version of this article appeared on Medscape.com.

Among adults with type 2 diabetes (T2D) older than 65 years, a body mass index (BMI) in the moderate overweight category (26-28) appears to offer better protection from cardiovascular death than does a BMI in the “normal” range, new data suggested.

On the other hand, the study findings also suggest that the “normal” range of 23-25 is optimal for middle-aged adults with T2D.

The findings reflect a previously demonstrated phenomenon called the “obesity paradox,” in which older people with overweight may have better outcomes than leaner people due to factors such as bone loss, frailty, and nutritional deficits, study lead author Shaoyong Xu, of Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, China, told this news organization.

“In this era of population growth and aging, the question arises as to whether obesity or overweight can be beneficial in improving survival rates for older individuals with diabetes. This topic holds significant relevance due to the potential implications it has on weight management strategies for older adults. If overweight does not pose an increased risk of cardiovascular mortality, it may suggest that older individuals are not necessarily required to strive for weight loss to achieve so-called normal values.”

Moreover, Dr. Xu added, “inappropriate weight loss and being underweight could potentially elevate the risk of cardiovascular events, myocardial infarction, cerebral infarction, and all-cause mortality.”

Thus, he said, “while there are general guidelines recommending a BMI below 25, our findings suggest that personalized BMI targets may be more beneficial, particularly for different age groups and individuals with specific health conditions.”

Asked to comment, Ian J. Neeland, MD, director of cardiovascular prevention, University Hospitals Harrington Heart & Vascular Institute, Case Western Reserve University, Cleveland, Ohio, pointed out that older people who are underweight or in lower weight categories may be more likely to smoke or have undiagnosed cancer, or that “their BMI is not so much reflective of fat mass as of low muscle mass, or sarcopenia, and that is definitely a risk factor for adverse outcomes and risks. ... And those who have slightly higher BMIs may be maintaining muscle mass, even though they’re older, and therefore they have less risk.”

However, Dr. Neeland disagreed with the authors’ conclusions regarding “optimal” BMI. “Just because you have different risk categories based on BMI doesn’t mean that’s ‘optimal’ BMI. The way I would interpret this paper is that there’s an association of mildly overweight with better outcomes in adults who are over 65 with type 2 diabetes. We need to try to understand the mechanisms underlying that observation.”

Dr. Neeland advised that for an older person with T2D who has low muscle mass and frailty, “I wouldn’t recommend necessarily targeted weight loss in that person. But I would potentially recommend weight loss in addition to resistance training, muscle building, and endurance training, and therefore reducing fat mass. The goal would be not so much weight loss but reduction of body fat and maintaining and improving muscle health.”
 

U-Shaped Relationship Found Between Age, BMI, and Cardiovascular Disease (CVD) Risk

The data come from the UK Biobank, a population-based prospective cohort study of adults in the United Kingdom. A total of 22,874 participants with baseline T2D were included in the current study. Baseline surveys were conducted between 2006 and 2010, and follow-up was a median of 12.52 years. During that time, 891 people died of CVD.

Hazard ratios were adjusted for baseline variables including age, sex, smoking history, alcohol consumption, level of physical exercise, and history of CVDs.

Compared with people with BMI a < 25 in the group who were aged 65 years or younger, those with a BMI of 25.0-29.9 had a 13% higher risk for cardiovascular death. However, among those older than 65 years, a BMI between 25.0 and 29.9 was associated with an 18% lower risk.

A U-shaped relationship was found between BMI and the risk for cardiovascular death, with an optimal BMI cutoff of 24.0 in the under-65 group and a 27.0 cutoff in the older group. Ranges of 23.0-25.0 in the under-65 group and 26.0-28 in the older group were associated with the lowest cardiovascular risk.

In contrast, there was a linear relationship between both waist circumference and waist-to-height ratio and the risk for cardiovascular death, making those more direct measures of adiposity, Dr. Xu told this news organization.

“For clinicians, our data underscores the importance of considering age when assessing BMI targets for cardiovascular health. Personalized treatment plans that account for age-specific BMI cutoffs and other risk factors may enhance patient outcomes and reduce CVD mortality,” Dr. Xu said.

However, he added, “while these findings suggest an optimal BMI range, it is crucial to acknowledge that these cutoff points may vary based on gender, race, and other factors. Our future studies will validate these findings in different populations and attempt to explain the mechanism by which the optimal nodal values exist in people with diabetes at different ages.”

Dr. Neeland cautioned, “I think more work needs to be done in terms of not just identifying the risk differences but understanding why and how to better risk stratify individuals and do personalized medicine. I think that’s important, but you have to have good data to support the strategies you’re going to use. These data are observational, and they’re a good start, but they wouldn’t directly impact practice at this point.”

The data will be presented at the European Congress on Obesity taking place May 12-15 in Venice, Italy.

The authors declared no competing interests. Study funding came from several sources, including the Young Talents Project of Hubei Provincial Health Commission, China, Hubei Provincial Natural Science Foundation of China, the Science and Technology Research Key Project of the Education Department of Hubei Province China, and the Sanuo Diabetes Charity Foundation, China, and the Xiangyang Science and Technology Plan Project, China. Dr. Neeland is a speaker and/or consultant for Boehringer Ingelheim, Novo Nordisk, Bayer, and Eli Lilly and Company.
 

