Cardiology News

Sunday night. Las Vegas. Jason Aldean had just started playing.

My wife and I were at the 2017 Route 91 Harvest Festival with three other couples; two of them were our close friends. We were sitting in the VIP section, a tented area right next to the stage. We started hearing what I was convinced were fireworks.

I’ve been in the Army for 20 some years. I’ve been deployed and shot at multiple times. But these shots were far away. And you don’t expect people to be shooting at you at a concert.

I was on the edge of the VIP area, so I could see around the corner of the tent. I looked up at the Mandalay Bay and saw the muzzle flash in the hotel window. That’s when I knew.

I screamed: “Somebody’s shooting at us! Everybody get down!”

It took a while for people to realize what was going on. When the first couple volleys sprayed into the crowd, nobody understood. But once enough people had been hit and dropped, everyone knew, and it was just mass exodus.

People screamed and ran everywhere. Some of them tried to jump over the front barrier so they could get underneath the stage. Others were trying to pick up loved ones who’d been shot.

The next 15 minutes are a little foggy. I was helping my wife and the people around us to get down. Funny things come back to you afterward. One of my friends was carrying a 16-ounce beer in his hand. Somebody’s shooting at him and he’s walking around with his beer like he’s afraid to put it down. It was so surreal.

We got everybody underneath the tent, and then we just sat there. There would be shooting and then a pause. You’d think it was over. And then there would be more shooting and another pause. It felt like it never was going to stop.

After a short period of time, somebody came in with an official badge, maybe FBI, who knows. They said: “Okay, everybody up. We’ve got to get you out of here.” So, we all got up and headed across the stage. The gate they were taking us to was in full view of the shooter, so it wasn’t very safe.

As I got up, I looked out at the field. Bodies were scattered everywhere. I’m a trauma surgeon by trade. I couldn’t just leave.

I told my two best friends to take my wife with them. My wife lost her mind at that point. She didn’t want me to run out on the field. But I had to. I saw the injured and they needed help. Another buddy and I jumped over the fence and started taking care of people.

The feeling of being out on the field was one of complete frustration. I was in sandals, shorts, and a t-shirt. We had no stretchers, no medical supplies, no nothing. I didn’t have a belt to use as a tourniquet. I didn’t even have a bandage.

Worse: We were seeing high-velocity gunshot wounds that I’ve seen for 20 years in the Army. I know how to take care of them. I know how to fix them. But there wasn’t a single thing I could do.

We had to get people off the field, so we started gathering up as many as we could. We didn’t know if we were going to get shot at again, so we were trying to hide behind things as we ran. Our main objective was just to get people to a place of safety.

A lot of it is a blur. But a few patients stick out in my mind.

A father and son. The father had been shot through the abdomen, exited out through his back. He was in severe pain and couldn’t walk.

A young girl shot in the arm. Her parents carrying her.

A group of people doing CPR on a young lady. She had a gunshot wound to the head or neck. She was obviously dead. But they were still doing chest compressions in the middle of the field. I had to say to them: “She’s dead. You can’t save her. You need to get off the field.” But they wouldn’t stop. We picked her up and took her out while they continued to do CPR.

Later, I realized I knew that woman. She was part of a group of friends that we would see at the festival. I hadn’t recognized her. I also didn’t know that my friend Marco was there. A month or 2 later, we figured out that he was one of the people doing CPR. And I was the guy who came up and said his friend was dead.

Some people were so badly injured we couldn’t lift them. We started tearing apart the fencing used to separate the crowd and slid sections of the barricades under the wounded to carry them. We also carried off a bunch of people who were dead.

We were moving patients to a covered bar area where we thought they would be safer. What we didn’t know was there was an ambulance rally point at the very far end of the field. Unfortunately, we had no idea it was there.

I saw a lot of other first responders out there, people from the fire department, corpsmen from the Navy, medics. I ran into an anesthesia provider and a series of nurses.

When we got everybody off the field, we started moving them into vehicles. People were bringing their trucks up. One guy even stole a truck so he could drive people to the ED. There wasn’t a lot of triage. We were just stacking whoever we could into the backs of these pickups.

I tried to help a nurse taking care of a lady who had been shot in the neck. She was sitting sort of half upright with the patient lying in her arms. When I reached to help her, she said: “You can’t move her.”

“We need to get her to the hospital,” I replied.

“This is the only position that this lady has an airway,” she said. “You’re going to have to move both of us together. If I move at all, she loses her airway.”

So, a group of us managed to slide something underneath and lift them into the back of a truck.

Loading the wounded went on for a while. And then, just like that, everybody was gone.

I walked back out onto this field which not too long ago held 30,000 people. It was as if aliens had just suddenly beamed everyone out.

There was stuff on the ground everywhere – blankets, clothing, single boots, wallets, purses. I walked past a food stand with food still cooking on the grill. There was a beer tap still running. It was the weirdest feeling I’d ever had in my life.

After that, things got a little crazy again. There had been a report of a second shooter, and no one knew if it was real or not. The police started herding a group of us across the street to the Tropicana. We were still trying to take cover as we walked there. We went past a big lion statue in front of one of the casinos. I have a picture from two years earlier of me sitting on the back of that lion. I remember thinking: Now I’m hunkered down behind the same lion hiding from a shooter. Times change.

They brought about 50 of us into a food court, which was closed. They wouldn’t tell us what was going on. And they wouldn’t let us leave. This went on for hours. Meanwhile, I had dropped my cell phone on the field, so my wife couldn’t get hold of me, and later she told me she assumed I’d been shot. I was just hoping that she was safe.

People were huddled together, crying, holding each other. Most were wearing Western concert–going stuff, which for a lot of them wasn’t very much clothing. The hotel eventually brought some blankets.

I was covered in blood. My shirt, shorts, and sandals were soaked. It was running down my legs. I couldn’t find anything to eat or drink. At one point, I sat down at a slot machine, put a hundred dollars in, and started playing slots. I didn’t know what else to do. It didn’t take me very long to lose it all.

Finally, I started looking for a way to get out. I checked all the exits, but there were security and police there. Then I ran into a guy who said he had found a fire exit. When we opened the fire door, there was a big security guard there, and he said: “You can’t leave.”

We said: “Try to stop us. We’re out of here.”

Another thing I’ll always remember – after I broke out of the Tropicana, I was low crawling through the bushes along the Strip toward my hotel. I got a block away and stood up to cross the street. I pushed the crosswalk button and waited. There were no cars, no people. I’ve just broken all the rules, violated police orders, and now I’m standing there waiting for a blinking light to allow me to cross the street!

I made it back to my hotel room around 3:30 or 4:00 in the morning. My wife was hysterical because I hadn’t been answering my cell phone. I came in, and she gave me a big hug, and I got in the shower. Our plane was leaving in a few hours, so we laid down, but didn’t sleep.

As we were getting ready to leave, my wife’s phone rang, and it was my number. A guy at the same hotel had found my phone on the field and called the “in case of emergency” number. So, I got my phone back.

It wasn’t easy to deal with the aftermath. It really affected everybody’s life. To this day, I’m particular about where we sit at concerts. My wife isn’t comfortable if she can’t see an exit. I now have a med bag in my car with tourniquets, pressure dressings, airway masks for CPR.

I’ll never forget that feeling of absolute frustration. That lady without an airway – I could’ve put a trach in her very quickly and made a difference. Were they able to keep her airway? Did she live?

The father and son – did the father make it? I have no idea what happened to any of them. Later, I went through and looked at the pictures of all the people who had died, but I couldn’t recognize anybody.

The hardest part was being there with my wife. I’ve been in places where people are shooting at you, in vehicles that are getting bombed. I’ve always believed that when it’s your time, it’s your time. If I get shot, well, okay, that happens. But if she got shot or my friends ... that would be really tough.

A year later, I gave a talk about it at a conference. I thought I had worked through everything. But all of those feelings, all of that helplessness, that anger, everything came roaring back to the surface again. They asked me how I deal with it, and I said: “Well ... poorly.” I’m the guy who sticks it in a box in the back of his brain, tucks it in and buries it with a bunch of other boxes, and hopes it never comes out again. But every once in a while, it does.

There were all kinds of people out on that field, some with medical training, some without, all determined to help, trying to get those injured people where they needed to be. In retrospect, it does make you feel good. Somebody was shooting at us, but people were still willing to stand up and risk their lives to help others.

We still talk with our friends about what happened that night. Over the years, it’s become less and less. But there’s still a text sent out every year on that day: “Today is the anniversary. Glad we’re all alive. Thanks for being our friends.”

Dr. Sebesta is a bariatric surgeon with MultiCare Health System in Tacoma, Wash.

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

Sunday night. Las Vegas. Jason Aldean had just started playing.

My wife and I were at the 2017 Route 91 Harvest Festival with three other couples; two of them were our close friends. We were sitting in the VIP section, a tented area right next to the stage. We started hearing what I was convinced were fireworks.

I’ve been in the Army for 20 some years. I’ve been deployed and shot at multiple times. But these shots were far away. And you don’t expect people to be shooting at you at a concert.

I was on the edge of the VIP area, so I could see around the corner of the tent. I looked up at the Mandalay Bay and saw the muzzle flash in the hotel window. That’s when I knew.

I screamed: “Somebody’s shooting at us! Everybody get down!”

It took a while for people to realize what was going on. When the first couple volleys sprayed into the crowd, nobody understood. But once enough people had been hit and dropped, everyone knew, and it was just mass exodus.

People screamed and ran everywhere. Some of them tried to jump over the front barrier so they could get underneath the stage. Others were trying to pick up loved ones who’d been shot.

The next 15 minutes are a little foggy. I was helping my wife and the people around us to get down. Funny things come back to you afterward. One of my friends was carrying a 16-ounce beer in his hand. Somebody’s shooting at him and he’s walking around with his beer like he’s afraid to put it down. It was so surreal.

We got everybody underneath the tent, and then we just sat there. There would be shooting and then a pause. You’d think it was over. And then there would be more shooting and another pause. It felt like it never was going to stop.

After a short period of time, somebody came in with an official badge, maybe FBI, who knows. They said: “Okay, everybody up. We’ve got to get you out of here.” So, we all got up and headed across the stage. The gate they were taking us to was in full view of the shooter, so it wasn’t very safe.

As I got up, I looked out at the field. Bodies were scattered everywhere. I’m a trauma surgeon by trade. I couldn’t just leave.

I told my two best friends to take my wife with them. My wife lost her mind at that point. She didn’t want me to run out on the field. But I had to. I saw the injured and they needed help. Another buddy and I jumped over the fence and started taking care of people.

The feeling of being out on the field was one of complete frustration. I was in sandals, shorts, and a t-shirt. We had no stretchers, no medical supplies, no nothing. I didn’t have a belt to use as a tourniquet. I didn’t even have a bandage.

Worse: We were seeing high-velocity gunshot wounds that I’ve seen for 20 years in the Army. I know how to take care of them. I know how to fix them. But there wasn’t a single thing I could do.

We had to get people off the field, so we started gathering up as many as we could. We didn’t know if we were going to get shot at again, so we were trying to hide behind things as we ran. Our main objective was just to get people to a place of safety.

A lot of it is a blur. But a few patients stick out in my mind.

A father and son. The father had been shot through the abdomen, exited out through his back. He was in severe pain and couldn’t walk.

A young girl shot in the arm. Her parents carrying her.

A group of people doing CPR on a young lady. She had a gunshot wound to the head or neck. She was obviously dead. But they were still doing chest compressions in the middle of the field. I had to say to them: “She’s dead. You can’t save her. You need to get off the field.” But they wouldn’t stop. We picked her up and took her out while they continued to do CPR.

Later, I realized I knew that woman. She was part of a group of friends that we would see at the festival. I hadn’t recognized her. I also didn’t know that my friend Marco was there. A month or 2 later, we figured out that he was one of the people doing CPR. And I was the guy who came up and said his friend was dead.

Some people were so badly injured we couldn’t lift them. We started tearing apart the fencing used to separate the crowd and slid sections of the barricades under the wounded to carry them. We also carried off a bunch of people who were dead.

We were moving patients to a covered bar area where we thought they would be safer. What we didn’t know was there was an ambulance rally point at the very far end of the field. Unfortunately, we had no idea it was there.

I saw a lot of other first responders out there, people from the fire department, corpsmen from the Navy, medics. I ran into an anesthesia provider and a series of nurses.

When we got everybody off the field, we started moving them into vehicles. People were bringing their trucks up. One guy even stole a truck so he could drive people to the ED. There wasn’t a lot of triage. We were just stacking whoever we could into the backs of these pickups.

I tried to help a nurse taking care of a lady who had been shot in the neck. She was sitting sort of half upright with the patient lying in her arms. When I reached to help her, she said: “You can’t move her.”

“We need to get her to the hospital,” I replied.

“This is the only position that this lady has an airway,” she said. “You’re going to have to move both of us together. If I move at all, she loses her airway.”

So, a group of us managed to slide something underneath and lift them into the back of a truck.

Loading the wounded went on for a while. And then, just like that, everybody was gone.

I walked back out onto this field which not too long ago held 30,000 people. It was as if aliens had just suddenly beamed everyone out.

There was stuff on the ground everywhere – blankets, clothing, single boots, wallets, purses. I walked past a food stand with food still cooking on the grill. There was a beer tap still running. It was the weirdest feeling I’d ever had in my life.

After that, things got a little crazy again. There had been a report of a second shooter, and no one knew if it was real or not. The police started herding a group of us across the street to the Tropicana. We were still trying to take cover as we walked there. We went past a big lion statue in front of one of the casinos. I have a picture from two years earlier of me sitting on the back of that lion. I remember thinking: Now I’m hunkered down behind the same lion hiding from a shooter. Times change.

They brought about 50 of us into a food court, which was closed. They wouldn’t tell us what was going on. And they wouldn’t let us leave. This went on for hours. Meanwhile, I had dropped my cell phone on the field, so my wife couldn’t get hold of me, and later she told me she assumed I’d been shot. I was just hoping that she was safe.

People were huddled together, crying, holding each other. Most were wearing Western concert–going stuff, which for a lot of them wasn’t very much clothing. The hotel eventually brought some blankets.

I was covered in blood. My shirt, shorts, and sandals were soaked. It was running down my legs. I couldn’t find anything to eat or drink. At one point, I sat down at a slot machine, put a hundred dollars in, and started playing slots. I didn’t know what else to do. It didn’t take me very long to lose it all.

Finally, I started looking for a way to get out. I checked all the exits, but there were security and police there. Then I ran into a guy who said he had found a fire exit. When we opened the fire door, there was a big security guard there, and he said: “You can’t leave.”

We said: “Try to stop us. We’re out of here.”

Another thing I’ll always remember – after I broke out of the Tropicana, I was low crawling through the bushes along the Strip toward my hotel. I got a block away and stood up to cross the street. I pushed the crosswalk button and waited. There were no cars, no people. I’ve just broken all the rules, violated police orders, and now I’m standing there waiting for a blinking light to allow me to cross the street!

I made it back to my hotel room around 3:30 or 4:00 in the morning. My wife was hysterical because I hadn’t been answering my cell phone. I came in, and she gave me a big hug, and I got in the shower. Our plane was leaving in a few hours, so we laid down, but didn’t sleep.

As we were getting ready to leave, my wife’s phone rang, and it was my number. A guy at the same hotel had found my phone on the field and called the “in case of emergency” number. So, I got my phone back.

It wasn’t easy to deal with the aftermath. It really affected everybody’s life. To this day, I’m particular about where we sit at concerts. My wife isn’t comfortable if she can’t see an exit. I now have a med bag in my car with tourniquets, pressure dressings, airway masks for CPR.

I’ll never forget that feeling of absolute frustration. That lady without an airway – I could’ve put a trach in her very quickly and made a difference. Were they able to keep her airway? Did she live?

The father and son – did the father make it? I have no idea what happened to any of them. Later, I went through and looked at the pictures of all the people who had died, but I couldn’t recognize anybody.

The hardest part was being there with my wife. I’ve been in places where people are shooting at you, in vehicles that are getting bombed. I’ve always believed that when it’s your time, it’s your time. If I get shot, well, okay, that happens. But if she got shot or my friends ... that would be really tough.

A year later, I gave a talk about it at a conference. I thought I had worked through everything. But all of those feelings, all of that helplessness, that anger, everything came roaring back to the surface again. They asked me how I deal with it, and I said: “Well ... poorly.” I’m the guy who sticks it in a box in the back of his brain, tucks it in and buries it with a bunch of other boxes, and hopes it never comes out again. But every once in a while, it does.

There were all kinds of people out on that field, some with medical training, some without, all determined to help, trying to get those injured people where they needed to be. In retrospect, it does make you feel good. Somebody was shooting at us, but people were still willing to stand up and risk their lives to help others.

We still talk with our friends about what happened that night. Over the years, it’s become less and less. But there’s still a text sent out every year on that day: “Today is the anniversary. Glad we’re all alive. Thanks for being our friends.”

Dr. Sebesta is a bariatric surgeon with MultiCare Health System in Tacoma, Wash.

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

Sunday night. Las Vegas. Jason Aldean had just started playing.

My wife and I were at the 2017 Route 91 Harvest Festival with three other couples; two of them were our close friends. We were sitting in the VIP section, a tented area right next to the stage. We started hearing what I was convinced were fireworks.

I’ve been in the Army for 20 some years. I’ve been deployed and shot at multiple times. But these shots were far away. And you don’t expect people to be shooting at you at a concert.

I was on the edge of the VIP area, so I could see around the corner of the tent. I looked up at the Mandalay Bay and saw the muzzle flash in the hotel window. That’s when I knew.

I screamed: “Somebody’s shooting at us! Everybody get down!”

It took a while for people to realize what was going on. When the first couple volleys sprayed into the crowd, nobody understood. But once enough people had been hit and dropped, everyone knew, and it was just mass exodus.

People screamed and ran everywhere. Some of them tried to jump over the front barrier so they could get underneath the stage. Others were trying to pick up loved ones who’d been shot.

The next 15 minutes are a little foggy. I was helping my wife and the people around us to get down. Funny things come back to you afterward. One of my friends was carrying a 16-ounce beer in his hand. Somebody’s shooting at him and he’s walking around with his beer like he’s afraid to put it down. It was so surreal.

We got everybody underneath the tent, and then we just sat there. There would be shooting and then a pause. You’d think it was over. And then there would be more shooting and another pause. It felt like it never was going to stop.

After a short period of time, somebody came in with an official badge, maybe FBI, who knows. They said: “Okay, everybody up. We’ve got to get you out of here.” So, we all got up and headed across the stage. The gate they were taking us to was in full view of the shooter, so it wasn’t very safe.

As I got up, I looked out at the field. Bodies were scattered everywhere. I’m a trauma surgeon by trade. I couldn’t just leave.

I told my two best friends to take my wife with them. My wife lost her mind at that point. She didn’t want me to run out on the field. But I had to. I saw the injured and they needed help. Another buddy and I jumped over the fence and started taking care of people.

The feeling of being out on the field was one of complete frustration. I was in sandals, shorts, and a t-shirt. We had no stretchers, no medical supplies, no nothing. I didn’t have a belt to use as a tourniquet. I didn’t even have a bandage.

Worse: We were seeing high-velocity gunshot wounds that I’ve seen for 20 years in the Army. I know how to take care of them. I know how to fix them. But there wasn’t a single thing I could do.

We had to get people off the field, so we started gathering up as many as we could. We didn’t know if we were going to get shot at again, so we were trying to hide behind things as we ran. Our main objective was just to get people to a place of safety.

A lot of it is a blur. But a few patients stick out in my mind.

A father and son. The father had been shot through the abdomen, exited out through his back. He was in severe pain and couldn’t walk.

A young girl shot in the arm. Her parents carrying her.

A group of people doing CPR on a young lady. She had a gunshot wound to the head or neck. She was obviously dead. But they were still doing chest compressions in the middle of the field. I had to say to them: “She’s dead. You can’t save her. You need to get off the field.” But they wouldn’t stop. We picked her up and took her out while they continued to do CPR.

Later, I realized I knew that woman. She was part of a group of friends that we would see at the festival. I hadn’t recognized her. I also didn’t know that my friend Marco was there. A month or 2 later, we figured out that he was one of the people doing CPR. And I was the guy who came up and said his friend was dead.

Some people were so badly injured we couldn’t lift them. We started tearing apart the fencing used to separate the crowd and slid sections of the barricades under the wounded to carry them. We also carried off a bunch of people who were dead.

We were moving patients to a covered bar area where we thought they would be safer. What we didn’t know was there was an ambulance rally point at the very far end of the field. Unfortunately, we had no idea it was there.

I saw a lot of other first responders out there, people from the fire department, corpsmen from the Navy, medics. I ran into an anesthesia provider and a series of nurses.

When we got everybody off the field, we started moving them into vehicles. People were bringing their trucks up. One guy even stole a truck so he could drive people to the ED. There wasn’t a lot of triage. We were just stacking whoever we could into the backs of these pickups.

I tried to help a nurse taking care of a lady who had been shot in the neck. She was sitting sort of half upright with the patient lying in her arms. When I reached to help her, she said: “You can’t move her.”

“We need to get her to the hospital,” I replied.

“This is the only position that this lady has an airway,” she said. “You’re going to have to move both of us together. If I move at all, she loses her airway.”

So, a group of us managed to slide something underneath and lift them into the back of a truck.

Loading the wounded went on for a while. And then, just like that, everybody was gone.

I walked back out onto this field which not too long ago held 30,000 people. It was as if aliens had just suddenly beamed everyone out.

There was stuff on the ground everywhere – blankets, clothing, single boots, wallets, purses. I walked past a food stand with food still cooking on the grill. There was a beer tap still running. It was the weirdest feeling I’d ever had in my life.

After that, things got a little crazy again. There had been a report of a second shooter, and no one knew if it was real or not. The police started herding a group of us across the street to the Tropicana. We were still trying to take cover as we walked there. We went past a big lion statue in front of one of the casinos. I have a picture from two years earlier of me sitting on the back of that lion. I remember thinking: Now I’m hunkered down behind the same lion hiding from a shooter. Times change.

They brought about 50 of us into a food court, which was closed. They wouldn’t tell us what was going on. And they wouldn’t let us leave. This went on for hours. Meanwhile, I had dropped my cell phone on the field, so my wife couldn’t get hold of me, and later she told me she assumed I’d been shot. I was just hoping that she was safe.

People were huddled together, crying, holding each other. Most were wearing Western concert–going stuff, which for a lot of them wasn’t very much clothing. The hotel eventually brought some blankets.

I was covered in blood. My shirt, shorts, and sandals were soaked. It was running down my legs. I couldn’t find anything to eat or drink. At one point, I sat down at a slot machine, put a hundred dollars in, and started playing slots. I didn’t know what else to do. It didn’t take me very long to lose it all.

Finally, I started looking for a way to get out. I checked all the exits, but there were security and police there. Then I ran into a guy who said he had found a fire exit. When we opened the fire door, there was a big security guard there, and he said: “You can’t leave.”

We said: “Try to stop us. We’re out of here.”

Another thing I’ll always remember – after I broke out of the Tropicana, I was low crawling through the bushes along the Strip toward my hotel. I got a block away and stood up to cross the street. I pushed the crosswalk button and waited. There were no cars, no people. I’ve just broken all the rules, violated police orders, and now I’m standing there waiting for a blinking light to allow me to cross the street!

I made it back to my hotel room around 3:30 or 4:00 in the morning. My wife was hysterical because I hadn’t been answering my cell phone. I came in, and she gave me a big hug, and I got in the shower. Our plane was leaving in a few hours, so we laid down, but didn’t sleep.

As we were getting ready to leave, my wife’s phone rang, and it was my number. A guy at the same hotel had found my phone on the field and called the “in case of emergency” number. So, I got my phone back.

It wasn’t easy to deal with the aftermath. It really affected everybody’s life. To this day, I’m particular about where we sit at concerts. My wife isn’t comfortable if she can’t see an exit. I now have a med bag in my car with tourniquets, pressure dressings, airway masks for CPR.

I’ll never forget that feeling of absolute frustration. That lady without an airway – I could’ve put a trach in her very quickly and made a difference. Were they able to keep her airway? Did she live?

The father and son – did the father make it? I have no idea what happened to any of them. Later, I went through and looked at the pictures of all the people who had died, but I couldn’t recognize anybody.

The hardest part was being there with my wife. I’ve been in places where people are shooting at you, in vehicles that are getting bombed. I’ve always believed that when it’s your time, it’s your time. If I get shot, well, okay, that happens. But if she got shot or my friends ... that would be really tough.

A year later, I gave a talk about it at a conference. I thought I had worked through everything. But all of those feelings, all of that helplessness, that anger, everything came roaring back to the surface again. They asked me how I deal with it, and I said: “Well ... poorly.” I’m the guy who sticks it in a box in the back of his brain, tucks it in and buries it with a bunch of other boxes, and hopes it never comes out again. But every once in a while, it does.

There were all kinds of people out on that field, some with medical training, some without, all determined to help, trying to get those injured people where they needed to be. In retrospect, it does make you feel good. Somebody was shooting at us, but people were still willing to stand up and risk their lives to help others.

We still talk with our friends about what happened that night. Over the years, it’s become less and less. But there’s still a text sent out every year on that day: “Today is the anniversary. Glad we’re all alive. Thanks for being our friends.”

Dr. Sebesta is a bariatric surgeon with MultiCare Health System in Tacoma, Wash.

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

Patients reporting moderate or extreme pain a year after a myocardial infarction (MI) – even pain due to other health conditions – are more likely to die within the next 8 years than those without post-MI pain, new research suggests.

In the analysis of post-MI health data for more than 18,300 Swedish adults, those with moderate pain were 35% more likely to die from any cause during follow-up, compared with those with no pain, and those with extreme pain were more than twice as likely to die.

Furthermore, pain was a stronger predictor of mortality than smoking.

“For a long time, pain has been regarded as merely a symptom of disease rather than a disease” in its own right, Linda Vixner, PT, PhD, of Dalarna University in Falun, Sweden, said in an interview.

Updated definitions of chronic pain in the ICD-11, as well as a recent study using data from the UK Biobank showing that chronic pain is associated with an increased risk of cardiovascular disease, prompted the current study, which looks at the effect of pain on long-term survival after an MI.

“We did not expect that pain would have such a strong impact on the risk of death, and it also surprised us that the risk was more pronounced than that of smoking,” Dr. Vixner said. “Clinicians should consider pain an important cardiovascular risk factor.”

The study was published online in the Journal of the American Heart Association.
 

‘Experienced pain’ prognostic

The investigators analyzed data from the SWEDEHEART registry of 18,376 patients who had an MI in 2004-2013. The mean age of patients was 62 years and 75% were men. Follow-up time was 8.5 years (median, 3.37).

Self-reported levels of experienced pain according to the EuroQol five-dimension instrument were recorded 12 months after hospital discharge.

Moderate pain was reported by 38.2% of patients and extreme pain by 4.5%.

In the extreme pain category, women were overrepresented (7.5% vs. 3.6% of men), as were current smokers, and patients with diabetes, previous MI, previous stroke, previous percutaneous coronary intervention, non-ST-segment–elevation MI, and any kind of chest pain. Patients classified as physically inactive also were overrepresented in this category.

In addition, those with extreme pain had a higher body mass index and waist circumference 12 months after hospital discharge.

Most (73%) of the 7,889 patients who reported no pain at the 2-month follow-up after MI were also pain-free at the 12-month follow-up, and 65% of those experiencing pain at 2 months were also experiencing pain at 12 months.

There were 1,067 deaths. The adjusted hazard ratio was 1.35 for moderate pain and 2.06 for extreme pain.

As noted, pain was a stronger mortality predictor than smoking: C-statistics for pain were 0.60, and for smoking, 0.55.

“Clinicians managing patients after MI should recognize the need to consider experienced pain as a prognostic factor comparable to persistent smoking and to address this when designing individually adjusted [cardiac rehabilitation] and secondary prevention treatments,” the authors write.

Pain should be assessed at follow-up after MI, they add, and, as Dr. Vixner suggested, it should be “acknowledged as an important risk factor.”
 

Managing risks

“These findings parallel prior studies and my own clinical experience,” American Heart Association volunteer expert Gregg C. Fonarow, MD, interim chief of the division of cardiology at the University of California, Los Angeles, and director, Ahmanson-UCLA Cardiomyopathy Center, told this news organization.

“There are many potential causes for patient-reported pain in the year after a heart attack,” he said, including a greater cardiovascular risk burden, more comorbid conditions, less physical activity, and chronic use of nonsteroidal anti-inflammatory medications or opioids for pain control – all of which can contribute to the increased risk of mortality.

Factors beyond those evaluated and adjusted for in the observational study may contribute to the observed associations, he added. “Socioeconomic factors were not accounted for [and] there was no information on the types, doses, and frequency of pain medication use.”

“Clinicians managing patients with prior MI should carefully assess experienced pain and utilize this information to optimize risk factor control recommendations, inform treatment decisions, and consider in terms of prognosis,” he advised.

Further studies should evaluate whether the associations hold true for other patient populations, Dr. Fonarow said. “In addition, intervention trials could evaluate if enhanced management strategies in these higher-risk patients with self-reported pain can successfully lower the mortality risk.”

Dr. Vixner sees a role for physical activity in lowering the mortality risk.

“One of the core treatments for chronic pain is physical activity,” she said. “It positively influences quality of life, activities of daily living, pain intensity, and overall physical function, and reduces the risk of social isolation” and cardiovascular diseases.

Her team recently developed the “eVISualisation of physical activity and pain” (eVIS) intervention, which aims to promote healthy physical activity levels in persons living with chronic pain. The intervention is currently being evaluated in an ongoing registry-based, randomized controlled trial.

The study was supported by Svenska Försäkringsföreningen, Dalarna University, Region Dalarna. Dr. Vixner and coauthors have reported no relevant financial relationships. Dr. Fonarow has disclosed consulting for Abbott, Amgen, AstraZeneca, Bayer, Cytokinetics, Eli Lilly, Johnson & Johnson, Medtronic, Merck, Novartis, and Pfizer.

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

Patients reporting moderate or extreme pain a year after a myocardial infarction (MI) – even pain due to other health conditions – are more likely to die within the next 8 years than those without post-MI pain, new research suggests.

In the analysis of post-MI health data for more than 18,300 Swedish adults, those with moderate pain were 35% more likely to die from any cause during follow-up, compared with those with no pain, and those with extreme pain were more than twice as likely to die.

Furthermore, pain was a stronger predictor of mortality than smoking.

“For a long time, pain has been regarded as merely a symptom of disease rather than a disease” in its own right, Linda Vixner, PT, PhD, of Dalarna University in Falun, Sweden, said in an interview.

Updated definitions of chronic pain in the ICD-11, as well as a recent study using data from the UK Biobank showing that chronic pain is associated with an increased risk of cardiovascular disease, prompted the current study, which looks at the effect of pain on long-term survival after an MI.

“We did not expect that pain would have such a strong impact on the risk of death, and it also surprised us that the risk was more pronounced than that of smoking,” Dr. Vixner said. “Clinicians should consider pain an important cardiovascular risk factor.”

The study was published online in the Journal of the American Heart Association.
 

‘Experienced pain’ prognostic

The investigators analyzed data from the SWEDEHEART registry of 18,376 patients who had an MI in 2004-2013. The mean age of patients was 62 years and 75% were men. Follow-up time was 8.5 years (median, 3.37).

Self-reported levels of experienced pain according to the EuroQol five-dimension instrument were recorded 12 months after hospital discharge.

Moderate pain was reported by 38.2% of patients and extreme pain by 4.5%.

In the extreme pain category, women were overrepresented (7.5% vs. 3.6% of men), as were current smokers, and patients with diabetes, previous MI, previous stroke, previous percutaneous coronary intervention, non-ST-segment–elevation MI, and any kind of chest pain. Patients classified as physically inactive also were overrepresented in this category.

In addition, those with extreme pain had a higher body mass index and waist circumference 12 months after hospital discharge.

Most (73%) of the 7,889 patients who reported no pain at the 2-month follow-up after MI were also pain-free at the 12-month follow-up, and 65% of those experiencing pain at 2 months were also experiencing pain at 12 months.

There were 1,067 deaths. The adjusted hazard ratio was 1.35 for moderate pain and 2.06 for extreme pain.

As noted, pain was a stronger mortality predictor than smoking: C-statistics for pain were 0.60, and for smoking, 0.55.

“Clinicians managing patients after MI should recognize the need to consider experienced pain as a prognostic factor comparable to persistent smoking and to address this when designing individually adjusted [cardiac rehabilitation] and secondary prevention treatments,” the authors write.

Pain should be assessed at follow-up after MI, they add, and, as Dr. Vixner suggested, it should be “acknowledged as an important risk factor.”
 

Managing risks

“These findings parallel prior studies and my own clinical experience,” American Heart Association volunteer expert Gregg C. Fonarow, MD, interim chief of the division of cardiology at the University of California, Los Angeles, and director, Ahmanson-UCLA Cardiomyopathy Center, told this news organization.

“There are many potential causes for patient-reported pain in the year after a heart attack,” he said, including a greater cardiovascular risk burden, more comorbid conditions, less physical activity, and chronic use of nonsteroidal anti-inflammatory medications or opioids for pain control – all of which can contribute to the increased risk of mortality.

Factors beyond those evaluated and adjusted for in the observational study may contribute to the observed associations, he added. “Socioeconomic factors were not accounted for [and] there was no information on the types, doses, and frequency of pain medication use.”

“Clinicians managing patients with prior MI should carefully assess experienced pain and utilize this information to optimize risk factor control recommendations, inform treatment decisions, and consider in terms of prognosis,” he advised.

Further studies should evaluate whether the associations hold true for other patient populations, Dr. Fonarow said. “In addition, intervention trials could evaluate if enhanced management strategies in these higher-risk patients with self-reported pain can successfully lower the mortality risk.”

Dr. Vixner sees a role for physical activity in lowering the mortality risk.

“One of the core treatments for chronic pain is physical activity,” she said. “It positively influences quality of life, activities of daily living, pain intensity, and overall physical function, and reduces the risk of social isolation” and cardiovascular diseases.

Her team recently developed the “eVISualisation of physical activity and pain” (eVIS) intervention, which aims to promote healthy physical activity levels in persons living with chronic pain. The intervention is currently being evaluated in an ongoing registry-based, randomized controlled trial.

The study was supported by Svenska Försäkringsföreningen, Dalarna University, Region Dalarna. Dr. Vixner and coauthors have reported no relevant financial relationships. Dr. Fonarow has disclosed consulting for Abbott, Amgen, AstraZeneca, Bayer, Cytokinetics, Eli Lilly, Johnson & Johnson, Medtronic, Merck, Novartis, and Pfizer.

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

Patients reporting moderate or extreme pain a year after a myocardial infarction (MI) – even pain due to other health conditions – are more likely to die within the next 8 years than those without post-MI pain, new research suggests.

In the analysis of post-MI health data for more than 18,300 Swedish adults, those with moderate pain were 35% more likely to die from any cause during follow-up, compared with those with no pain, and those with extreme pain were more than twice as likely to die.

Furthermore, pain was a stronger predictor of mortality than smoking.

“For a long time, pain has been regarded as merely a symptom of disease rather than a disease” in its own right, Linda Vixner, PT, PhD, of Dalarna University in Falun, Sweden, said in an interview.

Updated definitions of chronic pain in the ICD-11, as well as a recent study using data from the UK Biobank showing that chronic pain is associated with an increased risk of cardiovascular disease, prompted the current study, which looks at the effect of pain on long-term survival after an MI.

“We did not expect that pain would have such a strong impact on the risk of death, and it also surprised us that the risk was more pronounced than that of smoking,” Dr. Vixner said. “Clinicians should consider pain an important cardiovascular risk factor.”

The study was published online in the Journal of the American Heart Association.
 

‘Experienced pain’ prognostic

The investigators analyzed data from the SWEDEHEART registry of 18,376 patients who had an MI in 2004-2013. The mean age of patients was 62 years and 75% were men. Follow-up time was 8.5 years (median, 3.37).

Self-reported levels of experienced pain according to the EuroQol five-dimension instrument were recorded 12 months after hospital discharge.

Moderate pain was reported by 38.2% of patients and extreme pain by 4.5%.

In the extreme pain category, women were overrepresented (7.5% vs. 3.6% of men), as were current smokers, and patients with diabetes, previous MI, previous stroke, previous percutaneous coronary intervention, non-ST-segment–elevation MI, and any kind of chest pain. Patients classified as physically inactive also were overrepresented in this category.

In addition, those with extreme pain had a higher body mass index and waist circumference 12 months after hospital discharge.

Most (73%) of the 7,889 patients who reported no pain at the 2-month follow-up after MI were also pain-free at the 12-month follow-up, and 65% of those experiencing pain at 2 months were also experiencing pain at 12 months.

There were 1,067 deaths. The adjusted hazard ratio was 1.35 for moderate pain and 2.06 for extreme pain.

As noted, pain was a stronger mortality predictor than smoking: C-statistics for pain were 0.60, and for smoking, 0.55.

“Clinicians managing patients after MI should recognize the need to consider experienced pain as a prognostic factor comparable to persistent smoking and to address this when designing individually adjusted [cardiac rehabilitation] and secondary prevention treatments,” the authors write.

Pain should be assessed at follow-up after MI, they add, and, as Dr. Vixner suggested, it should be “acknowledged as an important risk factor.”
 

Managing risks

“These findings parallel prior studies and my own clinical experience,” American Heart Association volunteer expert Gregg C. Fonarow, MD, interim chief of the division of cardiology at the University of California, Los Angeles, and director, Ahmanson-UCLA Cardiomyopathy Center, told this news organization.

“There are many potential causes for patient-reported pain in the year after a heart attack,” he said, including a greater cardiovascular risk burden, more comorbid conditions, less physical activity, and chronic use of nonsteroidal anti-inflammatory medications or opioids for pain control – all of which can contribute to the increased risk of mortality.

Factors beyond those evaluated and adjusted for in the observational study may contribute to the observed associations, he added. “Socioeconomic factors were not accounted for [and] there was no information on the types, doses, and frequency of pain medication use.”

“Clinicians managing patients with prior MI should carefully assess experienced pain and utilize this information to optimize risk factor control recommendations, inform treatment decisions, and consider in terms of prognosis,” he advised.

Further studies should evaluate whether the associations hold true for other patient populations, Dr. Fonarow said. “In addition, intervention trials could evaluate if enhanced management strategies in these higher-risk patients with self-reported pain can successfully lower the mortality risk.”

Dr. Vixner sees a role for physical activity in lowering the mortality risk.

“One of the core treatments for chronic pain is physical activity,” she said. “It positively influences quality of life, activities of daily living, pain intensity, and overall physical function, and reduces the risk of social isolation” and cardiovascular diseases.

Her team recently developed the “eVISualisation of physical activity and pain” (eVIS) intervention, which aims to promote healthy physical activity levels in persons living with chronic pain. The intervention is currently being evaluated in an ongoing registry-based, randomized controlled trial.

The study was supported by Svenska Försäkringsföreningen, Dalarna University, Region Dalarna. Dr. Vixner and coauthors have reported no relevant financial relationships. Dr. Fonarow has disclosed consulting for Abbott, Amgen, AstraZeneca, Bayer, Cytokinetics, Eli Lilly, Johnson & Johnson, Medtronic, Merck, Novartis, and Pfizer.

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

Physicians tend to be compulsive multitaskers. We switch from one task to another all the time – even in front of patients. We think we are more efficient and productive, and that we are accomplishing more in less time. In fact, there is no credible evidence that this is true, and a mountain of evidence showing exactly the opposite.

According to this study and others, multitasking results in an average of 2 hours per day of lost productivity. It decreases the quality of work performed and increases cortisol levels, which impedes cognitive functioning, leading to a further decrease in productivity in a vicious cycle, making you increasingly ineffective and destroying your motivation and mood.

On the surface, the reasons for this are not intuitively obvious. After all, simple and routine tasks are easy to perform simultaneously; we can all walk and chew gum at the same time or eat a snack while watching TV. The problems arise when we try to multitask more complex tasks that require thought and decision-making.

It turns out that the pressures of our modern world have evolved faster than our brains. We are still hard-wired for monotasking. When we think we are completing two tasks simultaneously, we are actually performing individual actions in rapid succession. Each time you switch tasks, your brain must turn off the cognitive rules of the previous task and turn on new rules for the next one. When you switch back, the process repeats in reverse. Each of those mental gear shifts takes time and costs us productivity. According to one psychologist, even brief mental blocks created by shifting between tasks can cost as much as 40% of someone’s productive time. We are also far more likely to make mistakes while we are doing it.

Furthermore, you are stifling your creativity and innovation because you don’t focus on one task long enough to come up with original insights. Multitasking also slows down your general cognitive functions, in the same way that keeping many windows are open on your computer slows down the entire system. A study from my alma mater, the University of California, San Francisco, concluded that multitasking negativity affects memory in both younger and older adults (although the effects were greater in older adults) .

So, what to do? The fact remains that, all too often, there really are too many tasks and not enough hours in the day. How can you get through them without falling into the multitasking trap?

The first rule is to prioritize. In his book “The Seven Habits of Highly Effective People,” Stephen Covey makes an important distinction between tasks that are important and those that are merely urgent. Tasks that are important and urgent tend to make time for themselves, because they must be taken care of immediately.

Jobs that are important but not urgent are the ones we tend to try to multitask. Because there is no immediate deadline, we think we can do two or more of them simultaneously, or we fall into the other major productivity trap: procrastination. Neither of those strategies tends to end well. Identify those important but not urgent tasks and force yourself to go through them one by one.

Urgent but unimportant tasks are the productivity thieves. They demand your attention but are not worthy of it. Most tasks in this category can be delegated. I have written about physicians’ workaholic and perfectionist tendencies that drive our conviction that no one else can do anything as well as we can. Does that unimportant task, even if urgent, really demand your time, skills, education, and medical license? Is there someone in your office, or possibly an outside contractor, who could do it just as well, and maybe faster?

In fact, that is the question you should ask every time a project triggers your urge to multitask: “Who could be doing this job – or at least a major part of it – instead of me?”