A version of this article appeared on Medscape.com.

Among adults with type 2 diabetes (T2D) older than 65 years, a body mass index (BMI) in the moderate overweight category (26-28) appears to offer better protection from cardiovascular death than does a BMI in the “normal” range, new data suggested.

On the other hand, the study findings also suggest that the “normal” range of 23-25 is optimal for middle-aged adults with T2D.

The findings reflect a previously demonstrated phenomenon called the “obesity paradox,” in which older people with overweight may have better outcomes than leaner people due to factors such as bone loss, frailty, and nutritional deficits, study lead author Shaoyong Xu, of Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, China, told this news organization.

“In this era of population growth and aging, the question arises as to whether obesity or overweight can be beneficial in improving survival rates for older individuals with diabetes. This topic holds significant relevance due to the potential implications it has on weight management strategies for older adults. If overweight does not pose an increased risk of cardiovascular mortality, it may suggest that older individuals are not necessarily required to strive for weight loss to achieve so-called normal values.”

Moreover, Dr. Xu added, “inappropriate weight loss and being underweight could potentially elevate the risk of cardiovascular events, myocardial infarction, cerebral infarction, and all-cause mortality.”

Thus, he said, “while there are general guidelines recommending a BMI below 25, our findings suggest that personalized BMI targets may be more beneficial, particularly for different age groups and individuals with specific health conditions.”

Asked to comment, Ian J. Neeland, MD, director of cardiovascular prevention, University Hospitals Harrington Heart & Vascular Institute, Case Western Reserve University, Cleveland, Ohio, pointed out that older people who are underweight or in lower weight categories may be more likely to smoke or have undiagnosed cancer, or that “their BMI is not so much reflective of fat mass as of low muscle mass, or sarcopenia, and that is definitely a risk factor for adverse outcomes and risks. ... And those who have slightly higher BMIs may be maintaining muscle mass, even though they’re older, and therefore they have less risk.”

However, Dr. Neeland disagreed with the authors’ conclusions regarding “optimal” BMI. “Just because you have different risk categories based on BMI doesn’t mean that’s ‘optimal’ BMI. The way I would interpret this paper is that there’s an association of mildly overweight with better outcomes in adults who are over 65 with type 2 diabetes. We need to try to understand the mechanisms underlying that observation.”

Dr. Neeland advised that for an older person with T2D who has low muscle mass and frailty, “I wouldn’t recommend necessarily targeted weight loss in that person. But I would potentially recommend weight loss in addition to resistance training, muscle building, and endurance training, and therefore reducing fat mass. The goal would be not so much weight loss but reduction of body fat and maintaining and improving muscle health.”
 

U-Shaped Relationship Found Between Age, BMI, and Cardiovascular Disease (CVD) Risk

The data come from the UK Biobank, a population-based prospective cohort study of adults in the United Kingdom. A total of 22,874 participants with baseline T2D were included in the current study. Baseline surveys were conducted between 2006 and 2010, and follow-up was a median of 12.52 years. During that time, 891 people died of CVD.

Hazard ratios were adjusted for baseline variables including age, sex, smoking history, alcohol consumption, level of physical exercise, and history of CVDs.

Compared with people with BMI a < 25 in the group who were aged 65 years or younger, those with a BMI of 25.0-29.9 had a 13% higher risk for cardiovascular death. However, among those older than 65 years, a BMI between 25.0 and 29.9 was associated with an 18% lower risk.

A U-shaped relationship was found between BMI and the risk for cardiovascular death, with an optimal BMI cutoff of 24.0 in the under-65 group and a 27.0 cutoff in the older group. Ranges of 23.0-25.0 in the under-65 group and 26.0-28 in the older group were associated with the lowest cardiovascular risk.

In contrast, there was a linear relationship between both waist circumference and waist-to-height ratio and the risk for cardiovascular death, making those more direct measures of adiposity, Dr. Xu told this news organization.

“For clinicians, our data underscores the importance of considering age when assessing BMI targets for cardiovascular health. Personalized treatment plans that account for age-specific BMI cutoffs and other risk factors may enhance patient outcomes and reduce CVD mortality,” Dr. Xu said.

However, he added, “while these findings suggest an optimal BMI range, it is crucial to acknowledge that these cutoff points may vary based on gender, race, and other factors. Our future studies will validate these findings in different populations and attempt to explain the mechanism by which the optimal nodal values exist in people with diabetes at different ages.”

Dr. Neeland cautioned, “I think more work needs to be done in terms of not just identifying the risk differences but understanding why and how to better risk stratify individuals and do personalized medicine. I think that’s important, but you have to have good data to support the strategies you’re going to use. These data are observational, and they’re a good start, but they wouldn’t directly impact practice at this point.”

The data will be presented at the European Congress on Obesity taking place May 12-15 in Venice, Italy.

The authors declared no competing interests. Study funding came from several sources, including the Young Talents Project of Hubei Provincial Health Commission, China, Hubei Provincial Natural Science Foundation of China, the Science and Technology Research Key Project of the Education Department of Hubei Province China, and the Sanuo Diabetes Charity Foundation, China, and the Xiangyang Science and Technology Plan Project, China. Dr. Neeland is a speaker and/or consultant for Boehringer Ingelheim, Novo Nordisk, Bayer, and Eli Lilly and Company.
 