If your multitasking urges are deeply ingrained – particularly those that involve phones, laptops, and the cloud – you might consider employing electronic aids. SelfControl, for example, is a free, open-sourced app that lets you block your own access to distracting websites, your email servers, social media, or anything else on the Internet. You list the sites you wish to block and set a period of time to block them. Until the set time expires, you will be unable to access those sites, even if you restart your computer or delete the application.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at dermnews@mdedge.com.

Physicians tend to be compulsive multitaskers. We switch from one task to another all the time – even in front of patients. We think we are more efficient and productive, and that we are accomplishing more in less time. In fact, there is no credible evidence that this is true, and a mountain of evidence showing exactly the opposite.

According to this study and others, multitasking results in an average of 2 hours per day of lost productivity. It decreases the quality of work performed and increases cortisol levels, which impedes cognitive functioning, leading to a further decrease in productivity in a vicious cycle, making you increasingly ineffective and destroying your motivation and mood.

On the surface, the reasons for this are not intuitively obvious. After all, simple and routine tasks are easy to perform simultaneously; we can all walk and chew gum at the same time or eat a snack while watching TV. The problems arise when we try to multitask more complex tasks that require thought and decision-making.

It turns out that the pressures of our modern world have evolved faster than our brains. We are still hard-wired for monotasking. When we think we are completing two tasks simultaneously, we are actually performing individual actions in rapid succession. Each time you switch tasks, your brain must turn off the cognitive rules of the previous task and turn on new rules for the next one. When you switch back, the process repeats in reverse. Each of those mental gear shifts takes time and costs us productivity. According to one psychologist, even brief mental blocks created by shifting between tasks can cost as much as 40% of someone’s productive time. We are also far more likely to make mistakes while we are doing it.

Furthermore, you are stifling your creativity and innovation because you don’t focus on one task long enough to come up with original insights. Multitasking also slows down your general cognitive functions, in the same way that keeping many windows are open on your computer slows down the entire system. A study from my alma mater, the University of California, San Francisco, concluded that multitasking negativity affects memory in both younger and older adults (although the effects were greater in older adults) .

So, what to do? The fact remains that, all too often, there really are too many tasks and not enough hours in the day. How can you get through them without falling into the multitasking trap?

The first rule is to prioritize. In his book “The Seven Habits of Highly Effective People,” Stephen Covey makes an important distinction between tasks that are important and those that are merely urgent. Tasks that are important and urgent tend to make time for themselves, because they must be taken care of immediately.

Jobs that are important but not urgent are the ones we tend to try to multitask. Because there is no immediate deadline, we think we can do two or more of them simultaneously, or we fall into the other major productivity trap: procrastination. Neither of those strategies tends to end well. Identify those important but not urgent tasks and force yourself to go through them one by one.

Urgent but unimportant tasks are the productivity thieves. They demand your attention but are not worthy of it. Most tasks in this category can be delegated. I have written about physicians’ workaholic and perfectionist tendencies that drive our conviction that no one else can do anything as well as we can. Does that unimportant task, even if urgent, really demand your time, skills, education, and medical license? Is there someone in your office, or possibly an outside contractor, who could do it just as well, and maybe faster?

In fact, that is the question you should ask every time a project triggers your urge to multitask: “Who could be doing this job – or at least a major part of it – instead of me?”

If your multitasking urges are deeply ingrained – particularly those that involve phones, laptops, and the cloud – you might consider employing electronic aids. SelfControl, for example, is a free, open-sourced app that lets you block your own access to distracting websites, your email servers, social media, or anything else on the Internet. You list the sites you wish to block and set a period of time to block them. Until the set time expires, you will be unable to access those sites, even if you restart your computer or delete the application.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at dermnews@mdedge.com.

Physicians tend to be compulsive multitaskers. We switch from one task to another all the time – even in front of patients. We think we are more efficient and productive, and that we are accomplishing more in less time. In fact, there is no credible evidence that this is true, and a mountain of evidence showing exactly the opposite.

According to this study and others, multitasking results in an average of 2 hours per day of lost productivity. It decreases the quality of work performed and increases cortisol levels, which impedes cognitive functioning, leading to a further decrease in productivity in a vicious cycle, making you increasingly ineffective and destroying your motivation and mood.

On the surface, the reasons for this are not intuitively obvious. After all, simple and routine tasks are easy to perform simultaneously; we can all walk and chew gum at the same time or eat a snack while watching TV. The problems arise when we try to multitask more complex tasks that require thought and decision-making.

It turns out that the pressures of our modern world have evolved faster than our brains. We are still hard-wired for monotasking. When we think we are completing two tasks simultaneously, we are actually performing individual actions in rapid succession. Each time you switch tasks, your brain must turn off the cognitive rules of the previous task and turn on new rules for the next one. When you switch back, the process repeats in reverse. Each of those mental gear shifts takes time and costs us productivity. According to one psychologist, even brief mental blocks created by shifting between tasks can cost as much as 40% of someone’s productive time. We are also far more likely to make mistakes while we are doing it.

Furthermore, you are stifling your creativity and innovation because you don’t focus on one task long enough to come up with original insights. Multitasking also slows down your general cognitive functions, in the same way that keeping many windows are open on your computer slows down the entire system. A study from my alma mater, the University of California, San Francisco, concluded that multitasking negativity affects memory in both younger and older adults (although the effects were greater in older adults) .

So, what to do? The fact remains that, all too often, there really are too many tasks and not enough hours in the day. How can you get through them without falling into the multitasking trap?

The first rule is to prioritize. In his book “The Seven Habits of Highly Effective People,” Stephen Covey makes an important distinction between tasks that are important and those that are merely urgent. Tasks that are important and urgent tend to make time for themselves, because they must be taken care of immediately.

Jobs that are important but not urgent are the ones we tend to try to multitask. Because there is no immediate deadline, we think we can do two or more of them simultaneously, or we fall into the other major productivity trap: procrastination. Neither of those strategies tends to end well. Identify those important but not urgent tasks and force yourself to go through them one by one.

Urgent but unimportant tasks are the productivity thieves. They demand your attention but are not worthy of it. Most tasks in this category can be delegated. I have written about physicians’ workaholic and perfectionist tendencies that drive our conviction that no one else can do anything as well as we can. Does that unimportant task, even if urgent, really demand your time, skills, education, and medical license? Is there someone in your office, or possibly an outside contractor, who could do it just as well, and maybe faster?

In fact, that is the question you should ask every time a project triggers your urge to multitask: “Who could be doing this job – or at least a major part of it – instead of me?”

If your multitasking urges are deeply ingrained – particularly those that involve phones, laptops, and the cloud – you might consider employing electronic aids. SelfControl, for example, is a free, open-sourced app that lets you block your own access to distracting websites, your email servers, social media, or anything else on the Internet. You list the sites you wish to block and set a period of time to block them. Until the set time expires, you will be unable to access those sites, even if you restart your computer or delete the application.

Dr. Eastern practices dermatology and dermatologic surgery in Belleville, N.J. He is the author of numerous articles and textbook chapters, and is a longtime monthly columnist for Dermatology News. Write to him at dermnews@mdedge.com.

Health benefits of prolonged “water fasting” (zero calories) or Buchinger fasting (200-300 calories/day) don’t last, according to authors of a review of eight studies.

Five days of fasting lowered weight by about 6%, but this weight was regained after 3 months of regular eating, the investigators found. The article was published in Nutrition Reviews.

“Water fasting led to improvements in blood pressure, cholesterol, and blood sugar levels, but these were short-lived,” senior author Krista A. Varady, PhD, told this news organization.

“Levels returned to baseline ... quickly after participants started eating. Most benefits disappeared in 3-4 months,” said Dr. Varady, professor of nutrition at the University of Illinois, Chicago.

“My overall conclusion,” she said, “is that I guess you could try it, but it just seems like a lot of work, and all those metabolic benefits disappear. I would encourage someone hoping to lose weight to try intermittent fasting instead of water fasting, because there’s a lot more data to show it can help with weight management.

“People should consult their doctor if they have diabetes or any other major obesity-related conditions before doing water fasting,” Dr. Varady cautioned.

“Healthy people with obesity can probably fast safely for 5 days on their own (if they don’t have any other conditions). However, no one should undertake one of these fasts for more than 5 days without medical supervision,” she stressed.
 

Eight studies of water and Buchinger fasting

Although several favorable effects of prolonged fasting have been observed, benefits must be weighed against risks, Dr. Varady and her coauthors wrote.

Most medically supervised fasting programs have reported only minor adverse events, which included hunger, headaches, nausea, vomiting, dry mouth, and fatigue. However, more severe events have been documented, including edema, abnormal results on liver function tests, decreased bone density, and metabolic acidosis.

The researchers aimed to determine the effect of prolonged fasting on weight, blood pressure, lipid levels, and glycemic control, as well as safety and the effects of refeeding.

They examined two types of prolonged fasting: water fasting and Buchinger fasting, which involves consuming 250 mL of fruit or vegetable juice for lunch and 250 mL of soup for dinner every day of the 5- to 20-day fast.

Buchinger fasting is popular in Central Europe. Water fasting “institutes” exist in the United States, such as one in California, Dr. Varady noted.

The researchers excluded fasting during Ramadan or fasting practiced by Seventh Day Adventists.

They identified four studies of water fasting and four studies of Buchinger fasting (of which one study of 1,422 participants assessed fasting for 5, 10, 15, and 20 days).

The review showed that prolonged fasting for 5-20 days produced large increases in circulating ketones, weight loss of 2%-10%, and decreases in systolic and diastolic blood pressure.

People who fasted 5 days typically lost 4%-6% of their weight; those who fasted 7-10 days lost 2%-10% of their weight; and those who fasted 15-20 days lost 7%-10% of their weight.

LDL cholesterol and triglyceride levels decreased in some trials.

Fasting glucose levels, fasting insulin levels, insulin resistance, and A1c decreased in adults without diabetes but remained unchanged in patients with type 1 or type 2 diabetes.

Some participants experienced metabolic acidosis, headaches, insomnia, or hunger.

About two-thirds of the weight lost was of lean mass, and one-third was of fat mass. The loss of lean mass loss suggests that prolonged fasting may increase the breakdown of muscle proteins, which is a concern, the researchers noted.

Few of the trials examined the effects of refeeding. In one study, normal-weight adults lost 6% of their weight after 5 days of water-only fasting but then gained it all back after 3 months of eating regularly.

In three trials, participants regained 1%-2% of their weight 2-4 months after fasting; however, those trials instructed participants to follow a calorie-restricted diet during the refeeding period.

Three to 4 months after the fast was completed, none of the metabolic benefits were maintained, even when weight loss was maintained.

The study did not receive external funding. Dr. Varady has received author fees from Hachette Book Group for “The Every Other Day Diet” and from Pan Macmillan Press for “The Fastest Diet.” The other authors have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Health benefits of prolonged “water fasting” (zero calories) or Buchinger fasting (200-300 calories/day) don’t last, according to authors of a review of eight studies.

Five days of fasting lowered weight by about 6%, but this weight was regained after 3 months of regular eating, the investigators found. The article was published in Nutrition Reviews.

“Water fasting led to improvements in blood pressure, cholesterol, and blood sugar levels, but these were short-lived,” senior author Krista A. Varady, PhD, told this news organization.

“Levels returned to baseline ... quickly after participants started eating. Most benefits disappeared in 3-4 months,” said Dr. Varady, professor of nutrition at the University of Illinois, Chicago.

“My overall conclusion,” she said, “is that I guess you could try it, but it just seems like a lot of work, and all those metabolic benefits disappear. I would encourage someone hoping to lose weight to try intermittent fasting instead of water fasting, because there’s a lot more data to show it can help with weight management.

“People should consult their doctor if they have diabetes or any other major obesity-related conditions before doing water fasting,” Dr. Varady cautioned.

“Healthy people with obesity can probably fast safely for 5 days on their own (if they don’t have any other conditions). However, no one should undertake one of these fasts for more than 5 days without medical supervision,” she stressed.
 

Eight studies of water and Buchinger fasting

Although several favorable effects of prolonged fasting have been observed, benefits must be weighed against risks, Dr. Varady and her coauthors wrote.

Most medically supervised fasting programs have reported only minor adverse events, which included hunger, headaches, nausea, vomiting, dry mouth, and fatigue. However, more severe events have been documented, including edema, abnormal results on liver function tests, decreased bone density, and metabolic acidosis.

The researchers aimed to determine the effect of prolonged fasting on weight, blood pressure, lipid levels, and glycemic control, as well as safety and the effects of refeeding.

They examined two types of prolonged fasting: water fasting and Buchinger fasting, which involves consuming 250 mL of fruit or vegetable juice for lunch and 250 mL of soup for dinner every day of the 5- to 20-day fast.

Buchinger fasting is popular in Central Europe. Water fasting “institutes” exist in the United States, such as one in California, Dr. Varady noted.

The researchers excluded fasting during Ramadan or fasting practiced by Seventh Day Adventists.

They identified four studies of water fasting and four studies of Buchinger fasting (of which one study of 1,422 participants assessed fasting for 5, 10, 15, and 20 days).

The review showed that prolonged fasting for 5-20 days produced large increases in circulating ketones, weight loss of 2%-10%, and decreases in systolic and diastolic blood pressure.

People who fasted 5 days typically lost 4%-6% of their weight; those who fasted 7-10 days lost 2%-10% of their weight; and those who fasted 15-20 days lost 7%-10% of their weight.

LDL cholesterol and triglyceride levels decreased in some trials.

Fasting glucose levels, fasting insulin levels, insulin resistance, and A1c decreased in adults without diabetes but remained unchanged in patients with type 1 or type 2 diabetes.

Some participants experienced metabolic acidosis, headaches, insomnia, or hunger.

About two-thirds of the weight lost was of lean mass, and one-third was of fat mass. The loss of lean mass loss suggests that prolonged fasting may increase the breakdown of muscle proteins, which is a concern, the researchers noted.

Few of the trials examined the effects of refeeding. In one study, normal-weight adults lost 6% of their weight after 5 days of water-only fasting but then gained it all back after 3 months of eating regularly.

In three trials, participants regained 1%-2% of their weight 2-4 months after fasting; however, those trials instructed participants to follow a calorie-restricted diet during the refeeding period.

Three to 4 months after the fast was completed, none of the metabolic benefits were maintained, even when weight loss was maintained.

The study did not receive external funding. Dr. Varady has received author fees from Hachette Book Group for “The Every Other Day Diet” and from Pan Macmillan Press for “The Fastest Diet.” The other authors have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Health benefits of prolonged “water fasting” (zero calories) or Buchinger fasting (200-300 calories/day) don’t last, according to authors of a review of eight studies.

Five days of fasting lowered weight by about 6%, but this weight was regained after 3 months of regular eating, the investigators found. The article was published in Nutrition Reviews.

“Water fasting led to improvements in blood pressure, cholesterol, and blood sugar levels, but these were short-lived,” senior author Krista A. Varady, PhD, told this news organization.

“Levels returned to baseline ... quickly after participants started eating. Most benefits disappeared in 3-4 months,” said Dr. Varady, professor of nutrition at the University of Illinois, Chicago.

“My overall conclusion,” she said, “is that I guess you could try it, but it just seems like a lot of work, and all those metabolic benefits disappear. I would encourage someone hoping to lose weight to try intermittent fasting instead of water fasting, because there’s a lot more data to show it can help with weight management.

“People should consult their doctor if they have diabetes or any other major obesity-related conditions before doing water fasting,” Dr. Varady cautioned.

“Healthy people with obesity can probably fast safely for 5 days on their own (if they don’t have any other conditions). However, no one should undertake one of these fasts for more than 5 days without medical supervision,” she stressed.
 

Eight studies of water and Buchinger fasting

Although several favorable effects of prolonged fasting have been observed, benefits must be weighed against risks, Dr. Varady and her coauthors wrote.

Most medically supervised fasting programs have reported only minor adverse events, which included hunger, headaches, nausea, vomiting, dry mouth, and fatigue. However, more severe events have been documented, including edema, abnormal results on liver function tests, decreased bone density, and metabolic acidosis.

The researchers aimed to determine the effect of prolonged fasting on weight, blood pressure, lipid levels, and glycemic control, as well as safety and the effects of refeeding.

They examined two types of prolonged fasting: water fasting and Buchinger fasting, which involves consuming 250 mL of fruit or vegetable juice for lunch and 250 mL of soup for dinner every day of the 5- to 20-day fast.

Buchinger fasting is popular in Central Europe. Water fasting “institutes” exist in the United States, such as one in California, Dr. Varady noted.

The researchers excluded fasting during Ramadan or fasting practiced by Seventh Day Adventists.

They identified four studies of water fasting and four studies of Buchinger fasting (of which one study of 1,422 participants assessed fasting for 5, 10, 15, and 20 days).

The review showed that prolonged fasting for 5-20 days produced large increases in circulating ketones, weight loss of 2%-10%, and decreases in systolic and diastolic blood pressure.

People who fasted 5 days typically lost 4%-6% of their weight; those who fasted 7-10 days lost 2%-10% of their weight; and those who fasted 15-20 days lost 7%-10% of their weight.

LDL cholesterol and triglyceride levels decreased in some trials.

Fasting glucose levels, fasting insulin levels, insulin resistance, and A1c decreased in adults without diabetes but remained unchanged in patients with type 1 or type 2 diabetes.

Some participants experienced metabolic acidosis, headaches, insomnia, or hunger.

About two-thirds of the weight lost was of lean mass, and one-third was of fat mass. The loss of lean mass loss suggests that prolonged fasting may increase the breakdown of muscle proteins, which is a concern, the researchers noted.

Few of the trials examined the effects of refeeding. In one study, normal-weight adults lost 6% of their weight after 5 days of water-only fasting but then gained it all back after 3 months of eating regularly.

In three trials, participants regained 1%-2% of their weight 2-4 months after fasting; however, those trials instructed participants to follow a calorie-restricted diet during the refeeding period.

Three to 4 months after the fast was completed, none of the metabolic benefits were maintained, even when weight loss was maintained.

The study did not receive external funding. Dr. Varady has received author fees from Hachette Book Group for “The Every Other Day Diet” and from Pan Macmillan Press for “The Fastest Diet.” The other authors have disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Approximately one-quarter of adults who experience long COVID report activity limitations that do not change over time, based on data from national sample of nonhospitalized individuals.

Symptoms of long COVID, an ongoing medical condition that occurs in the wake of COVID-19 infection, include respiratory, neurologic, cardiovascular, or other complications that may last for weeks, months, or years after infection.

Current estimates of the incidence of long COVID in the United States range from 7.5% to 41%, according to Nicole D. Ford, PhD, of the Centers for Disease Control and Prevention, Atlanta, and colleagues. Long COVID has shown a significant effect on patients’ quality of life, functional status, and ability to work, but the impact on activity limitation in particular has not been examined, the researchers said.

In a study published in the Centers for Disease Control and Prevention’s Morbidity and Mortality Weekly Report (MMWR), the researchers reviewed data from surveys conducted between June 1 and 13, 2022, and June 7 and 19, 2023. The data came from the Census Bureau’s Household Pulse Survey (HPS), a cross-sectional national survey designed to measure the social and economic effects of COVID-19 on U.S. households. Surveys were conducted in 2-week cycles (2 weeks on, 2 weeks off). Questions about long COVID were added to the survey beginning on June 1, 2022, and questions about activity limitations from long COVID were added on Sept. 14, 2022, including questions about participants’ abilities to perform daily activities before and after COVID-19 infection.

Overall, the prevalence of long COVID decreased from 7.5% to 6.0% in U.S. adults aged 18 years and older during the study period. However, when stratified by age group, the decline was significant only in adults older than 60 years, and 1 in 10 adults with a history of COVID-19 reported long COVID at the end of the study period.

Among respondents with long COVID, 26.4% of respondents for time period of June 7-19, 2023, reported significant activity limitations, which remained unchanged over time, with no clear pattern in activity limitations across age groups, the researchers said.

Prevalence of long COVID was highest for individuals in middle adulthood (aged 30-39 years, 40-49 years, and 50-59 years) and lowest for younger adults (18-29 years) and older adults (aged 60 years and older). The prevalence of long COVID decreased by 1.16% per survey cycle between the June 1-13 and Jan. 4-16 cycles, but then remained stable, with a decrease of 0.01% per cycle between June 1-13, 2022, and Jan. 4-16, 2023.

Previous studies have shown that activity limitations resulting from long COVID can significantly affect quality of life and functional status, as well as the ability to work or care for others. A recent study in the United Kingdom showed that quality of life scores among long COVID patients were similar to those of individuals with advanced cancer, and more than half of the long COVID patients reported moderately severe functional impairment. “The larger economic and societal impact of long COVID could be far-reaching if working-age adults are unable to maintain employment or care for children or aging parents,” the researchers said.

The current study findings were limited by several factors including potential coverage bias in the survey sample, the relatively low survey response rate, and the inability to collect data on duration of symptoms, COVID-19 vaccination status, treatment during acute infection, and time since COVID-19 illness; any of these factors could affect the reported prevalence of long COVID, the researchers noted.

However, the results suggest the need for continued attention to COVID-19 prevention efforts, including not only staying current with recommended COVID-19 vaccination, but also planning for symptom management and health care service needs of long COVID patients, they concluded.
 

More data are needed to tease out patterns

“Physicians and patients are still trying to understand long COVID and its implications for the health of affected individuals,” said Noel Deep, MD, in an interview.

The current study shows a prevalence of long COVID in approximately 11% of COVID patients, which is a significant number, said Dr. Deep, a general internist in private practice in Antigo, Wisc., who was not involved in the study. Dr. Deep also serves as chief medical officer and a staff physician at Aspirus Langlade Hospital in Antigo.

The study also was useful to illustrate a decline in the incidence of people affected by long COVID symptoms in the United States and in other countries, he said.

Dr. Deep noted that despite the persistent prevalence of long COVID symptoms overall, he was encouraged by the findings that older adults “who tend to have other underlying health conditions that could put them at a higher risk for adverse health outcomes” reported fewer long COVID symptoms than younger adults.

However, he noted that the high incidence of long COVID symptoms in able-bodied individuals in their 30s and 40s may affect their the economic situations as well as their ability to care for elderly relatives and children who might be dependent on them.

“Physicians and other clinicians should be aware of the symptoms and impacts caused by long COVID,” Dr. Deep said in an interview. “These individuals usually present with a myriad of vague and varying symptoms. Physicians should be cognizant of this situation, ask about previous infection with COVID-19, and utilize the resources of long COVID clinics where available,” he said.

Several factors can affect the assessment and management of patients with long COVID symptoms in primary care practices, said Dr. Deep. First and foremost are the time constraints of detailed evaluation and testing, he said.

Second, primary care clinicians need to be aware of the different symptoms that may be indicative of long COVID including fatigue, neurocognitive symptoms such as brain fog or memory disturbance, respiratory symptoms, and cardiovascular symptoms, as well as olfactory and gustatory symptoms. “These symptoms can be confounded by underlying health conditions, especially in elderly individuals,” he noted.

“Recommendations and guidelines are evolving regarding the evaluation and management of patients with long COVID that should help physicians and other clinicians in the future,” said Dr. Deep.

In the meantime, having a high index of suspicion, paying attention to the symptoms described by the patient, and taking a proper history with regard to previous COVID-19 infection should help overcome some of these challenges, he said.

The study received no outside funding. The researchers had no financial conflicts to disclose. Dr. Deep had no financial conflicts to disclose and serves on the Editorial Advisory Board of Internal Medicine News.

Approximately one-quarter of adults who experience long COVID report activity limitations that do not change over time, based on data from national sample of nonhospitalized individuals.

Symptoms of long COVID, an ongoing medical condition that occurs in the wake of COVID-19 infection, include respiratory, neurologic, cardiovascular, or other complications that may last for weeks, months, or years after infection.

Current estimates of the incidence of long COVID in the United States range from 7.5% to 41%, according to Nicole D. Ford, PhD, of the Centers for Disease Control and Prevention, Atlanta, and colleagues. Long COVID has shown a significant effect on patients’ quality of life, functional status, and ability to work, but the impact on activity limitation in particular has not been examined, the researchers said.

In a study published in the Centers for Disease Control and Prevention’s Morbidity and Mortality Weekly Report (MMWR), the researchers reviewed data from surveys conducted between June 1 and 13, 2022, and June 7 and 19, 2023. The data came from the Census Bureau’s Household Pulse Survey (HPS), a cross-sectional national survey designed to measure the social and economic effects of COVID-19 on U.S. households. Surveys were conducted in 2-week cycles (2 weeks on, 2 weeks off). Questions about long COVID were added to the survey beginning on June 1, 2022, and questions about activity limitations from long COVID were added on Sept. 14, 2022, including questions about participants’ abilities to perform daily activities before and after COVID-19 infection.

Overall, the prevalence of long COVID decreased from 7.5% to 6.0% in U.S. adults aged 18 years and older during the study period. However, when stratified by age group, the decline was significant only in adults older than 60 years, and 1 in 10 adults with a history of COVID-19 reported long COVID at the end of the study period.

Among respondents with long COVID, 26.4% of respondents for time period of June 7-19, 2023, reported significant activity limitations, which remained unchanged over time, with no clear pattern in activity limitations across age groups, the researchers said.

Prevalence of long COVID was highest for individuals in middle adulthood (aged 30-39 years, 40-49 years, and 50-59 years) and lowest for younger adults (18-29 years) and older adults (aged 60 years and older). The prevalence of long COVID decreased by 1.16% per survey cycle between the June 1-13 and Jan. 4-16 cycles, but then remained stable, with a decrease of 0.01% per cycle between June 1-13, 2022, and Jan. 4-16, 2023.

Previous studies have shown that activity limitations resulting from long COVID can significantly affect quality of life and functional status, as well as the ability to work or care for others. A recent study in the United Kingdom showed that quality of life scores among long COVID patients were similar to those of individuals with advanced cancer, and more than half of the long COVID patients reported moderately severe functional impairment. “The larger economic and societal impact of long COVID could be far-reaching if working-age adults are unable to maintain employment or care for children or aging parents,” the researchers said.

The current study findings were limited by several factors including potential coverage bias in the survey sample, the relatively low survey response rate, and the inability to collect data on duration of symptoms, COVID-19 vaccination status, treatment during acute infection, and time since COVID-19 illness; any of these factors could affect the reported prevalence of long COVID, the researchers noted.

However, the results suggest the need for continued attention to COVID-19 prevention efforts, including not only staying current with recommended COVID-19 vaccination, but also planning for symptom management and health care service needs of long COVID patients, they concluded.
 

More data are needed to tease out patterns

“Physicians and patients are still trying to understand long COVID and its implications for the health of affected individuals,” said Noel Deep, MD, in an interview.

The current study shows a prevalence of long COVID in approximately 11% of COVID patients, which is a significant number, said Dr. Deep, a general internist in private practice in Antigo, Wisc., who was not involved in the study. Dr. Deep also serves as chief medical officer and a staff physician at Aspirus Langlade Hospital in Antigo.

The study also was useful to illustrate a decline in the incidence of people affected by long COVID symptoms in the United States and in other countries, he said.

Dr. Deep noted that despite the persistent prevalence of long COVID symptoms overall, he was encouraged by the findings that older adults “who tend to have other underlying health conditions that could put them at a higher risk for adverse health outcomes” reported fewer long COVID symptoms than younger adults.

However, he noted that the high incidence of long COVID symptoms in able-bodied individuals in their 30s and 40s may affect their the economic situations as well as their ability to care for elderly relatives and children who might be dependent on them.

“Physicians and other clinicians should be aware of the symptoms and impacts caused by long COVID,” Dr. Deep said in an interview. “These individuals usually present with a myriad of vague and varying symptoms. Physicians should be cognizant of this situation, ask about previous infection with COVID-19, and utilize the resources of long COVID clinics where available,” he said.

Several factors can affect the assessment and management of patients with long COVID symptoms in primary care practices, said Dr. Deep. First and foremost are the time constraints of detailed evaluation and testing, he said.

Second, primary care clinicians need to be aware of the different symptoms that may be indicative of long COVID including fatigue, neurocognitive symptoms such as brain fog or memory disturbance, respiratory symptoms, and cardiovascular symptoms, as well as olfactory and gustatory symptoms. “These symptoms can be confounded by underlying health conditions, especially in elderly individuals,” he noted.

“Recommendations and guidelines are evolving regarding the evaluation and management of patients with long COVID that should help physicians and other clinicians in the future,” said Dr. Deep.

In the meantime, having a high index of suspicion, paying attention to the symptoms described by the patient, and taking a proper history with regard to previous COVID-19 infection should help overcome some of these challenges, he said.

The study received no outside funding. The researchers had no financial conflicts to disclose. Dr. Deep had no financial conflicts to disclose and serves on the Editorial Advisory Board of Internal Medicine News.

Approximately one-quarter of adults who experience long COVID report activity limitations that do not change over time, based on data from national sample of nonhospitalized individuals.

Symptoms of long COVID, an ongoing medical condition that occurs in the wake of COVID-19 infection, include respiratory, neurologic, cardiovascular, or other complications that may last for weeks, months, or years after infection.

Current estimates of the incidence of long COVID in the United States range from 7.5% to 41%, according to Nicole D. Ford, PhD, of the Centers for Disease Control and Prevention, Atlanta, and colleagues. Long COVID has shown a significant effect on patients’ quality of life, functional status, and ability to work, but the impact on activity limitation in particular has not been examined, the researchers said.

In a study published in the Centers for Disease Control and Prevention’s Morbidity and Mortality Weekly Report (MMWR), the researchers reviewed data from surveys conducted between June 1 and 13, 2022, and June 7 and 19, 2023. The data came from the Census Bureau’s Household Pulse Survey (HPS), a cross-sectional national survey designed to measure the social and economic effects of COVID-19 on U.S. households. Surveys were conducted in 2-week cycles (2 weeks on, 2 weeks off). Questions about long COVID were added to the survey beginning on June 1, 2022, and questions about activity limitations from long COVID were added on Sept. 14, 2022, including questions about participants’ abilities to perform daily activities before and after COVID-19 infection.

Overall, the prevalence of long COVID decreased from 7.5% to 6.0% in U.S. adults aged 18 years and older during the study period. However, when stratified by age group, the decline was significant only in adults older than 60 years, and 1 in 10 adults with a history of COVID-19 reported long COVID at the end of the study period.

Among respondents with long COVID, 26.4% of respondents for time period of June 7-19, 2023, reported significant activity limitations, which remained unchanged over time, with no clear pattern in activity limitations across age groups, the researchers said.

Prevalence of long COVID was highest for individuals in middle adulthood (aged 30-39 years, 40-49 years, and 50-59 years) and lowest for younger adults (18-29 years) and older adults (aged 60 years and older). The prevalence of long COVID decreased by 1.16% per survey cycle between the June 1-13 and Jan. 4-16 cycles, but then remained stable, with a decrease of 0.01% per cycle between June 1-13, 2022, and Jan. 4-16, 2023.

Previous studies have shown that activity limitations resulting from long COVID can significantly affect quality of life and functional status, as well as the ability to work or care for others. A recent study in the United Kingdom showed that quality of life scores among long COVID patients were similar to those of individuals with advanced cancer, and more than half of the long COVID patients reported moderately severe functional impairment. “The larger economic and societal impact of long COVID could be far-reaching if working-age adults are unable to maintain employment or care for children or aging parents,” the researchers said.

The current study findings were limited by several factors including potential coverage bias in the survey sample, the relatively low survey response rate, and the inability to collect data on duration of symptoms, COVID-19 vaccination status, treatment during acute infection, and time since COVID-19 illness; any of these factors could affect the reported prevalence of long COVID, the researchers noted.

However, the results suggest the need for continued attention to COVID-19 prevention efforts, including not only staying current with recommended COVID-19 vaccination, but also planning for symptom management and health care service needs of long COVID patients, they concluded.
 

More data are needed to tease out patterns

“Physicians and patients are still trying to understand long COVID and its implications for the health of affected individuals,” said Noel Deep, MD, in an interview.

The current study shows a prevalence of long COVID in approximately 11% of COVID patients, which is a significant number, said Dr. Deep, a general internist in private practice in Antigo, Wisc., who was not involved in the study. Dr. Deep also serves as chief medical officer and a staff physician at Aspirus Langlade Hospital in Antigo.

The study also was useful to illustrate a decline in the incidence of people affected by long COVID symptoms in the United States and in other countries, he said.

Dr. Deep noted that despite the persistent prevalence of long COVID symptoms overall, he was encouraged by the findings that older adults “who tend to have other underlying health conditions that could put them at a higher risk for adverse health outcomes” reported fewer long COVID symptoms than younger adults.

However, he noted that the high incidence of long COVID symptoms in able-bodied individuals in their 30s and 40s may affect their the economic situations as well as their ability to care for elderly relatives and children who might be dependent on them.

“Physicians and other clinicians should be aware of the symptoms and impacts caused by long COVID,” Dr. Deep said in an interview. “These individuals usually present with a myriad of vague and varying symptoms. Physicians should be cognizant of this situation, ask about previous infection with COVID-19, and utilize the resources of long COVID clinics where available,” he said.

Several factors can affect the assessment and management of patients with long COVID symptoms in primary care practices, said Dr. Deep. First and foremost are the time constraints of detailed evaluation and testing, he said.

Second, primary care clinicians need to be aware of the different symptoms that may be indicative of long COVID including fatigue, neurocognitive symptoms such as brain fog or memory disturbance, respiratory symptoms, and cardiovascular symptoms, as well as olfactory and gustatory symptoms. “These symptoms can be confounded by underlying health conditions, especially in elderly individuals,” he noted.

“Recommendations and guidelines are evolving regarding the evaluation and management of patients with long COVID that should help physicians and other clinicians in the future,” said Dr. Deep.

In the meantime, having a high index of suspicion, paying attention to the symptoms described by the patient, and taking a proper history with regard to previous COVID-19 infection should help overcome some of these challenges, he said.

The study received no outside funding. The researchers had no financial conflicts to disclose. Dr. Deep had no financial conflicts to disclose and serves on the Editorial Advisory Board of Internal Medicine News.

Patients with a severe form of ventricular arrhythmia who may be referred for catheter ablation are often first tested for coronary artery disease (CAD) or ischemia. But such testing seldom makes a difference to downstream management or outcomes, researchers conclude based on registry data.

The findings, they say, question such routine CAD/ischemia testing in patients like those studied, who had episodes of monomorphic ventricular tachycardia (VT) storm but not an acute coronary syndrome (ACS) and ultimately went to ablation.

Of 97 such patients, about 44% underwent CAD/ischemia testing by invasive angiography, myocardial functional imaging, or both. But the tests didn’t predict important ablation outcomes, including pre- or postablation VT inducibility. Nor did they significantly affect the likelihood or outcomes of preablation revascularization or 2-year survival.

The findings “argue against performing routine evaluations to rule out coronary [disease] or myocardial ischemia as culprits in monomorphic VT storm” in patients without evidence of ACS, write Feras Alkhalaileh, MD, Heart and Vascular Institute, Cleveland Clinic, and colleagues in their report published in JACC: Clinical Electrophysiology.

They suggest it’s “reasonable” not to perform tests for CAD or ischemia in such patients, senior author Ayman A. Hussein, MD, from the same center, said in an interview. Although such tests may be considered “case by case,” performed routinely they “aren’t going to add much to patient care, and as a matter of fact, may delay proper care and expose them to risks,” Dr. Hussein said.

It’s “reasonable” to test for CAD or ischemia in patients with polymorphic VT storm, which is likely ischemia-driven, he observed. In contrast, monomorphic VT storm is likely caused by myocardial scar, which revascularization cannot treat. “Because there’s scar substrate, we find that ischemic evaluations are technically without much yield.”

These issues are “not very controversial” among cardiac electrophysiologists, Dr. Hussein said, but it remains “common practice” for other specialists to order angiography or ischemia testing for patients with monomorphic VT storm, typically in the cardiac care unit (CCU), before considering ablation.

“Sometimes, as electrophysiologists, we don’t get to see them before an ischemic evaluation has already been done,” he added.

It’s “very hard to convince interventional cardiologists, CCU intensivists, or general cardiologists” that a VT may not be caused by ischemia, said electrophysiologist Roderick Tung, MD, University of Arizona College of Medicine, Phoenix, who was not involved in the current study.

In patients with monomorphic VT storm, “by the time we’re consulted, they’ve already had a cath. And it’s probably just not necessary,” Dr. Tung said. “That’s why this is such a great paper, because it has an immediate message [for nonelectrophysiologist clinicians and] the potential to change clinical practice.”

The study included 97 patients with monomorphic VT storm from a prospective VT-ablation registry covering about 7 years at a major referral center. Their mean age was 64 years, and 88% were men. Two-thirds were known to have ischemic cardiomyopathy and were in NYHA functional class II.

As reported, 10% of the cohort underwent coronary angiography after presentation with monomorphic VT storm, 26% had CT or PET myocardial functional imaging, and 9% had both tests.

Only four patients ultimately underwent coronary revascularization; no acute coronary occlusions were involved. Monomorphic VT recurred in all four cases, the report notes.

The 43 and 54 patients who did or did not get the CAD/ischemia tests, respectively, showed no significant procedural differences in extent of scar modification, prevalence of clinical or hemodynamically stable VT, or use of mechanical circulatory support; or in postablation, VT inducibility or overall mortality during follow-up averaging 24.3 months.

To address possible concerns about selection bias in the main cohort, all of whom underwent ablation, a secondary analysis was conducted with 91 patients with known asymptomatic coronary disease and monomorphic VT storm who were selected from the registry without regard to whether they underwent catheter ablation.

Of that cohort, 21 went to invasive angiography and 25 underwent stress testing; six of the latter went on to coronary angiography, the report states. Monomorphic VT later recurred in four of the five patients, who then underwent coronary revascularization.

Such patients with known coronary disease, Dr. Hussein said, are those “possibly more likely to get an ischemic evaluation.” And yet, “regardless of whether they had ablation, the yield of ischemic evaluations in these patients was low.”

By far most of the CAD/ischemia tests in the study’s primary cohort were performed using noninvasive imaging, notes an editorial accompanying the new report. “This raises the possibility of false negatives with very proximal and multivessel CAD, and with balanced ischemia,” write Saurabh Kumar, BSc (Med)/MBBS, PhD, and Ashwin Bhaskaran, MBBS, MSc, University of Sydney.

Ideally, the issues addressed by the study should be tested in large randomized, controlled trials, they state. “Achieving sufficient recruitment to address this clinical question may be difficult, leaving clinicians with the challenge of applying observational data to their patients.”

A version of this article appeared on Medscape.com.

Patients with a severe form of ventricular arrhythmia who may be referred for catheter ablation are often first tested for coronary artery disease (CAD) or ischemia. But such testing seldom makes a difference to downstream management or outcomes, researchers conclude based on registry data.

The findings, they say, question such routine CAD/ischemia testing in patients like those studied, who had episodes of monomorphic ventricular tachycardia (VT) storm but not an acute coronary syndrome (ACS) and ultimately went to ablation.

Of 97 such patients, about 44% underwent CAD/ischemia testing by invasive angiography, myocardial functional imaging, or both. But the tests didn’t predict important ablation outcomes, including pre- or postablation VT inducibility. Nor did they significantly affect the likelihood or outcomes of preablation revascularization or 2-year survival.

The findings “argue against performing routine evaluations to rule out coronary [disease] or myocardial ischemia as culprits in monomorphic VT storm” in patients without evidence of ACS, write Feras Alkhalaileh, MD, Heart and Vascular Institute, Cleveland Clinic, and colleagues in their report published in JACC: Clinical Electrophysiology.

They suggest it’s “reasonable” not to perform tests for CAD or ischemia in such patients, senior author Ayman A. Hussein, MD, from the same center, said in an interview. Although such tests may be considered “case by case,” performed routinely they “aren’t going to add much to patient care, and as a matter of fact, may delay proper care and expose them to risks,” Dr. Hussein said.

It’s “reasonable” to test for CAD or ischemia in patients with polymorphic VT storm, which is likely ischemia-driven, he observed. In contrast, monomorphic VT storm is likely caused by myocardial scar, which revascularization cannot treat. “Because there’s scar substrate, we find that ischemic evaluations are technically without much yield.”

These issues are “not very controversial” among cardiac electrophysiologists, Dr. Hussein said, but it remains “common practice” for other specialists to order angiography or ischemia testing for patients with monomorphic VT storm, typically in the cardiac care unit (CCU), before considering ablation.

“Sometimes, as electrophysiologists, we don’t get to see them before an ischemic evaluation has already been done,” he added.

It’s “very hard to convince interventional cardiologists, CCU intensivists, or general cardiologists” that a VT may not be caused by ischemia, said electrophysiologist Roderick Tung, MD, University of Arizona College of Medicine, Phoenix, who was not involved in the current study.

In patients with monomorphic VT storm, “by the time we’re consulted, they’ve already had a cath. And it’s probably just not necessary,” Dr. Tung said. “That’s why this is such a great paper, because it has an immediate message [for nonelectrophysiologist clinicians and] the potential to change clinical practice.”

The study included 97 patients with monomorphic VT storm from a prospective VT-ablation registry covering about 7 years at a major referral center. Their mean age was 64 years, and 88% were men. Two-thirds were known to have ischemic cardiomyopathy and were in NYHA functional class II.

As reported, 10% of the cohort underwent coronary angiography after presentation with monomorphic VT storm, 26% had CT or PET myocardial functional imaging, and 9% had both tests.

Only four patients ultimately underwent coronary revascularization; no acute coronary occlusions were involved. Monomorphic VT recurred in all four cases, the report notes.

The 43 and 54 patients who did or did not get the CAD/ischemia tests, respectively, showed no significant procedural differences in extent of scar modification, prevalence of clinical or hemodynamically stable VT, or use of mechanical circulatory support; or in postablation, VT inducibility or overall mortality during follow-up averaging 24.3 months.

To address possible concerns about selection bias in the main cohort, all of whom underwent ablation, a secondary analysis was conducted with 91 patients with known asymptomatic coronary disease and monomorphic VT storm who were selected from the registry without regard to whether they underwent catheter ablation.

Of that cohort, 21 went to invasive angiography and 25 underwent stress testing; six of the latter went on to coronary angiography, the report states. Monomorphic VT later recurred in four of the five patients, who then underwent coronary revascularization.