A version of this article appeared on Medscape.com.

Among adults with type 2 diabetes (T2D) older than 65 years, a body mass index (BMI) in the moderate overweight category (26-28) appears to offer better protection from cardiovascular death than does a BMI in the “normal” range, new data suggested.

On the other hand, the study findings also suggest that the “normal” range of 23-25 is optimal for middle-aged adults with T2D.

The findings reflect a previously demonstrated phenomenon called the “obesity paradox,” in which older people with overweight may have better outcomes than leaner people due to factors such as bone loss, frailty, and nutritional deficits, study lead author Shaoyong Xu, of Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, China, told this news organization.

“In this era of population growth and aging, the question arises as to whether obesity or overweight can be beneficial in improving survival rates for older individuals with diabetes. This topic holds significant relevance due to the potential implications it has on weight management strategies for older adults. If overweight does not pose an increased risk of cardiovascular mortality, it may suggest that older individuals are not necessarily required to strive for weight loss to achieve so-called normal values.”

Moreover, Dr. Xu added, “inappropriate weight loss and being underweight could potentially elevate the risk of cardiovascular events, myocardial infarction, cerebral infarction, and all-cause mortality.”

Thus, he said, “while there are general guidelines recommending a BMI below 25, our findings suggest that personalized BMI targets may be more beneficial, particularly for different age groups and individuals with specific health conditions.”

Asked to comment, Ian J. Neeland, MD, director of cardiovascular prevention, University Hospitals Harrington Heart & Vascular Institute, Case Western Reserve University, Cleveland, Ohio, pointed out that older people who are underweight or in lower weight categories may be more likely to smoke or have undiagnosed cancer, or that “their BMI is not so much reflective of fat mass as of low muscle mass, or sarcopenia, and that is definitely a risk factor for adverse outcomes and risks. ... And those who have slightly higher BMIs may be maintaining muscle mass, even though they’re older, and therefore they have less risk.”

However, Dr. Neeland disagreed with the authors’ conclusions regarding “optimal” BMI. “Just because you have different risk categories based on BMI doesn’t mean that’s ‘optimal’ BMI. The way I would interpret this paper is that there’s an association of mildly overweight with better outcomes in adults who are over 65 with type 2 diabetes. We need to try to understand the mechanisms underlying that observation.”

Dr. Neeland advised that for an older person with T2D who has low muscle mass and frailty, “I wouldn’t recommend necessarily targeted weight loss in that person. But I would potentially recommend weight loss in addition to resistance training, muscle building, and endurance training, and therefore reducing fat mass. The goal would be not so much weight loss but reduction of body fat and maintaining and improving muscle health.”
 

U-Shaped Relationship Found Between Age, BMI, and Cardiovascular Disease (CVD) Risk

The data come from the UK Biobank, a population-based prospective cohort study of adults in the United Kingdom. A total of 22,874 participants with baseline T2D were included in the current study. Baseline surveys were conducted between 2006 and 2010, and follow-up was a median of 12.52 years. During that time, 891 people died of CVD.

Hazard ratios were adjusted for baseline variables including age, sex, smoking history, alcohol consumption, level of physical exercise, and history of CVDs.

Compared with people with BMI a < 25 in the group who were aged 65 years or younger, those with a BMI of 25.0-29.9 had a 13% higher risk for cardiovascular death. However, among those older than 65 years, a BMI between 25.0 and 29.9 was associated with an 18% lower risk.

A U-shaped relationship was found between BMI and the risk for cardiovascular death, with an optimal BMI cutoff of 24.0 in the under-65 group and a 27.0 cutoff in the older group. Ranges of 23.0-25.0 in the under-65 group and 26.0-28 in the older group were associated with the lowest cardiovascular risk.

In contrast, there was a linear relationship between both waist circumference and waist-to-height ratio and the risk for cardiovascular death, making those more direct measures of adiposity, Dr. Xu told this news organization.

“For clinicians, our data underscores the importance of considering age when assessing BMI targets for cardiovascular health. Personalized treatment plans that account for age-specific BMI cutoffs and other risk factors may enhance patient outcomes and reduce CVD mortality,” Dr. Xu said.

However, he added, “while these findings suggest an optimal BMI range, it is crucial to acknowledge that these cutoff points may vary based on gender, race, and other factors. Our future studies will validate these findings in different populations and attempt to explain the mechanism by which the optimal nodal values exist in people with diabetes at different ages.”

Dr. Neeland cautioned, “I think more work needs to be done in terms of not just identifying the risk differences but understanding why and how to better risk stratify individuals and do personalized medicine. I think that’s important, but you have to have good data to support the strategies you’re going to use. These data are observational, and they’re a good start, but they wouldn’t directly impact practice at this point.”

The data will be presented at the European Congress on Obesity taking place May 12-15 in Venice, Italy.

The authors declared no competing interests. Study funding came from several sources, including the Young Talents Project of Hubei Provincial Health Commission, China, Hubei Provincial Natural Science Foundation of China, the Science and Technology Research Key Project of the Education Department of Hubei Province China, and the Sanuo Diabetes Charity Foundation, China, and the Xiangyang Science and Technology Plan Project, China. Dr. Neeland is a speaker and/or consultant for Boehringer Ingelheim, Novo Nordisk, Bayer, and Eli Lilly and Company.
 