Such patients with known coronary disease, Dr. Hussein said, are those “possibly more likely to get an ischemic evaluation.” And yet, “regardless of whether they had ablation, the yield of ischemic evaluations in these patients was low.”

By far most of the CAD/ischemia tests in the study’s primary cohort were performed using noninvasive imaging, notes an editorial accompanying the new report. “This raises the possibility of false negatives with very proximal and multivessel CAD, and with balanced ischemia,” write Saurabh Kumar, BSc (Med)/MBBS, PhD, and Ashwin Bhaskaran, MBBS, MSc, University of Sydney.

Ideally, the issues addressed by the study should be tested in large randomized, controlled trials, they state. “Achieving sufficient recruitment to address this clinical question may be difficult, leaving clinicians with the challenge of applying observational data to their patients.”

A version of this article appeared on Medscape.com.

Patients with a severe form of ventricular arrhythmia who may be referred for catheter ablation are often first tested for coronary artery disease (CAD) or ischemia. But such testing seldom makes a difference to downstream management or outcomes, researchers conclude based on registry data.

The findings, they say, question such routine CAD/ischemia testing in patients like those studied, who had episodes of monomorphic ventricular tachycardia (VT) storm but not an acute coronary syndrome (ACS) and ultimately went to ablation.

Of 97 such patients, about 44% underwent CAD/ischemia testing by invasive angiography, myocardial functional imaging, or both. But the tests didn’t predict important ablation outcomes, including pre- or postablation VT inducibility. Nor did they significantly affect the likelihood or outcomes of preablation revascularization or 2-year survival.

The findings “argue against performing routine evaluations to rule out coronary [disease] or myocardial ischemia as culprits in monomorphic VT storm” in patients without evidence of ACS, write Feras Alkhalaileh, MD, Heart and Vascular Institute, Cleveland Clinic, and colleagues in their report published in JACC: Clinical Electrophysiology.

They suggest it’s “reasonable” not to perform tests for CAD or ischemia in such patients, senior author Ayman A. Hussein, MD, from the same center, said in an interview. Although such tests may be considered “case by case,” performed routinely they “aren’t going to add much to patient care, and as a matter of fact, may delay proper care and expose them to risks,” Dr. Hussein said.

It’s “reasonable” to test for CAD or ischemia in patients with polymorphic VT storm, which is likely ischemia-driven, he observed. In contrast, monomorphic VT storm is likely caused by myocardial scar, which revascularization cannot treat. “Because there’s scar substrate, we find that ischemic evaluations are technically without much yield.”

These issues are “not very controversial” among cardiac electrophysiologists, Dr. Hussein said, but it remains “common practice” for other specialists to order angiography or ischemia testing for patients with monomorphic VT storm, typically in the cardiac care unit (CCU), before considering ablation.

“Sometimes, as electrophysiologists, we don’t get to see them before an ischemic evaluation has already been done,” he added.

It’s “very hard to convince interventional cardiologists, CCU intensivists, or general cardiologists” that a VT may not be caused by ischemia, said electrophysiologist Roderick Tung, MD, University of Arizona College of Medicine, Phoenix, who was not involved in the current study.

In patients with monomorphic VT storm, “by the time we’re consulted, they’ve already had a cath. And it’s probably just not necessary,” Dr. Tung said. “That’s why this is such a great paper, because it has an immediate message [for nonelectrophysiologist clinicians and] the potential to change clinical practice.”

The study included 97 patients with monomorphic VT storm from a prospective VT-ablation registry covering about 7 years at a major referral center. Their mean age was 64 years, and 88% were men. Two-thirds were known to have ischemic cardiomyopathy and were in NYHA functional class II.

As reported, 10% of the cohort underwent coronary angiography after presentation with monomorphic VT storm, 26% had CT or PET myocardial functional imaging, and 9% had both tests.

Only four patients ultimately underwent coronary revascularization; no acute coronary occlusions were involved. Monomorphic VT recurred in all four cases, the report notes.

The 43 and 54 patients who did or did not get the CAD/ischemia tests, respectively, showed no significant procedural differences in extent of scar modification, prevalence of clinical or hemodynamically stable VT, or use of mechanical circulatory support; or in postablation, VT inducibility or overall mortality during follow-up averaging 24.3 months.

To address possible concerns about selection bias in the main cohort, all of whom underwent ablation, a secondary analysis was conducted with 91 patients with known asymptomatic coronary disease and monomorphic VT storm who were selected from the registry without regard to whether they underwent catheter ablation.

Of that cohort, 21 went to invasive angiography and 25 underwent stress testing; six of the latter went on to coronary angiography, the report states. Monomorphic VT later recurred in four of the five patients, who then underwent coronary revascularization.

Such patients with known coronary disease, Dr. Hussein said, are those “possibly more likely to get an ischemic evaluation.” And yet, “regardless of whether they had ablation, the yield of ischemic evaluations in these patients was low.”

By far most of the CAD/ischemia tests in the study’s primary cohort were performed using noninvasive imaging, notes an editorial accompanying the new report. “This raises the possibility of false negatives with very proximal and multivessel CAD, and with balanced ischemia,” write Saurabh Kumar, BSc (Med)/MBBS, PhD, and Ashwin Bhaskaran, MBBS, MSc, University of Sydney.

Ideally, the issues addressed by the study should be tested in large randomized, controlled trials, they state. “Achieving sufficient recruitment to address this clinical question may be difficult, leaving clinicians with the challenge of applying observational data to their patients.”

A version of this article appeared on Medscape.com.

Medical education has changed drastically over the years. As theories and practices continue to change, what was once standard 10 or 20 years ago has been replaced with newer ideologies, processes, or technology. It seems likely, then, that you may disagree with some of the things that you learned as medical school has evolved.

This news organization asked physicians what they learned in med school that they now contest. Many of their answers include newer philosophies and practice methods.
 

Treat appropriately for pain

Jacqui O’Kane, DO, a 2013 med school graduate, was taught to avoid prescribing controlled medications whenever possible.

“Initially this attitude made sense to me,” says Dr. O’Kane, “but as I became an experienced physician – and patient – I saw the harm that such an attitude could cause. Patients on controlled medication long-term were often viewed as drug-seekers and treated as such, even if their regimen was largely regarded as appropriate. Likewise, those who could benefit from short-term controlled prescriptions were sometimes denied them because of their clinician’s fear.”

Today, Dr. O’Kane believes controlled medications should seldom be the first option for patients suffering pain, anxiety, or insomnia. But, she says, “they should remain on the table and without judgment for those who fail first-line treatment or for whom alternatives are contraindicated.”

Amy Baxter, MD, believes that the amount of time spent on pain education in school needs to change.

“Doctors in the U.S. get only 12 hours of pain education, and most of it is on pharmacology,” says Dr. Baxter, who graduated from med school in 1995. “In addition to incorrect information on home opioids and addiction, I was left with the impression that medication could treat chronic pain. I now have a completely different understanding of pain as a whole-brain warning system. The goal shouldn’t be pain-free, just more comfortable.”
 

Practice lifestyle and preventive medicine

Dolapo Babalola, MD, went to medical school eager to learn how to care for the human body and her family members’ illnesses, such as the debilitating effects of arthritic pain and other chronic diseases.

“I was taught the pathology behind arthritic pain, symptoms, signs, and treatment – that it has a genetic component and is inevitable to avoid – but nothing about how to prevent it,” says Dr. Babalola, a 2000 graduate.

Twenty years later, she discovered lifestyle medicine when she began to experience knee pain.

“I was introduced to the power of health restoration by discovering the root cause of diseases such as inflammation, hormonal imbalance, and insulin resistance due to poor lifestyle choices such as diet, inactivity, stress, inadequate sleep, and substance abuse,” she says.

Adebisi Alli, DO, who graduated in 2011, remembers being taught to treat type 2 diabetes by delaying progression rather than aiming for remission. But today, “lifestyle-led, team-based approaches are steadily becoming a first prescription across medical training with the goal to put diabetes in remission,” she says.
 

Patient care is at the core of medicine

Tracey O’Connell, MD, recalls her radiology residency in the early to mid-90s, when radiologists were integral to the health care team.

“We interacted with referrers and followed the course of patients’ diseases,” says Dr. O’Connell. “We knew patient histories, their stories. We were connected to other humans, doctors, nurses, teams, and the patients themselves.”

But with the advent of picture archiving and communication systems, high-speed CT and MRI, digital radiography, and voice recognition, the practice of radiology has changed dramatically.

“There’s no time to review or discuss cases anymore,” she says. “Reports went from eloquent and articulate documents with lists of differential diagnoses to short checklists and templates. The whole field of patient care has become dehumanizing, exactly the opposite of what humans need.”

Mache Seibel, MD, who graduated almost 50 years ago, agrees that patient care has lost its focus, to the detriment of patients.

“What I learned in medical school that is forgotten today is how to listen to patients, take a history, and do an examination using my hands and a stethoscope,” says Dr. Seibel. “Today with technology and time constraints, the focus is too much on the symptom without context, ordering a test, and getting the EMR boxes filled out.”
 

Physician, heal thyself

Priya Radhakrishnan, MD, remembers learning that a physician’s well-being was their responsibility. “We now know that well-being is the health system’s responsibility and that we need to diagnose ourselves and support each other, especially our trainees,” says Dr. Radhakrishna. She graduated in 1992. “Destigmatizing mental health is essential to well-being.”

Rachel Miller, MD, a 2009 med school graduate was taught that learning about health care systems and policy wasn’t necessary. Dr. Miller says they learned that policy knowledge would come in time. “I currently disagree. It is vital to understand aspects of health care systems and policy. Not knowing these things has partly contributed to the pervasiveness of burnout among physicians and other health care providers.”
 

Practice with gender at the forefront

Janice L. Werbinski, MD, an ob.gyn., and Elizabeth Anne Comen, MD, a breast cancer oncologist, remember when nearly all medical research was performed on the 140-lb White man. Doctors learned to treat patients through that male lens.

“The majority of the anatomy we saw in medical school was on a male figure,” says Dr. Comen, author of “All in Her Head,” a HarperCollins book slated to be released in February 2024. She graduated from med school in 2004. “The only time we saw anatomy for females was in the female reproductive system. That’s changing for the better.”

Dr. Werbinski chose a residency in obstetrics and gynecology in 1975 because she thought it was the only way she could serve female patients.

“I really thought that was the place for women’s health,” says Dr. Werbinski, cochair of the American Medical Women’s Association Sex & Gender Health Coalition.

“I am happy to say that significant awareness has grown since I graduated from medical school. I hope that when this question is asked of current medical students, they will be able to say that they know to practice with a sex- and gender-focused lens.”
 

Talk about racial disparities

John McHugh, MD, an ob.gyn., recalls learning little about the social determinants of health when he attended med school more than 30 years ago.

“We saw disparities in outcomes based on race and class but assumed that we would overcome them when we were in practice,” says Dr. McHugh, an AMWA Action Coalition for Equity member. “We didn’t understand the root causes of disparities and had never heard of concepts like epigenetics or weathering. I’m hopeful current research will help our understanding and today’s medical students will serve a safer, healthier, and more equitable world.”

Curtiland Deville, MD, an associate professor of radiation oncology, recalls having few conversations around race; racial disparities; and diversity, equity, and inclusion.

“When I went to medical school, it often felt like you weren’t supposed to talk about the differences in race,” says Dr. Deville, who graduated in 2005. But today, in the post-2020 era between COVID, during which health disparities got highlighted, and calls for racial justice taking center stage, Dr. Deville says many of the things they didn’t talk about have come to the forefront in our medical institutions.
 

Information at your fingertips

For Paru David, MD, a 1996 graduate, the most significant change is the amount of health and medical information available today. “Before, the information that was taught in medical school was obtained through textbooks or within journal articles,” says Dr. David.

“Now, we have databases of information. The key to success is being able to navigate the information available to us, digest it with a keen eye, and then apply it to patient care in a timely manner.”

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

Medical education has changed drastically over the years. As theories and practices continue to change, what was once standard 10 or 20 years ago has been replaced with newer ideologies, processes, or technology. It seems likely, then, that you may disagree with some of the things that you learned as medical school has evolved.

This news organization asked physicians what they learned in med school that they now contest. Many of their answers include newer philosophies and practice methods.
 

Treat appropriately for pain

Jacqui O’Kane, DO, a 2013 med school graduate, was taught to avoid prescribing controlled medications whenever possible.

“Initially this attitude made sense to me,” says Dr. O’Kane, “but as I became an experienced physician – and patient – I saw the harm that such an attitude could cause. Patients on controlled medication long-term were often viewed as drug-seekers and treated as such, even if their regimen was largely regarded as appropriate. Likewise, those who could benefit from short-term controlled prescriptions were sometimes denied them because of their clinician’s fear.”

Today, Dr. O’Kane believes controlled medications should seldom be the first option for patients suffering pain, anxiety, or insomnia. But, she says, “they should remain on the table and without judgment for those who fail first-line treatment or for whom alternatives are contraindicated.”

Amy Baxter, MD, believes that the amount of time spent on pain education in school needs to change.

“Doctors in the U.S. get only 12 hours of pain education, and most of it is on pharmacology,” says Dr. Baxter, who graduated from med school in 1995. “In addition to incorrect information on home opioids and addiction, I was left with the impression that medication could treat chronic pain. I now have a completely different understanding of pain as a whole-brain warning system. The goal shouldn’t be pain-free, just more comfortable.”
 

Practice lifestyle and preventive medicine

Dolapo Babalola, MD, went to medical school eager to learn how to care for the human body and her family members’ illnesses, such as the debilitating effects of arthritic pain and other chronic diseases.

“I was taught the pathology behind arthritic pain, symptoms, signs, and treatment – that it has a genetic component and is inevitable to avoid – but nothing about how to prevent it,” says Dr. Babalola, a 2000 graduate.

Twenty years later, she discovered lifestyle medicine when she began to experience knee pain.

“I was introduced to the power of health restoration by discovering the root cause of diseases such as inflammation, hormonal imbalance, and insulin resistance due to poor lifestyle choices such as diet, inactivity, stress, inadequate sleep, and substance abuse,” she says.

Adebisi Alli, DO, who graduated in 2011, remembers being taught to treat type 2 diabetes by delaying progression rather than aiming for remission. But today, “lifestyle-led, team-based approaches are steadily becoming a first prescription across medical training with the goal to put diabetes in remission,” she says.
 

Patient care is at the core of medicine

Tracey O’Connell, MD, recalls her radiology residency in the early to mid-90s, when radiologists were integral to the health care team.

“We interacted with referrers and followed the course of patients’ diseases,” says Dr. O’Connell. “We knew patient histories, their stories. We were connected to other humans, doctors, nurses, teams, and the patients themselves.”

But with the advent of picture archiving and communication systems, high-speed CT and MRI, digital radiography, and voice recognition, the practice of radiology has changed dramatically.

“There’s no time to review or discuss cases anymore,” she says. “Reports went from eloquent and articulate documents with lists of differential diagnoses to short checklists and templates. The whole field of patient care has become dehumanizing, exactly the opposite of what humans need.”

Mache Seibel, MD, who graduated almost 50 years ago, agrees that patient care has lost its focus, to the detriment of patients.

“What I learned in medical school that is forgotten today is how to listen to patients, take a history, and do an examination using my hands and a stethoscope,” says Dr. Seibel. “Today with technology and time constraints, the focus is too much on the symptom without context, ordering a test, and getting the EMR boxes filled out.”
 

Physician, heal thyself

Priya Radhakrishnan, MD, remembers learning that a physician’s well-being was their responsibility. “We now know that well-being is the health system’s responsibility and that we need to diagnose ourselves and support each other, especially our trainees,” says Dr. Radhakrishna. She graduated in 1992. “Destigmatizing mental health is essential to well-being.”

Rachel Miller, MD, a 2009 med school graduate was taught that learning about health care systems and policy wasn’t necessary. Dr. Miller says they learned that policy knowledge would come in time. “I currently disagree. It is vital to understand aspects of health care systems and policy. Not knowing these things has partly contributed to the pervasiveness of burnout among physicians and other health care providers.”
 

Practice with gender at the forefront

Janice L. Werbinski, MD, an ob.gyn., and Elizabeth Anne Comen, MD, a breast cancer oncologist, remember when nearly all medical research was performed on the 140-lb White man. Doctors learned to treat patients through that male lens.

“The majority of the anatomy we saw in medical school was on a male figure,” says Dr. Comen, author of “All in Her Head,” a HarperCollins book slated to be released in February 2024. She graduated from med school in 2004. “The only time we saw anatomy for females was in the female reproductive system. That’s changing for the better.”

Dr. Werbinski chose a residency in obstetrics and gynecology in 1975 because she thought it was the only way she could serve female patients.

“I really thought that was the place for women’s health,” says Dr. Werbinski, cochair of the American Medical Women’s Association Sex & Gender Health Coalition.

“I am happy to say that significant awareness has grown since I graduated from medical school. I hope that when this question is asked of current medical students, they will be able to say that they know to practice with a sex- and gender-focused lens.”
 

Talk about racial disparities

John McHugh, MD, an ob.gyn., recalls learning little about the social determinants of health when he attended med school more than 30 years ago.

“We saw disparities in outcomes based on race and class but assumed that we would overcome them when we were in practice,” says Dr. McHugh, an AMWA Action Coalition for Equity member. “We didn’t understand the root causes of disparities and had never heard of concepts like epigenetics or weathering. I’m hopeful current research will help our understanding and today’s medical students will serve a safer, healthier, and more equitable world.”

Curtiland Deville, MD, an associate professor of radiation oncology, recalls having few conversations around race; racial disparities; and diversity, equity, and inclusion.

“When I went to medical school, it often felt like you weren’t supposed to talk about the differences in race,” says Dr. Deville, who graduated in 2005. But today, in the post-2020 era between COVID, during which health disparities got highlighted, and calls for racial justice taking center stage, Dr. Deville says many of the things they didn’t talk about have come to the forefront in our medical institutions.
 

Information at your fingertips

For Paru David, MD, a 1996 graduate, the most significant change is the amount of health and medical information available today. “Before, the information that was taught in medical school was obtained through textbooks or within journal articles,” says Dr. David.

“Now, we have databases of information. The key to success is being able to navigate the information available to us, digest it with a keen eye, and then apply it to patient care in a timely manner.”

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

Medical education has changed drastically over the years. As theories and practices continue to change, what was once standard 10 or 20 years ago has been replaced with newer ideologies, processes, or technology. It seems likely, then, that you may disagree with some of the things that you learned as medical school has evolved.

This news organization asked physicians what they learned in med school that they now contest. Many of their answers include newer philosophies and practice methods.
 

Treat appropriately for pain

Jacqui O’Kane, DO, a 2013 med school graduate, was taught to avoid prescribing controlled medications whenever possible.

“Initially this attitude made sense to me,” says Dr. O’Kane, “but as I became an experienced physician – and patient – I saw the harm that such an attitude could cause. Patients on controlled medication long-term were often viewed as drug-seekers and treated as such, even if their regimen was largely regarded as appropriate. Likewise, those who could benefit from short-term controlled prescriptions were sometimes denied them because of their clinician’s fear.”

Today, Dr. O’Kane believes controlled medications should seldom be the first option for patients suffering pain, anxiety, or insomnia. But, she says, “they should remain on the table and without judgment for those who fail first-line treatment or for whom alternatives are contraindicated.”

Amy Baxter, MD, believes that the amount of time spent on pain education in school needs to change.

“Doctors in the U.S. get only 12 hours of pain education, and most of it is on pharmacology,” says Dr. Baxter, who graduated from med school in 1995. “In addition to incorrect information on home opioids and addiction, I was left with the impression that medication could treat chronic pain. I now have a completely different understanding of pain as a whole-brain warning system. The goal shouldn’t be pain-free, just more comfortable.”
 

Practice lifestyle and preventive medicine

Dolapo Babalola, MD, went to medical school eager to learn how to care for the human body and her family members’ illnesses, such as the debilitating effects of arthritic pain and other chronic diseases.

“I was taught the pathology behind arthritic pain, symptoms, signs, and treatment – that it has a genetic component and is inevitable to avoid – but nothing about how to prevent it,” says Dr. Babalola, a 2000 graduate.

Twenty years later, she discovered lifestyle medicine when she began to experience knee pain.

“I was introduced to the power of health restoration by discovering the root cause of diseases such as inflammation, hormonal imbalance, and insulin resistance due to poor lifestyle choices such as diet, inactivity, stress, inadequate sleep, and substance abuse,” she says.

Adebisi Alli, DO, who graduated in 2011, remembers being taught to treat type 2 diabetes by delaying progression rather than aiming for remission. But today, “lifestyle-led, team-based approaches are steadily becoming a first prescription across medical training with the goal to put diabetes in remission,” she says.
 

Patient care is at the core of medicine

Tracey O’Connell, MD, recalls her radiology residency in the early to mid-90s, when radiologists were integral to the health care team.

“We interacted with referrers and followed the course of patients’ diseases,” says Dr. O’Connell. “We knew patient histories, their stories. We were connected to other humans, doctors, nurses, teams, and the patients themselves.”

But with the advent of picture archiving and communication systems, high-speed CT and MRI, digital radiography, and voice recognition, the practice of radiology has changed dramatically.

“There’s no time to review or discuss cases anymore,” she says. “Reports went from eloquent and articulate documents with lists of differential diagnoses to short checklists and templates. The whole field of patient care has become dehumanizing, exactly the opposite of what humans need.”

Mache Seibel, MD, who graduated almost 50 years ago, agrees that patient care has lost its focus, to the detriment of patients.

“What I learned in medical school that is forgotten today is how to listen to patients, take a history, and do an examination using my hands and a stethoscope,” says Dr. Seibel. “Today with technology and time constraints, the focus is too much on the symptom without context, ordering a test, and getting the EMR boxes filled out.”
 

Physician, heal thyself

Priya Radhakrishnan, MD, remembers learning that a physician’s well-being was their responsibility. “We now know that well-being is the health system’s responsibility and that we need to diagnose ourselves and support each other, especially our trainees,” says Dr. Radhakrishna. She graduated in 1992. “Destigmatizing mental health is essential to well-being.”

Rachel Miller, MD, a 2009 med school graduate was taught that learning about health care systems and policy wasn’t necessary. Dr. Miller says they learned that policy knowledge would come in time. “I currently disagree. It is vital to understand aspects of health care systems and policy. Not knowing these things has partly contributed to the pervasiveness of burnout among physicians and other health care providers.”
 

Practice with gender at the forefront

Janice L. Werbinski, MD, an ob.gyn., and Elizabeth Anne Comen, MD, a breast cancer oncologist, remember when nearly all medical research was performed on the 140-lb White man. Doctors learned to treat patients through that male lens.

“The majority of the anatomy we saw in medical school was on a male figure,” says Dr. Comen, author of “All in Her Head,” a HarperCollins book slated to be released in February 2024. She graduated from med school in 2004. “The only time we saw anatomy for females was in the female reproductive system. That’s changing for the better.”

Dr. Werbinski chose a residency in obstetrics and gynecology in 1975 because she thought it was the only way she could serve female patients.

“I really thought that was the place for women’s health,” says Dr. Werbinski, cochair of the American Medical Women’s Association Sex & Gender Health Coalition.

“I am happy to say that significant awareness has grown since I graduated from medical school. I hope that when this question is asked of current medical students, they will be able to say that they know to practice with a sex- and gender-focused lens.”
 

Talk about racial disparities

John McHugh, MD, an ob.gyn., recalls learning little about the social determinants of health when he attended med school more than 30 years ago.

“We saw disparities in outcomes based on race and class but assumed that we would overcome them when we were in practice,” says Dr. McHugh, an AMWA Action Coalition for Equity member. “We didn’t understand the root causes of disparities and had never heard of concepts like epigenetics or weathering. I’m hopeful current research will help our understanding and today’s medical students will serve a safer, healthier, and more equitable world.”

Curtiland Deville, MD, an associate professor of radiation oncology, recalls having few conversations around race; racial disparities; and diversity, equity, and inclusion.

“When I went to medical school, it often felt like you weren’t supposed to talk about the differences in race,” says Dr. Deville, who graduated in 2005. But today, in the post-2020 era between COVID, during which health disparities got highlighted, and calls for racial justice taking center stage, Dr. Deville says many of the things they didn’t talk about have come to the forefront in our medical institutions.
 

Information at your fingertips

For Paru David, MD, a 1996 graduate, the most significant change is the amount of health and medical information available today. “Before, the information that was taught in medical school was obtained through textbooks or within journal articles,” says Dr. David.

“Now, we have databases of information. The key to success is being able to navigate the information available to us, digest it with a keen eye, and then apply it to patient care in a timely manner.”

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

This transcript has been edited for clarity.

Dr. O’Donoghue: We’re going to discuss a very important and emerging topic, which is the use of low-dose colchicine. I think there’s much interest in the use of this drug, which now has a Food and Drug Administration indication, which we’ll talk about further, and it’s also been written into both European and American guidelines that have been recently released.

Many people are talking about where this fits into our current armamentarium, and I think there probably is no better person to discuss this than Paul Ridker, who’s been at the forefront of research into anti-inflammatory therapeutics.
 

Lifestyle lipid-lowering paramount

Dr. O’Donoghue: As we think about the concept behind the use of colchicine, we’ve obviously done a large amount of research into lipid-lowering drugs, but where does colchicine now fit in?

Dr. Ridker: Let’s make sure we get the basics down. Anti-inflammatory therapy is going to be added on top of quality other care. This is not a replacement for lipids; it’s not a change in diet, exercise, and smoking cessation. The new data are really telling us that a patient who’s aggressively treated to guideline-recommended levels can still do much better in terms of preventing heart attack, stroke, cardiovascular death, and revascularization by adding low-dose colchicine as the first proven anti-inflammatory therapy for atherosclerotic disease.

I have to say, Michelle, for me, it’s been a wonderful end of a journey in many ways. This story starts almost 30 years ago for quite a few of us, thinking about inflammation and atherosclerosis. The whole C-reactive protein (CRP) story is still an ongoing one. We recently showed, for example, that residual inflammatory risk in some 30,000 patients, all taking a statin, was a far better predictor of the likelihood of more cardiovascular events, in particular cardiovascular death, than was residual cholesterol risk.

Think about that. We’re all aggressively giving second lipid-lowering drugs in our very sick patients, but that means inflammation is really the untapped piece of this.

The two clinical trials we have in front of us, the COLCOT trial and the LoDoCo2 trial – both New England Journal of Medicine papers, both with roughly 5,000 patients – provide very clear evidence that following a relatively recent myocardial infarction (that’s COLCOT) in chronic stable atherosclerosis (that’s LoDoCo2), we’re getting 25%-30% relative risk reductions in major adverse cardiovascular events (MACEs) on top of aggressive statin therapy. That’s a big deal. It’s safe, it works, and it’s fully consistent with all the information we have about inflammation being part and parcel of atherosclerosis. It’s a pretty exciting time.
 

Inflammatory pathway

Dr. O’Donoghue: It beautifully proves the inflammatory hypothesis in many ways. You led CANTOS, and that was a much more specific target. Here, in terms of the effects of colchicine, what do we know about how it may work on the inflammatory cascade?

Dr. Ridker: Our CANTOS trial was proof of principle that you could directly target, with a very specific monoclonal antibody, a specific piece of this innate immune cascade and lower cardiovascular event rates.

Colchicine is a more broad-spectrum drug. It does have a number of antineutrophil effects – that’s important, by the way. Neutrophils are really becoming very important in atherosclerotic disease progression. It’s an indirect inhibitor of the so-called NLRP3 inflammasome, which is where both interleukin-1 (that’s the target for canakinumab) and IL-6 are up-regulated. As you know, it’s been used to treat gout and pericarditis in high doses in short, little bursts.

The change here is this use of low-dose colchicine, that’s 0.5 mg once a day for years to treat chronic, stable atherosclerosis. It is very much like using a statin. The idea here is to prevent the progression of the disease by slowing down and maybe stabilizing the plaque so we have fewer heart attacks and strokes down the road.

It’s entering the armamentarium – at least my armamentarium – as chronic, stable secondary prevention. That’s where the new American College of Cardiology/American Heart Association guidelines also put it. It’s really in as a treatment for chronic, stable atherosclerosis. I think that’s where it belongs.
 

When to start colchicine, and in whom?

Dr. O’Donoghue: To that point, as we think about the efficacy, I think it’s nice, as you outlined, that we have two complementary trials that are both showing a consistent reduction in MACEs, one in the post–acute coronary syndrome (ACS) state and one for more chronic patients.

At what point do you think would be the appropriate time to start therapy, and who would you be starting it for?

Dr. Ridker: Michelle, that’s a great question. There’s a very interesting analysis that just came out from the LoDoCo2 investigators. It’s kind of a landmark analysis. What they show is that 1 year, 2 years, 3 years, and 4 years since the initiating myocardial infarction, the drug is very effective.

In fact, you could think about starting this drug at your clinic in patients with chronic, stable atherosclerotic disease. That’s just like we would start a statin in people who had a heart attack some time ago, and that’s absolutely fine.

I’m using it for what I call my frequent fliers, those patients who just keep coming back. They’re already on aggressive lipid-lowering therapy. I have them on beta-blockers, aspirin, and all the usual things. I say, look, I can get a large risk reduction by starting them on this drug.

There are a few caveats, Michelle. Like all drugs, colchicine comes with some adverse effects. Most of them are pretty rare, but there are some patients I would not give this drug to, just to be very clear. Colchicine is cleared by the kidney and by the liver. Patients who have severe chronic kidney disease and severe liver disease – this is a no-go for those patients. We should talk about where patients in that realm might want to go.

Then there are some unusual drugs. Colchicine is metabolized by the CYP3A4 and the P-glycoprotein pathway. There are a few drugs, such as ketoconazole, fluconazole, and cyclosporine, that if your primary care doctor or internist is going to start for a short term, you probably want to stop your colchicine for a week or two.

In people with familial Mediterranean fever, for whom colchicine is lifesaving and life-changing and who take it for 20, 30, or 40 years, there’s been no increase in risk for cancer. There have been very few adverse effects. I think it’s interesting that we, who practice in North America, basically never see familial Mediterranean fever. If we were practicing in Lebanon, Israel, or North Africa, this would be a very common therapy that we’d all be extremely familiar with.

Dr. O’Donoghue: To that point, it’s interesting to hear that colchicine was even used by the ancient Greeks and ancient Egyptians. It’s a drug that’s been around for a long time.

In terms of its safety, some people have been talking about the fact that an increase in noncardiovascular death was seen in LoDoCo2. What are your thoughts on that? Is that anything that we should be concerned about?

Colchicine safety and contraindications

Dr. Ridker: First, to set the record straight, a meta-analysis has been done of all-cause mortality in the various colchicine trials, and the hazard ratio is 1.04. I’ll remind you, and all of us know, that the hazard ratios for all-cause mortality in the PCSK9 trials, the bempedoic acid trials, and the ezetimibe trials are also essentially neutral. We’re in a state where we don’t let these trials roll long enough to see benefits necessarily on all-cause mortality. Some of us think we probably should, but that’s just the reality of trials.

One of most interesting things that was part of the FDA review, I suspect, was that there was no specific cause of any of this. It was not like there was a set of particular issues. I suspect that most people think this is probably the play of chance and with time, things will get better.

Again, I do want to emphasize this is not a drug for severe chronic kidney disease and severe liver disease, because those patients will get in trouble with this. The other thing that’s worth knowing is when you start a patient on low-dose colchicine – that’s 0.5 mg/d – there will be some patients who get some short-term gastrointestinal upset. That’s very common when you start colchicine at the much higher doses you might use to treat acute gout or pericarditis. In these trials, the vast majority of patients treated through that, and there were very few episodes long-term. I think it’s generally safe. That’s where we’re at.

Dr. O’Donoghue: Paul, you’ve been a leader, certainly, at looking at CRP as a marker of inflammation. Do you, in your practice, consider CRP levels when making a decision about who is appropriate for this therapy?

Dr. Ridker: That’s another terrific question. I do, because I’m trying to distinguish in my own mind patients who have residual inflammatory risk, in whom the high-sensitivity CRP (hsCRP) level remains high despite being on statins versus those with residual cholesterol risk, in whom I’m really predominantly worried about LDL cholesterol, that I haven’t brought it down far enough.

I do measure it, and if the CRP remains high and the LDL cholesterol is low, to me, that’s residual inflammatory risk and that’s the patient I would target this to. Conversely, if the LDL cholesterol was still, say, above some threshold of 75-100 and I’m worried about that, even if the CRP is low, I’ll probably add a second lipid-lowering drug.

The complexity of this, however, is that CRP was not measured in either LoDoCo2 or COLCOT. That’s mostly because they didn’t have much funding. These trials were done really on a shoestring. They were not sponsored by major pharma at all. We know that the median hsCRP in these trials was probably around 3.5-4 mg/L so I’m pretty comfortable doing that. Others have just advocated giving it to many patients. I must say I like to use biomarkers to think through the biology and who might have the best benefit-to-risk ratio. In my practice, I am doing it that way.
 

Inpatient vs. outpatient initiation

Dr. O’Donoghue: This is perhaps my last question for you before we wrap up. I know you talked about use of low-dose colchicine for patients with more chronic, stable coronary disease. Now obviously, COLCOT studied patients who were early post ACS, and there we certainly think about the anti-inflammatory effects as potentially having more benefit. What are your thoughts about early initiation of colchicine in that setting, the acute hospitalized setting? Do you think it’s more appropriate for an outpatient start?

Dr. Ridker: Today, I think this is all about chronic, stable atherosclerosis. Yes, COLCOT enrolled their patients within 30 days of a recent myocardial infarction, but as we all know, that’s a pretty stable phase. The vast majority were enrolled after 15 days. There were a small number enrolled within 3 days or something like that, but the benefit is about the same in all these patients.

Conversely, there’s been a small number of trials looking at colchicine in acute coronary ischemia and they’ve not been terribly promising. That makes some sense, though, right? We want to get an artery open. In acute ischemia, that’s about revascularization. It’s about oxygenation. It’s about reperfusion injury. My guess is that 3, 4, 5, or 6 days later, when it becomes a stable situation, is when the drug is probably effective.

Again, there will be some ongoing true intervention trials with large sample sizes for acute coronary ischemia. We don’t have those yet. Right now, I think it’s a therapy for chronic, stable angina. That’s many of our patients.

I would say that if you compare the relative benefit in these trials of adding ezetimibe to a statin, that’s a 5% or 6% benefit. For PCSK9 inhibitors – we all use them – it’s about a 15% benefit. These are 25%-30% risk reductions. If we’re going to think about what’s the next drug to give on top of the statin, serious consideration should be given to low-dose colchicine.

Let me also emphasize that this is not an either/or situation. This is about the fact that we now understand atherosclerosis to be a disorder both of lipid accumulation and a proinflammatory systemic response. We can give these drugs together. I suspect that the best patient care is going to be very aggressive lipid-lowering combined with pretty aggressive inflammation inhibition. I suspect that, down the road, that’s where all of us are going to be.

Dr. O’Donoghue: Thank you so much, Paul, for walking us through that today. I think it was a very nice, succinct review of the evidence, and then also just getting our minds more accustomed to the concept that we can now start to target more orthogonal axes that really get at the pathobiology of what’s going on in the atherosclerotic plaque. I think it’s an important topic.

Dr. O’Donoghue is an associate professor of medicine at Harvard Medical School and an associate physician at Brigham and Women’s Hospital, both in Boston. Dr. Ridker is director of the Center for Cardiovascular Disease Prevention at Brigham and Women’s Hospital. Both Dr. O’Donoghue and Dr. Ridker reported numerous conflicts of interest.

This transcript has been edited for clarity.

Dr. O’Donoghue: We’re going to discuss a very important and emerging topic, which is the use of low-dose colchicine. I think there’s much interest in the use of this drug, which now has a Food and Drug Administration indication, which we’ll talk about further, and it’s also been written into both European and American guidelines that have been recently released.

Many people are talking about where this fits into our current armamentarium, and I think there probably is no better person to discuss this than Paul Ridker, who’s been at the forefront of research into anti-inflammatory therapeutics.
 

Lifestyle lipid-lowering paramount

Dr. O’Donoghue: As we think about the concept behind the use of colchicine, we’ve obviously done a large amount of research into lipid-lowering drugs, but where does colchicine now fit in?

Dr. Ridker: Let’s make sure we get the basics down. Anti-inflammatory therapy is going to be added on top of quality other care. This is not a replacement for lipids; it’s not a change in diet, exercise, and smoking cessation. The new data are really telling us that a patient who’s aggressively treated to guideline-recommended levels can still do much better in terms of preventing heart attack, stroke, cardiovascular death, and revascularization by adding low-dose colchicine as the first proven anti-inflammatory therapy for atherosclerotic disease.

I have to say, Michelle, for me, it’s been a wonderful end of a journey in many ways. This story starts almost 30 years ago for quite a few of us, thinking about inflammation and atherosclerosis. The whole C-reactive protein (CRP) story is still an ongoing one. We recently showed, for example, that residual inflammatory risk in some 30,000 patients, all taking a statin, was a far better predictor of the likelihood of more cardiovascular events, in particular cardiovascular death, than was residual cholesterol risk.

Think about that. We’re all aggressively giving second lipid-lowering drugs in our very sick patients, but that means inflammation is really the untapped piece of this.

The two clinical trials we have in front of us, the COLCOT trial and the LoDoCo2 trial – both New England Journal of Medicine papers, both with roughly 5,000 patients – provide very clear evidence that following a relatively recent myocardial infarction (that’s COLCOT) in chronic stable atherosclerosis (that’s LoDoCo2), we’re getting 25%-30% relative risk reductions in major adverse cardiovascular events (MACEs) on top of aggressive statin therapy. That’s a big deal. It’s safe, it works, and it’s fully consistent with all the information we have about inflammation being part and parcel of atherosclerosis. It’s a pretty exciting time.
 

Inflammatory pathway

Dr. O’Donoghue: It beautifully proves the inflammatory hypothesis in many ways. You led CANTOS, and that was a much more specific target. Here, in terms of the effects of colchicine, what do we know about how it may work on the inflammatory cascade?

Dr. Ridker: Our CANTOS trial was proof of principle that you could directly target, with a very specific monoclonal antibody, a specific piece of this innate immune cascade and lower cardiovascular event rates.

Colchicine is a more broad-spectrum drug. It does have a number of antineutrophil effects – that’s important, by the way. Neutrophils are really becoming very important in atherosclerotic disease progression. It’s an indirect inhibitor of the so-called NLRP3 inflammasome, which is where both interleukin-1 (that’s the target for canakinumab) and IL-6 are up-regulated. As you know, it’s been used to treat gout and pericarditis in high doses in short, little bursts.

The change here is this use of low-dose colchicine, that’s 0.5 mg once a day for years to treat chronic, stable atherosclerosis. It is very much like using a statin. The idea here is to prevent the progression of the disease by slowing down and maybe stabilizing the plaque so we have fewer heart attacks and strokes down the road.

It’s entering the armamentarium – at least my armamentarium – as chronic, stable secondary prevention. That’s where the new American College of Cardiology/American Heart Association guidelines also put it. It’s really in as a treatment for chronic, stable atherosclerosis. I think that’s where it belongs.
 

When to start colchicine, and in whom?

Dr. O’Donoghue: To that point, as we think about the efficacy, I think it’s nice, as you outlined, that we have two complementary trials that are both showing a consistent reduction in MACEs, one in the post–acute coronary syndrome (ACS) state and one for more chronic patients.

At what point do you think would be the appropriate time to start therapy, and who would you be starting it for?

Dr. Ridker: Michelle, that’s a great question. There’s a very interesting analysis that just came out from the LoDoCo2 investigators. It’s kind of a landmark analysis. What they show is that 1 year, 2 years, 3 years, and 4 years since the initiating myocardial infarction, the drug is very effective.

In fact, you could think about starting this drug at your clinic in patients with chronic, stable atherosclerotic disease. That’s just like we would start a statin in people who had a heart attack some time ago, and that’s absolutely fine.

I’m using it for what I call my frequent fliers, those patients who just keep coming back. They’re already on aggressive lipid-lowering therapy. I have them on beta-blockers, aspirin, and all the usual things. I say, look, I can get a large risk reduction by starting them on this drug.

There are a few caveats, Michelle. Like all drugs, colchicine comes with some adverse effects. Most of them are pretty rare, but there are some patients I would not give this drug to, just to be very clear. Colchicine is cleared by the kidney and by the liver. Patients who have severe chronic kidney disease and severe liver disease – this is a no-go for those patients. We should talk about where patients in that realm might want to go.

Then there are some unusual drugs. Colchicine is metabolized by the CYP3A4 and the P-glycoprotein pathway. There are a few drugs, such as ketoconazole, fluconazole, and cyclosporine, that if your primary care doctor or internist is going to start for a short term, you probably want to stop your colchicine for a week or two.

In people with familial Mediterranean fever, for whom colchicine is lifesaving and life-changing and who take it for 20, 30, or 40 years, there’s been no increase in risk for cancer. There have been very few adverse effects. I think it’s interesting that we, who practice in North America, basically never see familial Mediterranean fever. If we were practicing in Lebanon, Israel, or North Africa, this would be a very common therapy that we’d all be extremely familiar with.

Dr. O’Donoghue: To that point, it’s interesting to hear that colchicine was even used by the ancient Greeks and ancient Egyptians. It’s a drug that’s been around for a long time.

In terms of its safety, some people have been talking about the fact that an increase in noncardiovascular death was seen in LoDoCo2. What are your thoughts on that? Is that anything that we should be concerned about?

Colchicine safety and contraindications

Dr. Ridker: First, to set the record straight, a meta-analysis has been done of all-cause mortality in the various colchicine trials, and the hazard ratio is 1.04. I’ll remind you, and all of us know, that the hazard ratios for all-cause mortality in the PCSK9 trials, the bempedoic acid trials, and the ezetimibe trials are also essentially neutral. We’re in a state where we don’t let these trials roll long enough to see benefits necessarily on all-cause mortality. Some of us think we probably should, but that’s just the reality of trials.

One of most interesting things that was part of the FDA review, I suspect, was that there was no specific cause of any of this. It was not like there was a set of particular issues. I suspect that most people think this is probably the play of chance and with time, things will get better.