A version of this article appeared on Medscape.com.

Nontraditional risk factors such as migraine and autoimmune diseases have a significantly greater effect on stroke risk in young adults than traditional risk factors such as hypertension, high cholesterol, and tobacco use, new research showed.

The findings may offer insight into the increased incidence of stroke in adults under age 45, which has more than doubled in the past 20 years in high-income countries, while incidence in those over 45 has decreased.

Investigators believe the findings are important because most conventional prevention efforts focus on traditional risk factors.

“The younger they are at the time of stroke, the more likely their stroke is due to a nontraditional risk factor,” lead author Michelle Leppert, MD, an assistant professor of neurology at the University of Colorado School of Medicine, Aurora, Colorado, said in a news release.

The findings were published online in Circulation: Cardiovascular Quality and Outcomes.
 

Traditional Versus Nontraditional

The researchers retrospectively analyzed 2618 stroke cases (52% female; 73% ischemic stroke) that resulted in an inpatient admission and 7827 controls, all aged 18-55 years. Data came from the Colorado All Payer Claims Database between January 2012 and April 2019. Controls were matched by age, sex, and insurance type.

Traditional risk factors were defined as being a well-established risk factor for stroke that is routinely noted during stroke prevention screenings in older adults, including hypertension, diabetes, hyperlipidemia, sleep apnea, cardiovascular disease, alcohol, substance use disorder, and obesity.

Nontraditional risk factors were defined as those that are rarely cited as a cause of stroke in older adults, including migraines, malignancy, HIV, hepatitis, thrombophilia, autoimmune disease, vasculitis, sickle cell disease, heart valve disease, renal failure, and hormonal risk factors in women, such as oral contraceptives, pregnancy, or puerperium.

Overall, traditional risk factors were more common in stroke cases, with nontraditional factors playing a smaller role. However, among adults aged 18-34 years, more strokes were associated with nontraditional than traditional risk factors in men (31% vs 25%, respectively) and in women (43% vs 33%, respectively).

Migraine, the most common nontraditional risk factor for stroke in this younger age group, was found in 20% of men (odds ratio [OR], 3.9) and 35% of women (OR, 3.3).

Other notable nontraditional risk factors included heart valve disease in both men and women (OR, 3.1 and OR, 4.2, respectively); renal failure in men (OR, 8.9); and autoimmune diseases in women (OR, 8.8).
 

An Underestimate?

The contribution of nontraditional risk factors declined with age. After the age of 44, they were no longer significant. Hypertension was the most important traditional risk factor and increased in contribution with age.

“There have been many studies demonstrating the association between migraines and strokes, but to our knowledge, this study may be the first to demonstrate just how much stroke risk may be attributable to migraines,” Dr. Leppert said.

Overall, women had significantly more risk factors for stroke than men. Among controls, 52% and 34% of women had at least one traditional and nontraditional risk factors, respectively, compared with 48% and 22% in men.

The total contribution of nontraditional risk factors was likely an underestimate because some such factors, including the autoimmune disorder antiphospholipid syndrome and patent foramen ovale, “lacked reliable administrative algorithms” and could not be assessed in this study, the researchers noted.

Further research on how nontraditional risk factors affect strokes could lead to better prevention.

“We need to better understand the underlying mechanisms of these nontraditional risk factors to develop targeted interventions,” Dr. Leppert said.

The study was funded by the National Institutes of Health/National Center for Advancing Translational Sciences Colorado Clinical and Translational Science Award. Dr. Leppert reports receiving an American Heart Association Career Development Grant. Other disclosures are included in the original article.

A version of this article appeared on Medscape.com.

Nontraditional risk factors such as migraine and autoimmune diseases have a significantly greater effect on stroke risk in young adults than traditional risk factors such as hypertension, high cholesterol, and tobacco use, new research showed.

The findings may offer insight into the increased incidence of stroke in adults under age 45, which has more than doubled in the past 20 years in high-income countries, while incidence in those over 45 has decreased.

Investigators believe the findings are important because most conventional prevention efforts focus on traditional risk factors.

“The younger they are at the time of stroke, the more likely their stroke is due to a nontraditional risk factor,” lead author Michelle Leppert, MD, an assistant professor of neurology at the University of Colorado School of Medicine, Aurora, Colorado, said in a news release.

The findings were published online in Circulation: Cardiovascular Quality and Outcomes.
 

Traditional Versus Nontraditional

The researchers retrospectively analyzed 2618 stroke cases (52% female; 73% ischemic stroke) that resulted in an inpatient admission and 7827 controls, all aged 18-55 years. Data came from the Colorado All Payer Claims Database between January 2012 and April 2019. Controls were matched by age, sex, and insurance type.

Traditional risk factors were defined as being a well-established risk factor for stroke that is routinely noted during stroke prevention screenings in older adults, including hypertension, diabetes, hyperlipidemia, sleep apnea, cardiovascular disease, alcohol, substance use disorder, and obesity.

Nontraditional risk factors were defined as those that are rarely cited as a cause of stroke in older adults, including migraines, malignancy, HIV, hepatitis, thrombophilia, autoimmune disease, vasculitis, sickle cell disease, heart valve disease, renal failure, and hormonal risk factors in women, such as oral contraceptives, pregnancy, or puerperium.