Again, I do want to emphasize this is not a drug for severe chronic kidney disease and severe liver disease, because those patients will get in trouble with this. The other thing that’s worth knowing is when you start a patient on low-dose colchicine – that’s 0.5 mg/d – there will be some patients who get some short-term gastrointestinal upset. That’s very common when you start colchicine at the much higher doses you might use to treat acute gout or pericarditis. In these trials, the vast majority of patients treated through that, and there were very few episodes long-term. I think it’s generally safe. That’s where we’re at.

Dr. O’Donoghue: Paul, you’ve been a leader, certainly, at looking at CRP as a marker of inflammation. Do you, in your practice, consider CRP levels when making a decision about who is appropriate for this therapy?

Dr. Ridker: That’s another terrific question. I do, because I’m trying to distinguish in my own mind patients who have residual inflammatory risk, in whom the high-sensitivity CRP (hsCRP) level remains high despite being on statins versus those with residual cholesterol risk, in whom I’m really predominantly worried about LDL cholesterol, that I haven’t brought it down far enough.

I do measure it, and if the CRP remains high and the LDL cholesterol is low, to me, that’s residual inflammatory risk and that’s the patient I would target this to. Conversely, if the LDL cholesterol was still, say, above some threshold of 75-100 and I’m worried about that, even if the CRP is low, I’ll probably add a second lipid-lowering drug.

The complexity of this, however, is that CRP was not measured in either LoDoCo2 or COLCOT. That’s mostly because they didn’t have much funding. These trials were done really on a shoestring. They were not sponsored by major pharma at all. We know that the median hsCRP in these trials was probably around 3.5-4 mg/L so I’m pretty comfortable doing that. Others have just advocated giving it to many patients. I must say I like to use biomarkers to think through the biology and who might have the best benefit-to-risk ratio. In my practice, I am doing it that way.
 

Inpatient vs. outpatient initiation

Dr. O’Donoghue: This is perhaps my last question for you before we wrap up. I know you talked about use of low-dose colchicine for patients with more chronic, stable coronary disease. Now obviously, COLCOT studied patients who were early post ACS, and there we certainly think about the anti-inflammatory effects as potentially having more benefit. What are your thoughts about early initiation of colchicine in that setting, the acute hospitalized setting? Do you think it’s more appropriate for an outpatient start?

Dr. Ridker: Today, I think this is all about chronic, stable atherosclerosis. Yes, COLCOT enrolled their patients within 30 days of a recent myocardial infarction, but as we all know, that’s a pretty stable phase. The vast majority were enrolled after 15 days. There were a small number enrolled within 3 days or something like that, but the benefit is about the same in all these patients.

Conversely, there’s been a small number of trials looking at colchicine in acute coronary ischemia and they’ve not been terribly promising. That makes some sense, though, right? We want to get an artery open. In acute ischemia, that’s about revascularization. It’s about oxygenation. It’s about reperfusion injury. My guess is that 3, 4, 5, or 6 days later, when it becomes a stable situation, is when the drug is probably effective.

Again, there will be some ongoing true intervention trials with large sample sizes for acute coronary ischemia. We don’t have those yet. Right now, I think it’s a therapy for chronic, stable angina. That’s many of our patients.

I would say that if you compare the relative benefit in these trials of adding ezetimibe to a statin, that’s a 5% or 6% benefit. For PCSK9 inhibitors – we all use them – it’s about a 15% benefit. These are 25%-30% risk reductions. If we’re going to think about what’s the next drug to give on top of the statin, serious consideration should be given to low-dose colchicine.

Let me also emphasize that this is not an either/or situation. This is about the fact that we now understand atherosclerosis to be a disorder both of lipid accumulation and a proinflammatory systemic response. We can give these drugs together. I suspect that the best patient care is going to be very aggressive lipid-lowering combined with pretty aggressive inflammation inhibition. I suspect that, down the road, that’s where all of us are going to be.

Dr. O’Donoghue: Thank you so much, Paul, for walking us through that today. I think it was a very nice, succinct review of the evidence, and then also just getting our minds more accustomed to the concept that we can now start to target more orthogonal axes that really get at the pathobiology of what’s going on in the atherosclerotic plaque. I think it’s an important topic.

Dr. O’Donoghue is an associate professor of medicine at Harvard Medical School and an associate physician at Brigham and Women’s Hospital, both in Boston. Dr. Ridker is director of the Center for Cardiovascular Disease Prevention at Brigham and Women’s Hospital. Both Dr. O’Donoghue and Dr. Ridker reported numerous conflicts of interest.

This transcript has been edited for clarity.

Dr. O’Donoghue: We’re going to discuss a very important and emerging topic, which is the use of low-dose colchicine. I think there’s much interest in the use of this drug, which now has a Food and Drug Administration indication, which we’ll talk about further, and it’s also been written into both European and American guidelines that have been recently released.

Many people are talking about where this fits into our current armamentarium, and I think there probably is no better person to discuss this than Paul Ridker, who’s been at the forefront of research into anti-inflammatory therapeutics.
 

Lifestyle lipid-lowering paramount

Dr. O’Donoghue: As we think about the concept behind the use of colchicine, we’ve obviously done a large amount of research into lipid-lowering drugs, but where does colchicine now fit in?

Dr. Ridker: Let’s make sure we get the basics down. Anti-inflammatory therapy is going to be added on top of quality other care. This is not a replacement for lipids; it’s not a change in diet, exercise, and smoking cessation. The new data are really telling us that a patient who’s aggressively treated to guideline-recommended levels can still do much better in terms of preventing heart attack, stroke, cardiovascular death, and revascularization by adding low-dose colchicine as the first proven anti-inflammatory therapy for atherosclerotic disease.

I have to say, Michelle, for me, it’s been a wonderful end of a journey in many ways. This story starts almost 30 years ago for quite a few of us, thinking about inflammation and atherosclerosis. The whole C-reactive protein (CRP) story is still an ongoing one. We recently showed, for example, that residual inflammatory risk in some 30,000 patients, all taking a statin, was a far better predictor of the likelihood of more cardiovascular events, in particular cardiovascular death, than was residual cholesterol risk.

Think about that. We’re all aggressively giving second lipid-lowering drugs in our very sick patients, but that means inflammation is really the untapped piece of this.

The two clinical trials we have in front of us, the COLCOT trial and the LoDoCo2 trial – both New England Journal of Medicine papers, both with roughly 5,000 patients – provide very clear evidence that following a relatively recent myocardial infarction (that’s COLCOT) in chronic stable atherosclerosis (that’s LoDoCo2), we’re getting 25%-30% relative risk reductions in major adverse cardiovascular events (MACEs) on top of aggressive statin therapy. That’s a big deal. It’s safe, it works, and it’s fully consistent with all the information we have about inflammation being part and parcel of atherosclerosis. It’s a pretty exciting time.
 

Inflammatory pathway

Dr. O’Donoghue: It beautifully proves the inflammatory hypothesis in many ways. You led CANTOS, and that was a much more specific target. Here, in terms of the effects of colchicine, what do we know about how it may work on the inflammatory cascade?

Dr. Ridker: Our CANTOS trial was proof of principle that you could directly target, with a very specific monoclonal antibody, a specific piece of this innate immune cascade and lower cardiovascular event rates.

Colchicine is a more broad-spectrum drug. It does have a number of antineutrophil effects – that’s important, by the way. Neutrophils are really becoming very important in atherosclerotic disease progression. It’s an indirect inhibitor of the so-called NLRP3 inflammasome, which is where both interleukin-1 (that’s the target for canakinumab) and IL-6 are up-regulated. As you know, it’s been used to treat gout and pericarditis in high doses in short, little bursts.

The change here is this use of low-dose colchicine, that’s 0.5 mg once a day for years to treat chronic, stable atherosclerosis. It is very much like using a statin. The idea here is to prevent the progression of the disease by slowing down and maybe stabilizing the plaque so we have fewer heart attacks and strokes down the road.

It’s entering the armamentarium – at least my armamentarium – as chronic, stable secondary prevention. That’s where the new American College of Cardiology/American Heart Association guidelines also put it. It’s really in as a treatment for chronic, stable atherosclerosis. I think that’s where it belongs.
 

When to start colchicine, and in whom?

Dr. O’Donoghue: To that point, as we think about the efficacy, I think it’s nice, as you outlined, that we have two complementary trials that are both showing a consistent reduction in MACEs, one in the post–acute coronary syndrome (ACS) state and one for more chronic patients.

At what point do you think would be the appropriate time to start therapy, and who would you be starting it for?

Dr. Ridker: Michelle, that’s a great question. There’s a very interesting analysis that just came out from the LoDoCo2 investigators. It’s kind of a landmark analysis. What they show is that 1 year, 2 years, 3 years, and 4 years since the initiating myocardial infarction, the drug is very effective.

In fact, you could think about starting this drug at your clinic in patients with chronic, stable atherosclerotic disease. That’s just like we would start a statin in people who had a heart attack some time ago, and that’s absolutely fine.

I’m using it for what I call my frequent fliers, those patients who just keep coming back. They’re already on aggressive lipid-lowering therapy. I have them on beta-blockers, aspirin, and all the usual things. I say, look, I can get a large risk reduction by starting them on this drug.

There are a few caveats, Michelle. Like all drugs, colchicine comes with some adverse effects. Most of them are pretty rare, but there are some patients I would not give this drug to, just to be very clear. Colchicine is cleared by the kidney and by the liver. Patients who have severe chronic kidney disease and severe liver disease – this is a no-go for those patients. We should talk about where patients in that realm might want to go.

Then there are some unusual drugs. Colchicine is metabolized by the CYP3A4 and the P-glycoprotein pathway. There are a few drugs, such as ketoconazole, fluconazole, and cyclosporine, that if your primary care doctor or internist is going to start for a short term, you probably want to stop your colchicine for a week or two.

In people with familial Mediterranean fever, for whom colchicine is lifesaving and life-changing and who take it for 20, 30, or 40 years, there’s been no increase in risk for cancer. There have been very few adverse effects. I think it’s interesting that we, who practice in North America, basically never see familial Mediterranean fever. If we were practicing in Lebanon, Israel, or North Africa, this would be a very common therapy that we’d all be extremely familiar with.

Dr. O’Donoghue: To that point, it’s interesting to hear that colchicine was even used by the ancient Greeks and ancient Egyptians. It’s a drug that’s been around for a long time.

In terms of its safety, some people have been talking about the fact that an increase in noncardiovascular death was seen in LoDoCo2. What are your thoughts on that? Is that anything that we should be concerned about?

Colchicine safety and contraindications

Dr. Ridker: First, to set the record straight, a meta-analysis has been done of all-cause mortality in the various colchicine trials, and the hazard ratio is 1.04. I’ll remind you, and all of us know, that the hazard ratios for all-cause mortality in the PCSK9 trials, the bempedoic acid trials, and the ezetimibe trials are also essentially neutral. We’re in a state where we don’t let these trials roll long enough to see benefits necessarily on all-cause mortality. Some of us think we probably should, but that’s just the reality of trials.

One of most interesting things that was part of the FDA review, I suspect, was that there was no specific cause of any of this. It was not like there was a set of particular issues. I suspect that most people think this is probably the play of chance and with time, things will get better.

Again, I do want to emphasize this is not a drug for severe chronic kidney disease and severe liver disease, because those patients will get in trouble with this. The other thing that’s worth knowing is when you start a patient on low-dose colchicine – that’s 0.5 mg/d – there will be some patients who get some short-term gastrointestinal upset. That’s very common when you start colchicine at the much higher doses you might use to treat acute gout or pericarditis. In these trials, the vast majority of patients treated through that, and there were very few episodes long-term. I think it’s generally safe. That’s where we’re at.

Dr. O’Donoghue: Paul, you’ve been a leader, certainly, at looking at CRP as a marker of inflammation. Do you, in your practice, consider CRP levels when making a decision about who is appropriate for this therapy?

Dr. Ridker: That’s another terrific question. I do, because I’m trying to distinguish in my own mind patients who have residual inflammatory risk, in whom the high-sensitivity CRP (hsCRP) level remains high despite being on statins versus those with residual cholesterol risk, in whom I’m really predominantly worried about LDL cholesterol, that I haven’t brought it down far enough.

I do measure it, and if the CRP remains high and the LDL cholesterol is low, to me, that’s residual inflammatory risk and that’s the patient I would target this to. Conversely, if the LDL cholesterol was still, say, above some threshold of 75-100 and I’m worried about that, even if the CRP is low, I’ll probably add a second lipid-lowering drug.

The complexity of this, however, is that CRP was not measured in either LoDoCo2 or COLCOT. That’s mostly because they didn’t have much funding. These trials were done really on a shoestring. They were not sponsored by major pharma at all. We know that the median hsCRP in these trials was probably around 3.5-4 mg/L so I’m pretty comfortable doing that. Others have just advocated giving it to many patients. I must say I like to use biomarkers to think through the biology and who might have the best benefit-to-risk ratio. In my practice, I am doing it that way.
 

Inpatient vs. outpatient initiation

Dr. O’Donoghue: This is perhaps my last question for you before we wrap up. I know you talked about use of low-dose colchicine for patients with more chronic, stable coronary disease. Now obviously, COLCOT studied patients who were early post ACS, and there we certainly think about the anti-inflammatory effects as potentially having more benefit. What are your thoughts about early initiation of colchicine in that setting, the acute hospitalized setting? Do you think it’s more appropriate for an outpatient start?

Dr. Ridker: Today, I think this is all about chronic, stable atherosclerosis. Yes, COLCOT enrolled their patients within 30 days of a recent myocardial infarction, but as we all know, that’s a pretty stable phase. The vast majority were enrolled after 15 days. There were a small number enrolled within 3 days or something like that, but the benefit is about the same in all these patients.

Conversely, there’s been a small number of trials looking at colchicine in acute coronary ischemia and they’ve not been terribly promising. That makes some sense, though, right? We want to get an artery open. In acute ischemia, that’s about revascularization. It’s about oxygenation. It’s about reperfusion injury. My guess is that 3, 4, 5, or 6 days later, when it becomes a stable situation, is when the drug is probably effective.

Again, there will be some ongoing true intervention trials with large sample sizes for acute coronary ischemia. We don’t have those yet. Right now, I think it’s a therapy for chronic, stable angina. That’s many of our patients.

I would say that if you compare the relative benefit in these trials of adding ezetimibe to a statin, that’s a 5% or 6% benefit. For PCSK9 inhibitors – we all use them – it’s about a 15% benefit. These are 25%-30% risk reductions. If we’re going to think about what’s the next drug to give on top of the statin, serious consideration should be given to low-dose colchicine.

Let me also emphasize that this is not an either/or situation. This is about the fact that we now understand atherosclerosis to be a disorder both of lipid accumulation and a proinflammatory systemic response. We can give these drugs together. I suspect that the best patient care is going to be very aggressive lipid-lowering combined with pretty aggressive inflammation inhibition. I suspect that, down the road, that’s where all of us are going to be.

Dr. O’Donoghue: Thank you so much, Paul, for walking us through that today. I think it was a very nice, succinct review of the evidence, and then also just getting our minds more accustomed to the concept that we can now start to target more orthogonal axes that really get at the pathobiology of what’s going on in the atherosclerotic plaque. I think it’s an important topic.

Dr. O’Donoghue is an associate professor of medicine at Harvard Medical School and an associate physician at Brigham and Women’s Hospital, both in Boston. Dr. Ridker is director of the Center for Cardiovascular Disease Prevention at Brigham and Women’s Hospital. Both Dr. O’Donoghue and Dr. Ridker reported numerous conflicts of interest.

Higher daily step counts were associated with reduced risk of all-cause mortality and cardiovascular (CV) mortality, with benefit beginning with any amount over about 4,000 and 2,300 steps, respectively, in a new meta-analysis.
 

More steps were better – additional benefit was seen with increasing increments of 500 or 1,000 steps.

Leonardo Patrizi/E+/Getty Images

“One of our main aims was to overcome all the inconsistencies in previous studies, where the optimal number of daily steps for health benefits was usually between 6,000 and 10,000,” Maciej Banach, MD, PhD, of the Medical University of Lodz (Poland), said in an interview.

“As a preventive cardiologist, I saw that many of my patients were discouraged and said it’s impossible when I told them that making lifestyle changes included taking at least 7,000 daily steps,” he said.

“But our study in relatively healthy individuals, not patients, showed even a lower number – for example, around 4,000 – may be associated with a significant reduction of mortality.

“I tell people to start early, be regular, and don’t worry about the initial baseline number, because it’s important to start and it’s important to improve,” he said. “Our study showed that if we increase the number of steps per day, every 500- to 1,000-step increase might still be associated with an additional mortality reduction of 7%-15%.”

The study was published online in the European Journal of Preventive Cardiology.
 

Every move counts

The investigators searched the literature through June 2022 and selected 17 cohort studies with 226,889 participants and a median follow-up of 7.1 years for inclusion in the analysis: 10 studies reported all-cause mortality, 4 reported CV mortality, and 3 reported both outcomes.

The mean age of the participants was 64.4 years, and half were women. Daily step counts in the included studies were objectively measured for at least 7 consecutive days.

As noted, a 1,000-step increment was associated with a 15% decrease in risk of all-cause mortality (hazard ratio, 0.85); a 500-step increment was associated with a 7% decrease in CV mortality (HR, 0.93).

Compared with the reference quartile (median steps/day, 3,967), quartile 1 (median steps, 5,537) was associated with a 48% lower risk of all-cause mortality; quartile 2 (median steps, 7,370), with a 55% lower risk; and quartile 3 (median steps, 11,529), with a 67% risk reduction.

Similarly, compared with the lowest quartile of steps per day used as reference (median steps, 2,337), higher quartiles of steps per day (Q1, 3,982; Q2, 6,661; and Q3, 10,413) were linearly associated with a reduced risk of CV mortality (16%, 49%, and 77%, respectively).

In a restricted cubic splines model, a nonlinear dose-response association was observed between step count and all-cause and CV mortality, with a progressively lower risk of mortality with an increase in step count.

Dose-response curves were similar for men and women. However, there was a difference by age: Among people aged 60 years or older, the size of the risk reduction was smaller. Among the older adults, there was a 42% risk reduction for those who walked between 6000 and 10,000 steps daily, compared with a 49% reduction in risk among younger adults who walked between 7,000 and 13,000 steps a day.

For both groups, daily step counts higher than 5,000 resulted in a “dramatically” lower risk of all-cause mortality.

An analysis that compared the impact of climate regions on the associations showed no significant effect on all-cause mortality. People in all climate zones benefited when the daily step count exceeded approximately 5,500.

Even given the encouraging study results, “we know very well that every kind of exercise is critically important,” Dr. Banach said. It is easier to focus on step counts because the counts can be monitored and calculated with smartwatches, pedometers, and other tools. That also makes it easier to check associations and outcomes for large groups of patients.

“But in fact, we should not be focusing on one type of exercise, such as walking or running,” he said. “We can dance, ride bicycles, and do many other different exercises that mobilize our hearts.

“We also know that in all these activities, including steps, people have different capabilities – for example, some can walk more slowly, others faster and with more intensity.”

Dr. Banach recommended following the European and U.S. physical activity guidelines that advise, in addition to muscle-strengthening activities, 150 minutes of moderate-intensity aerobic training weekly, or 75 minutes of vigorous-intensity aerobic activity, or an equivalent combination of moderate- and vigorous-intensity aerobic activity.

From the results he sees in patients, he believes the combination approach is probably best for the heart.

Furthermore, it’s important to exercise regularly, something that’s easier if individuals enjoy what they’re doing. “The type of training or whether you are completely inactive or very active at the start doesn’t matter, because any improvement, any addition to the to the baseline values will have health benefits,” he concluded.
 

Higher goals helpful

Three experts commented on the study; all noted that the results are in line with previous studies, that the observational nature of the study is a limitation, and that additional randomized, controlled trials are needed to confirm the findings.

Evan Brittain, MD, an associate professor of medicine at Vanderbilt University Medical Center, Nashville, Tenn., expressed some additional concerns.

Dr. Brittain was principal investigator of a recent study that found that the relationship between steps per day and incident disease was inverse and linear for obesity, sleep apnea, gastroesophageal reflux disease, and major depressive disorder. Daily step counts above 8,200 were associated with protection from incident disease.

He noted that, in the current study, “the authors chose to make the least active quartile (25%) the reference group (only 3,967 steps/day for all-cause mortality and only 2,337 steps/day for CV mortality analysis), which somewhat lowers the bar for finding a significant benefit at higher step counts.

“Moreover, in the spline analyses, zero steps per day is used as the comparison, which is not a practical, real-world comparison,” he said. “As a result, those data are very hard to interpret, and I think are overstated.”

Like Dr. Banach, Dr. Brittain said he would continue to advise following guideline recommendations to get 150 minutes per week of moderate-intensity activity. However, he added that although it is reasonable to advise patients that benefits do accrue with daily step counts of less than 10,000, “I would not want patients to misconstrue from this study that getting more than only 2,330 steps per day is a beneficial goal.”

Martin Halle, MD, a professor in the department of prevention and sports medicine at the Technical University of Munich (Germany), said: “From a clinical, medical, and health perspective, the general population should aim for 5,000 steps, which is about 3-4 kilometers [about 2 miles] of walking, and intensity counts – the faster you walk, the better.

“I recommend doing 100 steps fast and 100 steps slow and then 100 steps fast and 100 steps slow,” said Dr. Halle, who is past president of the European Association of Preventive Cardiology. This approach not only motivates people, “but they improve their exercise capacity substantially and very quickly, just within weeks.”

European Society of Cardiology vice president and European Journal of Preventive Cardiology editor-in-chief Massimo Piepoli, MD, PhD, agreed that “little is better than nothing and more is even better. This applies to healthy subjects, as well as patients with chronic diseases.

“Five hundred steps is a very short distance (such as walking two blocks or walking the dog for about 10-15 minutes every day),” he said. Yet, increasing step counts in increments of 500 “is associated with a significant reduction in cardiovascular mortality both in men and women, particularly in older individuals.

“We do not need to depend on expensive gym facilities,” he added. “But at the same time, we need to live in and to promote the building of neighborhoods where it is possible to walk in a safe and healthy environment.”

The research received no external funding. Dr. Banach has reported financial relationships with Amgen, Daiichi Sankyo, Esperion, Freia Pharmaceuticals, Kogen, KRKA, Polpharma, NewAmsterdam, Novartis, Novo Nordisk, Polfarmex, Sanofi Aventis, Teva, Valeant, Viatris, and Zentiva, and is chief marketing and development officer at Longevity Group and chief marketing officer at Nomi Biotech.

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

Higher daily step counts were associated with reduced risk of all-cause mortality and cardiovascular (CV) mortality, with benefit beginning with any amount over about 4,000 and 2,300 steps, respectively, in a new meta-analysis.
 

More steps were better – additional benefit was seen with increasing increments of 500 or 1,000 steps.

Leonardo Patrizi/E+/Getty Images

“One of our main aims was to overcome all the inconsistencies in previous studies, where the optimal number of daily steps for health benefits was usually between 6,000 and 10,000,” Maciej Banach, MD, PhD, of the Medical University of Lodz (Poland), said in an interview.

“As a preventive cardiologist, I saw that many of my patients were discouraged and said it’s impossible when I told them that making lifestyle changes included taking at least 7,000 daily steps,” he said.

“But our study in relatively healthy individuals, not patients, showed even a lower number – for example, around 4,000 – may be associated with a significant reduction of mortality.

“I tell people to start early, be regular, and don’t worry about the initial baseline number, because it’s important to start and it’s important to improve,” he said. “Our study showed that if we increase the number of steps per day, every 500- to 1,000-step increase might still be associated with an additional mortality reduction of 7%-15%.”

The study was published online in the European Journal of Preventive Cardiology.
 

Every move counts

The investigators searched the literature through June 2022 and selected 17 cohort studies with 226,889 participants and a median follow-up of 7.1 years for inclusion in the analysis: 10 studies reported all-cause mortality, 4 reported CV mortality, and 3 reported both outcomes.

The mean age of the participants was 64.4 years, and half were women. Daily step counts in the included studies were objectively measured for at least 7 consecutive days.

As noted, a 1,000-step increment was associated with a 15% decrease in risk of all-cause mortality (hazard ratio, 0.85); a 500-step increment was associated with a 7% decrease in CV mortality (HR, 0.93).

Compared with the reference quartile (median steps/day, 3,967), quartile 1 (median steps, 5,537) was associated with a 48% lower risk of all-cause mortality; quartile 2 (median steps, 7,370), with a 55% lower risk; and quartile 3 (median steps, 11,529), with a 67% risk reduction.

Similarly, compared with the lowest quartile of steps per day used as reference (median steps, 2,337), higher quartiles of steps per day (Q1, 3,982; Q2, 6,661; and Q3, 10,413) were linearly associated with a reduced risk of CV mortality (16%, 49%, and 77%, respectively).

In a restricted cubic splines model, a nonlinear dose-response association was observed between step count and all-cause and CV mortality, with a progressively lower risk of mortality with an increase in step count.

Dose-response curves were similar for men and women. However, there was a difference by age: Among people aged 60 years or older, the size of the risk reduction was smaller. Among the older adults, there was a 42% risk reduction for those who walked between 6000 and 10,000 steps daily, compared with a 49% reduction in risk among younger adults who walked between 7,000 and 13,000 steps a day.

For both groups, daily step counts higher than 5,000 resulted in a “dramatically” lower risk of all-cause mortality.

An analysis that compared the impact of climate regions on the associations showed no significant effect on all-cause mortality. People in all climate zones benefited when the daily step count exceeded approximately 5,500.

Even given the encouraging study results, “we know very well that every kind of exercise is critically important,” Dr. Banach said. It is easier to focus on step counts because the counts can be monitored and calculated with smartwatches, pedometers, and other tools. That also makes it easier to check associations and outcomes for large groups of patients.

“But in fact, we should not be focusing on one type of exercise, such as walking or running,” he said. “We can dance, ride bicycles, and do many other different exercises that mobilize our hearts.

“We also know that in all these activities, including steps, people have different capabilities – for example, some can walk more slowly, others faster and with more intensity.”

Dr. Banach recommended following the European and U.S. physical activity guidelines that advise, in addition to muscle-strengthening activities, 150 minutes of moderate-intensity aerobic training weekly, or 75 minutes of vigorous-intensity aerobic activity, or an equivalent combination of moderate- and vigorous-intensity aerobic activity.

From the results he sees in patients, he believes the combination approach is probably best for the heart.

Furthermore, it’s important to exercise regularly, something that’s easier if individuals enjoy what they’re doing. “The type of training or whether you are completely inactive or very active at the start doesn’t matter, because any improvement, any addition to the to the baseline values will have health benefits,” he concluded.
 

Higher goals helpful

Three experts commented on the study; all noted that the results are in line with previous studies, that the observational nature of the study is a limitation, and that additional randomized, controlled trials are needed to confirm the findings.

Evan Brittain, MD, an associate professor of medicine at Vanderbilt University Medical Center, Nashville, Tenn., expressed some additional concerns.

Dr. Brittain was principal investigator of a recent study that found that the relationship between steps per day and incident disease was inverse and linear for obesity, sleep apnea, gastroesophageal reflux disease, and major depressive disorder. Daily step counts above 8,200 were associated with protection from incident disease.

He noted that, in the current study, “the authors chose to make the least active quartile (25%) the reference group (only 3,967 steps/day for all-cause mortality and only 2,337 steps/day for CV mortality analysis), which somewhat lowers the bar for finding a significant benefit at higher step counts.

“Moreover, in the spline analyses, zero steps per day is used as the comparison, which is not a practical, real-world comparison,” he said. “As a result, those data are very hard to interpret, and I think are overstated.”

Like Dr. Banach, Dr. Brittain said he would continue to advise following guideline recommendations to get 150 minutes per week of moderate-intensity activity. However, he added that although it is reasonable to advise patients that benefits do accrue with daily step counts of less than 10,000, “I would not want patients to misconstrue from this study that getting more than only 2,330 steps per day is a beneficial goal.”

Martin Halle, MD, a professor in the department of prevention and sports medicine at the Technical University of Munich (Germany), said: “From a clinical, medical, and health perspective, the general population should aim for 5,000 steps, which is about 3-4 kilometers [about 2 miles] of walking, and intensity counts – the faster you walk, the better.

“I recommend doing 100 steps fast and 100 steps slow and then 100 steps fast and 100 steps slow,” said Dr. Halle, who is past president of the European Association of Preventive Cardiology. This approach not only motivates people, “but they improve their exercise capacity substantially and very quickly, just within weeks.”

European Society of Cardiology vice president and European Journal of Preventive Cardiology editor-in-chief Massimo Piepoli, MD, PhD, agreed that “little is better than nothing and more is even better. This applies to healthy subjects, as well as patients with chronic diseases.

“Five hundred steps is a very short distance (such as walking two blocks or walking the dog for about 10-15 minutes every day),” he said. Yet, increasing step counts in increments of 500 “is associated with a significant reduction in cardiovascular mortality both in men and women, particularly in older individuals.

“We do not need to depend on expensive gym facilities,” he added. “But at the same time, we need to live in and to promote the building of neighborhoods where it is possible to walk in a safe and healthy environment.”

The research received no external funding. Dr. Banach has reported financial relationships with Amgen, Daiichi Sankyo, Esperion, Freia Pharmaceuticals, Kogen, KRKA, Polpharma, NewAmsterdam, Novartis, Novo Nordisk, Polfarmex, Sanofi Aventis, Teva, Valeant, Viatris, and Zentiva, and is chief marketing and development officer at Longevity Group and chief marketing officer at Nomi Biotech.

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

Higher daily step counts were associated with reduced risk of all-cause mortality and cardiovascular (CV) mortality, with benefit beginning with any amount over about 4,000 and 2,300 steps, respectively, in a new meta-analysis.
 

More steps were better – additional benefit was seen with increasing increments of 500 or 1,000 steps.

Leonardo Patrizi/E+/Getty Images

“One of our main aims was to overcome all the inconsistencies in previous studies, where the optimal number of daily steps for health benefits was usually between 6,000 and 10,000,” Maciej Banach, MD, PhD, of the Medical University of Lodz (Poland), said in an interview.

“As a preventive cardiologist, I saw that many of my patients were discouraged and said it’s impossible when I told them that making lifestyle changes included taking at least 7,000 daily steps,” he said.

“But our study in relatively healthy individuals, not patients, showed even a lower number – for example, around 4,000 – may be associated with a significant reduction of mortality.

“I tell people to start early, be regular, and don’t worry about the initial baseline number, because it’s important to start and it’s important to improve,” he said. “Our study showed that if we increase the number of steps per day, every 500- to 1,000-step increase might still be associated with an additional mortality reduction of 7%-15%.”

The study was published online in the European Journal of Preventive Cardiology.
 

Every move counts

The investigators searched the literature through June 2022 and selected 17 cohort studies with 226,889 participants and a median follow-up of 7.1 years for inclusion in the analysis: 10 studies reported all-cause mortality, 4 reported CV mortality, and 3 reported both outcomes.

The mean age of the participants was 64.4 years, and half were women. Daily step counts in the included studies were objectively measured for at least 7 consecutive days.

As noted, a 1,000-step increment was associated with a 15% decrease in risk of all-cause mortality (hazard ratio, 0.85); a 500-step increment was associated with a 7% decrease in CV mortality (HR, 0.93).

Compared with the reference quartile (median steps/day, 3,967), quartile 1 (median steps, 5,537) was associated with a 48% lower risk of all-cause mortality; quartile 2 (median steps, 7,370), with a 55% lower risk; and quartile 3 (median steps, 11,529), with a 67% risk reduction.

Similarly, compared with the lowest quartile of steps per day used as reference (median steps, 2,337), higher quartiles of steps per day (Q1, 3,982; Q2, 6,661; and Q3, 10,413) were linearly associated with a reduced risk of CV mortality (16%, 49%, and 77%, respectively).

In a restricted cubic splines model, a nonlinear dose-response association was observed between step count and all-cause and CV mortality, with a progressively lower risk of mortality with an increase in step count.

Dose-response curves were similar for men and women. However, there was a difference by age: Among people aged 60 years or older, the size of the risk reduction was smaller. Among the older adults, there was a 42% risk reduction for those who walked between 6000 and 10,000 steps daily, compared with a 49% reduction in risk among younger adults who walked between 7,000 and 13,000 steps a day.

For both groups, daily step counts higher than 5,000 resulted in a “dramatically” lower risk of all-cause mortality.

An analysis that compared the impact of climate regions on the associations showed no significant effect on all-cause mortality. People in all climate zones benefited when the daily step count exceeded approximately 5,500.

Even given the encouraging study results, “we know very well that every kind of exercise is critically important,” Dr. Banach said. It is easier to focus on step counts because the counts can be monitored and calculated with smartwatches, pedometers, and other tools. That also makes it easier to check associations and outcomes for large groups of patients.

“But in fact, we should not be focusing on one type of exercise, such as walking or running,” he said. “We can dance, ride bicycles, and do many other different exercises that mobilize our hearts.

“We also know that in all these activities, including steps, people have different capabilities – for example, some can walk more slowly, others faster and with more intensity.”

Dr. Banach recommended following the European and U.S. physical activity guidelines that advise, in addition to muscle-strengthening activities, 150 minutes of moderate-intensity aerobic training weekly, or 75 minutes of vigorous-intensity aerobic activity, or an equivalent combination of moderate- and vigorous-intensity aerobic activity.

From the results he sees in patients, he believes the combination approach is probably best for the heart.

Furthermore, it’s important to exercise regularly, something that’s easier if individuals enjoy what they’re doing. “The type of training or whether you are completely inactive or very active at the start doesn’t matter, because any improvement, any addition to the to the baseline values will have health benefits,” he concluded.
 

Higher goals helpful

Three experts commented on the study; all noted that the results are in line with previous studies, that the observational nature of the study is a limitation, and that additional randomized, controlled trials are needed to confirm the findings.

Evan Brittain, MD, an associate professor of medicine at Vanderbilt University Medical Center, Nashville, Tenn., expressed some additional concerns.

Dr. Brittain was principal investigator of a recent study that found that the relationship between steps per day and incident disease was inverse and linear for obesity, sleep apnea, gastroesophageal reflux disease, and major depressive disorder. Daily step counts above 8,200 were associated with protection from incident disease.

He noted that, in the current study, “the authors chose to make the least active quartile (25%) the reference group (only 3,967 steps/day for all-cause mortality and only 2,337 steps/day for CV mortality analysis), which somewhat lowers the bar for finding a significant benefit at higher step counts.

“Moreover, in the spline analyses, zero steps per day is used as the comparison, which is not a practical, real-world comparison,” he said. “As a result, those data are very hard to interpret, and I think are overstated.”

Like Dr. Banach, Dr. Brittain said he would continue to advise following guideline recommendations to get 150 minutes per week of moderate-intensity activity. However, he added that although it is reasonable to advise patients that benefits do accrue with daily step counts of less than 10,000, “I would not want patients to misconstrue from this study that getting more than only 2,330 steps per day is a beneficial goal.”

Martin Halle, MD, a professor in the department of prevention and sports medicine at the Technical University of Munich (Germany), said: “From a clinical, medical, and health perspective, the general population should aim for 5,000 steps, which is about 3-4 kilometers [about 2 miles] of walking, and intensity counts – the faster you walk, the better.

“I recommend doing 100 steps fast and 100 steps slow and then 100 steps fast and 100 steps slow,” said Dr. Halle, who is past president of the European Association of Preventive Cardiology. This approach not only motivates people, “but they improve their exercise capacity substantially and very quickly, just within weeks.”

European Society of Cardiology vice president and European Journal of Preventive Cardiology editor-in-chief Massimo Piepoli, MD, PhD, agreed that “little is better than nothing and more is even better. This applies to healthy subjects, as well as patients with chronic diseases.

“Five hundred steps is a very short distance (such as walking two blocks or walking the dog for about 10-15 minutes every day),” he said. Yet, increasing step counts in increments of 500 “is associated with a significant reduction in cardiovascular mortality both in men and women, particularly in older individuals.

“We do not need to depend on expensive gym facilities,” he added. “But at the same time, we need to live in and to promote the building of neighborhoods where it is possible to walk in a safe and healthy environment.”

The research received no external funding. Dr. Banach has reported financial relationships with Amgen, Daiichi Sankyo, Esperion, Freia Pharmaceuticals, Kogen, KRKA, Polpharma, NewAmsterdam, Novartis, Novo Nordisk, Polfarmex, Sanofi Aventis, Teva, Valeant, Viatris, and Zentiva, and is chief marketing and development officer at Longevity Group and chief marketing officer at Nomi Biotech.

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

Datascope/Maquet/Getinge has announced a recall of the Cardiosave Hybrid and Rescue Intra-Aortic Balloon Pumps (IABPs) because they may shut down unexpectedly due to electrical failures in the power management board or solenoid board (power source path).

“Using an affected pump may cause serious adverse health events, including unstable blood pressure, injury (e.g., inadequate blood supply or a vital organ injury), and death,” the Food and Drug Administration said in the recall notice.

The FDA has identified this as a class I recall, the most serious type of recall due to the risk for serious injury or death. To date, Datascope/Maquet/Getinge received 26 complaints, but no reports of injuries or death.

The devices are indicated for acute coronary syndrome, cardiac and noncardiac surgery, and complications of heart failure in adults.

The recall includes a total of 4,586 Cardiosave Hybrid or Rescue IABP units distributed from March 2, 2012, to May 19, 2023. Product model numbers for the recalled Cardiosave Hybrid and Cardiosave Rescue are available online.

On June 5, Datascope/Maquet/Getinge sent an “important medical device advisory” to all affected customers. The letter advises customers to be sure there is an alternative IABP available to continue therapy and provide alternative hemodynamic support if there is no other means to continue counterpulsation therapy.

Customers with questions about this recall should contact their company representative or call technical support at 1-888-943-8872, Monday through Friday, between 8:00 a.m. and 6:00 p.m. ET.

Last March, Datascope/Getinge recalled 2,300 Cardiosave Hybrid or Rescue IABPs because the coiled cable connecting the display and base on some units may fail, causing an unexpected shutdown without warnings or alarms to alert the user.

The Cardiosave IABPs have also been previously flagged by the FDA for subpar battery performance and fluid leaks.

Any adverse events or suspected adverse events related to the recalled Cardiosave Hybrid/Rescue IABPs should be reported to the FDA through MedWatch, its adverse event reporting program.
 

A version of this article appeared on Medscape.com.

Datascope/Maquet/Getinge has announced a recall of the Cardiosave Hybrid and Rescue Intra-Aortic Balloon Pumps (IABPs) because they may shut down unexpectedly due to electrical failures in the power management board or solenoid board (power source path).

“Using an affected pump may cause serious adverse health events, including unstable blood pressure, injury (e.g., inadequate blood supply or a vital organ injury), and death,” the Food and Drug Administration said in the recall notice.

The FDA has identified this as a class I recall, the most serious type of recall due to the risk for serious injury or death. To date, Datascope/Maquet/Getinge received 26 complaints, but no reports of injuries or death.

The devices are indicated for acute coronary syndrome, cardiac and noncardiac surgery, and complications of heart failure in adults.

The recall includes a total of 4,586 Cardiosave Hybrid or Rescue IABP units distributed from March 2, 2012, to May 19, 2023. Product model numbers for the recalled Cardiosave Hybrid and Cardiosave Rescue are available online.

On June 5, Datascope/Maquet/Getinge sent an “important medical device advisory” to all affected customers. The letter advises customers to be sure there is an alternative IABP available to continue therapy and provide alternative hemodynamic support if there is no other means to continue counterpulsation therapy.

Customers with questions about this recall should contact their company representative or call technical support at 1-888-943-8872, Monday through Friday, between 8:00 a.m. and 6:00 p.m. ET.

Last March, Datascope/Getinge recalled 2,300 Cardiosave Hybrid or Rescue IABPs because the coiled cable connecting the display and base on some units may fail, causing an unexpected shutdown without warnings or alarms to alert the user.

The Cardiosave IABPs have also been previously flagged by the FDA for subpar battery performance and fluid leaks.

Any adverse events or suspected adverse events related to the recalled Cardiosave Hybrid/Rescue IABPs should be reported to the FDA through MedWatch, its adverse event reporting program.
 

A version of this article appeared on Medscape.com.

Datascope/Maquet/Getinge has announced a recall of the Cardiosave Hybrid and Rescue Intra-Aortic Balloon Pumps (IABPs) because they may shut down unexpectedly due to electrical failures in the power management board or solenoid board (power source path).

“Using an affected pump may cause serious adverse health events, including unstable blood pressure, injury (e.g., inadequate blood supply or a vital organ injury), and death,” the Food and Drug Administration said in the recall notice.

The FDA has identified this as a class I recall, the most serious type of recall due to the risk for serious injury or death. To date, Datascope/Maquet/Getinge received 26 complaints, but no reports of injuries or death.

The devices are indicated for acute coronary syndrome, cardiac and noncardiac surgery, and complications of heart failure in adults.

The recall includes a total of 4,586 Cardiosave Hybrid or Rescue IABP units distributed from March 2, 2012, to May 19, 2023. Product model numbers for the recalled Cardiosave Hybrid and Cardiosave Rescue are available online.

On June 5, Datascope/Maquet/Getinge sent an “important medical device advisory” to all affected customers. The letter advises customers to be sure there is an alternative IABP available to continue therapy and provide alternative hemodynamic support if there is no other means to continue counterpulsation therapy.

Customers with questions about this recall should contact their company representative or call technical support at 1-888-943-8872, Monday through Friday, between 8:00 a.m. and 6:00 p.m. ET.

Last March, Datascope/Getinge recalled 2,300 Cardiosave Hybrid or Rescue IABPs because the coiled cable connecting the display and base on some units may fail, causing an unexpected shutdown without warnings or alarms to alert the user.

The Cardiosave IABPs have also been previously flagged by the FDA for subpar battery performance and fluid leaks.

Any adverse events or suspected adverse events related to the recalled Cardiosave Hybrid/Rescue IABPs should be reported to the FDA through MedWatch, its adverse event reporting program.
 

A version of this article appeared on Medscape.com.