Overall, traditional risk factors were more common in stroke cases, with nontraditional factors playing a smaller role. However, among adults aged 18-34 years, more strokes were associated with nontraditional than traditional risk factors in men (31% vs 25%, respectively) and in women (43% vs 33%, respectively).

Migraine, the most common nontraditional risk factor for stroke in this younger age group, was found in 20% of men (odds ratio [OR], 3.9) and 35% of women (OR, 3.3).

Other notable nontraditional risk factors included heart valve disease in both men and women (OR, 3.1 and OR, 4.2, respectively); renal failure in men (OR, 8.9); and autoimmune diseases in women (OR, 8.8).
 

An Underestimate?

The contribution of nontraditional risk factors declined with age. After the age of 44, they were no longer significant. Hypertension was the most important traditional risk factor and increased in contribution with age.

“There have been many studies demonstrating the association between migraines and strokes, but to our knowledge, this study may be the first to demonstrate just how much stroke risk may be attributable to migraines,” Dr. Leppert said.

Overall, women had significantly more risk factors for stroke than men. Among controls, 52% and 34% of women had at least one traditional and nontraditional risk factors, respectively, compared with 48% and 22% in men.

The total contribution of nontraditional risk factors was likely an underestimate because some such factors, including the autoimmune disorder antiphospholipid syndrome and patent foramen ovale, “lacked reliable administrative algorithms” and could not be assessed in this study, the researchers noted.

Further research on how nontraditional risk factors affect strokes could lead to better prevention.

“We need to better understand the underlying mechanisms of these nontraditional risk factors to develop targeted interventions,” Dr. Leppert said.

The study was funded by the National Institutes of Health/National Center for Advancing Translational Sciences Colorado Clinical and Translational Science Award. Dr. Leppert reports receiving an American Heart Association Career Development Grant. Other disclosures are included in the original article.

A version of this article appeared on Medscape.com.

Nontraditional risk factors such as migraine and autoimmune diseases have a significantly greater effect on stroke risk in young adults than traditional risk factors such as hypertension, high cholesterol, and tobacco use, new research showed.

The findings may offer insight into the increased incidence of stroke in adults under age 45, which has more than doubled in the past 20 years in high-income countries, while incidence in those over 45 has decreased.

Investigators believe the findings are important because most conventional prevention efforts focus on traditional risk factors.

“The younger they are at the time of stroke, the more likely their stroke is due to a nontraditional risk factor,” lead author Michelle Leppert, MD, an assistant professor of neurology at the University of Colorado School of Medicine, Aurora, Colorado, said in a news release.

The findings were published online in Circulation: Cardiovascular Quality and Outcomes.
 

Traditional Versus Nontraditional

The researchers retrospectively analyzed 2618 stroke cases (52% female; 73% ischemic stroke) that resulted in an inpatient admission and 7827 controls, all aged 18-55 years. Data came from the Colorado All Payer Claims Database between January 2012 and April 2019. Controls were matched by age, sex, and insurance type.

Traditional risk factors were defined as being a well-established risk factor for stroke that is routinely noted during stroke prevention screenings in older adults, including hypertension, diabetes, hyperlipidemia, sleep apnea, cardiovascular disease, alcohol, substance use disorder, and obesity.

Nontraditional risk factors were defined as those that are rarely cited as a cause of stroke in older adults, including migraines, malignancy, HIV, hepatitis, thrombophilia, autoimmune disease, vasculitis, sickle cell disease, heart valve disease, renal failure, and hormonal risk factors in women, such as oral contraceptives, pregnancy, or puerperium.

Overall, traditional risk factors were more common in stroke cases, with nontraditional factors playing a smaller role. However, among adults aged 18-34 years, more strokes were associated with nontraditional than traditional risk factors in men (31% vs 25%, respectively) and in women (43% vs 33%, respectively).

Migraine, the most common nontraditional risk factor for stroke in this younger age group, was found in 20% of men (odds ratio [OR], 3.9) and 35% of women (OR, 3.3).

Other notable nontraditional risk factors included heart valve disease in both men and women (OR, 3.1 and OR, 4.2, respectively); renal failure in men (OR, 8.9); and autoimmune diseases in women (OR, 8.8).
 

An Underestimate?

The contribution of nontraditional risk factors declined with age. After the age of 44, they were no longer significant. Hypertension was the most important traditional risk factor and increased in contribution with age.

“There have been many studies demonstrating the association between migraines and strokes, but to our knowledge, this study may be the first to demonstrate just how much stroke risk may be attributable to migraines,” Dr. Leppert said.

Overall, women had significantly more risk factors for stroke than men. Among controls, 52% and 34% of women had at least one traditional and nontraditional risk factors, respectively, compared with 48% and 22% in men.

The total contribution of nontraditional risk factors was likely an underestimate because some such factors, including the autoimmune disorder antiphospholipid syndrome and patent foramen ovale, “lacked reliable administrative algorithms” and could not be assessed in this study, the researchers noted.

Further research on how nontraditional risk factors affect strokes could lead to better prevention.

“We need to better understand the underlying mechanisms of these nontraditional risk factors to develop targeted interventions,” Dr. Leppert said.

The study was funded by the National Institutes of Health/National Center for Advancing Translational Sciences Colorado Clinical and Translational Science Award. Dr. Leppert reports receiving an American Heart Association Career Development Grant. Other disclosures are included in the original article.

A version of this article appeared on Medscape.com.

Genetic testing may be considered in patients with early-onset atrial fibrillation (AF), particularly those with a positive family history and lack of conventional clinical risk factors, because specific genetic variants may underlie AF as well as “potentially more sinister cardiac conditions,” a new white paper from the Canadian Cardiovascular Society suggested.

“Given the resources and logistical challenges potentially imposed by genetic testing (that is, the majority of cardiology and arrhythmia clinics are not presently equipped to offer it), we have not recommended routine genetic testing for early-onset AF patients at this time,” lead author Jason D. Roberts, MD, associate professor of medicine at McMaster University in Hamilton, Ontario, Canada, told this news organization.

“We do, however, recommend that early-onset AF patients undergo clinical screening for potential coexistence of a ventricular arrhythmia or cardiomyopathy syndrome through careful history, including family history, and physical examination, along with standard clinical testing, including ECG, echocardiogram, and Holter monitoring,” he said.

The white paper was published online in the Canadian Journal of Cardiology.

Routine Testing Unwarranted

The Canadian Cardiovascular Society reviewed AF research in 2022 and concluded that a guideline update was not yet warranted. One area meriting consideration but lacking sufficient evidence for a formal guideline was the clinical application of AF genetics.

Therefore, the society formed a writing group to assess the evidence linking genetic factors to AF, discuss an approach to using genetic testing for early-onset patients with AF, and consider the potential value of genetic testing in the foreseeable future.

The resulting white paper reviews familial and epidemiologic evidence for a genetic contribution to AF. As an example, the authors pointed to work from the Framingham Heart Study showing a statistically significant risk for AF among first-degree relatives of patients with AF. The overall odds ratio (OR) for AF among first-degree relatives was 1.85. But for first-degree relatives of patients with AF onset at younger than age 75 years, the OR increased to 3.23.

Other evidence included the identification of two rare genetic variants: KCNQ1 in a Chinese family and NPPA in a family with Northern European ancestry. In case-control studies, a single gene, titin (TTN), was linked to an increased burden of loss-of-function variants in patients with AF compared with controls. The variant was associated with a 2.2-fold increased risk for AF.

The two main classes of AF variants identified in candidate gene approaches were linked to ion channels and ventricular cardiomyopathy. For example, loss-of-function SCN5A variants are implicated in Brugada syndrome and cardiac conduction system disease, whereas gain-of-function variants cause long QT syndrome type 3 and multifocal ectopic Purkinje-related premature contractions. Each of these conditions was associated with an increased prevalence of AF.

Similarly, genes implicated in various other forms of ventricular channelopathies also have been implicated in AF, as have ion channels primarily expressed in the atria and not the ventricles, such as KCNA5 and GJA5.

Nevertheless, in most cases, AF is diagnosed in the context of older age and established cardiovascular risk factors, according to the authors. The contribution of genetic factors in this population is relatively low, highlighting the limited role for genetic testing when AF develops in the presence of multiple conventional clinical risk factors.

Cardiogenetic Expertise Required

“Although significant progress has been made, additional work is needed before [beginning] routine integration of clinical genetic testing for early-onset AF patients,” Dr. Roberts said. The ideal clinical genetic testing panel for AF is still unclear, and the inclusion of genes for which there is no strong evidence of involvement in AF “creates the potential for harm.”

Specifically, “a genetic variant could be incorrectly assigned as the cause of AF, which could create confusion for the patient and family members and lead to inappropriate clinical management,” said Dr. Roberts.

“Beyond cost, routine introduction of genetic testing for AF patients will require allocation of significant resources, given that interpretation of genetic testing results can be nuanced,” he noted. “This nuance is anticipated to be heightened in AF, given that many genetic variants have low-to-intermediate penetrance and can manifest with variable clinical phenotypes.”

“Traditionally, genetic testing has been performed and interpreted, and results communicated, by dedicated cardiogenetic clinics with specialized expertise,” he added. “Existing cardiogenetic clinics, however, are unlikely to be sufficient in number to accommodate the large volume of AF patients that may be eligible for testing.”

Careful Counseling

Jim W. Cheung, MD, chair of the American College of Cardiology Electrophysiology Council, told this news organization that the white paper is consistent with the latest European Heart Rhythm Association/Heart Rhythm Society/Asia Pacific Heart Rhythm Society/Latin American Heart Rhythm Society expert consensus statement published in 2022.

Overall, the approach suggested for genetic testing “is a sound one, but one that requires implementation by clinicians with access to cardiogenetic expertise,” said Cheung, who was not involved in the study. “Any patient undergoing genetic testing needs to be carefully counseled about the potential uncertainties associated with the actual test results and their implications on clinical management.”

Variants of uncertain significance that are detected with genetic testing “can be a source of stress for clinicians and patients,” he said. “Therefore, patient education prior to and after genetic testing is essential.”

Furthermore, he said, “in many patients with early-onset AF who harbor pathogenic variants, initial imaging studies may not detect any signs of cardiomyopathy. In these patients, regular follow-up to assess for development of cardiomyopathy in the future is necessary.”

The white paper was drafted without outside funding. Dr. Roberts and Dr. Cheung reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

Genetic testing may be considered in patients with early-onset atrial fibrillation (AF), particularly those with a positive family history and lack of conventional clinical risk factors, because specific genetic variants may underlie AF as well as “potentially more sinister cardiac conditions,” a new white paper from the Canadian Cardiovascular Society suggested.

“Given the resources and logistical challenges potentially imposed by genetic testing (that is, the majority of cardiology and arrhythmia clinics are not presently equipped to offer it), we have not recommended routine genetic testing for early-onset AF patients at this time,” lead author Jason D. Roberts, MD, associate professor of medicine at McMaster University in Hamilton, Ontario, Canada, told this news organization.

“We do, however, recommend that early-onset AF patients undergo clinical screening for potential coexistence of a ventricular arrhythmia or cardiomyopathy syndrome through careful history, including family history, and physical examination, along with standard clinical testing, including ECG, echocardiogram, and Holter monitoring,” he said.

The white paper was published online in the Canadian Journal of Cardiology.

Routine Testing Unwarranted

The Canadian Cardiovascular Society reviewed AF research in 2022 and concluded that a guideline update was not yet warranted. One area meriting consideration but lacking sufficient evidence for a formal guideline was the clinical application of AF genetics.

Therefore, the society formed a writing group to assess the evidence linking genetic factors to AF, discuss an approach to using genetic testing for early-onset patients with AF, and consider the potential value of genetic testing in the foreseeable future.

The resulting white paper reviews familial and epidemiologic evidence for a genetic contribution to AF. As an example, the authors pointed to work from the Framingham Heart Study showing a statistically significant risk for AF among first-degree relatives of patients with AF. The overall odds ratio (OR) for AF among first-degree relatives was 1.85. But for first-degree relatives of patients with AF onset at younger than age 75 years, the OR increased to 3.23.

Other evidence included the identification of two rare genetic variants: KCNQ1 in a Chinese family and NPPA in a family with Northern European ancestry. In case-control studies, a single gene, titin (TTN), was linked to an increased burden of loss-of-function variants in patients with AF compared with controls. The variant was associated with a 2.2-fold increased risk for AF.

The two main classes of AF variants identified in candidate gene approaches were linked to ion channels and ventricular cardiomyopathy. For example, loss-of-function SCN5A variants are implicated in Brugada syndrome and cardiac conduction system disease, whereas gain-of-function variants cause long QT syndrome type 3 and multifocal ectopic Purkinje-related premature contractions. Each of these conditions was associated with an increased prevalence of AF.

Similarly, genes implicated in various other forms of ventricular channelopathies also have been implicated in AF, as have ion channels primarily expressed in the atria and not the ventricles, such as KCNA5 and GJA5.

Nevertheless, in most cases, AF is diagnosed in the context of older age and established cardiovascular risk factors, according to the authors. The contribution of genetic factors in this population is relatively low, highlighting the limited role for genetic testing when AF develops in the presence of multiple conventional clinical risk factors.

Cardiogenetic Expertise Required

“Although significant progress has been made, additional work is needed before [beginning] routine integration of clinical genetic testing for early-onset AF patients,” Dr. Roberts said. The ideal clinical genetic testing panel for AF is still unclear, and the inclusion of genes for which there is no strong evidence of involvement in AF “creates the potential for harm.”

Specifically, “a genetic variant could be incorrectly assigned as the cause of AF, which could create confusion for the patient and family members and lead to inappropriate clinical management,” said Dr. Roberts.

“Beyond cost, routine introduction of genetic testing for AF patients will require allocation of significant resources, given that interpretation of genetic testing results can be nuanced,” he noted. “This nuance is anticipated to be heightened in AF, given that many genetic variants have low-to-intermediate penetrance and can manifest with variable clinical phenotypes.”

“Traditionally, genetic testing has been performed and interpreted, and results communicated, by dedicated cardiogenetic clinics with specialized expertise,” he added. “Existing cardiogenetic clinics, however, are unlikely to be sufficient in number to accommodate the large volume of AF patients that may be eligible for testing.”

Careful Counseling

Jim W. Cheung, MD, chair of the American College of Cardiology Electrophysiology Council, told this news organization that the white paper is consistent with the latest European Heart Rhythm Association/Heart Rhythm Society/Asia Pacific Heart Rhythm Society/Latin American Heart Rhythm Society expert consensus statement published in 2022.

Overall, the approach suggested for genetic testing “is a sound one, but one that requires implementation by clinicians with access to cardiogenetic expertise,” said Cheung, who was not involved in the study. “Any patient undergoing genetic testing needs to be carefully counseled about the potential uncertainties associated with the actual test results and their implications on clinical management.”

Variants of uncertain significance that are detected with genetic testing “can be a source of stress for clinicians and patients,” he said. “Therefore, patient education prior to and after genetic testing is essential.”

Furthermore, he said, “in many patients with early-onset AF who harbor pathogenic variants, initial imaging studies may not detect any signs of cardiomyopathy. In these patients, regular follow-up to assess for development of cardiomyopathy in the future is necessary.”

The white paper was drafted without outside funding. Dr. Roberts and Dr. Cheung reported no relevant financial relationships.

A version of this article appeared on Medscape.com.

Genetic testing may be considered in patients with early-onset atrial fibrillation (AF), particularly those with a positive family history and lack of conventional clinical risk factors, because specific genetic variants may underlie AF as well as “potentially more sinister cardiac conditions,” a new white paper from the Canadian Cardiovascular Society suggested.

“Given the resources and logistical challenges potentially imposed by genetic testing (that is, the majority of cardiology and arrhythmia clinics are not presently equipped to offer it), we have not recommended routine genetic testing for early-onset AF patients at this time,” lead author Jason D. Roberts, MD, associate professor of medicine at McMaster University in Hamilton, Ontario, Canada, told this news organization.

“We do, however, recommend that early-onset AF patients undergo clinical screening for potential coexistence of a ventricular arrhythmia or cardiomyopathy syndrome through careful history, including family history, and physical examination, along with standard clinical testing, including ECG, echocardiogram, and Holter monitoring,” he said.

The white paper was published online in the Canadian Journal of Cardiology.

Routine Testing Unwarranted

The Canadian Cardiovascular Society reviewed AF research in 2022 and concluded that a guideline update was not yet warranted. One area meriting consideration but lacking sufficient evidence for a formal guideline was the clinical application of AF genetics.

Therefore, the society formed a writing group to assess the evidence linking genetic factors to AF, discuss an approach to using genetic testing for early-onset patients with AF, and consider the potential value of genetic testing in the foreseeable future.

The resulting white paper reviews familial and epidemiologic evidence for a genetic contribution to AF. As an example, the authors pointed to work from the Framingham Heart Study showing a statistically significant risk for AF among first-degree relatives of patients with AF. The overall odds ratio (OR) for AF among first-degree relatives was 1.85. But for first-degree relatives of patients with AF onset at younger than age 75 years, the OR increased to 3.23.

Other evidence included the identification of two rare genetic variants: KCNQ1 in a Chinese family and NPPA in a family with Northern European ancestry. In case-control studies, a single gene, titin (TTN), was linked to an increased burden of loss-of-function variants in patients with AF compared with controls. The variant was associated with a 2.2-fold increased risk for AF.

The two main classes of AF variants identified in candidate gene approaches were linked to ion channels and ventricular cardiomyopathy. For example, loss-of-function SCN5A variants are implicated in Brugada syndrome and cardiac conduction system disease, whereas gain-of-function variants cause long QT syndrome type 3 and multifocal ectopic Purkinje-related premature contractions. Each of these conditions was associated with an increased prevalence of AF.

Similarly, genes implicated in various other forms of ventricular channelopathies also have been implicated in AF, as have ion channels primarily expressed in the atria and not the ventricles, such as KCNA5 and GJA5.

Nevertheless, in most cases, AF is diagnosed in the context of older age and established cardiovascular risk factors, according to the authors. The contribution of genetic factors in this population is relatively low, highlighting the limited role for genetic testing when AF develops in the presence of multiple conventional clinical risk factors.

Cardiogenetic Expertise Required

“Although significant progress has been made, additional work is needed before [beginning] routine integration of clinical genetic testing for early-onset AF patients,” Dr. Roberts said. The ideal clinical genetic testing panel for AF is still unclear, and the inclusion of genes for which there is no strong evidence of involvement in AF “creates the potential for harm.”

Specifically, “a genetic variant could be incorrectly assigned as the cause of AF, which could create confusion for the patient and family members and lead to inappropriate clinical management,” said Dr. Roberts.

“Beyond cost, routine introduction of genetic testing for AF patients will require allocation of significant resources, given that interpretation of genetic testing results can be nuanced,” he noted. “This nuance is anticipated to be heightened in AF, given that many genetic variants have low-to-intermediate penetrance and can manifest with variable clinical phenotypes.”

“Traditionally, genetic testing has been performed and interpreted, and results communicated, by dedicated cardiogenetic clinics with specialized expertise,” he added. “Existing cardiogenetic clinics, however, are unlikely to be sufficient in number to accommodate the large volume of AF patients that may be eligible for testing.”

Careful Counseling

Jim W. Cheung, MD, chair of the American College of Cardiology Electrophysiology Council, told this news organization that the white paper is consistent with the latest European Heart Rhythm Association/Heart Rhythm Society/Asia Pacific Heart Rhythm Society/Latin American Heart Rhythm Society expert consensus statement published in 2022.

Overall, the approach suggested for genetic testing “is a sound one, but one that requires implementation by clinicians with access to cardiogenetic expertise,” said Cheung, who was not involved in the study. “Any patient undergoing genetic testing needs to be carefully counseled about the potential uncertainties associated with the actual test results and their implications on clinical management.”

Variants of uncertain significance that are detected with genetic testing “can be a source of stress for clinicians and patients,” he said. “Therefore, patient education prior to and after genetic testing is essential.”

Furthermore, he said, “in many patients with early-onset AF who harbor pathogenic variants, initial imaging studies may not detect any signs of cardiomyopathy. In these patients, regular follow-up to assess for development of cardiomyopathy in the future is necessary.”

The white paper was drafted without outside funding. Dr. Roberts and Dr. Cheung reported no relevant financial relationships.

A version of this article appeared on Medscape.com.